Clinical Pharmacology and Forensic Toxicology

PHYSIOLOGY OF VITAL ORGANS: A REVIEW
SHRIKANT KULKARNI
The knowledge of basic physiology of alla the vital organs is very much
essential inorder to effecly achieve the therapeutic protocols and also to understand the
pathological changes that are taking place in body of the patient.The following
description is an attempt to revise the basic physiology of important vital organs in the
body.
BRAIN:
The brain is the center of the nervous system and is a highly complex organ. Enclosed
in the cranium. In spite of the fact that it is protected by the thick bones of the skull,
suspended in cerebrospinal fluid, and isolated from the bloodstream by the blood-brain
barrier, the delicate nature of the brain makes it susceptible to many types of damage
and disease. The most common forms of physical damage are closed head injuries such
as a blow to the head, a stroke, or poisoning by a wide variety of chemicals that can act
as neurotoxins. Infection of the brain is rare because of the barriers that protect it, but is
very serious when it occurs.
The most important biological function of the brain is to generate behaviors that
promote the welfare of an animal. Brains control behavior either by activating muscles,
or by causing secretion of chemicals such as hormones. Even single-celled organisms
may be capable of extracting information from the environment and acting in response
to it. However, sophisticated control of behavior on the basis of complex sensory input
requires the information-integrating
Several brain areas have maintained their identities across the whole range of
vertebrates, from hagfishes to humans.
• The medulla, along with the spinal cord, contains many small nuclei involved in
a wide variety of sensory and motor functions.
• The hypothalamus is a small region at the base of the forebrain, whose
complexity and importance belies its size. It is composed of numerous small
nuclei, each with distinct connections and distinct neurochemistry. The
hypothalamus is the central control station for sleep/wake cycles, control of
KVC Sponsored CVE training programme on “Clinical Pharmacology & Forensic

Toxicology” organized by the Dept.of Pharmacology &Toxicology,Veterinary
College,Bidar,from 24th -29th August,2009
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eating and drinking, control of hormone release, and many other critical
biological functions.
• The thalamus is a collection of nuclei with diverse functions. Some of them are
involved in relaying information to and from the cerebral hemispheres. Others
are involved in motivation. The subthalamic area (zona incerta) seems to
contain action-generating systems for several types of "consummatory"
behaviors, including eating, drinking, defecation, and copulation.
• The cerebellum modulates the outputs of other brain systems to make them
more precise. Removal of the cerebellum does not prevent an animal from
doing anything in particular, but it makes actions hesitant and clumsy. This
precision is not built-in, but learned by trial and error. Learning how to ride a
bicycle is an example of a type of neural plasticity that may take place largely
within the cerebellum.
• The tectum, often called "optic tectum", allows actions to be directed toward
points in space. In mammals it is called the "superior colliculus", and its best
studied function is to direct eye movements. It also directs reaching movements,
though. It gets strong visual inputs, but also inputs from other senses that are
useful in directing actions, such as auditory input in owls, input from the
thermosensitive pit organs in snakes, etc.
• The pallium is a layer of gray matter that lies on the surface of the forebrain. In
reptiles and mammals it is called cortex instead. The pallium is involved in
multiple functions, including olfaction and spatial memory. In mammals, where
it comes to dominate the brain, it subsumes functions from many subcortical
areas. The hippocampus, this part of the brain is involved in spatial memory and
navigation in fishes, birds, reptiles, and mammals.[35]
• The basal ganglia are a group of interconnected structures in the forebrain. The
primary function of the basal ganglia seems to be action selection. They send
inhibitory signals to all parts of the brain that can generate actions, and in the
right circumstances can release the inhibition, so that the action-generating
systems are able to execute their actions. Rewards and punishments exert their
most important neural effects within the basal ganglia.
• The olfactory bulb is a special structure that processes olfactory sensory signals,
and sends its output to the olfactory part of the pallium.
HEART:
The heart is a muscular organ in all vertebrates responsible for pumping blood through
the blood vessels by repeated, rhythmic contractions. The heart is composed of cardiac
muscle, an involuntary striated muscle tissue which is found only within this organ. In
mammals, the function of the right side of the heart (see right heart) is to collect de-

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oxygenated blood, in the right atrium, from the body (via superior and inferior vena
cavae) and pump it, via the right ventricle, into the lungs (pulmonary circulation) so
that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This
happens through the passive process of diffusion. The left side (see left heart) collects
oxygenated blood from the lungs into the left atrium. From the left atrium the blood
moves to the left ventricle which pumps it out to the body (via the aorta). On both
sides, the lower ventricles are thicker and stronger than the upper atria. The muscle
wall surrounding the left ventricle is thicker than the wall surrounding the right
ventricle due to the higher force needed to pump the blood through the systemic
circulation.
The heart is effectively a syncytium, a meshwork of cardiac muscle cells

interconnected by contiguous cytoplasmic bridges. This relates to electrical stimulation
of one cell spreading to neighboring cells. Some cardiac cells are self-excitable,
contracting without any signal from the nervous system, even if removed from the heart
and placed in culture. Each of these cells has its own intrinsic contraction rhythm. A
region of the heart called the sinoatrial node SA node, or pacemaker, sets the rate and
timing at which all cardiac muscle cells contract. The SA node generates electrical
impulses, much like those produced by nerve cells. Because cardiac muscle cells are
electrically coupled by inter-calated disks between adjacent cells, impulses from the SA
node spread rapidly through the walls of the artria, causing both artria to contract in
unison. The impulses also pass to another region of specialized cardiac muscle tissue, a
relay point called the atrioventricular (AV) node, located in the wall between the right
artrium and the right ventricle. Here, the impulses are delayed for about 0.1s before
spreading to the walls of the ventricle. The delay ensures that the artria empty
completely before the ventricles contract. Specialized muscle fibers called Purkinje
fibers then conduct the signals to the apex of the heart along and throughout the
ventricular walls. The Purkinje fibres form conducting pathways called bundle
branches. The impulses generated during the heart cycle produce electrical currents,
which are conducted through body fluids to the skin, where they can be detected by
electrodes and recorded as an electrocardiogram (ECG).
LUNGS:
The lung or pulmonary system is the essential respiration organ in air-breathing

animals. Two lungs are located in the chest on either side of the heart. Their principal
function is to transport oxygen from the atmosphere into the bloodstream, and to
release carbon dioxide from the bloodstream into the atmosphere. This exchange of
gases is accomplished in the mosaic of specialized cells that form millions of tiny,
exceptionally thin-walled air sacs called alveoli. Once air progresses through the mouth

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or nose, it travels through the oropharynx, nasopharynx, the larynx, the trachea, and a
progressively subdividing system of bronchi and bronchioles until it finally reaches the
alveoli where the gas exchange of carbon dioxide and oxygen takes place. The drawing
and expulsion of air (ventilation) is driven by muscular action. In addition to their
function in respiration, the lungs also:
• alter the pH of blood by facilitating alterations in the partial pressure of carbon

dioxide
• filter out small blood clots formed in veins
• filter out gas micro-bubbles occurring in the venous blood stream such as those
created after scuba diving during decompression.[4]
• influence the concentration of some biologic substances and drugs used in
medicine in blood
• convert angiotensin I to angiotensin II by the action of angiotensin-converting
enzyme
• may serve as a layer of soft, shock-absorbent protection for the heart, which the
lungs flank and nearly enclose.
Avian lungs do not have alveoli as mammalian lungs do. They contain millions of
tiny passages known as para-bronchi, connected at both ends by the dorsobronchi. The
airflow through the avian lung always travels in the same direction - posterior to
anterior. This is in contrast to the mammalian system, in which the direction of airflow
in the lung is tidal, reversing between inhalation and exhalation. By utilizing a
unidirectional flow of air, avian lungs are able to extract a greater concentration of
oxygen from inhaled air. Birds are thus equipped to fly at altitudes at which mammals
would succumb to hypoxia. This also allows them to sustain a higher metabolic rate
than an equivalent weight mammal.
LIVER:
The liver is the largest glandular organ of the body. This organ plays a major role in
metabolism and has a number of functions in the body, including glycogen storage,
decomposition of red blood cells, plasma protein synthesis, hormone production, and
detoxification. It lies below the diaphragm in the thoracic region of the abdomen. It
produces bile, an alkaline compound which aids in digestion, via the emulsification of
lipids. It also performs and regulates a wide variety of high-volume biochemical
reactions requiring highly specialized tissues, including the synthesis and breakdown of
small and complex molecules, many of which are necessary for normal vital The liver
is necessary for survival; there is currently no way to compensate for the absence of
liver function. The physiological functions of liver are:

