10th Ecc Uk Annual Congress Course Notes 2013 PDF

Contents
Page
Speakers at Congress ii & iii
Lecture Stream 1 Carriage Suite Thursday

Taking the difficulty out of dyspnoea Humm 1
Pulmonary pathology in diagnostic imaging Kinns 11
Acute kidney injury: An update Humm 21
Surgical management of haemoabdomen Stanley 35
Caesarian: 90 seconds Stanley 39
Dehiscences: Incisional and intestinal Stanley 47
Pharyngeal stick injuries and other penetrating traumas Stanley 55
Lecture Stream 2 Billiard Room Thursday
CPR current recommendations ODwyer 61
Ischemia and reperfusion injury Breton 71
Bad adrenals: Hypo and hyperadrenocorticism Breton 79
Getting a diagnostic study: Pitfalls and tips for excellence Kinns 89
Nursing care of the head trauma patient ODwyer 95
Post-operative care of the airway surgery patient Breton 107
Nursing patients presenting with ocular emergencies Petersen-Jones 113
Lecture Stream 3 Drawing Room Thursday
Contributing to clinical and financial outcomes Faulkner 117
Contributing to client satisfaction Faulkner 127
The psychology of persuasion Faulkner 137
Transfusion medicine in a war zone Rawlinson 143
Comparative transfusion medicine Humm 145
Disaster medicine: What can we do better? Breton 151
Lecture Stream 1 Carriage Suite Friday
Contrast radiology in emergency practice Kinns 157
Top ten easily missed key radiographic findings Kinns 169
Orofacial trauma Stanley 175
Traumatic ophthalmic emergencies Petersen-Jones 185
Non-traumatic ophthalmic emergencies Petersen-Jones 189
Managing parvovirus cases Boag 199
Lecture Stream 2 Billiard Room Friday
Diabetic emergencies Breton 207
Seizures: Stages, types and care Breton 215
Medical management of the whelping bitch ODwyer 221
An RTA enters your clinic: Step by step of what to do Breton 229
Nutritional options for the critical patient Brown 237
Critical care of the cat: The acute renal patient ODwyer 245
Nursing the post anaesthesia recovery patient ODwyer 253
Lecture Stream 3 Drawing Room Friday
Improved management of extensive wounds Stanley 263
Chylothorax: Better news? Stanley 275
Antibiotics: Use and misuse Humm 281
Advanced therapeutics for renal disease Humm 287
Oxyglobin: Its back! Boag 299
Fundus examination Petersen-Jones 305
Index 315
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10th Emergency & Critical Care UK Annual Congress 2013
TAKING THE DIFFICULTY OUT OF DYSPNOEA
Karen Humm MA VetMB CertVA DACVECC FHEA MRCVS

Department of Clinical Science and Services, RVC
khumm@rvc.ac.uk
Introduction
Dyspnoeic patients are very stressful to deal with. Owners are generally distressed, the
patient appears to be suffering and we are often unsure how to approach diagnostics in an
unstable patient. These notes discuss how a logical approach to clinical examination of the
dyspnoeic patient allows understanding of whether the patient has an upper respiratory,
lower airway, parenchymal or pleural space cause of their dyspnoea. Once this is
understood then a list of differentials can be created and treatment given as required. The
most important initial therapy is oxygen and methods of administration are discussed as well
as how to perform thoracocentesis.
Initial assessment
Any patient presenting in respiratory distress should have flow-by or mask administration of
oxygen during their physical examination. Mask administration is superior but often not
tolerated, particularly by cats. Stress should be kept to a minimum as any struggling will
lead to increased oxygen demand, so therefore if a mask isnt tolerated then do not persist
with it. Initial physical examination may need to be very brief but a quick effective
auscultation of the thorax is vital in almost all circumstances as if there is pleural fluid or air
then stabilisation will not be achieved by oxygen therapy alone.
Initially observing patient and listening to them from a distance is very useful. Increased
inspiratory effort suggests upper respiratory tract, pulmonary parenchymal or pleural space
disease. Increased expiratory effort suggests lower airway disease which less commonly
causes dyspnoea (feline allergic airway disease or feline asthma would be an example
however). Patients with pleural space disease can also have a very rapid shallow breathing
pattern. Noise audible when observing the patient without performing thoracic auscultation
suggests upper respiratory tract pathology such as laryngeal paralysis. Finally the patients
abdominal movement should be observed. The abdominal and thoracic walls should move
in the same direction. The abdomen will move markedly in patients with increased
respiratory effort as the diaphragm is pushing the abdominal contents more rapidly and more
caudally than usual. This is often described as increased abdominal effort but actually the
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movement is passive as abdominal contraction can only aid expiration. If the abdominal wall
moves inwards as the thoracic wall moves outwards this is known as paradoxical abdominal
movement. There are several possible causes for this including marked upper respiratory
tract obstruction, stiff lungs as seen in patients with pulmonary fibrosis, diaphragmatic
rupture or paralysis and it can also be seen in some patients with marked respiratory
distress. Cyanotic mucous membranes indicate extremely poor oxygen delivery to the
peripheral tissues.
After assessing the patient in this way thoracic auscultation should be performed.
Auscultation of the lung fields can reveal crackles or harsh lung sounds (commonly heard
with parenchymal (alveolar) disease such as pulmonary oedema, pneumonia or contusions.
Auscultating the thorax of patients with upper respiratory tract noise can be difficult as this
noise is referred. To determine if the noise auscultated originates in the upper respiratory
tract or the thorax the clinician should auscultate over both the laryngeal region and the
thorax and where the noise is loudest is the origin. Dull or quiet lung sounds with increased
respiratory effort suggest pleural space disease. If the dullness is more pronounced dorsally
this suggests pneumothorax whereas ventral dullness suggests pleural fluid such as
pyothorax. Diaphragmatic rupture patients can be confusing to auscultate as there can be
areas of dullness and some areas of increased respiratory sounds, also the heart sounds
may be most audible in an unusual position. It is important to note this as, unlike
pneumothorax and pleural fluid patients, thoracocentesis is generally not indicated (as even
if pleural fluid is present it is generally not a significant amount).
The cardiovascular and neurological systems also need to be carefully and quickly
assessed. This is particularly important as congestive heart failure is a common cause of
dyspnoea in both dogs and cats and so the heart should be carefully auscultated to check
for a murmur or gallop (both can be intermittent in cats and so repeated auscultation is wise)
or arrhythmia. Intravenous access is very useful in patients allowing effective drug and fluid
administration as well as blood sampling at the time of catheter placement. However, it is
not generally essential in the patient in respiratory distress and can cause undesirable
stress. The use of calm restraint, alternative veins such as the lateral saphenous and EMLA
cream will aid placement, but the procedure should be abandoned if causing excessive
stress.
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Stabilisation of the respiratory system
Oxygen administration
Respiratory distress is triggered by hypoxia, hypercapnia or a marked increase in the work of

breathing (which often leads to hypoxia and/or hypercapnia). Hypoxia is by far the most
common of these causes; therefore oxygen supplementation is of key importance in
managing any patient with respiratory distress. If there is uncertainty whether a patient is in
respiratory distress supplemental oxygen should be administered while physical examination
is performed.
Oxygen source
The source of oxygen for patients in respiratory distress will vary between practices
depending on their facilities. However most practices will use one (or more) of 3 options:
Direct from a cylinder using oxygen tubing

Breathing system attached to an anaesthetic machine
Piped source:
o Using oxygen tubing
o Using a breathing system
Humidification
Oxygen is supplied in canisters of dry gas. When administered to patients at high rates it
can lead to increased viscosity of respiratory secretions, impaired muco-ciliary clearance,
mucosal desiccation and an increased risk of respiratory tract infection. Therefore if oxygen
is to be administered for any period of time greater than an hour or so, it should be
humidified. This is particularly important in patients with nasal or tracheal catheters or those
undergoing mechanical ventilation as the administered oxygen bypasses the upper airway,
the natural site of humidification in an animal. Humidification is achieved simply by allowing
oxygen to bubble through sterile water. Bubble humidifiers are cheap to buy (approximately
2 each from Flexicare Medical Ltd.) and will fit onto oxygen ports. If a humidifier is not
available regular nebulisation can be performed but this requires more expensive equipment.
Oxygen administration methods
Oxygen makes up approximately 21% of the gaseous component of room air. Various
methods of increasing this fraction are available, each with different advantages and
disadvantages. For both short and long term options the percentage inspired oxygen
achieved will be affected by the size of the patient, their respiratory rate and the flow rate of
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oxygen used. Rough guides for administration rates have been given but they only a useful
starting point and adjustments may need to be made on a patient by patient basis.
Short term methods of oxygen administration
Mask administration
Using a mask to provide oxygen to a patient is simple and effective. A flow rate of 1 (for cats
and small dogs) to 10 (for giant breeds) litres/minute should be used. A high percentage of
inspired oxygen of 80-90% has been attained in experimental studies in anaesthetized dogs
using a tight fitting mask. However, in the vast majority of conscious dyspnoeic patients a
tight fitting mask is not tolerated and therefore the actual percentage of inspired oxygen in
clinical patients will be more like 35-55%. Calmer patients will tolerate a mask gently held
over the muzzle allowing free movement, but many patients, particularly cats, will not allow a
mask near their head. Struggling with a patient to administer oxygen is counterproductive as
their oxygen demand will be increased by the stress and increased muscular activity.
Collapsed or weak patients are ideal candidates for mask oxygen administration as they do
not move (although unconscious patients need intubation to protect their airway from the risk
of aspiration). A tight fitting mask can easily lead to hyperthermia in patients and if lower
oxygen flow rates are used than the patients minute volume re-breathing can occur resulting
in hypercapnia.
Flow-by
Flow-by administration is not an efficient means of oxygen administration. Anaesthetised

dogs administered oxygen via a tube which ended 2cm from their nose with flow rates of 4-
10 litres/minute had an inspired oxygen percentage of approximately 40%. In the conscious
patient it is likely this is lower due to the increased distance of the oxygen tubing from the
nose and movement of the patient. However, flow-by is usually ready within seconds, is
non-invasive and is less stressful than mask administration. Flow rates of 2-10 litres/minute
should be used and the oxygen outlet should be held as close to the patients nose (or
mouth if they are panting) as possible without causing distress. Sometimes a patient will
tolerate flow by when tubing is directed to the side of their mouth rather than in front of it.
Longer term oxygen administration
Once an initial physical examination and any emergency stabilisation has been performed it
is often beneficial to allow a patient to calm in a kennel. Oxygen administration can be
continued with flow by or mask administration but this requires a member or staff to remain
with the patient and both interventions can be stressful for the animal.
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Nasal catheters
Oxygen can be supplied direct into the respiratory tract via nasal catheters in both dogs and
cats. Feeding tubes are commonly used as catheters with a 5 French catheter being
suitable for a cat and an 8 or 10 French for most dogs. Before placement the catheter
should be pre-measured against the animal from the nostril to the lateral canthus of the eye.
A mark should be made on the catheter as it is to be inserted up to this point. A few drops of
0.5% proxymetacaine (the local anaesthetic commonly used for anaesthetising the cornea)
or 2% lidocaine should be administered into the nostril 10 minutes prior to placement of the
cannula. The patient needs to be gently but firmly restrained with their nose pointing
dorsally. The catheter should be advanced into the ventral meatus in the nares as the dorsal
and middle meatuses end at the ethmoid turbinate rather than the nasopharynx. Pushing
the nasal planum dorsally while aiming the cannula ventro-medially can aid correct
placement. The catheter should be gently but rapidly advanced as patients often move and
sneeze during this part of the procedure. If the catheter is not in the ventral meatus it will not
advance the pre-measured distance. Once the catheter is in the correct position it should be
fixed in place with a Chinese finger trap suture, sutures attached to butterfly wings of tape
securely attached to the catheter or with tissue glue. The catheter should loop round the
alar cartilage with fixation close to the nasal orifice to prevent dislodgement. Ideally the
catheter should then be looped dorsally between the eyes. This decreases the chance of
the patient removing it. In very brachycephalic dogs and many cats the bend that is required
to bring the catheter between the eyes is too acute and it will kink. In these cases the
catheter needs to be secured to the just below the ear.
Obviously a patient has to be tolerant to allow a nasal catheter to be placed. The procedure
should be abandoned if an animal becomes distressed as this may lead to marked
worsening of their hypoxia. The procedure is also contraindicated in coagulopathic animals.
Once in situ catheters can be displaced by determined patients and so a buster collar may
be required which again can be stressful. However, if a patient will tolerate placement and
maintenance of nasal oxygen catheters they can provide a consistent inspired oxygen
percentage of 40-50% with an oxygen flow rate of 50-100ml/kg/min. The placement of a
second nasal catheter can increase this percentage further to 60-70%. Unfortunately, if a
patient consistently pants then the mixing with room air in the pharynx leads to a decrease in
the percentage inspired oxygen.
Nasal prongs / cannulas
Prongs designed for oxygen supplementation in humans can be used for dogs. They come
in 2 sizes (paediatric and adult) and are supplied by Flexicare Medical Ltd at a cost of
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approximately 4 per set. The prongs advance approximately 1cm into the nostril and will
provide a percentage inspired oxygen of approximately 40%. They are minimally invasive
but are therefore easily displaced by an intolerant patient. Administration of proxymetacaine
into each nostril approximately 10 minutes before placing the prongs can be useful as can
taping the prong tubing together (but not to the dog) over the dorsal aspect of the muzzle.
As with a nasal catheter this method is less efficacious in the panting patient.
Tracheal catheter
Some texts describe administering oxygen via a tracheal catheter on a longer term basis,
particularly for patients with facial or upper airway injury. A standard intravenous catheter
can be used or a long stay catheter of increased length placed as described above under
short-term oxygen administration. In the authors hands this is not an effective method for
longer term administration as the catheter is difficult to secure and prevent from kinking.
Buster collar oxygen hood
Oxygen can be administered into an enclosed buster collar (either practice-made or

commercially produced (available from DLC Australia Pty Ltd)) to both cats and dogs. If
the oxygen collar is made in the practice a small gap should be left at the top of the collar to
allow venting of humid air and carbon dioxide. Despite the vent hole, many dogs and some
cats with these collars become hyperthermic, particularly in hot conditions. The inside of the
collar can also become very humid with condensation building up. Placement of the collar
may be poorly tolerated, however most dogs and cats do settle if left in a kennel with one on.
The percentage inspired oxygen achieved depends on the size of the gaps in the collar as
well as flow rate etc. A high flow rate should be used initially to fill the collar with oxygen and
then a rate of approximately 1 litre is suitable for a medium size dog. This rate gave a
percentage inspired oxygen of approximately 40% in healthy anaesthetised dogs.
Oxygen cage
Collapsible or lightweight oxygen cages are commercially available in various sizes (e.g.
from J.A.K. Marketing Ltd or DLC Pty Ltd Australia). They have adaptors for breathing
systems and are simple to use. Some models have no means of thermoregulatory or
humidity control and others only means of heating patients. As the cages are completely
sealed hyperthermia can rapidly develop in some patients, particularly dogs. Some
practices also have permanent fixed oxygen cages although again they are rarely
temperature or humidity controlled. Once a cage is opened the level of oxygen within it
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rapidly drops to room level. This can mean that if a patient is frequently being handled their
inspired oxygen fraction is barely increased.
An oxygen cage can be made in the practice when required by placing cling-film over the
front of a cage although the gaps present and the large volume of the cage relative to the
patient within it, means that very high flow rates are required and often the partial pressure
of oxygen is barely increased.
Endotracheal intubation and ventilation
It is very rare that an animal in respiratory distress requires anaesthetising and intubation
allowing provision of 100% oxygen. This most commonly occurs in patients with upper
respiratory tract obstruction when intubation allows by-passing of the obstruction. Judging
when intubation is required can be difficult. Less invasive oxygen administration techniques
in conjunction with stabilisation should be attempted first and the patients response
assessed. If a patient still has marked respiratory distress despite treatment then intubation
and ventilation may be required. Arterial blood gas analysis will give objective information
on the level of hypoxia which is very useful in deciding whether mechanical ventilation is
required. However obtaining an arterial sample from an extremely dyspnoeic patient can be
very difficult. Pulse oximetry can be useful as a haemoglobin oxygen saturation of less than
93% despite oxygen supplementation suggests severe respiratory compromise and
ventilation is likely to be required. Obtaining an accurate reading on a conscious patient can
be difficult though. If the cause of respiratory distress is not upper respiratory tract in origin
the prognosis for patients that require intubation and ventilation is unfortunately very poor.
Oxygen toxicity
Exposure of the lungs to an inspired oxygen fraction greater than 60% for greater than
approximately 12 hours can lead to oxygen toxicity. This causes damage to the alveoli
potentially worsening any lung disease present. Ideally therefore oxygen administration
should be kept below 60%. This is usually greater than that achieved by most methods of
oxygen administration in the practice situation.
Thoracocentesis
This can be lifesaving and diagnostic imaging is not necessary to confirm pleural space
disease prior to performing thoracocentesis. Confidence can be gained by a brief
examination with a portable ultrasound machine looking for free pleural fluid or
pneumothorax (see later), but this is not essential. Thoracic radiography should not be
performed if a patient is in respiratory distress as positioning or restraint could lead to
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marked distress and can on occasion be fatal. Thoracocentesis performed on a patient

without pleural fluid or pneumothorax does not lead to complications in the vast majority of
patients. Therefore, trust your physical examination and perform thoracocentesis if you think
it is necessary.
In small to medium dogs (<20-25kg) and cats a butterfly catheter, three way tap and syringe
can be used. In larger breed dogs butterfly catheters often do not penetrate the pleural
space. A large gauge catheter such as a 16G can be used in these dogs. It can be
attached via the stylet (slightly awkwardly as there is no luer lock fitting) to a three way tap
attached to a syringe. The stylet can be removed once the catheter has been inserted into
the pleural space making attachment to a three way tap easier and decreasing the risk of
trauma to the lung, but often this results in kinking of the catheter and therefore ineffective
drainage as well as having a period of time when there is a port from the pleural space
externally leading to iatrogenic pneumothorax. Often, therefore, keeping the stylet in situ is
more effective.
To perform thoracocentesis the patient needs to be effectively but sympathetically restrained

with flow-by or mask oxygen. Most dogs and cats prefer to lie in a sternal position but they
may prefer to stand. The patient should be clipped and the skin aseptically prepared over
the caudal thorax dorsally if air is suspected and ventrally if fluid is suspected. This
differentiation is much less important in small dogs and cats. The needle should be
introduced at a 90 angle perpendicular to the skin between the 8th and 9th rib, in the ventral
third of the chest if fluid is suspected and in the dorsal third if air is suspected. Aiming in the
middle of the intercostal space is the simplest approach. The caudal aspect of the rib should
be avoided to avoid the intercostal vessels and nerves.
Lidocaine can be infused in the area prior to thoracocentesis, but generally is not necessary
and causes as much pain if not more than the procedure itself. The painful part appears to
be going through the skin, so this can be done in one movement. If you have an assistant
(making the procedure much simpler) they can then put negative pressure on the syringe at
this point. The needle is then slowly advanced and once in the pleural space fluid will
appear in the syringe or there will be a loss of negative pressure with a pneumothorax. The
needle should then be flattened against the thoracic wall with the bevel facing inwards. As
much fluid or air as possible should be removed. If a sanguinous fluid is obtained then it
should be checked to see if it clots and if it does the thoracocentesis should be immediately
stopped. If the patient struggles, the procedure will be difficult. Sedation with 0-1-0.3mg/kg
butorphanol can be useful.
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Further reading
BSAVA Manual of Canine and Feline Cardiorespiratory Medicine 2nd Edition (2010) Eds Luis
Fuentes V, Johnson LR, and Dennis S. BSAVA, Gloucester
BSAVA Manual of Canine and Feline Emergency and Critical Care 2nd Edition (2007) Eds
King LG and Boag A. BSAVA, Gloucester
Small Animal Critical Care Medicine (2009) Eds Silverstein DC and Hopper K. Saunders
Elsevier, St Louis, Missouri
Textbook of Respiratory Disease in Dogs and Cats (2004) Ed King LG. Saunders, St Louis,
Missouri
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Notes page
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PULMONARY PATHOLOGY IN DIAGNOSTIC IMAGING

Jennifer Kinns BSc VetMB Dip ECVDI DACVR MRCVS
RCVS Recognised specialist in diagnostic imaging
IDEXX Telemedicine
Jennifer-kinns@Idexx.com
Thoracic imaging is a key component of the diagnostic work-up of patients presenting with
acute respiratory signs. Though diagnoses such as pneumothorax or pericardial effusion
should be possible with a thorough clinical examination, there are typically a number of
differentials for the patient presenting with compromise of the upper or lower respiratory
system. Radiographs can significantly narrow the differentials and may allow a definitive
diagnosis. This lecture will review the basic lung patterns and look at the key roentgen
findings associated with specific lesions of the acute thorax. Lesions will be illustrated with
case examples from clinical practice.
Thoracic radiographs
Radiographs must be of diagnostic quality to allow interpretation. If a patient is in acute

respiratory distress it may be necessary to stabilise prior to attempting radiographs, as a
poorly positioned study could confound interpretation. It is important to obtain at least two
view of the thorax. A lesion can be missed on a single projection, and having orthogonal
projections allows you to localize a lesion. At least a lateral (R or L) and a VD or DV view is
recommended. Straight views are important for consistent evaluation of intra-thoracic
structures. The size of the heart, for example, cannot be evaluated on a rotated lateral or
ventrodorsal projection. The thoracic limbs should always be pulled forward so that they do
not obscure the cranial lungs. The radiograph should include the entire lung so that lesions
in the caudodorsal margin, for example, are not missed. Correct exposure is essential.
Overexposed films do not allow evaluation of the pulmonary parenchyma, and
underexposed films can make a normal animal look abnormal and do not permit good
evaluation. Generally a high kVp and low mAs technique is recommended. This is because
the lungs have a high inherent contrast (a lower kVp will increase contrast) and respiratory
motion can be a problem (so you want to reduce the length of exposure to the shortest
possible time).
Review of pulmonary patterns
An alveolar pattern occurs when the alveoli within the lung are filled with soft tissue or fluid so
that the only air present within that area of lung is within the bronchial tree. As the bronchi are
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therefore surrounded by a soft tissue opacity they are seen much more clearly. This is
described as an air bronchogram. The bronchus is not always visible, and an area of soft
tissue opacity (without the clearly defined margins of a mass) or a lobar sign (in which the
margin of the affected lobe is clearly delineated) also indicate alveolar disease.
A bronchial pattern describes the increased thickness of the bronchial walls that is caused
by cellular or fluid infiltration. It can also be caused when air in the peribronchial region has
been replaced with soft tissue or fluid (peribronchial cuffing). On radiographs thickened end
on bronchi appear as a ring with a hole in the middle (often described as donuts).
Thickened bronchi seen longitudinally appear as two parallel lines extending toward the
periphery of the lung. These are often described as tramlines.
An interstitial pulmonary pattern can be structured or unstructured. A diffuse unstructured

interstitial pulmonary pattern is the most difficult to recognize, and also the easiest to over-
diagnose. The appearance occurs with poor pulmonary inflation and under-exposure. A true
interstitial pattern occurs due to fluid or increased cellularity within the interstitium. Many
disease processes, such as oedema, will appear interstitial initially and progress to alveolar.
The radiographic appearance of an interstitial pattern is a generalized increased opacity.
The borders of the pulmonary vessels are unclear, and there is a generalized fuzziness to
the pulmonary parenchyma. A structured interstitial pattern includes nodular infiltrate. A soft
tissue nodule generally has to be at least 3mm in size before it can be seen on radiographs,
though digital imaging may make smaller lesions more conspicuous. Round opacities
smaller than this are therefore likely to represent end on vessels or pulmonary osteomas
(small foci of mineralization that are often seen in the lungs of older dogs). If the lung is filled
with tiny soft tissue nodules this is referred to as a miliary pattern.
Radiographic findings of thoracic pathology
Pneumonia
Bacterial bronchopneumonia results from spread of exudative inflammation to the lung

parenychma from the bronchial and peribronchial tissues. Bronchopneumonia can be a
primary infectious process or can occur secondary to aspiration of gastric contents. The
associated alveolar pattern is mostly ventral in distribution and primarily affects the cranial
and right middle lung lobes. It may be possible to elucidate an underlying cause such as
megaoesophagus, by other radiographic findings. Viral pneumonia is less distinct in
character. An unstructured interstitial pattern may be present diffusely or caudally.
Secondary bacterial infection can occur with an alveolar pattern that may be patchy in
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distribution. Haematogeneous septic pneumonia is also more diffuse and patchy in

distribution and can be interstitial or alveolar.
Bronchial disease
Acute bronchitis (also referred to as tracheobronchitis) generally starts as a viral infection

and recognizable changes of the lower airway can be subtle or absent. A bronchial pattern
may be present if the presentation is acute on chronic.
Allergic bronchitis (asthma) is most commonly recognised in feline patients, and is the most
common lower airway presentation in this species. The radiographic findings are variable, and
the degree of radiographic severity does not correlate well with the severity of clinical signs. An
acute flare up of underlying disease is not necessarily associated with any radiographic
worsening. Radiographic findings include a variable bronchial pattern and hyperinflation (which
is seen on radiographs as a flattening of the diaphragm, increased distance between the
cardiac apex and the diaphragm, and caudal extension of the caudodorsal lung margins to
beyond T13). Secondary lung lobe collapse occurs relatively frequently and predominantly
affects the right middle lung lobe. This appears as a triangular soft tissue opacity within the
right thorax, with associated mediastinal shift to the right. Spontaneous rib fractures occur
relatively frequently in asthmatic cats during bouts of acute dyspnoea.
Eosinophilic bronchopneumopathy is a condition that is typically seen in young dogs. On

radiographs these animals usually have a marked bronchial pattern that can improve very
quickly with appropriate treatment. The pathology is not confined to the bronchi, and a mixed
pattern with additional unstructured interstitial and alveolar changes may be present. Ill-defined
soft tissue nodules may be present. These patients often have severe associated respiratory
signs, particularly coughing, and may be presented on emergency due to the severity of the
signs. Differentiating this from infectious bronchitis may require cytologic evaluation of the
airway, though the marked radiographic response to treatment helps to confirm the diagnosis.
Aspiration of respiratory toxins or smoke inhalation will appear as a bronchial pattern but
may progress to involve the interstitium particularly when heat in addition to smoke damage is
present. Serial radiographs are recommended if there is clinical worsening as these lesions
can progress with time.
Bronchieactasis describes irreversible, saccular or cylindrical dilations of the bronchi and

bronchioles, which may contain large quantities of bronchial secretions. It can be the result of
chronic respiratory disease but a congenital predisposition has also been found in dogs ciliary
dyskinesia. Radiographic features include widening and unevenness of the bronchial lumen, a
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failure of the airway to taper normally and thickening of the wall where there is additional
bronchitis. Though the condition itself is associated with chronic morbidity, the presentation may
be acute as a result of secondary pneumonia (the widening of the bronchi and ciliary
dysfunction reduces airway clearance and predisposes to bacterial infection). Radiographs
may demonstrate bronchial widening, often with a blunt rather than tapering terminal profile, in
addition to the classic findings of bronchopneumonia.
It should be remembered that a radiographic bronchial pattern can occur secondary to

peribronchial inflammation or oedema. Occasionally cardiac failure can appear radiographically
primarily as a bronchial pattern due to peribronchial oedema, and this should be considered if
there is concurrent cardiac enlargement.
Parasitic infection
Angiostrongylus vasorum is increasingly seen as a cause of acute respiratory signs in the

UK. The radiographic appearance consists of a bronchial or interstitial pattern with a patchy
and particularly a peripheral alveolar pulmonary pattern. The peripheral alveolar infiltrate is
quite characteristic of this infection. Following successful treatment the alveolar pattern may
be replaced with a diffuse ill-defined interstitial pattern.
Lung lobe torsion
Lung lobe torsion is a relatively rare diagnosis but one which requires surgical intervention.
There are characteristic radiographic findings, though it can be difficult to make a confirmed
diagnosis on initial radiographs. These patients typically present acutely with dyspnoea or
coughing, but if the diagnosis is not made in the early stages the condition can become sub-
acute or chronic. Classic associated radiographic findings are pleural effusion (typically mild
and haemorrhagic), lobar soft tissue opacity, a mediastinal shift away from the affected lobe
due to enlargement and interstitial emphysema within the affected lobe which appears as
numerous tiny radiolucent foci. If the bronchus is visible it may be turned in the wrong
direction or blunted. Some or all of these findings may be present. The left cranial (small
dogs, especially pugs) or right middle lung lobe (larger dogs; borzoi are predisposed) are
most often affected, though will be displaced by the torsion. If lung lobe torsion is a
differential that is suspected but not confirmed on initial radiographs it can be helpful to
obtain images in a different position (dorsoventral in addition to ventrodorsal and left in
addition to right lateral). Follow up radiographs obtained in 12-24 hours may also confirm
the diagnosis. In some cases advanced imaging such as thoracic CT may be necessary to
confirm the diagnosis prior to surgery.
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Pleural effusion
A patient may present acutely with pleural effusion, which can occur secondary to a number
of underlying disease processes. The radiographic features of pleural effusion are
consistent across the effusion types, though certain findings may help to determine the
underlying cause. The roentgen signs of pleural effusion are pleural fissures, peripheral soft
tissue/fluid opacity, and lung lobe retraction. Depending on the volume of effusion,
superimposition of fluid may give a hazy appearance to the lungs on the ventrodorsal view.
With a large amount of fluid there is also often subjective mediastinal widening due to cranial
accumulation of fluid, and it can be difficult to differentiate this from a mediastinal lesion.
Haemothorax most often occurs secondary to trauma. Careful evaluation for additional
signs of trauma such as rib fractures or cutaneous emphysema is therefore important. An
absence of other radiographic signs of traumatic injury does not exclude this aetiology as
blunt trauma can result in haemorrhage without thoracic wall injury. Underlying
coagulopathy should therefore be excluded. The exudative effusion associated with
pyothorax can primarily localise within one side of the thorax as it does cross the
mediastinum as readily. This is therefore a primary differential for a unilateral effusion,
though other types of fluid can be assymetric. Pyothorax can occur secondary to
oesophageal perforation, and this may be indicated by evidence of oesophageal foreign
material, mediastinal fluid or gas and additional association pulmonary alveolar pattern.
Pleural effusion associated with neoplasia can be unilateral or bilateral. A neoplastic lesion
may or may not be evident on initial radiographs. Careful evaluation for an aggressive rib
lesion, pulmonary mass or nodules, a mediastinal mass or an irregular pleural margin is
important in all cases of pleural effusion, particularly in older patients. Effusion associated
with right sided cardiac failure (which could occur secondary to pericardial effusion) is often
accompanied by peritoneal effusion, and in canine patients the acute presentation is rarely
as a consequence of the pleural effusion alone. Cardiomegaly (right sided or global),
distension of the caudal vena cava and evidence of a loss of peritoneal serosal detail would
be expected. Cats will often have pleural effusion secondary to left sided congestive cardiac
failure, and cardiac failure should always be considered as a differential for effusion in feline
patients. Pleural effusion can also be seen in associated with peritoneal disease, in
particular pancreatitis, though the acute presentation is typically abdominal and the effusion
may be appreciated on the edge of the abdominal radiographs. Simultaneous pleural and
peritoneal effusion is most often due to neoplastic or cardiovascular disease.
Page 15 of 334
It can be very helpful to repeat radiographs after removal of pleural fluid, particularly if there
is a large volume. This will allow additional evaluation of the mediastinum, pulmonary
parenchyma and cardiovascular structures.
Pneumothorax
Pneumothorax is most often diagnosed on clinical examination, but radiographs may be

obtained to confirm this diagnosis and to help determine an underlying cause if there is no
history of trauma. The radiographic appearance of pneumothorax is peripheral hyperlucency
with associated lung lobe retraction. There is often apparent elevation of the cardiac
silhouette on the lateral views due to displacement in to the dependent hemithorax. Care
should be taken not to mis-interpret superimposition of skin folds (with the adjacent relative
lucency) as a pneumothorax. The free gas is most often located ventral to the cardiac
silhouette on the lateral views and within the caudodorsal thorax.
Spontaneous pneumothorax occurs in the absence of trauma, and determining the cause
can be challenging. Spontaneous pneumothorax can occur as a result of ruptured
pulmonary bullae. Bullae appear as thin walled structures with a hyperlucent centre. They
can be extremely difficult to diagnose radiographically and the presence of bullae and
number of lesion is often under-estimated on radiographs. This is one instance when an
expiratory radiograph can be helpful, as the bullae may be more conspicuous when the
surrounding interstitium is more opaque. Thoracic CT would be recommended prior to
surgery to evaluate for bullae, though even this advanced modality has limited sensitivity and
specificity for bullae.
Other cavitated pulmonary lesions can present acutely as a pneumothorax. Cavitated

pulmonary neoplasia is a thick walled lesion or soft tissue mass with areas of gas lucency.
Primary or metastatic lesions can be cavitated. Pulmonary abscesses can also rupture,
though this is much less common as a cause of pneumothorax. Pneumothorax can also
occur with severe pulmonary pathology such as feline asthma.
Tension pneumothorax is a specific condition resulting from a check-valve mechanism at

the origin of the pleural air. The increased pleural pressure causes the lung to collapse
maximally. A unilateral tension pneumothorax will result in a mediastinal shift away from that
side. This condition can be rapidly fatal and requires immediate thoracocentesis.
Thoracic trauma
As described above (haemothorax), the radiographic features of thoracic trauma include

pleural effusion and rib fractures. Pneumothorax is common, and can occur in association
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with pelvic trauma without direct trauma to the thorax. Pneumothorax from trauma results
from lung tearing, but traumatic bullae can also occur and may fill with haemorrhage in
addition to gas. Pulmonary contusion appears as patchy areas of interstitial or alveolar
pattern, the location of which depends on the area of impact. It can be diffuse and patchy or
localised to one lobe.
Cardiac failure
The characteristic appearance of acute left sided congestive cardiac failure in canine
patients is of cardiomegaly with an interstitial or alveolar pulmonary pattern which is
predominantly located within the caudal pulmonary parenchyma, but can be patchy.
Peribronchial oedema can also result in an apparent bronchial pattern. The distribution of the
pulmonary changes can be asymmetric in cases of mitral endocardiosis. Venous distention
is associated with the pulmonary oedema and congestive failure. However, vascular
distention may not be apparent if diuretics were administered prior to radiographs, and can
be subtle. The characteristic appearance of left-sided cardiac enlargement associated with a
endocardiosis is of a loss of the caudal cardiac waist and deviation of the mainstem bronchi
secondary to left atrial enlargement. A bulge is also often apparent in the region of the left
auricular appendage. When congestive failure occurs secondary to dilated cardiomyopathy
in canine patients, left-sided cardiac enlargement also typically predominates. In some
predisposed breeds (the Doberman for example) the cardiac enlargement can be
radiographically mild at the time of failure.
Cardiac failure in feline patients has a less characteristic pulmonary distribution. An

interstitial or alveolar pattern may be diffuse or patchy and can be cranial or caudal, dorsal or
ventral in distribution. Peribronchial cuffing is also more commonly seen in feline cardiac
failure. A degree of pleural effusion is also typical with feline cardiac failure, and vascular
distention may be less apparent than in dogs.
Congenital cardiac disease can also present as acute cardiac failure, and the pulmonary
changes are as described above. The specific abnormality of the cardiac silhouette depends
on the type of anomaly. Detailed description of congenital disease is beyond the scope of
this lecture.
Follow-up radiographs can be helpful to assess the response to treatment for cardiac failure,
and to monitor cardiac size in patients with known cardiac disease.
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Non cardiogenic oedema
Non-cardiogenic oedema has a variety of causes with a classic radiographic appearance.

This is a marked caudodorsal alveolar pulmonary pattern. Neurogenic oedema is a form of
noncardiogenic oedema which occurs secondary to seizure or head trauma. The patient may
present in acute respiratory distress after recovery from seizure. Non-cardiogenic oedema
could also occur secondary to electrocution, transient upper respiratory obstruction or
anaphylaxis.
ARDS
Acute respiratory distress syndrome (ARDS) is a process of pulmonary inflammation and

oedema causing acute respiratory failure. It can occur as a sequela of bronchopneumonia,
sepsis or shock and presents as progressive hypoxaemia, tachypnoea and respiratory
distress. The radiographic appearance is typically a patchy alveolar pulmonary pattern which
can be both dorsally and ventrally distributed and affect all lung lobes. Initially the
appearance may be more interstitial, and peribronchial cuffing may be present. The
diagnosis is made by exclusion and correlation with additional clinical evaluation.
Neoplasia
Neoplasia does not typically present acutely. However, rupture of a cavitated pulmonary
lesion, acute haemorrhage associated with pulmonary neoplasia or metastasis (particularly
haemangiosarcoma) or airway obstruction with a neoplastic lesion may present acutely. The
radiographic findings will depend on the nature of the acute change.
Pulmonary thromboembolism
Pulmonary thromboembolism is associated with numerous systemic diseases including

hyperadrenocorticism, pancreatitis, renal disease and IMHA. A large embolus will result in
acute respiratory distress. The clinical signs are typically severe, while the radiographic
changes may be subtle or absent, particularly acutely. A pulmonary artery may be enlarged
proximally or blunted, and the associated lung may appear more lucent than adjacent lobes.
However, the absence of any radiographic changes does not exclude emboli, which should
be particularly considered if the clinical signs are disproportionately severe as compared to
radiographic findings in patients with underlying disease.
Diaphragmatic hernia
Traumatic diaphragmatic rupture may result in acute respiratory distress. Radiographically

there is typically pleural effusion and evidence of abdominal structures within the thoracic
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cavity (gas filled loops of bowel for example) and potentially absence of normal structures
from the cranial abdomen. Congenital diaphragmatic hernias such as peritoneopericardial
diaphragmatic hernia rarely present with acute respiratory signs and this finding may be
incidental.
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Notes page
Page 20 of 334
ACUTE KIDNEY INJURY: AN UPDATE

khumm@rvc.ac.uk
What is AKI?
Acute renal failure is an imprecise term which has now been replaced by the term acute
kidney injury (AKI) in human medicine and the veterinary world is following. AKI is defined
as a rapid (usually within 48 hours) reduction in renal function. Two similar human schemes
exist to aid recognition of AKI, the RIFLE scheme and the AKIN criteria. RIFLE is an
acronym for Risk, Injury, Failure, Loss and End-stage renal disease. Patients are
placed into one of these groups dependent on changes in their serum creatinine, GFR
(glomerular filtration rate) and/or urine output. As urea can be increased due to a number of
non-renal reasons (such as a recent high protein meal or gastrointestinal haemorrhage), it is
not included in AKI criteria. The first 3 grades R, I and F define the severity of AKI with
grades L and E defining clinical outcome. Patients in the Risk class may not have renal
dysfunction but its sensitivity is high, with specificity increasing during progression through
the more advanced classes. Higher stages correlate with increased mortality. The AKIN
(Acute Kidney Injury Network) scheme is a modified form of the RIFLE scheme which aims
to increase sensitivity by decreasing the change in serum creatinine required to be classed
as an AKI patient. It is simpler as the last two categories (L and E) have been removed and
GFR is not used for grouping of patients.
Both the RIFLE and the AKIN schemes have been adapted and retrospectively applied to
dogs and higher grades correlate with increased mortality (Lee and others, 2011 and Thoen
& Kerl, 2011) (see figures 1 and 2). These canine schemes are simplified as it is extremely
rare to measure GFR in our patients, but the VAKI (veterinary acute kidney injury) scheme
(Thoen and Kerl, 2011) does require two separate blood samples to assess for increases in
creatinine. Unfortunately no system currently exists for cats. The International Renal Interest
Society (IRIS; www.iris-kidney.com) has adopted another slightly different stratification
scheme for veterinary AKI (Figure three) (It is important to note that the IRIS classification
system for chronic kidney disease should not be applied during acute episodes of renal
dysfunction although AKI criteria can be applied to patients with acute on chronic kidney
disease). It is important that a veterinary standard is decided upon to allow consistent
categorisation of the severity of injury, therapeutic decision-making, and easier classification
for research and collaborative efforts.
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The biggest challenge of using the VAKI criteria in veterinary patients is that a baseline
creatinine prior to AKI is often lacking. Any previously recorded results can be invaluable,
particularly if they are recent. The incidence of AKI in general practice is unknown and many
mild cases of AKI probably go unrecognised. It is important to note that creatinine could still
be within the reference range for a patient with AKI when using the schemes described in
the previous paragraph.
Figure 1: RIFLE scheme used by Lee and others (2011)

Class Creatinine (mol/l)
Risk 116-174
Injury 175-347.9
Failure 347.9
Figure 2: Veterinary Acute Kidney Injury (VAKI) staging system used by Thoen and Kerl
(2011)
VAKI stage Criteria
0 Creatinine increase <150% from baseline
1 Creatinine increase of 150199% from baseline

OR
Creatinine increase of 26.5 mol/L from
baseline

OR
An absolute creatinine value >354 mol/L
AKIN (Acute kidney injury network), GFR (Glomerular filtration rate).
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Figure 3: IRIS AKI Grading Criteria
AKI Serum
Clinical Description
Grade Creatinine
Non Azotaemic AKI:

aDocumented AKI: (Historical, clinical, laboratory, or imaging evidence
of acute kidney injury, clinical oliguria/anuria, volume
<140 mol/l
Grade I responsiveness) and/or
bProgressive non azotaemic increase in serum creatinine; 26.4
mol/l (0.3 mg/dl)within 48 hours
cMeasured oliguria (<1 ml/kg/hr) or anuria over 6 hrs
Mild AKI:
aDocumented AKI and static or progressive azotaemia
Grade 141-220
bProgressive azotaemic increase in serum creatinine; 26.4 mol/l
II mol/l
(0.3 mg/dl) within 48 hours, or volume responsiveness
cMeasured oliguria (<1 ml/kg/hr) or anuria over 6 hrs
Grade 221-
III 445mol/l
Moderate to Severe AKI:
Grade 446-890
a
Documented AKI and increasing severities of azotaemia and
IV mol/l
functional renal failure
Grade
>890 mol/l
V
(Volume responsive is an increase in urine production to >1 ml/kg/hr over 6 hours; and/or
decrease in serum creatinine to baseline over 48 hours)
Each grade of AKI is further sub-graded on the basis of:
1. Non oliguric (NO) or oligoanuria (O)
2. Requirement for renal replacement therapy (RRT)
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Pathogenesis of AKI
AKI is often described in 4 phases:
1. The initiation phase: The period of the insult to the kidney. Clinical signs are often
not apparent.
2. The extension phase: The renal damage increases due to alterations in blood flow,
cytokine release and hypoxia.
3. Maintenance phase: Stage when AKI is generally detected. The course of phase 3 is
variable and can last days or even weeks. GFR decreases dramatically leading to
rapid rises in creatinine and urea. It is often during this stage that anuria develops.
4. The recovery stage: Renal repair occurs with marked variation in return to function.
The critical decisions and interventions by the practitioner, particularly in phases one and
two affect outcome and support the patient to the recovery phase.
Causes of AKI
There are many possible causes of AKI (figs 4 and 5). Discovering the cause of AKI is
important, not only as specific therapy may be required but also because the underlying
cause often affects the course of injury and prognosis. This necessitates careful history
taking and physical examination. This should also allow differentiation between acute and
chronic renal dysfunction, although AKI can occur in a previously stable chronic kidney
disease (CKD) patient secondary to an abrupt loss of renal function. This condition is known
as acute on chronic kidney disease (AOCKD).
Figure 4: Causes of Acute Kidney Injury (Most common causes in bold)
Decreased renal perfusion

Shock
NSAIDs, ACE inhibitors
Deep anaesthesia
Severe trauma
Severe hyperthermia or hypothermia
Prolonged urinary tract obstruction

Urethral obstruction
Ureteral obstruction
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Increased renal vascular resistance

Hyperviscosity/polycythemia
Systemic inflammatory response syndrome (SIRS)

Sepsis
Multiple organ dysfunction
Pancreatitis
Hypertension
Vascular
Renal vessel thrombosis
Coagulopathy
Disseminated intravascular coagulation
Vasculitis
Hepato-renal syndrome
Hypoxia Severe
Submersion injury
Severe pneumonia
Failure of fresh gas flow during anaesthesia
Drug and Toxin Associated see Figure 5
Infectious
Leptospirosis
Pyelonephritis
Feline infectious peritonitis (FIP)
Babesiosis
Borreliosis (Lyme nephritis)
Leishmaniasis
Bacterial endocarditis
Neoplasia
Tumour lysis syndrome
Lymphoma
Nephroblastoma
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Immune-mediated
Transfusion Reaction
Systemic lupus erythematosus
Figure 5: Substances known to have nephrotoxic potential (Most common in bold)

Antimicrobials Aminoglycosides
Cephalosporins
Penicillins
Sulfonamides
Quinolones
Tetracyclines
Vancomycin
Carbapenems
Polymyxin B
Rifampin
TMPS
NSAIDs ALL
ACE inhibitors ALL
Diuretics ALL
Chemotherapeutic Agents Cisplatin
Carboplatin
Doxorubicin
Methotrexate
Immunosuppressive drugs Cyclosporine
Azathioprine
Antiprotozoals TMPS
Thiacetarsamide
Pentamidine
Dapsone
Antifungal drugs Amphotericin B
Antiviral drugs Acyclovir
Foscarnet
Radiocontrast Agents Ionic contrast medium, High osmolarity contrast media
Page 26 of 334
Calcium antagonists Bisphosphonates

Galium nitrate
Organic compounds Ethylene glycol
Pesticides
Herbicides
Solvents
Carbon tetrachloride and other chlorinated hydrocarbons
Superphosphate fertiliser
Miscellaneous toxins Lilies (all parts of the plant although Arum/Calla lilies are
non-toxic)
Grapes, raisins and sultanas
Vitamin D intoxication (psoriasis cream or rodenticide)
Vitamin D3 Analogue
Cortinarius mushrooms
Snakes envemonation
Bee sting
Endogenous toxins Haemoglobin
Myoglobin
Heavy metals Mercury
Lead
Bismuth Salts
Copper
Nickel
Silver
Gold
Chromium
Arsenic
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Miscellaneous Drugs Allopurinol

Cimetidine
Apomorphine
Dextran 40
Pencillamine
EDTA
Streptokinase
Tricyclic antidepressants
Lipid lowering agents
Lithium
Phosphorous containing urinary acidifiers
Diagnosing AKI
Differentiating intrinsic, pre-renal and post-renal azotaemia

Urine specific gravity is key in determining whether a patient has an intrinsic renal azotaemia
with a value between 1.008 and 1.015 expected if this is the case. If a patient has a urine
specific gravity greater than 1.015 this suggests a pre-renal component to the azotaemia.
The patient should be assessed for signs of dehydration (e.g. decreased skin turgor, dry
mucous membranes, an acute drop in body weight, increased PCV/TP) or decreased
perfusion (e.g. tachycardia, abnormal pulse quality, mucous membrane pallor, hypotension).
Correction of hypoperfusion and dehydration if present is vital to remove any pre-renal
component of a raised creatinine.
Urine specific gravity may not allow identification of pre-renal azotaemia in all circumstances
however. Patients with severe AKI will have little urine concentrating ability and therefore
dehydration and hypovolaemia have to be identified by physical examination as described
above. Also, some disease processes such as hypoadrenocorticism and hypercalcaemia
prevent appropriate urine concentration despite the kidneys otherwise functioning
adequately. Glucosuria and colloid fluid therapy can lead to increased urine specific gravity
preventing identification of a renal azotaemia.
Potential causes of post renal azotaemia such as urethral obstruction or uroabdomen can be
recognised by careful bladder palpation and basic diagnostic imaging for evidence of
abdominal free fluid. Fluid obtained by abdominocentesis has elevated concentrations of
potassium, urea and creatinine compared with serum concentrations in cases of
Page 28 of 334
uroabdomen. Ureteral obstruction can be more difficult to detect but ureteroliths are
generally radio-opaque calcium oxalate in cats and so abdominal radiography will aid
detection. Rarely, post renal causes of renal dysfunction can lead to AKI especially when
there is permanent damage to the nephrons due to prolonged obstruction.
Differentiating AKI and Chronic Kidney Disease

It can sometimes be initially confusing as to whether an azotaemia patient has AKI or CKD
but Figure 6 aids distinction.
Figure 6: Differentiating between AKI and CKD
Findings on Presentation Acute kidney injury Chronic kidney disease
Body condition score Normal Decreased
PCV Normal Reduced (non-regenerative

anaemia)
Renal Size Normal /Increased Normal/ Reduced
Thirst Decreased /Normal Increased
Urine output Decreased/Increased Increased
Renal Pain Present Absent
Uraemic ulceration Initially absent May be present
Soft tissue mineralisation Absent Present (End stage)
General Diagnostics
An emergency minimum database (EMD) consisting of packed cell volume (PCV), total
protein (TP), venous blood gas analysis and electrolytes is very informative and can also be
used to aid monitoring of critical patients. PCV and TP aid assessment of the patients
hydration status although animals with CKD often have a non-regenerative anaemia.
Inclusion of urea and creatinine within the EMD not only allows initial assessment of renal
function but also allows assessment via the AKI criteria if repeated samples are taken.
Electrolyte disturbances are common in AKI patients. Hyperkalaemia can be seen in anuric
and oliguric patients, with concentrations greater than 6 mmol/l often causing severe cardiac
dysfunction. Unfortunately the presence or absence of hyperkalaemia cannot be assumed
from physical examination or electrocardiography (ECG). However, once diagnosed, an
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ECG can be used to monitor the effectiveness of any treatment for hyperkalaemia. Animals
suffering from significant polyuria during AKI can have marked hypokalaemia with levels less
than 2.5 mmol/l causing muscle weakness including respiratory muscle depression. Both
hyper- and hyponatremia can occur due to loss of free water in the renal filtrate and
dysregulation of sodium handling within the nephron. Ionised or total calcium measurement
can aid diagnosis of ethylene glycol toxicity as it is chelated to form calcium oxalate in the
presence of the toxin leading to hypocalcaemia, which can be severe enough to cause
cardiovascular depression worsening the effects of hyperkalaemia if present. Patients with
AKI often suffer from a severe metabolic acidosis due decreased renal excretion of acid. A
pH of less than 7.1 is critical as this can lead to significant cardiovascular depression and
damage to enzymatic pathways.
A complete blood count will not allow definitive identification of the cause of AKI but can
support certain diagnoses (e.g. the presence of a neutrophilia or significant toxic changes
may be noted in patients suffering from pyelonephritis or sepsis and a mild
thromobocytopenia is common in patients with Leptospirosis). Blood smear analysis may
also be useful in patients where haemoglobinaemia is suspected as a possible cause of AKI
as an aid to revealing its underlying cause. Similarly, a biochemistry profile can suggest an
underlying cause. ALT, ALP, GGT and total bilirubin measurements are useful in increasing
the suspicion of diseases such as leptospirosis. Hyperglobulinaemia may indicate an
aetiology for AKI such as feline infectious peritonitis (FIP) or multiple myeloma prompting
further testing for these conditions.
Uraemia can result in platelet dysfunction increasing the risk of bleeding following blood
sampling. If continuous renal replacement therapy or peritoneal dialysis is being considered
care should be taken to avoid, or at least minimise, jugular venous puncture due to the
necessity for placement of jugular catheters to allow therapy.
Urinalysis
Urinalysis is vital in all cases of suspected AKI. Patients with AKI usually have isosthenuria
with a USG of 1.007-1.015. Cystocentesis prior to fluid therapy should be performed when
possible; however fluids should not be withheld from critical patients if the bladder is not
large enough. A catheterised sample can be obtained if the bladder is small although this
increases the risk of sample contamination affecting bacterial culture.
Dipstick analysis may reveal glucosuria without systemic hyperglycaemia which is strongly
suggestive of renal injury to the proximal tubule. This is not a consistent finding in patients
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with AKI but can support the diagnosis. Dipstick readings for leucocytes are not reliable and
so in house sediment examination should be performed in these patients. Sediment
analysis may reveal crystalluria, with monohydrate calcium oxalate crystals being compatible
with ethylene glycol toxicity. Urine sediment may also contain evidence of acute tubular
injury with fine or coarse granular casts with hyaline casts also reported. Bacteria may be
seen suggesting urinary tract infection which should prompt urine culture and antibiotic
sensitivity testing.
A quantitative colony count of > 103 cfu/ml in cats and male dogs and >105 cfu/ml in female
dogs with a typical urinary pathogen in a catheterised sample indicates that a true urinary
tract infection is very likely. False negative results are possible with concurrent antibiotic
therapy or prolonged storage. Occasionally urine culture via cystocentesis can be negative
despite the presence of pyelonephritis. Pyelocentesis is more sensitive for the diagnosis of
infection; however complications such as haemorrhage, urinoma and sepsis mean that it
should only be attempted by experienced clinicians.
Specific Testing
Leptospirosis is not uncommon in dogs though very rare in cats. There are many different
serovars (variations in sub-species) with prevalence of serovars varying between countries.
Vaccination is not cross-protective between different serovars and therefore a vaccinated
animal can still become infected. Leptospirosis is generally diagnosed by micro-
agglutination testing (MAT) which detects antibodies. Unfortunately sub-clinical infections
and vaccination can lead to antibody formation which can cross-react with different serovars,
but values greater than 1:800 are highly suggestive of infection. If lower titres are present
but suspicion is strong a second MAT should be performed within 2 to 4 weeks with an
increasing level being suggestive of active infection. In unvaccinated dogs titres may initially
be low, 1:100 - 1:200, rising to 1:800 to 1:1600 or greater. PCR testing for Leptospira
interrogans is now available providing more rapid results. Ideally both blood and urine
samples are analysed and need to be collected prior to the patient receiving antibiotics.
Immuno-fluorescent antibody microscopy (IFA) is also available but will detect animals that
have carrier status.
Ethylene glycol urine tests are available but false positives can occur if propylene glycol
(often used as a carrier for certain drugs such as diazepam) is present in the body. The
lower limit of detection of many tests is close to the toxic dose in cats meaning they may
suffer from AKI even in the face of a negative test. A Woods lamp can reveal urine
fluorescence with some preparations of ethylene glycol but this is not always evident. Many
Page 31 of 334
texts discuss the presence of an elevated osmolar gap (measured serum osmolality
calculated osmolality) in the diagnosis of ethylene glycol intoxication where the calculated
osmolality = 2 x [Na mmol/L] + [glucose mmol/L] + [urea mmol/L]. Unfortunately serum
osmolality measurement isnt available commercially in the UK.
If the patient has travelled abroad, practitioners may want to consider diagnostic tests to
screen for Ehrlichia canis, Borrelia burgdorferi, Rickettsia rickettsii (Rocky Mountain spotted
fever) and Leishmania spp.
Diagnostic Imaging
Radiography can be used to assess renal size with normal kidney length 2.4 to 3.0 times the
height of the second lumbar vertebrae in cats and 2.5-3.5 times in dogs. Radio-opaque
nephroliths, ureteroliths or urethroliths causing post-renal azotaemia may also be detected.
Care should be taken to include the caudal urethra in male dogs.
Ultrasound
Ultrasonography can be used to assess for renal pelvic dilatation which can be seen in
patients with pyelonephritis but also those with volume overload or those treated with higher
rate fluid therapy or diuretics. The renal parenchyma can also be assessed by
ultrasonography for evidence of chronic or end stage disease such as small, shrunken
kidneys with hydronephrosis or evidence of polycystic kidney disease. Normal renal size on
ultrasound is related to body weight in dogs with an expected range of 3.0 - 4.3 cm in cats.
With skill the detection of ureteral dilatation or obstruction is also possible. Increased renal
echogenicity relative to the liver with presence of the halo sign (increased cortical and
medullary echogenicity with areas of lesser echointensity at the corticomedullary junction
and central medullary regions) is highly suggestive of ethylene glycol exposure. The
retroperitoneal and peritoneal space should be assessed for free fluid which can be seen
with urinary tract rupture causing post-renal azotaemia and also in patients with marked fluid
overload. Ultrasound guidance can aid sampling for fluid analysis.
Fine needle aspiration of the kidneys may aid diagnosis of lymphoma in the presence of
renomegaly with compatible ultrasonographic signs. As discussed above AKI patients may
be more prone to haematoma formation and bleeding and this should be monitored for
closely post sampling. Although ultrasound guided renal biopsy can confirm conditions
such as ethylene glycol toxicity and acute tubular necrosis, it rarely changes treatment
protocols and is associated with possible further renal injury.
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Contrast studies
Intravenous urography can worsen renal injury as contrast agents are potential nephrotoxins
but it has been used to assess function in patients suffering AKI. Retrograde urethrography
can be useful to document urinary tract rupture or obstruction. Antegrade pyelography can
also rule out ureteric obstruction or rupture.
Conclusion
AKI criteria should now allow easier definition and identification of acute renal injury. It can
be identified with the use of a minimum database, urinalysis and a good physical exam and
history.
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Notes page
Page 34 of 334
SURGICAL MANAGEMENT OF HEMOABDOMEN

Bryden J Stanley, BVMS, MACVSc, MVetSc, Diplomate ACVS
College of Veterinary Medicine, Michigan State University, USA
stanle32@cvm.msu.edu
Hemoabdomen or hemoperitoneum is seen frequently in small animal practice, almost

exclusively in dogs. It is defined as the accumulation of blood within the peritoneal cavity
(and sometimes retroperitoneal space).
Anatomy
Three main arteries perfusing the splanchnic viscera are the celiac artery, cranial mesenteric
artery and caudal mesenteric artery. Blood supply to and drainage from the viscera differ
due to the portal system, which collects the oxygen-poor, nutrient-dense blood into the liver
via the confluence of cranial mesenteric, caudal mesenteric and splenic veins, ultimately
forming the portal vein. Thus, unlike most other areas in the body, not all arteries have a
satellite vein. Take the time to learn the blood supply before operating, rather than learning it
in a hurry at 2 oclock in the morning.
Etiologies
Traumatic: Different types of trauma include blunt abdominal trauma and penetrating
injuries. Blunt abdominal trauma (mostly from motor vehicle accidents) is a leading cause of
morbidity and mortality in humans. Treatable abdominal injury is seen frequently dogs and
cats, who may be less susceptible to fatal conditions, possibly due to increased compliance
of their bodies. Injury to intra-abdominal structures can be from compressive/concussive
forces or deceleration forces. Concussive/compressive injuries tend to cause parenchymal
fracturing and subcapsular haematomas to solid viscera, as well as rupture of diaphragm
and bladder. Deceleration forces cause stretching and shearing between fixed and non-fixed
structures. Classic deceleration injuries include avulsion of vascular and urinary pedicles,
and tearing of hepatic ligaments.
In many cases, injury is not limited to the abdominal cavity, thus thoracic wall and contents
should be routinely evaluated for all trauma cases, even if the trauma appears restricted to
the abdomen. This is especially true for motor vehicle accidents. Rib fractures (with or
without flail), traumatic myocarditis and pulmonary contusions can be the primary
mechanism of cardiovascular instability in cases with blunt abdominal trauma. Radiography
Page 35 of 334
and ECG should be the minimum diagnostic checks of the thorax, and the patient should
continue to be monitored over several hours.
The most common sites of abdominal bleeding in blunt trauma cases are spleen, liver and
kidney trauma. Spleen and liver bleeds are associated with parenchymal fractures. Although
marked hemoabdomen results from caudal mesenteric artery or renal artery avulsion, these
animals can be saved with immediate resuscitation and intervention. The celiac and cranial
mesenteric arteries arise deep and dorsal within the cranial abdomen, and are very unlikely
to be ruptured. Avulsion of these pedicles will usually result in fatal exsanguination in small
animals, although in the human literature there are reports of superior mesenteric artery
rupture that have been saved by complex bypass or grafting procedures.
Penetrating trauma can occur with bite wounds, machinery trauma, ballistic and other
hunting injuries and malicious knife wounds. Bleeding can be acute and severe if a major
artery is lacerated, or slower with parenchymal or body wall penetrations. Even when the
patient is stable, all penetrations need to be explored due to the risk of peritonitis from
intestinal penetration.
Spontaneous: Most spontaneously-occurring hemoabdomens are caused by neoplasia. The

spleen is the organ most often affected (half benign, half malignant) followed by liver, kidney,
adrenal glands and body wall. Other causes of spontaneous hemoabdomen in small animals
are related to coagulopathies, but in humans conditions such as rupture of an abdominal
aortic aneurysm, ectopic pregnancy or ovarian cyst are seen
Iatrogenic: Occasionally, ligatures are not secure, knots are not tied properly, organs are
inadvertently lacerated, or other technical errors are made in surgery. Uterine ligatures
following spay, and splenic artery ligatures are probably the most common sources of
leaking vessels, although any type of abdominal surgery has the potential to cause
hemorrhage from inadequate ligation (e.g, nephrectomy, cryptorchid castration). I have even
seen significant bleeding from the falciform ligament.
Signs
The abdominal cavity in small animals is highly distensible, and can hold many liters of blood
a dog or cat can easily exsanguinate before adequate pressure builds to equalize the
arterial pressure. If an animal has signs of hemorrhagic shock, aggressive crystalloid fluid
therapy is instituted and baseline CBC, biochemistries, blood typing and blood gases are
performed. Monitoring vitals and ECG and oxygen is set up. It is then crucial to ascertain if
the animal continuing to bleed into its abdomen or thorax. A FAST (focused assessment with
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sonography for trauma) scan with abdominocentesis may provide a quick diagnosis. Packed
cell volume of the fluid should be obtained. Cytology (+_ culture) of the fluid may also be
prudent in cases of penetrating trauma. Some animals can sustain a certain amount of
transient hemorrhage (spontaneous, traumatic or iatrogenic) that may respond to aggressive
fluid therapy. Resuscitative efforts, however, often can include colloids, blood products (if
coagulopathy is suspected, fresh frozen plasma can be given), and pressors. If there is a
history of mild trauma (e.g., a short fall), but signs of blood loss are inappropriately severe,
then one should be aware that neoplasia (e.g., splenic haemangiosarcoma), may predispose
the animal to parenchymal rupture. Non-responding animals should be instrumented with a
central venous access, urethral catheter, and an arterial line (while you can still find one).
Tight abdominal bandaging has been proposed by some, but to be effective they cause
significant discomfort to the animal and take a long time to place.
The main indications for surgical intervention are continued cardiovascular deterioration in
the face of resuscitative efforts, or evidence of penetrating trauma. If the cause iatrogenic,
most cases go immediately to surgery.
Approach
Once the decision to operate has been made, the sooner the bleeding is attenuated, the
better. Although there are many hemostatic and vessel sealing devices available (hemoclips,
ligaclips, pressure enhanced ultrasound, bipolar, monopolar cautery, gelfoam, glues), the
security that comes with precisely placed suture ligation is hard to beat.
Anesthesia needs to be performed with care - these animals often require less anesthetic
drugs, and maintaining pressures during anesthesia can be challenging. Blood transfusion
(whole blood or packed red blood cells) is commenced as soon as possible the true
hematocrit of the patient is invariably lower than what is seen at presentation, and
restoration of vascular volume with fluids is continued. If the animal is stable enough, some
criticalists will wait until bleeding has been attenuated before they administer blood
components.
Nearly always, a ventral midline celiotomy is the procedure of choice. It is the quickest way
to enter the abdomen and the exposure is excellent. An incision should be made from
xiphoid to pubis, using electrocautery once the skin is incised. Hemostasis on the way in is
critical in these cases as they may be heading towards DIC and can ooze significant
amounts from the subcutaneous tissues if they are, or become, coagulopathic. Self-retaining
abdominal retractors will facilitate exposure. The abdomen is drained through a Poole
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suction tip taking care not to be rough with the tissues. Sterile, filtered autotransfusion can
be performed if neoplasia is ruled out I can count the number of times I have done this on
one hand. If the etiology of the hemoabdomen is known (e.g., post-operative splenectomy or
ovariohysterectomy), then immediate inspection of the suspect ligatures is indicated.
In other cases, the source of the bleeding may be readily identified by the presence of a
large clot organizing around the lacerated or leaking vessel. Look for this first, as it enables
1) rapid anatomical localization, and 2) the opportunity to clamp the vessel(s) before
removing the clot. In cases of traumatic avulsion of a major artery that is difficult to isolate
(e.g., renal) this could save 5-10 minutes of ongoing blood loss. If no obvious clot exists,
then a systematic exploration should commence. Typically, the spleen is examined and
exteriorized. An abnormal, hemorrhaging spleen is obvious as one enters the abdomen,
whereas an unaffected spleen in the face of hemoabdomen tends to be small and
contracted. Once the spleen has been examined, it can remain exteriorized and the
descending colon used to dam the viscera off to inspect the left kidney, adrenal and body
wall. Going cranially, the short gastric vessels (a common site of avulsion in gastric dilation
volvulus), left liver lobes, the papillary process of the caudate liver lobe and esophageal area
can be identified. Moving through and examining the liver lobes from left to right leads one to
the stomach and duodenum. The duodenum can be used to dam of the viscera and inspect
the right kidney, adrenal and body wall. When a lacerated vessel is identified, occlusion of
the vascular pedicle will temporarily control hemorrhage whilst inspection of the abdomen
continues.
Severe hepatic bleeding may be attenuated somewhat by occlusion of the hepatic artery and
portal vein (Pringle maneuver) - placement of an atraumatic clamp (e.g., Satinsky, Debakey
bulldog) at the ventral border of the epiploic foramen. This will allow some time to perform a
liver lobectomy, although leakage through the hepatic sinuses from the caudal vena cava
can still be significant. Automatic stapling equipment and harmonic scalpel devices have
greatly facilitated the removal of liver lobes and spleens, and are worthwhile investments for
the trauma surgeon. The kidney and ureter is generally removed by hand ligation of the
artery and vein. The entire abdomen should be inspected before lavage and closure.
Aggressive management and monitoring should continue into the post-operative period.
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CAESARIAN: 90 SECONDS
Since the advent of anesthesia in the second half of the 19th century, surgery has become a
more leisurely affair. However, there are times where urgency still needs to be impressed
upon the surgeonand delivery by caesarian is one of those times. There is general
agreement that the earlier a truly distressed fetus is removed and support is instigated, the
better the outcome.
Normal canine gestation is 64 days from ovulation. The most accurate ways of determining
due date are: the date of the pre-ovulatory luteinizing hormone surge (parturition should
occur 64-66 days later), the pre-ovulatory rise in progesterone (62-68 days following levels
rising above 1.5 ng/ml and fetal ultrasonography before day 39. Closer to parturition, a drop
in rectal temperature to less than 37.8 (labor should start within 24 hours), ultrasonographic
measurement of specific fetal and placental dimensions, and transcutaneous uterine and
fetal monitoring (placed 1 week before delivery) have been used. The most common late
gestation monitoring is the drop in body temperature, and this is what we used for the rare
planned C-section (e.g., brachycephalic with history of previous dystocia), in the absence of
pre-ovulatory data.
Normal feline reproduction is similar to dogs, but has been far less studied. The queen is an
induced ovulator in most cases coitus must happen for ovulation to occur and the corpora
lutea to develop. Parturition is around 66 days after coitus, but can be quite variable, with
breed differences.
Normal parturition
Stage 1 labor consists of uterine contractions. The bitch may be anxious, restless, display
nesting behavior, anorexia, shivering, occasionally vomiting and diarrhea. Stages 2 and 3
alternate as each fetus is expelled, with visible abdominal straining seen in Stage 2 as the
fetus is delivered, and the placenta being expelled in Stage 3. Parturition in dogs may last
from a few hours to up to 24 hours. As a general rule, active straining to expel a fetus should
not exceed 30 minutes and the interval between puppies should not exceed 4 hours. The
body temperature of the dam returns to normal about 12 hours after whelping, and the
uterus takes about 4-6 weeks to involute. During the period of involution, a diminishing
amount of lochia (dark red-brown, odorless vaginal discharge) is seen.
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Cats experience the same stages of delivery as dogs, and are mostly done with their
deliveries in less than 6 hours. The body temperature indicator of impending parturition is not
as accurate in cats. Extremely rarely, cats can appear to be finished with their deliveries, but
then begin again after a day or so.
Antenatal care is not routinely performed as it is in humans and mares, so often the first time
the vet has ever seen the animal is during dystocia. Once pregnancy is diagnosed, it is an
excellent idea to provide an antenatal program for the bitch (or queen) and an education
consultation for the owners, so that they know what to expect in the days leading up to and
during a normal delivery. This will also establish a relationship between you, the owner and
the patient, so that in the event of a dystocia, you are all more relaxed and prepared.
Dystocia
Dystocia is the abnormally slow or difficult delivery of the fetus. The word derives from the
Greek dystokia: dys-badly and tokos-childbirth. Says it all, really. Although the majority of
dogs and cats will deliver normally, dystocia is seen regularly (estimates between 15-20%),
with certain dog breeds over-represented - brachycephalics, and also some giant breeds.
Dystocia is not as common in cats, has been reported to be about 6% - and again over-
represented in pure and exotic breeds.
The causes of dystocia have been divided into maternal and fetal. Maternal causes include
primary uterine inertia, small pelvic canal, and less commonly, uterine torsion, and vaginal
septum or stricture. Fetal causes of dystocia are either fetal oversize (singleton, anasarca or
other anomaly), or fetal malposition. Secondary uterine inertia is not a cause of dystocia, but
is myometrial fatigue resulting from obstruction due to one of the causes listed above.
Primary uterine inertia can be complete or partial, and is the commonest cause of
dystocia. With complete primary uterine inertia, no puppies or kittens are delivered. In partial
primary uterine inertia, part of the litter is delivered, but then the uterus fatigues before
parturition is complete. The reasons for primary uterine inertia are thought to be:
- Very large or very small litter size leading to inadequate uterine stimulation;
- Systemic disorders
- Low plasma oxytocin
- Low prostaglandin/high progesterone levels
It can be challenging to recognize complete primary inertia. There are often no signs at all,
or there can be a lack of Stage 1 transitioning to Stage 2. Certainly, a prolonged known
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gestational period, failure to deliver 36 hours after rectal temperature drop or signs of
toxemia can indicate complete primary inertia.
Signs of partial primary inertia are prolonged (> 4 hours) interval between pups, and no
significant abdominal straining.
Diagnostics
A well lubricated digital vaginal exam and also rectal examination can determine if there is a
fetus in the birth canal, and the state of the vagina (with respect to tone, and contractions).
Sometimes malposition can be detected. The two most valuable diagnostic tools, however,
that aid decision-making are radiography and ultrasonography. Lateral and ventro-dorsal
abdominal views will allow us to determine the number of fetuses and their position. Breech
is considered normal in dogs and cats, but if the fetus is transversely presented, or breech
with hips flexed or the neck is flexed, then the malposition can cause fetopelvic
disproportion. Very large fetuses (e.g., singletons) and anasarcas can also be determined.
Gas in the fetal sacs and fetus indicates fetal death and is evident as early as 6 hours
following demise. Fetuses that have been dead for several days will show skeletal collapse.
Ultrasound is not as accurate for determining the number of fetuses, but provides an
excellent indication of fetal viability. Normal fetal heart rates in a conscious dam are around
220 bpm, and fetal limb movement is evident. The fetus is considered to be in distress if the
fetal heart rate drops to less than 190 bpm in the conscious dam. Severe fetal distress (150-
160) is an indication for immediate C-section
Treatment of dystocia
Once dystocia is recognized, it should be treated as soon as possible. At our institution,
immediate C-section is indicated if:
- there is obstruction to the birth canal, or
- there is unresolvable fetal malposition, or
- there is meconium staining in the vagina, or
- there is bloody or other abnormal vaginal discharge before the first pup, or
- the fetal heart rate is between 150 and 170, or
- the fetal heart rate is between 170 and 190, AND there is no movement, or
- it has been 4 hours since the last pup, or
- there has been more than 30 minutes of active abdominal straining, or
- the bitch has signs of systemic disease.
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If, on the basis of your diagnostics, there is no obstruction to the birth canal, there is no fetal
malposition or fetal monster, and fetal heart rates are normal or if they are between 170 and
190 but they are moving, and it has been less than 4 hours since the last pup delivered, then
medical management can be considered. Medical management typically consists of fluids
and electrolyte correction (animals are rarely hypoglycemic or hypocalcemic), and oxcytocin
0.2 U/5kg IM or SQ. If a fetus is delivered, oxytocin can be repeated every 30-40 minutes.
Most dogs, however, will go to caesarian
Caesarian
The word caesarian derives from the Latin root caedere or caesus, to incise or cut. The
following describes a team approach developed over many colony and client C-sections
where delivery of a healthy pup and saving the dam were critical. The key to success with C-
sections is in the team. Everything associated with prioritizing both fetuses and mother -
anesthesia induction and maintenance, clipping and preparing for surgery, the surgical
technique and neonatal resuscitation - all happen in very close concert. It is understood that
not all facilities have a plethora of people to help at all times, so extra and willing folk (e.g.,
the owners, receptionist, kennel maid, delivery man) may have to be recruited. The time to
removal of first fetus (often the most compromised) is critical.
A note on drugs: xylazine, methoxyflurane, ketamine, thiamylal and thiopentone have been
clearly associated with decreased neonatal vigor. Alphaxalone should be an excellent
choice.
10 step MSU protocol for emergency delivery by caesarian:
1. Assemble team
Round up folk and designate a resuscitation team leader. The anesthetist, surgeon (and
assistant if possible) must never forget that time is crucial. Experienced anesthesia support
greatly facilitates this mission.
2. Teams split
Anesthesia team: stays with animal and starts preparing animal (see Step 3.)
Surgery team: immediately gets the instrument pack and drape pack together, and opens
up packs with extra laparotomy sponges, hemostatic forceps (for umbilical clamping), and
towels. Do not use 4x4 gauzes unless you have time to count them, before the bitch arrives.
Surgeon and assistant surgeon scrub, gown and glove and open up pack in the operating
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room (OR)and wait. The surgical team should be ready and waiting to drape as soon as
the bitch is in position.
Resuscitation team: gets equipment together see below under Neonatal Resuscitation.
3. Preoxygenate, clip and prep