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• A large part of amino acid synthesis
• The liver performs several roles in carbohydrate metabolism:
o Gluconeogenesis (the synthesis of glucose from certain amino acids,
lactate or glycerol)
o Glycogenolysis (the breakdown of glycogen into glucose)
o Glycogenesis (the formation of glycogen from glucose)
• The liver is responsible for the mainstay of protein metabolism, synthesis as
well as degradation
• The liver also performs several roles in lipid metabolism:
o Cholesterol synthesis
o Lipogenesis, the production of triglycerides (fats).
• The liver produces coagulation factors I (fibrinogen), II (prothrombin), V, VII,
IX, X and XI, as well as protein C, protein S and antithrombin.
• In the first trimester fetus, the liver is the main site of red blood cell production.
By the 32nd week of gestation, the bone marrow has almost completely taken
over that task.
• The liver produces and excretes bile (a greenish liquid) required for emulsifying
fats. Some of the bile drains directly into the duodenum, and some is stored in
the gallbladder.
• The liver also produces insulin-like growth factor 1 (IGF-1), a polypeptide
protein hormone that plays an important role in childhood growth and continues
to have anabolic effects in adults.
• The liver is a major site of thrombopoietin production. Thrombopoietin is a
glycoprotein hormone that regulates the production of platelets by the bone
marrow.
• The breakdown of insulin and other hormones
• The liver breaks down hemoglobin, creating metabolites that are added to bile
as pigment (bilirubin and biliverdin).
• The liver breaks down toxic substances and most medicinal products in a
process called drug metabolism. This sometimes results in toxication, when the
metabolite is more toxic than its precursor. Preferably, the toxins are conjugated
to avail excretion in bile or urine.
• The liver converts ammonia to urea.
• The liver stores a multitude of substances, including glucose (in the form of
glycogen), vitamin A (1–2 years' supply), vitamin D (1–4 months' supply),
vitamin B12, iron, and copper.
• The liver is responsible for immunological effects- the reticuloendothelial
system of the liver contains many immunologically active cells, acting as a
'sieve' for antigens carried to it via the portal system.
• The liver produces albumin, the major osmolar component of blood serum.

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• The liver synthesizes angiotensinogen, a hormone that is responsible for raising
the blood pressure when activated by renin, a kidney enzyme that is released
when the juxtaglomerular apparatus senses low blood pressure.
KIDNEY:
The kidneys are paired organs, which have the production of urine as their primary
function. They are part of the urinary system, but have several secondary functions
concerned with homeostatic functions. These include the regulation of electrolytes,
acid-base balance, and blood pressure. In producing urine, the kidneys excrete wastes
such as urea and ammonium.
summary of physiologic activities in nephrons and collecting ducts during

formation of urine
Component of Nephron Physiologic Process

Glomerulus Passive formation of ultrafiltrate of plasma devoid of most protein.
Bowman's capsule Collection of glomerular filtrate
Proximal tubule Active Reabsorption of: Glucose, proteins & amino acids,
vitamins, ascorbic acid,acetoacetate, hydroxybutyrate, uric acid,
sodium, potassium, calcium ( by PTH), phosphate ( by PTH),
sulfate, bicarbonate
Passive Reabsorption of: Chloride, water, urea
Active Secretion of: Hydrogen ion
Henle's loop Generation of medullary hyperosmolality
Descending limb Passive Reabsorption of: Water
Passive Secretion of: Sodium, urea
Thin ascending limb Passive Reabsorption of: Urea, sodium, impermeable to water
Thick ascending limb Active Reabsorption of: Chloride, calcium
Passive Reabsorption of: Sodium, impermeable to water,
potassium
Distal tubule Active Reabsorption of: Sodium ( by aldosterone), calcium,
HCO3, small amounts of glucose
Passive Reabsorption of: Chloride, water ( by ADH)
Active Secretion of: Hydrogen ion, ammonia, uric acid Passive
Secretion of: Potassium
Collecting ducts Active Reabosorption of: Sodium ( by aldosterone)
Passive Reabsorption of: Chloride, water ( by ADH)
Active Secretion of: Hydrogen ion
Passive Secretion of: Potassium
*****

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THERAPEUTIC PROTOCOLS IN OCULAR AILMENTS
M.VIJAY KUMAR
Ocular antimicrobial therapy differs from treating infections in other tissues

because drugs can be administered directly to the eye, achieving high drug
concentrations. However,owing to the limited number of veterinary ophthalmic
preparations available for topical ophthalmic use, practitioners need to make rational
antimicrobial choice and extralabel drug use for successful therapy.practitioners should
avoid using the antimicorbials to treat noninfectious ocular conditions such as uveitis or
allergic conjunctivitis.unwarranted antimicrobials have no affect on an antiiflammatory
disease process and encourage antimicrobial resistance. Common bacterias affecting
eye include Staphylococcus intermdius, Streptococcus spp.( Dogs), Chlamydophilia
felis, Mycoplasma felis(cats), Staphylococcus spp,Streptococcus zooepidemicus,
Pseudomonas spp., Aspergillus spp., Fusarium spp (Equines), Moraxella bovis (Cattle),
Mycoplasma conjunctivae Branhamella ovis(Goats) and Chlamydophilia pecorum
,Branhamella spp (Sheep).
Routes of drug administration :
The 3 primary methods of delivery of ocular medications to the eye are :

Topical, Local ocular (ie, subconjunctival, intravitreal, retrobulbar, intracameral) and
Systemic. The most appropriate method of administration depends on the area of the eye
to be medicated - extraocular structures, cornea, anterior segment (anterior chamber and
iris), posterior segment (ciliary body, retina, vitreous), and retrobulbar or orbital tissues.
The conjunctiva, cornea, anterior chamber, and iris are usually best treated with topical
therapy. In contrast, the eyelids can be treated with topical therapy but more frequently
require systemic therapy. The posterior segment always requires systemic therapy, as
most topical medications do not penetrate to the posterior segment. Retrobulbar and
orbital tissues are most frequently treated systemically.
1. Topical-most common route of administration:
Degree of penetration of topically applied medications depends on integrity of

normal defense mechanisms of the eye. Drug absorption is greatly enhanced by ocular
inflammation. Medications put in the conjunctival sac can penetrate the cornea,
conjunctiva, or be absorbed systemically via the nasolacrimal system. Topical
administration is also affected by the Vehicle, molecular size of the drug, drug
concentration, pH, electrolyte composition and preservatives.

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Corneal epithelium is the main site of resistance to drug penetration. The cornea may
be thought of as a fat-water-fat sandwich. As a result, the epithelium and endothelium
are relatively impermeable to electrolytes but are readily penetrated by fat-soluble
substances. The stroma is readily penetrated by electrolytes but not by fat-soluble
substances. Drugs that have the ability to exist in equilibrium in solution as ionized
(water soluble; polar) and unionized (lipid soluble; nonpolar) forms are ideal for topical
use, i.e., chloramphenicol, fluoroquinolones. Topical administration is used for
treatment of eyelids, conjunctiva, cornea, iris, and anterior uvea. Following which, up to
80% of the applied drug(s) is absorbed systemically across the highly vascularized
nasopharyngeal mucosa. Because absorption via this route bypasses the liver, there is no
large first-pass metabolism seen after administration PO.
2. Sub conjunctival (bulbar conjunctiva):
This technique requires only topical anesthesia and a tuberculin syringe with a
25- or 27-gauge needle. Volumes should not exceed 0.25 ml in cats and Dogs and 1.0
ml in horses and cows. Subconjunctival medication reaches the cornea by slowly
leaking out of the injection site. Intraocular drug levels are attained by diffusion through
the cornea and sclera. Subconjunctival administration is used for diseases of the cornea,
anterior, uvea, anterior vitreous, and sclera. Subconjunctival or sub-Tenon’s therapy,
while not a true form of systemic medication, has potentially increased drug absorption
and contact time. Medications both leak on to the cornea from the entry hole of injection
and diffuse through the sclera into the globe. Drugs with low solubility such as
corticosteroids may provide a repository of drug lasting days to weeks. Appropriate
amounts must be used, as large amounts, especially of long-acting salts, can cause a
significant inflammatory reaction. For sub-Tenon’s injections, 0.5 ml/site is usually safe
and effective in small animals and ≤1 ml in large animals such as the horse and cow.
3.Retrobulbar medications:
They are used infrequently for therapeutics. In cattle, the retrobulbar tissues can
be anaesthetized with local anesthetic (lidocaine) for enucleations. Whenever any
medication is placed into the orbit, extreme care must be taken to ensure that the
medication is not inadvertently injected into a blood vessel, the optic nerve, or one of
the orbital foramen. Retrobulbar injection has a high risk of adverse effects and should
not be used unless the clinician is experienced and the animal is appropriately
restrained.
4. Intravitreal-used infrequently:
Antibiotics and antifungal drugs have been effectively used in microgram