Many laboring bitches can be clipped and even have an initial prep while conscious and
receiving oxygen. Take care to avoid clipper rash and nipple damage there is no need to
clip too wide. As soon as the bitch is catheterized, clipped and vacuumed, she can be taken
into the OR for induction.
4. Move to OR, induce, and line block

We use IV propofol induction followed by endotracheal intubation with administration of
oxygen only. A generous line block with lidocaine is infused into both deep and superficial
layers. The bitch is maintained on IV Propofol only with no (or minimal) isoflurane until
fetuses are removed. Dorsal recumbency is fine, supine hypotension is not an issue in cats
and dogs. Animal receives the final prep following line block.
5. Drape and incise

The surgeon needs to work quietly and surely, in unhurried movements, but not pausing
always be thinking of the next step in the procedure. It is probably slightly easier if surgeon
stands on right side of dog. Towels are quartered around the midline, covering the nipples,
and secured with towel clamps. The towel clamps should not penetrate through the skin.
Barrier and fenestrated drapes follow. Incise firmly from 2-3 cm cranial to umbilicus to pubis
(but drape up to xiphoid). Clamp any significant bleeders with hemostats but no other
hemostasis no electrocautery yet, no ligatures. Careful nick in linea right in the middle of
the incision length, then fingers protecting uterus and lifting linea, cut with Mayo scissors, up
and down. The linea is usually quite wide and obvious in these girls.
6. Deliver the first pup

Gently bring body of uterus up, be careful of your fingertips on the broad ligament, as the
uterine and ovarian vessels are ginormous. If there are only a few pups, you can also
exteriorize both uterine horns. Pack off with a couple of laparotomy sponges on either side of
the uterus. Transverse or longitudinal incision in body, with #15 blade, extend with
Metzenbaums. Open sacs by lifting up with Debakey forceps and cutting with blade or
scissors pup will present immediately. Hold up with head down, two hemostats on
umbilicus, leaving at least 2-3 cm of cord with pup. Cut between clamps and hand off onto
sterile, warmed towel.
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7. Deliver the rest

Immediately upon delivery of the first pup, the assistant should start applying gentle yet
persistent traction on the placenta, while the surgeon starts to milk the next fetus down from
the opposite horn. The placenta will slowly start to separate if torn off too quickly, bleeding
will ensue and some placenta may be retained. Each pup is delivered in a similar manner to
the first, with the placenta being brought out immediately afterwards, alternating from one
horn to the other. After one or two pups are delivered, the uterine horns are usually easily
exteriorized. If there is no neonatal movement or if there are signs of meconium staining,
these should be reported as the pup is handed off. The presence of a clearly dead fetus
indicates culture and sensitivity.
As soon as the pups are delivered, inhalation anesthesia can be started (sometimes a little is
needed before this), and the urgency (of the surgical team) is lessened.
8. Reconcile placentae, flush and suction

Reconcile the number of placentae with the number of pups. Check that you have all fetuses
extracted, and there is not a small, mummified fetus high in one horn. No more than a quick
flush and suction of the uterine horns is typically needed. By this time, you should notice
some involution of the uterus beginning to occur.
9. Close uterus
The uterus can be closed in a snug, single layer, simple continuous suture pattern, using a
3-0 monofilament absorbable suture. The muscular organ starts to contract and longitudinal
ridges appear in the body and horns. This will attenuate hemorrhage from the placentation
sites, so it is important to note that it occurs. If the uterus remains flaccid, oxytocin should
be administered.
10. Close
Following uterine closure, the abdomen can be lavaged and suctioned, using a new suction
tip. A routine three-layer closure is performed, using an intradermal suture pattern in the
skin. Finally, the abdominal skin is rinsed thoroughly with warm saline to rinse off any
residual scrub or solution from the surgical prep.
Neonatal resuscitation
The resuscitation team needs to gather equipment together beforehand: oxygen source,
bulb syringe and/or gentle suction tube, umbilical clips, warm towels, radiant heat lamp or
circulating water heating mat and epinephrine. Naloxone if an opiate was used on the dam.
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Try to have a person dedicated to each pup or kitten for resuscitation. The technique of
swinging or flicking the neonate to clear the respiratory passages is no longer performed
this action can lead to intracranial hemorrhage and laryngeal edema. Holding in a head-
down position while transferring the pup from the womb to the resuscitation table to facilitate
drainage from the pharynx is a good idea. At the time of handing off, the resuscitation person
should ensure that the hemostat on the umbilicus is not inadvertently poking into the
abdomen. The hemostat can generally be removed in 10-20 minutes, with or without being
replaced by an umbilical clip.
The oral cavity, pharynx and nares are gently suctioned to clear amniotic fluid from the area,
and the pups should be kept warm and rubbed gently. They are very prone to burning with
direct contact, so radiant heat or circulating water mats are preferred. Healthy pups will
generally start squeaking shortly after delivery. If the neonate is poorly responsive, then
oxygen can be delivered by mask or careful intubation (not flow by), and more vigorous
rubbing. Use of atropine and doxapram is controversial, as they increase myocardial oxygen
consumption. The use of glucose under the tongue is also of unknown value. As a final
resort for a non-vital neonate, 10ug/kg epinephrine can be administered through the
umbilical vein, and gentle external cardiac compression commenced. Overall survival is
variable and dependent on the condition of the fetuses at delivery.
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Notes page
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DEHISCENCES: INCISIONAL AND INTESTINAL

The word dehisce derives from the Latin dhiscere- to gape or yawn. Incisional dehiscence
is defined as a separation of the layers of a surgically closed wound, and can comprise of
just the skin, or can include the deeper tissue layers that were originally approximated.
Intestinal dehiscence is full thickness. It is more common for part of the suture line to
dehisce, but at times the entire effort can dishearteningly fall apart. There is always a reason
for dehiscence, be it technical failure, infection or due to underlying risk factors, and if these
can be minimized, then the risk of dehiscence decreases. Both incisional and intestinal
dehiscences typically occur within a week of the original surgery.
Incisional dehiscence
Breakdown of the incision can comprise of just the skin, or can include the deeper tissue
layers that were originally approximated. If the original surgical closure included the body
wall (e.g., celiotomy) and the linea alba has dehisced, then herniation of omentum and
sometimes intestines will occur. Incisional herniation occurs when the skin incision is still
intact and the herniated abdominal contents go no further than the subcutaneous area. An
incisional hernia is diagnosed on clinical presentation of a soft fluctuant swelling under the
skin. The contents are usually reducible into the abdominal cavity (unless strangulation or
incarceration have occurred), and one can palpate the edges of the body wall defect.
Ultrasound and radiography can confirm the presence of an incisional hernia. Evisceration
occurs when the linea, subcutaneous and skin suture lines are all dehisced and abdominal
contents are protruding through the skin. Evisceration of abdominal contents leads to self-
trauma and rapid clinical deterioration. Evisceration is self-evident and is an emergency.
Immediate re-operation and resection is indicated, as well as aggressive management
for peritonitis.
The first step in a suspected incisional dehiscence is to examine not only the wound, but
also the whole patient, even if you have just seen the patient 5 days ago. Obesity, old age,
exogenous or endogenous corticosteroids, malignancy, radiation therapy, hepatic and renal
disease, anemia can all cause a delay in the wound healing processes that may predispose
to dehiscence. Less common systemic causes of dehiscence in veterinary medicine are
severe malnutrition, diabetes, neuropathies and vascular insufficiencies.
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Careful probing and manipulation of the dehiscing wound itself should reveal the extent of
wound breakdown this is important, because it may be more extensive than what was
initially apparent. One should always be looking for an underlying reason for the failure, such
as incorrect suturing technique, poor suture material choice, poor apposition of tissues, poor
timing of initial closure, tension, movement, inappropriate activity, self-mutilation and
infection. This is critical, because recognition of the inciting cause of failure can avoid a
similar mistake being repeated. Additionally, in cases of post-celiotomy incisions, always
ascertain the integrity of the body wall closure.
There are many cases when a small area of relatively superficial dehiscence can be allowed
to heal by second intention. For example, following total ear canal ablations, where it can
sometimes be difficult to accurately appose tissues; or following a reconstruction where
there are three suture lines coming together in a mobile area with some judgement, these
can be cleaned, sutures removed, and allow a protective scab to form. This approach will
only work when the dehisced area is small, superficial, and not infected.
Some small dehiscences can be dealt with by en bloc resection of all affected tissues. Again,
this is only useful in small dehiscences, but can be quite effective when the area is grossly
infected. One of the disadvantages of this approach in a relatively healthy wound is that one
is removing the very cells that have infiltrated into the region to modulate wound healing.
In most cases, the wound and periwound are cleansed and explored. This is best performed
under general anesthesia and using strict aseptic protocols. Following draping, ineffectual
sutures are removed and a piece of the deep tissue selected for aerobic and anaerobic
culture (other cultures may be indicated later, or could be performed at this time if the wound
has an atypical appearance). There are times when biopsy for histopathology is also
indicated, e.g., if the dehiscence follows a tumor removal and there may be neoplastic cells
at the margins of the resected tissues. Sharp dissection of all necrotic and obviously
devitalized tissues should be performed (dbridement). With a dehisced wound, this can
generally be done in one session, but occasionally dbridement has to be repeated in
several days. Do not remove obviously viable tissue that is trying to heal, as macrophages,
fibroblasts and other cells integral to wound healing will be present. Wound lavage or
irrigation is also indicated at this time, although it is the first step to be forgotten! Irrigation
fluid should ideally be buffered and sterile, and copious in quantity. Pulsatile lavage units are
extremely effective at removing microscopic debris and stimulating blood flow to the wound.
The resultant wound should have a noticeably improved appearance, showing evidence of
good perfusion.
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Almost always, the best course of action for the cleansed, debrided and irrigated wound is to
manage it as an open wound for one to several days, prior to performing a delayed primary
or secondary closure. Further complications are more likely when immediately closure is
attempted. Dressing choice during open wound management will depend on the stage of
wound healing, the amount of exudate, and what is feasible in practice. Early wounds may
benefit from alginate and foam dressings for a few days, or even a wet-to-dry dressing, if
grossly infected. Negative pressure wound therapy is extremely effective at preparing a
wound for closure, as it stimulates formation of vascular granulation tissue (the sign of a
healthy wound). When the wound appears healthy enough to close, re-culturing is always
suggested. However, it is generally only performed in critical or complicated cases, as in
most cases the causes of dehiscence have been ascertained, and most practitioners can
recognize a healthy wound. It is important to reconsider the factors that may have led to the
original dehiscence, so that they are not repeated (e.g., tension on the closure, inadequate
immobilization). Dehisced wounds should be closed in two layers, with interrupted sutures.
The minimum number of sutures to obtain a strong closure should be used, and buried
sutures should be synthetic, absorbable and nonbraided. All attempts to minimize tension
and movement should be employed, including internal and external coaptation, and
restriction of activity. Consider the use of a tension-relieving technique, or small flap. Finally,
drainage should be provided to the area, preferably in the form of an active unit.
Intestinal dehiscence
One of the most critical of all abdominal surgery complications is the breakdown of an
intestinal suture line, leakage of contents into the peritoneal cavity, and ensuing septic
peritonitis. Gastric dehiscence is uncommon, due to the rich vascular supply and the typical
two-layer closure. Most dehiscences will occur within 3 5 days of surgery. An initially
improved post-operative patient will become lethargic, and inappetant. Heart rate and
temperature may rise, and vomiting, abdominal pain and distention can (but will not always)
develop. Younger animals can mask their clinical deterioration quite well, so close
examination and lab values are indicated. Haematology values tend to show an increase in
the WBC and percent bands, and decrease in platelets. Toxic changes will be seen
associated with the left shift. With colonic dehiscence, marked deterioration will occur within
hours. Diagnostics should include abdominal radiography, and abdominocentesis.
Ultrasonography can be useful to determine presence of early abdominal effusion. If
abdominocentesis is not diagnostic, diagnostic peritoneal lavage is indicated. Remember
that air can be present in the abdominal cavity for up to a week following abdominal surgery,
as well as mature neutrophils and a few bacteria. The appearance of degenerate neutrophils
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and intracellular bacteria in the face of clinical deterioration are an indication to re-operate.
The only other possible differential is a fulminating pancreatitis.
Treatment of intestinal dehiscence is immediate re-operation, with aggressive supportive

therapy, including fluids, antibiotics, and any further drugs to maintain cardiovascular
function. The original incision is re-opened, retracted, and thorough inspection of all
abdominal contents is warranted. The appearance of the serosal surfaces within the
peritoneal cavity can be variable, depending on how effectively the contamination has been
localized by the omentum and anatomical location. Cases of any type of intestinal
dehiscence require resection and anastomosis. The only exception might be in the proximal
duodenum, where to resect would require a Bilroth II procedure. An omental wrap or serosal
overlay is indicated, as the patient is now high-risk. Copious, copious, lavage and suction,
exit culture, placement of abdominal drains and placement of gastric decompression drains
are performed. Intensive post-operative monitoring and support is instituted
cardiorespiratory support, vascular volume maintenance, maintenance of renal perfusion,
appropriate antibiotics, and nutritional support. Younger animals can cope with this insult
quite well once the inciting cause has been addressed, but older or debilitated animals will
require intensive critical care.
Prevention
There are several principles of intestinal surgery that will decrease the chances of
experiencing an intestinal dehiscence. It is always worth remembering these when
performing intestinal (or any hollow viscus) surgery:
Recognizing the high-risk patient: Although complications of gastrointestinal

surgery can occur in any patient, there are some patients at increased risk. Patients
with pre-existing peritonitis or sepsis, hypoproteinemia, uraemia,
hyperadrenocorticism, immunosuppressed state, advanced liver disease, negative
nitrogen balance, coagulopathies, extensive neoplastic disease, etc., may not heal as
quickly or effectively, and carry a greater risk of dehiscence. These patients should
be aggressively prepared for surgery and may require intensive post-operative care.
Intestinal suture lines should be augmented with a serosal overlay or an omental
wrap, thus bringing in blood supply, a source of macrophages and mesothelial cells
to the sutured area. A serosal overlay pexies two sections of healthy bowel over the
suture line, carefully avoiding kinking of the jejunal festoons. An omental wrap covers
the suture line with a wrap of omentum, held in place with several tacking sutures.
Both these techniques effectively reinforce the suture line. High-risk patients should
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be considered for feeding tube placement before leaving the abdomen. The
abdominal wall closure needs to be secure and long lasting in these cases. An
interrupted or continuous, carefully spaced linea closure with a monofilament (slowly
absorbable or nonabsorbable) suture should be placed. Subcutaneous and skin layer
should follow.
Assessment of intestinal viability A decision to resect bowel requires an accurate

assessment of its viability. The standard subjective criteria for viable intestine are,
colour, arterial pulsations, peristalsis and bleeding from a cut edge. The bowel should
be moistened and warm when assessing these characteristics. These are not all
completely accurate, but the error is made in favour of resecting too much, rather
than leaving non-viable bowel behind. Other tests of perfusion used clinically include
intravenous fluorescein dye injection, Doppler ultrasonic flow probes and pulse
oximetry. If viability is questionable, resection is the prudent choice. Around 75 -
80% of the small intestines can be resected before permanent short bowel syndrome
is seen.
Antibiotic prophylaxis / antibiotic therapy In most cases of abdominal surgery

where a hollow organ is entered, prophylactic antibiotics are indicated. A first
generation cephalosporin is commonly used for gastric and small intestinal surgery,
administered as a slow intravenous bolus around induction. The dose is repeated
every 2 hours until the end of surgery. If infection is present, this broad-spectrum
therapy should be continued into the post-operative period, until the results of culture
and sensitivity provide an effective choice of antibiotic. A second generation
cephalosporin (such as cefoxitin) is preferred for the colon or rectal procedures. In
cases of gross contamination, an exit culture may be warranted.
Instrumentation Appropriate instrumentation greatly facilitates surgery of the

gastrointestinal tract. Self-retaining abdominal retractors (such as Balfours, Gossets,
or Nelsons) are essential. Hand-held retractors (e.g., malleable, Faraboeufs, Army-
Navy) are useful to expose deeper structures and protect other areas. Doyen non-
crushing intestinal forceps are useful for occluding the lumen of the bowel without
compromising perfusion of the bowel wall. Suction devices connected to continuous
and regulated suction is also a great asset in surgery. A Poole suction tip is preferred
when draining abdominal fluid, while Yankeur and Frasier tips will facilitate finer
procedures. The ability to dial the suction down minimizes trauma of bowel wall.
Metzenbaum scissors and Babcock forceps should routinely be included in the
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surgery pack. Fine, multitoothed forceps such as Debakey or Cooley are the least
traumatic for handling bowel edges - avoid large toothed forceps. Intestinal stapling
equipment, automatic ligating staplers are quick, fun and provide a secure
anastomosis, but are moderately expensive. A ceiling-mounted, double-lighting
system with fully articulated arms is invaluable. Fully mobile articulated arms are
preferred, or track mounted.
Surgical technique Always handle bowel gently. Excessive handling and drying of
the intestines can cause a vagal response and postoperative ileus; the serosa also
becomes irritated and inflamed. Keep the abdominal contents moistened with warm,
sterile saline at all times, as they have a tendency to dry out under the operating
room lights. Hands are excellent for examining the intestines and occluding the bowel
lumen. Correctly placed Doyen forceps can also be used to occlude lumen, if used
carefully, watching where the tips of the forceps are. Electrocautery should not be
used on the bowel wall haemorrhage from transected or incised bowel will soon
clot with gentle pressure from moistened gauze. Likewise, bleeding from vasa recti or
arcuate vessels should be attenuated with fine ligatures of 5-0 monofilament suture,
not electrocautery. When suturing bowel, use a simple interrupted or continuous
suture pattern, very snug. The tension on the suture line in an intestinal anastomosis
should be minimal.
Suture material A monofilament, absorbable suture material with a consistent,

known rate of absorption and minimal reactivity is suitable for use in the small
intestine. Polydioxanone and polyglyconate are most commonly used. Non-
absorbable monofilament sutures such as nylon, polypropylene and polybutester are
also suitable choices. Braided sutures are not recommended they harbour bacteria
from the intestinal lumen and they also cause more trauma as they pass through the
tissue. Chromic gut is not indicated due to its unpredictable rate of absorption,
especially in the presence of inflammation. Gut will also incite a significant
inflammatory response. A fine suture material is always indicated, usually 4-0 or 5-0,
and occasionally 3-0 in size.
Suture patterns Single layer, direct apposition of the bowel is preferred for rapid
healing, rather than an inverting, everting or two-layered suture pattern. This is true
for small and large bowel, but stomach wall is usually sutured in two layers a
simple continuous full thickness layer, followed by an inverting layer in the serosa
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and muscularis. Gastrointestinal sutures need to be tied snugly. Accurate apposition

is tricky to obtain, due to the tendency for the redundant mucosa to protrude outward
from the lumen. Mucosal eversion can be minimized by trimming the mucosa before
suturing, modifying the bite to a modified Gambee bite, and also using a simple
continuous pattern.
Abdominal lavage and suction Copious quantities of warm, sterile saline followed
by suctioning before closure is essential following GI surgery. Thorough abdominal
lavage will reduce contaminating bacteria and debris, removes residual blood, warms
the abdomen, moistens all organs and enables a final check of the cavity. Obviously,
water-impermeable barrier draping should be consistently used as part of the draping
protocol. The addition of antibiotics or antiseptics to the final lavage solution has no
proven benefit, and can be irritating to serosal surfaces.
Checklists It has been well documented in human surgery that complications are
decreased by adherence to checklists. Checklists should be mandatory in large, busy
hospital settings, and are even useful in smaller clinics. Checklists will ensure that
the correct patient is in the Operating Room, the procedure is appropriate to that
patient, informed consent has been granted by the owner, and costs have been
discussed. They will also confirm that antibiotics have been given when indicated,
what tissues are submitted for histopathology and other laboratory testing. The
checklist should be read out before the procedure and following the procedure.
When faced with a dehiscing wound, always try to learn from the experience. Think carefully
about what may have been performed, that may have avoided this consequence. This
includes not just wound closure techniques, but also management techniques and
identification of high-risk patients. Prevention is always better than cure, but an opportunity
to learn should never be wasted.
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Notes page
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PHARYNGEAL STICK INJURIES AND OTHER PENETRATING TRAUMAS

In small animal practice, dogs are the most likely species to experience foreign body stick
trauma through the oral cavity, probably due to their tendency to run through bush, catching
and retrieving things, and using their mouth as the primary prehensile appendage. Less
frequently, but still well documented, cats will sustain penetrating injuries to the mouth and
pharynx. Objects can be lodged within the oral cavity, nasal cavity, or pharynx; or break off
with a section remaining in the retropharyngeal tissues. Linear objects may migrate and
cause issues at distant sites over time. Oropharyngeal stick injuries are sustained fairly
sporadically, but can be quite spectacular in presentation at times, causing significant initial
discomfort to the animal and marked distress to the owner. Although wooden sticks are the
most common cause of penetration (especially in dogs), needles, fishhooks and bones are
also seen (more so in cats).
There does not appear to be a typical breed or predisposing age for this condition. Although
it was originally assumed that puppies and adolescent dogs would be at risk, this has not
been shown in the literature, or at our Veterinary Teaching Hospital. The average age is
actually around 5-6 years, with medium and large size dogs more commonly presented.
There is possibly a higher incidence in males, probably due to their stupidity.
Animals with oropharyngeal stick penetration tend to present to the veterinarian in two
separate and quite clinically distinct categories: those that have just experienced the
traumatic penetration (and these can be either peracute or acute), and those with the chronic
foreign body and characteristic draining tract.
Acute
The presenting signs of an acute case (in the literature this has been termed as less than 7
days) include:
Oral irritation - evidenced by pawing at the muzzle or rubbing face on the floor. Dogs
sometimes can initially appear maddened. This sign is transient and owners may
perceive an improvement after a few days.
Reluctance to manipulate the jaws open, due to pain or discomfort.
Hypersalivation
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Blood-tinged saliva
Dysphagia
Gagging
Stertorous pharyngeal noise, which may be accompanied by dyspnea
Epistaxis
Exophthalmos and periorbital swelling
Ocular discharge
Lameness (very rarely with pharyngeal sticks - only if the impalement is involving
cervical spinal, brachial plexus, or shoulder area).
Chronic
Unfortunately, more than 75% of dogs are presented as chronic cases - from weeks to
months following original insult. Following initial impalement; the stick may break off, or be
only partially removed by the owner or other individual. This leaves a residual foreign body in
the retropharyngeal tissues. The oropharyngeal mucosa tends to heal very quickly, often in a
matter of days, thus concealing the original entry site. This can make diagnosis more
challenging. Additionally, there is often no specific history of oropharyngeal trauma. Once
settled in the retropharyngeal tissues, the heavily contaminated foreign body can then
abscess, leading to swelling and a draining tract. If it is wooden, it will develop similar radio-
opacity as muscle as it absorbs water. Some of these foreign bodies can also migrate
considerable distances, causing nothing but trouble on the way. There have been reports of
brain abscessation, atlanto-axial osteomyelitis, quadriparesis from spinal canal migration
and pyothorax. We have also seen chronic brachial plexus irritation due to chronic stick
impalement. Chronic oropharyngeal stick injuries can therefore be quite variable in their
presentation. Animals can demonstrate one or several of the following signs:
Swelling. This is typically in the ventral cervical region, also intermandibular, and
sometimes facial, especially for retrobulbar penetrations.
Draining tract. Again this is typically in the ventral cervical area, but may be quite
small and not always detected by the owner. The nature of the discharge can vary
from serous, serosanguineous, or purulent, depending on current and prior therapies.
Lethargy/dullness
Pain and sometimes even a change in character. Animals can become head shy or
perceived as bad-tempered when their head and neck area are patted or stroked.
Difficulty or resentment upon manipulating the jaws open
Halitosis
Subcutaneous emphysema
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Lameness, usually a unilateral thoracic limb

Neck pain
Neurological signs (including quadriparesis)
Diagnosis
An accurate and thorough history can play a pivotal role in obtaining the diagnosis. In acute
penetrations, determining the historical chain of events is not too challenging. However, in
chronic situations, if clinical signs are at all compatible with a possible prior oropharyngeal
penetration (see clinical signs listed previously); owners need to be questioned in detail for
any possible episode where impalement may have occurred. This may even extend to
contacting a prior owner or shelter. Sometimes intense questioning will act to jog owners
memory about a possible episode of impalement, and we have had several instances when
a family discussion at home has recalled a long-forgotten mishap (e.g., a painful yelp out in
the woods, hunting injury).
Careful cervical palpation under anesthesia or sedation should be done, but it is usually
unrewarding, unless the foreign body lies quite superficially. It is also possible to confuse
fibrous tissue with a foreign body in chronic cases, thus palpation has limited diagnostic tool
usefulness. Bloodworm should be done routinely, and a nonregenerative anemia is a
common finding. This can be attributed to the effects of chronic inflammation. The following
diagnostics are useful:
Oropharyngeal examination under anesthesia. This is more rewarding in acute
cases. This should be done carefully and thoroughly, using probes, and allowing
plenty of time for a full oropharyngeal examination. Particular areas to concentrate on
include the sublingual tissues (both sides), the piriform recesses, the dorsal pharynx
(dorsal to the esophagus, with rostral retraction of the soft palate), caudal to the
tonsillar crypts, and the roof of the mouth (sometimes sticks can get jammed across
the two dental arcades of the maxilla).
Esophageal endoscopy should always be performed, as the stick may have
penetrated through the proximal esophageal wall, which can negatively impact
prognosis, especially if this traumatic penetration is missed. Endoscopy should
always include a retroflexed view of the choanae.
Radiography. Typically, plain radiography is unrewarding as a diagnostic tool. The
commonest foreign body is wooden and generally takes on the same density as
muscle as it absorbs water. However radiographs are indicated to detect other
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conditions such as mediastinitis, pulmonary or pleural involvement, and also will

identify metallic, or other radio-opaque foreign bodies.
Sinography. This tool, preferably with CT but also with fluoroscopy can prove quite
useful if a draining tract exists. To maximize the likelihood of the iodinated contrast to
highlight the filling defect around the foreign body, it is important to have the animal
off antibiotics, and perform the test when the animal has had an obvious draining
tract for at least a week. Fluoroscopic sinography was performed almost routinely
before CT and MRI capabilities were available.
Computed tomography (CT) and magnetic resonance imaging (MRI) have almost
revolutionized our diagnostic capabilities when hunting for acute and especially
chronic foreign bodies, including those originating from the oropharynx. The
sensitivities of these imaging tools, especially with contrast agents and other
enhancing modes, along with the technology to reformat images in 3D, make either
CT or MRI almost mandatory in locating challenging, chronic foreign bodies. MRI is
also quite sensitive in visualizing the inflammation around the foreign body. These
tools also make it easier for the surgeon to spatially locate the object within the body,
thus causing less tissue trauma during exploration.
Ultrasonography can locate a variety of foreign bodies, and is recommended if
advanced imaging tools are not available. Ultrasound is not as effective at
determining anatomic location as the previously mentioned imaging modalities.
In rare circumstances, cases will require more specific work up relevant to the clinical
presentation and are not discussed here, e.g., myelography for upper neurologic
presentations.
Treatment
Almost all oropharyngeal stick injuries should be explored surgically, firstly, due to the
degree of contamination that occurs when the stick is driven into the tissues, secondly, due
to the amount of debris associated with the bark, and thirdly due to the risk of laceration of a
vital structure if removed by simple traction. A possible exception to this statement may be a
peracutely presented small oral stick injury that can be removed cleanly per os, without
debris (such as bark) being left behind. In this situation the oral and retropharyngeal tissues
may heal well by just flushing the defect and leaving the mucosa unsutured. In such a
situation, the owners would need to be fully informed about the possibility of subsequent
abscessation.
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The approach to acute penetrations is usually directly over the stick, if palpable, or the
ventral midline if non-palpable. Imaging will further aid the surgical approach. The
advantages of a surgical cut-down has been brought home to me several times over the
years where if I had applied traction on the stick to remove it, I would have lacerated major
arteries. Orbital foreign bodies are usually retrieved via a modifed lateral orbitotomy, through
the zygomatic arch.
Once the skin has been opened and explored down to the stick in acute injuries, the
resulting wound can be copiously flushed, and as much bark or other debris removed as
possible. This can take some time, and one needs to be fairly meticulous about it. The
external wound can either left open (and subsequently closed as a delayed primary or
secondary closure), or closed with drains. The oral/pharyngeal mucosa should be closed if
possible, but only if drainage of the retropharyngeal tissues is provided. Due to a poorer
prognosis associated with esophageal penetrations, they are always debrided and closed,
even if the perforation is small. It can sometimes be difficult to suture the caudal pharynx, but
sublingual penetrations can readily be closed. The use of closed suction grenades or pumps
to provide drainage of the retropharyngeal tissues is strongly recommended (unless you
cant close the pharyngeal wound), rather than passive drain systems. Be aggressive with
acute penetrating injuries, and it will avert subsequent problems associated with
chronicity.
With chronic injuries, any draining tract is usually explored by meticulous dissection using
probes and catheters. A very generous clip should be performed, extending from mid-thorax
to the mandible. The usual approach is through a ventral midline cervical incision. Be
prepared for disappointment, and manage the owners expectations in this regard. In the
literature, final outcome is not always related to the retrieval of a foreign body. Once the tract
is explored, and hopefully a foreign body retrieved (put the champagne on ice), there is
usually a very contaminated open wound. A macerated tissue culture is performed at this
time. Both aerobic and anaerobic cultures should be undertaken; and with the plant material
that has often been festering in the wound, it is prudent to take tissue cultures for
Actinomyces and acid-fast organisms such as Nocardia, Mycobacteria. These results may
prove to be useful in the final treatment of this region, and are especially indicated in the
event a foreign body is not located. The area can be fairly aggressively debrided (depending
on location), and generally managed open for a few days with negative pressure wound
therapy or wet-dry dressings, before closing with drains, or allowing to heal by second
intention.
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Post-operative course and expectations

These wounds, even once the foreign body is retrieved, are still obviously contaminated, and
usually infected, due to origin of the stick and mode of wounding (through the oral cavity).
Even following foreign body removal, continued discharge can be a problem in about 25% of
cases; fragmentation may have occurred, greatly hindering extraction of all foreign material.
Additionally, chronic granulomatous inflammatory tissue has become established and in
itself can perpetuate clinical signs of drainage. It is for these reasons that delayed closure or
healing by second intention is recommended. Revisional aggressive debridement may be
required, and this possibility should be communicated to the owners.
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CPR CURRENT RECOMMENDATIONS

Louise ODwyer MBA BSc(Hons) VTS(ECC) DipAVN(Medical&Surgical) RVN
PetMedics Veterinary Hospital, Manchester, M28 2LY, UK
louise.odwyer@sky.com
Introduction
2011, celebrated the 50th anniversary of the first articles published about CPR based on the
work of Dr. Guy Knickerbocker, at the J. Hopkins Medical School in Baltimore, Maryland,
USA.
Sadly, after more than 50 years, with an impressive advance in technology, basic science
and pharmacology, the rates of success have not improved dramatically, and still we do not
have a clear understanding about which are the best interventions and what protocols we
should adopt.
The published reports of success rates in veterinary medicine after cardiac arrest and CPR
are around 13% in dogs and 15.4% in cats, and the rate of hospital discharge following
successful CPR is < 16%.
Cardiopulmonary resuscitation is a very complex and challenging situation, and because of

that, periodic re-examination of the protocols and recommendations by experts, institutions,
and senior leaders in that field occur, leading to changes that sometimes may be perceived
as drastic. Even the name has been changed, and different denominations have been
proposed. However, by the last consensus, it seems that the term CPR is more simple and
easy to understand for everyone, even if it does not describe completely all the interventions
and manoeuvres that will be attempted.
Every five years the American Heart Association (AHA) releases International Liaison
Committee on Resuscitation (ILCOR)-based updates on CPCR - this information is a review
of the previous 5 years of research to determine if there is any new evidence that impacts
guidelines for CPCR; the AHA guidelines are available free online through the Circulation
journal. This information is primarily based on human research, and application in veterinary
medicine may be inappropriate or simply wrong. However, the good news is that a group of
very well-known and dedicated specialists and professionals put together the Reassessment
Campaign on Veterinary Resuscitation (RECOVER) in order to publish the first evidence-
based consensus CPR guidelines for veterinary medicine.
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RECOVER identified 5 areas to be investigated:
Preparedness/prevention
Basic life support (BLS)

Advanced life support (ALS)
Monitoring
Post-arrest care
Preparedness/Prevention
RECOVER recognised that training the team is critical for success and expecting the
unexpected is part of the preparation, this training should include regular drills in the training
refreshers.
CPR Team
The ideal number of participants in a resuscitation attempt is three to five. In a small
practice, when staffing is limited, it may be helpful to train the receptionists and kennel help
to be a part of the CPR team. Each person can be taught to carry out a specific task.
The team leader is usually the veterinary surgeon; if the vet is not available, then the person
with the most experience in performing CPR should lead the team. People will be needed to
provide ventilation, chest compressions, establish IV lines, administer drugs, attach
monitoring equipment, record the resuscitation effort and monitor the effectiveness of the
team's efforts. Practice a protocol for reception, intervention, and monitoring for all people
in the hospital including reception staff if necessary.
Practice drills should be held monthly. A stuffed animal can be used as the patient during
these drills. Each person should understand what his or her responsibilities would be during
an arrest. After each practice session or true resuscitation, a self-evaluation should be
performed.
Resuscitation Area
One of the first decisions to be made is where will the resuscitation attempt take place.
Some people prefer to perform CPR wherever the patient is located and bring the
resuscitation equipment and supplies to the patient. Others prefer to designate an area in
the clinic. When selecting an area, take into consideration the space available; is there
enough room for a CPR team (3 plus people) and equipment? An oxygen source should be
readily available. Good lighting is a must; it facilitates endotracheal intubation and
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visualization of veins, and, if open-chest massage is attempted, it will allow visualization of

internal structures. If CPR is to be performed on a table, then the height of the table should
be adjustable. If a table is too tall for the person performing chest compressions, he/she may
find it difficult to perform effectively. If the height of the table is not adjustable, then a
footstool should be made available or CPR should be performed on the floor. Avoid grated
surgical prep tables if at all possible. They have too much "give," which can be
counterproductive when performing chest compressions. If you have no choice and must
use a prep table, then put a board on or below the grate to provide extra support. The table
must have a solid surface. If some form of crash cart is not used, then the drugs, ECG, and
defibrillator should be in close proximity. A shelf and a few drawers may be set aside for the
emergency supplies.
Crash Cart/Kit
A crash cart/kit may be as simple as a plastic box or as elaborate as a mobile tool chest.
Crash carts/kits help to make the resuscitation endeavour more efficient by having all the
supplies readily available. If a cart is used, then in addition to the endotracheal tubes, drugs,
catheters, syringes etc., equipment may be stored on the cart such as suction machine,
ECG, and defibrillator. The crash cart or kit should be checked at the beginning of each shift
and restocked immediately after each use.
CPR Protocol
Clinic staff can respond more efficiently if a protocol is established as to how CPA will be
managed. The protocol can be organized either as a numerical list of steps or an algorithm
(flowchart). It is also helpful to have a chart of drug dosages, which is based on the patient's
body weight. If a computer is available, a program can be set up using a spreadsheet. By
entering the patient's body weight, all the emergency drug doses can be calculated, printed,
and placed in the patient's record. A drug dosage chart can also be based upon a small,
medium, large, or giant patient. The protocols should be reviewed periodically to ensure that
they are up-to-date.
Recognition of CPA
The existence of cardiac arrest must be recognized early if we are to effectively resuscitate
the patient. The ABCs should be rapidly checked in the apnoeic unresponsive patient. The
absence of a palpable pulse, audible heart sound, or effective ventilation (agonal breaths
should not be considered effective breaths); all supports the assessment of cardiopulmonary
arrest. Even under the best of circumstances it may be difficult to palpate a pulse; therefore,
not much time should be spent trying to assess pulses. If there is any question that CPA has
taken place the patient should be treated as such until proven otherwise. If in doubt
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commence CPR, time should not be wasted looking at patients checking for pulses,
auscultating the thorax or looking for respirations. In patients under anaesthesia, aggressive
CPR should be commenced ASAP; we know patients under anaesthesia have an increased
chance of survival than any other patient.
Basic Life Support
Basic Life Support (BLS) should be initiated as quickly as possible following diagnosis of
CPA using the Circulation, Airway, Breathing (CAB) concept. Circulation should be
addressed first, as ventilation will be ineffective if there is no cardiac output, and evidence
suggests that outcome worsens as delay to the initiation of chest compressions increases.
Circulation: Chest Compressions
Patients with CPA have no forward blood flow out of the heart and no delivery of oxygen to
the tissues. An immediate consequence is the exhaustion of cellular energy stores, cell
depolarization and thus loss of organ function. This quickly results in increasing severity of
ischemic organ injury and sets the stage for escalating reperfusion injury upon reinstitution of
tissue blood flow. The initial goals of chest compressions are to provide (1) pulmonary blood
flow for oxygen uptake and CO2 elimination, and (2) tissue perfusion for oxygen delivery to
restore cellular metabolic activity. Experimental evidence suggests that even well-executed
external chest compressions produce at best 30% of normal cardiac output, making proper
technique critical. Chest compressions should be started as soon as possible after diagnosis
or suspicion of CPA. Delay in the start of high quality chest compressions reduces the
likelihood of return of spontaneous circulation (ROSC). Chest compressions should be done
with the dog or cat in lateral recumbency with a compression depth of 1/3-1/2 the width of
the chest at a rate of 100-120 compressions per minute regardless of size or species. Use of
aids to ensure correct compression rate, such as a metronome or a song with the correct
tempo (e.g., Staying Alive) is recommended. Leaning on the chest between compressions
must be avoided to allow full elastic recoil. Chest compressions should be delivered without
interruption in cycles of 2 minutes, and a new compressor should take over after each cycle
to reduce the effect of rescuer fatigue. Any interruption in compressions should be as short
as possible, as it takes approximately 60 seconds of continuous chest compressions before
coronary perfusion pressure (CPP) reaches its maximum. CPP in turn is a critical
determinant of myocardial blood flow and the likelihood of ROSC.
The physiology of blood flow generation is fundamentally different during CPR compared to
spontaneous circulation. Two distinct theories exist to explain how chest compressions lead
to systemic blood flow. The cardiac pump theory is based on the concept that the left and
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right ventricles are directly compressed, increasing the pressure in the ventricles, opening
the pulmonic and aortic valves and providing blood flow to the lungs and the tissues
respectively. Recoil of the chest between compressions due to the elastic properties of the
rib cage creates negative pressure within the chest, improving filling of the ventricles before
the next compression. The thoracic pump theory is based on the concept that external chest
compressions raise overall intrathoracic pressure, forcing blood from intrathoracic vessels
into the systemic circulation, with the heart acting as a passive conduit. Given the chest wall
stiffness in medium and large dogs, blood flow generated by the thoracic pump mechanism
likely predominates in these patients. Therefore, it is recommended that the chest be
compressed over the highest point on the lateral thoracic wall with the patient in lateral
recumbency (i.e., the widest part of the chest). In contrast, in very keel chested dogs (e.g.,
sight hounds); it is reasonable to do chest compressions directly over the heart as the
cardiac pump mechanism likely predominates. In markedly barrel chested dogs (e.g.,
English Bulldogs), compressions over the sternum with the patient in dorsal recumbency
may be more effective in eliciting the thoracic pump mechanism than lateral chest
compressions. In these and other large dogs with low chest compliance, considerable
compression force is necessary for CPR to be effective. The compressor should maintain
locked elbows with one hand on top of the other, and the shoulders should be directly above
the hands. This allows compressions to be done using the core muscles rather than the
biceps and triceps, reducing fatigue and maintaining optimal compression force. If the
patient is on a table and the elbows cannot be locked, a stool should be used or the patient
should be placed on the floor.
Most cats and small dogs tend to have higher thoracic compliance and narrower chests than
larger dogs, making the cardiac pump mechanism achievable in these patients; therefore,
chest compressions should be done directly over the heart. Compressions may be
performed using the same two-handed technique as described above for large dogs, or may
be done using a single handed technique where the compressing hand is wrapped around
the sternum and compressions are achieved from both sides of the chest by squeezing.
Circumferential compressions of the chest using both hands may also be considered.
Airway and Breathing: Ventilation
If an endotracheal tube and laryngoscope are available, the patient should be intubated as
soon as possible. Both dogs and cats can be intubated in lateral recumbency, so chest
compressions should continue during endotracheal tube placement. If an endotracheal tube
is not readily available, mouth to snout ventilation will provide improved oxygenation and
CO2 removal. The patients mouth should be held closed firmly with one hand. The neck is
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extended to align the snout with the spine, opening the airway as completely as possible.
The rescuer makes a seal over the patients nares with his/her mouth and blows firmly into
the nares to inflate the chest. The chest should be visually inspected during the procedure
and the breath continued until a normal chest excursion is accomplished. An inspiratory time
of approximately 1 second should be targeted.
In non-intubated patients ventilated using the mouth to snout technique, ventilation cannot
be performed simultaneously with chest compressions. Therefore, 30 chest compressions
should be delivered, immediately followed by two breaths. Alternating compressions and
ventilations should be continued for 2-minute cycles, and the rescuers rotated every cycle to
prevent fatigue. Chest compressions and ventilations should be performed simultaneously in
intubated patients because the inflated cuff of the endotracheal tube allows alveolar
ventilation during a chest compression and interruptions in chest compressions are
minimized. Intubated patients should be ventilated at a rate of 10 breaths per minute with an
inspiratory time of approximately 1 second. If a spirometer is available, a tidal volume of
approximately 10 ml/kg should be targeted. This low minute ventilation is adequate during
CPR since pulmonary blood flow is reduced. Care should be taken not to hyperventilate the
patient, as low arterial CO2 tension leads to cerebral vasoconstriction, decreasing oxygen
delivery to the brain.
Advanced Life Support (ALS)
Once BLS procedures have been implemented, the CPR team should initiate Advanced Life
Support (ALS), which includes monitoring, drug therapy, and electrical defibrillation. Drug
therapy is preferably administered by the intravenous or intraosseous route. Therefore,
placement of a peripheral or central intravenous or intraosseous catheter is recommended,
but should not interfere with continuation of BLS.
Monitoring
Many commonly employed monitoring devices are of limited use during CPR due to their
susceptibility to motion artefact and the likelihood that decreased perfusion will compromise
accurate readings. Low yield monitoring devices include pulse oximeter and indirect blood
pressure monitors, including Doppler and oscillometric devices. The two most useful
monitoring devices during CPR are the electrocardiogram (ECG) and end tidal CO2 monitor
(ETCO2).
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Electrocardiogram (ECG)
Although the ECG is highly susceptible to motion artefact and is of limited use during on-
going chest compressions, an accurate rhythm diagnosis is essential to guide drug and
defibrillation therapy. The goal of ECG monitoring during CPR is to diagnose which of the
three most common arrest rhythms are present: (1) asystole, (2) pulseless electrical activity
(PEA), or (3) ventricular fibrillation (VF). The ECG should be quickly evaluated while
compressors are being rotated between 2-minute cycles of CPR, the rhythm diagnosis
should be called out to the group by the team leader, and differing opinions on the diagnosis
should be solicited. Discussion about the rhythm diagnosis should not prevent rapid
resumption of chest compressions.
End-Tidal Carbon Dioxide (ETCO2)
ETCO2 data can be used in multiple ways during CPR, and regardless of the technology
used is highly resistant to motion artefact. The presence of measureable CO2 by ETCO2
monitoring is supportive of (but not definitive for) correct placement of the endotracheal (ET)
tube. Because ETCO2 is proportional to pulmonary blood flow, it can also be used as a
measure of chest compression efficacy under conditions of constant quality of ventilation.
Upon return of spontaneous circulation (ROSC), ETCO2 dramatically increases due to the
rapid increase in circulation, and therefore is a valuable early indicator of ROSC during CPR.
Drugs
Epinephrine (Adrenaline) is a strong alpha-adrenergic. Alpha-adrenergic drugs work on
alpha-receptors causing arterial vasoconstriction. Diastolic blood pressure is increased,
which results in augmented coronary and cerebral blood flow. The drug also causes
constriction of large veins, which would increase intrathoracic blood volume and thus
"cardiac output." Initial doses of epinephrine should be 0.01 mg/kg (low dose). In the case of
a prolonged arrest, a dose of 0.1 mg/kg (high dose) might be considered. Epinephrine
should be re-administered every three to five minutes. To minimize under and over dosing,
epinephrine should be administered during every other BLS cycle.
Vasopressin is the naturally occurring antidiuretic hormone. In doses higher than required
for the antidiuretic hormone effect, vasopressin acts as a direct peripheral smooth muscle
vasoconstrictor. Vasopressin is an effective vasoconstrictor and may be used as an
alternative to epinephrine in the treatment of cardiac arrest. The suggested dose is 0.08
U/kg IV. It may be used as a substitute or in combination with epinephrine every threefive
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minutes.
Atropine is indicated in the treatment of asystole. It plays the central role in the prevention
and management of CPA associated with intensive vagal stimulation, which can occur
during certain surgical procedures. The recommended dose is 0.04 mg/kg given once.
Crystalloid fluids: Fluids are indicated only if the patient is hypovolemic. Lactated Ringer's
or a Lactated Ringer's-like solution is a reasonable choice. In one study, dextrose solutions
were implicated in increased morbidity and mortality in association with cardiac arrest,
therefore, dextrose should not be used. The dose of fluids in the dog is about 40 ml/kg and
20 ml/kg in the cat. The fluids should be given rapidly intravenously, in boluses sufficient to
maintain effective circulating volume. When anaemia or hypoproteinaemia is present, whole
blood or plasma or a synthetic colloid may be indicated.
Reversal agents: such as naloxone, flumazenil, and atipamezole may be considered if an

opioid, benzodiazepine or alpha-2-agonist respectively has been administered recently prior
to the cardiac arrest.
Sodium bicarbonate (NaHCO3) is used to correct metabolic acidosis, which is generated by

anaerobic metabolism in hypoxic tissues. NaHCO3 may be given empirically at a dose of 1
mEq/kg if the cardiac arrest is greater than 1015 minutes.
Calcium is not currently recommended in the routine treatment of cardiac arrest. Calcium
may be indicated when the patient is hyperkalaemic or hypocalcaemic. The dose of calcium
is 0.1 ml/kg of 10% calcium chloride or 0.4 ml/kg of 10% calcium gluconate.
Route of Drug Administration
It appears that a central vein is the best route for drug administration. With this route drugs
are administered close to the heart. Peripheral venous drug administration tends to deliver
the drug to the heart in a lower blood concentration and at a slower rate as compared to the
central venous route. Experimental studies in animals demonstrate that drug delivery after
peripheral injection is enhanced by following the injection with 1030 ml saline flushes and
elevation of the extremity. The circulation time was shorter and the peak concentration was
higher.
An alternative to intravenous is intraosseous. This route requires the placement of an

intramedullary cannula inserted into the femur (through the greater trochanter), humerus
(through the greater tubercle), and wing of the ilium or tibial crest. Medications and IV fluids
can be injected into the medullary canal and rapid uptake is provided by the abundant
endosteum-medullary blood supply.
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The intratracheal route has been advocated for drug administration when venous access is
not available. Some studies have indicated that drug uptake from the tracheal surface during
resuscitation is sporadic, undependable, and delayed. The drugs that may be administered
by this route include epinephrine, atropine, and vasopressin. If this route is to be used, then
the dose of the drug should be doubled and added to sterile saline or water for volume. The
drugs are injected down the endotracheal tube via a long catheter that extends beyond the
endotracheal tube and down to the level of the carina.
Intracardiac injections are not recommended because of the potential problems that can
occur with this route. Problems include myocardial trauma, lacerated coronary arteries,
pericardial effusion, and refractory ventricular fibrillation when the heart muscle is injected
with epinephrine. The American Heart Association recommends that this route be used
when no other is available and others feel its use is indicated only during open-chest heart
massage.
Defibrillation
Defibrillation is the treatment of choice for ventricular fibrillation (VF) and pulseless
ventricular tachycardia (PVT). If the patient has VF or PVT and the duration is less than 4
minutes or if VF is diagnosed during a rhythm check between BLS cycles, the heart is
defibrillated immediately. However, if the duration of VF or PVT has been suspected to be
greater than 4 minutes, then a 2-minute cycle of BLS must be performed prior to
defibrillation.
Following the application of a contact gel and the defibrillator charged to the desired energy
level, BLS is stopped and the patient placed in dorsal recumbency. The defibrillator paddles
are placed firmly over the heart on each side of the chest; the defibrillator is discharged after
clearing the area around the patient of people. The energy necessary for defibrillation is 46
joules/kg and 24 joules/kg for monophasic and biphasic defibrillation, respectively. The
monophasic and biphasic internal defibrillation energy level is 0.20.5 joules/kg. In the past,
it was suggested to rapidly repeat defibrillation up to three times if the patient had a
refractory VF or PVT. It is now suggested that a full 2-minute cycle of CPR be performed
before re-evaluating the ECG and defibrillating again.
The precordial thump is a method of mechanical defibrillation where the patient is struck with
the heel of the hand directly over the heart in the hopes of converting the patient. While there
is minimal efficacy for this technique, it should be considered only if a defibrillator is not
available.
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Post-Resuscitation Care
After the arrest the patient should be monitored closely. Special attention should be paid to
the cardiovascular, pulmonary, and central nervous system. It's helpful to monitor as many
parameters as possible for each system; this gives you a clear overview of the patient
status.
References available upon request.
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ISCHEMIA AND REPERFUSION INJURY

Amy N. Breton, CVT, VTS (ECC)
Veterinary Emergency and Specialty Center of New England, Waltham, MA USA
abreton@vescone.com
Introduction
Ischemia is defined as an inadequate blood supply to a part of the body, usually caused by a
partial or total blockage of an artery. Reperfusion injury occurs when tissue perfusion and
oxygenation is restored to an affected area. Ischemia-reperfusion (I/R) injury is a complex
cascade of events which results in devastating effects to the body including death.
The Ischemic Cascade
The I/R injury chain of events can be broken down into two parts: ischemic cascade and
reperfusion injury. A series of events occurs during an ischemic event, which make up the
ischemic cascade. Within five minutes of ischemia occurring, disturbances in cell
electrolyte balance start. The ischemic cascade usually goes on for two to three hours, but
can last for days, even after perfusion is restored to the affected area.
In order to fully understand the ischemic cascade, it is important to remember adenosine

triphosphate (ATP) and how it functions. ATP is a multifunctional nucleotide (structural
factor of DNA and RNA) which is considered the most important nucleotide responsible for
transporting energy within a cell for metabolism. One of the fastest ways ATP is produced is
by a process called oxidative phosphorylation, thus denoting that ATP needs oxygen in order
to be produced. Despite the importance of ATP, cells do not stockpile it. When ischemia
occurs, oxygenation to cells ceases and therefore the formation of ATP occurs through the
less efficient anaerobic production.
When oxygen becomes unavailable to the cells an anaerobic glycolysis starts. This can be a
lifesaving way for the cells to obtain energy, however this process is extremely wasteful.
During the anaerobic process pyruvic acid and hydrogen atoms combine with nicotinamide
adenine dinucleotide (NAD) to form NADH and H+. If the buildup of NADH and H+
becomes too large, then the anaerobic process would stop, thus stopping the energy
production to the cells. However, NADH and H+ combine together to form lactic acid, which
diffuses into the cells rapidly so that the process can continue. If this process goes on for
too long, as in the case of ischemia, lactic buildup can occur which indicates worsening
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illness. As a consequence of lactic acidosis pH will decrease, which will injure and inactivate
mitochondria. There is some thought that lactic acid may also interfere with the recovery of
ATP post-ischemia. With any ischemic patient, a lactate level should be obtained. Values
under 2mmol/L are normal. Death itself is an ischemic event because death will cause an
oxygen deprivation to the tissues. Lactic acid buildup is the major cause of rigor mortis.
When the formation of ATP fails, the cells become depolarized, which causes calcium and
sodium (normal extracellular electrolytes) to enter the cells. Potassium (normally found in
the cells) starts to leak rapidly into the extracellular space. Excessive calcium overexcites
the cells, which in turn, creates free radicals and many calcium-dependent enzymes. The
amount of ischemic damage is often due to the amount of calcium that enter the cells as well
as the duration of time it stays in the cells. The longer calcium stays in the cells, the greater
the amount of harmful chemicals it can create.
One of the most important events involving calcium is the conversion of xanthine
dehydrogenase (XDH) to xanthine oxidase (XO). Xanthine oxidase does require oxygen to
be activated. During ischemia oxygen is not present, so XO accumulates without getting
used. It is later during reperfusion that XO causes damage to the cells.
As the mitochondria break down, they release toxins causing apoptosis. Apoptosis is the
bodys way of safely disposing of dead cell parts and is essentially the cells destroying
themselves. One of the other important events during ischemia is that nuclear factor-kB
(NFkB) is activated, which leads to the production of inflammatory mediators. Nuclear
factor-kB becomes activated during times of stress. NFkB will activate inflammatory
cytokines and their receptors, as well as platelet activating factor. This allows for neutrophils
to enter through the endothelium. The neutrophils that are activated are generally stiffer
because of the hypoxia and acidosis which occurred. Because of the alteration of the cell
membrane and the sheer number of neutrophils, capillary plugging may occur. This is where
neutrophils will clog up the capillaries. Even after reperfusion, the distribution of blood back
to the affected area may not produce enough force to clear the clog.
Reperfusion Injury
Despite the harsh effects that ischemia alone has on the body, it does not cause nearly as
much damage as reperfusion does. The longer the onset of the ischemic event; the greater
the insult.
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One of the first events is that oxygen can finally bind with XO that had been building up
during ischemia. Xanthine oxidase combines with oxygen and hypoxanthine to form
superoxide (O2-), a radical. Superoxide is not that damaging, but it can inactivate iron-sulfur
containing enzymes, thereby liberating free iron in the cell, which can generate the highly
reactive hydroxyl (-OH) radical. Hydroxyl is considered a reactive oxygen species (ROS).
Free radicals are radicals that have moved from the vicinity where they were created. Free
radicals are highly reactive and are usually involved in chemical reactions. A reactive
oxygen species (ROS) is an oxygen containing molecule which may or may not be a free
radical, but is very active chemically. ROS molecules will react quickly with other molecules.
At high levels they have the ability to damage cellular macromolecules, such as DNA and
RNA, as well as cause endothelial injury, microvascular dysfunction and apoptosis (cell
death). Formation of ROS can occur in 10 to 30 seconds after the onset of reperfusion.
During ischemia, neutrophils start to leak into the endothelium because of the activation of
NFkB as well as XO. Reperfusion accelerates the influx of neutrophils to the affected area.
They respond because of the inflammatory response which takes place. Neutrophil
activation itself can lead to the formation of even more ROS. The inflammatory cascade is
kicked into high gear during reperfusion. In short, neutrophils and macrophages start to
attack the reperfused tissues. Inflammatory cytokines are released from the activation of
neutrophils. Cytokines are small secreted proteins which help to mediate an inflammatory
response and are released from the activated monocytes, macrophages and neutrophils.
When the body becomes overwhelmed with inflammatory cells, the result can cause a
cytokine influx (hypercytokinemia), resulting in a continuous loop between cytokines and
immune cells in which too many cytokines are made. The exact mechanism behind this is
not fully understood.
COMPLICATIONS OF I/R INJURY
The ischemic insult sets the body up for a damaging chain of events, while reperfusion
actually sets the chain of events into motion. The end result can be overwhelming, and
while death occurring directly from I/R injury is still debated, I/R injury can definitely set the
body up for events which lead to death.
Disseminated Intravascular Coagulation (DIC):

DIC is a pathological process where the blood starts to coagulate throughout the whole
body. The end result is that it depletes the body of platelets and coagulation factors, causing
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the body to be at risk for increased bleeding. Petechiae, ecchymoses and excessive
bleeding are often noted with DIC. DIC can be triggered whenever there is a major
disruption in the intravascular system. In the case of I/R injury, when the endothelial cells
are damaged, it exposes substances that activate the clotting cascade. Eventually an
unbalance occurs between clotting and bleeding, which is DIC. DIC can also occur because
the low pH will inhibit heparin and antithrombin III. Both are needed for appropriate
coagulation to occur.
Systemic Inflammatory Response Syndrome (SIRS):

The cytokines produced during reperfusion injury act as the mediators of SIRS. SIRS is an
inflammatory response of the entire body and can result in death. The diagnosis of SIRS
can be made if the animal has two or more of the following criteria:
Heart rate: >160 bpm in the dog and >250 bpm in the cat or < 140 bpm in the cat
Respiratory rate: >20 bpm in the dog and >40 bpm in the cat
White blood cell count: >12,000 or <4,000 or > 10% bands
Multiple Organ Dysfunction Syndrome (MODS):

Just as it sounds, it is the altered organ function of two or more organ systems. MODS is
usually a response to the damaged endothelial cells from the overwhelming numbers of
cytokines. MODS usually occurs as a complication from sepsis or SIRS, however in 1/3rd of
human patients no primary cause for MODS could be found. If MODS occurs in conjunction
with SIRS, the prognosis becomes very poor. The number of organs involved decreases the
chances of survival.
Rhabdomyolysis:
Rhabdomyolysis is the rapid breakdown of muscle fibers due to traumatic injury to the
skeletal muscles.
The principal result is the release of muscle fiber contents, such as myoglobin, into the blood
stream. Myoglobin is then circulated through the bloodstream and eventually through the
kidneys where it blocks the structures of the kidneys causing acute tubular necrosis or
kidney failure. Ischemia to the muscles can predispose the body to rhabdomyolysis.
Interestingly enough, in human medicine, the hypoxia associated with giving propofol has
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been shown to cause several children and adolescents to develop rhabdomyolsis.

Treatment must be aggressive in order to help the kidneys eliminate the myoglobin.
TREATMENT
There is no known definitive cure for I/R injury. Many doctors and scientists agree that if
we can stop the key components of the ischemic cascade we can likely stop the effects of
I/R injury. Most also agree stopping the cascade at the earliest possible point would
produce the best results.
Treatment has been focused on blocking the formation of ROS, blocking calcium production,
as well as stopping the production of neutrophils.
ROS Formation:
Dimethylsulphoxide (DMSO) is an effective scavenger of the hydroxyl radical. It can

penetrate membranes, such as the mitochondria, to act at intra-cellular sites of free radical
production. In veterinary medicine there have been mixed studies regarding the efficacy of
DMSO. This is because DMSO can cause methyl radicals and methylperoxy radicals when
it scavenges the hydroxyl radical. While these other radicals are not as potent they still have
the ability to cause injury to the cell membranes. How much injury they cause is unknown
which is why the efficacy of DMSO for the treatment of I/R injury is largely unknown.
In the past several years both human and veterinary researchers have had several
promising studies using N-acetylcysteine (NAC). NAC is a powerful scavenger of the
hydroxyl radical. While most studies involving rats, rabbits and mice have all shown to be
promising regarding this drug, the most recent veterinary related study in 2008 showed that
the use of NAC failed to decrease the effects of I/R injury in the liver in the canine model.
Though most studies do appear promising it is clear that more research needs to be done.
Deferoxamine (DFO) has been studied for over 20 years in human medicine and is now
being looked at in veterinary medicine. Research has shown promising results in both fields
with one of the most recent study in 2009 showing that DFO helped to significantly protect
the rat in cases of ischemic stroke. This is because DFO is an iron chelator and therefore
inhibits the hydroxyl radical to form.
Allopurinol is capable of inhibiting xanthine oxidase from forming and also aids against
neutrophil infiltration. Unfortunately the best results have been when it has been used as a
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pretreatment against I/R injury. Since it is almost impossible to predict when I/R injury will
occur in veterinary medicine it makes it less than ideal to use.
Other Options:
Lidocaine may prove to be a safe and cost effective treatment option against I/R injury in
veterinary medicine. Lidocaine may act as a sodium and calcium channel blocker, ROS
scavenger and an inflammatory mediator. Since lidocaine also has beneficial analgesic
properties some literature supports starting all at-risk post-op veterinary patients on it until
there are no longer signs of pain, shock or ileus (such as in the case of GDV). Ketamine
may also prove to be a cost effective and safe treatment against I/R injury. Ketamine inhibits
NMDA receptors, as well as reduces the adhesion of neutrophils and decreases the cytokine
production.
Similar to lidocaine, ketamine also has analgesic properties and is frequently used in
veterinary medicine in post-surgical constant rate infusion analgesic combinations such as
morphine-lidocaine-ketamine. It may be that ketamine can be used in a similar fashion for
those post-surgery patients that are at-risk for developing side effects from I/R injury.
A study in 2008 suggested that prednisolone may suppress hepatic I/R injury. Steroid
therapy has been proven to help suppress liver injury by an increasing tissue blood flow and
suppression of oxygen free radicals and cytokine production. The study results showed that
prednisolone can help to prevent I/R injury in the rat liver. Throughout the history of
ischemia/reperfusion injury there has always been some debate as to whether steroids are
beneficial. This latest study has re-opened the debate.
The use of colloids may have some benefits in reducing the I/R injury effects. This is likely
because high molecular weight colloids can help to decrease microvascular permeability.
There have been numerous positive studies with evidence to show that high weight
molecular fluids may play a role in the treatment of I/R injury.
Lastly, therapeutic hypothermia has been in the news because it has been shown to help
minimize the harmful effect of the inflammatory cascade as well as decrease the production
of ROS during reperfusion. While this has yet to be applied in veterinary medicine, it may be
something for the future. In 2007 Dr. Lance Beckers research from the University of
Pennsylvania was released showing cooling the body during cardiac arrest increase the
chance of survival by 16%. Since 2007 an injectable ice/salt mixture has been created which
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allows emergency personal and paramedics to quickly cool human patients to help slow and
even prevent the effects of I/R injury.
References available on request
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Notes page
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BAD ADRENALS: HYPO- AND HYPERADRENOCORTICISM

Veterinary Emergency & Specialty Center of New England, Waltham, MA USA
abreton@vescone.com
Adrenals
The body contains two adrenal glands, with one lying close to each kidney. The adrenal
glands are part of the endocrine system and help to produce several hormones.
Glucocorticoids are released by the adrenal glands and are regulated by adrenocorticotropic
hormone (ACTH) from the pituitary gland. The term corticosteroids are applied to hormones
of the glucocorticoid class (those that affect glucose) that are released from the adrenals.
The most important corticosteroids produced are cortisol and corticosterone. They help
increase blood glucose levels by reducing glucose uptake in the cells, aid in
gluconeogenesis and help to convert fatty acids back to glucose. When there is an
excessive amount of corticosteroids the inflammatory and immune process can be reduced
which can lead to poor healing. This process is known as hypoadrenocorticism (Cushing's
Syndrome/Disease). A decrease in production is known as hypoadrenocorticism (Addison's
Disease).
The adrenals also produce aldosterone; a mineralocorticoid (affects "minerals" also known
as electrolytes) which regulates acid/base function of the kidney. It also helps to control the
excretion of sodium, chloride and potassium.
Lastly the adrenal glands are responsible for producing both male and female sex hormones
and while they produce seemingly insignificant quantities, it may explain why some animals
still display some level of sexual behaviour even after being neutered.
The body regulates cortisol through a negative feedback loop. When cortisol is needed
due to a stressful situation in the body, the hypothalamus signals the pituitary gland to
release ACTH. This signals the adrenal glands to produce cortisol. As cortisol levels rise
in the body it causes the hypothalamus to decrease its signal to the pituitary gland. This
causes less ACTH to be produced which therefore decreases the release of cortisol.
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Adrenal insufficiency
The production of mineralocorticoids and/or corticosteroids becomes decreased. The cause

of the decrease can be from bacteria or parasitic agents (histoplasma, cryptococcus)
causing inflammation in the adrenals, haemorrhage (Waterhouse-Friderichsen syndrome
due to massive sepsis), neoplasia, iatrogenic causes or may be idiopathic. Most dogs
diagnosed with hypoadrenocorticism are young to middle aged females (mean 45 years).
Certain breeds seem to have a higher risk: Standard Poodles, West Highland Terriers,
Bearded Collies, Great Danes, Portuguese Water dogs, Labrador retrievers, Rottweilers,
and Wheaton Terriers.
Roughly 90% of the adrenal function is compromised once clinical signs finally become
evident. As the mineralocorticoids are decreased the sodium, chloride and potassium levels
within the body become unregulated. The kidneys no longer secrete appropriate amounts of
potassium which leads to hyperkalaemia. The renal tubules do not reabsorb sodium and
chloride as well resulting in both being excreted rapidly in the urine. Aldosterone has a
direct effect on the extracellular fluid because of a direct relationship with how much sodium
is reabsorbed or excreted. Conversely, in the patients with hypoadrenocorticism
extracellular fluid volume will decrease as sodium decreases, thus causing the patient to
become dehydrated. Any small change in sodium, even by a few milliequivalents on blood
work, will stimulate thirst and water intake.
The hyperkalaemia will often cause ECG changes resulting in high-peaked T waves and
bradycardia. It can also cause abdominal pain, weakness (due to the cardiac effects), and
diarrhoea and in severe cases flaccid paralysis of the limbs, respiratory paralysis, circulatory
and cardiac failure.
As the sodium decreases the pet will become depressed, lethargic and cerebral oedema
may occur. Seizures and coma may occur though these signs are often a reflection of how
fast the sodium declined rather than the actual concentration. If the sodium decreases slow
enough the pet may have few clinical signs.
As the corticosteroid levels decrease gluconeogensis may not occur which can result in a
mild to moderate hypoglycaemia; leading to more lethargy of the pet.
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Overproduction
With hypoadrenocorticism the production of mineralocorticoids, corticosteroids and/or sex

hormones becomes increased. The most common cause of the increase is due to a
cortocotroph adenoma or hyperplasia of the pituitary gland. The cortocotroph are the cells
of the anterior lobe of the pituitary gland that produce adrenocorticotropic hormone (ACTH)
and is known as pituitary-dependent hyperadrenocorticism (PDH). This accounts for 85-90%
of all dogs with Cushing's Disease. The adenoma of the pituitary gland causes bilateral
adrenal cortical hypertrophy and hyperplasia. While not as common it can occur in cats.
Functional adrenal gland neoplasia (most commonly due to a pheochromocytoma) is rare
and accounts for only 10-15% of the cases. Tumours of the adrenal gland causing
hyperadrenocorticism are known as adrenal tumour hyperadrenocorticism (ATH). Rarely
Cushing's can occur due to an iatrogenic cause from the excessive use of glucocorticoids.
Poodles, dachshunds, beagles, German shepherds, and many terrier breeds are
predisposed to developing Cushing's though no genetic link has been found at this time.3 A
familial predisposition is particularly noted in the Dachshund. The median age of dogs with
pituitary-dependent hyper-adrenocorticism is 10 years. Dogs with adrenal tumours causing
Cushing's Disease tend to have a median age of 11.3 years. Females are slightly more
predisposed than males (60% vs. 40%). While there are no studies proving a correlation
between weight and developing Cushing's Disease roughly 75% of dogs will weigh less than
9 lb. (20 kg).
Hypoadrenocorticism
Signs/symptoms
Hypoadrenocorticism may occur acutely or chronically. If the pet has time to get use to the
shifting electrolytes and decrease in hormones then they typically present with more non-
descript signs: weight loss, hypothermia, shivering, weakness, anorexia, lethargy, vomiting,
polyuria and polydipsia. Some patients will also have weight loss, diarrhoea and melena.
Cats typically experience lethargy, anorexia, vomiting, weight loss, polyuria and polydipsia.
When the body does not have a chance to get use to the decreases in hormones the pet
typically presents with severe dehydration, hypovolemic shock, and bradycardia.
Upon presentation pets are usually depressed and at least mildly dehydrated.
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Pets that experience an acute onset of hypoadrenocorticism will often present with signs of
hypovolemic shock: pale/tacky oral membranes, decreased capillary refill time, weak pulses,
bradycardia, shaking, collapse, seizures or coma. These patients require emergency
treatment.
Diagnosis
A complete blood count (CBC), blood chemistry panel, electrolyte panel, blood gas and
ACTH stimulation test are all necessary if Addison's is suspected.
Typically a mild anaemia may be present, but may be masked by dehydration. The CBC is
typically normal. On a blood chemistry a hyponatremia, hyperkalaemia and a
sodium/potassium ratio less than 27:1 is usually present. Azotemia, hypocalcaemia and
hypoglycaemia are present in about 30% of pets. Pets may also experience metabolic
acidosis and have a urine specific gravity < 1.030.
Definite diagnosis requires the adrenocorticotropic hormone (ACTH) stimulation test. ACTH
is a hormone produced in the pituitary gland that stimulates the adrenal glands to release
cortisol and aldosterone. During the test, a small amount of synthetic ACTH (cosyntropin,
cortrosyn) is injected either IM or IV, and the amount of cortisol the adrenals produce in
response is measured. In pets with hypoadrenocorticism, both the pre- and post- ACTH
cortisol concentrations are usually less than 1 g/dL, with some references stating that
under 2.5 g/dL is diagnostic.
Treatment
An adrenal crisis is an acute medical emergency and requires the staff to work quickly in
order for the patient to have the best chance of survival. Patients may present weak, ataxic,
shaking, non-responsive and in shock. Dealing with the Addisonian crisis requires treating
the patient's shock. Focus should be on treatment the hypotension and hypovolemia.
A short, large gauge intravenous (IV) catheter should be placed and fluid therapy started.
Since the patient is usually hypotensive and vasconstricted blood should be removed from
the IV catheter once it is placed, as subsequent venipuncture may prove challenging. If
hypoadrenocorticism is suspected then 0.9% sodium chloride (NaCl) should be considered
choice because it offers a higher amount of sodium and lower amount of potassium
compared to other isotonic crystalloids (Lactated Ringer's solution (LRS), Normosol-R
(Norm-R)). Any balanced isotonic crystalloid is an acceptable fluid choice in most Addison's
disease patients.
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Patients with severe hyperkalaemia (severe bradycardia, ECG abnormalities), should be

given regular insulin and dextrose to help decrease serum potassium levels. Calcium
gluconate can also be given. While it does not decrease serum potassium levels it does
protect the heart against the effects of hyperkalaemia. Typically these treatments are not
needed as serum potassium is usually lowered fast enough through the dilution effects from
the IV fluids.
Bicarbonate therapy is usually not necessary as the metabolic acidosis is usually mild.
However, if the bicarbonate level remains less than 12 mEq/L even after fluid resuscitation,
the bicarbonate administration should be considered.
If the patient is stable or after they are stabilized the focus should shift to providing
glucocorticoid replacement. All glucocorticoids react with the ACTH stimulation test except
dexamethasone. Ideally blood for the ACTH test should be performed before glucocorticoids
are given. If the patient is not stable before the ACTH test can be completed then
dexamethasone sodium phosphate should be given IV. Dexamethasone is long acting,
about thirty times more potent than hydrocortisone, but offers no mineralocorticoid activity.
If the pet is stable enough for the ACTH test to be completed then prednisolone sodium
succinate is the glucocorticoid of choice. Prednisolone is a glucocorticoid that has some
mineralocorticoid activity. Some suggest hydrocortisone sodium succinate be administered
instead of prednisolone because of its combination of mineralocorticoid and glucocorticoid
activities. Hydrocortisone has only 25% of the glucocorticoid potency of prednisolone, but
offers more mineralocorticoid effects than prednisolone.
Other treatments should be tailored to the pet's condition. Patient may need to be started on
dextrose supplementation if they are hypoglycaemic. Antibiotics should be considered in
patients with severe melena or hemorrhagic diarrhoea. Antiemetics can be administered to
help combat nausea and vomiting. Colloids may need to be administered in patients with
hypoalbuminemia and hypotension.
Nursing care
Patients should be monitored for signs that they are not responding to the glucocorticoid
therapy. This may include weakness, lethargy, anorexia, vomiting, ataxia, hypotension
and/or tachy- or bradycardia. Physical exam parameters (heart rate, pulse, respiratory rate,
effort, mucous membranes, capillary refill time) and blood pressure should be checked every
2-6 hours depending on how critical the pet is. If the patient was experiencing ECG
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abnormalities then they should be placed on continuous ECG monitoring or have periodic
ECG checks minimally every hour or two.
Pets should be weighed twice a day to monitor rehydration. Urine output should also be
monitored to ensure the kidneys are functioning properly as well as for fluid therapy. Due to
the severity of dehydration urine output may be lower than volume input because until the
pet is adequately hydrated.
Blood pressure is extremely important in hypoadrenocorticism patients and should be

monitored minimally every 4-6 hours. Normalization of blood pressure, defined by a of MAP
of 80-120 mmHg or systolic between 110-160 mmHg, is goal.
Electrolytes, renal function and glucose should be all monitored regularly to assess the
response to the glucocorticoid therapy.
Lastly it is important that patients must be given appropriate nutrition. Nurses need to tempt
patients to eat and alert the veterinarian if the patient is nauseas or experiencing vomiting.
Long term care
With diligent monitoring by the owner and appropriate medication hypoadrenocorticism has a
good prognosis. Therapy is required for life and dosage may need to be altered throughout
the pets lifetime.
Patients will need to be given both mineralocorticoid and glucocorticoid supplements the rest
of their lives. Oral prednisone or prednisolone is the glucocorticoid treatment of choice in
both dogs and cats. In times of stress the prednisone may need to be increased. It is
important that the dose is tapered to the lowest effective dose as high doses may result in
hyperadrenocorticism. The decision to use glucocorticoids is based mainly on
gastrointestinal signs.
The main option for mineralocorticoid replacement in the United Kingdom is fludrocortisone
acetate (Florinef). Only 50% of dogs on fludrocortisone require supplemental prednisone.
Fludrocortisone is dosed orally and is given twice a day. It contains both glucocorticoid and
mineralocorticoid properties.
In the United States the options for mineralocorticoid therapy are fludrocortisone acetate or
desoxycorticosterone pivalte (DOCP). If available, the most economical option is DOCP
(Percorten-V, Novartis) which requires the pet to have an injection every 21-30 days. It
does not have any glucocorticoid activity. Almost all dogs on DOCP require prednisone at
least every other day. Both DOCP and fludrocortisone should be tapered to effect.
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Hyperadrenocorticism
Signs/symptoms
Hyperadrenocorticism is a chronic disease process. Signs/symptoms occur because of the

long term high doses of the naturally occurring corticosteroids. While signs rarely, if ever,
cause an emergency for the pet, they do play a role in decreasing the quality of life.
Appetite is often increased as a result of either the increase in corticosteroids or the damage
caused directly to the hypothalamic appetite centre as in the case caused by neoplasia.
Owners will often report their pets as ravenous and pets who normally do not ingest foreign
material or raid garbage cans may start doing so.
Approximately 80-85% of pets will display polyuria and polydipsia. This often leads to pets
having accidents in the house which frequently prompts the owner to bring them in for a
veterinary consult.
Pets will develop muscle weakness due to the high cortisol levels which, in turn, weakens
the muscle of the abdomen until they start to atrophy. This results in abdominal distension,
curving of the spine (lordosis) and muscle trembling. The liver will increase in size due to the
increase deposits of lipid and glycogen into the liver which adds to the increase in abdominal
size and distension.
Pets with Cushing's will often be poor healers and have skin disease. Cushing's should be
suspected in pets that have poor hair growth, balding, thin skin and pyoderma. The skin
disease is often a result of the catabolic action of excessive cortisol which causes certain
proteins, such as collagen and elastin, to be molecularly changed.
While rare, cats will often develop the same symptoms as dogs. However, only 10% of dogs
with Cushings disease develop diabetes mellitus while 80% of cats will develop diabetes
mellitus.
Approximately 80% of dogs will develop hypertension. Despite treatment approximately

40% remain hypertensive despite adequate control Cushing's disease. If the hypertension is
significant treatment should be considered.
Rarely pets will develop respiratory changes which can include tachypnea and even more
rare, pulmonary thromboembolism. The thought is that the increase in abdominal fat,
generalized weakened muscles (including respiratory muscles) and enlarged liver can all
lead to respiratory disturbances. Pulmonary thromboembolism may occur due to the
decrease level of antithrombin III and the increase of several other factors and fibrinogen.
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Diagnosis
A sterile urine culture should be obtained and submitted to a laboratory for a urinalysis and
culture. Most commonly dogs with Cushing's disease have a lower urine specific gravity of
less than 1.020. The exact cause of the dilution is unknown, but it is suspected it's due to
cortisol's effect on the antidiruetic hormone. Approximately 50% of dogs will have a urinary
tract infection.
A urine cortisol and creatinine ratio (UC:CR) has been found to be a good screening test for
dogs because it requires just a free catch urine. Stress can cause false elevations in urine
cortisol levels so owners are often instructed to catch samples at home. Because there are
numerous other diseases that can cause elevations in UC:CR it is more important to note
that a negative test can be good in helping to rule hyperadrenocorticism out. An elevated
test will need further testing to diagnose the cause of the elevation.
The most common tests that truly diagnose hyperadrenocorticism are the ACTH stimulation
test and the low dose dexamethasone suppression test (LDDST). Neither test is 100%
specific and therefore incorrect diagnoses can occur when running either test. It is important
therefore, that the test results are looked at with the full diagnostic picture.
The LDDST test (sensitivity 95%) is based on the negative feedback system between the
pituitary and adrenal glands. In normal dogs, the administration of dexamethasone will
cause the pituitary gland to decrease its secretion of ACTH which, in turn decreases the
release of cortisol. In pets with Cushing's, there will be no change in the level of cortisol
after the administration of dexamethasone. To perform an initial blood sample is taken as a
baseline. Dexamethasone is administered at a usual dose of 0.01 mg/kg of IV. Post
administration samples are drawn at 4 and 8 hours, though many references suggest that
just an 8 hour post is necessary. Obtaining a 4 hour allows for more information. The
LDDST test will not be accurate in where iatrogenic hyperadrenocorticism is the cause may
be falsely positive or negative. The LDDST is the test of choice for diagnosing feline
hyperadrenocorticism thought the test is performed using a higher dose of dexamethasone
(0.1 mg/kg IV).
Much like diagnosing hypoadrenocorticism, the ACTH stimulation test can be performed to
diagnose hyperadrenocorticism. If sample results come back with the post-ACTH 1822
g/dL it is possibly Cushing's. Samples with post-ACTH >22 g/dL are consistent with
Cushing's. Studies have shown this test to be between 73-95% sensitive.
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Even after blood tests it may be necessary to perform a high-dose dexamethasone

suppression (0.1mg/kg IV), endogenous ACTH concentration and/or abdominal ultrasound
to discriminate between PDH and ATH. Abdominal ultrasonography is very beneficial in
helping to determine the cause of hyperadrenocorticism. In one study of 71 dogs with
adrenal tumours approximately 86% of the cases were diagnosed correctly. Computer
tomography is better at diagnosing and evaluating adrenal glands, but it is not 100%
accurate either due to the size of the tumour and/or adrenal glands.
Treatment
Ultimately treatment is based on the cause of the hyperadrenocorticism. Pets that are
treated appropriately live long productive lives. Ultimately the treatment is based on the
severity of the disease, cost/affordability and owner compliance.
Mitotane (Lysodren) is the most common treatment for hyperadrenocorticism in dogs. It is a

derivative of an insecticide and works by causing necrosis in two out of the three layers of
the adrenal glands that release glucocorticoids. Mitotane can be used to treat either PDH or
ATH. There are two phases: Induction and Maintenance. After the initial induction phase
recheck ACTH levels are checked to see how the pet is responding to the medication. Pet
owners should watch for signs of anorexia, diarrhoea, vomiting, lethargy and weakness.
These signs occur due to the rapid decrease in serum cortisol levels. Owner should contact
their veterinarian immediately if they notice these signs. Approximately 25% of dogs may
exhibit signs. Adverse effects of mitotane include GI upset, hepatotoxicity, CNS toxicity, and
development of transient or permanent decrease in cortisol production.
For pets with PDH an adrenalectomy may be considered if they did not respond well to
medical management. Post-surgery replacement glucocorticoid and mineralocorticoid
therapy is begun and continued lifelong. A pet with an adrenal tumour may require surgery
unless it is nonresectable. Adrenalectomy is the preferred treatment of ATH because it
offers a potential cure. On average survival times have ranged from 2 months to more than 3
years. If complete surgical resection of a solitary pheochromocytoma is performed a cure
may be achieved. Mitotane may be used in patients with ATH in lieu of surgery or until
surgery is performed. Pets with other underlying disorders (clotting disorders, diabetes) are
not surgical candidates. Pets undergoing an adrenalectomy need a preoperative work up
that includes blood work and radiographs. Corticosteroids should be administered before
and after surgery and if both adrenals were removed then glucocorticoids and
mineralocorticoids will need to be administered for the life of the pet. Post operatively the
pet needs to be closely monitored with particular attention to electrolytes (sodium and
potassium) occurring.
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Trilostane, a synthetic inactive steroid, has also been successfully used to treat
hyperadrenocorticism by blocking the production of cortisol, aldosterone and sex hormones.
There is less literature and studies regarding trilostane and therefore it is not used as
commonly as mitotane. That being said it is thought to be comparable to mitotane with
regards to efficacy. An initial dose is usually given and recheck ACTH levels are performed.
The pets response to decreasing cortisol levels are monitored the same as when giving
mitotane.
Ketoconazole is an antifungal agent that works to decrease cortisol levels by inhibiting the
enzymes needed for glucocorticoid synthesis. Unlike mitotane and trilostane, ketoconazole
may cause a change in coat colour. Rare reported side effects include transient decreases
in cortisol levels, GI upset, and hepatotoxicity. It is administered indefinitely unless side
effects are noted or it is not considered effective.
Conclusion
As a veterinary technician it is important to understand signs, testing and treatment options

for adrenal disease. Often times owners dismiss may signs as "old age" or "they are just a
little off" not realizing the can help improve their pet's quality of life. Ultimately if owners are
diligent pets with adrenal disease can live long productive lives with treatment. Being able to
talk to owners about the disease and treatment will help improve owner compliance and
understanding which will help to improve the pet's prognosis.
References Available Upon Request
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GETTING A DIAGNOSTIC STUDY: PITFALLS AND TIPS FOR EXCELLENCE

IDEXX Telemedicine
The technical aspects of achieving a diagnostic radiographic study are easily overlooked,
particularly when presented with an emergency situation or an uncooperative patient.
However, if radiographs are of poor quality, through technical difficulties, poor positioning or
patient factors, the end result can be a study that is of limited diagnostic use. At worse,
critical lesions may be missed or a false diagnosis made. This can happen in general
practice and in top end referral practice. This lecture provides information for veterinary
surgeons and veterinary nurses on ensuring that diagnostic studies are obtained. It will be
illustrated with many examples from clinical practice, as well as brief practical
demonstrations aimed to avoid the pitfalls of radiology in general practice.
Get the patient ready

Even in an emergency the time taken to prepare the patient for the study will avoid the need
to repeat the radiographs, or accept a non-diagnostic study. Collars or harnesses should be
removed if covering the region of interest. Patient restraint is very important. If the patient is
un-cooperative the chances are that the positioning will be poor and the study may be
wasted. Sedation can greatly help in positioning, and in some cases (such as skull
radiographs) general anesthesia may be necessary. However, sedation is not always an
option for medical reasons, or due to client concerns. With many patients this would risk
producing a non-diagnostic or misleading study. However, it is possible in some
circumstances to position and restrain an awake patient and achieve good positioning, at
least for studies of the thorax and abdomen, with a few positioning aids.
Positioning Aids
Accurate positioning for radiographs is arguably the most important part of achieving a
diagnostic study, but may be the most challenging. Certain aids can massively reduce the
difficulty in restraint and correct positioning. They can also make the patient more
comfortable (reducing movement) and can help keep anesthetized patients warm!
Radiolucent foam troughs and foam pads can be used in the region of interest, and
sandbags are extremely helpful in patient restraint. Ties can be used for limb positioning.
This doesnt necessarily require much investment and homemade devices can work! With a
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co-operative assistant patient some methods of patient restraint will be demonstrated during
the lecture.
Positioning
The exact position required depends on the study that you are taking. There are several
excellent texts that relate to accurate positioning for each study, and I will not go in to detail
here. The rules are that the patient should be as straight as possible, and the entire region
of interest included, with the radiograph ideally collimated to that area. The region of
interest, such as in musculoskeletal imaging, should be parallel to the x-ray beam. Clinical
examples will be used to illustrate the effect that poor patient positioning can have on
diagnosis. Many of these may result in a false diagnosis of pathology, such as fracture.
Technique
Everyone is familiar with underexposed or overexposed radiographs. It is easy to accept this
as standard when it can result in poor quality radiographs. Although there is a wider range of
techniques that result in acceptable digital radiographs, an overexposed digital radiograph is
in some ways worse than an overexposed film screen radiograph, which can be reviewed
using a bright light. Overexposure in digital systems results in complete loss of data which
could be misinterpreted as free gas or lysis. Having a good technique chart for your system
can avoid this fundamental error.
Kilovoltage peak (kVp) indicates the penetrating power of the x-ray. The milliamperage / time
(mAs) determines the intensity of the primary beam. As a general rule the shortest time
possible should be selected to avoid motion artifact. If it is not possible to select time and mA
separately, an increased kV can be used to compensate for a lower mAs. A 15% increase in
kVp is equivalent to approximately a 50% increase in mAs. Particularly for abdominal
studies a lower kVp is ideal though, as this improves contrast resolution.
Grids should be used for any area thicker than 10cm. These reduce the amount of scatter
radiation that reaches the film and improve the quality of the study. The use of a grid
necessitates an increase in kVp.
Technique charts
Every practice should have a technique chart set up for their system. This should be
available to anyone who is taking radiographs. If one is already in place, it is worth reviewing
it periodically to ensure that the best possible images are obtained. It is relatively easy to
review your technique chart, and is strongly recommended if you are starting to see over-
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exposed (too dark) or under-exposed (too light) radiographs. As screens age it will be
necessary to update your charts. The following is an indication of how you can produce or
update your technique chart:
1. Select your mAs. Approximate mAs may be:

a. Extremity (table top, no grid) 2.5mAs
b. Thorax 5mAs
c. Abdomen 7.5mAs
d. Spine 10mAs
This is for a medium screen/film combination. For a slow (detail) combination
use double, and for a high speed combination approximately half.
2. Select your initial kVp. This is going to be approximately 2 x tissue thickness
(cm) + FFD (film focus distance, usually 40) + grid factor. Most grids are 8:1 for
which you add 8-10 kVp.
3. Expose a film. For an abdomen measuring 10cm thick you would use
(2x10)+40+8 = 68kVp
4. If the radiograph is too dark increase the kVp by 15%
5. If the radiograph is too light decrease the kVp by 15%
6. Make a chart
a. add 2kVp for each cm increase up to 80kVp
b. subtract 2kVp for each cm decrease
c. add 3kVp for each cm increase the places the kVp from 80-100
d. add 4kVp for each kVp that places kVp over 100
7. Repeat for each type of study (Thorax, Abdomen, Extremity, Spine)
Digital systems
Setting up technique on the digital system is slightly more complex. As well as having
appropriate exposure factors, the radiographs are also post processed according to the
region imaged. The post-processing is typically setup by the manufacture at the time of
installment but this can be reviewed, and it is important that the diagnostic result is not
compromised, for example by a technique that results in very high contrast but inability to
distinguish subtle lesions. If you are thinking of going digital then your choice of system can
have an enormous impact on the quality of your studies. Screen film does have a higher
inherent spatial resolution than digital radiography, and a poor quality digital system could
significantly reduce the diagnostic quality of your radiography.
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Trouble shooting
If your radiographs are already too dark or too light, reviewing a technique chart could be
very helpful. Other factors will play in to the apparently improperly exposed radiograph, and
darkroom factors (for regular screen film radiography) could be a problem. The flow chart
below may help you identify the source of a problem1.
Is the
radiograph too
dark or too
light?
Too dark Too light
Is the
peripheral
See Table 1 blackenng
adequate?
Periphery is Periphery is
grey black
Increase kVp
See Table 2 15%
1
Adapted from a chart that is available on the Animal Insides website www.animalinsides.com by kind
permission of Dr Matthew Wright
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Table 1: Film is too dark
Common Causes Processor and dark room Rare causes

problems (screen film)
Technique is too high Developer too strong X-ray machine

miscalibration
Try decreasing mAs by
50% or kVp by 15%
Double exposure Developer Temperature too X-ray machine timer

high malfunction
Tube height too low Processor timer malfunction
Light fog in the dark room
Safety light malfunction
Table 2: Film is too light
Common causes Processor problems (screen Rare causes

film)
Technique too low Developer exhausted X-ray tube miscalibration
Try 50% increase in mAs
Wrong technique chart Developer diluted X-ray tube failure
Wrong patient measurement Developer temperature too X-ray tube timer malfunction
low
X-ray tube too high Processor timer malfunction
X-ray tube not aligned to grid
What constitutes a diagnostic study?

Once you have got the positioning and technique right, with each patient you need to
determine which radiographs are necessary. There is a golden rule that applies to all but a
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select few cases always, always take orthogonal views. The best radiologist in the world
cannot isolate the location of a lesion from a single two dimensional radiograph, and a single
lateral view of the thorax will only ever provide evaluation of the lung lobes on one side
(potentially missing severe pneumonia or pulmonary metastases). A study of the thorax
should always be two views (right or left lateral and VD or DV), and arguably three views,
particularly if looking for metastases. An abdomen should also be two views (right or left
lateral and a VD) so that any lesion can be localized and not missed. For musculoskeletal
imaging, orthogonal views are essential and additional oblique or stressed views may be
necessary in some circumstances. There are exceptions a VD screening view of the hips,
lateral view of the elbows, or lateral view of the abdomen to look for calculi within the urinary
bladder but these should be kept to a minimum. It can certainly be difficult to achieve this
standard if you charge for each radiograph, and in many cases charging per study can work
out better without impacting the client. This is particularly true if you have a digital system,
where the cost to the practice of taking an extra film is minimal.
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NURSING CARE OF THE HEAD TRAUMA PATIENT

PetMedics Veterinary Hospital, Manchester, M28 2LY
Introduction
Head trauma is commonly seen in veterinary emergency clinics. Animals sustain head
trauma in numerous ways, including road traffic accidents, falling from heights, kicks from
horses, being stepped on by owners. Animals with head trauma required immediate medical
attention. The patient may also have concurrent injuries, such as circulatory or respiratory
problems, which need to be addressed during the initial treatment and stabilisation period.
There are two types of head trauma or brain injury: primary and secondary. Primary head
trauma, such as a skull fracture or cerebral haemorrhage, describes the injury to the brain
tissue from direct trauma and the forces applied to the brain at impact, these forces include
acceleration, deceleration and rotational forces. The brain is unable to tolerate these forces
because of its composition and lack of internal support. Secondary head trauma occurs
following the primary trauma. Following impact, a cascade of biomolecular events occur
causing continued and progressive brain pathology. The presence of haematomas and
oedema from the primary injury distorts normal brain parenchyma and decreases cerebral
blood flow. In addition, a series of cellular reactions occur at the time of impact, and continue
after the injury. An important goal of treating head trauma is to limit or prevent secondary
trauma.
Basic anatomy
The brain is encased within the skull, which does not allow any room for inflammation or
swelling. The skull cavity contains parenchymal tissue (the brain: 80% contents), blood
(10%) and cerebrospinal fluid (CSF, 10%). The main sections of the brain are the cerebrum,
cerebellum, and brainstem.
Pathophysiology
Like all organs, the function of the central nervous system (CNS) is dependent on sufficient
blood flow and oxygen and energy supply. The brain is a very active organ with a particularly
high oxygen and energy demand. It consumes about 20% of the total body oxygen and more
than 25% of the glucose. Neurones are also not able to retrieve their energy anaerobically to
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a sufficient extent. Since the brain has only very limited storage capacity for glucose and
oxygen, a minimal lack of energy can lead to brain damage.
Cerebral blood flow depends on the ratio between cerebral perfusion pressure (CPP), and
the cardiovascular resistance. In a healthy brain, the cerebral perfusion pressure is
monitored closely to maintain the oxygen and energy supply to the nerve cells. Through this
autoregulation, cerebral blood flow is kept constant despite changes in blood pressure and
cerebral vascular resistance. Cerebral blood flow is effectively self-regulated, with cerebral
perfusion pressure somewhere between 50-150mmHg. At CPPs above or below this range,
the cerebral blood flow becomes directly proportional. In various disease of the brain,
including traumatic brain injury, autoregulation may be impaired focally or generally, which
will also lead to direct dependence of cerebral blood flow of mean arterial pressure (MAP):
CPP = MAP - ICP
Intracranial pressure (ICP) is the pressure exerted between the skull and the intracranial
tissues, normal intracranial pressure being 5-10mmHg. Where there is inflammation or
bleeding in the brain, intracranial venous blood and CSF are shunted into the body in an
attempt to compensate for increasing intracranial pressure. If the body has done everything
it can to compensate but the ICP continues to increase, intracranial hypertension (ICH) can
develop. An increase in ICP results in decreased cerebral perfusion pressure (CPP) and
cerebral blood flow, decreased oxygen flow to, and diminished supply of brain cells with
oxygen and glucose. This leads to secondary changes and cell damage. Intracranial
hypertension will lead to alterations in levels of consciousness, respiratory and circulatory
abnormalities, and may cause death of the patient by brain herniation.
Severe, acute increases in ICP will trigger the Cushings Reflex, a characteristic rise in
MAP and reflex decrease in heart rate. Briefly, this occurs due to an initial drop in CPP
caused by the increase in ICP at a given MAP. The resulting decrease in CPP triggers
massive catecholamine release, which increases MAP, restoring CPP. The increase in MAP
triggers baroreceptors in the carotid body and aortic arch, which causes reflex vagal
stimulation, slowing the heart rate. The presence of the Cushings Reflex in a patient with
head trauma is a sign of a potentially life threatening increase in ICP and should be treated
promptly.
Initial assessment, diagnostics and monitoring
Initial assessment should involve evaluation of the patients respiratory and cardiovascular
systems.
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A Is the airway patient? Ensure that the airway is patient and there is no debris or swelling
in the oral cavity.
B Is the patient breathing normally? If the patient is unconscious and has apnoea or
dyspnoea, intubate the patient and perform manual ventilation, if needed.
C How is the circulation? What are the heart rate, pulse rate and blood pressure? Ensure
that the heart and pulse rates are synchronous. If there is a discrepancy,
electrocardiography should be performed to check for arrhythmias. If the heart rate or blood
pressure is not within normal limits, notify the veterinary surgeon. Emergency intervention,
which may consist of fluid resuscitation and/or pain management, may be indicated.
Physical examination
Once stable, a complete physical examination should be performed to document the

patients condition at presentation. Patients with severe head trauma can deteriorate quickly;
therefore, it is extremely important to note all changes in the patients condition. The head
and neck should be manipulated minimally during the physical examination. Manipulation
can displace fractures, worsen spinal cord injuries, or occlude the jugular vein, which can
decrease venous return from the brain and, in turn, increase ICP, leading to ICH. Patients
with head trauma should receive supplemental oxygen until proper oxygenation is confirmed.
A physical examination should start with the assessment of the patients level of
consciousness, changes to which can reveal the severity and progression of the injury. The
levels of consciousness are as follows:
Alert and responsive the patient exhibits normal behaviour.

Obtunded the patient is awake but responds less to stimuli
Stuporous the patient responds only to painful/noxious stimuli
Comatose the patient is unconscious and does not response to any stimuli
Examination of the eyes can provide important information about the severity of brain injury.
Any deviation from the normal eye position is called strabismus, which usually is caused by
damage to the cranial nerves or brainstem.
It is extremely important to check normal eye position. Rhythmic eye movement that is
vertical, rotary or horizontal, fast or slow, is called nystagmus. Physiologic nystagmus (or
oculocephalic reflex) can be initiated in healthy patients by moving the head horizontally or
vertically, resulting in rapid eye movement (also called fast phase) towards where the head
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is positioned. Absence of physiologic nystagmus indicates severe brainstem damage and

correlates with a poor prognosis. Any other type of nystagmus is considered abnormal.
In addition the pupils response to light (the pupillary light reflex (PLR)) should be assessed.
Shining a bright light into the eyes should cause the pupils to constrict they should dilate
when the light is removed. A slow PLR suggests a guarded to poor response. Absence of a
PLR suggests a grave response. Continual monitoring of the PLR can help assess the ICP.
Checking the size of the pupils is also important. With head trauma, the pupils can be
normal, constricted (miosis), dilated (mydriasis), or asymmetric (anisocoria). Miotic (pinpoint)
pupils are usually due to cerebral injury or oedema, indicating a guarded to fair prognosis,
but they can be associated with ocular causes, such as ocular injury, so this cause should
be investigated. Mydriasis can be associated with stress, medications, ophthalmic disease,
decreased cerebral perfusion and impending cardiopulmonary arrest, but also may indicate
permanent midbrain damage or brain herniation and is associated with a poor prognosis.
Mydriasis is not directly associated with brain injury but is important to recognise in
debilitated patients because it can be associated with cardiopulmonary arrest. Progression
from miosis to mydriasis indicates deteriorating neurological status and is an indication for
immediate, aggressive therapy. Anisocoria has several causes, including oculomotor nerve
damage or compression, direct eye injury, and uveitis (inflammation of the uvea). Mid-size
pupils that are unresponsive to light usually indicate a brainstem injury and grave prognosis.
Changes in the pupils size should be closely monitored and recorded in the medical
history/chart.
The menace response is the involuntary blink of the eyelids in response to movement
towards the eyes. If the menace response is intact, the patient will then blink when
something approaches the face, indicating sight. The staff member who evaluates this
response should be careful not to move air towards the face, which can cause the eyes to
blink, possibly leading to a false-positive test result. Neonates can be difficult to assess
because they may not yet have developed a menace response.
Blindness may indicate that either the nerves to the eyes and brain are too inflamed to work
or there is a problem with the eye(s). Vision problems usually indicate major nerve problems
with the head. Treatment decisions are not made based only on blindness. In many cases of
blindness due to trauma, vision can be restored.
The patients body position can be used to help the veterinary surgeon determine the
severity of the brain injury and the prognosis. In a position called opisthotonus or
decerebrate rigidity, the patient is recumbent and comatose with all limbs rigidly extended,
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and the head back. Opisthotonus indicates severe brainstem injury and usually carries a
grave prognosis. Decerebellate posture has a more favourable prognosis than decerebrate
rigidity, may indicate an acute cerebellar lesion or herniation. In decerebellate posture, the
patients forelimbs are extended and hind limbs flexed. Patients with this posture are usually
conscious and have responsive pupils. Close monitoring of the patient is important because
subtle changes in posture can indicate progression of the injury. Schiff-Sherrington
syndrome, which may appear similar to decerebrate posture, is characterised by extended,
rigid forelimbs and paralysed, flaccid hind limbs. This syndrome indicates a thoracolumbar
spinal lesion. It is extremely important to carefully assess the patient to avoid confusion and
misdiagnosis.
Neurological Assessment
The Modified Glasgow Coma Scale score (MGCS) or Small Animal Coma Scale/Score
(SACS) is a quantitative measure that has been shown to be associated with survival to 48
hours in dogs with TBI, and provides a score that can be used to assess initial neurologic
status as well as progression of signs. This scale incorporates three domains: level of
consciousness, posture, and pupillary size/response to light, with a score of 1-6 assigned to
each domain. The final score ranges from 3-18, with lower scores indicating more severe
neurologic deficits. The initial neurological examination should be interpreted bearing in mind
the patients systemic status, as shock can cause significant neurologic dysfunction.
Initial Diagnostics
Because patients with head trauma can deteriorate quickly, they must be closely monitored.
After the initial assessment, an intravenous (IV) catheter should be placed and blood drawn
for an extended database (venous and arterial blood gas values, CBC, and biochemistry).
Collection of blood from the jugular vein is contraindicated because occlusion of the vein
decreases venous outflow from the brain, therefore increasing ICP. The Packed Cell Volume
(PCV) and Total Solids (TS) value are used to check for haemorrhage. The blood glucose
level is monitored to ensure that the patient is not hypoglycaemic and is supplemented only
until the level is normal. Hyperglycaemia (iatrogenic or related to brain trauma) is associated
with severe head injuries in animals. To avoid hyperglycaemia, the blood glucose level
should be maintained in the normal range. Blood gas analysis is used to check ventilation,
oxygenation, perfusion, and acid-base status. The carbon dioxide (CO2) level should be
monitored because an increase in it can induce cerebral vasodilation and increase blood
flow to the brain, thereby increasing ICP and possibly causing ICH. The CO2 levels should
be maintained in the low normal range (40-45mmHg (venous); 35-40mmHg (arterial).
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Hypercapnia can increase ICP, which may necessitate mechanical ventilation of the patient.
Hypercapnia should also be avoided because it can cause cerebral vasoconstriction which
can lead to cerebral ischaemia.
Serial monitoring of the following is recommended: mucous membranes, capillary refill time,
heart rate, respiratory rate and effort, pulse rate and quality, lung sounds, temperature, the
hearts electrical activity, oxygenation (by pulse oximetry or arterial blood gas measurement)
and blood pressure. By closely monitoring these parameters, veterinary nurses can detect
changes in a patients status and notify the veterinary surgeon before they become life
threatening.
Based on extensive research on head trauma and hypotension, blood pressure should be
maintained at 100-150mmHg and MAP at 80-110mmHg. Hypotensive patients have
decreased cerebral perfusion, which may lead to brain ischaemia.
In the past, it was thought that the administration of IV fluids would increase ICP, causing
more brain trauma. Research has found that early and rapid establishment of euvolaemia
and avoidance of overhydration are essential. There has been much discussion about
whether crystalloid or colloid fluid therapy is better for rehydrating head trauma patients.
Either therapy can be used as long as hypovolaemia is treated and blood pressure is
maintained in the normal range.
Monitoring
The duration and frequency of episodes of hypoperfusion have been associated with poorer
outcomes in people with TBI. Serial monitoring of perfusion is essential for successful
management. Frequent qualitative assessment of tissue perfusion via mucous membrane
color, capillary refill time, heart rate and pulse quality, as well as quantitative assessment of
blood pressure, oxygenation, and ventilation are crucial. A minimal MAP of 80 mmHg should
be targeted to decrease the risk of inadequate CPP. If the Doppler technique is used for
monitoring, a minimum of 100 mmHg should be target, as it most closely reflects systolic
pressure in small animals. Continuous ECG monitoring should also be employed if possible;
if episodes of sinus bradycardia are noted, blood pressure should be assessed for evidence
of the Cushings Reflex, which warrants aggressive therapy directed at lowering ICP.
When the ICP is dangerously high, it can trigger the Cushing reflex, in which the patients
blood pressure increased and heart rate decrease (bradycardia). The Cushing reflex is life
threatening, so immediate identification and treatment are important. Affected patients
should be monitored by continuous electrocardiography and regular BP monitoring.
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Treatment
There are two main hyperosmolar treatments for an increase in ICP: mannitol or hypertonic
saline therapy. Mannitol is an effective therapy for patients with increased ICP, and has been
shown to reduce cerebral oedema, increase CPP and CBF, and improve neurologic
outcome in TBI. It has a rapid onset of action, with clinical improvement occurring within
minutes of administration, and these effects can last as long as 1.5-6 hours. Mannitol
boluses of 0.5-1.5 g/kg have been recommended for treatment of increased ICP in dogs and
cats. The diuretic effect of mannitol can be profound and can cause severe volume
depletion; therefore, treatment must be followed with isotonic crystalloid solutions and/or
colloids to maintain intravascular volume. Mannitol crystallizes easily at room temperature,
so it should be warmed before administration through a 0.22 m filter.
Hypertonic saline may be used as an alternative to mannitol in patients with TBI. Hypertonic
Saline has similar osmotic effects to mannitol, and can also improve hemodynamic status via
volume expansion and positive inotropic effects, as well as beneficial vasoregulatory and
immunomodulatory effects. In euvolemic patients with evidence of intracranial hypertension,
both mannitol and Hypertonic Saline can have beneficial effects. If an individual patient is not
responding to one drug, the other may yield a beneficial response.
Frusemide, a diuretic, has been used to help manage cerebral oedema. However, frusemide
can deplete intravascular fluid volume, resulting in systemic hypotension and a decrease in
cerebral perfusion pressure, leading to cerebral ischemia. Because frusemide can adversely
affect the patient outcome, it is one of the least used diuretics for treating an increase in ICP.
Frusemide can be used alone or with mannitol, but it is normally given once, whereas
mannitol can be given several times.
The use of corticosteroids is not recommended for treating head trauma patients. Research
in humans has found that the use of corticosteroids is detrimental to recovery. In a clinical
study involving more than 10000 people who sustained head injuries, corticosteroid therapy
was associated with worse outcomes. The Human Brain Trauma Foundation recommends
that corticosteroids not be given to patients with traumatic brain injuries. Veterinary medicine
has followed this recommendation.
Sedatives and analgesia is recommended is a patient is anxious, may worsen through its
injury through self- trauma, or seems painful. The sedative or analgesic which is used ideally
should be reversible with flumazenil (a benzodiazepine antagonist) or naloxone (an opiate
antagonist). Buprenorphine is ideal for treating pain because it does not depress the
respiratory system or central nervous system as much as fentanyl. Seizures are a common
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complication of head trauma. If a patient has seizures, traditional anticonvulsants (e.g.

diazepam, midazolam) should be administered. If the seizures are not controlled with these
medications, administration of propofol is recommended. Propofol, which includes
anaesthesia, can be given as a one off bolus (to see if the seizures stop) or a constant rate
infusion (CRI). If propofol is needed for long periods of time, the patient should be intubated
and given supplemental oxygen. The respiratory rate and effort, and heart rate, should be
monitored closely while the patient is under anaesthesia. An arterial blood gas reading
should be obtained to ensure adequate ventilation until the patient is awake. Monitoring the
end-tidal CO2 level is helpful if the clinic is not able to check the blood gas values.
Recent treatment developments
Polyethylene Glycol is an inorganic hydrophilic polymer that has a white matter sparing
effect after induced traumatic CNS injury when injected intravenously. It also been shown to
have antioxidant effects and to decrease free radical production. In experimental studies of
TBI, it reduced cellular damage and compromise of the BBB, and improved behavioral
recovery in rats when administered within 2-4 hours after brain injury. This drug shows
promise as a therapeutic agent for the treatment of TBI.
Controlled hypothermia and induction of coma reduce the metabolic rate and have been
reported in human head trauma patients, and recently in veterinary patients. Hypothermia
can be achieved by cooling a patient to a rectal temperature of 32-35C, which reduces
cerebral metabolic rate and oxygen consumption and leads to a decreased CBF and ICP.
This technique is not without its problems as it may result in the development of cardiac
arrhythmias, coagulopathies, electrolyte disturbances, hypovolaemia and insulin resistance.
Patient care
Patient care is an important part of what veterinary nurses can do for a head trauma patient,
who are usually recumbent. It is very important to turn these patients at least every 4 hours.
Patients should be maintained on a clean, dry, padded area to prevent decubital ulcers.
While the patient is recumbent, it is very important to elevate the cranial end of the body to
30 to 40 to decrease the ICP and thereby help prevent ICH. Elevating the head alone may
restrict the jugular veins, decreasing blood flow from the brain and thereby increasing the
ICP.
Because patients may not be able to blink, their eyes should be flushed with ocular wash
and lubricated with artificial tears at least every 4 hours to prevent dry eyes and formation of
ulcers.
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Obtunded or comatose patients may have difficulty swallowing, causing saliva and debris to
accumulate in their mouths; therefore, the mouth should be wiped out every 4 to 6 hours, as
needed, to remove secretions and keep it moist. An oral cleaning spray or solution can be
used to clean the mouth, and diluted glycerine can be used to keep the mouth moist. Rarely,
the mouth and oral pharynx may require suctioning to remove a large amount of secretions.
If the patient cannot walk or stand or use a litter tray, the bladder should be expressed at
least every 3 to 6 hours or an indwelling urinary catheter and closed system should be
placed to keep the patient clean and dry and to avoid development of an atonic bladder.
Recovery time can be prolonger, and nutrition is an important part of recovery. If the patient
can eat it should be helped into sternal and encouraged to eat every 4 to 6 hours. If the
patient is obtunded or comatose, a feeding tube, e.g. oesophageal or gastrotomy tube,
should be placed or the patient be given parenteral nutrition. Naso-oesophogeal tubes are
generally contraindicated as they may stimulate sneezing, which can cause a transient
increase in ICP.
Muscle wasting can occur in non-ambulatory patients; therefore, passive range of motion
exercises (PROM) may be indicated for all the limbs every 6 to 8 hours. PROM should be
performed with caution, or not at all, in patients that also have a spinal injury or a broken
limb. Consult the veterinary surgeon before starting PROM.
Conclusion
While head trauma patients can be difficult to manage, these patients are highly rewarding
and allow the nursing team to develop their nursing skills. Successful outcome for these
patients is very much dependent on close monitoring, attention to detail and focusing on
changes in the patient clinical signs, which may detect early deterioration and allow changes
to be made to the treatment plan.
References available on request.
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THE SMALL ANIMAL COMA SCALE FOR EVALUATING HEAD TRAUMA VICTIMS
CATEGORY/DESCRIPTION SCORE
MOTOR ACTIVITY
Normal gait; normal spinal reflexes 6
Hemiparesis. Tetraparesis or decerebrate activity 5
Recumbent; intermittent extensor rigidity 4
Recumbent; constant extensor rigidity 3
Recumbent; constant extensor rigidity with opisthotonus 2
Recumbent; hypotonia, depressed or absent spinal reflexes 1
BRAIN STEM REFLEXES
Normal PLR and oculocephalic reflexes 6
Slow PLR, normal to reduced oculocephalic reflexes 5
Bilateral unresponsive miosis; normal to reduced oculocephalic reflexes 4
Pinpoint pupils; reduced to absent oculocephalic reflexes 3
Unilateral, unresponsive mydriasis; reduced to absent oculocephlic reflexes 2
Bilateral unresponsive mydriasis; reduced to absent oculocephalic reflexes 1
LEVEL OF CONSCIOUSNESS
Occasional periods of alertness and response to environment 6
Depression or delirium; capable of responding to environment 5
Semicomatose; responsive to visual stimuli 4
Semicomatose; responsive to auditory stimuli 3
Semicomatose; responsive to noxious stimuli 2
Comatose; unresponsive to repeated noxious stimuli 1
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Total score Likely prognosis
3-8 Grave
9-14 Poor to guarded
15-18 Good
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Notes page
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POST OPERATIVE CARE OF THE AIRWAY SURGERY PATIENT

Amy Breton, CVT, VTS (ECC)
abreton@vescone.com
The Upper Airway
Nose
The air is warmed and moistened in this area. The paranasal sinuses in this area connect
with the nasal cavity through narrow openings and are thought to help lighten the weight of
the skull as well as for heat exchange.
There are numerous diseases or congenital problems that may require surgery on the nasal
area itself. Tumours in both the dog and cat may grow within the nasal passage and
paranasal sinuses.
Brachycephalic airway syndrome is used to described both dog and cat breeds that have
shortened skulls. The shortened skulls and consequently shortened nose results in
compressed nasal passages and distortion of pharyngeal tissues that can compromise air
flow. Brachycephalic airway syndrome is when these breeds also have stenotic nares and
elongated soft palate. At times these breeds may not be able to ventilate at well, if at all.
Surgery may be needed to reduce the length of the soft palate or open the nares.
Though not as common, foreign bodies and trauma to the nasal passage may also require
the pet to have surgery on its nasal passage. Whenever surgery is performed on the nasal
passage, some type of post-operative bleeding should be expected. The inflammation from
the surgery site often causes the delicate membranes to produce more secretions which
leak out of the nasal passage. The irritation from the surgery may make the pet feel as if
they have to sneeze leading to more bleeding.
Pharynx
From the nasal passage, the air passes into the pharynx and is divided into two chambers by
the soft palate; nasopharynx and oropharynx. Trauma can occur to the soft palate and is
often seen with dogs that enjoy chewing sticks. The biggest post-operative complication to
the area is swelling. To help aid in the reduction of inflammation it is important that pets are
kept quiet, free from barking and not allowed to excessively pant. If the area swells too
much the pet will not be able to ventilate appropriately.
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Larynx
The air enters the back of the throat into the larynx where its function is to regulate the flow
of only gases into the respiratory tract. The epiglottis seals off the entrance to the larynx and
glottis (the vocal cords and the opening between them). This prevents food from entering
the trachea. Bordering the glottis are the arytenoids. These are two small cartilage pieces at
the back of the larynx which the vocal cords are attached to.
The most common problems that require surgery are laryngeal paralysis (LP) or laryngeal
collapse. Laryngeal collapse usually occurs secondary to chronic upper airway obstruction,
disease or trauma. The cartilage loses its rigidity which results in a deviation of the cartilage
which can lead to permanent cartilage fatigue and deformity.
LP occurs because the nerves that control the movements of one or both arytenoid
cartilages of the larynx cease to function. While it commonly occurs usually because of an
idiopathic reason in dogs, it can occur in cats as well. The arytenoids stay in a neutral
position during inspiration and swallowing. The pet is no longer to open their airway during
times of increased need (stress, exercise) thus resulting in respiratory distress. Aspiration
pneumonia may develop even after surgery is performed. Post-operative dogs need to be
kept very quiet as surgical breakdown can occur in 4% to 8% of dogs.
Trachea
From the larynx the air enters into the trachea which is a permanently open tube made of
hyaline cartilage. Injury can occur to the trachea because of trauma (bite wounds),
venipuncture or intubation with a stylet or over inflation of the cuff.
One of the most common reasons a pet requires surgery on the trachea is due to tracheal
collapse. While more common in dogs, it can occur rarely in cats. Most commonly it occurs
in toy and miniature breed dogs and is considered idiopathic. Many times tracheal collapse
is medically managed, but if surgery is required the most common post-operative
complications include coughing, dyspnea, and laryngeal paralysis.
Post Operative
While the surgery was intended to alleviate any respiratory distress, swelling, breakdown of
the site or obstruction (mucous plug or blood clot) may cause the patient not to be able to
ventilate appropriately. Monitoring respiratory function is most important.
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Respiratory rate and effort are the easiest parameters to monitor. Look at the rate as well as
the effort. If you notice prolonged inspirations, it may indicate upper airway obstruction
(swelling, blood clot). Auscultation of the chest should occur each time a physical exam is
performed.
Mucous membrane colour is one of the easiest parameters to monitor and any presence of
cyanosis indicates a life threatening oxygenation issue which needs to be addressed
immediately.
A pulse oximetry (SpO2) machine measures the oxygen saturation of haemoglobin, which is
a very insensitive measure of oxygenation. The drawback to a pulse oximetry machine is
that, at times, it is not very accurate. Patient movement, poor perfusion, hair, or any colour
other than pink mucous membranes (icterus, cyanosis, anaemia) can cause the reading to
be inaccurate. However, the pulse oximetry machine continues to be a fairly quick and easy
test to use to determine overall oxygenation.
Partial pressure of oxygen in venous blood (PvO 2) is not very reliable and ideally should not
be used. If there is any change in cardiac output, oxygen consumption by the tissues and, to
a lesser extent, arterial oxygen content the PvO2 reading will be low. If you cannot obtain an
arterial sample, then you should obtain a venous sample from the jugular vein or vena cava
as these will often provide the most accurate results. Normal PvO 2 measurements are
above 40 mmHg. A PvO2 below 30 mmHg is concerning and requires intervention while a
PvO2 below 20 mmHg is an emergency.
Partial pressure of oxygen in arterial blood (PaO2) is still considered the gold-standard test
when monitoring for overall oxygenation ability of a patient. Normal PaO2, at sea level, is
between 80 and 110 mmHg. When PaO2 is less than 80 mmHg the patient is suffering from
hypoxemia and < 60 mmHg is life threatening hypoxia.
Post Operative Respiratory Distress
The cause of any dyspnea post-operative is usually related to one of three things:
obstruction, break-down or inflammation.
Sedation should be considered in patients that are very stressed. Animals that are barking,
jumping or panting may cause excessive inflammation to the surgery site or cause it to
dehisce. Before sedation takes place the patient should be assessed to ensure there isn't
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another underlying issue such as: pain, dirty litter box, full bladder or bowel, soiled bedding,
or uncomforted due to another reason.
If the patient still needs sedation once all other underlying issues have been ruled out then
the patient should be mildly sedated. While pain medication is important it is also important
to choose something that will not depress the respiratory system too much.
If oxygen is required until the underlying issue is addressed, oxygen cages offer the safest
long term oxygen delivery and also create the least amount of stress on the patient. Short
term methods for delivering oxygen include: oxygen hoods, face masks and flow-by. If a
patient received surgery on the nasal, pharynx or larynx area they may require tracheostomy
tube until inflammation can decrease and the area is healed.
Other Nursing Concerns
Tracheostomy tube care should be focused on preventing secretion build-up, providing

aseptic wound care and humidifying inspired air. The tracheostomy site itself should be
touched only by gloved hands (sterile gloves preferred) and the skin around it cleaned with a
0.05% chlorhexidine or betadine solution. Humidifying air should be provided every 1-2
hours through a humidifier or by instilling 0.5 to 3 mL of sterile saline into the tube.
Suctioning the tube itself helps to prevent accumulation of secretions. Suction catheters
should have more than one hole in their tip to prevent them from suctioning to the wall of the
trachea. The patient should be preoxygenated before suctioning occurs. The airway should
also be humidified just prior to suctioning and the procedure itself should be atraumatic and
sterile. Replacement of the tube itself should occur every 24 hours.
Cold compresses should be used in pets that experience some post-operative bleeding from
the nasal passage. Mucous or blood clots may need to be removed with a q-tip or warm
wash cloth to allow air to enter the nasal passage. If there is excessively bleeding a few
drops of epinephrine can be applied into the affected nostril.
Every post-operative patient should be closely monitored and should have a full physical
exam performed minimally every 4-6 hours. This should include a heart rate, respiratory rate
and effort, mucous membrane colour, capillary refill time, rectal temperature and
neurological status.
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Blood pressure should be monitored minimally every 6-8 hours. It is important that post-
operative upper airway patients do not experience hypo- or hypertension. If the patient has
hypotension it may because they are too sedated or not perfusing correctly. This can lead to
a patient who is not taking in adequate breaths or lying in a contorted position for their neck
which causes them not to ventilate appropriately. Hypertension can increase pressure to the
surgery area causing an increase in inflammation.
Most upper airway patients require small, frequent meals of soft food. Feeding hard food
and/or large meals may cause increase turbulence and abrasion of the surgery site as the
food is passing by. Food may need to be hand fed or fed in a raised bowl to avoid excessive
gulping or air and/or food.
Post-operative upper airway patients should never be restrained around their necks. This
includes placing a neck lead on a dog to walk it. Placing pressure on the neck can lead to
increase pressure in the area or directly injury the surgical site. It is imperative that dogs are
walked with harnesses and cats are never scruffed or held by their necks.
E-collars are usually not recommended unless the surgery was on the nasal passages. E-
collars will often rub on the neck area causing further irritation. A loose stockinette, bandage
or t-shirt can be used to avoid the patient scratching at the area. E-collars are usually
placed in any patient who has received surgery to its nasal passage as patients are often
irritated and want to rub or scratch at their nose.
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Notes page
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NURSING PATIENTS PRESENTING WITH OCULAR EMERGENCIES

Simon Petersen-Jones DVetMed PhD DVOphthal DipECVO MRCVS
Myers-Dunlap Chair in Canine Health
Michigan State University
peter315@cvm.msu.edu
Nursing management of ocular emergencies is very important to a successful outcome.
Taking a Client Phone Call about an Ocular Case
When speaking to an owner over the phone about an ocular case it is important to recognize
the emergency cases that need to come straight in and the urgent cases that should be seen
soon but maybe not immediately.
Owner complains about altered appearance Has the changed appearance developed
suddenly or have they noticed it coming on over a few days? Traumatic conditions such as
prolapse of the eye, trauma or penetrating wounds should be seen as soon as possible.
Owner complains that the eye is painful If there is acute ocular pain that could indicate
trauma, corneal ulceration or conditions such as acute glaucoma. Animals with these
conditions should be seen soon. If there is a history of primary lens luxation or primary
glaucoma these could be ocular emergencies that should be seen immediately. If there is
mild irritation with no other changes and no loss of vision then this is probably not an
emergency.
Change in appearance of the eye If there is an obvious crater on the cornea and there is
cloudiness this could indicate a deep ulcer. If this has come on quickly then the animal
should be seen very soon. If there is fluid or blood leaking from the eye then the animal
should be seem immediately.
Loss of Vision A sudden loss of vision that has not resulted from trauma and is not
associated with pain or a change in appearance of the eye is probably an urgent rather than
emergency case. Owners understandably are distressed and feel that the animal should be
seen immediately. However the conditions that cause such changes do not necessarily
need immediate treatment, compared to conditions such as prolapse of the globe which
need immediate treatment.
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First Aid Advice
Giving appropriate advice over the phone to owners of animals with ocular disease is
important. For example, if an owner calls and says their pets eye has popped out (a
prolapse of the globe or proptosis) instructing them to keep the cornea constantly moist
while they are coming in to the surgery is important. If they happen to have an ocular
lubricant or tear replacer at home they could use that. In most instances some cotton wool
soaked in boiled water is fine, or even a product such as KY gel could be used.
If an animal has a foreign body that is protruding from the eye or adjacent to the eye they
should not pull it out. While they are coming into the surgery it would be sensible to have a
passenger hold the animal and ensure that they do not rub at the eye or further traumatize it.
Restraint for Examination
Gentle restraint that does not result in any pressure on the eye or around the neck (which
can raise intraocular pressure) is important. Careful scruffing brachycelphalic breeds as
this had led to proptosis of the eye. When holding try to avoid pulling on the skin as this can
alter the lid position and make it difficult to assess.
In-Patients
Nurses should be familiar with and able to assess basic ocular reflexes and responses.
Menace response. This is an assessment of vision. A menacing movement is made to the

eye and should elicit a blink or head withdrawal. Care needs to be taken not to touch any
long hairs or create a current of air that can be felt on the cornea as this may give a false
positive.
Visual tracking An object such as a cotton wool ball is moved or thrown across an animals
visual field and their ability to follow the object is noted.
Pupillary light reflex A bright pen torch is used, and while the eyes are being examined for
any change in appearance the direct pupillary constriction should be noted as well as the
constriction of the pupil in the contralateral eye (the indirect response). When first examined
it is common for the PLR to appear sluggish. This is particular in nervous or stressed
animals where circulating adrenaline tends to dilate the pupil in a fight or flight response.
After a few minutes the PLR should become brisk. Loss of a PLR in an in-patient should be
reported immediately.
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Cleaning the eye and preparation for surgery
A traumatised eye should be handled with great care. If there is a deep corneal ulcer, a
penetrating wound etc. the eye is in a very delicate state. Direct pressure on the eye must
be avoided as this could worsen such an injury. If the animal struggles as well this will raise
the intraocular pressure and could cause a deep ulcer to rupture. Cotton wool balls
dampened in sterile eye wash can be used to clean discharges from the periocular area but
the eye itself should not be touched. When anaesthetized, the surgeon will typically prepare
the traumatized eye for surgery.
When preparing a patient for surgery the effect of drugs on intraocular pressure should be
considered. With many ocular conditions increasing the intraocular pressure by using
anaesthetic agents such as ketamine is contraindicated.
The cornea should always be kept moist. Eye lubricants are always placed in the eyes of
anesthetized animals. If intraocular surgery is to be performed the operated eye should not
be lubricated. A proptosed eye should however always be kept moist to prevent the
development or corneal ulceration (until it can be replaced and the lids sutured shut).
Post-operative care
Following ocular surgery it is important that the animal does not cough or retch as this can
raised intraocular pressure. For this reason early removal of an endotracheal tube is needed
before coughing. A quiet recovery from anaesthesia is also important so appropriate
sedation and pain-medication should be included. The Elizabethan collar should be fitted
before the animal has a chance to rub at the eyes.
Care must be taken not to apply any pressure around the neck as this can raise intraocular
pressure. We recommend attaching the leash to a harness rather than a collar and all choke
collars must be avoided. A loose collar for attaching the E-collar to is OK. If a harness is not
available looping a slip leash through one front leg can be done. The dog can be led and yet
there is no pressure on the neck.
Applying medications
Eye drops are applied by tipping the animals head up and allowing drops to fall from a few
centimetres above the eye on to the ocular surface. For ointments the lower lid is pulled
down and ~1/2 cm strip of ointment placed in the lower conjunctival fornix. Care should be
taken to avoid contacting the eye with the medication bottle or tube.
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Preventing self-trauma
Elizabethan collars are fitted to all animals with conditions such as corneal ulcers, ocular
injuries or following ocular surgery. Usually animals with conditions such as glaucoma or
uveitis do not require an E-collar.
Observing for deterioration in ocular condition
In-patients with ocular conditions should be monitored for any indication that the condition
has deteriorated. Examples are given below:
Glaucoma patient has increased pain, increased corneal opacity and redness of
the eye this may indicate a raised intraocular pressure and indicate that a change
in management may be required
Deep corneal ulcers fluid or blood leaking from the eye associated with increased
pain could indicate a corneal rupture and should be investigated
Any alteration in the appearance of the eye (such as corneal oedema, intraocular
haemorrhage etc.) should be noted and investigated
Any loss of vision should likewise be investigated immediately
Page 116 of 334

CONTRIBUTING TO CLINICAL AND FINANCIAL OUTCOMES

Brian Faulkner BSc (Hons), BVM&S, MBA, CertGP(BS), CertGP(SAM), MSc(Psych),
MRCVS
vetpsych.com
brian@vetpsych.com
The hallmark of a successful veterinary practice is that every employee, irrespective of their
job title contributes towards four essential outcomes; clinical resolution, client satisfaction,
financial resolution and team harmonynhappiness. This series of talks will discuss the
knowledge, the habits and the mindsets which enable members of staff who work in non-
clinical roles (referred to as non-clinical employees NCEs) to contribute to all of these
outcomes. The first half of this session will explore the ways NCEs can impact the
prevention and resolution of clinical issues and the second half will cover some money
issues relating to veterinary practice.
PART 1 Contributing to clinical outcomes

It is all too easy for vets, nurses, clients and NCEs to believe that NCEs dont make much of
a difference with respect to a pets health. This is not true as long as NCEs know where the
boundaries lie. This session will explore some of the skills, attitudes and knowledge NCEs
can use to impact the prevention and resolution of clinical issues based around 2 acronyms:
PREVENT IT and TREAT IT.
PREVENT IT
Nowadays many dogs and cats live to fifteen and rabbits to ten years and beyond. Whilst it
is entirely possible for pets to live this long without ever visiting a veterinary practice, it is
much more likely that they will do so if they receive a series of preventative healthcare
measures which minimise the probability and impact of illness. The PREVENT IT acronym
will help you remember all the things owners can do to increase the likelihood that their pet
lives as long as is possible. Below is a brief summary of what each letter stands for and why
it is important.
P is for PLANS. Most surgeries nowadays offer Pet Healthcare Plans which spread the cost
of regularly required preventative healthcare products and services such as vaccines,
wormers, external parasites. NCEs need to be familiar with the terms and conditions of their
PHP as well as how to sign up clients and dispense the correct products.
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R is for reproductive management. There are many benefits of proactively managing the
issues that can occur relating to a pets reproductive system. Some people want to breed
from their pets whilst others dont. It is important to be able to advise clients of the pros and
cons of breeding as well as neutering. However we also need to be able owners who wish to
breed their dog for the right reasons manage a successful pregnancy, birth and the post-
partum period.
E is Endoparasites. Endoparasites are parasites that live inside pets; in other words, worms.
There are about 12 different types of worm that affect pets in the UK, some of which, such
as lungworm, can be fatal. Your practice will recommend owners to worm their pets
regularly with a product or products which cover all the worms of concern.
V is for Vaccines. Vaccines are available for cats, dogs, rabbits and ferrets. Almost all of
the diseases we vaccinate against are fatal if contracted such as Canine Parvo virus, Feline
leukaemia to Myxomatosis. Pets need to be vaccinated against something every year to
remain protected.
E is for Ectoparasites. Ectoparasites are parasites that live on the outside of the pet. Whilst
fleas are the most common skin parasite, others such as lice, scabies and ticks are
important vectors of potentially life threatening diseases.
N is for nutrition. Possibly the single most useful thing owners can do to promote a long and
healthy life is feed their pet a high quality diet. You are what you eat applies to pets too.
T is for Teeth. Healthy teeth are about a lot more than a good cosmetic outcome. Dental
hygiene has been shown to have a massive impact on the amount of bacteria that circulate
around a pets blood stream which in turn causes liver, kidneys and lungs damage.
I is for Identification. There are various forms of identification ranging from collar tags to
microchips. I is also for Insurance. Financial planning is an essential component of effective
pet healthcare.
T is for training. Many dogs go through life behaving badly (running off, chewing furniture)
and becoming stressed (inappropriate toileting, howling) because they havent been
habituated or trained adequately.
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TREAT IT
We have already seen how NCEs can impact a pets health status by being knowledgeable
about and encouraging clients to comply with optimal preventative healthcare. NCEs can
also contribute to the outcomes of sick patients, especially in relation to what they do before
and after veterinary consultations. This section will use the acronym TREAT IT to highlight
the areas NCEs impact clinical processes.
T The primary consultation

R Re-check and follow up consultations
E Emergencies
A Admissions and booking in ops
T Therapeutics
I In-patients
T The euthanasia consultation
T The Primary consultation
Veterinary consultations can be categorised into the 5 following types:

Consult type Definition Examples
1 Primary consult The first time a patient is seen with a Routine veterinary
specific symptom or clinical consult
presentation (e.g. Vomiting, An out of hours consult
scratching, limping, etc.) A second opinion
2 Re-check consult The follow up after some initial Re-check after a primary
veterinary treatment Post-op check
3 Long term medic The regular planned follow up Prescription re-check
consultation consultation relating to an incurable
but manageable clinical condition
4 Vaccination The well-animal consult which The first vaccination
consultation includes a vaccination as part of a The annual booster
general preventative healthcare
strategy
5 Euthanasia Any consultation during which
consultation euthanasia is performed
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Primary consultations are the life-blood of a sustainable veterinary practice. A practice will
not thrive without a steady pipeline of consultations which relate to new medical
presentations (such as vomiting, scratching, limping, etc.) amongst veterinary patients.
Whilst each presentation is described as new, it is entirely possible of course that a patient
has had these symptoms before and then cured, and now the symptoms have now returned
for another reason.
The golden rule of veterinary reception: Always offer an appointment
R Re-checks and follow ups: When will I see you again?
In all medical professions there is a concept known as compliance. Compliance occurs

when clients follow-through on the requests made by the veterinary team; i.e. they comply
with the treatment recommended. Studies have shown that compliance rates amongst
veterinary clients are low, with some studies citing values as low as 30%.
Compliance affects three main areas of veterinary care; short term illnesses, long-term
illnesses and preventative healthcare. We have already discussed your practices policies
and protocols for Preventative Healthcare in the last module using the PREVENT IT
acronym. Compliance is also an issue in the two main types of clinical case (short term
illnesses and long term illnesses) both of which can be influenced by what happens at the
veterinary reception.
E Emergencies
What symptoms constitute emergencies?
Conditions Requiring Emergency Veterinary Attention in Dogs

Persistent retching and attempting to vomit. This could be symptomatic of a life-
threatening condition called Gastric Dilatation Volvulus (GDV), also known as Bloat.
This serious and potentially fatal condition happens when the stomach becomes filled
with excess gas then twists, preventing the gas from escaping.
Difficulty breathing
Inability to stand or use hind legs
Uncontrollable bleeding
Involvement in a road traffic accident
Straining to urinate or defecate
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Known ingestion of poisons

Drooling profusely, staggering, or experiencing a prolonged seizure.
Projectile vomiting
Extreme sluggishness
Labour that has not resulted in birth of a puppy within 2 hours
Conditions Requiring Emergency Veterinary Attention in Cats
Repeated trips to the litter box with little or no urine production, or straining to urinate.
Neutered males are more prone to urethral blockage than females, but in either case the
condition is a definite emergency since it can be fatal if untreated.
Known ingestion of poisons
Open-mouthed breathing or panting or any other difficulty breathing
Vomiting and/or diarrhoea leading to extreme dehydration.
Loss of appetite for more than 24 hours.
Inability to use or dragging hind legs.
Extreme lethargy and sluggishness.
Strange behaviour such as excessive hiding under a bed or in a closet.
Pain during eating.
Foul breath/drooling
Labour that has not resulted in birth of a kitten within 2 hours
A Admissions and booking in ops
NCEs often give advice to owners before an anaesthetic and surgery. It is essential to the
safety of the patients as well as the smooth operation of the business and ops that patients
arrive at the surgery having received and followed the correct instructions.
T Therapeutics
Prescribing and dispensing veterinary medicines

There are specific laws relating to the acquisition, storage, prescribing and dispensing of
veterinary medicines all of which is regulated by a government body called the Veterinary
Medicines Directorate (VMD). Firstly, all veterinary medications have been categorised. The
different categories determine where the medicines are stored within the practice as well as
who can prescribe and dispense them. The categories are determined It is important that we
know, understand and observe these regulations to ensure that we comply with the law.
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I In-patients
Most veterinary practices wish to generate in-patient procedures, be they day-patients or

patients which stay in on an overnight basis. Given that no one member of staff can (or
should!) be present 24/7, it is essential communication surrounding such patients is
particularly good. To achieve this requires the client and patient records to be up to date as
well as some basic paper-work in place. NCEs can help with this by ensuring that the client
details and the patient details are correct and complete on the record cards. They are often
also involved in generating the in-patient paper work as well as setting post-op / in-patient
communication expectations when the patient is being booked onto the diary in the first
place.
T The euthanasia consultation
It goes without saying that euthanasia is one of the most distressing times for a client. There
are many reasons which an animal may be euthanased, usually surrounding quality of life,
pain and debilitating illness. New members of staff also may not be used to the act of
euthanasia and find it distressing. It is important that they understand what actually happens
when an animal is euthanased in order that you can answer any questions that clients may
ask you before or afterwards, as well as be prepared for what you might see, hear or see if
you are ever asked to be involved.
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PART 2 Contributing to financial outcomes
This part of the talk relates to the objective of financial resolution whereby accounts are
generated and settled in a timely manner. In order to structure this module another
acronym PROFIT - will be used.
P Pets, people, profit
Pets, people, profit is the triple bottom line of veterinary practice. This means that success
in veterinary practice relates to achieving various outcomes including clinical outcomes,
client outcomes and commercial outcomes. In other words, there is nothing wrong with
aiming to generate a profit as long as it is seen within the wider context of what else we do
for our patients and the people we work with and for. Profit is the surplus left over when all
the costs have been paid out of the monies received by the business. Employees who are
not involved in managing the profit side of the business are always surprised at just how little
profit remains after all the costs of running a business have been paid. The main types of
costs in a veterinary business are the medicines and products used to treat the patients, the
staff costs and the overheads of running the business. The majority of veterinary practices
run at less than 10% profit. That means that for every 100 that goes into the till, less than
10 remains at the end. And even then that 10 doesnt all go into the business owners
pocket as profit is also needed to re-invest in the business, be it to expand into new
premises or buy new equipment.
R Recommendations
NCEs can influence the business side of practice by making recommendations in two areas;
1) recommending the practice protocols regarding the various preventative healthcare issues
which was discussed above and 2) by recommending that clients should book an
appointment on the diary. NCEs also need to be skilful at dealing with telephone price
checkers who represent potential new clients. A key part of being able to convert
prospective client calls into diary appointments is a sound understanding of the knowledge
discussed in PREVENT and TREAT IT above, but also having the prices of all these
standard services at their fingertips.
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O Offers and promotions
It is not uncommon for veterinary practices to run various offers and promotions in an
attempt to attract new clients or stimulate further sales. NCEs are usually asked and
expected to administer, promote and process the offers and the promotional campaign. It is
not uncommon however in veterinary practice for the explanation and the training with
respect to detail of the offers and the promotions to be less than ideal.
Often NCEs are cynical and sceptical of new initiatives for a variety of reasons;
They believe it is too complicated

They dont believe it will work since the last one didnt
They are concerned about the extra workload on an already busy schedule
Basic principles for implementing successful promotions
Keep it simple.
Ask for / use an offers and promotions brief an example of which is given below
should include some or all of the following depending on the nature of the promotion.
o What the promotion is

o When it begins
o When it ends
o Which clients it applies to
o Which products / services it applies to
o The purpose of the promotion or why it is perceived necessary
o The benefit to the pet / client if not obvious
o A step-by-step mechanism of what to do
o How clients will find out about the promotion
o Who staff are expected to do to make clients aware of the promotion
o Any tips on how to best to approach or not approach promoting the offer
o Any other relevant details and who to direct queries
Have all the price codes / pricelist items on the Practice Management System ready
to go
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F Financial resolution
Taking a payment and getting it into the practices bank account as cheaply and quickly as
possible is the ultimate objective of financial resolution. Some forms of payment are better at
achieving this than others. NCEs need to be aware of the pros and cons of the various
means of payments such that they can answer the question how would you like to be paid?
in a way that best suits the business if there is a choice. NCEs are also involved in sending
out invoices for outstanding balances and for chasing over-due accounts. They need to
know the practices protocols for achieving this.
I Insurance
Insurance claims represent a significant proportion of veterinary practice income. NCEs are
often expected by the clients to understand how their insurance policy works and to help
them make a claim. NCEs therefore need to be aware of the basic legislation surrounding
insurance, how to process the claims as well as any practice policies surrounding the
opportunity for direct claims in terms of the amounts and the insurance companies which
qualify.
T Team work
The last factor in achieving the goal of financial resolution in this acronym is team work.
Team work is essential since NCEs are often not involved in the conversations relating to
financial matters surrounding a case. The veterinary surgeons in particular can be very
proactive in helping NCEs deal with financial matters by doing the following; telling the
clients when their consultation bill is more than a certain figure before they leave the
consulting room as opposed to a NCE getting it in the ear for something they have no control
over; creating estimates for any proposed procedure that goes over this figure; escorting
clients out to reception after a consultation and handing them over to a NCE and instructing
them as to what follow appointments are required and the expectations regarding the
account (e.g. direct claim).
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Notes page
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CONTRIBUTING TO CLIENT SATISFACTION

MRCVS
vetpsych.com
brian@vetpsych.com
The acronym CLIENT will be used to focus on the key elements of a clients experience
before, during and after a veterinary consultation and how these relate to achieving client
satisfaction.
C Client focused culture

L Listening
I Intelligence
E Empathy
N Needs and wants
T Trust
CLIENT Client focused culture:
No veterinary practice can survive without a population of active clients. They are the
essential starting point of the following sequence of events which lead to a financial income:
A
population Appointments Veterinary In-patient Financial
of active on the diary Consultations procedures income
clients
In order to develop and maintain a population of active clients, especially in the face of stiff
competition, practices must know how to consistently satisfy their clients. Anyone who is
genuinely interested in achieving client satisfaction must realise that there is a difference
between customer service and client service.
Practices with a (genuinely) client-focused culture think about the practice-client relationship
in a specific way. They see clients at the centre of their raison detre; they see veterinary as
a people-business that serves people who have needs and wants in relation to the animals
they own. This is an entirely different mindset from a clinical culture for example, that sees
veterinary as an animal job built around the main (or even sole) function of making sick
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animals better. Practices that see the world through a clinical lens often assume that the
key to delivering client dissatisfaction is through delivering good clinical outcomes.
However, it is important to realise that most clients make judgements about the degree to
which they are satisfied about a veterinary service long before their pet shows any change in
its clinical status. If this were not true, why would we perform client satisfaction surveys
immediately after a consultation?
In order to deliver genuine client satisfaction, veterinary practices need to do more than just
deliver a smooth and straight-forward shopping experience; they need to work as a team in
order to collaborate with their clients as well as give them a smooth experience; they need to
work with them to determine and explain which strategies are actually available to the client;
they need to listen to the clients values, beliefs and feelings about those strategies. In
short, they need to reach a consensus about what represents the right thing for a fair price.
NCEs need to take the lead in delivering a smooth and straight-forward customer shopping
experience in terms of answering the telephone promptly, booking appointments and ops
efficiently, taking payments, processing paper work, maintaining the ambience of the waiting
room etc., all in a friendly and polite manner. It is up to the vets in the consulting room to
reach a consensus with clients about what represents the right thing for a fair price. Both
of these elements of client service are necessary.
CLIENT: L is for Listen
People can communicate with one of three different aims. The first aim is to talk about what
they want to talk about. The second aim is to appear polite by disciplining oneself not to
interrupt the other person; this is meant to portray to the other person that they are listening.
The third aim is to listen and attempt to genuinely understand what the other person is
thinking, feeling and wanting. This is called active listening and it is a learned skill. The
reason why it is called active listening is because it takes energy and effort to listen to the
tone and content of what the other person is saying. In veterinary practice, conversations
can be thought of as having two types of content. The first type of content is called clinical
content. The second type is called non-clinical content. Clinical content refers to the portion
of communication that relates to preventing, describing or resolving clinical symptoms. For
example, a client may be talking about specific veterinary concerns such as limping,
vomiting or scratching. Or how often should I worm my cat? Non-clinical content is much
more subtle. This type of content refers to what the client believes, values, expects, thinks
or wants in relation to the issue being discussed which is discussed using the acronym
ICEBERGs on the following page.
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CLIENT- I is for ICEBERGS
When we are actively listing we are taking the time to notice and analyse what someone else
believes, what they value and what they expect. We do this by comparing what the other
person thinks, feels, values and expects against what we think, feel, value and expect. To
be able to do this successfully we need to be able to resist the urge to interrupt, disagree,
contradict or correct the other person when they say something that we do not believe, feel,
value or expect. The first rule of active listening is not to want to jump in and change
someones mind; its to learn what their mind is.
The ICEBERGS acronym is a useful aide memoir. Like the proverbial iceberg, 90% of what
goes on in our mind happens below the surface i.e. at the subconscious level. Often without
realising it, we make choices guided by subconscious processes about what we believe to
be true, what we believe to be important (values), what we expect as well as beliefs about
what we are entitled to do (rights). Often these subconscious influences lead us to make our
minds up before considering alternative explanations or courses of action. Lets have a look
at each.
I Ideas and hypothesesfor example I think my dog has been poisoned!
C Concerns for example I am worried that my dog is in pain
E Expectations for example He just needs some ear drops
B Beliefs for example it is best to let them have a litter at least
once
E Evaluations for example the best thing to do is....
R Rights for example can I have a prescription for that please?
G Goals for example he is keeping me awake with his....
S Strategies for example I have always done it like this and it
works
Often clients will divulge ICEBERGS type information about themselves and their pets whilst
speaking with NCEs. These may be of value to the vet or nurse who is dealing with the
case.
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It is important to try and communicate this information to the rest of the practice team who
will be in contact with this client. This can be done in several ways. For example, make a
note on the client record or make a note on the diary when the appointment is made or take
a moment with the vet or nurse just prior to the client entering the consultation. It wont
always be possible to speak directly to the nurse or vet but sometimes that little snippet of
information can make a huge difference to the outcome of the consultation and the client
experience.
CLIENT- E is for Empathy
Empathy:
Empathy is the capacity to recognise, understand and demonstrate that you understand the
emotions that are being experienced by others. Empathy is not to be confused with
sympathy. Sympathy is associated with recognizing acknowledging negative emotions, such
as sadness, whereas empathy relates to recognising and acknowledging the entire range of
emotions, both positive and negative.
Good empathetic skills are a key feature of emotional intelligence. Emotional intelligence is
the ability to be intelligent with and about emotions whereby we use the information that
emotions give us to manage interpersonal situations more effectively. There are three key
core skills of emotional intelligence; 1) recognising emotions, 2) understanding why emotions
arise and 3) managing emotions in ourselves and others.
Lets start with Understanding why emotions arise.
There are 5 basic emotions recognised across all cultures:
Emotion Is a response to... Typical behavioural response
Fear Threat of loss (real or imaginary) Flight run away
Anger Being obstructed or treated unfairly Fight attack
Disgust Something offensive physical or verbal Expulsion (spitting or eviction)
Experience of losing someone / thing

Sadness Retreat and disengagement
valuable
Joy Experience of a sense of progress / Continued engagement and
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achievement exploration
All other emotions derive from these basic 5
Emotions arise due to the difference between what people expected or hoped would happen
and what they perceive is actually happening or just about to happen. Hopes and
expectations result from what people believe and value. For example, it is entirely possible
for two people to view the same scene and have completely different emotions about it. The
easiest way to demonstrate this is to thing about a sports contest with two sets of fans
cheering for opposite teams. When one team wins their fans perceive a sense of joy, whilst
the others perceive a sense of loss, possibly combined anger if they feel they have lost
unfairly due to some sense of foul play. For the same reason clients can become angry
when they lose a pet if they feel someone else was to blame for their loss.
This is why active listening is so important. We need to listen intently and actively in order
to detect the values and beliefs the other person is using. For example, the moment we
perceive someone as angry we automatically know (from the table above) that they probably
feel they have been treated unfairly. Sometimes what we consider to be a fair and
reasonable price (e.g. the cost of a flea product) is perceived as unfair to the client because
they do not believe that the value added is worth it.
Recognising emotions
Now that we know the core five emotions and why they arise, we now need to know how to
recognise each of them. Sometimes it is obvious what someone is feeling whereas other
times it can be more subtle. Even if it is apparent what they are feeling, it is important to
remember that it is not at always obvious why they are feeling it. Eye contact is always cited
as a crucial listening skill. This is true for several reasons. Firstly, it demonstrates to the
person you are communicating with that they have your attention and that your focus is on
them. For example, if possible, as soon as a client walks through the door, make eye contact
and greet them either vocally or with a nod of the head to let them know that you are aware
that they are there or that you are interested in helping them. The second reason why eye
contact is important is that it enables you to learn a lot about how the other person is feeling.
There are several keys areas of the body that reveal emotional status. Areas to pay
attention to are the face, the body demeanour (defensiveness versus openness) and the
tone of voice. The face is by far the most useful area to decipher what another person is
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feeling. Core emotions can be detected from the face by examining five areas of the face;
the eyebrows, the eyes, the nose, the mouth and the chin.
Managing emotions
The content of communication

When we analyse what people communicate, we can divide it into both emotional and non-
emotional components. The non-emotional component of communication relates to what is
being discussed and the emotional component of course relates to how someone feels
about what is being discussed. There is a commonly misquoted statistic that 93% of
communication is non-verbal. This is actually untrue. This myth arose as result of a mis-
interpretation of Albert Mehrabians study into communication in the 1960s. Mehrabian
actually stated that only 7% of the emotional content of communication occurs through
words with the remaining 93% of the emotional content of communication occurring via
body language. In contrast to the emotional component, the non-emotional component of
communication is most efficiently achieved using words, either spoken or written. Words are
the most effective way to describe and explain concepts. We can see this if we mute the
sound whilst watching a movie. By watching the characters, without hearing what they say,
we have a fair idea of what each feels about some of the incidents that are occurring in the
movie. However, we would not be able to understand even the majority of the story just by
watching.
Managing future emotions