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dosages. Generally injected at the pars plana for infectious endophthalmitis.
5. Systemic-P.O., I.V. or I.M:
Systemic administration is required for treatment of diseases of the retina,

optic nerve, and vitreous,for posterior segment therapy and to complement topical
therapy for the anterior segment. The blood-ocular barriers can limit absorption of less
lipophilic drugs, but inflammation initially allows greater drug concentrations to reach
the site. As the eye starts to heal, these barriers become more effective and can limit
further drug penetration. This should be considered when treating posterior segment
disease, eg, blastomycosis in small animals with hydrophilic drugs such as itraconazole.
Ocular dosage forms:
Topical ophthalmic drugs are formulated as ointments, suspensions and

solutions. Deciding which formulations to be used depends on the several practical
considerations. Ocular contact time of ointment is longer than solutions or
suspensions,so they are more practical when the owner cannot follow a frequent
administration regimen. Avoid ointments on penetrating wounds or descemetocele, and
prior to intraocular surgery, as their petroleum base elicits severe granulomatous
reaction when in direct contact with intraocular tissue. The application frequency of
topical antimicrobials depends on the disease and drug formulation. one drop of an
antimicrobial solution applied four times daily is usually sufficient in the treatment of
uncomplicated corneal ulcers and bacterial conjunctivitis. When ointment is used a
5mm strip is applied to the conjunctiva a minimum of three times a day. If more than
one drug is involved in the therapeutic regimen, then 3 to 5 minutes should be allowed
between application of each medication to avoid dilution or chemical incompatibility.
Antimicrobial therapy is typically continued for seven days or until the ocular infection
is resolved.
Antibacterial ocular drug therapy:
Topical antibiotics are indicated for the treatment of corneal ulcers, corneal
perforations, conjunctivitis and blepharitis. Ideal choice of appropriate therapy begins
with identification of the organism and its sensitivity. Culture or cytologic examination
of material from the affected area is necessary. Minor bacterial conjunctivitis infection
may not justify routine culture and may be amendable to initial therapy with broad
spectrum antibiotics. Normal ocular flora is predominantly gram positive; a
predominance of gram negative organisms is indicative of an abnormal condition.
1. Chloramphenicol: Broad spectrum, bacteriostatic. Soluble in both water and fat so

it penetrates intact cornea with topical administration-thus may be considered for initial

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treatment of intraocular infections (penetrates the cornea).it is good first choice
antimicrobial for corneal ulcers and bacterial conjunctivitis. It is having poor efficacy
against gram negative bacteria and pseudomonas spp. Frequency of administration- q4
hrs for full therapeutic levels. Toxicity- risk of aplastic anemia.
2. Aminoglycosides:
a. Neomycin: Usually found in combination with other antibiotics. Broad spectrum-

bacteriocidal, impairs protein synthesis. Frequency of administration-BID-TID.
Toxicity- Topical-localized sensitivity; conjunctival irritant. Systemic-ototoxicity-
possible head tilt.
b. Gentamicin: Broad spectrum bactericidal activity including Streptococcus,

Staphylococcus, Proteus spp, and Pseudomonas aeruginosa. Effective topically and
subconjunctivally for external ocular infections. It is available as solution and ointment
because of its chemical characteristics does not readily cross lipid membranes, but
readily enters the stroma when the corneal epithelium is damaged. Renal toxicity with
concurrent oral therapy, may be toxic to surface epithelium.
c. Tobramycin.: Two to four times more effective against Pseudomonas spp. and
betalactamase producing staphylococci than gentamicin and effective against
gentamicin-resistant microbes.
3. Polypeptides:
a. Bacitracin: Bactericidal, active against gram positive microorganisms. Used in

combination with other antibiotics. Poor corneal penetration.
b. Polymyxin B: Poor penetration. Bactericidal. Effective mainly against gram-negative

bacilli and Pseudomonas spp. Should not be given subconjunctivally.
The combination of neomycin,bacitracin and polymixin B is known as “triple

antibiotic” which is first choice antimicrobial for bacterial conjuctivits,corneal ulcers
and prophylaxis against surface infection.
4. Cephalosporins:
a.Cefazolin: Broad spectrum, first generation cephalosporin.Topical use for gram +

cocci resistant to other antimicrobials. Can be administered subconjunctivally-does
penetrate intact cornea. Usually diluted to 50 - 100 mg/ml concentration. Mix with
artificial tears to a concentration of 33 mg/ml for treatment of meibomitis
5. Fluoroquinolones: Eg: Ciprofloxacin HCl ,Levofloxacin, Ofloxacin etc. Broad

spectrum, active against gram positive and gram negative microorganims. Drug of

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choice for betalactamase producing staphylococcus and aminoglycoside resistant
pseudomonas spp. Generally preferred in corneal, conjunctival, and intraocular
infections. Excellent corneal penetration.not effective against streptococci spp. Because
of their spectrum of activity these agents should never be used as empirical treatment.
Antiviral ocular drug therapy:
Antiviral agents are indicated for treatment of herpetic keratitis in cats. Corticosteriods
should never be used in the suspected ocular eye infections as they further aggravate the
condition. The topical antiviral agents are static in action and topically irritating, so
frequent administration is necessary and client compliance and patient tolerance are
issues.
1. Idoxuridine: 0.5% ointment and 0.1% solution. Frequency of administration is 1

drop every 4hrs until corneal re-epithelialization occurs. Does not penetrate the cornea
unless the epithelial barrier is broken. Acts by altering the viral replication by
substituting for thymidine in the viral DNA chain therefore prolonged or too frequent
administration may damage the corneal epithelium and prevent the ulcer healing.
2. Vidarabine: 3%Ointment-it is poorly lipid soluble, so corneal penetration is

minimal unless ulceration is present. Penetrates the cornea better than Idoxuridine.
Frequency of administration is to apply small amount of ointment 5 times daily until
corneal re-epithelialization is complete, the every 12 hrs for 7 days. Acts by Preventing
extension of the DNA chain by causing a premature stop to DNA replication
3.Trifluridine: 1%Solution-Current drug of choice for feline herpetic keratitis.

Antiviral potency reported as over twice that of idoxuridine and 5 times greater than
Vidarabine. Like idoxuridine, trifluridine inhibits nucleic acid synthesis,penetrates the
intact cornea, ulceration and uveitis increase its intraocular penetration.it is administered
4-9 times daily for 2 days, and then the frequency is reduced over the next 2-3 weeks.
4. Others: Lysine, Acyclovir, Interferons
Antifungal ocular drug therapy :
Ocular antifungal agents belong to one of three classifications: polyenes,

imidazoles, and pyrimidines.Topical antifungal agents are used more commonly to treat
fungal keratitis in horses than in small animals. Penetration of the intact cornea is poor
with all antifungals.
1. Polyenes :

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a. Natamycin : Used mainly against Candida spp. and Fusarium spp. (only approved
agent in the market)
b. Amphotericin B: Fungistatic, generally used systemically for fungal endophthalmitis,

may be given as an intravitreal injection in mcg dosages.
2. Imidazoles
a. Miconazole 1%: Drug of choice for most veterinary fungal keratitis cases, but no
longer readily available in IV preparation. Tolerated well as subconjunctival injection.
1 ml SID x 3-5 days if tolerated. Treatment frequency of a fungal keratitis may warrant
1 to 4hour treatment intervals. Lotions or sprays that contain ethyl alcohol should not be
applied to the eye.
b.Fluconazole: Synthetic triazole, fungistatic. Strength 2 mg/ml IV preparation.

Currently drug of choice for topical use, subpalpebral lavage unit, and intracameral
(100 μg) injection. Treatment frequency for fungal keratitis may warrant 2 to 4hr
treatment intervals.
Anti-inflammatory ocular drug therapy:
1. Corticosteroids: Subconjunctival injection of corticosteroids provide a greater local

anti-inflammatory effect than can be achieved by topical or systemic administration.
Posterior segment inflammation requires systemic corticosteroid therapy. In general,
topical therapy should be continued two weeks beyond resolution of clinical signs.
Local side effects of corticosteroid use include delayed corneal healing, increased
corneal collagenase activity, and an increased incidence of bacterial and mycotic
keratitis. In addition, topical corticosteroids may result in systemic changes. These
include reduced baseline cortisol levels, suppression of the adrenocorticotropic hormone
response curve, and altered carbohydrate metabolism. Frequency of administration-
dependent on clinical signs and the type of steroid used..
2. Nonsteroidal anti-inflammatory ocular drugs : They include salicylic acids

(aspirin),Propionic acids , Indomethacin ,Phenylbutazone, Flunixin meglumine etc . 1.
Aspirin: Most effective when used prior to prostaglandin release. Dosages: Dog-10 to
20 mg/kg, BID; Cat-10 mg/kg, q 48 hrs.
2. Carprofen : Used in similar ways as aspirin. May have fewer side effects. Do not
use in Labrador retrievers - may cause liver disease. Dosages: 2.2mg/kg BID. Not
approved for use in cats.
3. Etodolac : Dosage: Dog-10 - 15 mg/kg, PO SID. Should not be used in Dogs < 5 kg