Just as prevention is better than cure in terms of physical symptoms, the same applies to
emotional states. The most important principle in for managing future emotions is to manage
expectations. Remember that we just saw how emotions are the difference between
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expectations and reality; managing expectations therefore manages future emotions. This
can be achieved by explaining what is going to happen for example when a patient is
admitted. Often when we ask people any questions? we are checking their expectations.
Managing emotions right here and now
The first step in dealing with someone who is upset (i.e. in an emotional status) is to
demonstrate that you get the emotion that they are experiencing as well as conveying
some sense of understanding why they are feeling it. With face-to-face communications, the
most effective way to do demonstrate that you recognise and understand an emotion is to
maintain gentle eye contact and nod as the other person tells their story. Your own face,
along with a nod and a few sympathetic noises, is the most effective first choice in conveying
that you understand and that you care than the words you use.
CLIENT- Needs and wants
Needs and wants
There is a saying in customer service that the customer is king! This means that the
customer has the power to make demands about their various needs and wants. Therefore,
the acronym for this section is HRH which is more commonly translated as His / Her Royal
Highness but here it stands for the clients need and want to be
H- Heard R-Respected H-Helped
Heard People need and want to be heard. Often people need to feel heard before
they will accept help. This is because they may be struggling to either come to terms or
make sense of something in terms of the what, how and why they feel what they do about
it. Sometimes when this happens people prefer to go quiet and think things through whilst
at other times they have the urge to talk to someone about it. The following statements are
frequently cited when someone wanted and needed to talk but didnt feel heard;
I wanted you to listen but you started giving advice

I wanted you to listen but you started telling me why I shouldn't feel the way I do. My
"irrational feelings" will make sense if you take time to listen and understand me.
I wanted you to listen but you started trying to solve my problem. I feel misunderstood
and patronised.
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Just because I want you to listen does not mean I am helpless; I may need help but I
am not helpless.
Respected Respect occurs when we believe that other people are entitled to their
opinions and to do what they want to do as long as it is legal, ethical and moral. The
challenge with respect is that many people confuse the difference between having the right
to an opinion and believing their opinion is right. When we believe our opinion is right to
the point that everyone elses must therefore be wrong, it leads to a tendency to disrespect
other people. The first step in respecting others is resisting our urge to judge them and their
opinions as wrong or inferior if they are different from our own. Often when we take the
time to make sure that we completely understand why they believe what they do, we realise
that people hold opinions for completely rational reasons at least rational to them.
Helped There are various attitudes we can hold with respect to helping other people.
The first attitude is to demonstrate a tendency to volunteer and offer help when you see
someone in need. This type of helpfulness is often referred to as the kindness, which is
borne out of being considerate. The second type of helpfulness is responding to a request
or a plea for assistance.
CLIENT- Trust
Trust is an emotion which occurs between two people or groups of people, whereby both
rely on the actions of the other to ensure or avoid some future event occurring. In order for
people to trust us, they must believe we are trustworthy i.e. worthy of their trust.
Trustworthiness is determined by two factors; the confidence someone has in our character
and the confidence they have in our competence.
Trustworthiness = character + competence
People have confidence in our character when we believe we will do the right thing. In
other words, we trust a persons character (or a corporations culture) when we have
confidence that their intentions and motivations are good. We believe that they mean well
and are genuinely keen to fulfil their side of the bargain and that they have no intention to
harm or exploit us. In contrast, mistrust occurs when we arent sure whether another party
will actually fulfil their obligations and keep our best interests in the forefront of their mind.
Distrust is stronger; it occurs when we are actually believe that the other party has an
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agenda that is directly at odds with our own or that they are unlikely to fulfil their obligations
or stated intentions.
We have confidence in someones competence when we believe they can do the right
thing. This has nothing to do with what we think of them as a person; it is more to do with
their actual skills and abilities. To truly trust and feel comfortable with another person, we
need to have confidence in their intentions and their abilities.
Clients must believe that we will not take advantage of them. Clients are at our mercy so to
speak since we know more than them about the technical side of our work and how much
effort and expertise are actually required to resolve a particular issue. Clients must trust
that our intention is to want to get the patient as well as possible, as quickly as possible, as
easily as possible as cost effectively for them as possible as opposed to not caring, delaying
or complicating the process for our own gains.
It is important to realise though that both components of the trust equation (character and
competence) are directly within our control; we can make choices that increase the trust
other people have in our character as well as our competence. In other we can control and
direct our behaviour in ways that either builds or weakens trust. As a NCE working within
veterinary practice there are many things we can do that builds or weakens trust with our
colleagues as well as our clients. The table below offers a list of behaviours that helps to
build trust between team members.
Character Competence
Never agree to something you cant or wont Know your job description and duties
be able to do
Actually do what you said you would do Ask if you dont know how to do something
that you know you should be able to do
Be on time Volunteer to show others how to do jobs they
are struggling to master
Give clients the benefit of the doubt until
proven otherwise.
Act in the interests of the client, not yourself
Look professional
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Maintain eye contact
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Notes page
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THE PSYCHOLOGY OF PERSUASION

MRCVS
vetpsych.com
brian@vetpsych.com
Persuasion is the process whereby you motivate someone to do something, (which they may
not have done) until you interacted with them. Persuasion can take many forms; one-on-
one conversation, a vaccine reminder, a radio ad or a threat. Persuasion can be both
negative and positive; i.e. it can be coercive and manipulative or it can be ethical and
constructive. Given that the veterinary profession is governed by a clear Code of Conduct, it
goes without saying that any attempts to persuade another party should not breach any
ethical or moral boundaries.
Ethos, Logos, Pathos: Three Ways to Persuade
Over 2,000 years ago the Greek philosopher Aristotle argued that there were three basic
ways to persuade an audience of your position: ethos, logos, and pathos.
Ethos: The use of character, image or reputation
The Greek word ethos is related to our word ethics or ethical, but a more accurate modern
translation might be image. Aristotle uses ethos to refer to the speakers character as it
appears to the audience. Aristotle says that if we believe that a speaker has good sense,
good moral character, and goodwill, we are inclined to believe what that speaker says. I.e.
we trust them.
Trust is an emotion which occurs between two people or groups of people, whereby both
rely on the actions of the other to ensure or avoid some future event occurring. In order for
people to trust us, they must believe we are trustworthy i.e. worthy of their trust.
Trustworthiness is determined by two factors; the confidence someone has in our character
and the confidence they have in our competence.
Trustworthiness = character + competence
People have confidence in our character when we believe we will do the right thing. In
other words, we trust a persons character (or a corporations culture) when we have
confidence that their intentions and motivations are good. We believe that they mean well
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and are genuinely keen to fulfil their side of the bargain and that they have no intention to
harm or exploit us. In contrast, mistrust occurs when we arent sure whether another party
will actually fulfil their obligations and keep our best interests in the forefront of their mind.
Distrust is stronger; it occurs when we are actually believe that the other party has an
agenda that is directly at odds with our own or that they are unlikely to fulfil their obligations
or stated intentions.
In order to be trustworthy, NCEs should also appear to have the appropriate expertise or
authority to speak knowledgeably about the subject matter. Ethos is often the first thing we
notice, so it creates the first impression that influences how we perceive the rest. For
example, when a NCE wears a uniform with a logo and a name badge or when a vet puts on
a white coat, they immediately gain a greater sense of authority in the eyes of the other
person than someone who wears everyday clothing such as trainers, jeans and T-shirts.
Logos: Logical Arguments
In our society, logic and rationality are highly valued. However, excessive formal logic and
reference to scientific data and theory is often referred to as jargon. It is therefore important
that we persuade others using a more rhetorical type of reasoning.
Aristotle described two types argument package (or enthymeme) based on two types of
logical argument; deductive logic and inductive logic.
Deductive logic works by showing how an undisputed premise (i.e. something both parties
believe is true) supports a conclusion. Aristotle used the following example of pure logic:
All men are mortal

Socrates is a man
Therefore, Socrates is mortal.
However, the skill in using this technique as a persuasive technique (as opposed to a logical
argument) depends on beginning with a premise, an assertion or a belief that the other
person actually believes in. This is called using the logic in the room; i.e. your basic
premise may not work on every audience every time but it must work on the person you are
addressing.
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Below is an example of how to use the deductive logic in the room
Begin with a common belief / value The most important thing is that animals dont suffer
Apply it to a specific circumstance That tooth is really sore
Conclude with the inevitable choice That tooth has to come out
Inductive logic works differently. It works by showing how multiple examples support a
conclusion.
Once again we have to use the logic in the room by using examples that will be persuasive
to the people we are addressing.
Below is an example of how to use the inductive logic in the room
Provide multiple examples (facts, Studies show that Lepto is still around, especially if
comparisons, stories) dogs lap out of puddles. In fact we saw a dog with it
last week.
Demonstrate how they are connected Lepto is a genuine threat in this area (and especially
in dogs that lap out of puddles), like yours!
Conclude with the obvious choice We need to vaccinate him!
In inductive logic, at least three pieces of supporting evidence seems to be the magic
number; i.e. the use of three examples, facts, comparisons and stories.
By the way.......in the days before the laws and methods of the scientific approach,
philosophers used to debate how the world worked using deductive logic packages; i.e.
because such-'n-such is (assumed to be) true and such-'n-such is also (assumed to be) true
and everybody agrees on this other thing, then-poof, stands to reason, this is a fact! The
problem was many of their basic assumptions were flawed and their subsequent theories
were like building a house of cards on sand; neither the foundational assumptions nor the
supporting material was very robust. The most classic example of how this technique back
fired was the assumption that the earth was at the centre of our solar system and all models
that predicted the movement of the planets based on this basic premise were therefore
flawed.
This all changed in the fifteenth and sixteenth centuries when the first scientists such as
Hume, Locke, Bacon, Newton, Hayley etc. (who went on to form "The Royal Society")
rejected deductive logic as a technique. Instead they switched to inductive techniques with
the aim of building evidence to support a hypothesis. They came up with the simple basis of
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the science which has remained ever since; observe the occurrence of events, formulate a
hypothesis about what and why they are happening and then conduct experiments to test
your hypothesis. If the results of the experiments were consistent with the hypothesis,
evidence is assumed to have been collected in support of your theory. This is the basis of
evidence based science. You might be tempted to believe that no-one nowadays therefore
believes anything unless supported by evidence. The problem is that what some people call
evidence other people call coincidence. For example, if an owner gives their pet a
homeopathic remedy and it gets better they are likely to conclude that the homeopathic
medicine worked! Thus homeopathy works! This is why both deductive and inductive
arguments are powerful as persuasive techniques; people are very easily persuaded by
relatively weak evidence or by clinging to unquestioned beliefs as the basis of proof about
cause and effect. Vets do it too; I used this drug once, it worked, its better than that other
drug I used to use!
Thus many persuasive arguments are often based on probabilities rather than certain truth.
This is true of many of the problems we face in veterinary practice. We cannot know with
absolute certainty what the best solution is, yet we must act anyway. Persuasion therefore
involves convincing people to accept our assumptions as probably true and to follow our
recommendations.
Pathos: The Emotions of the Audience
Most of us think that we make our decisions based on rational thought. However, Aristotle
pointed out that emotions such as anger, pity, fear, and their opposites, powerfully influence
our rational judgments. Many political appeals and the advertising we experience are
directed toward encouraging us to act due to emotion more than reason.
Appeals to the emotions and passions are often very effective and are very common in our
society. Such appeals are not always false or illegitimate. It is natural to feel strong emotions
about tragedies, victories, and other powerful events as well as about ones own image and
identity.
One form of emotional persuasion is called emotional blackmail which is common in

personal relationships as well as professional relationships. Susan Forward and Sue
Fraziers book entitled Emotional Blackmail is an excellent read, especially with respect to
how emotional blackmail is used in personal relationships. The following section is not to
advocate its use, but to help us to be aware of its existence and how it plays out. By being
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aware of when these strategies and techniques are being used on you, you are better able
to resist them.
Emotional blackmail is a powerful form of manipulation in which blackmailers threaten, either

directly or indirectly, to punish them to get what they want and win compliance. Knowing
that you want something or you want the other person to do something, blackmailers may
threaten to withhold or remove the valued resource, or make you feel like you must
constantly earn their compliance or approval. If you believe the blackmailer, you can fall into
a pattern of letting the blackmailer control your decisions and behaviour and become caught
in a sort of psychological fog.
Emotional blackmailers use fear, obligation and guilt in their relationships, ensuring that their
victim feel afraid to resist them, obligated to let them have their way or guilty if they don't.
Forward and Frazier use the acronym FOG, standing for Fear, Obligation, Guilt; feelings
which often result from being exposed to emotional blackmail.
Clients in veterinary practices use emotional blackmail on occasions. For example, it is not
uncommon for a client to call the practice and ask the receptionist for more ear drops. The
receptionist will duly explain that the ear drops cannot be given out over the counter as they
are a prescription only medicine; i.e. the vet needs to see the patient and decide which ear
drops are best suited. The client now has a choice; comply with the receptionists
recommendation to see the vet or try some manipulative persuasive techniques to try and
get what they want; thus begins the FOG manoeuver in fact they usually carry out the
sequence as GOF instead of FOG; guilt then obligation then fear. Heres how;
Guilt
The client may say they are unable to make an appointment for several days and then try
and make you feel guilty about not giving them the ear drops by making you feel that you are
now the cause of the pets unresolved pain; but his ear is really sore and I dont want him to
be in pain until I bring him in later this week!. The receptionist (or practice) has a choice;
comply with the clients wishes and give them the ear drops (but suffer the wrath of the VMD
for breaching dispensing regulations!) or continue to resist by stating the now increased
importance for an appointment since the pet is in pain! (It is of course entirely possible to
play the client at their own game and put the feelings of guilt back onto them; i.e. make them
feel that it is them that is causing the prolonged pain!.......however adopting this strategy is
unlikely to resolve the situation smoothly; fighting emotional blackmail with emotional
blackmail rarely resolves disputes nor builds relationships.
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Obligation
If the client doesnt decide to book the appointment they may continue to manipulate by
increasing the emotional pressure from feelings of guilt to feelings of obligation. They may
say things like I thought you were meant to care about animals! You lot are only interested
in money! or if the client doesnt have the money they may say you have to see my dog!
Obligations are trickier to resist because often the client will strike an obligation that we know
we must / should fulfil. At this point is the trick is to recognise the difference between what
obligations we must fulfil and how we can fulfil them. Our thought response to I thought
you were meant to care about animals may be I am aware I have a duty of care towards
the animals under my care but just giving out ear drops isnt the only way I can ethically and
legally fulfil my obligations.
Fear
The emotion of fear results from a threat of loss or harm. Clients who have been resisted
having used obligation may move onto fear. The classic threats are Ill report you to the
Royal College or Ill go to a practice that cares!
Page 143 of 334

TRANSFUSION MEDICINE IN A WAR ZONE

Sam Rawlinson (Col L/RAMC/V Rats) OBE, TD, BSc, Much, FRCP, FRCPath, FRCS
In this presentation I will try to give a broad overview of how we developed and refined our
ability to provide world class transfusion to the severely injured patients being treated in UK
military hospitals in Iraq and Afghanistan. I think it is important to highlight that the capability
I will be describing was produced as result of team work. I would particularly like to highlight
the outstanding contributions made by:
Maj Steve Smedley and his Blood Supply Team in Birmingham

Col Heidi Doughty
Joan Jones
The Defence Medical Services
The National Blood Service
UK and NATO Blood Transfusion Services
RAF
Operating in a war zone presents a number of challenges. Both Iraq and Afghanistan are
1000s of miles away from the UK. The environment we work in tends to be fairly rugged. The
facilities available change as we moved from being an expeditionary force to one deployed
in an enduring operation.
Our primary goal, as transfusionists is to give the transfusion support needed to treat
patients who have been severely injured in order to reduce both their mortality and the
morbidity associated with these injuries. We have to be able to deliver what-ever is needed,
when it is needed. This is made more difficult because blood components have short shelf-
lives, and casualty flow rates can vary considerably. It is also not uncommon for some to
need over 100 units of blood to treat a single patient.
General Hawleys axiom for medical services to group forward, group early but maintain
balance is highly relevant to transfusion services. The approach we adopted was to develop
our service using an evidence based approach. The evidence we used varied, but includes
Blood Quality Regulations, current literature, the benchmarking of other NATO blood
transfusion services, and various studies. In order to deliver this we evolved over time.
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The blood components used are principally supplied by the National Blood Service; they are
donated by UK donors, collected, tested and processed by the NBS, shipped by the Blood
Supply team and transported by the RAF (as priority cargo). The systems we have
introduced allow us to safely supply red cells, fresh frozen plasma, cryoprecipitate and
platelets from the UK to the UK Military Hospitals in both Iraq and Afghanistan. We are
currently the only country in the world which has the capability of supplying platelets
collected at home and delivered to a war zone.
Early experience showed that patients were more likely to survive if rapid and aggressive
transfusion support was given. As a result we developed a Massive Transfusion Protocol
that proactively delivered this. This approach has now been adopted throughout the UK.
It is fairly obvious that patients who are severely injured may need to be given blood before
they arrive in a hospital. In order to do this we modified a technique that had been used in
Dundee for a number of years to provide road side transfusion support. This system is called
Safe Return. It enables us to safely transport red cells and plasma in the helicopter with the
MERT team so that they can be transfused into severely injured soldiers at the front line.
This approach is now being used by several of the UK Helicopter Ambulances.
More recently we have also reverse engineered the processes used in Iraq and Afghanistan
so that they can be used in Dundee. The Code Red system allows us to have red cells,
plasma and platelets available to treat patients who are severely injured immediately on their
arrival in the A&E department in Ninewells Hospital.
Providing platelet support, when they only have a shelf life of 5 days (at 22oC), and demand
is so variable, is quite challenging. We have addressed this by holding a substantial stock of
UK platelets, and by introducing an In Theatre donor apheresis programme, using
Haemonetic apheresis machines. Initially we used a pre-selected and pre-tested volunteer
donor panel, and retrospectively test each donation collected. This was improved by
introducing a near donation testing system for the mandatory microbiological tests that was
validated by the Health Protection Agency.
Finally I think it is worth noting that whilst the service we offer has evolved substantially, and
is really quite impressive - there is always room for improvement.
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COMPARATIVE TRANSFUSION MEDICINE

khumm@rvc.ac.uk
Introduction
In 1946 the Blood Transfusion Service was launched in Britain. There are four national
blood services, one each in England, Wales Scotland and Northern Ireland. The English
transfusion service has now been renamed National Health Service Blood and Transplant
(NHSBT). Despite the fact that much of the original research into blood transfusions was
performed in animals (the first recorded blood transfusion was performed by Richard Lower
in 1665, transfusing blood from one dog to another), storing animal blood products for
therapeutic purposes was not legal in the UK until 2005. The NHSBT supplies
approximately 2 million units of blood a year to hospitals in England and Wales at a cost of
125 per unit of packed red blood cells (PRBC). Pet Blood Bank processes over 2000
donated canine whole blood units per year to supply to veterinary practices in the UK at
varying costs, but the current price for a unit of DEA 1.1 positive PRBC is 138.99 (ex. VAT).
There are many interesting similarities and differences between human and companion
animal transfusion medicine. These notes focus on blood types, platelet transfusions,
transfusion reactions and transfusion triggers.
Blood types
A blood type is determined by the presence or absence of antigens on the erythrocyte

surface. The antigens may be proteins, glycoproteins, glycolipids or carbohydrates
depending on the blood typing system used. In humans we generally consider the ABO and
Rhesus systems, classifying people as A+, AB- etc. However, there are 31 other blood
group systems recognised by the International Society of Blood Transfusion, including the
MNS system, the Kell system etc. The reason we focus on the ABO and Rhesus systems is
that these are the antigens most likely to cause a transfusion reaction with the discovery of
the ABO system in 1900 being a major breakthrough in transfusion medicine.
In dogs we focus on the DEA (dog erythrocyte antigen) system and in cats the AB system,
for similar reasons i.e. these are the antigens most likely to cause a reaction. However, in
2007 two new blood types were described, Mik in cats and Dal in dogs. It is likely that there
are many many more, but their clinical significance is probably minor. A cat which is Mik
negative receiving Mik positive blood can have a transfusion reaction on the first transfusion
and so some clinicians recommend cross matching all feline transfusions, although at the
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authors institute this is not performed and the actual prevalence of Mik positivity and
negativity is unknown.
As with the AB system in cats, administering a blood product which is not ABO type matched
in humans can result in a fatal transfusion reaction. This occurs in about 1 in 14000
transfusions and deaths unfortunately occur with legal action taken against medical staff
involved in some of these situations. The Serious Hazards Of Transfusion (SHOT) scheme
was set up in 1996 to collect anonymous data on adverse events resulting from transfusions
in the UK. It revealed that between October 1996 and September 1997 63 patients were
reported to have been administered the incorrect blood typed product resulting in 1 death
and 9 cases of major morbidity. The number of people involved in a transfusion in a human
hospital is probably far higher than in a veterinary hospital but undoubtedly errors do occur in
the veterinary world. SHOT devised guidelines to try to decrease the risk of adverse events
and these include appropriate training, checking the patient is correctly identified at sampling
and at administration of the product and also double checking of the laboratory blood typing
result. Improvements have resulted with the 2012 SHOT report (2012) showing that there
were 14 incidents in which ABO incompatible blood had been transfused (4 resulting in
serious morbidity). As over 3 million units are transfused each year the overall incidence of
transfusing ABO incompatible blood is approximately 1:250,000 units.
Platelet transfusion
The production of multiple products from one donation was a great step forward in
transfusion medicine. Component therapy is beneficial for any patient who has not lost
whole blood. It decreases the risk of adverse events in the recipient as they are only
administered what they require and also maximises the utility of each precious donation.
Traditionally the various products were separated out post donation through centrifugation.
This is generally what happens in veterinary blood banks and in the UK plasma, PRBC and
cryoprecipitate are all produced commercially in this way. Apheresis is a method of
producing specific blood products while returning that which is not required to the patient. It
is performed regularly with human donors, with 80% of platelets for transfusion provided in
this way. The donors blood passes through an apheresis machine which separates out the
platelets and returns the rest of the blood to the patient, this is known as plateletpheresis.
This is a very valuable method as the number of platelets in a standard donated blood unit is
not enough to produce a unit of platelets, requiring the platelets from many units to be
pooled. This means that typing of the unit is more difficult and also the risk of infection is
increased. Platelet donors can donate up to 4 units of platelets in one donation sitting and
can also donate more regularly.
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Platelet donations are most commonly used in humans for patients with bone marrow failure
e.g. post-chemotherapy. The idea of units of administering platelets is very attractive to
veterinary practitioners, particularly when considering patients with immune mediated
thrombocytopenia although the lifespan of platelets transfused into these patients is likely
very short. There are difficulties in platelet product production in our patients however.
Primarily once a unit of platelets is produced it needs to be stored at 20-24C and undergo
constant agitation. The product also only lasts 5 days and so the costs involved in producing
each unit are very high. It is likely that the demand would not be high enough for
commercial production in the UK although in the US commercial blood banks do supply
platelet products, with a unit of fresh platelet concentrate costing $420 from American Blood
Resources International.
Fresh whole blood is the product most commonly used in veterinary medicine to provide
platelets to thrombocytopenic animals. It is thought that platelet function is preserved for up
to 8 hours in whole blood collected in CPDA1 kept at room temperature post donation.
Chilling blood causes platelets to become dysfunctional resulting in rapid clearance from the
recipients circulation. Fresh platelet products can be produced in dogs, platelet rich plasma
(PRP) and platelet concentrate (PC) are produced from fresh whole blood by careful
centrifugation. Plateletpheresis is also performed to produce canine platelet concentrate by
at least one American blood bank. PRP and PC have to be stored at room temperature and
administered quickly, but their advantage over the use of whole blood for administration of
platelets is that a smaller volume unit is produced and it can be administered to non-anaemic
patients without causing polycythaemia.
Cryopreserved canine platelets are sold in the US and are produced by the addition of
DMSO to platelet concentrate with or without the addition of Thrombosol (a solution which
reversibly inhibits platelet activation). These platelets can then be stored at -80C for up to a
year. Although this massively increases platelet lifespan, platelet function, lifespan post-
transfusion and yield are decreased. Platelets can also be treated by lyophilisation to
increase their lifespan. This involves freezing the platelet product and then removing the
water from it i.e. freeze-drying it. Lyophilised platelets can be refrigerated for up to 24
months and are reconstituted with saline immediately prior to use. Their lifespan is thought
to be shorter post-transfusion than fresh platelets. Davidow and others (2012) compared the
use of fresh and lyophilised platelets in thrombocytopenic dogs and found no difference in
survival or need for further transfusion products between the two groups. Mild transfusion
reactions were suspected in a low number of dogs in both groups. To the authors
knowledge lyophilised platelets are not currently commercially available.
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Transfusion reactions
SHOT reports that approximately half of the complications of transfusions are due to human
error such as administering the incorrect blood product, administering an inappropriate
amount of product or incorrect handling or storage of the products. The rest of the
transfusion complications involve the patients response to a correctly administered
transfusion. Two large retrospective studies examining canine and feline transfusion
recipients reported acute transfusion reactions occurring in 13 and 9% respectively (Kerl and
others, 1993; Klasser and others, 2005). In cats fever was the most common sign seen in
5/11 cats but this detail was not available in the canine study. In humans non-haemolytic
febrile transfusion reactions are fairly common (affecting 1-2% of patients) but they are
generally not serious and can be controlled by slowing the transfusion or administering non-
steroidal anti-inflammatory drugs. To classify as suffering from this type of reaction the
patient must have an increase in temperature of >1C with no other cause of the fever
detected. A similar approach to diagnosis and management is recommended by the author
in dogs and cats. These reactions are thought to be secondary to cytokines which
accumulate during blood storage and leucoreduction has decreased their frequency but not
eradicated them. There are many other possible causes of transfusion reactions but
transfusion related acute lung injury (TRALI) is the most common cause of transfusion-
related mortality in humans. It is caused by antibodies directed against white blood cells
which result in leucoagglutination and non-cardiogenic pulmonary oedema. There are no
reports of TRALI in canine or feline patients however and given the severity of clinical signs
seen in some human patients it is likely therefore that it does not occur in the same way, if at
all, in our patients.
Transfusion Triggers
In human medicine there has long been an ability to give large volumes of blood products
meaning that a liberal approach to transfusion developed. In veterinary medicine we have
never been this fortunate and we also have to consider financial costs for our patients. The
human medical field was shaken when studies started to suggest that using the commonly
held transfusion trigger of a haemoglobin of 95-100g/l (equating to a haematocrit of
approximately 28-30%) may be associated with more harm than using a trigger of 70g/l
(equating to a haematocrit of approximately 21%). Studies are on-going to look at different
patient populations to assess whether different triggers are appropriate. In our world these
triggers would still probably be fairly generous; particularly in cats (although the reference
range for human haematocrit is more akin to a dogs than a cats at 37-51% for females and
43-52% for males). There is also a move within human medicine towards prescribing one
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unit of packed red blood cells at a time (unless there is large scale life threatening bleeding)
to prevent potentially unnecessary and detrimental administration of further units. Again this
is rarely a concern in the veterinary world. For our patients we tend to assess the need for
blood on a case by case basis, focusing on clinical signs, underlying disease process
(whether resolution is likely and over what time period as well as expected lifespan of the
patient) and cost to the owner; although transfusion triggers are discussed they are not
applied across the board. We do not treat the large numbers of chronically seriously unwell
patients that human medics do and so long term mild to moderate anaemia does not trouble
us so commonly.
Conclusions
Human transfusion medicine shows us what is possible and where veterinary transfusion
medicine may progress for example with platelet transfusion. We certainly can learn a lot
from the approach to transfusion safety and monitoring of transfusion reactions with the use
of guidelines decreasing the risks involved. However, there are advantages to the veterinary
system particularly when considering individual care of a patient with respect to deciding on
whether a transfusion is required.
Further reading and references
Blais M and others (2007) Canine Dal Blood Type: A Red Cell Antigen Lacking in Some
Dalmatians. Journal of Veterinary Internal Medicine 21(2) 281-286
Callan MB, Appleman EH, Sachais BS. (2009) Canine platelet transfusions. Journal of
Veterinary Emergency and Critical Care 19(5) 401-415
Davidow EB and others (2012) Use of fresh platelet concentrate or lyophilized platelets in
thrombocytopenic dogs with clinical signs of hemorrhage: a preliminary trial in 37 dogs.
Journal of Veterinary Emergency and Critical Care 22(1) 116-25
Fastag E, Varon J and Sternabch G (2012) Richard Lower: The Origins of Blood
Transfusion. The Journal of Emergency Medicine 44(6) 1146-1150
Hux BD, Martin LG. (2012) Platelet transfusions: treatment options for hemorrhage
secondary to thrombocytopenia. Journal of Veterinary Emergency and Critical Care 22(1)
73-80
Kerl ME, Hohenhaus AE. Packed red blood cell transfusions in dogs: 131 cases
(1989). J Am Vet Med Assoc 1993;202(9):14959.
Klaser DA, Reine NJ, Hohenhaus AE. Red blood cell transfusions in cats: 126
cases (1999). J Am Vet Med Assoc 2005;226(6):9203.
Weinstein, NM and others (2007) A Newly Recognized Blood Group in Domestic Shorthair
Cats: The Mik Red Cell Antigen. Journal of Veterinary Internal Medicine 21(2) 297-292
http://www.shotuk.org/home/
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Notes page
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DISASTER MEDICINE: WHAT CAN WE DO BETTER DURING A DISASTER?

abreton@vescone.com
Introduction: While there is never a perfect solution on how to handle each disaster there
have been some key lessons learned. Fifty-six percent of Americans own a pet; therefore
when a disaster strikes, animals usually are involved. Today veterinarians and technicians
are considered first responders and the community looks to them for help.
All Clinics Should Be Prepared: Veterinary clinics by themselves are generally not
prepared for a disaster. Unfortunately many practice owners continue to assume the local,
state or federal government will aid them in times of a disaster.
Lessons Learned: It is imperative that each individual veterinary clinic has its own disaster
plan just like every human hospital has a disaster plan in place. Veterinary clinics need to
work with their local communities to be incorporated into the local plan. The federal
government now has plans in place to offer federal aid to those clinics that provide services
to the community. While no plan is perfect, one thing is certain: any plan is better than no
plan. Numerous chapters, articles and even online videos have been published on how to
create your own clinic disaster plan and how to protect your clinic in case of a disaster.
Veterinarians Are The First Line Of Defence to Reuniting Pets & Owners: Lamar Dixon
was a fairground outside of New Orleans that held upwards of 6,000 or more animals
including livestock and exotics. Less than 1% of the dogs had identification tags or
microchips and the number was even less for cats. While it is true that contacting the
owners of those that had tags/chips created quite a challenge, the fact remains that most of
those owners were eventually tracked down.
Lessons Learned: Veterinarians have the ability to ensure that each pet that comes through
their doors has appropriate identification. While microchipping is effective, its only effective
if the owners remember to update their information. Reminding owners at the yearly visit is
important. Pet tag engravers can offer a clinic more revenue. If purchasing an engraver is
not an option, pre-paying for ID tags at a local pet store and offering them to owners is also
another idea. A computer can be set up in the clinic so owners can purchase them directly
online through a website the clinic trusts or a technician can sit down and fill out the
paperwork, take payment and mail away for a tag for the owner.
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Research Facilities & Zoos Are Not Exempt: For years research facilities and zoos have
created their own disaster plans. Most of these plans assume there will be only a temporary
interruption of services and that hardened structures could operate with emergency
generators thus keeping the facility operational. Unfortunately during Katrina this was not
the case. Most of the research and zoo employees were forced to relocate and the city saw
a complete shutdown of all resources. These facilities had to reach out to federal agencies
in order for the animals to be rescued. Millions of dollars of research was destroyed.
Lessons Learned: These facilities need to work more closely with the state and federal
government to create back up plans to their pre-existing disaster plans. Unfortunately
sometimes it is impossible to save all the animals in such facilities. No matter all the
planning, some animal casualties must be planned for.
Every State Must Have An Active SART Team: After the state of North Carolina suffered
more than 1 billion dollars worth of damage to their farm animal population during a
hurricane in 1999 they realized they needed to be better prepared. They formed the first
SART (state animal response team) and worked with the state using the basic principles of
human disaster response. They set up their own incident command system (ICS) which is
the cornerstone to every good disaster plan. ICS had been established by the California fire
department in the 1970s after they had lost more than 600,000 acres of land, 800 buildings
and 16 lives due to wild fires and a lack of organization. The system was integrated into
FEMA by President Carter in 1979.
Lessons Learned: Every state should have an active SART team. SART team members
should be minimally trained in ICS, haz-mat, personal protection equipment (PPE) and take
a beginner animals in disasters training class. All of these are offered online for free from
FEMA at: http://training.fema.gov/IS. SART teams should hold meetings and trainings and
keep an accurate record of members expertise (large animal, small, exotics). While
veterinarians/technicians may have their own clinic disaster plan in place it is important that
veterinarians/technicians become involved in their local and state animal response teams.
Take Your Pets With You: For years pet owners have been instructed to leave their pets
behind. During Katrina many local veterinary clinics offered to board pets during the storm
so that the people could evacuate. Unfortunately most of those veterinary clinics took on
water and many of those pets were trapped in cages and died.
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Lessons Learned: American Red Cross, HSUS and other large human/pet sheltering
organizations are working together for the first time to help solve the sheltering problem.
Pets and people must be evacuated together and should not be boarded at local clinics that
are affected by the disaster themselves. There is no perfect solution, but it is imperative that
veterinarians/technicians work with their local and state animal response teams so that they
can identify locations where sheltering can occur. If sheltering together is not possible, then
measures must be in place to create a shelter and care for the pets housing and medical
concerns.
Save Pets = Save People: Images of humans, felines and canines together on rooftops
waiting to be rescued were all over the news. Many people died because they refused to
leave their pets. As a result from the poor animal response to Hurricane Katrina many
veterinarians, animal organizations, state and local officials got together and helped create
the Pets Evacuation and Transportation Standards Act (PETS Act) which was signed into
law by President Bush on October 6th 2006.
Lessons Learned: The reason it was signed into law so quickly was simple. If you save the
pets you save the people. The PETS Act requires local and state emergency preparedness
authorities to include in their evacuation plans how they will accommodate household pets
and service animals in case of a disaster. Local and state authorities must submit these
plans in order to qualify for grants from the Federal Emergency Management Agency
(FEMA).
Veterinarians Are Not The Best Record Keepers: During Katrina 6000 animals entered
Lamar Dixon fairgrounds in 14 days (a rate of over 400 animals a day). When animals
arrived, one fact was simple: appropriate records and identification were not kept. Pets that
received veterinary care had a record, but the rest of the animals did not. It wasnt until
weeks later that the animals were categorized, identified and received an actual record.
Lessons Learned: Veterinarians are not the best record keepers. Does your practice have a
way to keep records without a computer? Can you generate receipts, prescription labels
and records without electricity? Does the SART or local animal response team have a way
to keep track of every single animal that they shelter or care for? It is important to develop a
system before a disaster hits.
Euthanasia/Disposal Plans Must Be In Place: As terrible as it sounds, plans must be in

place to euthanize and dispose of animals on a small and large scale. This may include
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plans on how to dispose of large (elephants, cattle, horses) and small (dogs, cats, chickens)
animals.
Lessons Learned: All good disaster plans account for euthanasia and disposal. Many local
veterinary clinics assume they will not be involved in a disaster and they then find
themselves in the front lines. As animals are brought in and more pets are euthanized, how
many bodies can your facility hold? If the local animal pet cemetery is inoperable, who will
dispose of the bodies? Many local and state animal response team forget to include
euthanasia and disposal plans for all species.
Volunteers Will Come/Are You Acting As A Volunteer? From the biggest to the smallest
disasters, volunteers will always come especially when it involves animals. All it takes is one
image of a cute helpless animal and the people start arriving. This was the case during 9/11
when people rushed down to help save the abandoned animals and during Katrina when
they just showed up and starting going through homes. Many veterinarians and technicians
just up and left their paying jobs to come help the animals of Katrina. While their intentions
are good, often at times volunteers cause more problems.
Lessons Learned: All good disaster plans account for volunteers. While not ideal, in large
scale disasters sometimes volunteers are needed. This was the case during Katrina. Some
of the volunteers were injured and did not have disability insurance. If you want to volunteer
the best way is to get involved with a team before a disaster. Many organizations offer
insurance to their members should they become injured or even sued. You must always
check with your employer to see if its okay if you volunteer and, if you elect to do so without
their consent, then you must accept the consequences afterwards. With the exception of the
federal disaster team, NVRT, employers are not required to hold your position if you
volunteer for a disastereven if the disaster is in your own town. If you are already involved
in disaster planning then your plan must account for volunteers.
Use the Media Effectively: During any disaster, no matter the size, the media will come.
By knowing what to say and who should speak to the media you can utilize them in a way
they will become your friend instead of your enemy.
Lessons Learned: Disaster plans must include how to deal with the media. Only one or two
people should be allowed to speak to the media. If you are not the person who is
designated to speak, then dont. Politely say no comment and refer to the person who is
designated as the public information officer (PIO). The PIO should be responsible for
organizing information about the disaster and communicate what is going on and if any
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resources are needed. While sometimes the media can be the enemy, they can also act as
a friend. In desperate times, the media has the ability to obtain resources quickly such as
food (for both pets/humans), shelter (for both pets/humans), equipment, cages, bowls,
medical supplies, volunteers, leashes and more.
Protect Yourself During A Disaster: Mental and physical health is generally forgotten
about during a disaster. Working 24 hour shifts and not eating well is considered normal.
Besides mental health issues, disasters can be dangerous for responders. Besides the
danger of being bitten by an animal, toxic substances, down power-lines and even angry
looters/mobs can pose a threat. All of these became a reality during Katrina.
Lessons Learned: Every disaster plan must include a plan to keep the responders safe. It
must include down-time for responders involved. Adequate food/water and sleeping area
should be provided to all those involved. Human medical treatment should be available to
responders if needed. Physical protection should be given to responders if needed. The
military reservists can be called upon if situations are dangerous. Ideally all disaster teams
should also have a safety officer who is trained to spot safety hazards and works towards
keeping the team safe. PTSD must be discussed with each responder. Responders should
be given information on how to take care of themselves during and after the disaster.
Protecting the Pets During A Disaster: Reports were all over the news of people stealing
fireman coats and sneaking into the world trade centre pile site. At Lamar Dixon the
numbers of animals started to decline over time. Some of these animals found their owners
and some of them were stolen.
Lessons Learned: Even though most people are well-intentioned during a disaster,
unfortunately there are some that are not. Disaster plans must include ways to prevent the
pets from harm or theft.
An Ounce Of Planning Is Worth A Pound of Prevention: Disaster planning must plan for
all types of disasters: natural and man-made. Most of the lessons learned were simply
because no planning had taken place before the disaster occurred. Scrambling at the last
minute only adds to the chaos that is already present.
Lessons Learned: Plan, plan and more planning. Keeping teams organized and trained
when there is not a disaster is difficult because disasters help to motivate people. It is
imperative that meetings are held and training occurs to keep people interested. Disaster
plans should be three-fold: local, state and federal and training must occur on all levels.
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Conclusion: While there is never a perfect disaster response, it is imperative that we learn
from each mistake that has made in the past. Planning is the key. Veterinarians and
technicians need to plan for themselves, for the clinic, for the community and for the state. It
is important we take an active role in planning to help animals in disasters.
References available on request.
Page 157 of 334

CONTRAST RADIOLOGY IN EMERGENCY PRACTICE

IDEXX Telemedicine
The use of radiographic contrast can provide important diagnostic information above that of
survey radiographs alone. Upper GI studies are the most frequently performed contrast
study in emergency practice, often to rule out the presence of gastrointestinal obstruction.
Contrast evaluation of the gastrointestinal and urinary tract should be possible in emergency
practice without specialist equipment or expertise. The methods discussed in this lecture
can be extremely useful if ultrasound is not available or referral is not an option for the client.
This lecture will discuss the indications for, methods and interpretation of contrast studies in
emergency practice. This is necessarily a limited overview, and further details on
procedures and interpretation may be elucidated from the references provided.
1. Contrast evaluation of the gastrointestinal tract
Upper GI study
The upper GI study is an excellent method for additional evaluation of the gastrointestinal
tract when ultrasound expertise is not available. The interpretation of an upper GI study is
arguably easier than ultrasound, and can be a more definitive means for excluding surgical
obstruction. It is essential that the procedure is performed with an adequate volume of
contrast and with orthogonal views obtained at regular intervals for this procedure to be
diagnostic.
Indications
Suspected gastrointestinal obstruction is the foremost indication for an upper GI study in

emergency practice. This can help determine if surgical intervention is necessary when
survey radiographs are not definitive or difficult to interpret. If the patient is clinically stable
and survey radiographs are inconclusive I would usually initially recommend follow up fasted
survey radiographs in 4-12 hours after any necessary fluid therapy and medical
management. Obstructive patterns are either static or progressive. It may also be possible
to determine if acute gastrointestinal signs presenting as an emergency are secondary to a
more chronic process such as neoplasia.
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Method
The stomach should ideally be empty of food prior to the study. This is not always going to
be the case in patients that are potentially obstructed, and the study will help to determine if
any gastric contents are retained ingesta or foreign material. Sedation should be avoided
due to the effects on gastrointestinal motility, but Acepromazine may be administered at 0.1-
0.25mg/kg IM if necessary.
For canine patients 5-10ml of 30% weight per volume of micropulverised liquid barium
should be administered by either orogastric tube (ideal) or oral syringe. If necessary
confirmation of the position of the tube can be obtained with a lateral radiograph. The larger
dose would be recommended in smaller animals. For feline patients 12-20ml/kg of contrast
is necessary for a diagnostic study. A lesser volume can markedly increase gastric emptying
time and lead to a false diagnosis of delay and limited gastric evaluation. Contrast should
never be mixed with food for this study. This will also lead to delayed gastric emptying and
there will be an irregular appearance to the contrast which can confound interpretation.
Immediately after contrast administration initial radiographs should be obtained. A lateral

and ventrodorsal view is necessary as a minimum. If there is any concern for a gastric
lesion dorsoventral and opposite lateral views will also be necessary as a filling defect
associated with a lesion of the wall may only be visible on one view. Follow up lateral and
ventrodorsal views are ideally recommended at 30 min, 1 hr, and 2 hrs and until contrast has
filled the colon and gastric emptying has occurred. Follow up radiographs obtained at 12
hours can help to confirm that all the contrast reaches the colon. If this sequence is not
followed a partially obstructive surgical lesion or focal intestinal abnormality could be missed.
In cats gastrointestinal transit is more rapid and images should also be obtained at 15min.
Other contrast agents can be used. Iodinated contrast is typically recommended if

gastrointestinal perforation is suspected. However this does not provide an ideal study.
Ionic iodinated contrast is hyperosmolar and will draw water in to the intestines leading to
gradual decreased opacification and intestinal dilation which can confuse interpretation.
Non-ionic agents are better, but are very expensive for this purpose.
Interpretation
Gastrointestinal obstruction is characterized by segmental distension of intestine that

persists over multiple time points. The distension can be very focal, or more diffuse on the
oral side of the obstruction. There will be a delay in passage of contrast beyond the point of
obstruction. However, some fluid may pass, and the presence of contrast beyond this does
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not exclude an obstructive process. A persistent filling defect is frequently (but not always)
seen in association with obstructive foreign material. With linear foreign material the focal
distension is often not present. Instead there is plication of intestine rather than normal
tubular contrast filled bowel. If obstruction is within the pyloric outflow tract there will be
delayed gastric emptying, and if there is foreign material there is often a filling defect in the
pyloric antrum. Gastric outflow obstruction can also occur with neoplasia, pyloric
hypertrophy or pylorospasm, in which case the outflow is persistently narrow on multiple
views and can have a beak like appearance.
Neoplastic or focal granulomatous inflammatory lesions of the stomach or intestines are

characterised by static filling defects within the wall. In the stomach these may only be seen
on the initial gastrogram phase of the study.
Normal canine gastric emptying occurs in 30-120 min. It can be delayed by systemic
disease and certain medications in addition to gastrointestinal disease. Contrast typically
reaches the colon by 30-120min and the small intestine empties in 180-300min. In cats
normal gastric emptying occurs in 15-60min and normal small intestinal transit is 30-60min.
BIPS
Small spherical opaque structures called BIPS (barium impregnanted polyethylene spheres)
are available for use in evaluation of gastrointestinal disease. They come in a large and
small size, and the pattern of passage of the BIPS can be associated with certain
gastrointestinal disease. However, the use of these has generally fallen out of favour and I
find them to be of limited use in evaluation of the gastrointestinal tract, as there are many
factors that influence their passage. A barium upper GI study is considered more reliable in
evaluating for obstructive disease.
Pneumocolonogram
Diagnosis of an obstructive pattern on survey radiographs relies on the differentiation of

small intestine from colon, and this is not always easy. A pneumocolonogram involves the
administration of gas (room air is fine) in to the colon. Mild distension of the colon with gas
will often confirm its location as compared to potentially distended bowel. Caution should be
taken to avoid over-distension of the colon, which can result in damage.
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Barium enema
Indications
A barium enema is rarely indicated in emergency practice but could be helpful to confirm a
suspected acute lesion such as intussusception or colon volvulus (torsion). This can also be
used instead of a pneumocolonogram to differentiate small intestine from colon.
Method
The patient is placed in right lateral recumbency with the pelvis and rectum elevated using a
foam wedge. Contrast can then be administered with a large Foley catheter and should be
allowed to fill the colon in a gravity dependent manner without forced distension. This limits
the chances of complication. A 20-25% weight/volume concentration of micropulverised
Barium suspension is recommended. A starting volume of 11-15 ml/kg is used in the dog
and 7-11 ml/kg in the cat. Lateral, oblique and ventrodorsal radiographs should be obtained
immediately after filling of the colon with the catheter clamped to prevent leakage. An initial
right lateral view will help to ensure that there is sufficient contrast filling.
Interpretation
Intussusception has a classic coiled spring appearance on contrast studies. With volvulus
the colon is typically distended with focal severe narrowing and displacement. An empty
colon should fill evenly with contrast, though the contrast will not always reach the ascending
colon and caecum in a normal animal. Focal narrowing of the lumen is an indication of
intramural or extramural thickening and luminal constriction. This could occur secondary to
neoplasia or less typically an inflammatory lesion. A neoplastic lesion will appear as a
sessile filling defect.
Oesophagram
Indications
An oesophagram can be used in evaluation of suspected oesophageal dysmotility,

obstruction or congenital anomaly. These patients often present with regurgitation as a
primary clinical sign, but dependent on the suspected aetiology there may be additional
gagging or associated neurologic deficits.
Survey thoracic radiographs should always be obtained in cases of suspected oesophageal

disease. Bone foreign bodies within the oesophagus may be readily visible without further
investigation. If diffuse megaoesophagus is present there is also no indication for an
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oesophagram, as this will only confirm the diffuse distension. However, a contrast study can
be an excellent way to confirm oesophageal distension if you are not sure radiographically.
There is a risk of aspiration with oesophagography. If the patient has a history of aspiration
the study is generally not recommended. Barium is fairly inert in the lungs, and while
aspiration of barium can look dramatic radiographically it is typically readily cleared to the
regional lymph nodes. Aspiration of food is much more likely to result in pneumonia.
Aspiration of ionic iodinated contrast can however be catastrophic. Hyperosmolar contrast
draws fluid in to the interstitium and aspiration can rapidly result in severe morbidity and
even death.
Method
The type of contrast recommended depends on the type of lesion suspected. Esophageal
motility disorders are best evaluated with barium fluid followed by barium soaked kibble
(soaked for 10 minutes prior to the study). It is possible that either fluid or food will result in
abnormal motility when the other type does not. This can also be true of diverticuli and
oesophageal strictures (including those resulting from vascular ring anomalies).
Suspected oesophagitis is best evaluated with barium paste, which will adhere to inflamed
mucosa. Barium paste can also be useful in delineating esophageal foreign material and
can be best for delineating a focal mass.
Non-ionic iodinated contrast media should be used if there is concern for esophageal
perforation. Ionic iodinated contrast media should never be used as the hyperosmolar
contrast can lead to significant pulmonary oedema. If endoscopy is planned immediately
after the contrast study this would also be an indication for non-ionic iodinated media.
Following survey orthogonal radiographs contrast is administered orally (by feeding syringe
for fluid/ paste or by hand for food) with the patient in right lateral recumbency. 60% weight
per volume of barium sulphate suspension should be used for fluid studies. For small to
medium dogs approximately 15 mL is recommended. 20-30 mL may be necessary for large
dogs. Approximately 5 ml is recommended for cats. A similar volume of paste is
recommended.
Immediately after contrast administration a lateral radiograph of the neck and thorax and
ventrodorsal view of the thorax should be obtained. It may be necessary to repeat the study
with an additional bolus. Given the midline location of the thoracic oesophagus, an oblique
ventrodorsal view angled from left ventral to right dorsal can be helpful in evaluation of the
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intrathoracic oesophagus. If evaluating for motility disorders or oesophageal stricture, this

process should be repeated with the barium soaked kibble.
All oesophageal studies must be performed with the patient awake, to limit aspiration and to
ensure that motility is not affected pharmacologically. Some patients may not be suitable for
oesophageal contrast studies.
Interpretation
An oesophageal foreign body, particularly if obstructive, will result in varying degrees of

oesophageal distention oral to the lesion. The foreign body typically results in a focal filling
defect. The foreign material can also become coated with contrast, and will remain static in
appearance after the remainder of contrast has passed to the stomach.
Strictures result in focal narrowing which is persistently seen on multiple images, typically
with distention oral to the lesion. It is possible that the stricture will limit passage of food but
not fluid. Cranial to the carina and cardiac silhouette focal narrowing in immature patients
may be associated with a vascular ring anomaly. Oesophageal stricture can occur
secondary to scarring from a previous foreign body and association necrosis.
Oesophageal diverticuli are focal outpouchings of the esophagus that can occur congenitally
or secondary to prior foreign body trauma or inflammation. It is not uncommon to see a focal
widening similar to a diverticulus within the cranial thoracic esophagus of brachycephalic
type breeds such as bulldogs, where this may be incidental.
Sliding hiatal hernias can appear transiently or persistently during an oesophagram study,
and the displaced stomach is often delineated by contrast enhancement coating of the rugal
folds. Gastroesophageal intussusception is a more serious and acute condition, with a
curved intraluninal filling defect within the caudal distended oesophagus, barium outline of
the rugal folds and no contrast within the stomach.
An oesophageal mass or abscess will result in a focal filling defect associated with the wall,
static over several images.
It should be noted that the caudal feline oesophagus has a normal herringbone pattern that
should not be confused with mucosal pathology.
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2. Contrast imaging of the urinary system
Contrast imaging of the urinary bladder, urethra, kidneys and ureters is possible in practice
and can provide much additional information over survey radiographs, particularly when
ultrasound is not available.
Cystography
Indications
Positive contrast and double contrast cystography can be used to evaluate a variety of
suspected lesions of the urinary bladder. In trauma patients, positive contrast cystography
can be very useful in evaluating for evidence of bladder rupture. This may also be used
when rupture is suspected following outflow obstruction. Positive contrast cystography can
also delineate a bladder mass or wall thickening. Double contrast cystography provides
excellent evaluation of the luminal bladder contents and the bladder wall in patients
presenting with haematuria or dysuria. This is more sensitive and specific than ultrasound or
survey radiographs in determining the number and size of cystic calculi. It can identify calculi
(urates for example) that are not evident on survey radiographs. It also provides excellent
delineation of the bladder wall.
Methods
Only iodinated contrast media should be used for positive contrast cystography. If the colon
is very full, fasting and a warm water enema may be necessary to avoid superimposition.
Survey radiographs should initially be obtained. Deep sedation or anesthesia is typically
necessary.
The urinary catheter is placed aseptically into the bladder and as much urine as possible is
withdrawn. A diluted solution of iodinated contrast (30 mgI/ml) should be used. The volume
of contrast that can be used depends on the urinary bladder. Most bladders will be filled with
approximately 5 mls/kg but if there is pathology of the bladder wall, as little as 1ml/kg can
result in bladder distention. The bladder should be palpated during filling to avoid over
distention. Right lateral, oblique and ventrodorsal radiographs are obtained immediately after
filling.
A double contrast cystogram can be performed immediately after a positive contrast

cystogram with the withdrawal of the majority of the contrast and subsequent filling of the
bladder with air. It is recommended that the patient is in left lateral recumbency for injection
of air to limit the risk of air embolus. Double contrast cystography is more ideally obtained by
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initially administering a small volume of contrast, rolling the patient to coat the mucosa,
followed by introduction of air to distend the urinary bladder. 1ml of contrast should be used
for a cat and between 1 and 6ml depending on the size of the dog. Undiluted contrast can be
used for double contrast cystography.
Interpretation
Initial leakage of contrast can appear as a small and indistinct plume adjacent to the urinary
bladder. With time, there will be contrast filling of the abdomen. However, very small tears
may not be appreciated without repositioning the patient, as compression of the lesion in
lateral recumbency could limit leakage.
On double contrast cystography, calculi appear as filling defects within the centre of the
contrast pool. They can be rounded or irregular. Gas bubbles move to the periphery of the
pool. Blood clots may be central and peripheral, but are typically irregular shapes. Mucosal
irregularity and bladder wall thickening can be appreciated in association with cystitis,
typically toward the apex. A bladder wall mass would appear as a filling defect on positive
contrast cystography and focal wall thickening on double contrast cystography.
Urethrogram
The urethra of the male canine or feline patient is relatively easily catheterized, and a
urethrogram can be very useful method to evaluate for luminal lesions or strictures that
would not otherwise be evident.
Indications
A history of urethral obstruction or stranguria can be evaluated with urethrography. In the

acute stages of obstruction, passage of a urinary catheter is of paramount importance, but
subsequent contrast evaluation can help determine the underlying cause or assist surgical
planning. A urethrogram can more accurately determine the size, number and location of
calculi within the urethra than would be evident radiographically. Radiolucent calculi, urethral
strictures, mass lesions or compression by an enlarged prostate can be evaluated.
Evaluation of the female urethra is more challenging as it is much shorter, and localization is
more limited. A positive contrast vaginocystourethrogram or urtherogram can be performed.
Methods
Heavy sedation or light anesthesia is necessary. Survey radiographs should be obtained,

and in the male canine this should include a right lateral view with the legs pulled forward
and centred on the region of the membranous urethra. A sterile Foley catheter is placed
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within the most distal aspect of the urethra. Iodinated contrast is injected into the urethra with
a radiograph obtained immediately after finishing the injection. 5 ml is recommended the cat,
and 10 ml, 20 ml of 30 ml for imaging of small, medium and large dogs respectively.
Approximately 50% of the contrast should be injected initially and a second radiograph
obtained after injection of the remaining contrast. This helps to determine if filling defects
represent static lesions or air bubbles.
Interpretation
Static luminal defects are most likely calculi. However, blood clots or mucosal plugs may
also be present. Some contrast filling of the prostate can occur as a normal finding.
However, narrowing of the urethra in the region of the prostate and irregular filling of the
prostate can be an indication of prostatic neoplasia or prostatitis. Inflammatory or neoplastic
lesions can result in focal or focally diffuse narrowing. Urethrospasm can occur as a clinical
finding, but is also seen secondary to contrast administration in a less heavily sedated
patient. This can be avoided with injection of 2 mL 2% lidocaine at the start of the study.
Intravenous pyelography (IVP)
This study is also known as intravenous urography (IVU). Intravenous contrast is filtered by
the kidney and cleared by the ureters, and allows a degree of functional in addition to
anatomic evaluation. The study requires radiographs be obtained in close succession. It is
unlikely to be obtained in an emergency setting, but may be recommended for further
evaluation if ultrasound is not available.
Indications
If ultrasound is not available, an IVP study can provide useful information regarding the
anatomic structure of the kidney. Differentials for renal enlargement can be better
discriminated by this study. Suspected ectopic ureters can also be evaluated by this method,
though interpretation can be challenging. The normal kidney will filter contrast within an
expected time frame, and any change to this indicates abnormalities of renal function.
There is some risk with any intravenous contrast administration. Contrast associated acute
renal failure has been described and the risk is limited by adequate hydration. This
procedure is also contraindicated in patients with severe azotaemia. In patients with mild
azotaemia an increase in the contrast dose may actually be necessary to perform a
diagnostic study.
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Methods
The patient must be adequately hydrated prior to the study, and dehydration should
therefore be corrected. This should not be performed if there is severe renal compromise.
Following survey radiographs an enema may be performed if there is sufficient faecal

material within the colon to compromise evaluation. This is particularly true in evaluation of
the distal ureters.
An intravenous catheter is necessary for contrast administration. A dose of 880 mgI/kg of

iodinated contrast is recommended. They should be given as a rapid bolus. The dose can be
increased by 10% of patients with mild azotaemia. Follow-up right lateral and ventrodorsal
radiographs should be obtained immediately and at 5 minutes, 15 minutes and 30 minutes. If
the study is carried out in evaluation for ectopic ureters, initial air filling of the urinary bladder
can help to visualize the ureterovesicular junction and additional oblique views are
recommended.
Interpretation
The immediate vascular phase is often not appreciated and is rapidly followed by the
nephrogram phase which results in enhancement of the renal parenchyma. This is followed
(within minutes) by a pyelogram phase in which the renal pelvis and ureters are filled with
contrast. There should be a gradual decrease in the opacity of the renal parenchyma.
The sequence of opacification can be abnormal with functional renal disease. Initial
opacification followed by progressively increasing opacity can occur with systemic
hypotension, renal obstruction or contrast induced renal failure for example.
Structural abnormalities can be differentiated. An irregular outline to an enlarged kidney on

survey radiographs could be secondary to neoplasia or polycystic disease. A neoplastic
lesion will typically results in an irregular area of abnormal contrast enhancement and
possible distortion or dilation of the renal pelvis and pelvic recesses. Polycystic disease
results in multiple well-defined rounded filling defects that do not enhance.
A smoothly marginated enlarged kidney could be secondary to acute inflammation, FIP, a

perirenal psuedocyst, hydronephrosis or neoplastic infiltration such as lymphoma. Acute
pyelonephritis typically results in pelvic dilation and mild ureteral dilation, while chronic
pyelonephritis causes blunting of the pelvic recesses in addition to mild ureteral dilation.
Hydronephrosis secondary to ureteral obstruction typically results in severe pelvic dilation,
dilation of the pelvic recesses and ureteral dilation to the level of obstruction. A perirenal
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pseudocyst appears as a large nonenhancing pocket around a typically small kidney. Other
acute inflammation or FIP may not have specific changes.
Ectopic ureters are typically, but not always, dilated. They bypass the normal
ureterovesicular entry to the urinary bladder and join the urethra or other more distal
location. It can be difficult to differentiate intra-mural tunnelling ectopic ureters from the
normal junction.
References
1. The handbook of veterinary contrast radiology. Seth T. Wallack. 2003. Published by

the author, San Diego Veterinary Imaging Inc., 361 North Sierra Avenue, Solana
Beach, CA 92075
2. Textbook of veterinary diagnostic radiology, sixth edition. Donald E. Thrall. 2012.
Elsevier.
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Notes page
Page 169 of 334

TOP TEN EASILY MISSED KEY RADIOGRAPHIC FINDINGS

IDEXX Telemedicine
The importance of making a correct radiographic diagnosis, particularly in an emergency

situation, cannot be under-estimated. Often radiographs are acquired to rule out or confirm
suspected lesions, and it is essential that these are not missed or mis-interpreted.
Unexpected diagnoses can completely change a treatment plan and may lead to emergency
intervention that was not otherwise considered necessary. Unfortunately some of the most
important radiographic diagnoses can be those that are most easily missed. This lecture will
review a Top ten of these key radiographic findings with discussion of how best to improve
diagnosis, illustrated by examples from clinical practice. The list is drawn from my
experience of reading cases for general and emergency practice and through appreciating
what is often missed by the attending clinician, even when experienced. It is of course not
exhaustive, and could go on almost indefinitely, but within the limitations of this lecture I
hope to provide some helpful advice to improve your ability to make the correct key
radiographic diagnosis.
1. Pneumoperitoneum
Even very small amounts of free peritoneal gas can indicate a need for surgical intervention.
The sooner that a diagnosis of a ruptured viscus is made, the greater the chances that the
patient will recover from surgical treatment of associated septic peritonitis. Free gas within
the abdomen typically localizes to certain areas, and careful evaluation of these in a patient
presenting with an acute abdomen can improve sensitivity to the diagnosis. Gas will almost
always move to the non-dependent aspect of the abdomen. It is typically localized adjacent
to the dorsal aspect of the diaphragm and along the dorsal margin of the liver lobes. This
location is very typical for gastric perforation. With small intestinal perforation the gas may
initially be localized to a focal area of the abdomen. Peritoneal gas pockets are initially often
small and rounded and do not conform to the intestinal margins. Gas may also be seen
along the body wall, and have a somewhat linear distribution. If in doubt, further imaging
can help to confirm or dismiss a suspicion of free gas. In a patient that is clinically stable,
follow up radiographs could be obtained in 2 hours. Increasing amounts of gas will almost
always be present within that time frame. However, if possible, it would always be best to
use the position of the patient to help confirm the diagnosis. A horizontal beam radiograph
obtained with the patient in left lateral recumbency is a much more sensitive way to look for
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free gas in the non-dependent aspect of the abdomen. If you cannot move the x-ray tube to
obtain a horizontal beam, adding an additional view (left lateral for example) may help.
2. Peritoneal effusion
Effusion within the abdomen can have many origins. In the acute abdomen this is most
often present as haemoabdomen associated with intra-abdominal neoplasia, peritonitis
associated with pancreatitis or uroabdomen. Effusion can also be associated with right
sided cardiac disease, portal hypertension, hypoalbuminaemia, carcinomatosis or other
causes of peritonitis. Detecting effusion on radiographs can be key in making a correct
diagnosis or adding an important differential. The diagnostic quality of your radiographs can
be really important in the ability to detect subtle changes in serosal detail that indicate mild
effusion. Evaluation for loss of delineation of the serosal margins of the intra-abdominal
organs is an important part of abdominal radiograph evaluation and will be illustrated by
case examples. Thin patients and young animals can have a normal decreased serosal
delineation leading to mis-diagnosis. Abdominal ultrasound can be used to confirm
suspected effusion, but is not always available in general practice.
3. Retroperitoneal effusion
The retroperitoneal space, housing the kidneys, adrenals, some lymph nodes and the great
vessels, is separated from the peritoneal cavity by the peritoneal membrane. While
retroperitoneal effusion is not very common, the ability to differentiate this from peritoneal
disease can really help to narrow a list of differentials in a patient presenting with abdominal
signs. Retroperitoneal effusion can be associated with haemorrhage, urine leakage,
neoplasia and acute renal inflammation. Radiographically it is distributed dorsally on the
lateral views, often with ventral displacement of the colon or small intestines. As it is
specifically retroperitoneal serosal detail that is limited, the margins of the kidneys will be
indistinct on the affected side, but the serosal margins of the peritoneal organs should
remain intact. If ultrasound is not available, further imaging such as an IVP study may be
helpful in further evaluation.
4. Linear foreign body

A linear foreign body is a surgical emergency. They may be more prone to perforation than
simple mechanical obstruction. Carpet material, for example, is highly abrasive to the
mucosal surface. They can also rapidly progress to involve the entire small intestine, as
peristalsis draws the anchored foreign material distally. While some may be diagnosed by
virtue of entrapment under or around the tongue, many linear foreign bodies can be
anchored in the pylorus. Unlike simple mechanical obstruction, linear foreign material does
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not necessarily result in focal intestinal distension. The key is to appreciate the radiographic
signs of plication. Elliptical gas lucencies, bunched intestine and the plicated serosal margin
of intestine can be appreciated. Clinical examples will be used to illustrate this often
challenging diagnosis. Beware the obese cat! Apparent bunching of intestine in the right
abdomen can be a normal distribution. If in doubt a contrast study or ultrasound (in
experienced hands) can confirm the diagnosis.
5. Mechanical Obstruction
The clinical signs of an obstructed patient (for which surgery is necessary) and severe
gastroenteritis can be similar, and radiographs are an important part of work-up. You dont
have to see the foreign body on radiographs for there to be a mechanical obstruction, but
when the foreign body is not identified it can be more challenging to interpret the intestinal
gas pattern. Segmental intestinal distension is the key roentgen sign that indicates a
mechanical obstruction. Several measurements have been reported to indicate abnormally
distended intestine, but diffuse distension can occur with functional ileus, and it is the
segmental nature of distension that is important in diagnosing a mechanical lesion. The
normal small bowel diameter in the dog has been reported as less than twice the width of a
rib or less than 1.6x the height of L5. In cats the intestines should not be more than 12mm
wide or twice the height of L4. In cases of early or partial obstruction the degree of
distension may be relatively mild. It can also be challenging to differentiate potentially
distended small intestine from colon (which can be significantly wider). Further imaging is
therefore often indicated prior to surgical intervention. A pneumocolonogram is a great way
to differentiate small intestine from colon, and does not involve the use of specialized
equipment or contrast. Repeating radiographs in 4-6 hours following a period of fluid
therapy is another excellent way to evaluate for progression of intestinal distension, or a
static focally gas distended loop, that would indicate obstruction. If the radiographic findings
remain equivocal an upper GI study could then be used. Properly carried out, this is an
excellent way to determine if obstruction is present. Barium can also have therapeutic in
addition to diagnostic benefit, and may help relieve the signs of gastroenteritis if no
obstruction is present. If the patient has to go to surgery the risk of barium peritonitis is very
low as the abdomen would be adequately lavaged at surgery. The risk of perforation from a
missed foreign body is much greater.
6. Renomegaly
Renal enlargement can occur with a number of conditions, not all resulting in biochemical
derangement that would immediately indicate a renal origin for the presenting clinical signs.
Smooth bilateral renal enlargement can occur with acute inflammation, amyloidosis, toxicity,
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hydronephrosis (can be bilateral if associated with urine outflow or ureterovesicular

obstruction) or in cats with FIP, perinephric psueodocysts or renal lymphoma. Irregular
bilateral enlargement can occur with polycystic disease, FIP or neoplasia (lymphoma can be
smooth or irregular). Unilateral enlargement may be more easily recognized as the size can
be compared with the other kidney. In dogs in particular the right kidney is often much
harder to delineate when normal as it is more cranially positioned and effaces with the liver
and unilateral enlargement can be harder to appreciate. Unilateral smoothly marginated
enlargement can occur with hydronephrosis, compensatory hypertrophy, a subcapsular
abscess or haemorrhage or in cats a perinephric psuedocyst. Irregular unilateral
enlargement is seen in association with neoplasia in particular, but can also occur with a
haematoma, cyst, abscess or granuloma.
Normal measurements for renal size have been reported, and rely on the ability to delineate
the renal margins on radiographs. This can be challenging if there is limited retroperitoneal
fat. The normal size of the canine kidney is 2.5-3.5 x the length of L2. Feline kidneys should
be approximately 2-3 x the length of L2. This is most reliable on the ventrodorsal view, as
magnification of the uppermost kidney can result in inaccurate measurement on lateral
views, particularly in obese patients. Appreciating the displacement of adjacent organs can
also help to determine if marked renal enlargement is present, and whether this is unilateral
or bilateral. The kidneys are retroperitoneal, and will therefore displace adjacent organs
ventrally. Left sided renal enlargement results in ventral displacement of the descending
colon, while ventral small intestinal displacement occurs with significant right renomegaly. A
large amount of retroperitoneal fat can result in the same displacement so this should be
excluded. Once renomegaly is suspected, additional diagnostics can be used to determine
the cause. If ultrasound expertise is available this is an excellent modality for helping to
differentiate the causes of renal enlargement. An IVP study would allow differentiation of
hydronephrosis from other causes and can also give information about the parenchyma.
7. Small liver
There are few differentials for a small liver. In young patients microhepatica is most often
associated with portosystemic shunting. This may be the only significant radiographic
finding in these patients. Liver atrophy in older patients is more often secondary to chronic
liver disease and cirrhosis. While liver enlargement is relatively easily diagnosed
radiographically, a small liver can easily be overlooked. The position of the stomach can be
used to estimate liver size. The gastric axis (line from the fundus to the pylorus on the
lateral view) should lie between an angle perpendicular to the vertebrae and parallel to the
ribs. Subjectively this leads to wide variation, and it can be very difficult to determine when
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the liver is truly small. Deep chested breeds will always have a cranially oriented gastric axis
which makes differentiation from a truly small liver more challenging. Correlation with
biochemistry will help to determine if the subjectively small liver may be significant, though in
patients with end stage cirrhosis the liver enzymes may be relatively normal as no further
damage is occurring. Liver function tests can then be helpful. Additional imaging may be
indicated if there is radiographic and clinical evidence of liver disease. Cirrhosis has a
relatively classic ultrasound appearance, though the absence of enlargement in conjunction
with the clinical findings will indicate chronic disease. In cases of suspected portosystemic
shunting, Doppler sonography, CT angiography, mesenteric angiography, MRI or nuclear
scintigraphy can be used for further evaluation.
8. Thoracic or skeletal lesions

Lesions outside the abdomen can occasionally be more important than the intra-abdominal
findings, and can be unexpected. Pulmonary metastases in a patient presenting with
vomiting, megaesophagus in a patient that had been thought to have been vomiting or
skeletal metastases in a patient straining to urinate will radically change the management
and prognosis of these patients. It is easy to focus on the abdomen in a patient that
presents with signs referable to this region. A systematic approach to reviewing abdominal
radiographs should mean that lesions of the adjacent caudal thorax or surrounding skeletal
structures are not missed. It is recommended that you begin reviewing abdominal
radiographs by evaluating these extra-abdominal structures; if necessary additional thoracic
radiographs or collimated skeletal images could be obtained to evaluate an area of concern.
9. Urethral calculi
Stones within the urethra are often overlooked if the patient is not presenting as acutely
obstructed, and can be missed if appropriate radiographs are not obtained. In male canine
patients presenting with urinary signs (stranguria, haematuria or obstruction) a lateral view of
the caudal abdomen and pelvis with the pelvic limbs pulled cranially should always be
obtained to assess the urethra. If bladder stones are noted as an incidental finding, this view
is also recommended to evaluate the urethra, as urethroliths then represent a risk for future
complication. Urethral calculi are also easily overlooked in female canine patients, when
they are not typically associated with obstruction. In the rare cases where an obstructive
urethral calculus is present in a female, it is critical to identify this prior to surgical
intervention for additional cystic calculi, as significant morbidity and mortality can otherwise
occur. In male cats the urethra terminates caudally, and an additional view is not helpful.
However, close evaluation of the caudal urethral region is important if radiographs have
been obtained of obstructed cats. If uretheral obstruction is suspected and no calculi are
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evident on survey radiographs, a retrograde positive contrast urethrogram will help to

exclude small or radiolucent calculi, or calculi superimposed on the pelvis which can be
difficult to appreciate otherwise.
10. Normal post-operative findings

Occasionally surgical structures can be over-interpreted as acute foreign material. Sutures,
staples and coils can all be mis-interpreted, and it is best to avoid having to explain to the
owner that what you were going in to remove was associated with a previous procedure.
Portosystemic shunt surgery is relatively rare, but the ameroid constrictor used to occlude
the anomalous vessel is large, and if you have not seen one before, can be easily mistaken
for a foreign body. Dystrophic mineralization of granulomas associated with spay sutures is
also relatively common. These focal areas of mineralization can easily be mistaken for
ureteral calculi. Radiographic examples of these structures will be used to demonstrate
these incidental findings. Immediate post-operative radiographs are more challenging.
When dehiscence or sepsis is suspected in the post-operative period, radiographs may be
obtained for evaluation. However, it is extremely difficult to differentiate normal post-
operative changes from signs of sepsis. Pneumoperitoneum may persist for several weeks,
and effusion is typically present after surgery. As these are also indications of perforation, it
is difficult to differentiate acute pathology from expected changes. Abdominocentesis is
therefore a more sensitive means of evaluating post-operative complication.
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OROFACIAL TRAUMA
Minor trauma to the face and mouth can often be managed to heal by second intention or
direct apposition, as the blood supply to the area is excellent. But even with abundant lip
tissue, closure of larger facial wounds can be challenging, due to tensile and shear forces
activated by the highly mobile anatomy. Luckily, there are several robust flaps that can be
easily developed to cover significant wounding to the face. We should be aware of these
options so that we can advise owners with an accurate prognosis.
Anatomy
The mucosa of the upper lip is more generous than that of the lower lip, which becomes
narrower rostrally. However, the lower lip is easier to mobilise rostrally than the upper lip.
The lower lip has a firm attachment to the gum between the lower canine and first premolar
the interdental ligament - it prevents the lower lip from sagging, and is important to restore
when reconstructing this area.
Between the inner mucosa and the skin of the lips and cheeks are two layers of muscles
the superficial orbicularis oris and the deeper buccinator. There are many superficial facial
muscles around here: the levator nasolabialis, caninus, levator labii maxillaris, platysma,
zygomaticus, sphincter colli profundus-pars palpebralis and frontalis. These muscles are
critical for facial expression in humans, but not as critical for dogs and cats. However,
including these superficial muscles into a reconstructive effort will bring bulk, protection and
good vascularity to the repair. The superficial temporal muscle of the head and the platysma
of the neck are well developed in the dog and also useful to include in skin flaps.
The blood supply to the lips, cheeks, and lesser extent head, is bountiful. The facial artery
divides to supply the cheeks through the superior and inferior labial, and the angularis oris
arteries. The infraorbital artery comes directly off the maxillary artery (which is the major
terminating branch of the external carotid, so - high pressure!) and supplies a rich arterial
network of blood to the upper lip and muzzle. The head is mostly supplied from the branches
of the superficial temporal artery, which is the minor terminating branch off the external
carotid. There are about six branches off the superficial temporal which cover most of the
head. This wonderful arborization and collateral circulation makes it easier to develop flaps
with a good chance of surviving.
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Initial wound management