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Monitor tear production-associated with development of KCS
4. Flunixin meglumine: Effective anti-inflammatory agent in the Horse and Dog ,

although not currently approved for use in Dogs. Dosages: Dog-0.75 to 1.20 mg/kg, IV,
SID, not to exceed 2 days. Commonly given 30 minutes prior to surgery to minimize
postoperative swelling and inflammation (i.e., lens extraction).; Not to be used. In cat.
5. Flurbiprofen: Used topically preoperatively to stabilize the blood-aqueous barrier in

inflammation (in diabetes mellitus), decrease production of ocular prostaglandins and
maintain pupil size. Can be used to treat anterior uveitis and in the presence of corneal
ulceration.
Ocular topical Anesthetics:
Drugs suitable for use as local anesthetics cause a reversible block of conduction
through nerve fibers by displacing calcium at binding sites in cell membranes. To be
effective, local anesthetics must have properties similar to drugs that penetrate the
cornea. They must be capable of existing in ionized (water-soluble) and nonionized
(lipid soluble) forms. Increased membrane permeability exists in an alkaline state. Local
anesthesia is less effective in inflamed tissue which has more acidic pH than normal.
Most topical anesthetics are effective within 30 seconds to 3 minutes to facilitate

procedures such as tonometry, corneal and conjunctival scrapings, and subconjunctival
injections. Microbial cultures should be taken prior to application of topical anesthetics
as inhibition of microorganisms has been attributed to topical anesthetic agents. The
agents used are Proparacaine - 0.5%, . Tetracaine - 0.5% to 2%. Topical anesthetics
should not be used on a regular basis with painful eyes because,animal may scratch off
corneal epithelium (feels no pain) and they may inhibit mitosis (thus healing) in
corneal cells.
a. Osmotic Agents (topical): 2-5% NaCl (hypertonic saline). Indicated primarily for
treatment of severe chronic corneal edema originating from superficial epithelial
disruption and for severe cornea bullae formation. Side effect-localized irritation.
b.Tear Film Supplements : All are indicated to control keratitis sicca. May provide
temporary comfort to corneal irritation resulting from distichia, entropion, or sutures,
and as a vehicle for delivery of medications. Tear supplements are available in solution
and ointment form and are intended to replace the aqueous or lipid layer of the tear film.
Preservative-free products generally recommended.
c.Lacrimogenics: These are drugs potentially capable of stimulating tear secretion.
1. Pilocarpine: Prescribed as 2 drops of 2% Pilocarpine per 4.5kg body weight added

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to the food twice daily. Maintain therapy for at least 1 month prior to recheck.Side
effect-emesis or anorexia-if this occurs-stop therapy for 24 hrs and start again at one
half the dose, gradually increasing to the starting dose.
2. Cyclosporine A 0.2% ointment : Cyclosporine is a potent suppressor of T-cell

growth factor and of the cytotoxic T-cell response to this growth factor.
3. Tacrolimus 0.02%, 0.03% ointment or solution:Effective alternative to

cyclosporine. T-cell surpressor with a distinct receptor site to cyclosporine.
Anticollagenase/Mucolytic Agents:Collagenase inhibitors are indicated for the

treatment of melting corneal ulcers.
1. Acetylcysteine : Anticollagenase (i.e,. Pseudomonas aeruginosa infection). Diluted

10 to 20% with artificial tears to a 5 to 8% concentration. Administered every 1 to 4 hrs
until desired effect is achieved. Overuse may result in localized inflammation and
excessive lysis of normal mucus, thus worsening corneal exposure.
2. Autogenous serum – anticollagenase: Use topically. Must be refrigerated and each

batch used for only 7 days - it is an excellent growth media for microorganisms.
*****

105
CARDIO VASCULAR EMERGENCIES: INTERPRETATION
AND CLINICAL MANAGEMENT
SANTOSH . P. SARANGAMATH
Cardiology is an interesting subject in recent times not only in human medicine

but in veterinary sciences as well. Recent diagnostic techniques and therapy have not
only improved the expectency of the life but also increased quality of life in dogs.
Overall the incidence of heart diseases in dogs is estimated to be 10 to 14 % and
majority of the geriatric patients (aged dogs) tend to suffer from valvular diseases.
Physical examination cardiac ailments requires great expertise, if history and signs are
included in the physical examination then probably more than 80 % of case diagnosis
can be made effectively.
Signalment:
Age: congenital heart diseases = < 2 years, cardiomyopathies + 2 to 7 years, Valvular

insufficiency=7 to 9 years. Breed: Patent ductus arteriosis= Pomaranian, coolie, poodle.
Aortic arch abnormilities = GSD, Grate dane. Mitral/trricuspid valvular insuffiency=
Daschund, Pomaranian, Poodle, Cocker spanial. Dialted cardiomyopahty= Doberman,
large breeds of dogs.
History: most patients with cardiac diseases have exercise intolerance at some level of
excertion. In most instances cardiac diseases begins somewhat insidiously with slow
progression over a period of several months to years. With right sided failure, ascites,
hepatomagaly occur initially where as with left sided failure coughing, pulmonary
odema and dyspnoea are commonly observed. History of fainting, syncope or collapse
can also be observed in dogs with arrythmias. Functional ability of the other organs too
get affected like kidney and liver.
Physical examination: most of the dogs look apparently normal, but they
progressively go down in condition and may look thin to cachetic in later stages.
Affected animals stand with abducted elbows indicating respiratory distress or
pulmonary oedema. Cyanosis of the visible mucous membrane may result from right to
left shunting of blood as in case of tetralogy of fallot, atrial septal defect and ventricular
septal defect. Increased capillary refill time may be noticed in conditions of shock,
mitral valve insufficiency. Superficial veins, jugular vein distension can be observed in
right sided failure or pericardial effusion.

105
Pulse: normal rate is 70-160 beats/min. Arrhythmia is characterized by irregular pulse
rate that is corellated with respiration. Pulse defecit is seen when there are more heart
beats than the femoral pulses. Greater the pulse deficit indicate more severe problem of
arrhythmia.
Ascultation: most important in assessing heart diseases. Both heart and lungs should
be asculted. 4 sounds are produced normally, but first 2 are heard frequently in dogs.
Murmers: are abnormal heart sounds as a result of vibration produced by the flow of
blood (turbulence in blood flow) in the heart or greater vessels.
Laboratory examination:
Combined with the history, physical examination, ECG tracings, Radiographs,

Ultrasonography, Phonocardiography and Angiography can usually pin down the
diagnosis of heart defect. The later diagnostics are special techniques which provide the
most exact view of the heart and great vessels,and can help clinicians to confirm a
diagnosis or evaluate the severity of the heart defect.
While performing clinical examination, observations such as pulse character,
mucous membrane color, capillary refill time, heart sounds are most important part of
initial work up. Detection of heart murmur during auscultation, coughing, dyspnoea,
ascites are some of the things which make clinicians to suspect cardiac involvement.
Some of the different conditions that can be diagnosed with the help of ECG in dogs
are:
• Evaluation of cardiac chamber enlargement

• Evaluation of Arrhythmias
• Evaluation of therapy- drug therapy e.g. Digitalis/ Propranolol/Quinidine etc
Interpretation of ECG:
The systemic Electrocardiographic interpretation can be done by monitoring
• Heart rate
• Heart rhythm
• Measurement of complexes and intervals
• Mean electrical axis of the heart
 COMMON ECG ABNORMALITIES:
A. HYPERTROPHY OF THE CARDIC CHAMBERS:

i) Right atrial hypertrophy : Tall “ P” wave, usually ≥ 0.4 mv on lead II
ii) Left atrial hypertrophy : wide “ P “ wave, usually ≥ 0.05 sec on lead II
iii) Right ventricular hypertrophy: Deep “ S” wave usually ≥ 0.35 mv

105
iv) Left ventricular hypertrophy : wide “ QRS” complexes usually ≥ 0.06 sec along
with height of the “R” wave is ≥ 2.5 mv in laed II
v) Biventricular Hypertrophy: Tall “ R” wave, wide “ QRS” complexes and deep
“S” wave in lead II
B. CONDUCTION ABNORMALITIES:
i)_Atrio-venticular heart block : occurs due to delay in transmission of impulses
from AVN to bundle of His
a) Ist degree AV Block: “PR” interval ≥ 0.13 sec.
b) II nd degree heart block: some “P” waves without “QRS” complex.
c) IIIrd degree heart block: more of “P” waves without ‘QRS” complex.
ii) Bundle Branch Block(BBB) : occurs due to interruptions in the transmission of

impulses through left and right bundle of His
a) Right BBB: wide “S” wave, QRS duration ≥ 0.08 sec
b) Left BBB : QRS duration ≥ 0.08 sec, but may be seen in left ventricular
hypertrophy, so, thoracic X-ray is must to differentiate this hypertrophy
C. EFFECT OF ELECROLYTE DISTURBANCES ON ECG

a) Hypokalaemia : Tal “T”ve, “P” wave flattened.
b) Hyperkalaemia: Prolonged “Q-T” interval and small biphasic “T” wave (+ ve or
– ve deflection)
c) Hypocalcaemia and Hypercalcaemia : prolonged “Q-T” interval and “ST”
segment elevation
D. ECTOPIC ARRYTHMIAS
a) Atrial fibrillation: most common arrhythmias seen in small animal, depolarization
occurs randomly throughout atria, here “P’ waves are replaced by “F” waves (saw
toothed waves) i.e. fine irregular movement of the base line observed as a result of
atrial fibrillation.
b) Ventricular fibrillation: it is a terminal event associated with cardiac arrest,

depolarization occurs randomly throughout ventricles, here large fine, irregular, bizarre
movement of base line without waves or complexes are observed.
ECG and radiography are the basic needs of the cardiac evaluation; the results
of these along with history and physical examination make clinician to arrive at a
definitive diagnosis. Although ECG is quite useful, it is not HIGHLY sensitive for
detecting hypertrophy of the heart chambers; it only supports a differential diagnosis
and should not be considered a definitive diagnostic test.