Upon presentation of acute trauma to the face it is critical to evaluate the cardiovascular and
neurological status of the animal, in case concurrent injuries exist (e.g., concussion, skull
fractures, nasal bone fractures, diaphragmatic hernia). The eyes should also be closely
examined (with an ophthalmoscope), patency of the nares assessed, and integrity of the
hard palate and other intraoral structures determined. Some of these examinations, such as
the oropharynx, are more easily accomplished when the animal is sedated or anesthetized
for cleansing and debridement.
All injuries should be clipped and cleansed as soon as possible, adhering to the basic tenets
of wound management clipping and cleansing of the periwound and wound, debridement
and lavage. Debris and necrotic tissue and clots should be removed through meticulous
debridement. Liberal and frequent lavage is beneficial, as dressing facial trauma can be
challenging. Placing a calcium alginate in the wound bed, and then stapling of a
polyurethane foam to the wound edges provides some protection and maintenance of a
reasonable wound environment. Newer, slow-release silver and povidone-iodine dressings
are becoming available as well. When bandage placement is simply not possible due
location, frequent application of hydrogel will suffice until reconstruction is possible.
Surgical considerations for facial reconstruction

We look at our pets faces more than other areas, and even if they are not as facially
expressive as humans, cosmetic outcome may be of greater concern to the owner compared
to other areas of the body. From the animals perspective, however, restoration of pain-free
function is probably the most important requirement. It is the owner, not the animal, who is
concerned about final cosmetic appearance. To some extent, cosmesis and function are
complementary. For example, restoring lip continuity is beneficial both for function (holding
food within the oral cavity) and appearance. But we still need to manage the owners
expectation of the final outcome. Most owners will readily accept a degree of cosmetic
disfigurement, if they recognize an improvement in quality of life following surgery. And
appearance, if not a perfect 10, is often considerably better than pre-operatively.
Due to the availability of tissues in dogs, mobilizing local tissues with tension-relieving
techniques and simple flaps will enable closure of many small to moderate defects. Cats
lack this redundancy and generally have a tighter face - usually a more elaborate plan is
required to reconstruct effectively. Most defects in dogs and cats can be repaired with a
carefully planned, single stage procedure, in contrast to human plastic surgery, where multi-
staged procedures are more common. Our patients have the advantage of having a dense
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fur coat to mask deficits and cover scars, and facial asymmetry is less obvious in the
elongated muzzle.
Skin flaps for the face

A skin flap is a portion of skin with an intact vascular (and generally cutaneous) attachment
to its donor site. If the facial defect cannot be closed by direct apposition, a local skin flap is
generally indicated because they can cover areas that are difficult to immobilize. Other
closure techniques such as free skin grafting, distant flaps or pretensioning over several
days are not as well suited to this area. Skin flaps will improve the regional circulation as
they bring their own blood supply, and for the same reason they are resistant to infection.
Flaps also provide immediate padding and protection, although as the hair grows back it will
resemble the donor area.
Subdermal plexus flaps

There are several extremely useful local subdermal plexus flaps that the surgeon can utilize
around head, including lip-to-lid procedures. Most flaps used clinically for facial
reconstructions (excluding palates) are musculocutaneous. Single pedicle advancement
flaps can be developed from either side of the muzzle, utilizing the loose upper labial skin to
facilitate a tension-free closure. These are useful in defects rostral to the eyes. In many
cases, a single pedicle advancement flap can be developed from both sides of the muzzle,
forming an H-plasty, to cover defects on the bridge of the nose. These flaps can also be
dissected on a deep plane, down to the bone if necessary, to provide more secure coverage
for defects that include nasocutaneous fistulation. For nasal planum restoration, staged,
bilateral rotation flaps can be brought in from the skin of the muzzle and upper lip.
Axial pattern flaps

These flaps incorporate a direct cutaneous artery and vein into its base, providing better
perfusion and allowing much larger flaps to be developed (compared to the subdermal
plexus flaps). Useful axial pattern flaps for the face and neck include: the omocervical, the
superficial temporal, and the angularis oris. (A somewhat less dependable axial pattern flap
is the caudal auricular). For the caudal muzzle area and between the eyes, the superficial
temporal axial pattern flap will provide a padded, hirsute and quite robust coverage. This
flap incorporates a consistent vascular pedicle (the cutaneous branch of the superficial
temporal artery), so is quite reliable. Additionally, the frontalis muscle and fascia that can be
transferred concomitantly provides support over any defect in the bone. It can also be used
to replace eyelids, using the conjunctiva as a lining to preserve corneal health. The flap is
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based at the level of the zygomatic arch and is developed over the top of the head,
extending to the middle of the dorsal orbital rim of the contralateral orbit.
More recently, the angularis oris facial flap allows for a large caudodorsal-oriented flap
based at the commissure of the lip to be developed and rotated into maxillofacial defects in
dogs and cats. It is perfused by three arteries (the superior and inferior labial, and the
angularis oris) that arborize and throw off yet another cutaneous perforator within its base.
This flap is extremely robust and versatile for large facial and muzzle defects, and also for
intraoral defects.
Lips and lids

Restoration of lip integrity and function can be achieved by ensuring meticulous positioning
of lip margins and strong anchorage to the gingival and mandibular tissues. Accurate
alignment of the mucocutaneous junction should always be performed as the first step of
reconstruction, usually with a figure-of-eight suture. This is also critical for the eyelid
margins, as both lid notches and suture material will cause corneal trauma, and interfere
with normal precorneal tear film distribution.
Incising wobbly lips and lids can be tricky, so stabilizing and stretching the lip onto a firm
surface (e.g., wooden tongue depressor, folded drape, or Jaeger lid plate) will facilitate
clean, accurate cutting. Proposed incision lines should be drawn with a sterile marker before
commencing surgery.
In highly mobile area such as the lips, it is vital that apposition is secure and free of tension,
in order to avoid dehiscence. Full thickness repairs should be undertaken in three or four
layers: submucosa, deep musculature, superficial musculature and subcutaneous tissue,
and skin. (Mucosa can be sutured separately after these layers are closed if desired). Fine
(4-0) rapidly absorbable, monofilament suture material (4-0) in a continuous pattern (for
fewer knots) is preferred.
As lip and lid surgeries are classified as clean-contaminated procedures, prophylactic

antibiotics are indicated (usually a single intravenous bolus of a broad spectrum antibiotic at
time of induction). Although self-trauma is not typical, an E-collar should be placed for the
post-operative week.
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Lip avulsions
Lower labial avulsions occur from shear trauma (high rise fall [cats], car accident, chasing
rabbits down a hole) and other trauma may be sustained concurrently, such as mandibular
fracture, tooth disruption or extraction, diaphragmatic hernia, pelvic fracture, etc. Disruption
usually occurs at the rostral gingival border, leaving little tissue with which to anchor the
hanging lower lip. To ensure healing without complication, the wound must be healthy, and
the lip secured firmly back to the gum. This involves thorough cleansing and debridement of
the wound, converting it, if possible, to clean-contaminated status. Drainage (usually a small
closed-suction device) should be provided as part of the wound repair. Sutures should be
meticulously placed from the buccal mucosa around the incisor teeth. In the absence of
incisors, transosseous sutures, placed through small holes drilled through the mandible are
required to secure the lip. An additional tension-relieving stent suture, traversing full
thickness, may be indicated in more dramatic avulsions.
Lip trauma
Full thickness segmental resection of the lip is indicated for debridement of complicated or
infected trauma (also for tumor resections). A wedge resection is easiest to close (in three or
four layers), as there is minimal disparity between edges. Mild disparity between edges can
be accommodated by placing tension at either end of the suture line. Significant disparity is
corrected by removing a Burows triangle from the dorsal end of the long side. A square
defect can be converted to a pentagon to facilitate closure, or closed as a Y. Large
rectangular defects will require a labial advancement flap.
Labial or buccal advancement flaps are flaps based adjacent to the commissure of the
mouth, and can be used to repair larger rostral maxillary or mandibular labial defects. These
full thickness flaps will result in a shorter oral commissure, but are very useful for large lip
loss. A shortened oral commissure generally does not cause a problem, and a second
procedure can easily be performed to lengthen it if necessary (rarely). The cheek tissue and
commissure is richly perfused and heals well. A full thickness incision parallel to the lip
margin is made, extending caudal to the commissure (it can actually arc down behind the
commissure a little if necessary). It is helpful to preserve about 5mm of labial mucosa
coming off the gingiva to facilitate mucosal suturing. The flap is elevated and advanced
rostral into the defect, and sutured in four layers. For lower lip reconstruction, the interdental
attachment must be recreated to avoid drooping of the lip.
For large, full thickness defects in the upper lip, a buccal rotation flap can be performed
where the commissure and buccal (cheek) mucosa is actually rotated to form the upper lip.
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Always remember the previously mentioned facial flap based on the angularis oris vascular
pedicle when confronted with very large facial and muzzle defects.
Eyelids
Most eyelid reconstructions in small animals have been adapted from human surgical
techniques. The lid anatomy is similar, except that the dog has a thinner tarsal plate and a
poorly developed lateral canthal ligament. The upper eyelid in both dogs and cats is a little
longer, more mobile, and larger overall. Closure is achieved by contraction of the orbicularis
oculi muscle (facial n.), which shapes the palpebral fissure into a slit due to the medial and
lateral canthal attachments. Blinking acts to distribute the precorneal tear film across the
cornea towards the superior and inferior lacrimal puncta. Upper lid integrity is critical to
maintaining corneal health the upper eyelid margin has greater movement over the cornea
than the lower eyelid and preservation of normal upper eyelid function and structure is
important to prevent exposure keratitis. Eyelid opening is mediated through the levator
palpebrae superioris (oculomotor n.) and Mullers muscle (sympathetic innervation). The
actual lid margins are hairless and contain the orifices of the Meibomian glands. The cilia
(upper lid only) are located about 1 2 mm from the free lid margin.
Principles of eyelid surgery

Lid skin can be shaved with small hair clippers, protecting the globe with lubricant and
moistened cotton balls. Povidone-iodine solution (not scrub), 0.02% (1:50), will provide
satisfactory antisepsis to the conjunctiva and lids. The surrounding skin can be prepared as
for routine surgery, but alcohol must not come into contact with the conjunctiva or corneal
surface (it will cause epithelial damage). Position the animal with the palpebral fissure
horizontal, the neck extended and the nose elevated. Vacuum bags are very useful for good
positioning.
Powerful illumination and moderate magnification (2.5x binocular loupes) is recommended

for accuracy (e.g., apposition of lid margins). Eyelid movement, especially the upper eyelid,
should be preserved or restored when possible. Accurate anatomic reconstruction is
required, and reconstructed eyelids should be lined with conjunctiva (flap or graft).
Meticulous alignment of eyelid margins must be achieved to prevent corneal damage and
allow even distribution of the precorneal tear film. Suture ends and knots should not contact
the cornea.
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Good quality and appropriate instrumentation improves technique considerably in eyelid

procedures. Fine gauge forceps (Brown-Adson, Bishop-Harmon, St Martin suturing forceps)
will minimize trauma when grasping eyelids and conjunctiva. Tenotomy scissors are useful
for the conjunctiva, or fine Metzenbaums. A #15 Bard-Parker blade or #64 or #69 Beaver
blades should be used for cold cutting. Monopolar electrocautery should be avoided near
the globe and conjunctiva, but fine bipolar or radiofrequency units can be useful. Micro
mosquito hemostats are also very handy for attenuating fine vessel bleeding. Sutures with
swaged needles should always be used - larger than 6-0 should be handled with Derf needle
holders and finer sutures with Castroviejo needle holders. It is also worth investing in a
Jaeger lid plate, which is used to immobilize the eyelid and protect the globe when making
incisions. A dedicated instrument holding case for protecting fine instruments is also
recommended.
Most full-thickness lid reconstructions are performed in two or three layers, with fine (5-0 or
6-0) suture material. Buried sutures are usually used and the lid margin should be
constructed with care the Meibomian gland orifices along the eyelid margin are useful
landmarks for ensure accurate apposition. A figure-of-eight suture with suture ends away
from the cornea should be used to reform the eyelid margin.
Eyelid Defects
Bite wounds or automobile trauma are the most common causes of eyelid lacerations in
dogs and cats, so the animal must be fully assessed, including neurologic examination for
concurrent injury. The globe should also be examined thoroughly for involvement. Post-
traumatic lid edema and chemosis can be marked, making examination difficult. Ice-packing
may help reduce swelling and NSAIDS are useful. Eyelids are highly vascular tissues so
they heal rapidly and are resistant to infection. When lacerations of the nasal (medial)
eyelids occurs, the lacrimal puncta should be cannulated and flushed to determine if the
nasolacrimal apparatus is involved. Eyelid wounds should be cleaned of all debris and
prepped debridement is not usually indicated.
Traumatic eyelid lacerations should not be left to heal by second intention, but rather should
be repaired as soon as possible. Defects of less than 1/3 of the eyelid margin can be closed
by direct apposition. Larger defects will require a major reconstructive effort, unless the
animal has excessive eyelid length (which is the case in many breeds of dog).
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Advancement flap This flap is most commonly used to repair lower lid defects. The square
flap is developed and Burows triangles created to prevent dog-ear formation. The bulbar
conjunctiva is undermined and mobilized into the defect to line the flap. The flap is
advanced into the defect and the conjunctival border sutured to the leading flap edge with a
continuous suture. Attention must be paid to the alignment of the flap and the remaining lid
margin there is a tendency for the flap to contract a little during healing, so there must be
no tension on the advancement. A temporary tarsorrhaphy (which reduces motion stresses
on the flap) will also ameliorate healing and cosmetic outcome. This flap is easy to perform,
but it does not replace the eyelid margin hair growth may cause corneal irritation at times.
H plasty (lower lid skin advancement flap of skin, with upper lid conjunctival flap) This is a
staged procedure for larger lower lid defects. A tarsoconjunctival flap (part of the tarsus and
conjunctiva) is developed from the fornix of the upper lid, and brought down to provide
conjunctival lining to the lower lid defect. The skin of the lower lid is then advanced with a
single pedicle advancement flap as described above. A temporary tarsorrhaphy is
performed for 14 21 days, at which time the intervening conjunctival bridge is divided, the
lid margin sutured, and the upper fornix repaired.
Cheek rotation flap A rotation flap can be mobilized from the cheek to close large triangular
eyelid defects. Conjunctiva must also be mobilized to line the defect. These flaps can
developed arcing down over the side of cheek, mobilizing skin from a lateral to medial
orientation, or the arc can extend down from the defect, mobilizing the flap from a ventral to
dorsal orientation. The rotation flap should be large, with the arc extending at least 4x the
base of the defect. Undermining should be performed carefully, beneath the superficial colli
(the panniculus layer) muscles.
Lip to lid procedure This one-stage procedure described uses a mucocutaneous

subdermal plexus flap from the upper lid to replace the entire lower lid. A long flap is
developed, based caudoventral to the eye, preserving a section of the upper lip
mucocutaneous junction just rostral to the oral commissure. This flap is transposed into the
eyelid defect through a bridging incision and sutured in two layers.
Reconstruction of large upper eyelid defects
Mustardes modified lid switch procedure provides extensive reconstruction of the upper lid
in two stages. The upper lid is replaced by a broad-based, full-thickness lower lid flap that is
rotated around the palpebral fissure into the defect, in a caterpillar fashion. Two weeks later,
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the base of that flap is divided and the rest of the flap inset into the remaining upper eyelid
defect. At this time, the lower lid defect is reconstructed with a cheek rotation flap. If any
remnant of upper lid is present, the vascular hinged pedicle of the lower lid flap should be on
the same side as the largest remnant. If the defect is central, or involves the entire lid, the
hinge should be on the lateral side. Avoid including the lacrimal puncta in the flap.
Reconstruction of the medial canthus and lids

Reconstruction of the medial one-half of the upper and lower eyelids and recreation of the
medial canthus can be performed using a superficial temporal axial pattern flap and the
nictitating membrane. This technique recreates lid margins and a medial canthus, with the
bulbar surface of the nictitans providing a conjunctival lining to protect the globe.
These techniques are just a few of many possible restorative options around the eye. There
are a large number of eyelid reconstructive techniques described in the human
ophthalmology literature. Many of these techniques can be adapted for use in the veterinary
patient. By utilizing and modifying these techniques, we may be able to save a perfectly
normal globe, rather than performing a more radical enucleation.
Post-operative care
Investment into preventing post-operative pitfalls will not only improve outcomes, but will
also inspire further attempts in reconstruction.
Pain Almost all our patients will require some form of analgesia. Fentanyl (pre-operative
patch or constant rate infusion), cocktails (hydromorphone and lidocaine; morphine,
ketamine and lidocaine), tramadol, butorphanol, carprofen and meloxicam are the most
commonly used analgesics in our hospital.
Hydration Dehydration will compromise flap perfusion significantly. Intravenous fluids

should be maintained until the animal is eating and drinking completely normally.
Antibiotics Antimicrobial coverage is generally given during a reconstructive surgery, but

continuing coverage will depend on wound status and results of cultures and sensitivity.
Sedation Acetyl promazine is an excellent sedative in most cases when used in

combination with pain medications. Often animals are exhausted by the trauma, the
hospitalization, and constant nursing care, but find it difficult to settle in the strange
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environment. Sedation will often enable a good sleep period as well as help prevent self-
mutilation.
Drainage Many of the reconstructions around the head and neck will heal more effectively
if some form of drainage is provided. Obliteration of dead space cannot generally be
achieved by bandaging in this area, so drainage is especially important. Active, closed-
suction drains are preferred, and are commercially available. They can also be made from
butterfly catheters and syringes or vacutainers. Drainage should be measured over each 24
hour period and continued until drainage decreases.
Protection - It is incredibly frustrating for vet and owner alike when a reconstructive effort is
ruined by patient self-trauma. Elizabethan collars are almost mandatory unless a suture line
extends to the neck. The collar should be large enough so that the animal cannot rub its
face on the ground. Bandaging paws may also help.
Feeding Many animals will not eat in the post-operative period, either because of
hospitalization stress, pain medications, sedation, pain, or a combination of these. Ensuring
an adequate nutritional plane is critical for wound healing in both cats and dogs. Cats have
the added risk of hepatic lipidosis if they are anorexic for more than a couple of days.
Anticipating loss of appetite and placing a gastrostomy or oesophagostomy feeding tube will
often prevent a drop in albumin, and optimize outcomes in surgery.
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TRAUMATIC OPHTHALMIC EMERGENCIES

Periocular Blunt, Sharp and Penetrating Injuries
Periocular trauma is common and may result in sight threatening injuries. Careful
examination of the globe for any damage is important (sharp and blunt trauma to the globe is
discussed below). Cats and dogs have an open orbit so penetrating injuries may reach the
orbit from several different directions not just rostrally. In dogs stick and bone penetrations
from the mouth may involve the orbit and result in swelling, haemorrhage and lead to
cellulitis or abscessation. Imaging of animals presenting with orbital swelling can include
orbital ultrasound or CT or MRI imaging.
Proptosis or Prolapse of the Globe
Prolapse of the globe is the result of trauma leading to rostral displacement of the globe
such that the eyelids may be behind the globe equator. There are 2 initial ocular
considerations when dealing with globe prolapse: firstly does the damage to the globe and
extraocular tissues render the eye unsalvageable? and secondly the rapidly progressive
damage to the cornea that will develop if the cornea is not kept moist (must be addressed
immediately). Prolapse can occur as a result of relatively minor trauma in brachycephalic
breeds and in some cases there may be little resultant damage to globe and extraocular
tissues. In non-brachycephalic breeds with globe prolapse often significant trauma has
occurred and such animals may have accompanying injuries such as skull fractures.
Initial telephone advice:

Tell owner to keep cornea moist with either ophthalmic lubricant ointment (if
available), or cotton wool saturated with saline or even tap water.
If prolapse just occurred in a brachycephalic dog without any great trauma to the
head the owner may try replacing the globe by applying gentle pressure on the globe
with water or saline soaked cotton wool (dog should still be brought in for
examination). Rapid replacement of the globe will reduce the degree of orbital
swelling that develops. In longer standing cases or in non-brachycephalics, or in
those suffering direct trauma to the globe this should NOT be attempted
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Cornea must be kept moist while transporting animal to the clinic
Initial treatment at the clinic:

Continue to keep cornea moist it must never be allowed to dry out
Ascertain a history any previous eye problems? What sort of trauma caused the
prolapse? Etc.
Complete a full physical examination for the presence of any other injuries
Examine the eye Corneal or sclera rupture? Hyphaema? PLR present or absent?
Any other intraocular damage? Is there obvious tearing of extraocular tissues?
o Significant tearing of extraocular tissues usually means the globe will need to
be removed. A bandage can be applied to the head to protect the eye until
surgery can be performed. Pain meds should be provided.
o If the extraocular tissues appear intact and there is not obvious severe
intraocular damage the prolapse should be reduced and a temporary
tarsorrhaphy performed.
Replacement of the globe and temporary tarsorrhaphy:
Any life threatening injuries should be identified and treated appropriately first. Unless
contraindicated, IV methylprednisolone can be given to reduce orbital swelling and for
possible neuroprotective effects. Under general anesthesia the lids are manipulated to allow
them to close over the globe a strabismus muscle hook may be used to pry the lids over
the globe. A lateral canthotomy may be required to allow repositioning of the globe. Gentle
pressure may be applied to the cornea to retropulse the globe while pulling the lids rostrally.
Preplacing of tarsorrhaphy sutures may be performed and these tightened over a scalpel
handle held across the cornea. As the sutures are tightened they press on the scalpel
handle which in turn presses on the cornea pushing the globe back into the orbit while the
lids are pulled rostrally. Tarsorrhaphy sutures should be positioned so they emerge through
the eyelid, at or just anterior to the eyelid margin. It is very important that they do not rub on
the cornea. Mattress suture pattern placed over stents are often used. These sutures can
be under tension until the swelling resolves and a stent will spread the pressure and help
prevent the sutures from cheese wiring through the eyelid skin. Two or three mattress
sutures are placed. It is best to leave a small gap at the medial canthus for application of
topical medications.
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Sharp trauma to the globe
Penetrating corneal wounds usually require specialized management. In general blunt

trauma resulting in globe rupture results in such severe intraocular damage that enucleation
is required. Sharp trauma resulting in penetrating wounds holds a better prognosis. Referral
for corneal repair surgery should be considered.
IMPORTANT:
DO NOT apply any pressure to the globe.
DO NOT measure IOP.
If the animal is struggling do not apply tight restraint around the neck as this can
raise IOP leading to possible rupture.
If the globe is ruptured or there is material adherent to the surface of a wound do not
attempt to remove it.
Examination of eye with corneal laceration:

Undertake careful examination to see if the lens is damaged. Small lens capsule punctures
can heal leaving a focal scar. Large lens capsule lacerations require lens removal
(phacoemulsification) otherwise it is likely that the eye will develop a severe uveitis leading
to secondary glaucoma. Complete examination might not be possible until the animal is
anesthetized.
Repair of corneal lacerations:

Magnification and appropriate instrumentation required
Careful cleaning of surface of laceration with balanced salt solution
Removal of clotted aqueous from the wound and any prolapsed iris.
Replace iris in anterior chamber
Reform anterior chamber with viscoelastic
Repair laceration with fine suture e.g. 8-0 or 9-0 Vicryl
Sutures need to be deep into cornea but not full thickness
Good anatomic reconstruction needed
Wound checked for leakage Fluorescein (Seidel test)
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Blunt trauma to globe
Compressive blunt trauma to the globe can result in serious damage and permanent loss of
vision. If an animal presents with vision loss following blunt trauma to the eye (for example
hit in the eye by a golf ball, squash ball, baseball bat etc.) the prognosis is very guarded.
A complete examination should include the following:

Discharge or blood from eye?
Is there a menace response?
Is there a dazzle response?
If you can see the pupil is there a direct reflex? An indirect reflex?
Examine as much of the eye as possible can the fundus be examined?
In an eye that is cloudy (e.g. intraocular haemorrhage, corneal oedema etc.) such that the
posterior segment cannot be examined then an ocular ultrasound should be performed.
Ocular Ultrasound This can be performed with a higher frequency probe (7.5 to 13 MHz is
ideal). A topical anaesthetic is place on the cornea and the globe imaged through the
cornea using regular ultrasound gel. Changes such as retinal detachment, posterior
segment haemorrhage, lens displacement and scleral rupture may be detected.
Common findings following blunt trauma

An eye blind following blunt ocular trauma may have the following lesions:
Hyphaema
Lens displacement
Corneal or sclera splits. The sclera commonly splits posteriorly adjacent to the optic
nerve.
Vitreal haemorrhage
Retinal detachment (+/- subretinal haemorrhage)
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NON-TRAUMATIC OPHTHALMIC EMERGENCIES

Orbital Abscessation/Cellulitis
Orbital infection is a common cause for exophthalmos. To detect orbital swelling always
examine eyes from above to compare position and palpate eye through closed lids to
compare retropulsion into orbit between affected and normal side.
If there is corneal exposure (an inability to close the eyelids - lagophthalmos) it is important
the cornea is kept lubricated during the work-up. A viscous tear replacement gel or ointment
is suitable. The major differential for an animal presenting with exophthalmos is a
retrobulbar tumour. Usually the history and presentation make it easy to distinguish between
retrobulbar cellulitis/abscess and a retrobulbar tumour.
Differentiating between retrobulbar abscess/cellulitis and a retrobulbar tumour
Retrobulbar abscess or Retrobulbar tumour

cellulitis
Onset Usually rapid over a few Gradual onset of

days exophthalmos
Demeanour Usually painful maybe Usually no indication of pain

depressed
Third eyelid protrusion Normally present Present except with

intraconal lesions
Pain on opening mouth? Usually very painful. May Not usually resented
need GA for oral exam
Appearance in mouth Swelling behind last molar, Usually see swelling behind
check for dental disease, last molar tooth
penetrating wounds
Blood work May see neutrophilia with left May be normal
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shift (sometime do not).
Ultrasound Not always possible to May be able to detect soft-

localize a fluid cavity tissue mass
depending on position
Signalment: usually young animals (mean age of 4 years)
History:
Acute onset
Owners may note anorexia and painful around mouth
Physical Examination:
Unilateral exophthalmos
Elevated 3rd eyelid
Congested episcleral vessels due to stasis of blood flow
Globe itself is usually normal
+/- serous to mucopurulent ocular discharge
Palpation of globe, periorbital area and opening of the mouth are usually VERY
PAINFUL!
Examine caudal to the ipsilateral last molar (often requires GA for a thorough
exam due to the pain) and may see a fluctuant swelling and/or hyperemia of the
oral mucosa.
Additional Diagnostics:
Ocular ultrasound: may see hypoechoic area caudal to the globe
Dental radiographs: can see lysis of tooth roots, radiolucent areas if tooth root
abscess
CT/MRI: usually not required, but if non-responsive or complicated case can use
to identify foreign bodies, orbital fractures, etc.
Treatment:
establish drainage
o Incise caudal to the last upper molar with a #15 Bard Parker blade- just
incise the oral mucosa
o Insert closed hemostats
o Advance with caution slowly through the pterygoid muscle and withdraw
(this area is highly innervated and vascularized)
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o May not see tremendous drainage does not mean it is not a retrobulbar
infection
o Collect samples for culture and sensitivity (aerobic and anaerobic) and
cytology
Broad-spectrum systemic antibiotics pending results of C&S. Often use
amoxicillin/clavulanic acid or cephalosporins initially.
Hot packs over the periorbital area if tolerated
Soft food
NSAIDs as needed for pain and inflammation, ex. carprofen or meloxicam
Lubrication of globe (if inadequate blink)- antibiotic ointment (if ulcer present) or
gel or ointment artificial tears every 6-8 hours
E-collar to prevent rubbing
Usually start to respond in 2-3 days
Prognosis: very good
Complications: Foreign body or unresolved dental disease, etc. will cause recurrence.
Deep Corneal Ulcers
Examination of an eye with a deep ulcer

An eye with an ulcer should be examined for predisposing factors. Perform a complete but
gentle eye examination (do not press on the globe i.e. do not measure intraocular pressure,
avoid retropulsion of globe to examine external surface of third eyelid etc.). Consider tear
production (usually wait until ulcer healed before performing Schirmer tear test). The depth
and extent of the ulcer should be assessed looking for evidence of corneal stromal
liquefaction (due to protease release from bacteria, neutrophils or from damaged
keratocytes). Identification of intraocular involvement such as an accompanying anterior
uveitis, hypopyon or even corneal perforation is important. Always take samples for culture
and cytology (microswab used at edge of ulcer for culture, material collected for cytology
with a spatula, swab or cytology brush) these should be taken from the edge of the ulcer
with great care.
The appearance of the cornea surrounding the ulcer should be considered:

is there vascularization?
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is the surrounding cornea edematous?

is there corneal liquefaction/melting?
does the edge of the ulcer have a smooth edge indicating the epithelium is attempting to
cover the ulcer?
Judgment of the depth of an ulcer
The thickness of the normal cornea is about 0.6 - 0.7mm. The edema associated with
ulceration may considerably increase the thickness of the cornea. But even with the
increased thickness of an edematous cornea judging the depth of an ulcer without
magnification is difficult. The ideal examination instrument is the slit-lamp biomicroscope,
which enables one to accurately visualize the depth of an ulcer. Unfortunately few practices
have this available. In the absence of a slit-lamp a magnifying loupe or even a direct
ophthalmoscope with a +20 - +30 lens selected is useful. The cornea should be examined in
profile as well as straight on. If the ulcer has extended down to Descemets membrane it will
appear clearer at the deepest portion (Descemets membrane does not become
edematous). Additionally, Descemets membrane does not take up fluorescein stain, so a
non-staining center to a deep ulcer may indicate that it extends to Descemets membrane.
Descemets membrane will sometimes bulge from the depth of such an ulcer, this is a
descemetocele.
Paradoxically the deeper and more serious ulcers are typically less painful than superficial
ulcers. This is because the corneal sensory nerve supply is more extensive in the superficial
corneal layers than the deeper layers.
Etiology of corneal ulceration

Trauma
Foreign bodies e.g. grass seed under nictitating membrane.
Chemical injuries detergents, spirit, alkalis (alkalis tend to melt corneal stroma and can
rapidly deepen e.g. ammonia, lime), acids (acids coagulate corneal protein and do not
deepen).
Thermal injuries
Cilia abnormalities ectopic cilia (when present often cause ulceration), distichiasis &
trichiasis (don't often cause ulceration).
Lid abnormalities entropion.
Tear film abnormalities keratoconjunctivitis sicca (ulceration is commonest with acute
onset KCS), corneal drying during anesthesia (e.g. cat anaesthetized with ketamine - this
is really an exposure problem).
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Exposure keratitis an inadequate blink can cause corneal dry spot formation and
ulceration.
Neurotrophic keratitis corneal anesthesia (lesion of ophthalmic branch of trigeminal
nerve) will often cause a superficial ulcerative keratitis of the area of cornea exposed
within the palpebral fissure.
Recurrent and refractory (non-healing) corneal erosions (considered elsewhere)
Bacterial corneal ulcers Bacterial contamination of corneal injuries can occur.
Bacteria can adhere to, and therefore colonize damaged epithelial cells and stroma. This
can lead to deepening of the ulcer. Material collected from the edge of such an ulcer is
useful for culture. Cytology smears are stained with Dif Qik, if organisms are seen then
a second smear is Gram-stained - this can give a rapid guide as to the type of bacteria
involved and help in selection of an appropriate antibiotic.
Treatment of the deeper ulcer

A deep ulcer, or one that is deepening, should be aggressively treated. The release of
proteases from bacteria (especially Pseudomonas aeruginosa), neutrophils or damaged
corneal cells can cause a rapid deepening of ulcers. Deeper ulcers, including
descemetocoeles require some form of surgical treatment in addition to medical therapy.
Medical therapy
Typically antibiotic selection will be of a broad-spectrum antibiotic. With a more severe ulcer
the animal is hospitalized, an Elizabethan collar fitted and antibiotics applied hourly initially.
A fluoroquinolone is a good initial choice. Where Gram-positive cocci are identified on
cytology from a severe ulcer topical cefazolin (resuspended to up to 100mg/ml) may be
added. For severe ulcers associated with infection with Gram-negative rods an alternative to
a fluoroquinolone, fortified gentamicin or tobramycin drops (8-20mg/ml) are suggested.
Anticollagenases such as acetylcysteine and EDTA have been suggested for the treatment
of melting ulcers, but are less commonly used now. Autologous serum has an antiprotease
action. Serum is separated from a clotted blood sample and applied every 1-2 hours. It
should be kept refrigerated and replaced daily. Topical atropine drops (1% 1 4 times daily)
are useful to treat reflex uveitis and overcome the pain due to reflex ciliary and iridal muscle
spasm. Pain meds may be included.
Surgical treatment
Conjunctival grafts, free or more usually attached, are very useful for the management of
serious sight threatening corneal ulcers and can be readily performed using a minimum of
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specialized equipment. It is important that surgical magnification is available to allow for

accurate repair. Binocular loupes or an operating microscope are suitable.
Indication for conjunctival grafts
Conjunctival grafts are usually reserved for the treatment of corneal ulcers that are deeper
than one half of the corneal thickness or where satisfactory healing without surgical
intervention is unlikely. They offer very significant advantages over techniques such as third
eyelid flaps and tarsorrhaphies. They:
provide support for weakened cornea
provide an immediate blood supply to the ulcer (except for free grafts)
provide antiproteases and antibacterial substances
with the exception of total conjunctival flaps, continued visualization of the cornea
and intraocular structures is possible
are readily performed and highly successful
The main disadvantage of their use is the resulting area of corneal opacity at the ulcer site,
however this is a minor drawback compared to the risks of corneal perforation and loss of
the eye if grafting is not performed.
Types of graft
The selection of graft depends on the extent and position of the ulcer and the health of the
surrounding cornea (for suture placement). The most versatile and useful graft is the pedicle
graft which can be used on large and even perforated ulcers. Other patterns of conjunctival
graft include; bridge, hood and total grafts and free island grafts.
Acute Glaucoma
An acute rise in intraocular pressure is very painful. This is particularly in dogs and is less
commonly seen/or appreciated in cats.
The animal may resent being touched on the head and be depressed and inappetent. There
may be corneal oedema and epsicleral congestion. There will be loss of vision in the
affected eye although the owner may not be aware of this if the other eye is unaffected and
visual.
Primary Anterior Lens Luxation
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Primary anterior lens luxation is commonest in terrier breeds between 3 to 6 years of age.
Typically the dislocation of a lens to the anterior chamber of the eye leads to a secondary
glaucoma. Examination of the other eye may show evidence of lens instability (ranging from
subluxation, the presence of an aphakic crescent, vitreous prolapse into the anterior
chamber to complete luxation.
Measuring the intraocular pressure accurately can be problematical. Try to measure the
pressure at the periphery of the cornea where there is not a lens pressed up against the
corneal endothelium.
Emergency treatment is to reduce the intraocular pressure. For primary lens luxation
intravenous mannitol is used: 1-2g/kg given over a 20 minute period. Do not allow dog to
drink and rehydrate itself too rapidly. Once the intraocular pressure is lowered the ongoing
damage to the intraocular structures is stopped. The displaced lens can then be removed.
Primary Glaucoma
Primary glaucoma in dogs is relatively common. Typical presentation is of an acute onset
although there may have been a history of intermittent signs of a raised intraocular pressure.
Gonioscopy is required to confirm the form of primary glaucoma typically the other (non-
glaucomatous) eye will be examined.
Emergency treatment is to reduce intraocular pressure. Usually there will be a response in

about 30 minutes from a topical prostaglandin analogue (such as latanoprost). If the
intraocular pressure is still elevated after 30 minutes then a second drop can be applied. If a
prostaglandin analogue does not reduce the intraocular pressure then an osmotic diuretic
(e.g. mannitol) can be used. In some instances a careful aqueocentesis may be needed.
Once the intraocular pressure is controlled, then longer-term treatment may include
continuation of medical management, possibly with the addition of a topical carbonic
anhydrase inhibitor and maybe a beta blocker; or a surgical intervention.
Secondary Glaucoma
Glaucoma secondary to lens luxation is discussed above. It may also be secondary to
anterior uveitis, intraocular tumours and conditions such as ocular melanosis.
Management will consist of identifying the underlying cause and treating if possible and
management to control intraocular pressure.
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Acute Uveitis
Acute anterior uveitis can result in pain and some degree of vision loss and affected animals
may present as an emergency. Initial management is to complete an eye examination
including intraocular pressure measurement and also to run diagnostics for potential causes
of uveitis.
Sudden-Onset Blindness
Owners will often present animals with a bilateral sudden-onset vision loss as an
emergency. Some of the conditions listed above can cause this presentation.
In dogs sudden acquired retinal degeneration syndrome (SARDS), is one possible cause.
Usually, apart for some changes to the papillary light reflexes (some seem almost normal
others are absent) the eyes look essentially normal. Diagnosis is by an electroretinogram
(ERG) that will reveal a lack of response from the retina. Some animals with pituitary
macroadenomas can present with apparent vision loss. In these cases the ERG is normal
and CT or MRI brain imaging is needed.
Retinal Detachment Bilateral retinal detachments results in sudden vision loss. Possible
causes include hypertension and in younger dogs a so-called steroid responsive retinal
detachment. The steroid responsive retinal detachments are of unknown aetiology. Blood
work is unremarkable and serology for tick-borne, fungal and other potential infectious
causes are negative. As the name suggests systemic steroid treatment of such cases can
lead to reattachment of the retina and restoration of vision. Some dogs develop retinal
attachments associated with the development of retinal tears of holes. In such instances
retinal reattachment is not likely and retinal reattachment surgery, if available would be
indicated.
Intraocular Haemorrhage. Bleeding within the eye can cause a loss of vision. It may result
from a number of conditions including coagulopathies, hyperviscosity syndrome and
hypertension. Congenital anomalies such as Collie eye anomaly and persistent hyperplastic
primary vitreous may also be associated with intraocular haemorrhage. In cases where the
bleeding precludes examination of the posterior segment of the eye ocular ultrasound is
indicated.
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Notes page
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Notes page
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MANAGING PARVOVIRUS CASES

Amanda Boag MA VetMB DipACVIM DipACVECC FHEA MRCVS
Clinical Director, Vets Now
amanda.boag@vets-now.com
Parvovirus is a common viral disease of our canine patients. It is a highly pathogenic virus
and principally causes severe gastrointestinal signs (vomiting and diarrhoea). Although it can
be fatal, with high quality, diligent care, high survival rates are possible (90%+). Regardless
of the therapies used, frequent monitoring and adjustment of therapy to the patients needs
is one of the key factors in treatment success yet this can be challenging to provide
practically as these patients should be kept isolated and the financial outlay to provide the
necessary care may be beyond some clients.
Clinical signs and diagnosis
Parvovirus is most commonly seen in dogs less than six months of age, generally between
the ages of 6 and 20 weeks. Infected patients typically have no or reduced natural immunity.
This may occur in unvaccinated animals due to either failure of passive transfer or early
waning of maternal antibodies. In older vaccinated animals it is possible that they have been
vaccinated too soon when the passively transferred maternal antibodies were still present
and prevented efficacious response to vaccination. Doberman Pinschers, Rottweilers,
American Pit Bull Terriers and German Shepherd Dogs are all thought to be more
susceptible than other breeds. It is also often stated that Rottweilers and Dobermans show
more severe signs although evidence for this is lacking. A seasonal occurrence has also
been shown in the USA, with three times as many cases seen in July to September
compared to November to June.
When CPV-2 (the most common pathogenic strain) first appeared in the 1970s, clinical
signs secondary to acute myocarditis (coughing, dyspnoea, pulmonary oedema) were often
seen. Now that antibodies are generally present throughout the adult population this
presentation is rare as maternal antibodies protect the puppies till they are beyond the age
where myocarditis occurs.
At the current time, signs relating to the GI tract are most commonly seen and occur as the
rapidly dividing cells of the intestinal crypts are destroyed. Although sometimes signs are
mild, more commonly there is sudden onset vomiting, depression, abdominal pain, anorexia
and pyrexia followed 12-48 hours later by severe diarrhoea. The destruction of the intestinal
crypts leads to intestinal bleeding and it is common for the diarrhoea to be bloody. Intestinal
protein loss frequently leads to panhypoproteinaemia. The rapidly dividing cells of the bone
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marrow are also affected leading to a concurrent profound neutropenia. The intestinal
damage coupled with the neutropenia means these patients are very vulnerable to bacterial
translocation. Systemic inflammatory response syndrome (SIRS), sepsis, septic shock and
multiple organ failure syndrome may occur in severe cases.
On clinical examination, hypoperfusion and dehydration are often both present to varying
degrees. Patient may be tachycardic with alterations in pulse quality, mucous membrane
and capillary refill time. Mental depression is also often frequently present and may relate to
poor perfusion, hypoglycaemia or both.
A clinical diagnosis is often made on the basis of signalment, knowledge of the puppys
environment and clinical signs. This is supported by the finding of neutropenia on a
haematology panel/blood smear. To confirm the diagnosis, in house faecal analysis ELISA
test kits are available which detect antigen via an immunochromatographic assay. These
tests allow rapid and inexpensive diagnosis and have a good sensitivity and specificity.
False positives can occur rarely if the dog has recently received a live CPV-2 vaccine (in the
past 5-15 days). False negatives can also occur if the sample is taken very early in the
disease, if faecal antigen levels are low or if large amounts of antibodies are present binding
the antigen.
Management preventing infection
Vaccination
On the basis that prevention is better than cure, vaccination still plays a vital role in
managing parvovirus cases and is very effective. Most adult dogs are now immune to CPV-
2, either via juvenile infection, sub-clinical adult infection or immunization and so most
puppies receive parvoviral antibodies via colostrum. The challenge often is that the duration
of protection from the maternal antibodies is variable dependent on the mothers level of
immunity it may be as short as 4-6 weeks if their mother has low antibody titers or as long
as 12-20 weeks if their mother has high titres. Vaccinations have also evolved over the years
and it is recommended that the manufacturers protocols are followed; however it should be
remembered that no protocol or vaccine is completely efficacious and vaccinated dogs do
still get the disease.
Environmental management
Infected dogs shed virus in the surrounding environment and the virus survives very well.
Thorough cleaning with agents such as bleach (dilute 1 part bleach to 32 parts water) or
pentapotassium bis(peroxymonosulphate) bis(sulphate), sulphamidic acid, sodium
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dodecylbenzenesulfonate and dipotassium peroxodisulphate (Virkon) is required. It is likely

to be impossible to clean soft furnishings effectively and so in a home environment, it is
recommended that no unvaccinated, nave animals should be introduced for one year. An
animal that has recovered should be kept away from other dogs for 2 to 4 weeks after
discharge with careful disposal of faeces. Dogs that were in contact with the puppy can be
given an inactivated vaccine booster to try and increase immunity.
Management general treatment
Symptomatic supportive treatment is the mainstay of therapy for parvovirus and even if other
drug therapy is not used high quality supportive care can give excellent survival rates.
Affected animals should be kept an isolation unit to avoid the risk of transmission to other in
patients.
Fluid therapy
Both hypovolaemia and dehydration are frequently present to some degree on presentation.
Furthermore during the course of the disease, fluid losses are difficult to predict and it is not
uncommon for patient to have a one or more periods of hypovolaemia that are addressed
and then redevelop. As most patients are puppies, assessment of both hydration and
perfusion can be more challenging than in the adult animal. In rare cases subcutaneous
fluids administered on an out-patient basis may be sufficient (and should be attempted if the
owners are unable to hospitalize) however hospitalisation is generally necessary.
Generally an isotonic balanced electrolyte solution is the first fluid of choice (e.g. Hartmanns
Solution, Lactated Ringers Solution or 0.9%NaCl). Aggressive fluid rates may be necessary
and initially, up to 90ml/kg can be given and the response assessed. In the more severely
affected patients with hypoalbuminaemia, vasculitis and/or septic shock, response to
crystalloid therapy can be disappointing and colloid therapy is required. Similarly bolus
doses of up to 20ml/kg may be used acutely to correct volume status. Once the
hypovolaemia is corrected, a longer term crystalloid fluid plan consisting of estimated
maintenance, replacement of hydration and on-going losses can be calculated. It must be
remembered though that this on-going support figure is very much a best guess and
patient should be monitored closely, at a minimum every 4 hours in early stages and
sometimes more frequently. Despite our best guess, a high proportion of these patients will
redevelop signs of poor perfusion at some point; prognosis will be better if this is identified at
the earliest possible stage and bolus doses of either crystalloid or colloid repeated.
Transfusion therapy may also be useful in selected patients; plasma can be used largely for
its clotting actor content in cases with prolonged enteral bleeding or DIC and whole blood is
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an option if the puppy is anaemic. The albumin found in plasma or whole blood is unlikely to
be of much benefit.
Electrolytes should also be closely monitored. Hypokalaemia is very common and once the
patient is on a stable fluid rate, potassium chloride should be added to the long term fluids.
Gastrointestinal losses can also result in hyponatraemia and hypochloraemia and if identified
these should be addressed by alterations of the fluid used. Blood glucose levels are often
low due to immature enzyme systems, sepsis, inadequate glycogen stores and decreased
caloric intake and glucose/dextrose supplementation is frequently required.
Maintaining catheter sterility can be challenging in these patients due to the copious volumes
of diarrhoea produced. Careful bandaging and regular checking of catheter sites is required.
Long stay jugular catheters should be considered; although there is a risk of thrombosis
(puppies with parvovirus are often hypercoagulable), this risk needs to be balanced against
the benefit of ensuring clean long term vascular access.
Antibiosis
Broad spectrum antibiosis is generally recommended for patient with parvovirus as even the
more stable patients are at risk of bacterial translocation. Certainly, dogs with evidence of
septic shock, and those that are pyrexic or severely neutropenic, require antibiosis. Afebrile
neutropenic dogs may be treated with an antibiotic such as potentiated amoxicillin. However,
in more severely affected patients with evidence of sepsis, broad spectrum antibiotics with
good activity against both Gram positive and negative organisms should be chosen.
Ampicillin and amikacin represent a good combination as long as care is taken to ensure
renal perfusion is optimized prior to therapy and patients UA is monitored for development of
casts. Second or third generation cephalosporins can also be considered as can
enrofloxacin although the risks of effects on cartilage development should be communicated
to the owner. Parenteral administration is preferred as vomiting and delayed gastric
emptying may result in poor reliability of oral preparations.
Anti-emetics
Nausea is an unpleasant sensation and in humans it is associated with a decreased quality

of life. Continued vomiting also leads to on-going fluid loss, electrolyte and acid base
disturbances and oesophagitis. Anti-emetics are therefore strongly recommended.
Metoclopramide, maropitant and ondansetron can all be effective and may be used in
combination. Although the latter is expensive, it is useful when vomiting is unresponsive to
other drugs.
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Gastric Protectants
H2-receptor antagonists (cimetidine, ranitidine) are frequently used however their use must
be questioned considering the data on their ability to change canine gastric pH. If gastric
ulceration or severe oesophagitis is thought to be present drugs with proven efficacy such as
omeprazole should be used. Sucralfate can also be used if vomiting is adequately controlled.
Nutrition
Providing nutrition is encouraged at the earliest possible opportunity although is often

delayed until vomiting is at least partially controlled. A naso-oesophageal or
oesophagostomy tube can be placed if the patient is reluctant to eat. A relatively recent
study has suggested that even if an animal is still vomiting naso-oesophageal feeding results
in earlier clinical improvement and significant weight gain (see recent literature). Great care
must be taken to monitor these patients for aspiration however especially as they are often
located in an isolation ward which has less frequent patient observation. Nasogastric tubes
can also be used to allow gastric decompression which may decrease nausea. Enteral
nutrition is preferred as it helps maintain mucosal integrity and decreases bacterial
translocation and although total or partial parenteral nutrition can be performed,
complications may develop.
Management specific treatment
Antiviral drugs
Feline interferon (type omega) (Virbagen Omega) is now licensed for treatment of parvovirus
in dogs in Europe, Japan, Australia and New Zealand. In one study of 94 clinical cases it
was found to decrease mortality rates by 4.4 fold and also decrease clinical signs compared
to dogs not given the drug. This study should be treated with slight caution however as the
mortality rate in the untreated dogs was very high for standard care (30%). The most
successful dosing regime appears to be 2.5 MU/kg administered intravenously once daily for
three consecutive days.
There has been recent interest in the use of oseltamivir (Tamiflu) for canine parvovirus. It is
a neuraminidase inhibitor and as parvovirus does not have a neuraminidase glycoprotein it is
difficult to see what benefit it would bring. A single clinical trial has been reported with
equivocal results (see recent literature).
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Immune plasma
Plasma containing parvoviral antibodies (e.g. from recovered dogs) is sometimes advocated.
There is one study evaluating its use (see recent literature) which showed no effect.
Recombinant granulocyte colony-stimulating factor
Human recombinant gCSF may increase the white blood cell count in severely leukopenic
patients, but again its use is controversial and it has not been shown to improve survival
rates. Recombinant canine gCSF may prove more useful (see recent literature)
Prognosis
Parvovirus is undoubtedly a severe disease with the potential for a fatal outcome. Prognosis
is good however if appropriate care can be provided. The single most effective treatments
are diligent fluid therapy coupled with antibiosis especially in the first few days. A number of
other drug therapies are either being marketed or are under evaluation and it is likely to be
worth using those backed by evidence if the client is willing; however if the client has limited
funds (as is sadly often the case with these patients) it is recommended that available
money is spent on nursing care and monitoring.
Recent literature
Clinical evaluation of a single dose of immune plasma for treatment of canine

parvovirus infection.
Bragg RF, Duffy AL, DeCecco FA, Chung DK, Green MT, Veir JK, Dow SW. J Am Vet Med Assoc.
2012 Mar 15;240(6):700-4.
OBJECTIVE: To evaluate the efficacy of administration of a single 12-mL dose of canine parvovirus
(CPV)-immune plasma for treatment of CPV enteritis.
DESIGN: Prospective, randomized, double-blinded, placebo-controlled clinical trial.
ANIMALS: 14 dogs with naturally occurring CPV enteritis.
PROCEDURES: Dogs were assigned to treatment groups on the basis of randomization tables and
were administered a single i.v. dose of CPV-immune plasma (treatment group) or an equivalent
volume of saline (0.9% NaCl) solution (placebo group) within 18 hours after admission to the hospital.
Treatment and outcome variables evaluated included neutrophil, monocyte, and CPV counts; number
of days of hospitalization; changes in body weight; and cost of treatment.
RESULTS: When dogs treated with CPV-immune plasma were compared with dogs treated with
saline solution, there were no significant differences detected among neutrophil or monocyte counts,
magnitude of viremia, weight change, number of days of hospitalization, or cost of treatment.
CONCLUSIONS AND CLINICAL RELEVANCE: Administration of a single 12-mL dose of immune

plasma soon after the onset of CPV enteritis in dogs was not effective in ameliorating clinical signs,
reducing viremia, or hastening hematologic recovery.
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Use of oseltamivir in the treatment of canine parvoviral enteritis.

Savigny MR, Macintire DK. J Vet Emerg Crit Care (San Antonio). 2010 Feb;20(1):132-42.
OBJECTIVE: To determine if oseltamivir with standard therapy for canine parvoviral enteritis
ameliorates disease morbidity, mortality, or both; to document significant adverse effects associated
with its use.
DESIGN: Prospective, randomized, blinded, placebo-controlled clinical trial.
SETTING: University veterinary teaching hospital.
ANIMALS: Thirty-five dogs.
INTERVENTIONS: Standard therapy was administered to all dogs. Treatment dogs also received
oseltamivir, while control dogs received an equivalent volume of placebo.
MEASUREMENTS AND MAIN RESULTS: Dogs were monitored daily according to a clinical scoring
system, physical parameters, and diagnostic evaluations. Dogs in the treatment group gained a
significant percentage of weight during hospitalization (mean, +2.6%; SD, 7.1%) versus the control
dogs (mean, -4.5%; SD, 6.9%) (P=0.006). Treatment dogs did not have any significant changes in
their white blood cell (WBC) count, while control dogs experienced a significant drop in their WBC
counts during their initial stay. In addition, it did not appear that oseltamivir use was associated with
any major adverse clinical effects.
CONCLUSIONS: While a clear advantage to the use of oseltamivir was not established, a significant
weight loss during hospitalization, as well as a significant decrease in WBC count were documented
in the control group. No major adverse effects were identified that could be associated with
oseltamivir administration. Based on these results, the true role of oseltamivir in the treatment of
parvoviral enteritis remains speculative, although it is believed that further investigation is warranted.
Hematologic improvement in dogs with parvovirus infection treated with recombinant

canine granulocyte-colony stimulating factor.
Duffy A, Dow S, Ogilvie G, Rao S, Hackett T. J Vet Pharmacol Ther. 2010 Aug;33(4):352-6.
Previously, dogs with canine parvovirus-induced neutropenia have not responded to treatment with
recombinant human granulocyte-colony stimulating factor (rhG-CSF). However, recombinant canine
G-CSF (rcG-CSF) has not been previously evaluated for treatment of parvovirus-induced neutropenia
in dogs. We assessed the effectiveness of rcG-CSF in dogs with parvovirus-induced neutropenia with
a prospective, open-label, nonrandomized clinical trial. Endpoints of our study were time to recovery
of WBC and neutrophil counts, and duration of hospitalization. 28 dogs with parvovirus and
neutropenia were treated with rcG-CSF and outcomes were compared to those of 34 dogs with
parvovirus and neutropenia not treated with rcG-CSF. We found that mean WBC and neutrophil
counts were significantly higher (P < 0.05) in the 28 dogs treated with rcG-CSF compared to disease-
matched dogs not treated with rcG-CSF. In addition, the mean duration of hospitalization was reduced
(P = 0.01) in rcG-CSF treated dogs compared to untreated dogs. However, survival times were
decreased in dogs treated with rcG-CSF compared to untreated dogs. These results suggest that
treatment with rcG-CSF was effective in stimulating neutrophil recovery and shortening the duration of
hospitalization in dogs with parvovirus infection, but indicate the need for additional studies to
evaluate overall safety of the treatment.
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Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and
outcome in dogs with severe parvoviral enteritis.
Mohr AJ, Leisewitz AL, Jacobson LS, Steiner JM, Ruaux CG, Williams DA. J Vet Intern Med. 2003
Nov-Dec;17(6):791-8.
A randomized, controlled clinical trial investigated the effect of early enteral nutrition (EN) on intestinal
permeability, intestinal protein loss, and outcome in parvoviral enteritis. Dogs were randomized into 2
groups: 15 dogs received no food until vomiting had ceased for 12 hours (mean 50 hours after
admission; NPO group), and 15 dogs received early EN by nasoesophageal tube from 12 hours after
admission (EEN group). All other treatments were identical. Intestinal permeability was assessed by
6-hour urinary lactulose (L) and rhamnose (R) recoveries (%L, %R) and L/R recovery ratios. Intestinal
protein loss was quantified by fecal alpha1-proteinase inhibitor concentrations (alpha1-PI). Median
time to normalization of demeanor, appetite, vomiting, and diarrhea was 1 day shorter for the EEN
group for each variable. Body weight increased insignificantly from admission in the NPO group (day
3: 2.5 +/- 2.8%; day 6: 4.3 +/- 2.3%; mean +/- SE), whereas the EEN group exhibited significant
weight gain (day 3: 8.1 +/- 2.7%; day 6: 9.7 +/- 2.1%). Mean urinary %L was increased, %R reduced,
and L/R recovery ratios increased compared to reference values throughout the study for both
groups. Percent lactulose recovery decreased in the EEN group (admission: 22.6 +/- 8.0%; day 6:
17.9 +/- 2.3%) and increased in the NPO group (admission: 11.0 +/- 2.6%; day 6: 22.5 +/- 4.6%, P =
.035). Fecal alpha1-PI was above reference values in both groups and declined progressively. No
significant differences occurred for %R, L/R ratios, or alpha1-PI between groups. Thirteen NPO dogs
and all EEN dogs survived (P = .48). The EEN group showed earlier clinical improvement and
significant weight gain. The significantly decreased %L in the EEN versus NPO group might reflect
improved gut barrier function, which could limit bacterial or endotoxin translocation.
Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled

field trial.
de Mari K, Maynard L, Eun HM, Lebreux B. Vet Rec. 2003 Jan 25;152(4):105-8.
The clinical efficacy of a recombinant feline interferon (IFN) (type omega) was evaluated under field
conditions for the treatment of dogs with parvoviral enteritis. In this multicentric, double-blind, placebo-
controlled trial, 94 dogs from one to 28 months old were randomly assigned to two groups which were
treated intravenously either with IFN (2.5 million units/kg) or placebo once a day for three consecutive
days, and monitored for clinical signs and mortality for 10 days. Each dog received individual
supportive treatment The data from 92 interpretable cases (43 IFN-treated and 49 placebo) showed
that the clinical signs of the IFN-treated animals improved significantly in comparison with the control
animals, and that there were only three deaths in the IFN group compared with 14 deaths in the
placebo group (P = 0.0096) corresponding to a 4.4-fold reduction. Alternative analyses of the data
taking into account the prior vaccination status of the dogs against canine parvovirus suggested that
the IFN therapy resulted in a 6.4-fold reduction in mortality (P = 0.044) in the unvaccinated cohort, a
significant reduction when compared with the vaccinated cohort.
Page 207 of 334

DIABETIC EMERGENCIES
abreton@vescone.com
Physiology
The pancreas is an organ that is a mixed gland (endocrine and exocrine parts). The exocrine
secretions enter the duodenum through the pancreatic duct. The endocrine secretions are
formed in tissue found within the exocrine tissue known as the islets of Langerhans. The
three hormones secreted from the islets of Langerhans are insulin, glucagon and
somatostatin.
The insulin is secreted in response to high blood glucose levels in the body. Ultimately the
insulin helps to lower the blood glucose by increasing the uptake of glucose into the cells
and storing the excessive glucose as glycogen in the liver for later use. It is also
responsible for breaking down fat and storing it as adipose tissue. Glucagon is secreted in
response to low blood glucose levels. It helps to raise the blood glucose by converting the
stored glycogen in the liver back to glucose. Somatostatin helps to regulate blood glucose
levels in conjunction with insulin and glucagon as well as helps to decrease gut motility and
secretion of digestive juices.
An insult to the pancreas occurs causing a degeneration in the islet cells. The insult could
be from an acute or chronic onset of pancreatitis, neoplasm or may be idiopathic. The end
result is that there is a reduction of the hormone insulin, the failure of the cells of the body to
be able to respond to insulin and/or the increase of glucagon resulting in hyperglycaemia.
The lack of insulin in the body along with the rising levels of glucagon result in
hyperglycaemia for an extended period of time within the body.
Hyperglycaemia
When blood glucose levels rise above 9.98 mmol/l in dogs and above 15.5 mmol/l in cats,
the kidneys are no longer able to filter out all the glucose which results in glucose spilling
into the urine. Glucose is therefore detectable on a urine test strip.
While blood glucose levels can reach above 33.2 mmol/l, the only significant side effect to
the extreme hyperglycaemia is dehydration of the tissue cells. The dehydration is likely
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because glucose does not diffuse easily through cellular pores which results in an increase
in osmotic pressure in extracellular fluids causing fluids to shift out of the cells.
The loss of glucose in the urine leads to osmotic diuresis in the renal tubules causing a
decrease in tubular reabsorption of fluid. This causes an increase in urine production,
increase in thirst (due to the decrease of fluids being reabsorbed) and intra- and extracellular
dehydration.
The chronic high glucose levels will lead to tissue injury of the blood vessels which causes
the blood vessels not to function normally. The exact mechanism of why this occurs is not
fully understood. When the blood vessels fail to function normally it leads to inadequate
blood supply to the tissues. As the blood sugar increases pet can experience one of two
types of emergencies: diabetic ketoacidosis (DKA) or hyperosmolar hyperglycaemic state
(HHS).
DKA
Because there is a lack of insulin in the body, the body shifts from carbohydrate metabolism
to fat metabolism. As the fat is metabolized for energy it produces pH falls below 7.0 coma
or death may occur. In cases of severe metabolic acidosis (<7.0) the pet may experience
Kussmaul respirations (slow, deep and gasping respiration). The ketones build up in the
body which eventually overwhelm the body. High numbers of ketones overwhelm the body's
buffering system which leads to an increase in hydrogen ions (H+), a decrease in
bicarbonate (HCO3-) and a decrease in blood pH. This leads to a metabolic acidosis. As
the pH decreases and the dehydration worsens, the body will experience electrolyte
abnormalities with sodium, potassium, phosphorous and magnesium.
Pets with DKA often present with symptoms including: polyuria, polydipsia, nausea,
weakness, vomiting and diarrhoea. Other signs may include shock, tachypnea,
hypothermia, hypotension and dehydration (dry oral membranes, decreased skin turgor,
sunken eyes). About 10% of cats may exhibit diabetic neuropathy with a plantigrade stance
(hocks touch the ground when the cat walks or stands). Approximately 40% of dogs may
present with cataracts in one or both eyes. Hepatomegaly and secondary pancreatitis is
common in both the dog and cat.
If the pH falls below 7.0 coma or death may occur. In cases of severe metabolic acidosis
(<7.0) the pet may experience Kussmaul respirations (slow, deep and gasping respiration).
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HHS
While not common, HHS can occur in both the dog and cat and is sometimes referred to as
"nonketonic hyperglycaemia". HHS is when the pet experiences profound hyperglycaemia
(>33.2 mmol/L), hyperosmolarity (>350 mOsm/L), extreme dehydration, CNS depression
and is absent of ketones and severe metabolic acidosis. Pets with HHS are more likely to
have some underlying kidney or cardiovascular disease. HHS pets may also be non-
insulin-dependent.
It's not fully understood why the pet does not experience ketonuria since the pathogenesis is
similar to that of an uncomplicated diabetic. It is thought that there are likely some
functioning cells that are still producing some insulin for the pet. The existence of some
insulin prevents the formation of ketones. As the blood sugar rises the pet begins to
experience severe signs of dehydration. As the dehydration continues the pet will start to
experience azotemia. The increase in osmolarity causes water to shift out of the cerebral
neurons which results in obtundation.
Pets with HHS are often lethargic, severely dehydrated, depressed and weak. They may
have gastrointestinal signs (anorexia, vomiting, and diarrhoea) which may progress to
neurological symptoms. They are often in shock and hypothermic. As it progresses the pet
may experience a coma and/or death.
Diagnosing HHA and DKA
Diagnosis is made based on laboratory findings. A complete blood count (CBC), blood
chemistry, electrolytes, urinalysis (sterile sample ideal) and blood gas should be performed.
In both the dog and cat a mild polycythemia (due to dehydration) or leukocytosis may be
noted.
A chemistry may reveal increased liver values, most commonly ALT and ALP. Increases in
blood glucose level, kidney enzymes and cholesterol are often noted. Electrolyte
derangements are more common in DKA and most commonly include hyponatremia,
hypomagnesaemia and hypokalaemia. If HHS is suspected serum osmolarity should be
calculated. To calculate out osmolarity the following equation should be used: Serum
Osmolarity = (2 x serum sodium [mEq/L]) + (BUN [mg/dl]/2.8) + (glucose [mg/dl]/18).
Normal serum osmolality is 290 to 310 mOsm/kg. Neurologic symptoms have been
documented in animals when osmolality exceeds 340 mOsm/kg.
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A urinalysis will always reveal glucosuria and, most likely, in the case of DKA, ketonuria.
Protein, bacteria (due to secondary urinary tract infection) and/or blood may also be present
in the urine. If DKA is suspected and ketones are not detected on a urine stick, testing
plasma on a urine strip should be performed. It has been shown that plasma will detect
ketones at times when urine may not.
Hypoglycaemia
Hypoglycaemia is one of the most common side effects of insulin therapy in a diabetic.
Clinical hypoglycaemic is defined as blood glucose levels less than 3.32 mmol/l. Diabetics
who experience a hypoglycaemic state do so because of one of two reasons: they were
incorrectly dosed with insulin or are experiencing a change in insulin requirements. Cats
frequently can experience "transient diabetes" causing their insulin requirements to change.
Approximately 20% of diabetic cats will experience transient diabetes. Changes in the pet's
weight, appetite, diet, and activity level can results in the pet needing a lower insulin dose.
Owners of new diabetics should be given written instructions on ways to avoid
hypoglycaemic episodes (give insulin after ensuring pet has eaten, have family member
double check dose, keep a check system on the refrigerator).
Hypoglycaemia mainly affects the nervous and musculoskeletal systems. Nervous tissue
relies heavily on glucose as its primary energy source. While emergency signs resulting
from hyperglycaemia take days if not weeks to occur, a pet experiencing hypoglycaemia is
always an immediate emergency. Pets that experience hypoglycaemia will often become
lethargic, weak, ataxic and appear "wobbly". Signs can be seen in blood glucose levels
between 50-60 mg/dl. Hypoglycaemia stimulates appetite so pets may start acting hungry or
eat things they normally may not. As the hypoglycaemia worsens (the blood sugar level
continues to decline) the symptoms will worsen and can lead to seizures, coma and death.
Treatment
Upon presentation of any emergency diabetic all emergent signs should be treated. Patients
may present severely lethargic, shock, obtunded, seizuring or in a coma. All known
diabetics should immediately have their blood glucose level tested to ensure the signs are
not from hypoglycaemia. In general, treatment should be focused on fluid therapy, insulin
therapy if hyperglycaemic, electrolyte correction and treatment of any metabolic acidosis. It
will take about 36-48 hours to normalize high glucose levels and pH levels and about 12-24
hours to normalize low glucose levels.
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DKA, HHS and hypoglycaemic diabetics will present with signs and symptoms that warrant
fluid therapy and medication administration (valium, dextrose). Therefore it is better if an
intravenous (IV) catheter is placed first even if the patient is seizuring. A central line should
be placed once the patient is a little more stable as this will allow for blood to be obtained
and fluid therapy to begin almost simultaneously. In the case of a DKA patient, placement of
a central line can usually occur first and is likely the only IV catheter placement needed.
Placement of a central line will allow for central venous pressure (CVP) to be monitored,
parental nutrition to be given and blood obtained for future lab work.
If the patient is experiencing HHS or is a DKA, baseline blood work should be obtained and
fluid therapy should begin. Fluid therapy may be started before blood work is obtained if the
patient is too critical and blood too difficult to obtain. The goal of fluid therapy is to re-
establish normal fluid balance. Just rehydrating the patient will aid in helping to decrease
plasma glucose levels by helping to improve kidney function. The choice of fluids is
ultimately the clinician's decision and should be based on electrolyte and acid-base status.
Many clinicians will start with 0.9% NaCl to help with hyponatremia that most DKA
experience. The current recommendations by the American Diabetes Association for
patients with HHS is to use 0.9% NaCl in patients with a low serum sodium concentration
and use 0.45% NaCl in patients with a normal or high serum sodium concentration. It is
generally recommended to correct about 75% of the dehydration over the first 24 hours and
the other 25% on the second day.
Potassium supplementation is usually added to the fluids of DKA patients. After 6-12 hours
the electrolytes and blood gas should be rechecked in any HHS or DKA patient. Some
clinicians will opt to change the fluids to a buffered solution with less sodium (LRS, P-lyte,
Norm R) if the patient's sodium level is >140 mmol/L.
Phosphate supplementation may be needed in a DKA patient due to a rapid decrease in

levels within 12-24 hours after insulin administration begins. Phosphorus levels < 1.5 mg/dL
can lead to anaemia, weakness, ataxia and seizures. Phosphorus should never be used in
conjunction with calcium containing fluids.
The use of bicarbonate therapy in DKA patients is controversial, but should be considered in
patients with a pH <7.1 or a serum HCO3 < 12 meq/L. Most of the time acidosis improves
once perfusion and glucose levels are normalized. Using a buffered solution (LRS, Norm-R)
also aids in the correction of any acidosis. Administration of bicarbonate can result in
coronary acidosis, a paradoxical CNS acidosis and therefore sudden death. If the patient is
not responding and still in a critical acidotic state then bicarbonate therapy can be initiated.
Bicarbonate must be administered slowly (over 2-6 hours) to avoid overwhelming the blood-
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brain barrier with rising levels of PCO2. The use of bicarbonate is not recommended in HHS
patients and not needed in hypoglycaemic patients.
If an owner calls stating their pet is a known diabetic who was overdosed on insulin or who is
exhibiting signs of hypoglycaemia (seizure, ataxia) they should be instructed to put karo
syrup, honey or even raw sugar on the gums and then drive to the veterinary hospital
immediately. Upon arrival, if the pet is experiencing hypoglycaemia an initial slow IV bolus
of 50% dextrose (0.5g/kg diluted with sterile saline or sterile water 1:4 or 1:2 ratio) should be
administered. The pet should then be placed on a CRI of 5% dextrose solution.
Blood sugars will be constantly checked every couple of hours. Hypoglycaemic pets should
slowly be wean off the dextrose CRI over a 12-24 hour period once they have high or normal
blood glucose levels. The cause of the hypoglycaemia must be investigated so that further
hypoglycaemic episodes do not occur. This may be a decrease in insulin, removal of insulin
all together or more careful medical management at home.
Insulin Therapy
Regular insulin is always chosen for the initial treatment of DKA and HHS because it offers a
quick onset of action and a short duration of effect. There are two routes regular insulin can
be given to patients: IV or IM. If given IV, it is typically given at a constant rate infusion (CRI).
Intramuscular doses are given intermittently, usually every 4-6 hours with blood glucose
checks occurring every 2 hours. If a DKA patient is on a CRI of insulin, a dextrose CRI
should be added once glucose levels reach between 8.32-16.64 mmol/L. Adding in dextrose
will help with the further breakdown of the remaining ketones and help to resolve acidosis of
a patient with DKA.
The goal of insulin therapy in a DKA is to drive blood glucose levels between 8.32-16.64
mmol/L. In the case of a pet with HHS, it is recommended that blood glucose concentration
remain at 13.87-16.64 mmol/L until hyperosmolarity is corrected. DKA patients are then
started on subcutaneous regular insulin until anorexia and ketosis has resolved. Pets are
then sent home on either an intermediate or long-acting maintenance insulin.
Nursing Care
Nursing care of diabetic emergencies can be intense. The primary nursing care of a diabetic
emergency patient revolves around monitoring the patient's response to the treatment.
Physical exam parameters and blood pressure should be checked every 2-6 hours
depending on how critical the pet is. Pets should be weighed twice a day to monitor
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rehydration. Since these pets are often on high rates of fluids they should be monitored
closely for signs of fluid overload (respiratory rate/effort, auscultation of lung sounds).
A urine catheter should be considered in down pets to aid in keeping them clean and to be
able to quantify urine output. Non-absorbent litter or obtaining a free catch can be done to
obtain accurate amounts of urine. Urine should be checked every 6-12 hours for ketones so
collection of urine is important for a variety of reasons. Ketones may persist up to 5 days in
the urine even after a resolution of the ketosis state.
Measuring CVP will help determine how much fluid can be administered to a patient without
causing fluid overload. Depending on the literature normal CVP measurements vary, but
most will agree it is somewhere between 1-10 cm H2O. Monitoring CVP is particular useful
in HHS and DKA patients.
It is important that patients have their blood pressure monitored minimally every 4-6 hours.
If the mean arterial pressure (MAP) falls below 60 mmHg, the kidneys and other organs are
not appropriately perfused putting them at risk for organ failure. Normalization of blood
pressure defined by a MAP of 80-120 mmHg or systolic between 110-160 mmHg, is goal.
Diabetic emergency patients require frequent blood draws and it is imperative that if the
patient does not have a central line, the integrity of the veins be kept in good health. Having
one ready to go and placing a pressure bandage on for every venipuncture is imperative.
If the patient is recumbent, the pet will need to be turned and kept dry and free of bed sores
and have passive range of motion must be performed every four to six hours.
Lastly it is important that patients be given appropriate nutrition. Malnutrition can delay
healing and cause large fluctuations in glucose/insulin regulation. Feeding tubes, force
feedings or parental nutrition should be considered in patients who are unwilling to eat.
At time of discharge clients need to have a discussion on how to care for their diabetic
animal. Hand-outs and one-on-one demonstrations on insulin handling and administration
are key to client compliance.
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Conclusion
As a veterinary technician you will likely encounter an emergency diabetic pet at some point.
Being able to communicate with the owner quickly and effectively will allow for faster
treatment of the pet. Being able to monitor the patient and notice subtle changes will help
the patient receive the appropriate course of treatment and allow for a faster recovery.
Page 215 of 334

SEIZURES: STAGES, TYPES AND CARE

abreton@vescone.com
Physiology
Seizures are thought to be the cause of hyperexcitable neurons that suddenly depolarize in
the prosencephalon (forebrain). There are two types of mechanisms that help to control the
firing of neurons within the brain: inhibitory circuits and the fatigue of synapes.
The inhibitory circuit works to help prevent the excessive spread of signals by inhibiting
either the input neurons or the intermediate neurons. Intermediate neurons gather and
process information in the brain and then transmit the information to the motor neurons
where it is carried to various parts of the body. Synaptic fatigue works by the simple process
of the synaptic transmissions slowly becoming weaker with the more neuron excitability they
experience. Ultimately it is the failure of these mechanisms to respond to the
hyperexcitable neurons which causes a seizure to occur. Ultimately seizures stop on their
own because of neuronal fatigue.
Causes
Causes can be broken down into two groups: Extracranial and Intracranial. Extracranial
causes are those that are not a direct insult to the brain itself. These include metabolic
disorders (hypoglycaemia, electrolyte disturbances, hyperthermia), toxicities (snake
envenomation, lead) and nutritional disorders (thiamine deficiency). Intracranial causes are
those that are caused by a direct insult to the brain such as trauma, idiopathic epilepsy and
neoplasia.
Idiopathic epilepsy is the most common cause of seizures in dogs. The diagnosis of
epilepsy is one of rule-outs and is a disease considered to be idiopathic. Epilepsy is defined
as a seizure with no underlying structural brain lesion or other neurological signs or
symptoms. Idiopathic epilepsy is presumed genetic and usually age dependant. Generally
most dogs that develop idiopathic epilepsy are between 6 months to 6 years of age.
Idiopathic epileptic seizures usually last between 30 seconds to 3 minutes. Neoplasia
should always be ruled out through radiographs, CT scan, ultrasonography and MRI. There
are numerous dog breeds where idiopathic epilepsy is considered genetic including: German
Page 216 of 334

Shepherd Dog, Keeshond, Beagle, English Springer Spaniel, Dachshund, Vizsla, Standard
Poodle, Labrador Retriever, Golden Retriever and Bernese Mountain Dog.
The most common extracranial cause of seizures in dogs is due to hypoglycaemia.

Hypoglycaemia most commonly occurs because of neoplasia (insulinoma), a functional form
due to rigorous exercise, an unexplained form in small/toy breed puppies 6-12 weeks of age,
large parasitic infection, gastrointestinal disturbances, hypothermia, starvation and
numerous systemic diseases. Because on initial presentation you cannot determine if it is
intra- or extracranial, it is always important to test a blood glucose level in all seizuring
patients.
In cats, the most common extracranial cause of seizures is hepatic encephalopathy. Hepatic
encephalopathy most commonly occurs secondary to a portosystemic shunt (PSS). Cats
will frequently demonstrate ptyalism (hypersalivation) as a sign. As ammonia and electrolyte
levels fluctuate, seizures, an altered mental status and changes in behaviour will come and
go. At times the cat may appear normal. Ultimately PSS correction, electrolyte
normalization and normalization of ammonia levels must occur in order for the seizures to
stop.
There is not one definitive "most common intracranial cause of seizures in cats. Intracranial
causes most likely to occur in cats are: brain tumours (meningiomas), trauma, infectious
central nervous diseases (feline infectious peritonitis, toxoplasmosis, feline leukaemia virus,
cryptococcosis, feline immunodeficiency virus) and idiopathic epilepsy (though occurs
significantly less than in the dog).
Types & Stages of Seizures
There are two main types of seizures: Generalized and Partial. Generalized seizures are
also known as "major motor" or "grand mal". It is more common in certain breeds, such as
German shepherds, Saint Bernards and Irish Setters, to experience severe generalized
seizures. Pets will often fall on the ground unconscious, extend their limbs rigidly and
convulse. Breathing may stop during this time. The convulsions usually last for only 10-30
seconds. After the major convulsions have ceased, the pet may experience jaw snapping or
clonic limb movements in the form of "running" or paddling. It is possible for the pet to
experience intermittent periods of convulsions and then paddling.
Partial seizures are also known as "focal motor" or "jacksonian". They are localized to a
certain area of the body such as the face or a limb. It is more common for Labrador
retrievers and cats to experience partial seizures then generalized. Pets that experience
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partial seizures will almost always experience their seizure activity in the same way. Most
commonly partial seizures "spread" into generalized seizures. Because partial seizures may
be subtle, pet owners may easily miss the seizure activity all together or mistake it as
something else. Partial seizures typically seen are: fly-biting, facial twitching, excessive
salivation and changes in behavior. Cats are unique and can display behaviour-like
symptoms such as vocalizing, piloerection, attacking objects, startling and running. Owners
may need to video tape the behaviour in order to confirm it is seizure activity.
There are three stages to seizures: Preictal, Ictus and Postictal. In the preictal stages (also
known as the prodromal stage) the pet may sense they are going to experience a seizure.
They may cling to the owner, act nervous, hide or vocalize. The ictus stage is when the pet
is experiencing the actual seizure. The postictal stage can last a couple seconds to minutes
and usually lasts less than an hour. Some pets may experience a seizure and appear
completely normal afterwards. Signs include: confusion, disorientation, restlessness,
pacing, vocalizing, depression and blindness. Status epilepticus (SE) is a condition where
multiple seizures occur without a complete recovery in-between. This condition is life-
threatening and is an emergency. There are a variety of definitions, but most agree that it is
either one continuous seizure lasting longer than 5 minutes or recurrent seizures without
regaining consciousness between seizures that lasts longer than 5 minutes. Ultimately the
continuous hyperexcitability of the neurons leads to hyperthermia, pulmonary oedema,
cardiac arrhythmias, and cardiovascular collapse. A hyperthermic SE patient experiences
that same complications as a malignant hyperthermic patient including disseminated
intravascular coagulation (DIC), systemic inflammatory response syndrome (SIRS), multiple
organ dysfunction, multiple organ dysfunction syndrome (MODS) and rhabdomyolysis.
While these patients can recover, the prognosis depends on the underlying issue and how
neurologically impaired the patient appears to be (pinpoint pupils, no response to
stimulation).
Treatment
Depending on the inciting cause of the seizure a variety of treatment options may be
available. It is important to come up with an official diagnosis for a seizuring patient
otherwise the treatment given may not be appropriate. Ultimately the goal with any
treatment is to stop the seizures and then treat the underlying condition second.
Diazepam continues to be the most useful anticonvulsant for stopping seizures. It is not
effective as an oral maintenance to prevent seizures, but is effective at stopping them. The
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preferred route is IV, but can also be administered IM or rectally in patients that it is difficult
to obtain venous access. For patients where seizures are continuing after multiple doses of
diazepam have been given, then phenobarbital or pentobaribtal can be administered.
In patient experiencing cluster seizures or SE, propofol can be administered. Propofol is an

injectable anaesthetic which will work to stop the hyperexcitability of the neurons by
decreasing brain metabolic activity. Unfortunately sometimes after the propofol wears off,
the patient can start seizuring again because it does little to affect the activity within the brain
itself. Certainly putting the pet under anaesthesia (isoflourane) will also stop the seizures.
Sometimes SE patients need to be kept under anaesthesia for several hours to stop the
hyperexcitability of the neurons. During that time any underlying cause of the seizures must
be corrected (electrolyte disturbances) and an anticonvulsant is usually administered.
Patients are then slowly woken back up with the hopes that the seizures do not reoccur.
Other drugs that can be considered to stop seizures are: midazolam and levetiracetam.
For some patients with idiopathic epilepsy or certain conditions (neoplasia), maintenance
anticonvulsant medication may be required to prevent seizure activity. With the advances in
veterinary medicine there are numerous anticonvulsant choices available. Phenobarbital is
still considered the standard maintenance anticonvulsant in dogs and cats. It works by
increasing the threshold of neurons to the initiation of a seizure and is a fast acting drug.
Owners should be informed of the common side effects which include: polyuria, polydipsia,
polyphagia, weight gain, sedation and ataxia. Less commonly hepatic failure may occur. In
cats facial pruritus and limb oedema have been noted, but these side effects stop with the
discontinuation of the drug.
Potassium Bromide (KBr) is a frequently used maintenance anticonvulsant. It is generally

used in conjunction with phenobarbital when phenobarbital alone doesn't work to control the
seizures adequately. The side effects are similar to that of phenobarbital, though it does
take a longer time for the body to rid itself of the drug once it has been discontinued.
An increasingly popular newer maintenance anticonvulsant is zonisamide. It has a high

margin of safety, but unfortunately the cost is somewhat prohibitive. Rare side effects
include mild sedation, ataxia and vomiting. Zonisamide has been shown to reduce seizure
activity by 50% in 7 of 12 dogs who were receiving phenobarbital, but still experiencing
breakthrough seizures. Currently there are no reports of use in cats.
Levetiracetam (Keppra) is a newer maintenance anticonvulsant. While it appears to have a

high safety margin, the mechanism of action is poorly understood. This drug has been
shown to be well tolerated in both dogs and cats and is a good add-on drug to use in
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conjunction with phenobarbital. A prospective trial evaluating levetiracetam as an add-on

therapy for dogs with refractory epilepsy showed a 54% decrease in seizures.
Felbamate (Felbatol) has a high safety margin in dogs. Little studies have been published
on the use of it in cats. It appears effective as both an add-on drug as well as the soul
maintenance anticonvulsant drug. Other drugs that can be used are gabapentin and
pregabalin. In both, the mechanism of action is not fully understood. Neither are
recommended to be used as the only maintenance anticonvulsant. Both drugs have been
only used in dogs.
Nursing Care
Initial stabilization of the patient should include stopping any seizure activity, stabilizing the
patient (airway, breathing, circulation), correcting any underlying emergency metabolic
disturbances (hypoglycaemia, hypocalcaemia) and normalizing any physical exam
parameters (temperature, heart rate).
An intravenous catheter should be placed to help support cardiac output and to administer
an anticonvulsant. When the catheter is placed baseline blood work should be drawn at the
same time. Minimally packed cell volume, total solids, blood glucose and electrolytes should
be run. It is important to obtain a body temperature immediately when the pet arrives. This
is particularly true in patients in SE because they can be suffering from secondary
hyperthermia. If the pet is experiencing hyperthermia (temperatures above 106F) then the
pet should be actively cooled until it is 103F. The most acceptable way to cool a patient is
to pour cool, not cold, water over them.
The most common physical exam findings of patients presenting with a seizure or that are in
SE are: hyperthermia, tachycardia, tachypnea, hyperaemic mucous membranes, and
capillary refill time of less than one second. Once the patient is not actively seizuring a blood
pressure should be obtained and an ECG should be performed. Hypotension can be seen in
patients with increased intracranial pressure from cerebral oedema which can form
secondary to SE. Normalization of blood pressure defined by a MAP of 80-120 mmHg or
systolic between 110-160 mmHg, is goal.
Oxygen supplementation improves tissue perfusion and decreases the risk of ischemia.
Seizuring patients often experience moments of apnoea and often are poorly circulating. In
the case of SE patient, severe tissue hypoxia can occur. Therefore oxygen should be
provided because most patients experience some level of ischemia and hypoxia. The most
effective ways to administer oxygen are through the use of a face mask (removing the
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diaphragm to allow for panting) or an oxygen hood. Flow-by oxygen is generally ineffective
and oxygen cages should be avoided because treatment cannot occur and the pet needs
adequate circulating air to cool.
Intravenous fluids may be administered to help with perfusion and cardiac output issues.
Dextrose may be given if the patient is suffering from hypoglycaemia. It is important that
intravenous dextrose is diluted with an isotonic crystalloid and given at a steady (not fast)
rate. Once the blood glucose levels are normal, they will be rechecked and monitored
closely. Mannitol may be administered if cerebral oedema is suspected. Cerebral oedema
can occur from brain swelling due to SE, trauma, metabolic or electrolyte disturbances.
Mannitol should be given through a filter to filter any crystallization that may occur and needs
to be given slowly intravenously.
Status epilepticus patients will require the most intensive nursing care. If the patient is
recumbent, the technician will need to lubricate the eyes, moisten the mucous membranes,
turn the pet, keep the pet dry and free of bed sores and perform passive range of motion.
Passive range of motion must be performed every four to six hours and patients should be
repositioned at that time. Adequate soft bedding should be used and bedding should be
cleaned and replaced once a day.
Ideally, unless DIC is present, a central line should be placed in SE patients to monitor
central venous pressures and for the administration of parental nutrition if needed later. A
central line should be considered in patients suffering from hypoglycaemia as these patients
require frequent blood draws. Technicians should monitor for signs of DIC in SE patients
such as increase bleeding times, petechiae or ecchymoses. A urinary catheter should be
placed in down pets to keep them clean and dry. If a SE patient was placed under
anaesthesia the endotracheal tube should be replaced every 24 hours. In addition the cuff
on the tubes should be deflated, repositioned and reinflated every four to six hours.
Throughout the pets hospitalization they should be constantly monitored and treatment
should be tailored to the pet accordingly.
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MEDICAL MANAGEMENT OF THE WHELPING BITCH

PetMedics Veterinary Hospital, Manchester, UK
Dystocia, the difficulty in passing the foetus through the pelvic canal, is a common small
animal emergency. Positive clinical outcomes can be expected only when the clinician has a
thorough knowledge and understanding of normal canine parturition, the pathogenesis and
underlying aetiology of dystocia, the criteria for diagnosing dystocia, and the appropriate
medical and surgical interventions.
Normal Parturition
The dams whelping date may be determined using breeding dates, time of lutenizing
hormone (LH) peak, ovulation date, or the first day of oestrus. Gestation duration in the bitch
is approximately 57-72 days (average 65 days) when established using breeding dates. This
period varies because the postcoital viability of canine sperm is at least 6 days and because
the ovulation date may not have been identified using progesterone or LH assays. Parturition
occurs 63 days after ovulation and 64-66 days after the LH peak. The gestation length after
the first day of dioestrus is 56-59 days, but this date is rarely known for dystocia patients.
Once the appropriate gestation time has passed, the complex cascade of events leading to
delivery begins.
Understanding the neuroendocrine cascade of parturition assists the clinician in managing

the dam and understanding the aetiology of dystocia. The accepted neuroendocrine model
of canine parturition is initiated by the foetus. The foetal hypothalamic-pituitary-adrenal axis
is activated by foetal stress and increased glucocorticoid concentration stimulates maternal
oestrogen production, contributes to the synthesis and release of prostaglandins, and
increases oxytocin receptors on the myometrium. Maternal oxytocin is initially released from
the hypothalamus in response to afferent stimulation of pressure receptors within the cervix
and vagina. Relaxin hormone, produced by the ovary and placenta, assists foetal passage
by allowing the interpubic ligament to elongate and the pubic bones to separate. The
prolactin (lactation hormone) level, which increases gradually during gestation, starting 21-
28 days after ovulation, rises suddenly with the decline in the progesterone level.
A decline in rectal temperature below 37.6C (99.7F) has been cited as the most consistent
change indicating that parturition will take place within the next 12-24 hours. This drop
coincides with the decrease in the plasma progesterone level below 2ng/ml. A recent study
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found no association between body temperature decline and impending parturition but did
find a significant increase in body temperature 12 hours after the onset of parturition was
identified. Limited conclusions may be drawn from this investigation owing to its small
number of subjects. It is possible that direct measurement of progesterone decline and
prostaglandin elevation is a more reliable indicator of parturition and that any elevation in the
bitchs temperature at the end of pregnancy without expulsion of foetuses could indicate
dystocia.
Each of the three stages of labour has predictable group of clinical signs and duration. Stage
1 labour begins with indiscernible uterine contractions and progressive cervical dilation. This
stage lasts 6-12 hours, but primiparous bitches may persist for up to 24 hours. Behavioural
signs associated with stage 1 labour begins with indiscernible uterine contractions and
progressive cervical dilation. This stage lasts 6-12 hours, but primiparous bitches may
persist for up to 24 hours. Behavioural signs associated with stage 1 labour include nesting,
panting and restlessness.
The second stage of labour is the active expulsion of the foetus from the birth canal; this
visible abdominal straining matches the strong uterine contractions. Clear vaginal discharge,
the allantoic fluid, is seen as stage 2 labour begins and precedes each puppy. The first
foetus is normally delivered within 30 minutes of the start of stage 2 labour but may not be
delivered for 2-4 hours due to weak or uncoordinated uterine contractions. Stage 2 labour
should be complete within 12-24 hours, with a foetus produced approximately every 30
minutes to 4 hours. One study described the delivery of a healthy puppy after a 34 hour
interval between puppies and 37 hour duration of stage 2 labour.
Stage 3 labour is the expulsion of the placenta, which takes place 5-15 minutes after the
delivery of the foetus. Multiple placentas may be passed after several puppies are delivered
close together. It is not uncommon for the bitch to bite the amniotic and allantoic
membranes, sever the umbilical cord, and ingest the placenta after parturition.
Post-partum findings in the bitch may include mild fever, transient vomiting and diarrhea, and
lochial discharge. Lochial discharge, produced by haemoglobin breakdown, is normal after
parturition and is associated with uterine involution. The discharge is green to red-brown,
odourless and persists for up to 6 weeks.
Criteria for diagnosis of dystocia

Veterinary and nursing staff are routinely confronted with telephone calls and enquiries
regarding canine parturition. The criteria listed are useful for advising owners when
examination of the whelping bitch is appropriate. The criteria are intentionally stringent to
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facilitate earlier examination of the dam by veterinary personnel and reduce neonatal
complications with prolonged dystocia.
Prolonged gestation: due date reached without signs of labour or temperature drop;
65 + 1 days after the LH peak or 63 + days after ovulation;
Temperature decreases below 37.6C (99.7F) for 12 to 24 hour without signs of
labour;
Temperature decreases and then increases to >37.6C (99.7F) or >39.2C
(102.5F) for 12 to 24 hours;
Clear vaginal discharge for more than 2 to 3 hours;
Green discharge without the production of a pup within 30 minutes;
Lack of strong progression to stage 2 labour after 6 to 8 hours;
Strong, active abdominal contractions for 30 mins without the expulsion of a puppy;
Stage 2 labour lasting >24 hours;
Membranes or part of foetus protruding from the vagina;
Signs of systemic illness in the dam.
Pathogenesis of Canine Dystocia
Dystocia has conventionally been described as being maternal or foetal in origin. Maternal
dystocia is encountered more frequently (60-70% of dystocia cases reviewed). The most
common cause of maternal dystocia is uterine inertia, representing 40-72% of all dystocias
attributed to the dam. Uterine inertia is the failure to expel the foetus from the uterus when
no obstruction exists; it can be classified as primary or secondary. Complete primary uterine
inertia occurs when stage 2 labour fails to start and no puppies are delivered. Partial primary
uterine inertia is defined as initiation of normal labour but failure to deliver all puppies.
Primary uterine inertia can develop because of litter size; either the litter is too small, or the
myometrium is over-stretched secondary to a large litter. More than 50% of studies bitches
with complete primary inertia had three or fewer puppies in the litter. Primary uterine inertia
is also attributed to inherited predispositions, nutritional or neuroendocrine imbalance, age-
related changes, nervous inhibition, and systemic disease. Secondary uterine inertia is the
exhaustion of uterine musculature after contracting against an obstruction and has been
reported as accounting for 3.2- 12.6% of dystocias. Obstructions can include maternal
changes or characteristics such as a narrow pelvis, congenital malformation, pelvic trauma,
neoplasia or abscess, vaginal stricture, uterine torsion, uterine or vaginal prolapse, and
vaginal hyperplasia.
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Several dog breeds are associated with increased risk for dystocia. Scottish terriers and
Boston terriers have inherited characteristics that predispose them to obstructive dystocia.
Secondary uterine inertia occurs in Scottish terrier bitches with dorsoventral pelvic flattening
and small vertical pelvic canal diameter. Boston terriers have similar pelvic measurements,
but foetal oversize is a contributing factor to obstruction. Accurate identification of breed
predispositions to dystocia has been limited by local breed popularity and failure of
investigators to obtain a representative sample of the dystocia patient population.
Management of Abnormal Parturition
Initial evaluation of the dam requires an accurate history and thorough physical examination.
Pertinent information includes breeding dates, ovulation date, vaginal cytology, and
preovulatory LH peak date, when available, to establish a whelping date. An accurate history
of the dams behaviour for the previous 24-48 hours will help define the stage of labour and
assist the clinician in deciding which interventions are indicated. Owners should also be
questioned about the dams previous reproductive history, age, and breed before any
treatments or manipulations performed before presentation. Standard historical information,
such as current medications, past or chronic medical conditions or surgeries, adverse
reactions to medications, and a systems review to check for signs of systemic disease, is
important for case management.
Physical examination of the bitch should be efficient yet thorough, and should cover all major
body systems, with particular focus on the cardiovascular system and urogenital tract.
Abdominal palpation is performed to check for the presence and position of pups, uterine
contractions, and signs of abdominal pain, which may indicate uterine pathology. Palpation
is not an accurate method of determining litter size. Mammary glands should be examined
for the presence of milk and degree of development. Long hair around the vulva should be
clipped and the skin cleaned in preparation for a vaginal examination. Sterile gloves are
used during the vaginal examination, during which the clinician may detect a foetus, vaginal
septa, masses, strictures, or pelvic abnormalities. Foetal presentation may also be
determined. Without vaginoscopy, cervical examination is impossible in most bitches, but
vaginal vault diameter and muscular tone are described as possible indicators of cervical
dilation.
Abdominal imaging is important in the continued workup and management of the dam.
Radiographs can detect mineralized foetal skeletons 43 to 54 days after breeding, or 45
days after the LH peak. Foetal mineralization can be used to estimate gestation; the foetal
pelvis, ribs, radius, and ulna appear on radiographs 11 days before parturition, and teeth
appear 4 days before parturition. Abdominal radiographs are valuable in identifying
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malpositioned puppies, and in providing an accurate foetal count and are important to rule
out the presence of an obstructive mass lesion (e.g. pelvic fracture, neoplasia). Radiography
is a poor modality to assess foetal viability because the typical changes denoting foetal
death (infrafoetal gas, collapse of the spinal column, and overlap of the skull bones) do not
appear until approximately 6-24 hours after foetal death.
Abdominal ultrasonography has not proven useful in estimating gestational age at or around
the time of parturition, however, it is an excellent method of assessing foetal viability
because it allows visualization of foetal movements and heart rates. An experienced
ultrasonographer can also estimate foetal size by measuring foetal biparietal and thoracic
diameters; these measurements can then be compared to the dams pelvic diameter on
radiographs to determine oversize. Ultrasonographic signs of foetal death include lack of
heartbeats or movement, increased echogenicity and decreased volume of foetal fluids, and
increased gas in the foetal stomach. Foetal bradycardia, or heart rate below 150-200 bpm,
can result from hypoxia and is an early indicator of foetal distress. Foetal bowel movements
detected by ultrasound can be another indicator of severe foetal distress (defined as foetal
heart rate <180bpm). An experimental model of surgically induced foetal hypoxia in 12
bitches demonstrated that late deceleration of foetal heart rates was an early indicator of
foetal hypoxia and decreased foetal blood ph.
Survey blood work with priority given to packed cell volume and total protein, blood urea
nitrogen, glucose and calcium level is beneficial to complete patient assessment.
Medical management of Dystocia
Medical management of the dam may be initiated before some of the above diagnostics are
completed. Management includes digital or foetal manipulation and the administration of
medications to augment uterine contractions.
When a foetus is detected within the vaginal canal, extraction may be attempted. Foetal
extraction should be accomplished using generous amounts of sterile, water-soluble
lubricant and digital manipulation. Based on vaginal anatomy, the foetus should be gently
pulled caudoventrally, with care not to exert excessive traction on the foetal limbs. The
puppys shoulders or pelvis may be rotated into the dorsoventral plane of the dams pelvis to
provide the greatest width for passage of the body. Use of instrumentation to manipulate and
extract the foetus is possible but is not recommended due to the risk of foetal and maternal
injury.
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When maternal and foetal obstructions have been ruled out, the stimulation of uterine
contractions may be initiated. This may be accomplished by having the owners walk the dam
or by the vet feathering the dams dorsal vaginal wall. Oxytocin administration is an
effective technique to augment labour. While there has been little investigation into the
optimum dose or route, the recommended dosage of oxytocin is 0.1 IU/kg IM(up to a
maximum 5IU with a dose range between 5 and 20 IU q. 30 minutes to effect. Concurrent
administration of IV calcium gluconate (0.25-1.5mg/kg of 10% solution) slow IV, may
augment oxytocins effect on myocardial contraction. Studies have found that oxytocin-
induced myometrial contractions are dependent on the influx of extracellular calcium. Lower
dosages of oxytocin (0.1 IU/kg may stimulate uterine contractions whilst avoiding the
possible negative effects of excessive oxytocin, which include uteroplacental blood flow
interruptions and ineffective, tetanic uterine contractions.
Administration of oxytocin as a dilute IV solution (10 IU of oxytocin per 1 litre of isotonic

crystalloid, 10 mU/ml) to effect at a slow drip rate is also reported.
The limitations of this technique are based on the inability to accurately monitor the dams
uterine contractions. Human obstetricians routinely use oxytocin as a continuous rate
infusion with several protocols well described. Regardless of the method of oxytocin
administration, the clinician should provide the dam with intravenous fluids to correct
hydration, electrolyte, and blood glucose abnormalities. There is evidence in humans that
mothers have higher rates of intravenous fluids have shorted duration of labour and
decreased need for oxytocin administration.
A particularly anxious dam may present a particular challenge. If stable, these patients may
be placed in a quiet, dimly lit, comfortable room with their owners while the labour is
managed (veterinary staff should check on the dam and owners every 15 20 minutes).
Intrapartum monitoring of the foetus and uterine activity allows the clinician to better
medically manage labour and identify the need for early surgical intervention. Human
medicine sets the standard for monitoring of uterine activity and foetal physiologic variables.
Current monitoring tools available to veterinary staff include B-mode ultrasonography,
Doppler (foetal heart rate) ultrasonography, and tocodynamometry, which can detect
changes in intrauterine pressure.
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Suggested Protocol for Medical Management of Canine Dystocia
1. Perform a physical examination and a sterile vaginal examination; attempt digital

manipulation of foetus if needed;
2. Place IV catheter; collect blood sample; measure PCV, TP, BUN, glucose, calcium
and electrolytes; start IV fluids; correct deficits as needed;
3. Obtain abdominal radiographs; conduct abdominal ultrasound or Doppler
ultrasonography for foetal heart rates;
4. Administer low-dose oxytocin (0.1 IU) IM. Continue monitoring foetal heart rates
every hour;
5. If 30-45 mins pass without delivery of a puppy, administer 0.25mg/kg calcium
gluconate (10%) IV slowly over 20 minutes whilst monitoring the ECG;
6. Follow calcium administration with a repeat dose of low-dose oxytocin or increase
oxytocin dose to 0.1 IU/kg IM;
7. If another 30-45 mins pass without the delivery of a puppy, administer a third dose of
oxytocin;
8. If no puppies are delivered within 30-45 minutes after the third dose of oxytocin,
proceed to caesarean section.
Criteria for Caesarean Section
Complete primary uterine inertia

Partial primary uterine inertia unresponsive to medical management
Secondary uterine inertia
Obstructive abnormality of the pelvic canal
Foetal malposition that cannot be corrected
Foetal death
Relative or absolute foetal oversize
Foetal distress: consistent foetal heart rates <150bpm or foetal bowel movements
can be seen on ultrasound.
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Notes page
Page 229 of 334

AN RTA ENTERS YOUR CLINIC: STEP BY STEP OF WHAT TO DO

Amy Breton, CVT, VTS (ECC)
Veterinary Emergency and Specialty Center of New England, Waltham, MA
abreton@vescone.com
Introduction
At some point every veterinary clinic will have the surprise emergency road-traffic-accident
(RTA) arrive. Its important to be able to deal with the client in an effective manner so that
treatment to the pet can occurs in a timely manner. Being able to take a step-by-step
approach to the trauma patient will allow you to provide fast and effective care.
Triage
All RTA pets are emergencies. This includes if the pet seems completely normal after
being hit. Adrenaline is usually released in large quantities when the pet experiences blunt
trauma. Adrenaline acts as a pain reliever and helps to elevate the heart rate. Because of
this, the pet may get hit and then immediately act as if nothing happened. Unfortunately this
can mask underlying signs such as pulmonary contusions or internal bleeding.
One of the fastest and most effective ways to triage is by using the RAP system:
Respiration, Alertness, Perfusion. Immediately upon entering the hospital a technician
should listen to the heart and lungs and check the mucous membranes and pulses. Most
times the pet is experiencing some type of shock and will need emergency treatment. Being
able to communicate to the owner what is going to happen is important.
Dealing with the client
Client reaction can be completely unexpected. Its important to remember to not become
emotionally involved yourself. Maintain a calm and professional attitude at all times. Clients
may express sadness, anger, indifference, confusion or be in a state of shock themselves.
No behaviour is inappropriate except one that involves a physical threat or a danger to you
or the clinic. Remember that if the client is yelling, they are likely upset about the situation,
not at you directly. Reacting to a client will only fuel their emotions. Clients act out because
they are unsure of the future of their pet and they are fearful.
Owners of these pets should be informed in a clear concise manner of WHY, WHAT
and HOW MUCH.
o WHY their pet needs emergency treatment
o WHAT is going to be done to their pet
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o HOW MUCH it is going to cost (rough estimate)

Owners must then be given a brief timeline of what to expect
Shock
In order to understand how to treat the RTA pet you must understand what shock is. Shock
is defined as the decline in vital organ function due to maldistribution of blood causing
oxygen and nutrients to be inadequately delivered. It is the bodys life-saving mechanism
because the body pulls blood from non-essential areas (legs, GI tract) and pushes it to
essential areas (heart, brain, lungs).
There are three main phases of shock: Early, Decompensatory, Terminal. In the early phase
the animal may actually appear normal. The circulatory system becomes compromised
causing baroreceptors in aortic arch and carotid arteries to detect a decrease in cardiac
output. The baroreceptors stimulate the sympathetic nervous system, which causes
catecholamines (epinephrine) to be released. The release of the catecholamines causes:
Heart Rate Increases (the key indicator that the pet is in the early stage of shock)
Cardiac Contractility Increases
Vasoconstriction Occurs
Blood Flow Decreases To GI Track, Muscle and Skin
Splenic Contraction (falsely elevated increase blood volume by 20% more)
Decrease Oxygen Delivery To The Tissues
Ultimately if treatment is not initiated in the early stage, the body may be able to either pull
itself out of shock or the shock may worsen. It is possible that the pet gets hit by a car and
immediately goes into the decompensatory or terminal stage of shock. This
decompensatory stage is marked by:
Multiple Organ Failure

Low Temperature
o Due to the continued poor perfusion and hypotension
Poor Pulses
Pale/Muddy Mucous Membranes
Prolonged Capillary Refill Time
Tachycardia
Depressed Mentation
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Unfortunately, most pets are not responsive to treatment if they are in the terminal phase of
shock. This phase is characterized by:
Bradycardia
o The heart is no longer able to keep up with the demand
Hypotension
Heart Failure
Severe Mental Depression
Abnormal Respiratory Pattern
Cardiopulmonary Arrest
It is important to note that in dogs the shock organ is the gastrointestinal track. This means
that post-shock dogs generally experience GI symptoms including ileus, diarrhoea or
melena. In cats the shock organ is the lung. Post-shock cats often experience respiratory
problems.
STEP-BY-STEP: A 10 Step Approach
Immediately upon a RTA pet arriving a veterinarian should be notified of arrival. This
does not mean that initial treatment should be put on hold while a veterinarian is
notified since it may take a couple of minutes for notification. Instead benign, non-
invasive treatments should begin.
1) Triage using R.A.P. Minimally obtain heart rate, pulse, mucous membrane colour
and note respiratory effort.
2) Notify the owner of WHY, WHAT, HOW MUCH
o Your dog is in shock. He needs treatment in order to save his life. We are
going to need to place an IV catheter, start fluids and perhaps run some blood
work. This will cost between $300-$600. Is this okay? The doctor will be out
to speak to you once we have Fido a little more stable
o Get a signed form that allows you to treat
3) Obtain blood pressure, pulse ox and attach ECG
4) Administer oxygen if in shock, respiratory distress or if you are unsure of pets

condition
5) Obtain official set of vitals (T, P, R) if there is time and if it is appropriate
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(If pet is in the decompensatory or terminal stage of shock procedure to step 6)
Initiate CPR immediately at any point if pet arrests
o Temperature
o Heart Rate With Pulses
o Respiratory Rate With Effort
o Mucous Membranes
o Mentation
o Capillary Refill Time
6) Place IV catheter(s), attach 3cc syringe and draw back to obtain ideally 3mls of blood
o Run PCV, TS, BG

o Run any other blood work prescribed by veterinarian
7) Start fluid therapy if appropriate and consider pain medication
8) Obtain approval for other treatments (radiographs, ultrasound, medications)
o Update owner on pets status

9) Veterinarian should have a basic diagnosis and prognosis and should speak to owner
at this point
10) Continue to work on stabilizing pet
o Prepare pet for hospitalization and further treatments
Treatment of RTA pet

It is important to obtain permission from the owner before treatment can begin. Having them
sign a consent form to treat and explaining exactly the procedures that are going to take
place will help to avoid confusion as well as help to protect the practice and staff involved.
The goal for any emergency is to return the circulatory system back to normal by working to
perfuse the organs and provide adequate oxygen delivery to them.
Providing oxygen is important for any patient in any type of shock or respiratory distress. If
you are unsure whether the pet needs oxygen, it is better to give it then to not. The goal is to
administer oxygen the most effective and least stressful way to the patient. Flow-by Oxygen
is effective, but usually only if owners are there to administer it because animals in general
do not like air blowing on their noses. The efficacy of flow-by is still debated because of the
extreme variables. The flow rate, the distance of the tubing from the patients nose and the
movement of the patient all contribute to how much oxygen the patient actually intakes.
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Administering oxygen via a face mask is more effective, but generally not tolerated if the
patient is alert at all. Studies have shown it to be very effective at administering 60% FiO2
very quickly. The disadvantage is, if the diaphragm is left on, the patient cannot
appropriately exhale CO2. Oxygen hoods have a particular advantage because they tend to
be more tolerated in alert animals and allow for patient movement. Roughly 75% of an
Elizabethan collar should be covered. The remaining 25% allows for ventilation and the
escape of CO2. The oxygen line is placed through the ecollar so that it rests in front of the
patient nose. FiO2 levels can get up to 80% very quickly. Lastly the oxygen cage is good at
providing oxygen support, but it is impossible to work with the patient while they are in the
cage.
Depending on the nature of the emergency it may not be able to get a full set of vitals right
away. The importance of obtaining a temperature or capillary refill time may not be as
important as initiating CPR. When appropriate all vitals should be obtained at some point.
In addition to performing a full physical exam all RTA patients should receive a blood
pressure, an ECG and a pulse ox.
Gaining venous access is important in all RTA pets. You should place 1-2 peripheral
catheters that are short and large diameter. As a general rule, healthy patients that are 2-5
pounds should receive a 22g, 1 over-the-needle catheter. Healthy patients that weight 5-20
pounds should receive a 20g, 1-1.25 over-the-needle catheter. Patients that weight 20-75
pounds should receive an 18g, 1.25 over-the-needle catheter. Anything greater than 75
pounds should have a 16g over-the-needle catheter placed. Exotics and neonates should
receive 24g over-the-needle catheters. Studies have shown that short, large diameter
catheters allow for higher fluid flows and increasing the diameter of the catheter by one size
can cut the time it takes to bolus a litre of fluids by half. This may mean the difference
between life and death to a patient. The above recommended IV catheter sizes are merely a
guideline. When a pet is hemodynamically unstable you may have to choose a smaller
gauge catheter because of smaller-then-normal vein size or poor integrity of the vessels.
The most common peripheral catheter locations are the cephalic, saphaneous and femoral.
Peripheral catheters can also be placed in the dorsal pedal vein, aural vein, umbilical vein
(neonates) and jugular vein (neonates/exotic). If venous access is too difficult to obtain
attempting a cut-down or placing an intra-osseous catheter should be considered.
When you place the peripheral catheter, you should attempt to draw blood from it first before
you flush or start any fluids. This is the fastest way to obtain blood without performing
another venipuncture stick. This method may not always be successful depending on the
patients perfusion. All emergency patients should have a PCV, TS BG and lactate run.
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Lactate is a measurement of anaerobic metabolism and becomes built up in the blood

stream during periods of poor perfusion. In some cases lactate may be the only indicator
that a perfusion problem of the microvascular system exists. Values under 2 mmol/L are
considered normal. If the pet initially has a high lactate, giving fluids should help correct the
hyperlactataemia. The veterinarian may prescribe other blood work for the pet (CBC,
Chemistry, blood gas). If blood cannot be obtained through the IV catheter, IV fluids should
be initiated. Once the patient is stable it may be easier to obtain blood from another
peripheral vein.
Pain can increase and even cause shock, so it is important treat the pain. Opioids are great
because they have limited effects on hemodynamics. Unfortunately there continue to be
many false thoughts about the benefits of pain (helps to inhibit patient movement, cant fully
assess the patient, etc.). It is has been proven that recovery time is greatly reduced when
pets experience less pain.
There are very few other treatments that need to be performed that are emergent.
Permission from the owner should be obtained for any other diagnostics. While obtaining
radiographs or an ultrasound may yield a better diagnostic picture, it is always important to
stabilize the patient first. A team member should alert the owner as to the pets status, what
is being done to help the pet and how long it will be until the veterinarian is able to speak
with them.
IV Fluids
There are two types of fluids that can be given: Crystalloids (the most common) and
Colloids. Interestingly enough there is no clear consensus that proves one type of fluid
reduces mortality. There are three types of crystalloids: Isotonic (LRS, Norm-R, P-Lyte,
Hypertonic (7-7.5% NaCl), Hypotonic (0.45% NaCl). Isotonic crystalloids are still the most
common used. They are similar to the bodys extracellular fluid by containing similar
electrolyte concentrations (sodium, chloride, potassium, magnesium, calcium and
bicarbonate-like anions). Isotonic crystalloids will distribute rapidly. Within 30 minutes 75-
98% of the fluids shift into the extravascular space. You need large volumes in order to
make a difference and the infusion must continuous.
Hypertonic fluids contain a higher osmotic pressure than isotonic. Useful when large
volumes cannot be given fast enough. Hypertonic saline causes fluid to shift from the
intracellular space to the extracellular space, which causes improved venous return and
cardiac output. One dose equals four times the volume of isotonic saline. The use of
hypertonic saline is also known as limited-volume resuscitation and is currently
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recommended in head trauma cases. It helps to reduce cerebral swelling without worsening
oedema.
Hypotonic fluids contain a lower osmotic pressure then isotonic (5% Dextrose in Water,
0.45% NaCl). Hypotonic fluids should NOT be used to treat shock because they contain too
much water and will redistribute quickly.
Colloids (hetastarch, albumin, plasma, blood) are high molecular weight fluids that do not
pass readily through the capillary membranes. Colloids help to increase oncotic pressure
because they keep fluids in the intravascular space. Roughly 50-80% of the infused volume
stays in the intravascular space. Most veterinarians reach for colloids when crystalloids fail.
What to do if the patient arrests
1) Start chest compressions FIRST

Studies have proven that starting chest compression before gaining
access to an airway offers the best chance of survival
Perform 100-120 bpm while pet is lying on their side
2) Intubate SECOND
One breath every 10 seconds
No studies have proven that administering 100% oxygen offers a better
chance of survival.
3) Obtain venous access (ideally at the same time as someone is trying to gain an
airway)
4) Consider drugs if needed
CPR drugs can be given via trachea, but have slower absorption times
and usually require 5 times larger dose.
ATROPINE: Bradycardia
EPINEPHRINE: Asystole
IV FLUIDS: Just enough to keep the catheter patient. Large volumes
should only be given for hypovolemic shock. Recent studies have shown
that large boluses for all other causes of arrest cause a decrease in
coronary perfusion.
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After stabilisation
The emergency patient turns into a hospitalized patient after the patient is stabilized. This is
defined by normal blood pressure, appropriate mentation, normal heart and respiratory rate,
pink mucous membrane colour, normal capillary refill time and normal temperature. If
available, lactate levels should be less than 2.5 mmol/L.
After a pet is RTA it may experience several problems due to the poor perfusion during
shock or any major inflammation caused by injury. Ischemia/Reperfusion injury (I/R) injury
can occur because of the decrease in blood supply to areas of the body (skin, muscles,
organs) during times of shock. During resuscitation, reperfusion occurs which sets the I/R
injury events into motion. I/R injury can lead to multiple organ dysfunction syndrome
(MODS) where two or more organs are involved or systemic inflammatory response
syndrome (SIRS). Ultimately disseminated intravascular coagulopathy (DIC) can be
experienced whenever there is a major change in the intravascular status, which is certainly
the case at times of shock. It is important that technicians watch for signs including:
petechiae, increased bleeding during venipuncture, fever, PU/PD or jaundice. These can all
be signs of the multitude of syndromes a post RTA can experience.
Conclusion
Dealing with the surprise emergency starts with the owner. Administering oxygen for any
shock or respiratory distress is important in helping to maintain adequate oxygenation to the
organs. Stabilization occurs through improving tissue perfusion by IV fluids. Once the
patient is more stable, further diagnostics can occur.
It is important to be organized and take a step-by-step approach with any RTA. Failure to do
so can cause added stress to the situation and may delay patient care. Having all members
of the team understand what steps need to be taken, can mean the difference between life
and death for the patient.
References available on request
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NUTRITIONAL OPTIONS FOR THE CRITICAL PATIENT

Andrew J Brown, MA, VetMB, DACVECC, MRCVS.
Vets Now, UK
andrew.brown@vets-now.com
Ensuring adequate nutritional intake is essential in critically ill patients. Malnutrition is

common in these patients, and has been associated with increased morbidity and mortality.
Multiple studies in people and animals have demonstrated that nutritional goals for both
humans and animals are not being met whilst in the ICU. The two primary reasons for this
malnutrition are non-delivery of sufficient calories and patient intolerance of the food. The
former may be a result of under-prescription of nutrition (or no nutrition at all) or a result of
frequent interruptions of feeding for nursing care, diagnostic procedures or client visits.
Recognition of a need for supplemental nutrition is the first and most key step to ensure that
patients are not malnourished. In the past, arbitrary recommendations such as supplement
nutrition once they have been anorexic for five days, have been made. Given our current
understanding of critically ill patients needs for adequate nutrition, this is clearly no longer
acceptable. However, we must consider that any route of nutritional delivery carries some
risk of complications. For example, studies in some human populations have documented a
worse outcome when receiving parenteral nutrition. Each patient has to therefore be
considered on an individual basis.
Assessing the Need for Nutrition
When deciding if an animal is going to require parenteral or enteral nutrition, it is important to

categorize hospitalised patients into one of the following:
1. Already malnourished
2. High risk of developing malnutrition
3. Low risk of developing malnutrition
Animals in the first group will require prompt nutrition whereas animals in the second group
may require nutrition within 2 or 3 days and should be monitored very closely.
Factors that should be considered when considering starting supplemental nutrition include:
Current nutritional state (see above)

Length of anorexia
Disease process (e.g. sepsis, trauma, pancreatitis)
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Ongoing protein losses (e.g. peritonitis, severe wounds)

Potential for imminent sedation/anaesthesia/surgery that will prevent eating
Additional metabolic demands (e.g. recent lactation)
Deciding on the Optimum Route of Nutritional Support
The enteral route of nutritional provision should always be considered in a patient. It is

typically the least expensive, the most convenient and has fewer complications than the
parenteral route. In addition, it is the most physiologically appropriate route. In patients that
are not able to tolerate any enteral nutrition, the parenteral route should be considered.
However, even in animals that require parenteral nutrition, use of the gut for delivery of a
small volume of enteral nutrition (trickle feeding) should be considered to promote health of
the gastrointestinal tract.
Options for delivery to the enteral tract include oesophageal, gastric and post-pyloric
(typically jejunal) feeding. Tubes may be placed with minimal invasiveness (e.g. naso-
oesophageal feeding tubes), require general anaesthesia (e.g. fluoroscopic guided
nasojejunal tubes) or require surgical placement. Consideration should be paid to whether
the patient is still vomiting (post-pyloric would be best), tolerance of anaesthesia/surgery and
how long the tube is likely to be used for. For example, a naso-oesophageal feeding tube is
ideal for the short-term, but investment in an oesophagostomy tube may be justified for
longer-term use. If a patient is undergoing general anaesthesia, then placement of a feeding
tube should be considered at that time.
Calculating Nutritional Needs
Energy calculations for patients at rest (RER or resting energy requirement) are:
For dogs RER = 30 x (Wt [kg]) +70
For cats RER = 40 x (Wt [kg])
RER is the resting energy requirement and should be calculated based upon the actual body
weight, not lean body weight. With patients affected by disease or suffering from injury the
energy requirement tends to be a little higher than this. Historically, the RER value was
multiplied by a factor (e.g. x2 for full thickness skin burns) to calculate the energy
requirement for a specific patient. Recent evidence suggests that this has over-estimated the
energy requirements of patients. Currently it is only possible to subjectively assess energy
requirements on a patient by patient basis using the RER as the minimum requirements.
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The aim is to provide 33-50% of the RER of the patient on day one and 66-100% on day
two. Full RER should be given on day 3.
Placement of a Naso-Oesophageal Tube
Equipment list:
Sedation (if required)

Feeding tube. If a specialist paediatric feeding tube is not available, then other soft
catheters can be used (3.5-8 Fr).
Lubricant gel.
Local anaesthetic drops, or 2% lidocaine
Permanent marker pen.
Suture material
Zinc oxide tape or similar.
Elizabethan collar
Procedure:
1. Depending on the dogs temperament, light sedation may be required

2. Administer topical anesthesia at least 3 minutes before starting this procedure. Draw
up 0.5-1ml of lidocaine (with or without adrenalin) into a 2 ml syringe. Remove the
needle from the syringe. Place the tip of the syringe into the patients nostril and
quickly inject the lidocaine into the nostril, so as to aerosolize the anaesthetic. Local
anesthetic drops can also be used
3. Pre-measure the feeding tube from the alar fold of the nose to the 8th intercostal
space, and mark with a permanent marker pen
4. An assistant should hold the dog, and keep its head steady and in a neutral position
5. With one hand steadying the nose of the dog, insert the lubricated feeding tube into
the nostril, aiming ventrally and medially as you advance the tube
6. Continue to advance the feeding tube until you reach the mark on the feeding tube
7. The feeding tube should be secured at the nostril with a Chinese finger trap
8. Depending on the shape of the dogs head, the feeding tube should run either
between the eyes or on the side of the face and be secured in place using pre-placed
tape wings that are sutured to the skin
9. An Elizabethan collar should be placed to avoid self-removal
10. A lateral thoracic radiograph should be performed to confirm correct placement
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Feeding:
The feeding tube can be used immediately following placement, and can be removed
at any time
Calculate the resting energy requirement of the dog (RER)
Administer 30-50% of the RER on the first day, and increase to 100% RER over 1-2
days
Use a liquid or semi-liquid diet warmed to room temperature
Flush the feeding tube with 5-10 mL of water before and after feeding
If the patient coughs or appears distressed after administering the water, do not
continue with the feed
Administer the diet intermittently (divided into 4-6 feeds per day) or deliver
continuously at a low rate using a syringe driver
If the dog vomits or regurgitates, hold off feeding for 6 hours and resume again at a
lower volume.
Complications:
Incorrect placement will lead to instillation of liquid food into the lungs with
development of pneumonia or pneumonitis.
Vomiting or regurgitation
Diarrhoea from the liquid diet
Tube dislodgement
Rhinitis (typically mild)
Notes:
Naso-oesophageal feeding tubes should not be placed if the patients have the following:
Coagulopathy
Nasal disease
Raised intracranial pressure (or suspicion of)
Megaoesophagous
Confirmation of correct tube placement by obtaining negative pressure when a syringe is

placed on the tube and suction applied or flushing a small volume of water into the tube to
ensure that coughing does not occur is not sensitive. Negative pressure does not rule out
bronchial placement and not all animals will cough when water is flushing into the airways.
A confirmatory radiograph should always be performed.
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Placement of an Oesophagostomy Tube
Oesophagostomy tubes can be placed to deliver long-term nutrition to anorexic dogs.

Although they require the dog to be briefly anaesthetized, the procedure itself is minimally
invasive.
Equipment list:
Drugs and equipment for general anaesthesia

Feeding tube. If a specialist polyurethane feeding tube is not available, then other
soft catheters or tubes can be used (14-24 Fr)
Permanent marker pen
Curved forceps (e.g. Carmalt)
No. 11 or 15 scalpel
Suture material
Zinc oxide tape or similar
Bandaging material
Elizabethan collar
Procedure:
1. Anaesthetise, intubate and place the dog in right lateral recumbency

2. Clip and aseptically prepare the lateral neck from the ramus of the mandible to the
thoracic inlet
3. A mouth gag can be inserted to aid placement
4. Insert the curved forceps into the mouth and advance down the oesophagous until
the mid-cervical region
5. Turn the tips of the forceps laterally so that the tips can be seen pressing up on the
skin
6. Ensure that the tips are away from any blood vessels (e.g. external jugular vein) and
make an incision through the skin onto the forceps
7. Whilst still pressing the tips of the forceps outwards, incise through the oesophagous
so that the tips of the forceps can be directly visualized
8. The feeding tube should be pre-measured and marked with a permanent marker pen
from the incision to the 8th intercostal space
9. Open the forceps, grasp the distal end of the feeding tube and then close the forceps
so that they click
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10. Withdraw the forceps bringing the distal end of the tube through the oesophagostomy
site and out of the mouth
11. Continue to pull more of the feeding tube out of the mouth, ensuring that you leave a
sufficient length outside of the oesophagostomy site to prevent inadvertent loss of all
the tube into the oesophagous (this will aid in the next step)
12. Open the curved forceps, and taking the distal end of the tube in your fingers,
advance it back into the mouth (back on itself). Advance until the tube goes beyond
the oesophagostomy site and the proximal end of the tube is seen to flip back on
itself
13. Pull the proximal end of the tube back until the mark on the tube is at the
oesophagostomy site
14. Suture the oesophagostomy tube in place using a Chinese finger-trap
15. Take a lateral thoracic radiograph to confirm correct placement
16. Cover the oesophagostomy site with a sterile dressing and lightly bandage in place
17. Check the oesophagostomy site daily for signs of infection. Clean the stoma with
swabs soaked in 4% chlorhexidine gluconate solution or similar, and reapply sterile
dressing.
Feeding:
The feeding tube can be used as soon as the dog has recovered from anaesthesia,
and can be removed at any time following placement
Calculate the resting energy requirement of the dog (RER)
Administer 30-50% of the RER on the first day, and increase to 100% RER over 1-2
days
Use a liquid or semi-liquid diet warmed to room temperature
Flush the feeding tube with 5-10 mL of water before and after feeding
If the patient coughs or appears distressed after administering the water, do not
continue with the feed
Divide the daily nutritional requirements into 4-6 feeds per day
If the dog vomits or regurgitates, hold off feeding for 6 hours and resume again at a
lower volume.
Complications:
Vomiting or regurgitation
Diarrhoea from the liquid diet
Tube dislodgement
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Stoma site infection

Oesophageal stricture or fistula
Notes:
Oesophagostomy feeding tubes should not be placed if the patients have the following:
Coagulopathy
Megaoesophagous
Oesophagitis
Persistent vomiting
Altered mentation
The feeding tube can be removed at any point. Remove the Chinese finger-trap suture, pull
the tube out and cover with a sterile dressing. Leave the oesophagous and skin to heal by
secondary intention.
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Notes page
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CRITICAL CARE OF THE CAT: THE ACUTE RENAL PATIENT

Louise ODwyer MBA BSc(Hons) VTS(ECC) DipAVN (Medical&Surgical) RVN
PetMedics Veterinary Hospital, Manchester, M28 2LY
23803455
The kidney's function is to eliminate metabolic waste materials and help maintain
homeostasis by manipulating the composition of blood plasma. The kidneys achieve
homeostasis by regulating acid-base, fluid and electrolyte balance and producing hormones
(erythropoietin, renin, and calcitriol). In the normal animal, sodium, potassium, chloride and
nitrogenous waste must be maintained within narrow concentration limits. The acute failure
of the kidneys to perform their function was previously known as acute renal failure. We now
recognize that an acute disruption of kidney function correlates with injury but may not
progress to permanent kidney failure. Thus, 'acute renal failure' is now termed acute kidney
injury (AKI). Acute kidney injury is characterized by the rapid loss of nephron function,
resulting in azotemia and fluid, electrolyte, or acid-base abnormalities. The decrease in
kidney function that occurs with AKI is multifactorial and includes cellular damage and
decreased intrarenal blood flow. This discussion will focus on the nursing management of
AKI.
Physiology
The functional unit of the kidney is the nephron. It is made up of a glomerulus, proximal
tubule, loop of Henle, distal tubule, and collecting duct. Up to 25% of the cardiac output goes
to the kidneys. Blood enters the glomerulus; the hydrostatic pressure in the glomerular
capillaries forces some plasma into Bowman's capsule. This fluid is called glomerular filtrate;
the glomerular filtrate moves into the proximal convoluted tubules and becomes tubular
filtrate. As the tubular filtrate passes through the tubules of the nephron, some of the
constituents (sodium, potassium, chloride, calcium, magnesium, glucose, amino acids,
bicarbonate and water) are reabsorbed and other constituents are secreted (hydrogen,
potassium and ammonia) from the peritubular capillaries into the tubular filtrate. Once the
tubular filtrate reaches the renal pelvis it is now known as urine and moves into the bladder
via the ureters.
Pathophysiology
Acute kidney injury is caused by a number of conditions or events. Some insult initiates a
cascade that leads to renal hypoperfusion and hypoxia causing tubular epithelia damage
and death. In addition, there may be a reduction in glomerular capillary hydrostatic pressure
and glomerular filtration rate; this reduction leads to decreased urine production and impairs
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regulation of water and solute elimination.
Acute kidney injury may be caused by decreased blood flow to the kidneys (prerenal),
disorders that disrupt structures in the kidneys (intrinsic renal) or disorders that interfere with
elimination of urine from the kidneys (post renal).
Common causes of AKI

Prerenal
Hypovolaemia
Dehydration
Hypotension
Intrinsic renal
Toxins
Ethylene glycol
Grapes/raisins
Lilies
Evenomation
Drugs
Cisplatin
NSAIDs
Aminoglycoside
Infectious
Leptospirosis
Pyelonephritis
Postrenal
Renal/urethral calculi
Prostatic disease
Ureteral, bladder, urethral perforation
FLUTD leading to urethral obstruction
Clinical Presentation & Assessment

History
The patient may report a history of sudden onset of anorexia, vomiting, diarrhea, changes in
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urination and listlessness. Additional complaints may include seizures, ataxia, or halitosis.
Owners should be thoroughly questioned about potential exposure to toxins, ingestion of
medications and recent medical procedures (including human preparations).
Clinical Examination
Abnormalities on clinical examination may include oral ulcerations including the tongue,
decreased skin elasticity and tacky mucous membranes, tachypnoea, bradycardia and
hypothermia. Abdominal palpation may reveal large, painful and/ or swollen kidneys.
Patients may have a large non-expressible bladder, suggestive of a urethral obstruction.
Patients with AKI generally do not display signs of chronic illness (muscle wasting, weight
loss, and poor hair coat). Patients previously treated with fluids may show signs suggestive
of fluid overload (generalized oedema, chemosis, and crackles on thoracic auscultation).
Laboratory Evaluation
Blood should be taken for a complete blood count (CBC), biochemistry profile, electrolytes,
and blood gases. In addition, a urine sample should be obtained for analysis and possible
culture.
A CBC may reveal anaemia, although AKI patients do not usually present with anaemia.
Changes may be seen in haematocrit and total protein, suggesting dehydration (decreased
PCV and TP). An increase in white cell count may suggest infection or inflammation.
Increases in serum creatinine, urea nitrogen, phosphorus, and potassium are usually
consistent with decreased urine output. Calcium may vary.
With the kidneys having a major role in electrolyte and acid base regulation both parameters
should be assessed. Hyperkalemia is the most common electrolyte abnormality. Moderate to
severe metabolic acidosis may be present.
A urine specific gravity of 1.0081.012 represents the inability of the kidneys to dilute or
concentrate urine. A concentrated urine suggests that the azotaemia is prerenal. Active urine
sediment (cast, red and white cells, bacteria and crystals) is seen in acute kidney injury.
Calcium oxalate crystals suggest ethylene glycol toxicity.
In hospital, tests are available for testing the presence of ethylene glycol toxicity.
Imaging
Survey radiographs may reveal the size and shape of the kidneys. In chronic renal failure the
kidneys may be small and irregular. In AKI, the kidneys may be normal or enlarged. A
distended bladder, abdominal or retroperitoneal fluid in the case of a perforation, Calculi and
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prostatomegaly may be evident.
Ultrasonography can help to evaluate renal architecture, for example bright (hyperechoic)
renal cortices may be seen in ethylene glycol toxicity, and also possible ureteral obstruction.
Other
Renal biopsy can be diagnostic and prognostic for intrinsic renal failure.
Treatment
When possible, treatment of the underlying cause should be undertaken. This may mean
discontinuation of a drug or drugs, correcting hypoperfusion or administering specific
antidotes for toxins. In general therapy includes correction of fluid imbalances, correction of
electrolyte and acid base disorders, promotion of diuresis, supportive care and nutritional
support.
Catheter Placement
A peripheral catheter is placed initially but a multilumen central catheter is advantageous. A
multilumen catheter will allow for the simultaneous administration of fluids, drugs, the
collection of blood samples and / or central venous pressure (CVP) measurements. Drugs
such as mannitol, with osmolalities greater than 700 mOsm, cannot be administered
peripherally without causing severe irritation to the vessel.
A urinary catheter will greatly facilitate care of the patient. It will allow the quantitation of
urine, which helps in addressing fluid needs. The catheter should be placed using aseptic
technique along with a closed urinary collection system; this will help to minimize urinary
catheter related infection.
Correction of Fluid Imbalances
The goal is to induce diuresis so as to decrease serum urea nitrogen and creatinine as well
as potassium.
If the patient is showing signs consistent with hypovolemia then fluid deficits will need to be
corrected immediately. This usually entails the administration of a crystalloid at up to "shock
doses" of 5055 ml/kg in the cat, this is commonly administered as a 15-20ml/kg bolus, or
fluid challenge and then the patients clinical response reassessed before subsequent
bolus are administered. If the patient's total protein or albumin is 3.0 mg/dl or 1.5 mg/dl
respectively then synthetic colloids might be used. Blood products are considered if the PCV
is less than 20%.
If the patient is simply dehydrated then the product of the percentage dehydration and the
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body weight equals the volume of fluids necessary to correct dehydration. In addition,
maintenance (normal losses) fluids at a dose of 5075 ml/kg/ day are added to the fluid
therapy plan. Finally, abnormal losses (vomiting, diarrhea, third space and excessive
urination) are included in the plan and replaced ml for ml. The total volume is replaced over
612 hours.
Care must be taken not to fluid overload the patient. The primary reason for fluid overload is
failure to adjust the fluid administration rate in the face of decreased urine production. The
oliguric or anuric patient is incapable of effectively excreting an excessive fluid load. Body
weight and indices of hydration should be monitored closely. An early sign of fluid overload
is an increasing respiratory rate and effort. Crackles may be auscultated. Chemosis and
subcutaneous edema are late signs. CVPs greater than 10 cm H2O or a significant increase
in a short period of time may be indicative of fluid overload.
Correction of Electrolyte and Acid Base Disorders
Life-threatening hyperkalemia and severe metabolic acidosis are common complications in

AKI. There are various options for treating hyperkalemia and are dependent on the severity
of the elevated potassium level. This includes promoting excretion or dilution with fluid
therapy; administration of sodium bicarbonate to correct acidosis and promote H+ and K+ ion
exchange across cells; administering glucose and insulin to promote the movement of K+
and glucose into the cell or calcium administration which antagonizes the cardiotoxic effects
of potassium. Ideally, electrolytes are monitored as frequently as dictated by the patient's
condition. Staff should be familiar with the electrocardiographic changes of hyperkalemia.
The signs are peaked T waves bradycardia, decreased P wave amplitude, prolongation of
the PR interval, and widening of the QRS complex.
Management of Anuria/Oliguria
Diuretics are indicated if diuresis has not occurred following volume restoration. Furosemide
is a loop diuretic, meaning it acts primarily in the ascending loop of Henle. It is a renal
vasodilator and a natriuretic (promotes the excretion of sodium) agent. If used in anuria high
does should be utilized. If diuresis does not occur then another diuretic or combination of
diuretics is used. If the patient is oliguric, then low doses are used and titrated to effect.
Furosemide has the potential for potentiating nephrotoxic effects of certain drugs
(aminoglycosides) and therefore should not be used in those cases. The technician should
be aware that furosemide could cause excessive diuresis and dehydration, hypovolaemia,
hypotension, hyponatraemia, metabolic alkalosis, vomiting and diarrhoea.
Mannitol has osmotic diuretic effects, it increases blood volume, and renal perfusion, it works
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in the glomerulus of the nephron, therefor it will only be effective if the patient is oliguric
rather than anuric. It is usually given as a slow bolus over 20 minutes. Significant diuresis
should be seen within 30 min, if not it may be repeated once more. Because it contributes to
hyperosmolality and ECF edema, its use is discontinued if it fails to work. If significant
diuresis occurs, then mannitol may be given as an intermittent bolus every 46 hours over
the next 2448 hours or may be administered as a constant infusion.
In low doses, dopamine has been used to increase the renal blood flow in dogs, but its
efficacy is dubious. There is little or no documentation on the efficacy of dopamine in dogs
and cats with AKI. Its routine use to increase urine production in oliguric or anuric AKI cannot
be justified.
These drugs may be used independently or in conjunction with each other. There are no
specific guidelines that dictate which order the drugs are used.
Dialysis
If anuria persists, then peritoneal or hemodialysis is considered. Both options are expensive
and time consuming. Peritoneal dialysis uses the principles of diffusion, osmosis and
ultrafiltration across the peritoneal membranes. A slightly hypertonic dialysate solution is
instilled into the patient's abdomen and allowed to dwell for a short period of time (one hour).
The patient's peritoneum acts as a semi-permeable membrane to allow the removal of
undesirable solutes via diffusion.
Supportive Care
Uraemic patients are prone to vomiting; therefore, centrally acting antiemetics such as
metoclopramide, maropitant (Cerenia), or ondansetron (Zofran) may be indicated. Because
patients are also at risk for the development of oesophagitis and ulcerative gastritis drugs
that inhibit gastric acid production may be beneficial, including histamine receptor
antagonists, such as famotidine and proton pump inhibitors, such as omeprazole (Losec)
and gastrointestinal protectants (Sucralfate).
Routine nursing principles apply as far as performing physical therapy in the recumbent
patient and keeping the patient warm, clean and dry. IV and urinary catheter care should be
performed every 48 and 8 hours respectively. The patient should be observed for potential
risk factors such as fluid overload, adverse drug reactions, infection, and catheter related
problems.
Physiological monitoring should include blood pressure (patient may be hyper or

hypotensive), central venous pressure (patient may be hypo or hypervolemic), ECG (looking
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for arrhythmias or signs suggestive of hyperkalemia), and "ins and outs" and / or frequent
body weight to assess fluid balance.
Nutritional Support
Dietary intake is compromised because of anorexia, vomiting and nausea. These patients
may be hypercatabolic; as a result nutritional support will be required. Enteral and parenteral
feeding has been utilized. Patients should be fed a diet that is comparable to the chronic
renal failure patient. The diet is high energy and moderate in protein. There are a variety of
commercial prescription diets that meet these requirements and can be blended for tube
feeding.
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Notes page
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NURSING THE POST ANAESTHESIA RECOVERY PATIENT

PetMedics Veterinary Hospital, Manchester, UK
Introduction
The Confidential Enquiry into Perioperative Small Animal Fatalities (CEPSAF; Brodbelt and
et al, 2006) examined perioperative small animal fatalities. The results revealed that the
postoperative period was a particularly common time for dogs, cats and rabbits to die. Over
60% of cats and rabbits, and nearly 50% of dogs died during this time period and of these
postoperative deaths approximately half of the patients died within 3 hours of termination of
the procedure. Cardiovascular and respiratory causes of death were the most common
causes of death in dogs and cats with a substantial majority being of unknown cause. The
results of the study suggest that improved monitoring of recovering patients could reduce the
number of fatalities in this group of patients. This lecture will look at the most important
aspects of post-operative care which are based around frequent patient monitoring and
anticipation of patient needs, this includes frequent and accurate patient assessment, which
will allow identification of arising problems and help guide therapy and also the use of
monitoring equipment.
Monitoring
Successful management of the post-operative, emergency and critically ill patient is

dependent on several factors: such as the training and skills of personnel and readiness of
facility. The implementation of a team approach thorough the use of established policies,
protocols and procedures; allows for coordinated resuscitative efforts. The survival of the
patient is also dependent on the collaborative efforts of the veterinarian and technician. The
success of the team is not only dependent on the knowledge base and skill level of each
member, but also on the consistency and repetition of their practice as a team. Thus, the
nurse or technician should be skilled in patient monitoring, based on clinical and
physiological parameters and knowledgeable at utilizing different types of monitoring
equipment.
Physiological Parameters
Neurological Status
The neurological status of a critical patient should be assessed in conjunction with the other
body systems. A patients mental status and gait should be noted, and any variation from
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ambulatory, bright, alert and responsive, will require further investigation. Patients may have
many variations in mental status from dullness and depression, to hyperexcitability and
seizures. Central nervous system depression may be a result of primary CNS disease, or as
a complication from metabolic disorders. Hypoglycaemic or patients with renal or hepatic
compromise my display depressed mentation.
Temperature
Pathophysiology: The body maintains temperature homeostasis by balancing heat
production with heat loss through a thermostatic feedback mechanism in the hypothalamus
of the brain. During illness or central nervous system disorder, this mechanism may be
altered. Chemical substances released in disease can reset the thermoregulatory centre,
increasing the metabolic rate, producing and conserving heat and elevating body
temperature. These chemicals may be pyrogens secreted by bacteria or cytokines
associated with inflammation. Primary brain disease (e.g., cerebral oedema, neurosurgery,
brain trauma, or tumours) can reset the thermostat to a higher level.
Hyperthermia creates increased tissue oxygen requirements. The body responds by

increasing ventilation to release body heat. Should the PCO2 decrease too low, cerebral
vasoconstriction and brain hypoxia can result. Cardiac work and oxygen demands increase.
Peripheral vasodilatation occurs in an effort to release heat. Damage to vascular cells can
lead to disseminated intravascular coagulation, sloughing of gastrointestinal mucosa,
bacterial translocation, and significant intravascular volume deficits.
Hypothermia results in a reduced metabolic rate and enzyme functions. There is a decrease
in oxygen consumption and a decrease in the ability of haemoglobin to release oxygen to
tissues. Hypothermia affects the cardiovascular system by causing peripheral
vasoconstriction, decreased heart rate and hypotension. Gastrointestinal motility is
decreased, and ileus may occur.
Assessment: Emergency patients should have temperature monitored several times daily.
Patients with infections, excessive panting, hyperactivity, and postoperative patients should
have their temperatures checked more frequently. Temperatures are ideally monitored from
the same site, usually rectally. Other sites of monitoring include the axillary and inguinal
region. These areas generally are 1degree lower than rectal temperature. Ear temperatures
can be obtained using an ear probe. Serial temperatures taken from the same area are more
important than single values.
Intervention: Any abnormal temperature must be reported. The veterinarian will determine
what aggressive methods are required to cool hyperthermic and warm hypothermic patients.
Hyperthermic patients may benefit from being placed in front of a low current of air (blowing
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from a fan), laying on the metal surface of the cage or a grate without bedding or with cool
towels, cool compresses in the inguinal and axillary regions, cool bathing, and receiving cool
intravenous fluids and enemas. Cooling measures should cease when the rectal
temperature reaches 39.8C in order to prevent overcooling.
For hypothermic patients circulating warm water blankets or forced air warming devices are
preferred over heating blankets and lamps because there is less chance of accidental
thermal burns. No surface heat should be provided without volume replacement, because
vasodilatation from the heat may exacerbate their condition. Severe or prolonged
hypothermia may require more aggressive approaches such as active core warming with IV
warmed fluids, warm peritoneal lavage or intracolonic lavage with warm isotonic fluids. The
recumbent patient should be turned every 2-4 hours to avoid thermal injury. Heating should
be discontinued after the rectal temperature is low normal.
Blood Pressure
Pathophysiology: Arterial blood pressure is a product of cardiac output (heart rate and
stroke volume) and peripheral vascular resistance. Systolic pressure is the pressure exerted
by the blood as a result of contraction of the left ventricle. Diastolic pressure is the pressure
exerted by the blood within the vessel when the ventricle is at rest. The difference between
the diastolic and the systolic pressure is called the pulse pressure. Mean arterial pressure
(MAP) is the diastolic pressure plus one-third the pulse pressure. Any factor that alters
cardiac output or peripheral vascular resistance will alter the blood pressure.
Procedure: Blood pressure can be measured by either direct or indirect methods.
Assessment: The normal blood pressure in the dog and cat averages 120 mmHg systolic
and 80 mmHg diastolic. The mean arterial pressure is normally 80-90 mmHg. Increases in
blood pressure can be caused by any condition that increases cardiac output, such as fever,
exercise, and septic shock. Decreases in blood pressure can be caused by cardiac failure,
hypovolemic shock, drugs (such as sedatives, opioids, and anaesthetics). Blood pressure
should be evaluated together with the animal's perfusion parameters, UO, and disease state.
As with any other monitoring parameter, repeated measurements are needed to detect a
trend in change. Renal perfusion over the short term is considered adequate if BP is
maintained above 60 mmHg.
Shivering, trembling, struggling, vasoconstriction, and inappropriate cuff size are common
causes of erroneous measurements when utilizing the oscillometric method. There is also a
decreased reliability when attached to animals less than 15 pounds. Erroneous results can
occur with the Doppler method due to malpositioning of transducer, inappropriate cuff size,
poor contact with coupling gel, and flexion of the limb.
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Intervention: Any blood pressure outside the normal value must be reported to the
veterinarian. Intervention by the veterinary team is performed after complete patient
assessment including LOC, CVP, perfusion and UO. Hypotension may be treated by
haemostasis, crystalloid or colloid infusion, and potentially positive inotropes or
vasopressors. Hypertension can be treated with pain relief, diuretics or possibly vasodilators.
Central Venous Pressure