105
CONGENITAL DEFECTS :
Subvalvular aortic stenosis : left ventricular out flow is obstructed below the arotic
valve and include incomplete fibrous ridges, discrete fibrous rings, such dogs usually
won’t bred, balloon catheter dilatation( like balloon angioplasty in humans) of the sub
aortic area is found to be helpful.
Pulmonic stenosis : right ventricular out flow obstructed along with pulmonic valve
dysplasia characterized by thickening of valves, various surgical procedures are
employed to correct this apart from the balloon catheter dilatation.
Patent ductus arteriosus : where in pulmonary artery gets fused with aorta, leading to
increased flow of blood from the aorta to pulmonary artery leading to increased
pulmonary flow, intern increased pulmonary venous return to ventricles resulting in
volume overload in ventricles ending up with left side congestive heart failure, surgical
ligation is the best method for clinical management though such animals are not used
for breeding purpose.
DILATED CARDIOMYOPATHY AND HYPERTROPIC CARDIOMYOPATHY
Most common disease in dogs and cats, initially anorexia, weakness, exercise
intolerence, coughing, pulmonary odema, syncope with progression to congestive heart
failure. Treatment should be directed towards (1) reducing the elevated ventricular
pressure in order to relieve congestion- i.e. oedema (2) increasing forward stroke
volume and (3) Optimizing heart rate and rhythm
Regardless of the underlying cause, decrease in filling pressure with alleviating
oedema is achived by administration of diuretics. Such animals should receive
furosemide parentrally at the rate of 2 – 3 mg/kg until it stabilizes.Refractory oedema
cases are most effectively controlled by adding a second diuretic that acts at different
site at kidney, i.e. spiranolactone at the dose rate of 1-2 mg/kg BID (PO) or thiazide
diuretic (hydrochlorothiazide) at the dose rate of 2-4 mg/kg BID (PO).
List of diuretics used in case of cardia ailments
Bendroflumethia Dog 0.2-0.4 mg/kg BID (PO) Hypovolemia, as for
zide Cat undetermined hydrochlorthiazide
Bumetanide Dog 0.01-0.5 mg/kg total (IV); Hypovolemia, hypokalemia,
0.03-0.06 mg/kg SID-BID (PO) metabolic alkalosis
Cat unknown
Chlorthiazide Dog 20-40 mg/kg BID-TID (PO) Hypovolemia, hypokalemia,
Cat 20-40 mg/kg BID (PO) metabolic acidosis
Furosemide Dog 2-4 mg/kg BID-TID (IV, IM, SQ, Hypovolemia, hypokalemia,
PO); metabolic alkalosis, deafness
2-8 mg/kg q 1h (IV) in severe
pulmonary edema
Cat 1-2 mg/kg BID-TID (PO, IM, IV),
do not exceed 2 mg/kg (IV)

105
Hydrochlorothiazide Dog 2-4 mg/kg BID (PO) Hypovolemia, hypokalemia,
Cat 1-2 mg/kg BID (PO) metabolic acidosis, GI,
hyperglycemia
Spironolactone Dog 1-2 mg/kg BID (PO) Hypovolemia, hyperkalemia,
Cat 1-2 mg/kg BID (PO) GI
Triamterene Dog 1-2 mg/kg daily (PO) Hypovolemia, hyperkalemia,
Cat unknown metabolic acidosis
The only universally applicable recommendation for increasing cardiac output is to

optimize heart rate and rhythm. Arteriolar dilators and positive ionotropic agents are
used to achive this, such as potent ionotropes like dobutamine ( 5 – 10µ/kg i.v) and
dopamine or amrinone ( 1-3mg/kg initially). Positive inotropic therapy functions to
enhance contractility. These agents have been thought to be indicated when
contractility is reduced (systolic dysfunction).
Once the patient condition stabilizes then digoxin is administered at 0.007
mg/kg orally once in 2 days. Vasodilators such as enapril ( 0.25-0.5 mg/kg orally b.i.d)
are administered. Digoxin has 3 benefiial effects such as it decreases sympathetic
response, increasing the myocardial contractility by inhibiting K-Na ATPase and it
slows the impulse conduction through AV node there by decreases the arrhythmias.
Other positive ionotropic drugs used include bipiridine compound class of
drugs. (amrinone and milrinone). Phemobendan, a benzimidazole compound, is also a
phosphodiesterase inhibitor which also has calcium sensitizing effect. Thus, this drug
increases the sensitivity of the cardiac myofibrils to the calcium, there by improving the
strength of contraction of the myocardium. Doasge of Pimobendan: Dog: 0.25/kg BID
on an empty stomach.
Therapy for common Cardiac Arrhythmias :
The best therapy for most of the arrhythmia is to eliminate the underlying
causes which may be of intrinsic cardiac disease (like myocardial diseases, infiltrative
diseases, Ischemia, Hypertension, congenital heart disease, conduction disorders etc,),
Hypoxia( systemic- anemia, anaesthesia, local-myocardial infarction), Metabolic
diseases (like Acid-Base disorders, Neurologic disease, Endocrine disorder), Infection (
sepsis, Pyrexia). Some of these can be ruled out by history, physical examination, blood
examination and other routine diagnostic tests. Most clinicians agree that the presence
of clinical signs (weakness, Syncope) in conjunction with an arrhythmia warrants anti-
arrhythmic therapy.
Some of the antiarrhythmic drugs used in dogs and cats are:

105
Amiodarone Dog 10-20 mg/kg SID (PO) for 7-10 days Pulmonary fibrosis, GI,
(loading dose), then 3-15 mg/kg SID hepatitis, leukopenias,
bradycardia
Cat Unknown
Aprindine Dog 0.5-2.0 mg/kg (IV); TID (PO) GI, seizure, hepatitis
Cat Unknown
Digoxin Dog 0.22 mg/m2 BID (PO) GI, depression, anorexia,
Cat 1/4 of 0.125 mg (PO) q 48h - SID bradycardia, arrhythmias
Flecainide Dog 1-5 mg/kg BID-TID (PO); Dr. Fox GI, weakness, confusion,
suggests 3-10 mg/kg TID (PO) 1-2 depression
mg/kg (IV) slowly
Cat Unknown
Lidocaine Dog 2-4 mg/kg slow (IV), repeat q 10 Seizures, CNS excitation
min. to maximum of 8 mg/kg; 25-75 (seizures), GI, arrhythmias,
ug/kg/min (CRI) hypotension
Cat 0.25-1.0 mg/kg slow (IV) over 5
minutes
Mexiletine Dog 2-5 mg/kg BID-TID (PO) (oral As for lidocaine
lidocaine) Dr. Fox suggests 5-10
mg/kg BID-TID (PO)
Cat unknown
Phenytoin Dog 5-10 mg/kg (IV) slow; 35 mg/kg Depression, seizures
TID (PO)
Cat None
Procainamide Dog 6-8 mg/kg (IV) over 5 min; 25-40 Weakness, hypotension,
ug/kg/min (CRI); 8-20 mg/kg q 4-6 negative inotropic, GI,
hr (IM), TID (PO) (slow release bradycardia
formulation)
Cat 8-20 mg/kg TID (PO)
Propafenone Dog 3-6 mg/kg q8 hrs Transient arrhythmia &
Cat unknown hypotension
Quinidine Dog gluconate 6-20 mg/kg QID (IM); As per procainamide,
Extentab (sulfate) 6-16 mg/kg TID interacts with digoxin
(PO); Quinaglute, Cardioquin 8-20
mg/kg TID-QID (PO); 5-10 mg/kg
(IV)
Cat Sulfate 5.5-11.0 mg/kg TID (PO)
Sotalol Dog 0.5-2 mg/kg BID (PO) As per beta-blockers
Cat Unknown
Tocainide Dog 5-10 mg/kg TID-QID (PO); (oral As for lidocaine
lidocaine) Dr. Hamlin suggests 25
mg/kg QID (PO)
Cat unknown
Beta blockers / calcium chnanel blockers:

In dogs, Digitalis glycosides are useful in slow downing HR associated with
sinus tachycardia, atrial fibrillation, or supraventricular arrhythmias. If does not

105
controlled with this, a beta blocker or a calcium channel blocker is added to the
therapeutic regimen. The use of beta-blockers therefore can counteract the excess
catecholamines typical of heart failure, actually resulting in improved systolic function
in the long term and increased survival time. Beta-blockers increase survival in people
with heart failure. They can protect against arrhythmic death (sudden death). Dosage
of certain beta blockers ( Propranolol, metopralol, Atenolol) are given below in dogs
and cats. Calcium channel blockers, including diltiazem also used as adjunct to digoxin
therapy for heart rate control.
Propranolol : dog: 0.2-1.0 mg/kg TID (PO); 0.02-0.06 mg/kg (IV) slowly , cat: 0.2-
1.0 mg/kg BID-TID (PO); 0.04 mg/kg (IV) slowly.
Metoprolol: dog: 0.25-1 mg/kg BID-TID (PO), cat: 0.25-1 mg/kg BID-TID (PO)
Atenolol : dog: 5-12.5 mg SID-BID (PO) or 0.25-1 mg/kg SID-BID (PO) , cat: 5-12.5
mg SID-BID (PO)
Carvedilol : Dog: up to 0.5mg/kg BID (PO), Cat: unknown
ACE Inhibitors : ACE inhibitors have been shown to improve the length of survival of
dogs with CHF secondary to Dilated Cardiomyopathy. Enapril is found to be
beneficial in the treatment of CHF. ACE inhibitors block production of angiotensin II
(potent arterial constrictor) and block production of aldosterone (which contributes to
fluid overload), thereby causing vasodilation and reduction of fluid retention. Through
both of these actions ACE inhibitors appear to delay the progression of heart failure. In
dogs with chronic mitral valve insufficiency (CMVI), ACE inhibitors reduced
mortality.Dosage; Enalapril in case of dog: 0.5 mg/kg SID-BID (PO), usually BID and
in cases of cats 0.5 mg/kg SID (PO), Benazapril in case of dogs is 0.5 mg/kg SID-
BID(PO), usually BID and in cats the dosage is 0.25-0.5 mg/kg SID (PO).
Nitrates : Nitropruside a potent vasodilator, its effectiveness in veterinary medicine is
not been clearly proven. However, transdermal placement of nitroglycerine is used in
combination with digoxin, lasix to stabilize the heart failure patient.
VALVULAR DEGENERATION ( ENDOCARDITIS) :
This is common in certain breeds like GSD, bull terrier, Grate Dane. Seen most
commonly in older dogs and dogs over 13 years will exibit murmurs upon
ascultation.Diagnosis requires echocardiography. Surgical intervention, including valve
reconstruction, valve replacement and annuloplasty of the mitral valve has been
successful in associated clinical signs.
*****

105
CLINICAL MANAGEMENT OF RESPIRATORY
DISORDERS
SANDEEP HALMANDGE
Diseases of respiratory tract are commonly encountered in routine clinical

practice and there fore form important clinical entity for the clinicians. The causes of
respiratory disorders are multiple and complex, but the factors of stress, viral infection
and bacterial infection are almost always involved in cases of severe disease. A wide
variety of different stressors and agents may be involved in the disease process.
Stress factors Viral agents Bacterial agents

Heat PI 3 Pasteurella
Cold IBR Haemophilus
Dust BVD Klebsiella
Dampness BRSV Mycobacterium
Injury Adenovirus Mycoplasma
Fatigue Rhinovirus Streptococcus
Dehydration Herpesvirus Others
Hunger MCF
Anxiety
Irritant gases
Nutritional deficiencies
Surgery
Principal manifestations of respiratory insufficiency:
The functional integrity of respiratory system depends on its ability to exchange

oxygen in place of carbon dioxide from the venous circulation. Therefore, failure of
adequate oxygenation of tissues is a sign of respiratory insufficiency and is termed as
HYPOXIA.
Clinical hypoxia can be of four types viz;
a) Reduced oxygen carrying capacity of the blood (Anaemic hypoxia) seen in nitrite
poisoning and carbon monoxide poisoning,
b) Insufficient alveolar ventilation (Anoxic hypoxia) seen in strangulation, lung disease
c) Reduced blood flow (Stagnant hypoxia) seen in congestive heart failure and
D) Inability of tissues to utilize oxygen (Histotoxic hypoxia) encountered in cyanide

105
poisoning.
Nasal discharge: Serous, mucoid, muco-purulent nasal discharge is usual indication of

respiratory tract disease. Mucoid and serous discharge indicate acute inflammatory
disease whereas, muco-purulent always suggest secondary bacterial invasion. Close
inspection of nasal cavity helps in determining the origin of nasal discharge. Unilateral
discharge suggests a local problem whereas, bilateral indicates systemic involvement.
Bleeding from the nose is referred as epistaxis and if it is profused

rhinnorhagia, Whereas, haemaptysis is coughing up of blood usually from lower
respiratory tract.
Polypnea is rapid breathing, Tachypnea is very rapid and shallow breathing and
Hyperapnea is an abnormal increase in rate and depth of breathing but not up to the
point of labored. Dyspnea is difficult or labored breathing and can be of two types:
Expiratory dyspnea is prolonged and forceful expiration associated with

chronic obstructive lower airway diseases (COPD).
Inspiratory dysnea is prolonged and forceful inspiratory effort associated with

obstruction of upper respiratory airway (Laryngeal paralysis, obstruction, collapse of
tracheal rings).
Abnormal respiratory sounds:
Crackles are popping/bubbling sounds originating from lungs and suggestive of

presence of oedematous exudate in alveoli and bronchi. Wheezes are continuous
squeaking/whistling sound caused by passing of air through narrowed airway. These
are suggestive of presence of tenacious exudate or narrowing of airways.
Pleuritic frictional sounds are produced due to rubbing of inflamed parietal and
visceral pleural surface against each other which are more pronounced during
expiration and are suggestive of pleurisy or diffused pulmonary emphysema. Absence
of lung sounds or silent lung is suggestive of space occupying lesion in the thoracic
cavity or consolidation of lungs.
Coughing :
It is an explosive expiration of air from lungs which is initiated by stimulation of cough

centre located in medulla oblongata due to irritation of sensory receptors of airways.
Productive cough is suggestive of presence of exudative lesion and there is expulsion
of mucus and inflammatory debris, whereas, non-productive cough indicate
inflammation with minimal exudation.

105
Cyanosis (Bluish discoloration) of visible mucosae is indicative of serious respiratory
insufficiency. Common causes of cyanosis include congenital heart diseases and all
types of hypoxias.
DIAGNOSTIC APPROACH TO RESPIRATORY TRACT DISORDERS:
Clinical examination of the patient:
Clinical examination of patient suspected for respiratory disorder will definitely carry a
history of poor working performance, early exhaustion, abnormal breath sounds and
presence of one or the other clinical evidence like nasal discharge, respiratory distress
at rest, coughing. A thorough physical and clinical evaluation of the patient will help
the clinician to pinpoint the ongoing illness of which auscultation is the most important
indispensable tool.
Special techniques :
Nasopharyngeal swab, percutaneous trans-tracheal aspiration, broncho-alveolar lavage

are used as special diagnostic techniques in the diagnosis of respiratory tract
dysfunction. Elevated absolute neutrophil count in broncho-alveolar lavage fluid
(BALF) is considered as diagnostic feature of COPD in horses. Similarly, presence of
haemo-siderophages in the BALF in thoroughbred horses is suggestive of pulmonary
haemorrhage.
Use of fiber-optic endoscope has improved the diagnostic skill of the physician and is
routinely being used in canine and equine practice. Flexible fiber-optic endoscope has
clinical advantage of non-invasiveness, visual inspection of airways and collection of
sample with minimal contamination.
Thoracic radiography is a valuable diagnostic tool for diseases of lungs and helps in
detecting atelectasis, consolidation of lung parenchyma, space occupying lesion and
pleural effusions. Ultrasonography has a limited use but can be used for guided
thoracocentesis.
Pulmonary function tests :
Capnography means measurement of carbon di-oxide content of breath. Measurement

of respiratory volume, residual air and vital capacity of lung is referred as
Spirography.
PRINCIPLES OF TREATMENT OF RESPIRATORY TRACT DISORDERS:
1. Selection of antibiotic:A course of antibiotic is essential to counteract the bacterial

invasion. The choice of antibiotic depends on cost effective ratio, sensitivity of

105
microorganisms and effective penetration of the drug. Parenteral use of any one of the
following can be of choice under field conditions.
• Combination of Sulpha-trimethoprim @ 20 mg/kg body weight.