Pathophysiology: Central venous pressure (CVP) is a function of four independent forces:
volume and flow of blood in the vena cava, distensibility and contractility of the right
chambers during filling, venomotor activity in the vena cava, and intrathoracic pressure.
When right heart function and intrathoracic pressure are normal, CVP can be used as a
reflection of intravascular volume. Changes in blood volume will result in pressure changes
in the vena cava and are reflected by the CVP.
Procedure: Central venous pressure monitoring set-up: Central venous pressure

measurement requires placement of a central catheter into the cranial vena cava with the tip
lying near the base of the heart (i.e., right atrium). The catheter is attached to IV extension
tubing, which is connected at right angles to a water manometer by a three-way stopcock.
Across from the IV extension tubing on the stopcock is an IV line and fluids. The zero on the
water manometer should be at the level of the right atrium. A horizontal line drawn between
the thoracic inlet and the manometer establishes the zero reference level.
The stopcock is off to the manometer when the patient is receiving intravenous fluids. To
measure CVP, the manometer is filled with fluid from the IV bag and then the stopcock is
turned off to the bag leaving a column of fluid within the manometer. The stopcock is then
opened towards the patient, allowing the fluid in the manometer to access the patient. The
fluid level in the manometer is allowed to equilibrate with the pressure in the jugular vein.
The fluid level may oscillate a few millimetres with each respiration or heartbeat. Three
values or readings are obtained to ensure consistent readings.
Assessment: Normal CVP measurements are reported as -1 to 5 cmH2O. However, critical

animals are resuscitated to supra-normal values and the CVP is optimally maintained
between 5-8 cmH2O. Values less than 5 are suggestive of insufficient intravascular volume.
Values over 14 cmH2O are of concern for right heart failure or significant volume overload.
Factors unrelated to right heart function and volume overload (such as pleural, pericardial or
mediastinal pressure, and increases in pulmonary hypertension) can also raise the CVP.
If readings do not fluctuate with respiration, the readings are inaccurate. Note what side the
animal is positioned and, future reading should be made with the animal lying on the same
side. Always use the same zero point reference (thoracic inlet), so that readings are
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comparable. Always obtain three or five consecutive reading at a time. Each reading should
be approximately close in measurement. Huge discrepancies in readings should alert the
nurses to trouble shoot the CVP set-up for kinks, clogs or changes in catheter or patient
position.
Intervention: The CVP can be used to guide aggressive intravascular fluid resuscitation.
When the CVP is low in a hypotensive animal, crystalloids and colloids are rapidly
administered until the CVP is between 5-8 cmH2O. At that time if hypotension persists,
positive inotropes or pressor agents are administered.
High CVP measurements warrant examination of the system for occlusion of the catheter. If
the system is patent, then fluid overload or right heart failure are suspected. The fluid rate is
lowered and the veterinarian will opt to administer diuretics or drugs specific for the cardiac
condition. Any CVP measurements outside of the target values set by the veterinary team
should be reported to the attending veterinarian.
Pulse Oximetry
Pathophysiology: Pulse oximetry is a quick and reliable non-invasive method of measuring
arterial oxygen saturation (SaO2). Oxygen saturation is the percentage of haemoglobin sites
that are chemically combined with oxygen. Oxygen saturation and pulse rate are determined
by passing two wavelengths of light, one red and one infrared, through body tissue to a
photo detector. The signal strength resulting from each light source determines the SaO2.
Pulse oximetry can be affected by the colour and thickness of body tissues, the probe
placement, the intensity of the light source (including fluorescent lights) and the absorption of
the arterial and venous blood in the body tissue.
Procedure: There are several types of probes that can be placed. The probes that are
clamps can be placed on the tongue or on a shaved, non-pigmented skin surface. The rectal
probe is placed against the rectal mucosa, which has been cleared of faeces. The pulse
oximeter is turned on and the SaO2 and pulse rate is digitally reported.
Assessment: Animals requiring oxygen therapy or under anaesthesia should have their
SaO2 monitored as well as monitoring for physical signs of hypoxia (e.g., decreased LOC,
tachycardia, arrhythmias, restlessness, altered blood pressure, increased respiratory rate,
and changes in MM colour). The use of pulse oximetry for monitoring oxygen saturation and
pulse rate can provide early warning of pulmonary or cardiovascular deterioration before it is
clinically apparent. Normal SaO2 is 98%. Values below 90% are correlated with PaO2 <60
mmHg and cyanosis is imminent. It is of most value when the arterial oxygen saturation is
between 90% and 95%.
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Limitations of pulse oximetry include its inability to differentiate carboxyhaemoglobin (seen

with carbon monoxide poisoning) from haemoglobin. The pulse oximeter cannot distinguish
a declining PaO2 that is above 100mmHg (e.g., a fall from 330 mmHg to100 mmHg will still
report a SaO2 of 100%) or the presence of methaemoglobin. Results can be erroneous in
animals with poor peripheral perfusion, heavily pigmented skin, hypothermia, icterus, and
anaemia.
Intervention: Any sudden decrease in the oxygen saturation with proper probe placement
requires immediate notification of the veterinarian and rapid assessment of the animal's
cardiopulmonary function. The oxygen concentration may need to be increased or the
method of ventilation improved.
Electrocardiogram
An electrocardiogram (ECG) provides valuable information on rate and rhythm and is

essential to assess arrhythmias. Arrhythmias are clinically important; they may cause or
exacerbate low cardiac output states. It may be impossible to resolve congestive heart
failure signs without controlling concurrent arrhythmias. Arrhythmias can contribute to
myocardial ischaemia.
The ECG is the gold standard for identification of an arrhythmia. It should be remembered
that the ECG is not sensitive in detecting cardiac chamber enlargement (echocardiography
and radiography are much more sensitive). An ECG provides no information about the ability
of myocardium to contract, nor does it provide any information about the heart valves or
endocardium. The ECG is the only way to diagnose the actual arrhythmia and hence provide
appropriate treatment for the patient. Cardiac arrhythmias can contribute to morbidity and
mortality in critically ill dogs and cats. Successful management of arrhythmias often involves
investigation and correction of an underlying non-cardiac disorder, and management of
contributing factors in cases with severe systemic illness. In animals with primary cardiac
disease, arrhythmia management is usually accomplished with drug therapy or cardiac
pacing.
Capnometry
Capnometry is a non-invasive mode of monitoring partial pressure of end-tidal CO2. It is
defined as the measurement and numeric display of End-tidal CO2 (ETCO2). Capnography
is the measurement and graphic display of expired carbon dioxide PCO2 versus time.
Exhaled CO2 is a reflection of CO2 production (metabolism), transport (blood and
circulation) and elimination (ventilation). Though a variety of techniques can be used to
measure CO2 (colorimetric, mass spectrometry, Raman analysis), the majority of
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capnographs rely on infrared absorption. Use of this technique can reliably and quantitatively
provide vital information regarding the respiratory status of operative and critically ill patients.
The normal capnogram consist of four phases:
1. Phase I: represents the beginning of exhalation, during which PCO2 remains almost
zero while gas from the anatomic dead space leaves the upper airway.
2. Phase II: depicts the waveform rising sharply as exiting alveolar gas mixes with dead-
space gas.
3. Phase III: the capnogram reaches a plateau representing gas from the alveolar
space:
a. The terminal and highest portion of plateau represents PetCO2.
b. The slope of phase III is determined by ventilation/perfusion (V/Q) status of lungs.
c. Patients that have increased dead space have a steeper phase III and may not
reach a plateau.
4. Phase IV: the waveform sharply declines as inspiration begins.
Image reproduced with permission from capnography.com
Normally, ETCO2 is 2-5 mmHg lower than PaCO2. Increase levels may be due to increased
production, depression of respiratory centre, or hypoventilation. Abnormally low levels of
ETCO2 most often are associated with hyperventilation or due to increased dead space. A
sudden or abrupt decrease in ETCO2 can be due to ventilator disconnection, leakage in
circuit, an obstructed ET, acute hypotension, hyperventilation or massive pulmonary
embolism. Accidental placement of ET into the oesophagus or ET dislodgement will result in
total absence of waveform.
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Elevation of baseline or phase I is indicative of CO2 rebreathing and suggests that either the
absorbance of the CO2 is exhausted or malfunctioning valves. Prolongation or slanting of
phase II occurs with obstruction of expiratory gas flow (kinked ET) or leak in breathing
system. Increases in the slope of phase III can be due to events that impede or obstruct
expiration.
ETCO2 is most commonly measured in intubated patients, however if nasal cannula are
placed they can be adapted (with the addition of a Y connector) to allow connection of the
patients to a capnograph, or nasal prongs with measure ETCO2 as well as delivering O2 can
be obtained. The capnogram using these nasal techniques may differ from that in
anaesthetised patients.
Urine Output
Pathophysiology: The main function of the kidneys is to excrete metabolic wastes and
reabsorb vital electrolytes and water. The volume and contents of the urine produced is a
result of the function of the population of nephrons, made up of the glomerulus and renal
tubules. The volume of urine produced is dependent upon the glomerular filtration rate
(GFR) and ability of the renal tubules to reabsorb sodium and water. The factors governing
the GFR are the size of the glomerular capillary bed, the permeability of the capillaries, and
the hydrostatic and oncotic pressure gradients across the capillary walls. The factors
governing the function of the tubular cells include: oxygen utilization, glucose availability, and
integrity of the cellular enzyme systems. Variations in these factors have predictable results.
For example, should the mean arterial blood pressure falls below 60 mmHg, the hydrostatic
pressure gradient declines across the glomerular capillary beds and glomerular filtration
almost stops (oliguria). Severe prolonged hypoxia can cause the dysfunction or death of the
glomerular and tubular cells, leading to inadequate urine production. In addition, interruption
of the tubular cell ability to reabsorb sodium results in high urine sodium and an increased
urine production.
Procedure: Accurate and frequent measurement of urine output requires bladder

catheterization. A closed urinary collection system utilizing a sterile collection bag and IV line
is attached with the bag maintained off the floor and below the level of the catheter. The
bladder is immediately emptied and the time recorded as the 0 time (start of collection). The
frequency of measuring UO is determined by the rate of onset and the severity of the
disease. In general, UO is measured every 2 hours. Daily examination of urine sediment is
performed to monitor for infection. Urinary catheters should be flushed with sterile saline and
inspected for kinks and clots in the line at least every 8 hours or if there is a sudden decline
in urine collected.
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An indirect method of estimating UO is to place incontinence sheets in the patient's cage to

collect the urine. The weight of a dry sheet is subtracted from the weight of a urine soaked
sheet. Each 1g increase in weight equals 1ml of urine. An alternate method is to place the
animal on a grate elevated off the cage floor. Urine is then collected and measured.
Fluid input and UO are recorded, including any fluids administered by enteral or parental
routes. Quantities of fluid lost through vomiting and diarrhoea are estimated and recorded.
Assessment: Normal UO is 1-2 ml/kg/hour. Oliguria is defined as UO <0.27 ml/kg/hr and

anuria is <0.08 ml/kg/hr. However, as urine falls below 1 ml/kg/hr, oliguria is anticipated.
Oliguria can be from prerenal, renal, or postrenal causes. Prerenal conditions such as
hypovolemia, cardiac failure, hypotension, excessive vasoconstriction or hypercalcemia can
lead to reduced GFR. Dehydration and hypotension will decrease UO (prerenal) until
adequate intravascular volume has been restored. Renal changes affect the glomeruli and/or
tubular cell function, with sepsis, trauma, toxins (such as aminoglycosides, amphotericin),
radiocontrast agents, infections (pyelonephritis) as potential aetiologies. Postrenal problems
cause interruption of the flow of urine through the ureters, bladder or urethra and include
renal calculi, blood clots, neoplasia or trauma.
True oliguria in an animal receiving IV fluid will result in a decreased PCV/TS due to
haemodilution. The CVP will increase and harsh or wet lung sounds may develop. The body
weight will increase rapidly as fluid accumulates. Increasing blood levels of urea nitrogen,
creatinine and potassium suggests renal failure or postrenal obstruction and warrants
immediate veterinary attention.
Excessive urine production is called polyuria and can be due to IV fluid overload or impaired
renal tubular absorption of sodium and water. Other conditions such as medullary wash out,
post obstructive diuresis and sepsis can causes polyuria and require large amounts of IV
fluids.
Intervention: The technician must evaluate the UO in relation to the haematocrit, total
solids, central venous pressure (CVP), blood pressure, heart rate, and body weight. Any
decrease in UO in an adequately hydrated and perfused animal warrants immediate
notification of the veterinary surgeon in charge of the case. The IV fluid rate is reduced and
the urinary collection system examined for post-renal causes of urine outflow obstruction. If
the origin of the condition is determined to be renal, the veterinarian may choose to
administer either mannitol or frusemide and dopamine to stimulate urine production.
A polyuric animal will require a greater quantity of intravenous fluids for maintenance of
normal hydration. Medullary washout often occurs and requires a slow tapering from IV fluids
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onto oral fluids to avoid significant dehydration. Potassium is commonly low in these animals
and required aggressive supplementation.
Blood Gas Analysis
Normal Blood Gas Values
Dog PaO2: 92mmHg (80-105)

PaCO2: 27mmHg (32-43)
SaO2: More than 95%
Cat PaO2: 105mmHg (95-115)

PaCO2: 31mmHg (26-36)
SaO2: More than 95%
PaO2/FiO2 ratio calculation
PaO2:FiO2 ratio can be used to evaluate pulmonary function at any FiO2, which provides an
advantage over the A-a gradient and the 120 rule. The value is acquired simply by dividing
the PaO2 by the FiO2.
PaO2/FiO2 = P:F ratio
Where the FiO2 is expressed as a decimal. With normal pulmonary function, the P:F ratio
should exceed 500mmHg. The P:F radio can be used to approximate the severity of
pulmonary dysfunction; values between 300 and 500mmHg are associated with mild
dysfunction, between 300 and 200mmHg are considered to have moderate dysfunction, and
less than 200mmHg are considered to have severe pulmonary dysfunction. The author finds
this method useful as it is quick and can be used at any FiO2. The main disadvantage being
the method disregards the effect of ventilation (PaCO2), but this is only an issue when
carrying out the calculation on room air.
References available upon request.
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IMPROVED MANAGEMENT OF EXTENSIVE WOUNDS

The management of complex traumatic wounds remains a challenge to both human and
veterinary wound care practitioners. Especially challenging to our profession are traumatic
injuries sustaining large losses of epidermis and dermis (i.e., full thickness skin loss). The
skin primarily protects the body from trauma, desiccation and UV damage. It also provides
immunosurveillance, controls invasion of microbial organisms and synthesizes pheromones
and vitamin D. It is the largest organ in the body. It contains receptors to touch, pressure,
vibration, tension, noxious stimuli, heat and cold. It also monitors temperature, but is limited
in its capacity for heat regulation. It is a remarkable structure, its viscoelasticity means it can
retract considerably upon wounding, yet also has the ability to cover significant distances
upon healing. It also provides veterinarians with new challenges to wound care every day!
In most cases of extensive traumatic wounding, immediate closure is not possible or

advisable, due to the degree of contamination and undeclared vascular integrity. When a
wounded animal is initially presented to the clinic, it is important to ascertain exactly how the
injury occurred, when it happened, and how the wound has been handled in the interim
period before presentation. If the owner calls before arriving, he should be advised to wrap
the wound with a clean sheet or bandage to prevent further contamination and ongoing
damage to the area. Depending on urgency of the presentation, the patient should be
stabilized as necessary and a full history and examination taken. The wound can be then
be classified and an initial treatment plan formulated.
Many traumatic injuries in small animals are a result of motor vehicle or other high impact
trauma and systemic evaluation should always be performed to rule out concomitant injuries.
This typically includes evaluation of cardiopulmonary systems, integrity of the abdominal wall
and contents, specifically including GI and urinary systems, and neurologic assessment.
Analgesia will be critical in the immediate post-wounding period and also for at least the first
week after wounding, before granulation tissue appears in the wound.
With large loss of full-thickness skin, be prepared for significant ongoing fluid losses through
the wound, inappetance, ileus, prolonged pain, hypoproteinemia, hypoalbuminemia, anemia,
lymphedema. Older or debilitated animals with significant wounding may take longer to heal,
and have increased risk of sepsis and associated systemic issues. It is important to be
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aware of these potential issues, assess comorbidities, anticipate their occurrence, and be
aggressive in prevention and treatment.
Wound Healing
It is of paramount importance that the processes of normal wound healing are understood,
so that we can recognize abnormal or delayed healing. We want to manage a wound to a
condition where it is either completely healed, or ready for a closure/reconstructive
procedure. Wound healing has been described in a series of phases to facilitate
understanding and learning of the different processes that are occurring. There is
considerable and variable overlap of these phases within a healing wound at any point in
time.
Inflammatory Phase: Immediate vasoconstriction of blood vessels occurs, with platelet

aggregation and subsequent thrombus (clot) formation. Then an increase in capillary and
venule permeability occurs and leucocytes become sticky and adhere to endothelium.
Within 30 60 minutes, the entire endothelium will be covered with adherent leucocytes.
Diapedesis of leucocytes occurs through the endothelial gaps and they concentrate at the
site of injury. Neutrophils predominate early in the post-wounding period. The main role of
the neutrophil is to phagocytose bacteria (enhanced by opsonization and complement
activation) and release enzyme-containing granules. They are a short-lived cell, and not
essential unless there is massive contamination, or infection. As monocytes enter the
wound, they become macrophages and are essential for wound healing. Early on,
macrophages are important in wound debridement through phagocytosis, and degradation of
the provisional extracellular matrix (blood clot, fibrin, cells). Later on, these long-lived cells
produce many cytokines that modulate wound healing. The inflammatory phase typically
lasts for 3-5 days, but can extend for much longer if the contamination is significant or there
is significant tissue trauma.
Proliferative Phase: The transition into the proliferative phase is often not grossly evident in
large wounds until the second week following wounding. Epithelialization begins with
mobilization of the basal cells of the epidermis at the wound edge. This mobilization occurs
early, within a couple of days, while the wound is still in the inflammatory phase. At this time,
the basal epithelial cells loosen their firm attachment to underlying dermis, start to mobilize
and migrate outward toward the wound. They undergo mitosis, enlargement, flattening as
they proliferate outwards. In large open wounds, epithelialization will only start to take off
once a smooth bed of granulation tissue is evident, and migration may take weeks.
Epithelialization is stopped by contact inhibition - in large wounds, the final epithelial
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coverage can be very thin and fragile, and prone to traumatic ulceration and excoriation.
Over the weeks, the epithelial cells differentiate and mature and finally the basement
membrane is replaced. Epithelialization does not bring dermal components, so adnexal
structures such as hair and glands are not present. Angiogenesis is stimulated by specific
angiogenic and growth factors. Capillary buds form, coalesce, and mature into arterioles and
venules within the granulation tissue. Once reconstitution is complete, involution of most of
the capillary network occurs through apoptosis. This is why granulation tissue is initially
bright red, and then becomes paler as the capillaries regress and more collagen is laid down
by fibroblasts. Fibroplasia is the production of extracellular matrix, collagen and elastin fibers
by fibroblasts. This is intimately associated with the capillary ingrowth discussed above.
Fibroblasts arise from undifferentiated mesenchymal cells in adjacent connective tissue.
They advance along fibrin framework preceding the capillary bud. Evidence of granulation
tissue (= fibroblasts, capillaries, collagen, extracellular matrix, macrophages), is seen grossly
about 7 to 9 days in healthy open wounds. Granulation tissue is extremely important in
wound healing as it is resistant to infection, provides a surface for epithelialization, plays a
role in contraction, and provides collagen required for wound healing. As granulation tissue
matures, some fibroblasts undergo apoptosis, and others assume a myofibroblast
phenotype, with well-developed actin filaments. These myofibroblasts play a role in
contraction of the wound.
Maturation Phase: Contraction occurs as the granulation tissue pulls the skin margins
inwards, resulting in a smaller area to be covered by epithelialization. Specialised cells of
granulation tissue (myofibroblasts) have contractile ability. They attach to each other, to the
extracellular matrix (via a peculiar connection called a fibronexus), and to the wound edges.
They then start to contract and pull the wound inwards, stopping when wound edges come
into contact, or when tension of surrounding skin equals that of myofibroblasts. Contraction
usually begins about 7 to 9 days after wounding in healthy wounds. Contraction can be quite
remarkable and progress to complete healing, even in quite large wounds. Remodeling is
the final process in wound healing. As fibroplasia progresses, the collagen fibers that are
orientated along the lines of tension become thicker, and the non-functionally orientated
fibers disappear. Type III collagen is replaced with type I collagen. A balance between
collagen production and collagen destruction, is partially mediated by collagenase secreted
by overlying epithelium (at about 3 weeks post wounding), but also certain matrix
metalloproteinases. Intermolecular cross-linking increases and the collagen bundles develop
a basket-weave appearance. Maturation and remodelling will continue for months, slowly
strengthening the wound; however, scar still remains about 15 to 20% weaker than
surrounding normal tissue.
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Factors that influence wound healing can be related to its management, host status, and
also factors local to the wound itself. Management factors include tension, motion, pressure,
inadequate debridement of devitalized tissues or eschar, desiccation and maceration. Host
factors that will delay wound healing include: protein deficiency, anemia, uremia,
endocrinopathy (Cushings, Addisons, diabetes), vitamin deficiency (C,A,E), corticosteroid
medication, chemotherapy, sepsis and old age. Local wound factors that will delay wound
healing include: oxygen tension, temperature, radiation therapy, neoplasia, infection, foreign
body, large amount of devitalized soft tissues, eschar and exposed bone.
Wound classification
Wounds can be classified as Clean, Clean-Contaminated, Contaminated or Dirty. Most
traumatic wounds in small animals fall into the Contaminated or Dirty classification and thus
should undergo open wound management for a period of time. The extracellular matrix,
cytokines and growth factors play a critical role in wound healing, as well as the cellular
elements of the wound and all should be protected as the wound transitions from the
inflammatory phase into the proliferative phase. We now realize how important it is to
provide the ideal environment for wound healing. In the early or Inflammatory Phase of
wound healing, debridement, irrigation and drainage are the most important events, but as
the wound enters the Proliferative Phase and becomes less exudative, the dressings
should maintain a warm and protected environment for wound healing to progress.
Basic tenets of wound management

Following attention to life-threatening issues, cardiovascular stabilization and analgesic
medication, four main tenets of open wound management are followed:
1. Cleansing
The periwound skin and the wound itself need to be clipped and cleansed. First, the wound
is protected whilst the periwound skin is prepared. Common ways of protecting the wound
include liberal application of a lubricating gel, or placing saline-moistened gauze in the
wound. This prevents irritation of the wound by clipped hairs, and detergent getting into the
wound. The skin is clipped generously around the wound, and the area (skin only) prepped
with surgical scrub and alcohol (as for an aseptic procedure). Neither alcohol nor scrub
should get into the open wound. Once the periwound skin is prepped, then wound itself can
be cleansed with either chlorhexidine 0.05% or povidone-iodine 0.1%- 1.0% solution (not
scrub).
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2. Debridement
Debridement is the removal of devitalized tissues from a wound. The term usually includes
removal of foreign debris from the wound. There are several types of debridement including
chemical, enzymatic and maggots, but the most effective and commonest type is surgical
debridement. Most animals will require profound analgesia/sedation or general anesthesia
for this procedure. Strict aseptic technique should be employed and tissue that is obviously
necrotic within the wound should be excised using a scalpel blade or fine sharp scissors.
Take care to avoid damage to vital structures within the wound. Any tissue that is of
questionable viability should be left in the wound for a later surgical debridement event.
Proper debridement can take time, i.e., several hours.
3. Lavage
Surgical debridement is usually followed with lavage (which actually provides some further
debridement). Copious lavage serves to decrease bacterial contamination. High-pressure
lavage (8 15 psi) appears more effective than low pressure lavage. A 20 ml syringe and
19g needle provides approximately 8 psi. Pulsatile lavage units are available and are
recommended over syringes and bottles. Large volumes are more beneficial than small
volumes. The ideal lavage solution is sterile, isotonic and buffered (e.g., lactated Ringers).
However, tap water is readily available, and appears to be just as effective clinically. The
end point for lavage is almost a waterlogged appearance usually 5 10 minutes.
Final Lavage Solutions:

Antiseptics have been shown to reduce bacterial numbers when used as a final lavage, or in
wet-dry dressings. They are indicated in highly contaminated wounds.
Chlorhexidine: has a wide antimicrobial activity and sustained residual activity. It is
minimally absorbed and toxicosis is rare. It is not inactivated in the presence of organic
matter. There has been ototoxicity reported, so should probably not be used for otitis, or in
cats. We recommend 0.05% solution.
Povidone-iodine: The mechanism of action is based on the amount of free iodine in
solution. Increasing the dilution gives increased relative amounts of free iodine and the
duration of action is around 4 to 6 hours. This means that 0.1% to 1.0% solutions have as
much antibacterial activity as 10% solutions (stock solution is 10% povidone-iodine, so dilute
1:10 or 1:100). Higher concentrations may be toxic to neutrophils, and povidone-iodine is
inactivated in the presence of exudates and organic matter. Systemic absorption of large
amounts may lead to adverse effects such as thyroid, acid-base disturbances. The
maximum effect is achieved with 0.1 to 1.0% solutions with lavage every 6 hours.
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Malic acid, benzoic acid, salicylic acid in propylene glycol: This is a low pH solution
excellent for debridement of necrotic tissues. It has minimal antibacterial action, but provides
acidic environment, discouraging bacteria.
Hypochlorous solutions (originally derived from Dakins solution) have become very popular
for wound cleansing in veterinary medicine recently. These appear to be quite effective and
should be evaluated in comparative studies.
A few words on hydrogen peroxide:

- minimal antibacterial activity
- toxic to fibroblasts
- inappropriate for use in open wounds
And finally, NEVER USE DETERGENTS IN OPEN WOUNDS!
4. Drainage: Dressing and Bandaging

The bandage has an extremely important role it exerts pressure, absorbs, protects,
immobilizes, and makes the animal more comfortable. Bandages are composed of three
layers, each with its own properties and functions. The contact layer of the wound dressing
is in contact with the open wound and interacts with it. It has the ability to modulate wound
healing in some cases. The intermediate (secondary) layer is bulky for absorbency and
padding. The outer (tertiary) layer holds the other layers in place, and provides protection.
Wound care practitioners are provided with an overwhelming plethora of choice with respect
to the contact layer, and many extrapolations are made between species, especially from the
human wound care industry to the veterinary practitioner. The contact layers will be
discussed in further detail. The contact layer acts to pack the wound, provide an appropriate
level of moisture for healing, maintain a warm temperature (35 37C), and ideal pH (~6).
The contact layer rests on the wound bed and may be adherent or non-adherent, occlusive,
semi-occlusive, non-occlusive (referring to moisture retention), or provide active negative
pressure.
Inflammatory phase dressings for early, exudative wounds:
Adherent wet-to-dry dressings: These dressings are indicated for the initial management
of the highly exudative open wound. They assist in the debridement of the wound, pulling off
dried exudate and debris as they are removed. The most commonly used adherent dressing
is the wet-to-dry bandage:
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Following surgical debridement and lavage, the wound is covered with sterile gauze sponges
barely moistened (wrung out) with sterile saline or an antibacterial solution such as 0.05%
chlorhexidine. The dressing is then covered with the secondary bandage layer of absorbent
material and finally by a protective tertiary layer. No plastic or occlusive covering should be
placed over the wound, as it will tend to retain moisture and macerate the wound. The wet-
to-dry bandage is allowed to dry and is removed dry. The bandage adheres onto the wound
during the drying process, thus removal of the bandage strips exudate and necrotic tissue
from the wound. The gauze should have wide mesh openings enabling entrapment of
necrotic debris and exudate as it is drawn into the drying gauze. The frequency of bandage
changes will vary from once to twice daily, depending on the amount of exudation and tissue
necrosis. Dry-to-dry dressings can be used in copious, low-viscosity exudates.
Although adherent dressings are effective in the early treatment of a wound, they have some
disadvantages: they are painful to change, they may injure cells and capillary buds upon
removal, they may desiccate the wound if they dry out too much, and they may macerate the
wound and strike through if they are too wet. Although they are very useful for the first
several days, these wet-to-dry dressings do not maintain an optimum environment for
wound healing after that time they are more of an aid to debridement and exudate
removal. Adherent dressings should be stopped once the wound has been adequately
debrided, even if it is before the appearance of granulation tissue.
Negative Pressure Wound Therapy: One of the mechanical adjuncts used in human
wound management to expedite the formation of granulation tissue and the healing of
difficult wounds involves the application of sub-atmospheric pressure to the wound. This
technique is known as vacuum-assisted closure (V.A.C.); negative pressure wound therapy,
or topical negative pressure therapy. Negative pressure is uniformly distributed to all tissues
within the wound in a sealed environment, thus converting an open wound into a controlled,
closed wound. This is achieved using open-cell polyurethane foam trimmed to the size of the
wound, and then placed on the defect. An adhesive plastic drape is applied over the foam
and adjacent skin to create a closed system. The vacuum is obtained through an evacuation
tube to the reservoir canister of a programmable vacuum pump.
Several mechanisms of action of topical negative pressure therapy have been investigated,
mostly regarding fluid movement and mechanical application of pressure. Application of a
controlled vacuum to the wound interface facilitates removal of excess interstitial fluid,
resulting in a decrease in wound edema. As interstitial pressure falls, the capillaries reopen
and blood flow to the wound and periwound tissue is increased. The mechanical deformation
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of the cells within and around the wound and shear forces that deform the extracellular
matrix have been shown to result in a higher mitotic rate and increased production of
granulation tissue.
The high rate of clinical success with negative pressure wound therapy in human medicine
has led to its adaptation not only by plastic surgeons, but also by thoracic surgeons (for
postoperative sternal infection and mediastinitis), general surgeons (for abdominal wall
defects) and urologic surgeons (for perineal, urologic and gynecologic wounds). Trauma and
orthopedic surgeons have started using V.A.C. to address complex wounds with extensive
soft tissue damage (e.g. wartime missile injuries) and wounds with exposed orthopedic
hardware, tendon and bone.
At MSU, we have been using the V.A.C. on traumatic wounds since 2005 with excellent
clinical results, both for wounds healing by second intention, and in preparing wound beds
for surgical reconstruction. We are particularly pleased with results on severe degloving
injuries, shear injuries with exposed bone, and wounds with orthopedic hardware. We have
conducted and published several studies, all of which appear to strongly validate this
modality in veterinary medicine.
Foam dressings are highly absorptive polyurethane or silastic foams that do not adhere to
the wound. They are extremely absorbent (even when compressed), and maintain a warm
(~35C), moist and well-oxygenated environment. Foam dressings are indicated in lightly
exudative wounds of relatively low viscosity. They are available as sheets, various shapes
and cavity forms as well. They can be left in the wound for much longer than traditional
dressings such as gauze - usually changed every three days. They are very comfortable and
not painful to remove, but may cause some maceration in highly exudative wounds, due to
their slightly occlusive nature.
Alginates are fiber sheets or rope made from brown seaweed (giant kelp), and are usually
composed of calcium alginate. They are non-occlusive, very absorbent and as they interact
with the wound they form a soft gel, which is haemostatic and also may entrap bacteria.
They are indicated in highly exudative wounds. They need to be left on the wound for around
three days to develop into the gel. This gel can then be easily removed from the wound, or
washed out. If the dressing is removed too early, before the gel has developed, fibers may
be left behind. Foam dressings and alginates can also be used together alginate as the
contact layer with the wound bed.
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Proliferative phase dressings for granulating wound beds:
Hydrogels consist of insoluble hydrophilic polymers with some absorptive capacity. They
provide a moist wound environment conducive to granulation tissue formation and
epithelialization. The partially hydrated gel that is in contact with the wound can donate or
absorb moisture, depending on wound conditions. These dressings are indicated in
granulating wounds, are non-painful, and can be left in place for 3 4 days. Formulations
include an amorphous gel product that is squeezed onto the wound and then covered with a
perforated film; or a sheet dressing. They have a tendency to produce hypergranulation
tissue, and are sometimes best used interchangeably with a film or petroleum-impregnated
dressing.
Hydrocolloids consist of a layer of insoluble gel (cellulose or gelatin) that absorbs and
retains wound fluid, backed by polyurethane foam backing. The gel that contacts the skin is
adherent, sealing the dressing. The gel in contact with the wound interacts with the wound
fluid and forms a non-adherent gel, providing a moist wound rich in growth factors,
promoting epithelialization. These are non-painful, and should be changed every 3 4 days.
Although promoted for many wounds in small animals, they are much more suited to chronic
or dry wounds or partial abrasions, rather than the exudative wounds. They also have a
tendency to produce hypergranulation tissue. I only use these in superficial burn wounds.
Perforated film dressings consist of a single layer of adhesive polyethylene film that allows
gas exchange, but is impermeable to bacteria and water. This maintains a moist wound
environment without maceration. This dressing can be used in mature granulating wounds,
or to cover other dressings (e.g., Hydrogels, foams, alginates). They accelerate
epithelialization, but may have a tendency to macerate if the wound is still exudative.
Petroleum-impregnated dressings are semi-occlusive and non-adherent, and indicated

once the wound is granulating. These dressings will promote contraction, but may delay
epithelialization.
Synthetic micropores are useful as post-operative dressings, or as a retention dressing, to

hold other dressings in place. They are non-adherent and semi-occlusive. If used on
granulating wounds without additional hydrogels, the wound may desiccate.
The main function of the intermediate layer in a bandage is its ability to absorb and store
exudate away from the wound. If a wound is highly productive, or if the bandage becomes
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soaked from the external environment, it will require frequent changing. This layer of the
bandage is primarily absorptive, so the material should have good capillary action. This layer
also protects against trauma, and acts as a splint to retard movement. It should be firmly and
evenly applied, conforming to the area. If the area is difficult to bandage (i.e., not a distal
extremity), looped sutures can be placed around the wound and the dressing and
intermediate layer laced onto the wound. Alternatively staples can be used, or tape.
Materials commonly used are synthetic cast padding material - very conforming and
excellent capillary action, cotton wool - good protection and absorption, but readily
saturated if wet, moderately conforming. Do not use plastic foam it will tend to become
saturated and unhygienic, will not absorb if compressed. Most importantly, it does not
breathe well and will macerate the wound.
The outer bandage layer serves to hold the other layers in place. This layer should be hardy,
porous, and may be adhesive or non-adhesive. Gauze cotton bandages (Kling) are useful as
the initial part of this layer to slightly compress the intermediate layer before placing the final
outer wrap, which is usually Vetrap or Elastikon. Elasticized bandages are ideal if applied
snugly and evenly, but can cause ischemic damage if too tight. Zinc oxide tape is not elastic
and is best used to prevent bandages from slipping (with the use of stirrups, or taping at
the top of the bandage).
Indications for systemic antibiotics:

Indicated for wounds with extensive deep tissue trauma.
Indicated for contaminated wounds in which primary closure must be attempted
(along with drain), due to exposure of vital structures.
Not indicated for open wounds that have been adequately debrided and lavaged.
Indiscriminate use will not decrease infection rates, but will ensure that infections that
do occur will be resistant to treatment.
Summary of Open Wound Management:

1. Clipping and cleansing of periwound and cleansing of open wound.
2. Debridement: Accurately excise necrotic tissue. Leave questionable tissue for later
debridement.
3. Thorough lavage - high volume, relatively high pressure, buffered solutions preferred.
4. Chlorhexidine 0.05% most efficacious as final antibacterial lavage, and for use in
wet-to-dry dressing.
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5. Wet-to-dry dressings and bandaging for early, highly exudative wounds. Alternatively,
NPWT for 3 days (or 6 days, occasionally longer), which will rapidly produce
granulation tissue, and one can go to Step 8.
6. (The above steps may need to be repeated daily in the early wound management
period, depending on contamination and soft tissue damage).
7. Once wound requires no further debridement, but is still exudative, change to
polyurethane foam or alginate dressings, until signs of early granulation tissue.
These dressings can be left in place for 3-4 days. Do not place occlusive material
over wound.
8. Once early granulation tissue is evident, an amorphous or sheet hydrogel dressing or
other semi-occlusive dressing can be used, changing every 3 4 days.
9. Mature granulating wounds or partial thickness excoriations can have a hydrogel or
perforated film dressing. Hydrocolloids can produce hypergranulation tissue.
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Notes page
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CHYLOTHORAX: BETTER NEWS?

Anatomy of the lymphatic vascular system

The lymphatic system consists of a tissue component and a vascular component. The tissue
portion plays a major role in immune defence mechanisms, whilst the vascular component of
the lymphatic system really acts as an auxiliary to the venous part of the vascular system.
The vascular component includes lymph capillaries, larger vessels and lymph transporting
ducts. As blood flows through capillary beds, significant amounts of fluid and proteins (up to
50% of the total circulating protein) escape into the interstitial compartment. This fluid
(generally clear and colourless) readily enters the lymphatic capillaries and returns slowly via
the lymphatic ducts to the systemic venous system cranial to the heart. Lymph typically
contains proteins and cells (polymorphonuclear cells, mononuclear cells and red blood
cells), but lymph from each region of the body has a characteristic composition. Lymphatic
villi in the intestines absorb emulsified fat and thus the lymphatic vessels (called lacteals)
appear milky or chylous. Small lymphaticovenous communications have been
demonstrated to nearly all the veins of the body, especially in the renal area. When a major
duct such as the thoracic duct is ligated, the lymphatic system opens up lymphaticovenous
anastomoses proximal to the obstruction. The small lymphatic capillaries are simple,
transparent endothelial tubes, but the larger lymphatic vessels are surrounded by poorly
organized smooth muscle and a thin fibrous adventitia. Upon gross inspection however,
even the larger vessels appear incredibly thin and difficult to identify. Flow of lymph depends
mainly upon movement of adjacent muscles, although some weak intrinsic contractions have
been noted. Large lymphatic vessels contain valves, and when obstructed, lacteals can
show a string of beads appearance.
Lymphatic drainage of the thoracic limbs and head and neck is via the lymph nodes to the
right and left tracheal trunks. The right tracheal trunk usually terminates into the venous
junction of the external jugular and the right subclavian. The left tracheal trunk usually
terminates into the thoracic duct. Lymphatic drainage of the pelvic limbs (via the iliac lymph
nodes) and the abdominal viscera (via the mesenteric lymph nodes) is to the cisterna chyli.
The cisterna chyli is a bipartite structure that lies retroperitoneally, closely associated with
the cranial abdominal aorta. The part that lies ventral to the aorta is plexiform, and extends
from the caudal pole of the left kidney to cranial mesenteric artery. It communicates via
variable connections to the part that lies dorsal to the aorta. This part is saccular, and
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extends from the left renal hilus to the celiac artery but can be quite erratic in location, and
sometimes even extends through the aortic hiatus of the diaphragm before it narrows into
the thoracic duct. The thoracic duct is the main channel for the return of lymph from the
caudal body and abdominal viscera; it is the cranial continuation of the cisterna chyli. Its
exact point of origin is variable, depending on the rather erratic location of the cisterna chyli.
It seems to begin mostly as a single duct, but can then become quite plexiform in nature -
most notably in the caudal thorax. It is closely associated with right dorsal aspect of the
thoracic aorta until the level of the sixth thoracic vertebra, where it traverses to the left side,
running cranioventrally to terminate in the junction of the left external jugular vein and the
cranial vena cava.
Aetiologies of chylothorax
Chylothorax is defined as the accumulation of chyle within the pleural cavity. It does not
occur commonly, but is seen on a regular basis in referral institutions, and can be
devastating for both animal and owner. Reported aetiologies for free chyle collecting in the
thorax in both dogs and cats include right-sided cardiac failure (cardiomyopathy, congenital
anomalies), pericardial disease, diaphragmatic malformation, diaphragmatic hernia,
mediastinal neoplasia (lymphoma, thymoma, heart based masses), granulomas,
lymphangiectasia, lung lobe torsion, jugular venous thrombosis, dirofilariasis, blastomycosis,
and traumatic or iatrogenic rupture of the thoracic duct. Generally when the thoracic duct has
been lacerated (trauma or surgery) the resulting chylothorax tends to resolve with simple
drainage, as the duct heals rapidly.
In most presentations, no specific underlying cause is identified and the condition is termed
idiopathic. Very little is known about the underlying pathology of idiopathic chylothorax. It
is suspected that some type of mediastinal lymphangiectasia causes a lymphatic
obstruction, possibly associated with a transmural insufficiency that allows chyle to leak
through the thin endothelial walls of the thoracic duct. Breeds of dogs reported to be
predisposed are Afghan hounds, Borzois, Salukis, and Mastiffs. However, it can be seen in
any breed or mixed breed, including Labrador Retrievers, Golden Retrievers, Shelties,
German Shepherd dogs, etc. Chylothorax is also seen in cats - there may be a
predisposition to Oriental breeds. Cats tend to develop fibrosing pleuritis more readily than
dogs with chylothorax, although with chronicity the pleurae become thickened in all animals.
Diagnosis of idiopathic chylothorax

Clinical signs of pleural effusion include: increased respiratory rate (sometimes with
abdominal effort), restrictive breathing pattern, lethargy, inappetance, exercise intolerance,
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coughing and occasionally vomiting. Physical examination typically reveals muffled heart
sounds, decreased lung sounds ventrally and increased dorsally, and occasionally cyanosis
(depending on severity). There is a lack of resonance upon thoracic percussion. Weight loss
occurs with chronicity.
Differential diagnosis of pleural effusion includes hydrothorax, hemothorax, pyothorax and

chylothorax. A thorough work up (which is largely to rule out an underlying cause) includes
complete blood count, serum biochemistry, heartworm test, thoracic and abdominal
radiography, abdominal ultrasonography, echocardiography, pleural fluid cytology and
analysis, pleural fluid culture. Thoracocentesis is required to obtain pleural fluid sample for
definitive diagnosis and will often provide relief of respiratory distress if a significant volume
of fluid is removed. The technique is typically performed through the right 5 th intercostal
space, with the animal in sternal recumbency, using a butterfly or veress needle, extension
tubing and a 3-way stopcock. Aseptic technique is indicated. Chyle is classed as a modified
transudate (protein > 2.5 g/dL, cell count 6,000-7,000), with predominant cell types
lymphocytes and non-degenerate neutrophils. With chronicity, more macrophages can be
present. The fluid has a characteristic milky white or milky pink appearance to it and special
staining will reveal the presence of chylomicrons. Definitive confirmation of chyle is obtained
by demonstrating increased triglycerides concentration and decreased cholesterol
concentration compared to the serum levels. Thoracic CT will provide a more thorough
assessment of intrathoracic structures, and is typically performed before definitive surgical
intervention is undertaken.
Management options
This condition can be extremely challenging to manage successfully. Failure to resolve the
pleural effusion is frustrating to client and clinician, and potentially devastating to the animal.
Over the years several numerous medical and surgical interventions have been employed,
with varying degrees of success. Medical management consists of dietary modification (to
decrease fat absorption into the lymphatic system), and pharmaceutical intervention (to
decrease chyle volume and thoracic duct flow) such as rutin or octreotide. Corticosteroids
and diuretics have also been used. During medical management protocols, the thorax must
be repeatedly drained to maintain comfort. Typically, idiopathic chylothorax is refractory to
medical management, and major surgical intervention is frequently required. The goal of
surgical intervention is to divert chyle flow away from the thoracic duct system, drain pleural
accumulation of chyle, or facilitate flow into the systemic venous system through pressure
changes. Many different procedures have been described including passive or active
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pleuroperitoneal shunting, pleurovenous shunting, pleurodesis, thoracic omentalization,

cyanoacrylate instillation, pericardectomy, thoracic duct ligation and cisterna chyli ablation.
Although the most effective choice of surgical intervention has yet to be definitively validated,
individual or en bloc ligation of the thoracic duct and all identifiable collaterals has been at
the core of surgical treatment. Thoracic duct ligation is typically performed through a right
caudal intercostal approach in the dog, and left caudal intercostal approach in the cat.
Complete resolution of chylothorax with thoracic duct ligation alone is reported in ~ 60% of
cases, even when pre- and post-ligation lymphangiography and vital staining (using
methylene blue) is performed to identify anatomic variations of the thoracic duct network. In
a low percentage of animals, a non-chylous effusion can continue.
Over the past decade, several adjunctive surgical procedures to thoracic duct ligation have
been reported that appear to have improved outcomes. These include cisterna chyli
ablation and pericardectomy. The aim of cisterna chyli ablation is to destroy the cisterna
chyli (the collecting reservoir into which the intestinal lymphatics drain, and from which chyle
drains into the thoracic duct) which completely disrupts the flow of chyle into the thoracic
duct. The aim of pericardectomy is to decrease right-sided venous pressure, thus facilitating
drainage of the chyle into the venous system. When either of these techniques is performed
concurrently with thoracic duct ligation, success rates for resolution of chylothorax increase.
Recent comparison of outcomes after various combination of these procedures suggest that
thoracic duct ligation + cisterna chyli ablation will have a superior outcome compared to
thoracic duct ligation + pericardectomy. Many surgeons will undertake all of these
procedures (i.e., thoracic duct ligation, cisterna chyli ablation and pericardectomy) in an
effort to optimize outcome for their patients.
Each of the previously mentioned procedures has been described with separate approaches
- typically a right 9th or 10th intercostal thoracotomy for thoracic duct ligation (left in cats),
followed by median celiotomy for cisterna chyli ablation, and a 4th or 5th intercostal
thoracotomy for the pericardectomy. Procedural modifications have now been developed
which decrease operative time and patient morbidity, without compromising outcome. Such
modifications include endoscopic approaches (either transdiaphragmatic through the
abdomen or thoracoscopic), and a single, paracostal approach to provide surgical access to
both the cisterna chyli and the thoracic duct. These techniques appear to substantially
decrease postoperative discomfort and hospitalization time. In the paracostal approach,
dogs are positioned in left lateral recumbency with the thoracolumbar region elevated by a
rolled towel bolster. A right-sided, dorsal, paracostal approach allows access to the
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dorsocranial right abdomen and the retroperitoneum where the cisterna chyli is located.
From this approach, the diaphragm can be retracted caudally; then incised parallel to its
costal attachment. By placing stay sutures into the pars costalis, the diaphragm can be
manipulated to expose the right caudal thorax and retropleural space and thus the thoracic
duct. Also from this single approach, the mesenteric lymphatics (either lymph node or
vessel) can be accessed to introduce dye to highlight the cisterna chyli and thoracic duct.
This vital staining is essential before undertaking any dissection near the thoracic and
abdominal aorta, as the nearly invisible thoracic duct and cisterna chyli are closely
associated with the aorta. Once the cisterna chyli and thoracic duct are identified by their
blue coloration from the vital staining, careful dissection around the thoracic duct can be
performed, and the duct and any collaterals can be ligated close to the diaphragm. At this
stage, the cisterna chyli tends to plump up and the structure can be more clearly exposed
with careful dissection, before its destruction by tearing it gently away from the underlying
aorta. Closure of the diaphragm and abdomen is routine. The paracostal approach, with its
low morbidity, can be performed bilaterally under one anesthesia, or staged if chylous
effusion persists due to the presence of a right-sided thoracic duct collateral. Pericardectomy
is usually performed through a right 5th intercostal thoracotomy or thoracoscopically. It
appears better to remove as much pericardium as possible, which is usually to the heart
base on the right and to the phrenic nerve on the left.
Another technique that has decreased the morbidity associated with repeated thoracic
drainage is the placement of a subcutaneous pleural port, leading to a fluted or fenestrated
thoracic catheter. Placement of this device eliminates the need for a post-operative thoracic
drain, and allows for early discharge from critical care into either the ward or into the home.
Drainage is then accomplished by the transcutaneous insertion of a 19 gauge Huber needle
into the port, and 3-way stopcock. Chylous effusion can sometimes persist for up to a month
in some cases of chylothorax, before finally resolving (continued leakage through the aortic
hiatus?), so the ability to repeatedly drain the pleural cavity with virtually no discomfort to the
animal is most valuable.
Overall success rates are probably around 80-90% when all three procedures (thoracic duct
ligation, cisterna chyli ablation, pericardectomy) are performed. If chylous effusion persists,
we recommend reoperation on the left side through a paracostal approach, or intermittent
drainage through the pleural port on a long-term basis. A few animals will develop a non-
chylous effusion. All animals with pleural effusion are susceptible to lung lobe torsion.
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Summary points
1. Idiopathic chylothorax is a serious condition that is poorly understood.
2. Further basic research is indicated to elucidate the underlying aetiology and
pathophysiology.
3. Further clinical research is indicated to validate the best combination of interventions
to maximize outcomes, including the cost-effectiveness of various lymphangiographic
procedures.
4. Although we have improved management over the last decade, we need to strive for
better outcomes.
5. It is prudent to provide means of regular, intermittent drainage (i.e., subcutaneous
pleural ports)
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ANTIBIOTICS; USE AND MISUSE

khumm@rvc.ac.uk
There are probably very few vets working in first opinion small animal practice who work a
day without prescribing an antibiotic for a patient. Recent studies showed that antibiotics are
prescribed in a third to half of veterinary small animal consultations with the broad spectrum
antibiotic potentiated amoxicillin being the most commonly prescribed drug in dogs and cats.
In rabbits fluroquinolones were the most commonly used antibiotics. Both studies showed
marked variation in antibiotic usage between individual vets which suggests that antibiotics
are being administered inappropriately in some cases.
The risks associated with antibiotic misuse are familiar to us but easy to forget or ignore
when in a consultation. When we administer an antibiotic to an animal we select for
resistant bacteria in every area of the patient that is colonised, predominantly the
gastrointestinal tract and the skin. The longer the antibiotic is administered for the greater
this selection pressure. Bacterial resistance is not caused by antibiotic use but it does result
in selection pressure for these organisms. If they are pathogenic this can be detrimental for
the patient and if they are commensal they can transfer resistance to pathogenic bacteria.
Resistance can be classified as inherent or acquired:
Inherent resistance refers to an inherent feature of the organism that makes it

resistant to a particular antibiotic. For example, anaerobic organisms are inherently
resistant to aminoglycosides because the drug needs to be actively transported into
the cell by an oxygen dependent carrier. Gram positive organisms lack an outer cell
membrane and therefore are inherently resistant to polymyxin B which targets cell
membrane. Mycoplasma has no cell wall and is therefore resistant to beta lactam
antibiotics, which target the cell wall.
Acquired resistance is unpredictable and can occur during the course of therapy. It
can also be shared among bacteria and can spread rapidly. There are two types of
acquired resistance:
Chromosomal resistance: DNA can be misreplicated in all species including
bacteria, resulting in mutation. This could lead to resistance to a particular
antibiotic which gives it a survival advantage. This type of resistance occurs
slowly as misreplication is not common and the likelihood of a mutation
causing antibiotic resistance will be very small.
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Plasmid mediated resistance: plasmids are small pieces of DNA carried by

some bacteria. These can carry genes that give resistance to one or several
antibiotics. Plasmids can be transferred between bacteria. This type of
resistance can spread very quickly.
Resistance can manifest in different ways. For example, it may allow production of enzymes
that inactivate the antimicrobial or it may lead to mutation of the target site so that the
antibiotic can no longer bind to the microbe. The use of an antibiotic does not create
resistance per se; however, if a few of the microbes have a mutation that renders them
resistant to the antibiotic, they will have a survival advantage and flourish in the presence of
the drug. This can have deleterious effects on the animal being treated and on the
community as a whole.
One of the most important approaches to reduce resistance is to observe our antimicrobial
usage and make the required changes:
1. Do not use antimicrobials when an alternate therapy is available; this includes no

therapy in some cases. For example, a dog with acute diarrhoea or a sneezing cat is
unlikely to need antibiotics if they are systemically well. It is also worth noting that
placement of a urinary catheter or thoracostomy tube does not in itself require the
administration of antibiotics. Tubes and lines will become colonised with bacteria
and administering antibiotics will select for a resistant population.
2. Design a treatment regime that minimises resistance:
If possible a narrow spectrum antibiotic should be used. Appropriate
antibiotic selection requires knowing the pathogen involved and the results of
culture and sensitivity testing. However, this may not be practical in some
cases and empirical choices will be made. Knowing the most likely
pathogens associated with different organ system infections helps in these
cases. BSAVA in conjunction with SAMSoc issued the PROTECT poster
where specific suggestions of appropriate antimicrobials for selected
bacterial diseases are made and the BSAVA website also offers advice on
antibiotic usage (see Further Reading).
The correct dosage at the correct frequency should be used; this will
maximise bacterial killing and minimise the window for resistance to develop
(dead bacteria cant mutate!). It is worth telling owners how frequently to
administer the drug in terms of every 12 hours rather than twice daily.
The duration of therapy is also important. Generally, the duration of therapy
should be 2-3 days beyond the resolution of clinical signs. However, this
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may not be as straightforward as it sounds particularly if there are no discreet

clinical signs that are easy to monitor. The longer the better approach is
inappropriate and evidence suggests that long courses of therapy lead to an
increase in the emergence of resistance. In humans five days of therapy are
used for intra-abdominal infections and community acquired pneumonia and
three days for uncomplicated cases of pneumonia. The extrapolation to
veterinary medicine is difficult, but it is likely that short courses of
antimicrobials are appropriate in most cases and reduce the risk of
resistance. Exceptions may include immune-compromised patients or where
the affected site has poor blood supply/healing. In general, for
uncomplicated infections, the duration of therapy should be less than 7 days.
Combination of antimicrobial therapy may be a powerful tool to increase the
spectrum in polymicrobial infections and occasionally, the combination of
antimicrobials may be effective against a given microbe when each drug on
its own is infective. This is called synergism. For example, the combination
of trimethoprim and a sulphonamide leads to synergism through their action
on different parts of the same metabolic pathway. Clavulanic acid increases
the spectrum of a beta lactam by inactivating the beta-lactamase activity of
the microbe. Beta lactams and aminoglycosides can be synergistic by killing
bacteria through different pathways. Despite the fact that these synergistic
actions are useful in some difficult cases, the combination of antibiotics
should not be done randomly and without the support of culture and
sensitivity testing. Increasing the antimicrobial spectrum without a good
reason is not good practice.
Routine use of antibiotics used to treat life threatening infections in humans
(fluoroquinolones, third and fourth generation cephalosporins) should be
avoided in veterinary medicine. These antibiotics should not be first choice
options and failure to adopt these measures may mean that restrictions are
placed on veterinary use of these drugs. Last resort antimicrobials such as
vancomycin and imipenem should not be used in veterinary patients.
Prophylactic use of antibiotics should be avoided. There are specific
situations where it is done:
Immunocompromised patients: in neutropaenic patients antimicrobials
may be given to reduce the gastrointestinal flora, which is the most
common source of infection in these patients (through gastrointestinal
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translocation). Trimethoprim sulphonamide is the first choice in these

cases.
Dentistry and prevention of chronic recurrent infections (e.g. skin)
Surgical prophylaxis: the aim of surgical prophylaxis is to reduce the
microbial load in the surgical wound to prevent a clinical infection.
The contaminating bacteria can access the wound from external
sources (the environment, the surgical instruments, personnel, etc.)
or from endogenous sources (the skin, mucosal surfaces, blood, etc.).
Surgical prophylaxis is not a substitute to adequate sterility. Clean
surgical wounds (such as those not involving the GI or respiratory
tract) do not require prophylactic antibiotic therapy unless the
consequences of infection are serious (e.g. hip replacement or
placement of a pacemaker). Clean contaminated wounds (e.g.
enterotomy where there is no spillage) are often managed with
prophylactic antimicrobial therapy as detailed below. Contaminated
wounds (e.g. bite wound or intestinal surgery with spillage) should be
treated as infected and managed with pre and post-surgical
antimicrobial therapy. Key considerations in surgical prophylaxis are:
Ideally, a dose of intravenous antibiotic is given at the time of
anaesthetic induction and another dose at the time of
completion. This will achieve tissue levels at the time of
bacterial contamination risk. If the surgery lasts longer than 3
hours, then additional doses can be given during the
procedure.
In the absence of a documented infection, there is no rationale
for continuing antibiotics post-operatively. If contamination
during the surgery is documented (for example, spillage in an
enterotomy) then antimicrobials should be continued beyond
the post-operative period.
Potentiated amoxicillin or a first generation cephalosporin are
good choices for surgical prophylaxis as they will cover the
pathogens that are most likely to infect the surgical wound. If
there is likely involvement of anaerobes (e.g. surgery of the
lower gastrointestinal tract) then metronidazole can be added.
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3. Decontamination: reducing bacterial exposure is one of the most important ways to

avoid future antimicrobial usage and resistance. This includes disinfection of the
environment, effective hand washing and use of gloves, and reducing exposure to
contaminated areas by separating work areas.
When selecting antimicrobials to treat infections consideration of which bacteria are likely to
be involved should be made and the antimicrobial with the narrowest spectrum that will be
effective against that pathogen should be used. This may require using cytology and culture
to diagnose the bacterial infection correctly. Then drug penetration of the affected tissue
should be assessed. In some cases, debridement of the area and removal of any necrotic
tissue will be required to improve tissue penetration. Any potential side effects of the
antimicrobial should also be considered at this stage. The PROTECT website discusses
appropriate antibiotic choices for many common bacterial diseases.
Acknowledgement
With thanks to Patricia Ibarrola with her help with these notes
Further Reading
BSAVA website PROTECT project (free access):

http://www.bsava.com/Advice/PROTECT/Antibacterialuseincompanionanimals/Antibacterialr
esistanceincompanionanimals/tabid/1677/Default.aspx
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Notes page
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ADVANCED THERAPEUTICS FOR RENAL DISEASE

khumm@rvc.ac.uk
Introduction
Acute kidney injury (AKI) is a common emergency presentation. My previous lecture Acute
Kidney Disease: An Update discusses diagnosis of AKI. These notes discuss the optimum
medical management of intrinsic acute kidney injury which can be performed in general
practice followed by details on renal replacement therapy. Patients suffering from AKI
progress through an initiation phase when the AKI-inducing insult occurs; an oliguric phase
when they develop olig- or an-uria, a polyuric phase and then a recovery phase. Our
patients usually present in the oliguric or polyuric phase.
Emergency management of the AKI patient

Many patients suffering from AKI require stabilisation. Therapy may also be necessary to
prevent worsening of the kidney injury. It is important to rapidly assess the patients
perfusion status and address hypoperfusion or dehydration with fluid therapy to improve
renal perfusion. Fluid therapy also often leads to the correction or improvement of
electrolyte and acid-base disturbances, particularly if they are mild and so therapy for these
can be withheld in many cases until the effect of fluid therapy is seen. This is not the case
for severe symptomatic hyperkalaemia however. Hyperkalaemia is a common electrolyte
disturbance in AKI patients, potentially leading to bradycardia and arrhythmias and this may
require rapid treatment if the effects are marked. The patients cardiovascular system
should be carefully assessed to decide whether calcium gluconate therapy is required.
Other electrolyte disturbances, such as hypo- and hyper-natraemia and chloraemia,
hyperphosphataemia and hypocalcaemia, are less likely to require therapy but this can be
considered after fluid therapy has been initiated. Metabolic acidosis is common in the AKI
patient and can be severe. If the patient has a venous pH lower than 7.15 bicarbonate
therapy may be necessary. The BSAVA Canine and Feline Emergency and Critical Care
manual is a good resource for details on therapeutics for electrolyte and acid-base
disturbances.
If a toxic cause is known or suspected for AKI then decontamination should be performed
and any known antidote administered. Specific therapies to eradicate any known or
suspected causes of AKI should be implemented. If there is any suspicion of pyelonephritis,
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broad-spectrum antibiotics that concentrate in the urine, such as amoxicillin-clavulanate or

ampicillin, should be administered intravenously until the disease has been ruled out via
negative urine culture. Dogs that do not have evidence of another cause of AKI should be
treated with antibiotics that target Leptospira spp. while diagnostics are pending.
Intravenous ampicillin or amoxicillin is commonly used initially to reduce multiplication,
shedding and transmission of the organism. Oral tetracyclines, such as doxycycline, or
fluoroquinolones are then used for elimination of the carrier state.
It is also extremely important to avoid any nephrotoxic drugs in these patients such as non-
steroidal anti-inflammatory drugs or radio-opaque contrast agents. Agents which cause
hypotension, including most general anaesthetics and many sedative agents, will decrease
GFR and so should also be avoided if possible. The patients blood pressure should be
measured as hypotension can be seen in hypovolaemic patients or those with other forms of
hypoperfusion and hypertension can occur secondary to AKI. Both conditions require
prompt treatment as they can exacerbate AKI and can also lead to damage to other organs.
Finally, in many patients with AKI the placement of a urethral catheter can be very helpful to
allow assessment of urine output and specific gravity, as well as potentially aiding treatment
of the underlying disease process in post-renal AKI. Urethral catheterisation can also
prevent urine scalding and discomfort in polyuric or immobile patients improving their
welfare.
Supportive therapies
Correction of underlying fluid deficits, electrolyte imbalances and acid-base disorders with
fluid therapy is the mainstay of supportive care for dogs and cats with AKI. Intravenous
fluids have traditionally been administered at high rates in an attempt to maximize renal
blood flow (RBF) and glomerular filtration rate (GFR). However, increasing fluid
administration does not always result in increased urine production and may lead to fluid
overload especially in oliguric and anuric patients. Furthermore, fluid overload has been
associated with increased mortality in humans with AKI. However, high rate fluid therapy is
appropriate if the patient is hypovolaemic, which, although uncommon, can occur in AKI
patients. Once hypovolaemia is corrected, fluid therapy should aim to provide the patients
daily maintenance fluid requirement (33 to 44 ml/kg/d), correct underlying dehydration and
provide for on-going losses such as vomiting and diarrhoea. After fluid deficits have been
replaced, polyuric patients should ideally then receive the volume of urine they are producing
in addition to their maintenance fluid requirements.
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It is very easy to fluid overload oliguric and anuric AKI patients. Placement of a urinary
catheter allows fluid balance to be assessed much more accurately. Patients with clinical
evidence of fluid overload e.g. weight gain, chemosis, peripheral oedema (particularly easy
to note as swelling around hock, Achilles tendons and inter-mandibular space),
exophthalmos, serous nasal discharge, ascites or pleural fluid and tachypnoea or dyspnoea
with pulmonary crackles and oedema do not require any fluid therapy until their overload has
resolved although they should be monitored closely during this period.
If oliguria or anuria persists once hydration and volume deficits have been corrected drug
therapy to increase urine production is required. Furosemide exerts its diuretic effects by
inhibiting the Na+-K+-2Cl- co-transporter located on the apical membrane of the renal tubular
cells of the thick ascending limp of the loop of Henle. The diuretic and natriuretic effects of
furosemide are dependent on its delivery to the nephrons. In AKI effective GFR is hugely
decreased and so furosemide may not be delivered to its site of action. The use of
furosemide in human patients with AKI is controversial. Large-scale human clinical trials
have not shown consistent results in the effectiveness of preserving RBF or shortening
hospital stay. Because similar results were also found in several veterinary studies, in which
healthy dogs and cats treated with furosemide did not show an increase in GFR or RBF, the
benefit of using furosemide in AKI patients may solely rely on its diuretic effect. Furosemide
administration may heighten the patients tolerance to on-going fluid therapy due to its ability
to alleviate and prevent fluid overload.
Mannitol elevates plasma osmolality resulting in expansion of the intravascular volume and it
is also an osmotic diuretic as it is filtered freely through the glomeruli and is not reabsorbed
by the renal tubules. There are currently no prospective clinical trials investigating the use of
mannitol in veterinary patients with AKI. Nevertheless, mannitol was shown to preserve
some form of autoregulation of RBF in experimentally induced renal ischaemia in healthy
anaesthetised dogs. In healthy awake cats, mannitol infusion failed to have any significant
impact on urine output, GFR and RBF. Because mannitol cannot be adequately excreted by
the kidneys in anuric and oliguric animals, it is contraindicated in volume-overloaded patients
as it may result in severe hyperosmolality and hypervolaemia leading to pulmonary oedema
and/or congestive heart failure.
Dopamine is a catecholamine neurotransmitter produced from L-Tyrosine. At an infusion

rate of 0.5-3 g/kg/min, dopamine activates both DA-1 and DA-2 receptors resulting in
vasodilation of the interlobular arteries, afferent arterioles and, to a lesser extent, efferent
arterioles, leading to an increase in GFR and RBF. Other proposed benefits of dopamine
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include natriuresis and diuresis. Adverse effects of dopamine infusion include

gastrointestinal ischaemia, inhibition of immune functions and, at higher doses,
tachyarrhythmia, and hypertension. A number of human studies have shown no beneficial
effects of low-dose dopamine for the treatment of AKI. Studies investigating the use of
dopamine in veterinary patients with AKI are limited. Due to the potential adverse effects of
dopamine and its lack of documented benefits on renal haemodynamics and urine output in
dogs and cats, the author does not recommend the routine use of dopamine infusion in
oliguric or anuric AKI patients.
Fenoldopam is a selective DA-1 agonist, which has shown promising results in human
clinical trials of AKI as a renal vasodilator. Canine and feline experimental models have
shown it to induce diuresis but clinical trials evaluating its efficacy in dogs and cats with AKI
have not yet been performed. Fenoldopam is currently not available in the UK.
Electrolyte and acid-base abnormalities

Severe to life-threatening hyperkalaemia is a common electrolyte abnormality in AKI patients
with oliguria and anuria. Besides ensuring adequate urine output, additional therapies with
calcium gluconate, insulin and glucose and sodium bicarbonate are indicated in
hyperkalaemic patients with bradycardia and bradydysrhythmias. However, the resolution of
hyperkalaemia by medical therapies is only transient if olig/anuria persists. These patients
often require frequent monitoring of electrolytes, repeated medical therapies (generally
insulin and glucose and/or sodium bicarbonate) and, in selected cases, renal replacement
therapies, to manage their on-going hyperkalaemia.
Hypokalaemia and hypernatremia are commonly encountered during the recovery phase of
AKI when patients are profoundly polyuric. Hypernatremia can be corrected with appropriate
volume replacement, whereas hypokalaemia requires potassium supplemented fluids. In
general, hypernatremia that persists for more than 48 hours should be corrected slowly at a
rate no greater than 0.5 mEq/l/hr in order to avoid the development of cerebral oedema.
Metabolic acidosis may be severe in patients with AKI due to the abrupt decrease in renal
excretion of hydrogen ions, ammonium, and phosphorus. Patients with ethylene glycol
toxicity also suffer from severe metabolic acidosis. Although the usual treatment for
metabolic acidosis is treatment of the underlying cause this is not possible in anuric and
oliguric patients without renal replacement therapy and so bicarbonate therapy may be
required if the patients pH is less than 7.1.
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Serial monitoring of electrolytes and acid-base status is important for appropriate adjustment
of therapies based on the results. Initially blood sampling may be required frequently in
unstable patients (often approximately 6 times a day) and so long-stay catheter placement
may be beneficial. Once the patient is stable then sampling is required less frequently.
Management of Polyuria and Patients in Recovery Phase

Patients recovering from anuric, oliguric or non-azotaemia AKI are often polyuric. This
recovery phase may last from weeks to months. In these patients, the matching of ins and
outs is vital in order to avoid a negative fluid balance. Daily assessment of hydration status
including skin turgor and body weight is essential. Once the patient is stable, eating and
drinking with azotaemia resolved or plateaued, fluid administration can be tapered slowly by
about 25% daily. During this period, urine production, serum creatinine and the patients
hydration status should be monitored diligently in order to ensure that the kidneys are
capable of maintaining fluid balance. If the decrease of urine production corresponds well
with the decrease of fluid administration and without weight loss and the return of azotaemia,
fluid therapy can be further tapered. It should be noted however, that azotaemia and
polyuria may not completely resolve if there is permanent damage to the kidneys and will not
resolve in patients suffering from an acute on chronic renal insult. In these patients,
monitoring body weight and signs of dehydration will guide whether fluid therapy can be
stopped.
Systemic Hypertension
Systemic hypertension is a common complication seen in approximately 80% of cats and
dogs with AKI. The likelihood of hypertension is not related to the severity of the patients
azotaemia. For that reason, blood pressure monitoring every 8 to 12 hours is recommended
in all AKI patients. In general, non-invasive blood pressure monitoring such as Doppler with
sphygmomannometry or oscillometric monitoring are economic and user-friendly methods to
assess blood pressure in most veterinary practices. The decision to initiate anti-
hypertensive therapies is based on the severity of hypertension and risk of target organ
damage (see ACVIM consensus statement below in Further Reading which is freely
available on the web for guidelines for treatment of hypertension).
Gastrointestinal complications
The pathogenesis of vomiting in AKI patients is multifactorial and usually involves direct
stimulation of the chemoreceptor trigger zone by uremic toxins and hypergastrinemia
resulting in elevation of hydrochloric acid secretion and associated gastric ulcers and
gastritis. For that reason, the administration of centrally mediated anti-emetics such as
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maropitant and antacids such as omeprazole or famotidine is beneficial in symptomatic

patients.
Nutritional management
AKI, like many disease processes, results in a catabolic state, which causes breakdown of
proteins leading to exacerbation of hyperphosphatemia, hyperkalaemia and elevation of
blood urea nitrogen. Because most animals with severe uraemia are often anorexic due to
gastrointestinal ulceration and nausea, nutritional support is recommended until medical
therapies have reduced the severity of azotaemia and gastrointestinal complications. If
patient is not vomiting, enteral supplementation can be administered via naso-oesophageal,
oesophagostomy or PEG feeding tubes. Naso-oesophageal tubes are generally the tube of
choice as they are tolerated well by most severely ill animals, relatively easy to place and do
not require general anaesthesia. The author does not recommend force feeding as it does
not generally provide adequate caloric support and may predispose patients to aspiration. It
is important to note that fluid infusion should be adjusted accordingly if enteral or parenteral
nutrition is provided to prevent fluid overload.
Renal Replacement Therapies

Renal replacement therapy (RRT) is a term used to describe treatments which attempt to
accomplish the functions performed by healthy kidneys whilst awaiting return of the patients
renal function or pending renal transplant. Renal replacement therapies always use a semi-
permeable membrane to achieve blood purification. They can be intermittent or continuous,
and can involve any of 4 mechanisms:
Diffusion: The movement of a solute from a fluid of high concentration to a fluid with
a lower concentration, generally from the blood into the dialysate (the fluid on the
other side of the semi-permeable membrane)
Convection (or solvent drag): The movement of large solutes through the force of
water from the blood into the dialysate. This is increased when the pressure
differential across the semi-permeable membrane is higher and the flow rate of the
blood is faster.
Adsorption: The attachment of solutes to a material surface. This happens to a
small extent on the dialyser membranes, but this effect is maximised in some
patients when an adsorbent (usually activated charcoal) is added to the circuit. This
technique is known as haemoperfusion.
Ultrafiltration: The movement of water from an area of higher pressure to lower
which would usually be from the blood into the dialysate
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Effectively RRT is a treatment that removes waste products, salts and excess water from the
body. The modalities of RRT used in veterinary medicine are peritoneal dialysis (PD), and
the extracorporeal therapies intermittent haemodialysis (IHD) and continuous renal
replacement therapy (CRRT). RRT is indicated in severe cases of AKI in which renal
function is expected to be reversible. There are no definitive guidelines for when RRT is
indicated in our patients, but animals which are anuric or severely uraemic with life-
threatening electrolyte abnormalities benefit most from RRT. Patients undergoing RRT
require close monitoring and technically challenging patient care in an intensive care setting.
Clinicians and nursing staff with advanced knowledge of renal physiology and the mechanics
for the specific RRT modality are required. Referral, if appropriate, should occur early, as a
delay in extracorporeal therapy results in higher morbidity and mortality in human studies.
Peritoneal dialysis
Of the 3 RRT techniques discussed this is the only one that does not require expensive
equipment but it should be realised that managing a patient with AKI through PD is not
simple and 24 hour committed intensive care is required for success. The method relies
upon the peritoneal membrane acting as the semi-permeable membrane, allowing diffusion
of excess body fluids and uraemic solutes from the blood into the infused peritoneal fluid.
Peritoneal catheters can be placed either with local anaesthetic in the unstable conscious
patient (trochar style catheters) or with the patient under general anaesthesia. For both
procedures sterility is of optimum importance and so the patient should be carefully clipped
and aseptically prepared. Surgical placement of catheters is preferable if possible as this
allows an omentectomy to be performed and optimal placement of drains decreasing the
likelihood of catheter blockage which is a common complication in PD. Commercially
prepared dialysate solutions are available but they can also be prepared in house as long
as a strict aseptic protocol is followed. Lactated Ringers solution with added dextrose can
be used with further details available in the JVECC review (Ross and Labato, 2013) noted
below in Further Reading. Dextrose is required to increase the tonicity of the dialysate
which facilitates the removal of water from the fluid overloaded patient and it also promotes
convection. Heparin also should be added to a dialysate solution for the first few days to
decrease the risk of catheter occlusion but systemic absorption is low and a coagulopathy
should not result.
Once the patient has a peritoneal catheter in situ it can be attached to a three way tap
allowing influx of the dialysate through one access point and drainage through another into a
sterile collecting system. Strict asepsis is required with a sterile technique required prior to
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changing dialysate bags or any lines. Connections should be covered with chlorhexidine
soaked dressings covered with sterile gauze or povidone-iodine connection shields.
Dialysate volumes are kept low for the first 48 hours to decrease the likelihood of leakage
but after this point 20-40ml/kg of body temperature dialysate can be infused over a ten
minute period. A dwell time of 30-40 minutes is recommended prior to fluid drainage. This
cycle can be repeated as frequently as required.
PD is not recommended in patients that have undergone recent abdominal surgery,

particularly gastrointestinal surgery as the risk of dehiscence is increased. Complications
include; dialysate retention due to catheter occlusion, hyperglycaemia, hypokalaemia,
dialysate leakage into the subcutaneous tissue, hypoalbuminaemia, over-hydration and
hypothermia. Many of these can be managed but bacterial peritonitis can be fatal or lead to
the owners electing to end attempts at RRT. The risk of this complication can be decreased
hugely by appropriate aseptic technique. Dialysis disequilibrium is a complication that can
occur with any of the RRT methods discussed. It occurs when the osmolality of the serum is
rapidly decreased leading to a difference in osmolality with the brain cells. Water flows into
the brain cells causing cerebral oedema, increased intracranial pressure and therefore
neurological dysfunction. This is very rare and particularly so in PD as it is generally not as
efficient as other RRT methods.
The outcome of patients undergoing PD is fair given the severity of their disease process.
Retrospective studies have shown that approximately 45% of cats (Cooper and Labato,
2011) undergoing PD due to AKI survive but the case selection affects these figures.
Continuous renal replacement therapy

CRRT involves removal of blood from the patient which is then passed through a dialysis
machine where unwanted solutes and fluid are removed via the processes of diffusion,
convection, ultrafiltration and absorption. Diffusion, ultrafiltration and convection occur due
to exposure of the blood to the dialysate (which is free of the unwanted solutes) through a
semi-permeable membrane. Adsorption is achieved through passage of the blood over an
adsorbent, generally activated charcoal. This allows removal of both endogenous and
exogenous toxins including ethylene glycol, barbiturates, non-steroidal anti-inflammatory
drugs and many anti-microbials.
CRRT is used for AKI patients but also can be used for patients with fluid overload or
intoxication. There are various different modes of CRRT that can be used but the most
common is continuous veno-venous haemodiafiltration (CVVHDF). This mode uses both
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convection and diffusion as methods of removing solutes. A large bore dialysis catheter is
placed in a central vein which has 2 access points and 2 lumens. Blood is both removed
and returned through this catheter. A pump is required to give consistent blood flow through
the dialysis machine. The blood is pumped through thousands of straw-like semi-permeable
membranes bathed in a dialysate. The dialysate flows in the opposite direction to the blood
to maximise detoxification. Anticoagulation is required to decrease the likelihood of blood
clotting in the filter.
CRRT is a slow and continuous process which facilitates removal of a large amount of fluid
without causing a sudden drop in serum osmolality and compromising cardiovascular
stability. It also filtrates larger molecules and prevents loss of white blood cells and platelets.
Bleeding is a common complication reported in humans. It can be either local around the
catheter or systemic. Lack of vascular access is a major issue for our patients as the
dialysis catheter is so large. This is important to remember if you are considering referring a
patient for CRRT as preserving a jugular vein is extremely helpful. Other complications
include blood clots in the filter (even if anti-coagulants are used), hypothermia, hypotension
electrolyte and acid-base imbalances, dialysis dysequilibrium and infection. There is a fairly
small retrospective study on CRRT looking at animals with both AKI and acute on chronic
renal disease which reported survival rates of approximately 40-45% (Diehl and Seshadri,
2008).
Intermittent Haemodialysis
IH involves a very similar process to CRRT but as the name suggests it is performed
intermittently. It utilises the same methods of solute and fluid removal as CRRT i.e.
diffusion, convection, ultrafiltration and adsorption, although diffusion usually predominates.
Generally it is provided for 3-6 hours a day for 2-3 days initially for AKI patients followed by 3
times weekly sessions. Because of the intermittent nature of the therapy it results in marked
variation in azotaemia, fluid load, hyperkalaemia etc. and so is thought to be more difficult for
critical patients to tolerate. It is not suitable for patients with cardiovascular instability. IH is
not available in the UK currently. Retrospective studies show a fairly impressive survival
rate of 86% for dogs suffering from Leptospirosis undergoing IH and approximately 60% in
cats with a variety of causes of AKI.
Prognosis
The overall mortality rate of AKI in cats and dogs is reported to be approximately 50%.
This figure is based on a referral population and hence may be an underestimation due to
the severity and complexity of these cases. However 50% may also be an overestimation
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due to the availability of advanced therapies, nursing care and increased commitment from
owners. In general, the outcome is largely dependent on the underlying cause and severity
of the disease. A retrospective study showed that dogs with leptospirosis were reported to
have a fair to good prognosis with an overall survival rate of 83%. On the other hand, dogs
with symptomatic AKI due to ethylene glycol have a grave prognosis. Other negative
prognostic indicators in dogs with AKI include initial creatinine of greater than 884 mol/l,
anaemia of less than 33% at the time of diagnosis, proteinuria and hypocalcaemia (less than
2.2 mmol/l). In addition, dogs with concurrent diseases or syndromes such as pancreatitis,
sepsis and disseminated intravascular coagulation (DIC) have a poorer prognosis.
Clinicopathological abnormalities such as hypoalbuminaemia and hyperkalaemia at initial
diagnosis are also associated with decreased survival in cats with AKI.
Summary
Acute kidney injury is a commonly encountered emergency or complication resulting in
significant morbidity and mortality. Identification of the inciting cause of AKI is important to
ensure any specific antidotes or treatments are administered and this information can also
help inform the owner of the patients likely prognosis. Supportive care in conjunction with
specific therapies can potentially reverse renal injuries and improve outcome of the patients.
Fluid therapy remains the mainstay of supportive therapy. The maintenance of fluid balance
requires diligent monitoring of the patients hydration status and formulation of fluid therapies
that are tailored to each patients needs. AKI patients that are severely azotaemic, anuric
and refractory to fluid therapy with potentially reversible renal function generally benefit from
RRTs.
Acknowledgements
With thanks to Ron Li and Adam Mugford who helped in the writing of these notes
Further reading and References

A clinical review of peritoneal dialysis
Alexa M.E. Bersenas
Journal of Veterinary Emergency and Critical Care 21(6) 2011, pp 605617
Guidelines for the Identification, Evaluation, and Management of Systemic Hypertension in
Dogs and Cats ACVIM consensus statement
S. Brown, C. Atkins, R. Bagley, A. Carr, L. Cowgill, M. Davidson, B. Egner, J. Elliott, R.
Henik, M. Labato, M. Littman, D. Polzin, L. Ross, P. Snyder, and R. Stepien
Page 297 of 334

Journal of Veterinary Internal Medicine 2007 21 pp.542558

Peritoneal Dialysis in Cats with Acute Kidney Injury: 22 Cases (2001 2006)
R.L. Cooper and M.A. Labato
Journal of Veterinary Internal Medicine 2011, 25 pp. 1419
Extracorporeal renal replacement therapy and blood purification in critical care. Larry D.
Cowgill and Julien Guillaumin. Journal of Veterinary Emergency and Critical Care 23(2) 194-
204
Use of continuous renal replacement therapy for treatment of dogs and cats with acute or
acute-on-chronic renal failure: 33 cases (20022006)
Shenandoah H. Diehl and Ravi Seshadri. Journal of Veterinary Emergency and Critical Care
18(4) 370-382
Current techniques in peritoneal dialysis. Linda A. Ross and Mary Anna Labato. Journal of
Veterinary Emergency and Critical Care 23(2) 230-240
Principles of Continuous Renal Replacement Therapy Self-Learning Packet 2005 Orlando
Regional Healthcare, Education & Development (free internet access)
http://www.orlandohealth.com/pdf%20folder/continuous%20renal%20replace.pdf
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Notes page
Page 299 of 334

OXYGLOBIN: ITS BACK!