• Ampicillin, Amoxycillin or Amoxicillin and Cloxacillin combination @ 10
mg/kg b.wt.
• Third generation cephalosporins like Ceftazidime, Ceftrioxone @ 10 – 20
mg/kg b.wt.
• Recently extended spectrum Cephalosporins are gaining importance in large
animal practice. Tazobactam is a new beta lactamase inhibitor and its combination
with Cetrioxone has been reported very effective in complicated respiratory tract
infections with gram positive, gram negative as well as few anaerobes belonging to
Clostridial group.
• Amikacin, Azithromicin have promosing role in small animal practice.
2. Environmental alterations: Provision of comfortable, well ventilated environment
during convalescence brings about early recovery.
3. Use of antihistamines is beneficial to antagonize the deleterious effects of histamine

and other substances.
4. Respiratory stimulants like CO2, nikethamide, leptazole, caffeine and amphetamine

are widely used. doxapram hydrochloride, a centrally acting respiratory stimulant is
commonly used to antagonize respiratory depression in equine practice.
5. Mucokinetic drugs and broncodialators have effective mucocilliary clearance and

better penetration of antibiotic in the treatment of respiratory diseases.
Bromohexine, theophylline are drugs of choice. β–adrenergic agonist
bronchodialator e.g. clenbuterol is used in the treatment of chronic obstructive
pulmonary disease.
6. Expectorants are indicated to expel the mucus from the respiratory tract. Sedative
expectorants containing ammonium chloride are used in exhaustive, tenacious
cough whereas; codeine or dextramethorphan containing expectorants are indicated
in non-productive cough to suppress the cough center.
DISEASES OF LUNG:
Pulmonary congestion and oedema:
Engorgement of pulmonary vascular bed and subsequent increase in the amount

of blood in lung parenchyma is called as pulmonary congestion which later on leads to
escape of fluid into interstitial space and alveoli referred as pulmonary oedema.

105
Etiology: Primary pulmonary congestion is due to inhalation of toxic fumes and
smoke, anaphylactic shock, hypostatic congestion of lungs (prolonged recumbency due
to downer cow syndrome, milk fever, fracture of long bone). Secondary congestion
occurs due to congestive heart failure.
Pulmonary oedema can occur due to acute anaphylaxis, pneumonic

pasteurellosis, gram negative sepsis in pigs, CHF, inhalation of toxic gases and fumes,
pulmonary form of African horse sickness and Barker syndrome in foals.
Pathogenesis: Reduced effective alveolar space, reduced vital capacity of lungs and
impaired oxygenation of blood are the hallmarks of pulmonary congestion and oedema.
The end effect is anoxic hypoxia.
Clinical signs: Increased depth of respiration to the point of extreme dyspnea, open
mouth breathing, typical stance with front legs spread wide apart and abducted elbows.
Presence of crackles (moist rales) on auscultation over lower parts of lungs is
characteristic.
Diagnosis:
• Clinical findings.
• Laboratory investigation like bacterial isolation from nasal swabs, eosinophilia on
haematological examination.
Treatment:
• Epinephrine in anaphylactic shock.

• Antihistamines like pheniramine maleate, promethazine.
• Diuretics like furosomide @ 1-2 mg/kg body weight im.
• Acetylsalicylic acid is more effective than antihistamines in providing symptomatic
relief
• Corticosteroids like Hydrocortisone @ 1 mg/kg body weight have beneficial effect
as anti-inflammatory agents.
Pulmonary emphysema:
It is distension of lungs caused by overdistension of alveoli with rupture of

alveolar wall with or without escape of air into interstitial space.
Etiology: Chronic obstructive pulmonary disease (COPD) in horses is the most

important cause of pulmonary emphysema. Moldy hay is linked with COPD in horses.
In cattle, acute interstitial pneumonia, lung worm infestation (Dyctiocaulus viviparous),
Traumatic pneumonitis due to foreign body and poisonous plants like Senecio
quadridentatus, Perilla frutesens are attributing factors for pulmonary emphysema.

105
Pathogenesis: Excessive dilatation of alveoli due to narrowing of airways leads to its
rupture and escape of air in to interstitial space is the most accepted hypothesis of
pulmonary emphysema. Other possible reason could be inherent weakness of alveolar
wall and supporting tissue unable to sustain the stress during forceful coughing or
exertion. Incomplete evacuation and imperfect oxygenation of blood are the net results
of pulmonary emphysema leading to hypoxia.
Clinical findings: Increased rate of respiration at rest is initial sign of pulmonary

emphysema. As the disease advances, expiratory dyspnea is evident which gets
pronounced during exercise. It is accompanied by expiratory grunt. On auscultation
presence of Paper crackling rales over lung parenchyma is sure indication of
pulmonary emphysema. Subcutaneous emphysema of wither is considered as sequalae
of pulmonary emphysema.
Diagnosis:
• Based on clinical findings and evidence of paper crackling rales on auscultation.

• Narrowing of bronchioles and presence of abundant exudate in airways during
endoscopic examination.
• High absolute neutrophil count in BALF.
Treatment: Reduction of inflammation of airways with NSAID, β-adrenergic
bronchodialators like clenbuterol @ 0.8 - 3.2 µg/kg bodyweight and Steroids are
indicated. But the prognosis is always guarded.Inhalant corticosteroids in the form of
intra-nasal spray have been found effective in controlling the signs of respiratory
distress. Sodium cromoglycate is also useful in the treatment of COPD in horses as it
prevents degranulation of mast cells.
Pneumonia:
Inflammation of lung parenchyma, accompanied with inflammation of

bronchioles and may get complicated with extension of infection to pleura leading to
pleuritis.
Etiology:
• Pneumonic pasteurellosis (Pasteurella hemolytica)

• Haemophilus somnus, Klebsiella pneumoniae, Mycobacterium tuberculosis var
bovis, Mycoplasma mycoides var bovis, Fusobacterium necrophorus. Other
microorganisms include Actinomyces pyogenus, Streptococcus sp., and Bedsonia
sp.
• Viral agents like rhinovirus, bovine herpes virus, bovine respiratory syncytial virus,
parainfluenza-3, adenovrus-1, 2 and 3.

105
• Chlamidia and Aspergillus fumigatus like fungal agents.
• Lungworms (Dictyocaulus viviparous)
Pathophysiology: all types of pneumonia is based on interference with gaseous
exchange between alveolar air and blood which results in anoxia and hyperapnea. This
is manifested clinically by Polypnea, dyspnea or Tachypnea. Later on consolidation of
lungs brings about change in quality of breath sounds. Depending on type of exudate,
there is evidence of crackles or wheezes on auscultation. Toxaemia in bacterial
pneumonia can be life threatening clinical emergency.
Clinical Findings: Rapid shallow breathing is initial cardinal sign of pneumonia which
changes to dyspnea in later stages loss of lung parenchyma functionas. Presence of
moist, soft but painful cough is suggestive of bacterial broncho-pneumonia. Whereas
dry, hacking and paroxysmal cough is indicative of viral etiology. Bilateral muco-
purulant nasal discharge, fever, rough hair coat, gaunt appearance, presence of crackles
or wheezes on auscultation are observed.
Diagnosis:
• Isolation and identification of causative agent from nasal swab, transtracheal

aspirate or BALF.
• Haematological investigation: Leucopenia is suggestive of viral involvement
whereas, leucocytosis is indicative of bacterial invasion. Prominent eosinophilia
(>20%) is suggestive of parasitic etiology.
• Detection of lung worm larvae in faecal sediment suggests verminous pneumonia
• Serological tests for confirmation of viral interstitial pneumonia
• Medical imaging techniques: Thoracic radiography is helpful in detecting radio-
opaque patches suggestive of consolidation of lungs. Ultrasonography also has been
proved useful diagnostic aid in detecting pulmonary abscessation and anaerobic
bacterial pleuro-pneumonia.
Treatment:
• Higher Antibiotics
• Antihistamines
• Potent anti-inflammatory agents or steroids
• Bronchodilators and other supportive therapy.
*****