Amanda Boag MA VetMB DipACVIM DipACVECC FHEA MRCVS
Clinical Director, Vets Now
amanda.boag@vets-now.com
Oxyglobin is one of a number of haemoglobin based oxygen carriers (HBOCs) that have
been developed and investigated over the last 30 years for use as an alternative to
transfusion therapy. It was withdrawn from the market in 2010 following a change in
ownership of the manufacturing company however production was resumed in early 2013
and it is now available once again for clinical use. It is the only HBOC licensed in the UK for
the treatment of canine patients and may also be used in feline patients, as there is no
equivalent licensed product available at this time. Although transfusion medicine is
continuing to develop rapidly in the UK and practitioners now have increasing access to
canine blood products, there may still be situations, especially in feline patients, where blood
is not readily and immediately available. Use of HBOCs in these situations can be life-
saving.
Whats in the bag?

Oxyglobin is a dark purple solution currently supplied in 60ml or 125ml bags which contain
13g/dl of ultrapurified, polymerised haemoglobin solution of bovine origin suspended in a
modified lactated Ringers solution. It has an osmolality of 300mOsm/L and a pH of 7.8. In its
original foil packing, it can be stored for up to 3 years from the date of production. Once
opened it should be used within 24 hours as exposure to light and air results in gradual
oxidation of the haemoglobin to methaemoglobin.
What does it do?

Oxyglobin increases plasma and therefore total haemoglobin concentration and
consequently increases arterial oxygen content and oxygen delivery to the tissues.
Furthermore the partial pressure of oxygen that results in 50% saturation of haemoglobin
(P50) is approximately 35 mmHg; this is higher than blood (approximately 28mmHg) and
suggests there will be a more efficient release of oxygen at tissue level. Its main therapeutic
use is therefore to increase tissue oxygen delivery in patients where this is compromised. Its
low viscosity may also be a benefit for this purpose where it may improve oxygen delivery to
tissues supplied by narrowed blood vessels. The half-life of Oxyglobin is dependent on the
dose administered but the improvement in oxygen carrying capacity seen following infusion
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is likely to be significantly reduced by 24 hours and over 90% will have been excreted by 5-7
days post-infusion.
Alongside that it should be remembered that the polymerised haemoglobin molecules are
large (range 65-500kDa with a mean of 200kDa) and the COP of oxyglobin is high (43
mmHg) and thus it is a very effective colloid and leads to significant intravascular volume
expansion; whilst in some patients (acute haemorrhage) this may be advantageous, in
others (chronic euvolaemic anaemia) there is a real risk of causing volume overload. It is
also possible to use it in the same way as any other colloid fluid as part of the treatment of
hypovolaemic shock (see recent literature at the end of these notes).
Finally, increased systemic (including pulmonary) vascular resistance as a result of intense

vasoconstriction is seen with the use of Oxyglobin. This is thought to be due to an
interaction between nitric oxide (a potent vasodilator) and the Oxyglobin solution although
the precise mechanism is unclear. This is potentially beneficial in patients where
inappropriate vasodilation is present e.g. septic patients but may result in reduced cardiac
output with detrimental effects in others (see recent literature at the end of these notes).
How do I use it?

As it does not contain any red cell membranes, there is no need to perform blood typing or
cross matching prior to its use and it can be infused through a standard fluid giving set. Its
compatibility with other drugs has not been well evaluated, so it should either be infused via
a dedicated line or the line should be flushed well before and after administration of other
drugs. In terms of doses, as mentioned above, it is a powerful colloid fluid and has a marked
effect on expanding intravascular volume. In patients that are hypovolaemic, bolus doses of
10-30ml/kg administered over a short time frame are appropriate. In patients with
euvolaemic anaemia slower infusion rates (1-2ml/kg/hr) should be used to avoid side effects
of volume overload.
It is only licensed for single use and there is theoretical concern that multiple doses could
lead to antibody formation and anaphylaxis. However a study in 2001 in dogs showed that
although antibodies are formed, they do not diminish the effectiveness and do not create an
anaphylactic response. Clinically multiple doses are often administered.
How do I monitor patients?

Following administration of Oxyglobin the packed cell volume (PCV) is no longer an
accurate estimation of the patients oxygen carrying capacity as a proportion of the
haemoglobin is present in the plasma. PCV may actually drop following Oxyglobin infusion
due to its volume expanding effects. However, even if PCV drops, haemoglobin levels and
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oxygen carriage will still be improved. The most appropriate parameter to monitor as an
estimation of oxygen carrying capacity is total haemoglobin (Hb). This should be measured
directly using a haemoglobinometer (e.g. HaemoCue AB, Angelholm, Sweden); the Hb value
provided by many in-house haematology machines is calculated from the haematocrit and
so is inaccurate following Oxyglobin infusion. When direct haemoglobin measurement is
not possible, regular monitoring of clinical perfusion parameters such as heart rate, pulse
quality, capillary refill time and mentation is vitally important. Mucous membrane colour is a
less useful parameter as the mucous membranes develop a red-brown discolouration
following Oxyglobin infusion. Respiratory rate and effort should also be monitored closely.
An increase in respiratory rate and effort can be a sign of volume overload especially in
patients given rapid infusions. It should also be remembered that any blood tests done
using colorimetric methods (many in house biochemistry tests and urine dipstick) are
inaccurate following Oxyglobin use. No interference is seen with haematological or
coagulation parameters.
Uses of Oxyglobin
Moderate to severe anaemia is a frequently identified problem in small animal emergency
and critically ill patients and may occur secondary to haemorrhage (e.g. trauma, bleeding
disorders), red cell destruction (e.g. immune mediated haemolytic anaemia) or lack of red
cell production (e.g. myelodysplasia). Successful treatment of these patients involves
identification and treatment of the underlying cause of the anaemia; however urgent
stabilisation is often required whilst diagnostic tests and definitive treatment are on-going.
Although the dose rate stated on the package insert is 15-30ml/kg, Oxyglobin should be
used in a flexible fashion with the total dose and infusion rate tailored to the individual
patient. The following case examples illustrate this.
Case study Chunky

Chunky was an 18 month old male entire Domestic short hair which presented as an
emergency; his owners had found him weak and collapsed, although he had also been a
little less lively in the previous 2-3 weeks. On physical examination he was very quiet but
responsive. His heart rate was 220 beats per minute with tall, narrow pulses. Mucous
membranes were white with a non-detectable capillary refill time. A grade I/VI heart murmur
was audible. Other than tachypnoea, the rest of the physical examination was unremarkable.
An initial attempt to take a jugular blood sample led to him becoming very distressed and
starting to open mouth breath. Only a very small amount of blood was obtained which was
used to perform a PCV/TS and make a blood smear. PCV was 8% with TS of 64 g/L
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(reference range 58-70 g/L). The blood smear was very thin but red cell morphology was
unremarkable and there was no evidence of regeneration. Platelet and white cell numbers
appeared adequate.
Patients like Chunky present a diagnostic and therapeutic dilemma. The history, physical
examination and basic blood work were most suggestive of a chronic non regenerative
anaemia and a full medical work-up was recommended. However the very low PCV put
Chunky at risk of deterioration if he became stressed during diagnostic tests. A fresh whole
blood transfusion given at a slow rate would be an excellent way to stabilise Chunky but can
be difficult to obtain. It is also essential that a blood type is obtained in cats prior to
transfusion and that the same type blood is administered. In Chunky, there was insufficient
blood available to perform a blood type. The decision was made to stabilise Chunky with an
Oxyglobin infusion. An infusion rate of 1ml/kg/hr was chosen as Chunky was considered to
have a euvolaemic anaemia i.e. normal intravascular volume with reduced red cell mass.
This rate was continued throughout his first night of hospitalisation.
The following morning, he was much brighter and was stable enough to proceed with
diagnostics including full blood work, blood type, imaging and anaesthesia for a bone
marrow sample. These tests confirmed Chunky was suffering from immune mediated bone
marrow disease and corticosteroid therapy was started. Sufficient blood was obtained to
perform a blood type and he also received a fresh whole blood transfusion for further support
whilst the medical treatment took effect. Chunky ultimately responded well to the medical
therapy.
Case study Baggins

Baggins was a 12 year old Domestic shorthair that was having surgery for removal of a liver
mass. Pre-operative haematology was unremarkable and the PCV at the start of surgery
was 31%.
Unfortunately Baggins suffered significant blood loss during the surgery. Although the
haemorrhage was rapidly controlled, post haemorrhage, Baggins was tachycardic and
Doppler blood pressure had dropped to 70mmHg. Feline blood was not immediately
available so the decision was made to stabilise with Oxyglobin. He was thought to be
suffering moderate hypovolaemic shock so a bolus dose of 20ml/kg of Oxyglobin was
administered over 30 minutes. This resulted in improvement in blood pressure and heart
rate. Fluid therapy was continued for the rest of the surgery and recovery period using
6ml/kg/hr of Hartmanns solution. A blood type was obtained in case Baggins needed to
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receive a transfusion but he remained stable. The surgery was completed without further
incident. Post-operatively his PCV was 18% but this increased gradually over the following 5
days and Baggins made a full recovery.
Summary
Oxyglobin is a very useful addition to our fluid therapy armoury. The two cases and the
paper described below illustrate the flexible ways in which Oxyglobin can be used both to
stabilise patients following acute blood loss, in patients with chronic anaemia and in patients
with hypovolaemic shock. Although it can never replace blood transfusions, it can be a vital
component of treatment especially in situations where obtaining blood in the necessary time
frame is not possible.
Recent literature
Comparison of Hb-200 and 6% hetastarch 450/0.7 during initial fluid resuscitation of 20 dogs
with gastric dilatation-volvulus. Haak CE, Rudloff E, Kirby R. J Vet Emerg Crit Care. 2012
Apr;22(2):201-10.
Objective: To compare the use of polymerized stroma-free bovine hemoglobin (Hb-200) and 6%
hetastarch 450/0.7 (HES 450/0.7) in 0.9% saline during fluid resuscitation of dogs with gastric
dilatation-volvulus (GDV).
Design: Prospective, randomized clinical case series.
Setting: Private specialty and referral clinic.
Animals: Twenty client-owned dogs presenting with GDV.
Interventions: Dogs presenting with GDV and abnormal perfusion parameters first received rapid IV
infusion of a buffered isotonic replacement crystalloid (15 mL/kg) and IV opioids. Patients were then
randomized to receive either Hb-200 (N = 10) or HES 450/0.7 (N = 10). Balanced isotonic
replacement crystalloids (10-20 mL/kg IV) were rapidly infused along with either Hb-200 or HES in 5
mL/kg IV aliquots to meet resuscitation end points.
Measurements and main results: Resuscitation was defined as meeting at least 2 of 3 criteria: (1)
capillary refill time 1-2 seconds, pink mucous membrane color, strong femoral pulse quality; (2) heart
rate (HR) 150/min; or (3) indirect arterial systolic blood pressure (SBP) > 90 mm Hg. HR, SBP,
packed cell volume, hemoglobin, glucose, venous pH, bicarbonate, base excess, anion gap, and
colloid osmotic pressure were compared at hospital entry and within 30 minutes post-resuscitation.
Compared to the HES group, the Hb-200 group required significantly less colloid (4.2 versus 18.4
mL/kg) and crystalloid (31.3 versus 48.1 mL/kg) to reach resuscitation end points (P = 0.001). Time to
resuscitation was significantly shorter in the Hb-200 group (12.5 versus 52.5 min).
Conclusions: Dogs with GDV receiving Hb-200 during initial resuscitation required smaller volumes
of both crystalloid and colloid fluids and reached resuscitation end points faster than dogs receiving
HES 450/0.7 (P = 0.02).
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Evaluation of the effects of bovine hemoglobin glutamer-200 on systolic arterial blood

pressure in hypotensive cats: 44 cases (1997-2008).Wehausen CE, Kirby R, Rudloff E. J Am Vet
Med Assoc. 2011 Apr 1;238(7):909-14.
Objective: To determine effects of bovine hemoglobin glutamer-200 (Hb-200) solution on systolic

arterial blood pressure (SAP) in hypotensive cats and describe potential adverse effects associated
with this treatment.
Design: Retrospective case series.
Animal: 44 cats.
Procedures: Medical records of hypotensive (Doppler SAP 80 mm Hg) cats that received Hb-200
treatment were reviewed. Volume and rate of Hb-200 administration, treatments for hypotension given
prior to Hb-200 administration, changes in SAP, potential adverse effects, and short-term outcome
were evaluated.
Results: 44 cats were included in the study. Mean SD SAP prior to Hb-200 administration was 52
11 mm Hg, despite other treatments. Forty-three cats received Hb-200 via IV bolus administration
(mean SD volume, 3.1 2.2 mL/kg [1.41 1.0 mL/lb] over 25.17 17.51 minutes); 1 cat received a
continuous rate infusion (CRI) only. The SAP increased to > 80 mm Hg in 33 of 44 (75%) cats. The
SAP increased > 20 mm Hg above baseline value in 29 of these 33 cats and in 4 cats in which SAP
did not exceed 80 mm Hg. A CRI (mean SD rate, 0.8 0.5 mL/kg/h [0.36 0.23 mL/lb/h]) of Hb-200
was administered to 37 cats (after bolus infusion in 36). Mean SAP during the CRI was 92 18 mm
Hg. Adverse effects included respiratory changes (n = 8 cats), vomiting (2), and pigmented serum
(30). Seventeen (39%) cats survived to discharge from the hospital, 6 died, and 21 were euthanized.
Conclusions and clinical relevance: Hb-200 effectively increased SAP in hypotensive cats with few
adverse effects.
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FUNDUS EXAMINATION
The term fundus describes the structures that can be seen ophthalmoscopically at the
posterior of the eye. Examination and assessment of this part of the eye is a skill that many
veterinarians find difficult. However, by following a few basic rules and with a little practice
fundus examination can be easy and once it is routinely performed an appreciation of the
range of normal appearances can rapidly be built up.
FACILITIES AND EQUIPMENT
1. A room that can be darkened.
Examining eyes in a darkened room makes the task much easier and enables a bright clear
image of the fundus to be obtained.
2. An ophthalmoscope
a) A direct ophthalmoscope
The majority of practices will have a direct ophthalmoscope only. Check that the optics are
clean and that it has fresh batteries (or in the case of rechargeable models is fully charged).
b) Indirect ophthalmoscope
Indirect ophthalmoscopy offers many advantages over direct ophthalmoscopy, but

unfortunately commercial indirect ophthalmoscopes are expensive and therefore not widely
used. A simple form of indirect ophthalmoscopy can be performed using a magnifying lens
and a pen light or tranilluminator. This simple monocular form of indirect ophthalmoscopy is
cheap and with practice can provide the viewer with a clear wide-field view of the fundus.
The disadvantages are that both hands are occupied so an assistant may be needed to hold
the animal's head in the correct position and hold the eyelids open. The Volk 2.2 Pan Retinal
lens is an excellent lens for indirect ophthalmoscopy.
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3. Mydriatic
Dilating the pupil using a mydriatic drug such as tropicamide makes any form of
ophthalmoscopy easier and allows the majority of the fundus to be examined.
OPHTHALMOSCOPY
Direct ophthalmoscopy
It may be useful to start off by performing distant direct ophthalmoscopy and then to move in
to examine the fundus (close direct ophthalmoscopy).
The ophthalmoscope is set to zero (for a person with normal eyesight), looking through the
viewing aperture the animal's eye is observed from arm's length. A fundus reflection is
obtained and any opacities in front of the fundus show up as dark shadows on the reflected
light which is coloured by the tapetal coloration. Once the tapetal reflection is in view the
examiner moves closer until the ophthalmoscope is within a few cm of the eye. The fundus
should now be in focus.
This technique gives a magnified view of a relatively small area of the fundus, the examiner
needs to move around to build up a mental montage of as much of the fundus as possible.
Tips for direct ophthalmoscopy

Set the ophthalmoscope at zero diopters, or adjusted to allow for your own refractive
error and select the widest beam of light
Rest the ophthalmoscope against your eyebrow so that your eye is as close to the
viewing hole as possible - it is best performed without glasses (imagine you are looking
through a keyhole)
Position the ophthalmoscope close to the animals eye
Alter the angle that you are looking into the eye to see different areas of the fundus
Try to look through your left eye for the animals left eye and vice versa (to prevent noses
clashing)
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Indirect ophthalmoscopy
This technique has some major advantages over direct ophthalmoscopy.

Comparison between direct and indirect ophthalmoscopy
Direct ophthalmoscopy Indirect ophthalmoscopy
most commonly used method in general method most commonly used by veterinary
practice ophthalmologists
relatively inexpensive equipment equipment more expensive, although indirect

ophthalmoscopy is possible using a pen light and 14
30 D lens.
image is upright image is inverted and reversed
magnified image but narrow field of view less magnification, but much greater field of view.
(scanning around is required to build up This allows for rapid and easy examination of large
a mental picture of the entire fundus) areas of the fundus. Magnification and field of view
can be altered by selection of lenses of different
strength - typically between 14 diopters (higher
magnification, narrower field of view) and 30 diopters
(lower magnification and wider field of view)
can be difficult to see fundus through superior view through opacities of the ocular media
opacities (e.g. corneal or lens)
Simple indirect ophthalmoscopy may be performed using a pen light and condensing lens
(between 15 and 30 diopters).
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Indirect ophthalmoscopy using a pen light and magnifying lens

Dilate the pupil
Hold the examining light by your temple so that it is possible to look along the beam of
light.
Position yourself at arms length from the patient so that the light is shining along the
animals visual axis. A good tapetal reflection should be seen.
Interpose the lens at right angles to the examining beam of light, about 5cm from the
cornea. An aerial image of the fundus should now be seen. Move the lens closer or
further from the cornea until the best image is achieved. I find it easiest to hold the edge
of the lens between finger and thumb and rest my little finger on the animals head. The
hand holding the lens then moves with any head movements.
To view other parts of the fundus the examiner must be prepared to either move him or
herself or to alter the position of the animals head. To view the dorsal fundus, for
example, the examiner needs to look up into the eye or lift the animals nose upwards,
and to view the medial fundus the examiner needs to view from the lateral side of the
eye. Therefore quite a lot of moving about may be required to view the entire fundus.
When changing the direction of viewing it is important to alter the lens so that it remains
at 90 degrees to the beam of the examining light.
NORMAL APPEARANCE OF THE FUNDUS
The fundus consists of:
optic nerve head
retina (including retinal pigment epithelium)
superficial retinal vasculature
choroid underlying the retina - including in the tapetal area the tapetum
in some instances the underlying sclera may be visible
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The appearance of the normal fundus varies considerably between individual animals,
particularly so in dogs. This wide range of normality must be appreciated before abnormality
can be detected.
Normal appearance of the canine fundus
Feature Range of appearances
optic nerve head position - just ventromedial to posterior pole, tapetal / non-tapetal
(disc) junction usually close to disc
shape - circular to triangular, may be irregular, surface slightly raised,

often with a central dip (physiological pit)
colour - pinkish white. White colour due to myelination and pink due to
blood vessels.
surface vasculature. Pattern varies, may be a partial or complete

vascular ring visible on the surface. Retinal vasculature travels over part
of the disc and radiates out from disc periphery
tapetal fundus Tapetal area may be reduced (particularly in miniature breeds) or even
absent (e.g. often in colour-dilute individuals). Not present at birth but
develops in the first three months of life.
position - The tapetum occupies the area of the fundus just dorsal to the
disc, but does not extend to the ora ciliaris retinae.
shape - Roughly triangular, may vary in extent. The junction with the
non-tapetal area may be sharply demarcated or irregular with islands of
tapetal tissue being seen in the non-tapetal area.
colour - Varies between grey, blue, reddish, green and yellow.

Developing tapetum first appears blue in colour and then slowly
develops adult coloration.
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non-tapetal fundus This describes the entire retinal area which does not have an underlying
tapetum.
colour - typically dark greyish brown to black in colour. A slight mottling

in pigmentation is common and should be distinguished from
depigmentation resulting from pathological processes. Some animals
(often those with a light coloured iris) have reduced or even absent
pigmentation in the choroid and retinal pigment epithelium. This results
in a reddish non-tapetal fundus or even a toroid" appearance due to
choroid blood vessels superimposed on a background of sclera.
superficial retinal Consist of arterioles and venues.

vasculature
Arterioles numbering up to 20 are smaller and radiate from the edge of
the disc.
The major venues (approximately three to six) come together to form a

venous circle on or within the substance of the optic disc.
The pattern of the vessels varies as does their tortuosity.
The feline fundus exhibits a range of different normal appearances, although it is less
variable in appearance than that of the dog.
Normal appearance of the feline fundus

Feature Range of appearances
optic nerve head position - usually well within tapetal area

(disc)
shape - circular, smaller than the dogs disc, surface slightly depressed
due to relative lack of myelination. May have a sieve-like appearance
due to lamina crib Rosa
colour - dull grey
surface vasculature - vasculature just dips over edge of disc. Not on

surface of disc (compare with dog)
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tapetal fundus Tapetum may be absent in some cats, usually associated with colour-
dilute animals. The area centralis, which is a cone-rich area for detailed
vision, is situated in the tapetal fundus lateral and slightly dorsal to the
optic disc. This area is comparatively devoid of blood vessels and the
colour may be a slightly different shade compared to the surrounding
area (e.g. in cats with a yellow tapetum the area centralis may appear
greenish).
position - The tapetum is positioned in the dorsal posterior area of the

fundus.
shape - Roughly triangular.
colour - yellow/green - blue or reddish in some individuals
non-tapetal fundus This describes the entire retinal area that does not have an underlying
tapetum.
colour - dark brown to black in colour. Colour-dilute animals may have a

corresponding reduction or even lack of ocular pigment allowing the
normal choroidal blood vessels to be seen and if there is a total lack of
pigment the sclera will show through between the vessels.
superficial retinal Consist of arterioles and venules radiating from the optic nerve head.
vasculature The vessels can be seen dipping over the edge of the optic nerve head.
Typically there are three major pairs of vessels; one pair runs dorsally to
then curve laterally, one runs ventrolaterally and the other
ventromedially. There are smaller arterioles extending from the edge of
the optic nerve head at sites between the three major arterioles.
Superficial retinal vessels tend to pass around the area centralis rather
than directly crossing it.
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ABNORMALITIES OF THE FUNDUS

The wide range of normal appearance of the fundus must be appreciated prior to diagnosing
abnormalities.
There are a limited number of changes in appearance that can develop in the fundus. The
following are a few such changes:
Retinal thinning
Retinal thinning over the tapetal fundus results in tapetal hyper-reflectivity. This is indicative
of retinal degeneration.
Causes:
focal degeneration, may be a post-inflammatory change, be associated with geographic

retinal dysplasia etc.
generalized thinning can result from diseases such as progressive retinal atrophy,
secondary to retinal damage from conditions such as glaucoma, result from sudden
acquired retinal degeneration (takes several weeks to develop) etc.
Change in tapetal colour

In addition to the wide range of normal tapetal colours, alterations in coloration may result
from inflammatory processes (chorioretinitis) or from changes in thickness of the overlying
retina, or from proliferation and pigmentation of the overlying retinal pigment epithelium
obscuring view of the underlying tapetum. Severe inflammatory changes may result in
destruction of the tapetum.
Retinal thickening
Thickening of the retina results in reduced reflection from the tapetum in the tapetal area.
The lesions may appear grey in colour. Lesions in the nontapetal area appear as whitish or
greyish lesions. Causes include: retinal edema and retinitis.
Pigmentary changes
Rough or long coated dogs usually have an irregular tapetal/nontapetal border. This can give
the appearance of darkly pigmented areas amongst islands of tapetal tissue. This is normal.
Inflammatory lesions can result in changes in pigmentation. In the nontapetal area

depigmentation may develop (allowing visualization of the underlying sclera) with patches of
pigment hypertrophy. Inflammatory lesions in the tapetal area may induce retinal pigment
Page 313 of 334

epithelium proliferation and pigmentation. The condition retinal pigment epithelial dystrophy
results in accumulation of light brown pigment clumps (lipofuscin) across the tapetal fundus
Vascular changes
hemorrhage at various layers from vitreous to choroid gives different appearances.
Possible causes include: trauma, coagulopathies, hypertension, inflammation
Changes in the superficial retinal blood vessels can include:

narrower or less obvious blood vessels e.g. anemia, retinal degeneration, post-
inflammatory change
wider blood vessels e.g. hyperviscosity syndrome, hypertension
segmental dilation and constriction of blood vessels e.g. hypertension, inflammatory
disease
creamy coloured very high circulating lipid levels
Underlying choroidal vessels may be exposed normal lack of pigmentation,

depigmentation following inflammation, Collie eye anomaly.
Retinal detachments
This may range from small flat detachments (affected area just appears fuzzy) to total
bullous detachments where a grey membrane with blood vessels on its surface is seen
bulging into the vitreous cavity. If retinal tearing occurs the torn retinal may fall ventrally to
appear as a veil which obscures the optic disc. Causes: congenital abnormalities (retinal
dysplasia, Collie Eye Anomaly), inflammatory, hypertension, associated with hypermature
cataract, neoplastic, trauma, idiopathic.
Optic disc changes

Excess myelination at the optic disc can give the appearance of pseudopapilledema.
Swelling of the disc may result from true papilledema or papillitis. Depression of the surface
of the disc may be congenital (e.g. coloboma) or acquired (e.g. glaucomatous cupping). The
feline optic disc is slightly depressed compared to the canine. The rabbit normally has a
deep optic pit.
Page 314 of 334

Notes page
Page 315 of 334

Index in CPR 235

endogenous 229, 230
Lucy Leicester BVet Med MRCVS in neonatal resuscitation 45
lucy@leicesterindexing.co.uk advanced life support (ALS) 6669
Afghanistan 143, 144
AKI see acute kidney injury
aldosterone 79, 80
alginate dressings 270
allergic bronchitis 13
A allopurinol
AB blood typing system (cats) 145, 146 in ischemia-reperfusion injury 7576
abdominal lavage 53 nephrotoxic potential 28t
ABO blood typing system (humans) 145, 146 alphaxalone 42
ACE inhibitors, nephrotoxic potential 26t ALS (advanced life support) 6669
acepromazine 158 alveolar pattern 1112, 14
acquired bacterial resistance 281282 American Heart Association 61, 69
ACTH (adrenocorticotropic hormone) 79 amikacin 202
ACTH stimulation test 82, 83, 86 aminoglycosides
active listening 128, 129, 131 furosemide and 249
acute bronchitis 13 nephrotoxic potential 26t
acute glaucoma 113, 116, 194195 amoxicillin/clavulanic acid 191, 202, 281, 284
acute kidney injury (AKI) amphotericin B, nephrotoxic potential 26t
causes 2428 ampicillin 202
vs CKD 29t anaerobic glycolysis 71
clinical presentation 246247 anaesthesia
diagnosis 2833, 247248 AKI and 24t
diuresis 249250, 289 in caesarian section 42, 43, 44
electrolyte disturbances 2930, 249, 287, CPR 64
290291 in haemoabdomen 37
emergency management 287288 nursing care during recovery 253262
fluid therapy 248249, 288289 in seizures 218
gastrointestinal complications 291292 analgesia
hypertension 25t, 85, 196, 288, 291 in head trauma 101
IRIS AKI Grading Criteria 23t in RTA 234
nutrition 251, 292 in traumatic wounds 263
pathophysiology 24 angiogenesis (wound healing) 265
prognosis 295296 Angiostrongylus vasorum 14
recovery phase 291 anisocoria 98
renal replacement therapies 250, 292295 anorexia 237
schemes for grading 2123 antenatal care 40
supportive care 250251 anterior lens luxation 194195
urethral catheterisation 288, 289 anterior uveitis 191, 195, 196
acute on chronic kidney disease (AOCKD) 26t anthelmintics 118
acute respiratory distress syndrome (ARDS) 18 antibiotics
acyclovir, nephrotoxic potential 26t in abdominal surgery 51
Addisonian crisis 8284 bacterial resistance 281282
adenosine triphosphate (ATP) 7172 combination therapy 283
adherent dressings 268269 in corneal ulcers 194
admissions 121 misuse 281
adrenal glands nephrotoxic potential 26t
adrenal insufficiency 80 in parvovirus infection 202
hyperadrenocorticism 81, 8588 prophylactic use 283284
hypoadrenocorticism 79, 80, 8184 in pyelonephritis 287288
physiology 7677 recommendations to reduce resistance 282
adrenalectomy 87 285
adrenaline restrictions on use 283
in advanced life support 67 in retrobulbar infection 191
Page 315 of 334
in traumatic wounds 272 post respiratory tract surgery 111
treatment regimens 282283 post-anaesthesia 255256
anticonvulsant therapy 217219 in seizures 219
anti-emetics 202, 250, 291292 Blood Quality Regulations 143
antifungal drugs, nephrotoxic potential 26t blood transfusions see transfusion medicine
antiprotozoal drugs, nephrotoxic potential 26t blood types 145146
antiseptics, for wound lavage 267268 BLS (basic life support) 6466
antiviral drugs blunt abdominal trauma 3536
nephrotoxic potential 26t body position, in head trauma 9899
in parvovirus infection 203 body temperature see also hyperthermia;
anuria 249250 hypothermia
AOCKD (acute on chronic kidney disease) 26t monitoring 254255
apheresis 144, 146147 and onset of parturition 221222
apomorphine, nephrotoxic potential 28t physiology 254
apoptosis 72 Borrelia burgdorferi 25t, 32
appointments 120 brachycephalic airway syndrome 107
ARDS (acute respiratory distress syndrome) 18 brain injury see head trauma
Aristotle 137, 138, 140 bronchial disease 12, 1314
arrhythmias 258 bronchiectasis 1314
arterial blood gases 109 bubble humidifiers 3
aspiration pneumonia 108, 161 buprenorphine 101
asthma 13 buster collars see Elizabethan collars
asystole 67, 68 butorphanol 8
atipamezole 68
ATP (adenosine triphosphate) 7172 C
atropine 45, 68, 194, 235 caesarian section
autologous serum 194 anaesthesia 42, 43, 44
azathioprine, nephrotoxic potential 26t indications for 4142, 227
azotaemia neonatal resuscitation 4445
differentiating 2829, 247 surgical approach 4344
intravenous pyelography and 165 team approach 42
calcium, role in ischemic injury 72
B calcium alginate dressings 270
babesiosis, AKI and 25t calcium antagonists, nephrotoxic potential 27t
bacterial corneal ulcers 193 calcium gluconate
bacterial endocarditis, AKI and 25t in advanced life support 68
bacterial resistance to antibiotics 281282 in AKI 287
bandage layer (dressings) 268, 272 in dystocia 226, 227
barium studies 157162 calculi
baroreceptors 230 cystic 163, 173
basic life support (BLS) 6466 ureteroliths 29
Bilroth II procedure 50 urethral 173174
BIPS (barium impregnated polyethylene canine parvovirus see parvovirus infection
spheres) 159 capnometry 258260
bisphosphonates, nephrotoxic potential 27t carbapenems, nephrotoxic potential 26t
bladder, contrast radiology 163164 carbon dioxide see CO2 measurement
blastomycosis 276 carboplatin, nephrotoxic potential 26t
blindness 98, 113, 196 cardiac arrhythmias 258
blood gas analysis 262 cardiac failure 2, 15, 17
blood glucose see diabetes mellitus; cardiac output, during chest compressions 64
hyperglycaemia; hypoglycaemia 65
blood pressure monitoring cardiopulmonary resuscitation
in advanced life support 66 advanced life support 6669
in AKI 291 basic life support 6466
in diabetic emergencies 213 chest compressions 63, 6465, 66, 235
in head trauma 100 crash kits 63
in hypoadrenocorticism 84 defibrillation 69
Page 316 of 334
fluid therapy 68, 234235 surgical management 277279
monitoring 6667 thoracic duct ligation 278
neonatal 4445 cimetidine 28t, 203
pharmacology 6769, 235 circulation, chest compressions and 6465
post-resuscitation care 70 cirrhosis 173
precordial thump 69 cisplatin
preparedness/prevention 6264 AKI and 246
protocols 63 nephrotoxic potential 26t
recognition of cardiopulmonary arrest 6364 cisterna chyli
RECOVER guidelines 6162 ablation 278279
in RTA 235 anatomy 275276
success rates 61 CKD (chronic kidney disease) 26t, 29t
team 62 cleansing wounds 266
ventilation 6566, 235 clients
catecholamines conversations in RTA 229230
in advanced life support 67 emotional blackmail 140142
endogenous 229, 230 emotions 130133, 229
catheters empathy and 130
intravenous see intravenous access ICEBERGS acronym 129130
nasal 5 listening to 128129
tracheal 6 managing expectations 132
urethral 288, 299 needs and wants 133134
cats new 123
AKI 240245 and practice culture 127128
cardiac failure 15, 17 respect 134
chylothorax 276 satisfaction 127135
criteria for emergencies 121 trust 134135
fluid therapy 248249 cluster seizures 218
fundus examination 310311t CO2 measurement
hepatic encephalopathy 216 capnometry 258260
post-shock respiratory problems 231 during CPR 67
transient diabetes 210 in head trauma 99100
celiotomy 37 coagulopathy
central venous pressure (CVP) 213, 256257 AKI and 25t
cephalosporins 26t, 51, 191, 202 spontaneous haemoabdomen and 36
cerebral haemorrhage 95 cold compresses 110
cerebral oedema 220 colloids
cerebral perfusion pressure (CPP) 96 HBOCs 299303
character 134, 135t, 137138 in hepatic ischemia-reperfusion injury 76
checklists 53 in RTA 235
chemical injuries, ocular 192 colon volvulus 160
chemotherapeutic agents, nephrotoxic potential colonic dehiscence 49
26t communication skills see also persuasion
chest compressions 63, 6465, 66 active listening 128, 129, 131
chlorhexidine 267 emotional vs non-emotional content 132
chloride, in parvovirus infection 202 empathy 130
chromosomal bacterial resistance 281 ICEBERGS acronym 129130
chronic kidney disease (CKD) 26t, 29t non-clinical content 128
chylothorax competence 135, 137
aetiologies 276 compliance 120
cisterna chyli ablation 278279 component therapy 146
diagnosis 277 computed tomography (CT)
idiopathic 276277 in chylothorax 277
lymphatic vascular system 275276 in hyperadrenocorticism 87
medical management 277 in orbital pathology 190
pericardectomy 278279 in oropharyngeal stick injuries 58
pleural ports 279 Confidential Enquiry into Perioperative Small
Page 317 of 334
Animal Fatalities 253 deductive logic 138, 139
congestive heart failure 2, 15, 17 deferoxamine (DFO) 75
consciousness, in head trauma 97 defibrillation 69
consent 232 dehiscence
consultations 119120 defined 47
contact layer (dressings) 268271 incisional 4749
continuous renal replacement therapy (CRRT) intestinal 4953
250, 294295 dental hygiene 118
contraction (wound healing) 265 Descemets membrane 192
contrast radiology desoxycorticosterone pivalte (DOCP) 84
barium enema 160 dexamethasone 83
BIPS 157159 dextran 40, nephrotoxic potential 28t
gastrointestinal obstruction 157, 158159, dextrose
171 contraindications 68
intravenous pyelography 165167 in diabetic emergencies 212
oesophagram 160162 in seizures 220
pneumocolonogram 159, 171 diabetes mellitus
upper GI studies 157159, 171 fluid therapy 210212
urethrogram 164165 in hyperadrenocorticism 85
urinary system 163167 hyperglycaemia 207210
controlled hypothermia 7677, 102 hyperosmolar hyperglycaemic state 209
cooling hyperthermic patients 254255 hypoglycaemia 210
corneal ulcers insulin therapy 212
assessing depth 192 ketoacidosis 208
conjunctival grafts 193194 nursing care 212213
deterioration 116 physiology 207
etiology 192193 diagnostic imaging see computed tomography;
examination 191 contrast radiology; fluoroscopy; magnetic
medical therapy 193 resonance imaging; radiography;
opthalmic examination 191 ultrasonography
coronary perfusion pressure 64 dialysis 250, 294295
corticosteroids see also glucocorticoids diaphragmatic rupture 2, 1819
contraindication in head trauma 101 diazepam, in seizures 217218
defined 79 digital radiography systems 91
endogenous 7980, 81, 85 dimethylsulphoxide (DMSO) 75
CPR see cardiopulmonary resuscitation direct ophthalmoscopy 305308, 306, 307t
CPV see parvovirus infection dirofilariasis 276
crash kits 63 disaster medicine
creatinine 22t animal identification 151
cryopreserved platelets 147 disaster plans 151, 152
crystalloid fluids, in advanced life support 68 euthanasia 153154
Cushing Reflex 96, 100 evacuation of pets 152153
Cushing's disease see hyperadrenocorticism health and safety 155
CVP (central venous pressure) 213, 256257 media and 154155
cyclosporine, nephrotoxic potential 26t PETS Act 153
cystic calculi 163, 173 planning 155
cystography 163164 record keeping 153
SART teams 152
D volunteers 154
Dal blood type (dogs) 145 dispensing 121
dapsone, nephrotoxic potential 26t disposal of bodies 153154
DEA (dog erythrocyte antigen) system 145 disseminated intravascular coagulation (DIC)
debridement, traumatic wounds 266 AKI and 25t
decerebellate posture 99 in ischemia-reperfusion injury 7374
decerebrate rigidity 9899 in RTA 236
decompensatory shock 230231 in status epilepticus 217
decubital ulcers 102 distichiasis 192
Page 318 of 334
distrust 134 emergencies, criteria 120121
diuretics emotional blackmail 140142
in AKI 249, 289 emotional intelligence 130
nephrotoxic potential 26t emotions
DKA (diabetic ketoacidosis) 208 basic five 130
DMSO (dimethylsulphoxide) 75 basis 131
DOCP (desoxycorticosterone pivalte) 84 managing 132133
dopamine, in AKI 250, 289290 recognising 131
double contrast cystography 163164 empathy 130
doxapram 45 endoparasites 118
doxorubicin, nephrotoxic potential 26t endoscopy, in oropharyngeal stick injuries 57
doxycycline 288 endotracheal intubation 7, 65
dressings energy needs, calculating 238239
alginates 270 enrofloxacin 202
contact layer 268271 enteral nutrition
for exudative wounds 268270 indications for 238
foam 270 naso-oesophageal feeding 203, 239240
for granulating wounds 272 oesophagostomy tubes 231243
hydrocolloid 271 in parvovirus infection 203, 206
hydrogels 271 entropion 192
intermediate layer 268, 271272 eosinophilic bronchopneumopathy 13
negative pressure wound therapy 269270 epilepsy 215216, 218
perforated film 271 epinephrine see adrenaline
petroleum-impregnated 271 epistaxis 56
synthetic micropore 271 epithelialization (wound healing) 264
wet-to-dry 268269 esophageal perforation 161
dysphagia 56 estimates 125
dyspnoea see respiratory distress ethos 137138
dystocia ethylene glycol
caesarian section 4145, 227 AKI and 246, 290
diagnosis 41, 222223 nephrotoxic potential 27t
foetal extraction 225 urine testing 3132
imaging 41, 224225 euthanasia 119, 122, 153154
medical management 225227 evacuation of pets 152153
pathogenesis 4041, 223224 evidence-based science 139140
dysuria 121, 163, 164, 173 evisceration 47
exophthalmos 56, 189, 190
E exotics, intravenous access 233
ECG see electrocardiography exposure, radiography 11, 9091, 93t
ectoparasites 118 exposure keratitis 192
ectopic cilia 192 exudative wounds, dressings for 268270
ectopic ureters 165, 167 eye contact 131, 133, 135t
EDTA, nephrotoxic potential 28t eye drops, administering 115
Ehrlichia canis 32 eyes see also ocular emergencies
electrocardiography discharge from 56, 190
in CPR 67 examination in head trauma 9899, 105t
in head trauma 100 foreign bodies 192
in hyperkalaemia 249 fundus 305313
post-anaesthesia 258
electrolyte disturbances F
in AKI 2930, 249, 287, 290291 famotidine 250
in diabetic emergencies 209 FAST (focused assessment with sonography for
in hypoadrenocorticism 80, 82 trauma) scans 3637
electroretinography 196 fear 142
Elizabethan collars feeding see nutrition
indications for 111, 115, 116, 184, 193 felbamate 219
as oxygen hoods 6, 233 feline infectious peritonitis (FIP) 25t, 166, 167
Page 319 of 334
fenoldopam 290
fentanyl 101 G
fetus see foetus gabapentin 219
fever, in transfusion reaction 148 galium nitrate, nephrotoxic potential 27t
fibroplasia 265 gastric axis 172
financial outcomes 123125 gastric dehiscence 49
fine needle aspiration, kidneys 32 gastric dilatation-volvulus (GDV) 120, 303
flow-by oxygen administration 1, 4, 8, 232233 gastric perforation 169
fludrocortisone acetate 84 gastric protectants 203
fluid overload 249, 289 gastroesophageal intussusception 162
fluid therapy gastrointestinal obstruction 157, 158159, 170
in acute hypoadrenocorticism 82 171
in advanced life support 68 gastrointestinal tract, as shock organ in dogs
in AKI 248249, 289 231
colloids see colloids generalized seizures 216
in CPR 68, 234235 gestation 39, 221
in diabetic emergencies 210212 glaucoma 113, 116, 194195
in dystocia 226 glomerular filtration rate (GFR) 21, 22t, 24, 260,
fluid overload 249 288, 289
in haemoabdomen 37 glucagon, physiology 207
in head trauma 100 glucocorticoids see also corticosteroids
in parvovirus infection 201202 defined 79
in RTA 234235 in hypoadrenocorticism 83, 84
in seizures 220 glucose see diabetes mellitus; hyperglycaemia;
flumazenil 68, 101 hypoglycaemia
fluoroquinolones 194, 202, 281, 283, 288 glucosuria 207, 208
fluoroscopy 58 granulation tissue 264265
foam dressings 270 granulocyte-colony stimulating factor, in
focal seizures 216217 parvovirus infection 204, 205
foetus grapes, nephrotoxic potential 27t
distress 41 guilt 141
ultrasonographic signs of death 225
foreign bodies H
gastrointestinal 158159, 171 haematology, in intestinal dehiscence 4950
linear 159, 170171 haemoabdomen
nasal 107 anatomy 35
ocular 192 iatrogenic 36
oesophageal 160, 162 radiographic signs 170
oropharyngeal stick injuries 5560 signs 3637
foscarnet, nephrotoxic potential 26t spontaneous 36
free peritoneal gas 169170 surgical approach 3738
free radicals 72, 73, 75, 76 traumatic 3536
fresh whole blood 147 haemoglobin, transfusion triggers 148
fundus haemoglobin based oxygen carriers (HBOCs)
abnormalities 312313 administration 300
mydriatic 306 case studies 301303
normal appearance 308311 indications 301
ophthalmoscopy 305308 literature review 303304
optic disc 309t, 310t, 313 mechanisms of action 299300
pigmentary changes 312313 monitoring 300301
retina thickness 312 specifications 299
retinal detachments 313 haemorrhagic shock 3637
tapetal colour changes 312 haemothorax 15
vasculature 313 halitosis 56
furosemide harmonic scalpel devices 38
in AKI 249, 289 HBOCs see haemoglobin based oxygen
in head trauma 101 carriers
Page 320 of 334
head trauma physiology 254
anatomy 95 in status epilepticus 217, 219
diagnostics 99100 in transfusion reaction 148
initial assessment 9699 treatment 254255
monitoring 100 hypertonic saline
neurological assessment 9899, 104105t in head trauma 101, 234235
nursing care 102103 in RTA 234235
overview 95 hyperviscosity syndrome 196
pathophysiology 9596 hypoadrenocorticism
prognoses 105t defined 79
treatment 101102 diagnosis 82
health and safety, disaster plans and 155 nursing care 8384
Health Protection Agency 144 physiological basis 80
heart failure 2, 15, 17, 276 signs 8182
heavy metals, nephrotoxic potential 27t treatment 8284
hepatic encephalopathy 216 hypocalcaemia, in AKI 30
hepato-renal syndrome, AKI and 25t hypochloraemia, in parvovirus infection 202
hernia hypochlorous solutions 268
diaphragmatic 1819, 276 hypoglycaemia
hiatal 162 in diabetic emergencies 210
incisional 47 in hypoadrenocorticism 80
HHS (hyperosmolar hyperglycaemic state) 209 seizures in 216
hiatal hernias 162 hypokalaemia
high-dose dexamethasone suppression 87 in AKI 30, 290
homeopathic remedies 140 in parvovirus infection 202
Human Brain Trauma Foundation 101 hyponatremia
humidification 3, 110 in AKI 30
hydrocolloid dressings 271 in parvovirus infection 202
hydrocortisone 83 hypopyon 191
hydrocortisone sodium succinate 83 hypotension
hydrogel dressings 271 in AKI 288
hydrogen peroxide 268 HBOCs and 304
hydronephrosis 166, 171172 in seizures 219
hyperadrenocorticism hypothermia
defined 79 AKI and 24t
diagnosis 8687 controlled 7677, 102
physiological basis 81 physiology 254
signs 85 treatment 255
treatment 8788 hypotonic fluids 235
hypercapnia 3, 99100 hypoxia
hypercytokinemia 73 AKI and 25t
hyperglobulinaemia, in AKI 30 defined 109
hyperglycaemia 99, 207210 respiratory distress and 3
hyperkalaemia in seizures 219220
in AKI 2930, 249, 287, 290
in hypoadrenocorticism 80, 82 I
hypernatremia 290 iatrogenic haemoabdomen 36
hyperosmolar hyperglycaemic state 209 ICEBERGS acronym 129130
hyperosmolar treatments see hypertonic saline; ictus 217
mannitol identification (pets) 118, 151
hypersalivation 55 idiopathic epilepsy 215216, 218
hypertension ileus 171, 231
AKI and 25t, 288, 291 imipenem 283
in hyperadrenocorticism 85 immune mediated thrombocytopenia 147
retinal detachments and 196 immune plasma, in parvovirus infection 204
hyperthermia immunosuppressive drugs, nephrotoxic
AKI and 24t potential 26t
Page 321 of 334
incident command systems 152
incisional dehiscence J
causes 4748 jugular venepuncture, contraindication in head
evisceration 47 trauma 99100
herniation 47
management 4849 K
indirect ophthalmoscopy 305, 307t, 308 Katrina (hurricane) 152, 153, 154
inductive logic 138, 139140 KBr (potassium bromide) 218
inflammatory phase (wound healing) 264, 266 keratoconjunctivitis sicca 192
inherent bacterial resistance 281 ketamine, in ischemia-reperfusion injury 76
in-patients, communication and 122 ketoacidosis 208
insulin ketoconazole 88
physiology 207 kidneys
therapy 212 AKI see acute kidney injury
insulinoma 216 intravenous pyelography 33, 165167, 170,
insurance 118, 125 172
interferon-omega, in parvovirus infection 203, normal measurements 172
206 physiology 245
intermediate layer (dressings) 268, 271272 radiography 166167, 171172
intermittent haemodialysis 295 Kussmaul respirations 208
International Renal Interest Society 21 kVp guidelines (radiography) 91
International Society of Blood Transfusion 145
interstitial pulmonary pattern 12 L
intestinal dehiscence lactate 7172, 233234
prevention 5053 lagophthalmos 189
systemic changes 4950 lameness 56
treatment 50 larynx 108
intestinal viability, assessment 51 leishmaniasis 25t, 32
intracardiac injections 69 lens luxation 194195
intracranial pressure (ICP) 96, 99100, 101 leptospirosis 25t, 30, 31, 288, 295, 296
intraocular haemorrhage 196 levetiracetam 218, 218219
intraocular pressure 115, 116, 194195 lidocaine
intra-osseous access 68, 233 in ischemia-reperfusion injury 76
intratracheal drug administration 69 local anaesthesia 5, 8, 43, 239
intravenous access lilies, nephrotoxic potential 27t
in acute hypoadrenocorticism 82 limited-volume resuscitation 234235
in advanced life support 68 line block 43
in AKI 248 linear foreign bodies 159, 170171
in diabetic emergencies 213 lipid lowering agents, nephrotoxic potential 28t
in parvovirus infection 202 lithium, nephrotoxic potential 28t
in respiratory distress 2 liver
in RTA 233 cirrhosis 173
in seizures 219 microhepatica 172
intravenous pyelography 33, 165167, 170, local anaesthesia
172 in caesarian section 43
intubation 7, 65 in nasal catheterisation 5
intussusception 160 in naso-oesophageal tube placement 239
Iraq 143, 144 in thoracocentesis 8
IRIS AKI Grading Criteria ( (for acute kidney lochial discharge 222
injury) 23t logic 138140
ischemia-reperfusion injury low dose dexamethasone suppression test
in cardiopulmonary arrest 64 (LDDST) 86
complications 7375 Lower, Richard 145
pathophysiology 7173 lungs
in RTA 236 auscultation 2
treatment 7577 evaluating function 262
islets of Langerhans 207 lobe collapse 13
Page 322 of 334
lobe torsion 14 ECG see electrocardiography
pulmonary metastases 173 HBOCs 300301
as shock organ in cats 231 post-anaesthesia 253262
luteinizing hormone (LH) 39 pulse oximetry 66, 109, 257258
lymphangiectasia 276 team approach 253
lymphatic vascular system 275276 urine output 260262
lymphoma, AKI and 25t mouth to snout ventilation 6566
lyophilised platelets 147 MRI see magnetic resonance imaging
mucous membrane colour 109
M multiple organ dysfunction syndrome (MODS)
magnetic resonance imaging (MRI) 58, 173, 25t, 74, 217
185, 196, 215 mydriasis 98, 105t
malnutrition 237 myocarditis 199
mannitol myoglobin, in AKI 7475
in acute glaucoma 194195
in AKI 249250, 289 N
in head trauma 101 N-acetylcysteine (NAC) 75
in seizures 220 naloxone 44, 68, 101
maropitant 202, 250 nasal oxygen 56
mAs guidelines (radiography) 91 naso-oesophageal feeding
mask oxygen administration 1, 4, 8 complications 240
Massive Transfusion Protocol 144 feeding method 240
maturation phase (wound healing) 265266 indications for 238
mean arterial pressure (MAP) 96, 100, 213, in parvovirus infection 203
219, 255 tube placement 239
mechanical obstruction, radiographic signs 171 nasopharynx 107
media, disaster plans and 154155 National Blood Service 143
megaoesophagus 160161, 173 National Health Service Blood and Transplant
Mehrabian, Albert 132 145
melena 231 NATO Blood Transfusion Services 143
menace response 98, 114 nausea 202
mentation negative pressure wound therapy 269270
in head trauma 97 neonates
post-anaesthesia 253254 intravenous access 233
metabolic acidosis 287, 290291 resuscitation 4445
methotrexate, nephrotoxic potential 26t neoplasia
metoclopramide 202, 250 adrenal gland 81
microhepatica 172173 AKI and 25t
midazolam, in dystocia 218 mediastinal 276
migration, foreign bodies 56 pleural effusion and 15
Mik blood type (cats) 145146 pulmonary 16, 18
mineralocorticoids 79, 80, 84 retrobulbar 189
miosis 98, 105t spontaneous haemoabdomen and 36
mistrust 134 nephroblastoma, AKI and 25t
mitotane 87 neuraminidase inhibitors 203
Modified Glasgow Coma Scale score (MGCS) neurological status
99 in head trauma 9899, 104105t
monitoring post-anaesthesia 252253
in advanced life support 6667 neurotrophic keratitis 193
in AKI 250251 neutering 118
blood gases 262 neutropenia 199200
blood pressure see blood pressure new clients 123
monitoring non-cardiogenic pulmonary oedema 18
body temperature 254255 non-clinical employees (NCEs)
capnometry 258260 admissions 121
CVP 213, 256257 clinical outcomes and 117122
in dystocia 226 criteria for emergencies 120121
Page 323 of 334
euthanasia and 122 oesophagostomy tubes 238, 241243
financial outcomes and 123125 oesophagus
offering appointments 120 diverticuli 162
in-patient information and 122 foreign bodies 162
prescribing and dispensing 121 megaoesophagus 160161, 173
preventative healthcare measures 117118 oesophagitis 160162, 250
non-tapetal fundus 310t, 311t oesophagostomy tube placement 241243
nose, surgical considerations 113116 oesophagram 160162
NSAIDs (non-steroidal anti-inflammatory drugs) strictures 162
24t, 26t offers (promotional) 124
nuclear factor-kB (NFkB) 72 oliguria 249250, 261
nursing care omental wrap 5051
in AKI 250251 omeprazole 203, 250
diabetic emergencies 212213 ondansetron 202, 250
in head trauma 102103 ophthalmoscopy 305308
in hypoadrenocorticism 8384 opioids
in ocular emergencies 113116 blood pressure and 255
post respiratory tract surgery 110111 in RTA 234
post-anaesthesia 253262 opisthotonus 9899
in seizures 219220 optic disc 309t, 310t, 313
nutrition oral irritation 55
in AKI 251, 292 orbital swelling 189191
assessing needs 237238 oropharyngeal stick injuries
calculating energy requirements 238239, acute 5556, 5859
240, 242 chronic 5658, 59, 60
in diabetic emergencies 213 diagnosis 5758
in head trauma 102 treatment 5860
malnutrition 237 oseltamivir, in parvovirus infection 203, 205
naso-oesophageal feeding 203, 239240 ovariohysterectomy, iatrogenic haemoabdomen
oesophagostomy tubes 241243 and 36
optimum route 238 overheads 123
in parvovirus infection 206 oxidative phosphorylation 71
post upper respiratory tract surgery 111 oxygen therapy
preventative healthcare measures 118 administration methods 37
nystagmus 9798 in dyspnoea 1
humidification 3
O in neonatal resuscitation 45
obligation 142 oxygen toxicity 7
octreotide 277 post respiratory tract surgery 110
ocular discharge 56 in RTA 232233
ocular emergencies see also eyes in seizures 219220
acute glaucoma 113, 116, 194195 during thoracocentesis 8
acute uveitis 196 oxygenation, monitoring 66, 109, 257258
deep corneal ulcers 191195 Oxyglobin see haemoglobin based oxygen
first aid advice 114 carriers
foreign bodies 192 oxytocin 226, 227
non-traumatic 189196
nursing care 113116 P
reflexes and responses 114 pain see analgesia
restraint 114 pancreas, physiology 207
retrobulbar infection 189191 pancreatitis
sudden-onset blindness 196 AKI and 25t
surgical considerations 115 peritoneal effusion 15, 170
telephone triage 113114 panhypoproteinaemia 199
traumatic 185188 PaO2 109
ocular examination, in head trauma 9899, PaO2/FiO2 ratio calculation 262
105t paranasal sinuses 107
Page 324 of 334
parenteral nutrition 237, 238 pleural ports 279
partial seizures 216217 plication, intestinal 171
parturition 3940, 221222 see also dystocia pneumocolonogram 159, 171
parvovirus infection pneumonia 1213
clinical signs 199200 pneumoperitoneum 169170, 174
diagnosis 200 pneumothorax 16
environmental management 200201 polycystic kidney disease 166
incidence 199 polycythemia, AKI and 25t
literature review 204206 polyethylene glycol 102
prognosis 204 polymyxin B, nephrotoxic potential 26t
treatment 201204 polyphagia 85
vaccination 200 polyuria 261262, 291
passive range of motion exercises (PROM) 102 portosystemic shunt 172, 173, 216
payment 125 positioning (radiography) 8990
PEA (pulseless electrical activity) 67, 69 positive contrast cystography 163
pedicle graft (corneal) 194 post-operative radiography 174
pencillamine, nephrotoxic potential 28t post-renal azotaemia 2829
penetrating trauma post-resuscitation care 70
abdominal 36 potassium
ocular 36 in AKI 2930, 249, 287, 290
oropharyngeal stick injuries 5560 in hypoadrenocorticism 80, 82
penicillins, nephrotoxic potential 26t in parvovirus infection 202
pentamidine, nephrotoxic potential 26t potassium bromide 218
perforated film dressings 271 potentiated amoxicillin 191, 202, 281, 284
pericardectomy 278279 povidone-iodine 267
perioperative fatalities 253 practice drills, for CPR 62
peritoneum precordial thump 69
dialysis 293294 prednisolone 76, 84
effusion 15, 170 prednisolone sodium succinate 83
peritonitis 169170 prednisone 84
pneumoperitoneum 169170, 174 pregabalin 219
persuasion see also communication skills pre-renal azotaemia 28
defined 137 primary anterior lens luxation 194195
emotions and 140142 primary consultations 119t, 120
ethos 137138 primary head trauma 95
logical arguments 138140 Pringle maneuver 38
Pet Blood Bank 145 processor problems (radiography) 93t
pet healthcare plans 117 profit 123
pet insurance 125 progesterone 221222
petroleum-impregnated dressings 271 prolactin 221
PETS (Pets Evacuation and Transportation proliferative phase (wound healing) 264265,
Standards) Act 153 266
pharynx promotions 124
stick injuries see oropharyngeal stick injuries propofol
surgical considerations 107 and myoglobin in humans 7475
phenobarbital 218 in seizures 102, 218
pheochromocytoma 81 proptosis 114
phosphorous containing urinary acidifiers, PROTECT project 285
nephrotoxic potential 28t proxymetacaine 5
physiotherapy, in head trauma 102 pseudopapilledema 313
pituitary-dependent hyperadrenocorticism 81 ptyalism 216
placenta, expulsion 222 pulmonary function, evaluating 262
planning, for disasters 155 pulmonary thromboembolism 18, 85
plasmid-mediated bacterial resistance 282 pulsatile lavage units 267
plateletpheresis 146, 147 pulse oximetry 66, 109, 257258
platelets 144, 146147 pulseless electrical activity 67, 69
pleural effusion 1, 1516, 276277 pupil size 98, 105t
Page 325 of 334
pupillary light reflex 98, 105t, 114, 196 renal replacement therapies (RRT) 250, 292
PvO2 109 295
pyelonephritis 25t, 31, 287288 renal vessel thrombosis, AKI and 25t
pyothorax 15 renomegaly 171172
pyrexia, in transfusion reaction 148 reperfusion injury 64, 7273
reproduction see also dystocia
Q gestation 39, 221
quinolones, nephrotoxic potential 26t parturition 3940, 221222
preventative healthcare measures 118
R reputation 137
radiocontrast agents, nephrotoxic potential 26t RER (resting energy requirement) 238239,
radiography 240, 242
achieving a diagnostic study 8994 research facilities, disaster plans 152
contrast see contrast radiology respect 134
dental 190 respiratory distress see also thorax
digital systems 91 in chylothorax 276277
in dystocia 41, 224225 initial assessment 12
exposure 11, 9091, 93t intravenous access 2
kidneys 32 oxygen therapy 1, 37, 8
linear foreign bodies 170171 physiological triggers 3
mechanical obstruction 171 post-operative 109110
microhepatica 172173 thoracocentesis 78
oropharyngeal stick injuries 57 respiratory toxins 13
patient preparation 89 resuscitation areas 6263 see also
peritoneal effusion 170 cardiopulmonary resuscitation
pneumoperitoneum 169170 retching 120
positioning 11, 8990 retina
post-operative 174 detachments 196, 313
pulmonary metastases 173 SARDS 196
renomegaly 171172 vasculature 310t, 311t
retroperitoneal effusion 170 retrobulbar infection 190
selecting views 9293 retrograde urethrography 33
technique 9091 retroperitoneal effusion 170
thoracic 1119, 173 rhabdomyolysis 217
troubleshooting 9293 Rhesus blood typing system 145
urethral calculi 173174 Rickettsia rickettsii 32
raisins, nephrotoxic potential 27t rifampin, nephrotoxic potential 26t
ranitidine 203 RIFLE scheme (for acute kidney injury) 21, 22t
RAP (respiration, alertness, perfusion) system rights 129
229 right-sided cardiac failure 276
reactive oxygen species 73, 75 road side transfusion support 144
receptionists see non-clinical employees road traffic accident see RTA
re-check consultations 119t Rocky Mountain spotted fever 32
recombinant granulocyte colony-stimulating RTA
factor, in parvovirus infection 204, 205 blood samples 233234
recommendations, non-clinical employees and client communication 229230, 231, 232
123 fluid therapy 234235
record keeping 153 ischemia-reperfusion injury 236
RECOVER (Reassessment Campaign on oxygen therapy 232233
Veterinary Resuscitation) guidelines 6162 shock 230231
regular insulin 212 step-by-step approach 231232
regurgitation 160 treatment 231236
relaxin 221 triage 229, 231
remodelling (wound healing) 265 rutin 277
renal failure
acute see acute kidney injury S
chronic 26t, 29t SARDS (sudden acquired retinal degeneration
Page 326 of 334
syndrome) 196 subcutaneous emphysema 56
SART (state animal response team) 152 sucralfate 203, 250
Schiff-Sherrington syndrome 99 suction devices 51, 53
science, history of 139140 sudden acquired retinal degeneration syndrome
secondary glaucoma 195 (SARDS) 196
secondary head trauma 95 sulfonamides, nephrotoxic potential 26t
sedation surgery
in head trauma 101 adrenalectomy 87
post respiratory tract surgery 109110 caesarian section 4145, 227
in thoracocentesis 8 chylothorax 277279
segmental intestinal distension 171 cisterna chyli ablation 278279
seizures conjunctival grafts 193194
causes 215216 haemoabdomen 3538
generalized 216 incisional dehiscence 4749
in head trauma 101102 intestinal dehiscence 4953
nursing care 219220 negative pressure wound therapy 269270
partial 216217 ocular 115
physiology 215 oesophagostomy tube placement 241243
stages 217 oropharyngeal stick injuries 5960
treatment 217219 pericardectomy 278279
sepsis perioperative fatalities 253
AKI and 25t post-operative radiography 174
peritonitis 169 prophylactic antibiotics 283284
radiographic signs 174 thoracic duct ligation 278
Serious Hazards Of Transfusion (SHOT) upper respiratory tract 107111
scheme 146, 148 sympathetic nervous system, catecholamines
shock and 229, 230
AKI and 24t sympathy 130
cats vs dogs 231 synthetic micropore dressings 271
decompensatory 230231 systemic inflammatory response syndrome
defined 230 (SIRS)
haemorrhagic 3637 AKI and 25t
in RTA 230231 in ischemia-reperfusion injury 74
signed consent 232 in parvovirus infection 200
sinography, in oropharyngeal stick injuries 58 in RTA 236
skeletal lesions (radiography) 173 in status epilepticus 217
skin, functions 263 systemic lupus erythematosus 26t
skull fracture 95
SLE (systemic lupus erythematosus) 26t T
Small Animal Coma Scale (SACS) 99, 104 table height (CPR) 63
105t tapetal fundus 309t, 311t
small intestinal perforation 169 tarsorrhaphy 194
smoke inhalation 13 team approach
sodium (serum) client satisfaction and 127128
in hypoadrenocorticism 80 financial resolution and 125
in parvovirus infection 202 perioperative fatalities and 253
sodium bicarbonate teeth, preventative healthcare measures 118
in advanced life support 68 telephone triage, ocular emergencies 113
in hypoadrenocorticism 83 tension pneumothorax 16
somatostatin, physiology 207 terminal shock 230231
spontaneous pneumothorax 16 tetracyclines 26t, 288
status epilepticus 217, 218, 220 therapeutics, non-clinical employees and 121
steroid responsive retinal detachments 196 thiacetarsamide, nephrotoxic potential 26t
stertor 56 third eyelid flap 194
stick injuries see oropharyngeal stick injuries third eyelid protrusion 189, 190
strabismus 97, 105t thoracic duct
streptokinase, nephrotoxic potential 28t anatomy 276
Page 327 of 334
ligation 278 dressings 268272
thoracic pump theory, chest compressions and exudative 268270
65 first aid advice 263
thoracocentesis 78, 277 granulating 271272
thorax see also respiratory distress lavage 267268
ARDS 18 negative pressure wound therapy 269270
auscultation 2 overview 263264
cardiac failure 2, 15, 17, 276 skin functions 263
chylothorax 275280 wound healing 264266
collapsed lung 13 triage 229, 231
diaphragmatic rupture 1819 trickle feeding 238
lung lobe torsion 14 tricyclic antidepressants, nephrotoxic potential
non-cardiogenic pulmonary oedema 18 28t
parasitic infection 14 trilostane 88
pleural effusion 1516 trimethoprim/sulfonamide 26t, 284
pneumonia 1213 tropicamide 306
pneumothorax 16 trust 134135, 137138
pulmonary metastases 173 tumour lysis syndrome, AKI and 25t
pulmonary patterns 1112
pulmonary thromboembolism 18 U
radiography 1119 UC:CR (urine cortisol and creatinine ratio) 86
trauma 1617 UK Blood Transfusion Services 143, 145
thrombocytopenia, immune mediated 147 ulcers
tidal volume, during CPR 66 corneal 191195
tocodynamometry 226 decubital 102
toxins, nephrotoxic potential 27t ultrasonography
trachea in dystocia 41, 225
catheters 6 in hyperadrenocorticism 87
intratracheal drug administration 65 kidneys 32
intubation 7, 65 in oropharyngeal stick injuries 58
surgical considerations 108 in peritoneal effusion 170
tracheobronchitis 13 in renomegaly 172
tracheostomy tubes 110 in retrobulbar swelling 189, 190
training (dogs) 118 upper GI studies 157159, 171
TRALI (transfusion related acute lung injury) upper respiratory tract surgery
148 complications 109110
transfusion medicine larynx 108
apheresis 144, 146147 nose 107
blood types 145146 nursing care 110111
comparative 145149 pharynx 107
component therapy 146 post-operative monitoring 108109
errors 146 trachea 108
in haemoabdomen 37 ureters
Massive Transfusion Protocol 144 ectopic 165, 167
in parvovirus infection 201202 ureteroliths 29
platelets 144, 146147 urethra
road side transfusion support 144 calculi 173174
TRALI 148 catheterisation 288, 289
transfusion reactions 26t, 145146, 148 urethrogram 164165, 173174
transfusion triggers 148149 urinalysis
in war zones 143144 in AKI 3031
traumatic brain injury see head trauma cortisol:creatinine ratio 86
traumatic wounds in diabetic emergencies 209
antibiotics 272 in hyperadrenocorticism 86
classification 266 urinary tract
cleansing 266 AKI see acute kidney injury
debridement 266 contrast radiology 163167
Page 328 of 334
differentiating azotaemia 2829 Z
dysuria 121 zonisamide 218
ectopic ureters 165, 167 zoos, disaster plans 152
infection 31
ureteroliths 29
urethral calculi 173174
urine output, monitoring 260262
uterine inertia 4041
uveitis 191, 195, 196
V
vaccination 118, 200
vacuum-assisted closure 269270
VAKI (veterinary acute kidney injury) scheme
21, 22, 22t
values (clients) 129
vancomycin 26t, 283
vascular ring anomaly 162
vasculitis, AKI and 25t
vasopressin 6768
ventilation (during CPR) 6566
ventricular fibrillation 67, 69
Veterinary Medicines Directorate 121
veterinary practice
client satisfaction 127135
compliance 120
consultations 119120
culture 127128
disaster plans 151
emergencies 120121
financial outcomes 123125
non-clinical employees 117125
pet healthcare plans 117
preventative healthcare measures 117118
veterinary receptionists see non-clinical
employees
vision 98, 113
visual tracking 114
volunteers, disaster plans 154
vomiting 202, 291
W
war zones, transfusion medicine in 143144
warming hypothermic patients 255
Waterhouse-Friderichsen syndrome 80
wet-to-dry dressings 268269
whelping bitches see dystocia; parturition
wound healing see also traumatic wounds
factors affecting 266
inflammatory phase 264, 266
maturation phase 265
proliferative phase 264265, 266
X
xanthine oxidase 72, 73
x-rays see radiography
Page 329 of 334


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Contents

Lecture Stream 1 Carriage Suite Thursday

TAKING THE DIFFICULTY OUT OF DYSPNOEA

Karen Humm MA VetMB CertVA DACVECC FHEA MRCVS

Stabilisation of the respiratory system

Respiratory distress is triggered by hypoxia, hypercapnia or a marked increase in the work of

Direct from a cylinder using oxygen tubing

Oxygen administration methods

Short term methods of oxygen administration

Flow-by administration is not an efficient means of oxygen administration. Anaesthetised

Longer term oxygen administration

Nasal prongs / cannulas

Buster collar oxygen hood

Oxygen can be administered into an enclosed buster collar (either practice-made or

Endotracheal intubation and ventilation

marked distress and can on occasion be fatal. Thoracocentesis performed on a patient

To perform thoracocentesis the patient needs to be effectively but sympathetically restrained

PULMONARY PATHOLOGY IN DIAGNOSTIC IMAGING

Radiographs must be of diagnostic quality to allow interpretation. If a patient is in acute

Review of pulmonary patterns

An interstitial pulmonary pattern can be structured or unstructured. A diffuse unstructured

Radiographic findings of thoracic pathology

Bacterial bronchopneumonia results from spread of exudative inflammation to the lung

distribution. Haematogeneous septic pneumonia is also more diffuse and patchy in

Acute bronchitis (also referred to as tracheobronchitis) generally starts as a viral infection

Eosinophilic bronchopneumopathy is a condition that is typically seen in young dogs. On

Bronchieactasis describes irreversible, saccular or cylindrical dilations of the bronchi and

It should be remembered that a radiographic bronchial pattern can occur secondary to

Angiostrongylus vasorum is increasingly seen as a cause of acute respiratory signs in the

Lung lobe torsion

Pneumothorax is most often diagnosed on clinical examination, but radiographs may be

Other cavitated pulmonary lesions can present acutely as a pneumothorax. Cavitated

Tension pneumothorax is a specific condition resulting from a check-valve mechanism at

As described above (haemothorax), the radiographic features of thoracic trauma include

Cardiac failure in feline patients has a less characteristic pulmonary distribution. An

Non cardiogenic oedema

Non-cardiogenic oedema has a variety of causes with a classic radiographic appearance.

Acute respiratory distress syndrome (ARDS) is a process of pulmonary inflammation and

Pulmonary thromboembolism is associated with numerous systemic diseases including

Traumatic diaphragmatic rupture may result in acute respiratory distress. Radiographically

ACUTE KIDNEY INJURY: AN UPDATE

Figure 1: RIFLE scheme used by Lee and others (2011)

0 Creatinine increase <150% from baseline

1 Creatinine increase of 150199% from baseline

3 Creatinine increase of 300% from baseline

AKIN (Acute kidney injury network), GFR (Glomerular filtration rate).

Figure 3: IRIS AKI Grading Criteria

Non Azotaemic AKI:

Figure 4: Causes of Acute Kidney Injury (Most common causes in bold)

Decreased renal perfusion

Prolonged urinary tract obstruction

Increased renal vascular resistance

Systemic inflammatory response syndrome (SIRS)

Drug and Toxin Associated see Figure 5

Figure 5: Substances known to have nephrotoxic potential (Most common in bold)

Calcium antagonists Bisphosphonates

Miscellaneous Drugs Allopurinol

Differentiating intrinsic, pre-renal and post-renal azotaemia

Differentiating AKI and Chronic Kidney Disease

Figure 6: Differentiating between AKI and CKD

Findings on Presentation Acute kidney injury Chronic kidney disease

Body condition score Normal Decreased

PCV Normal Reduced (non-regenerative