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CURRENT THERAPEUTIC PROTOCOLS IN HEPATIC
DISORDERS
M. VIJAY KUMAR
Liver disorder should always be considered when nonspecific clinical signs,

such as depression, weight loss, intermittent fever, and recurrent colic, are present
without an apparent cause. Differentiation between acute and chronic hepatitis or
failure based on the duration of clinical signs before presentation may be misleading
because the disease process is often advanced before clinical signs are evident.Liver
biopsy to determine the type of pathology, degree of hepatic fibrosis present, and the
regenerative capabilities of the liver parenchyma is necessary for developing a
treatment plan and giving an accurate prognosis. Chronic hepatitis patients sometimes
need to use antibiotics for unrelated infections and various other procedures and many
are not sure about the possible harmful effects some antibiotics may cause their liver.
The liver has very complicated functions and one of the most important
function is the detoxification of drugs such as antibiotics and its metabolites. Some
antibiotics can cause allergic reactions while others can cause direct damage to their
liver, which can be quite severe in patients with chronic liver disease. For patients with
a pre-existing liver disorder, the detoxification function of the liver is already
compromised and substances that would normally be metabolized could actually
accumulate in the liver or in the bloodstream.Liver disease may have a variable effect
on drug clearance. The effect is difficult to predict and almost impossible to quantify.
There are no tests for hepatic function that will reliably predict drug clearance. Changes
in hepatic function due to disease that may affect drug clearance are described by: :i)
decreased intrinsic clearance caused by loss of functional hepatic mass ii) Increased
fraction unbound of protein-bound drugs. Decreased drug protein binding caused by
decreased albumin; this may increase clearance of drugs that are highly protein bound
iii) decreased hepatic blood flow resulting in decreased drug clearance.
Antibiotics that accumulate in this manner could become toxic to the body and
its functions can change drastically from its original purpose. For the most part in
treating patients with preexisting liver disease who develop infections outside the liver,
one should use caution in prescribing drugs known to be dependent on liver for
inactivation or excretion. Usually a safer substitute drug can be found. One should also
take care to avoid use of hepatotoxic non-antibiotic drugs concomitantly. On the other
hand, drugs metabolized and/or excreted by the liver are theoretically ideal for
treatment of acute infections of liver and biliary tract.

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PRINCIPLES OF TREATMENT OF LIVER DISEASE
Objectives
• Eliminate causative agent
• Suppress mechanism that potentiate the disease
• Provide optimum conditions for hepatic regeneration
• Control manifestations of complication that occur
Specific therapies
• Drug-induced –recognition and withdrawal of the drug
• Bacterial hepatitis/cholangitis –antibiotics
• Idiopathic chronic hepatitis, lymphocytic cholangitis- steroids , azathioprine
• Hepatic fibrosis – steroids, colchicines
• Cholestasis- ursodeoxycholic acid (UCDA)
• Copper toxicity – decoppering agents
• Hepatic lipidosis – identify and treat pre-existing disease
Drugs
Antibiotics
Penicillin, ampicillin, cephalosporins, clindamycin, enrofloxacin
Tetracyclines are concentrated in the liver and the bile but are only bacteriostatics
Avoid drugs requiring hepatic metabolism ( or given reduced given dose)
Eg. Chloramphenicol, lincomycin
The following is a list of the most common antibiotics groups being used today. Each is
ordered according to their potential harmful effects on the liver, the top group being the
most potentially harmful and the last group being the least.
1.Tetracyclines: When used in larger doses, these can cause jaundice, fever, and fatty
liver. Metabolism by liver. All tetracyclines are concentrated in liver and excreted via
bile into intestine, where they are reabsorbed.

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Tetracyclines have adverse effects on several hepatic enzymes, thus to be avoided
completely in liver disease
2.Macrolides :
A.Erythromycin: It causes damage to the liver via cholestasis (bile retention) and
jaundice. The harmful effects usually start to show after 10 to 14 days use and the
incidence rate is approximately 5 to 10%. Metabolism by liver,major excretory
pathway and it is excreted into bile in active form. Avoid estolate form in liver disease
and other forms in usual dosage.
Oleandomycin and triacetyl oleandomycin: Metabolism by liver. No liver toxicity.
B.Lincosamides:
Lincomycin: Metabolism by liver. It is excreted and re-excreted via enterohepatic

circulation. Half-life of drug is doubled in liver disease accordingly drug dose should
be reduced, or drug avoided entirely.
Novobiocin: Metabolism by liver. Best to avoid in liver disease. This drug may induce
"jaundice" by five different methods, all generally uncommon.
Kanamycin : Not Metabolised by liver. No change in dose in case of parenteral liver

disease.in case of oral dose kanamycin at 8 Gm/day eventually builds serum levels to
therapeutic range. This effect is even greater with hepatic disease and azotemia.
Accordingly, patients on gut sterilization with kanamycin should be watched for
deafness and increasing nephropathy.
Neomycin: Not metabolised by liver. Not more than 6 Gm PO in liver disease for gut
sterilization. If azotemia also present,kanamycin is preferred.
Polymyxin- Colistin Group and Vancomycin: Minor metabolism by liver. No change

in dose in liver disease.
Chloramphenicol:
Metabolism by liver. Liver toxicity is rare. Use with caution in liver disease. If ascites
or jaundice is present, use under 25 mg/kg/ day or another drug.
Penicillins: These antibiotics cause the least liver damage. Generally, antibiotics in the
penicillin family are the most "liver friendly" and safe for chronic hepatitis patients to
use.
Penicillin G: Metabolism by liver: Only minor fraction is ordinarily handled by liver,

but in impaired renal function the liver may be a major excretion route via bile. Attains

105
significant liver tissue levels and also bile levels.Liver toxicity is rare. No change in
dose in liver diseases if renal function is good and reduce dose in circumstances of
combined kidney and liver disease.Generally the information for penicillin G applies
also for Alpha-phenoxy-peniclllins Methicillin., Oxacillin methicillin. Cloxacillin and
broad spectrum penicillins: ampicillin, hetacillin, carbenicillin and nafcillin.
Streptomycin and Dihydrostreptomycin: Metabolism by liver.Small fraction is

secreted into bile. Appreciable Liver tissue levels. Bile levels up to 10-20mcg/ ml on
high doses. No change in dose in liver disease.
Cephalosporins: Cephalothin: Metabolism by liver, 70-80% usually excreted

unchanged in urine. Advisable to decrease in presence of combined renal-hepatic
disease.
Cephaloridine: Metabolism by liver, but 70-75% of the drug is accounted for in

unchanged form in urine. Dose in liver disease Same as for cephalothin.
Nitrofurantoin: Metabolism by liver. Rarely, causes a hypersensitivity hepatitis with

cholestasis, focal necrosis, infiltrates,eosinophils.
Sulphonamides: Metabolism is significantly, but not solely by liver (acetylation,

glucuronidation, and/or oxidation), then excreted into urine. Significant liver tissue
levels and bile levels,similar to plasma. Best to avoid dose in liver disease. Pre-existing
nutritional liver disease may predispose to sulfonamide hepatotoxicity. Kidneys appear
to be more susceptible to damage by sulfas in patients with chronic liver disease.
Metronidazole and related drugs (tinidazole, ronidazole): are sometimes used in

patients with hepatic disease because of the anaerobic spectrum. They have been safe
drugs when prescribed according to standard dose recommendations, but when doses
have been exceeded, problems may arise. The most serious problem caused by
metronidazole has been attributed to CNS toxicity and include seizures, ataxia,
nystagmus, tremors, and rigidity.
Fluoroquinolones: The fluoroquinolones (enrofloxacin, marbofloxacin, orbifloxacin,

difloxacin) have had a good safety record Although some of these drugs are
metabolized, the clearance is low and probably not affected unless there is substantial
loss of hepatic function. These drugs are also cleared by the kidneys
Glucocoritcoids : Prednisolone 0.125 – 1mg/kg/day initially , then decrease dose to

alternate day therapy over 4-6 weeks Prednisone is metabolized to liver to active from ,
prednisolone
Advantages

105
• Improved well – being
• Appetite stimulation
• Anti – inflammatory
• Immunosuppression
• Anti- fibrotic
Disadvantages
• Superimposed steroid heptopathy
• Predispose to infection
• Catabolic
Azathioprine
• Alternative drug for immunosuppression,use alone or in combination with

steroids 1.0 mg/kg/day in dogs . 0.3 mg/kg/day in cats ; may decrease to alternate
day
Colchicine
Used experimentally to reduced hepatic fibrosis 0.03 mg/kg/day PO
Ursodeoxycholic acid
• Hydrophilic, beneficial bile salt
• Alter bile composistion and stimulates bile flow in intra- hepatic cholestsais
• Modulates immune response in liver
• Efficancy not yet proven in small animals
Decoppering agents
• D – penicillamine & trientine – very slowly chelate copper in circulation

and excrete it in urine
• Oral zinc acetate to block copper absorption
Vitamin E

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• Reduced continuation of oxidative damage in chronic hepatitis
• Supprotive and symptomatic therapies
• Control HE an aid hepatic regeneration
Diet
• Protein restriction and modification
• Rationale= reduced blood NH3 and aromatic amino acids, yet permit
regeneration
• Protein sources
• Pedigree hepatic support diet
• Home cooking : cottage cheese , vegetable protein (plus pasta or rice)
• Feed 1.4 – 2.2 gm protein /kg/ day in 3-4 small meals
• If hypoalbuminaemic, increases protein amount useless encephalopathic
Carbohydrates
• Easily digestible – eg. Boiled rice
Fats
• Increased amount may aggravate encephalopathay,Some necessary for

palatability,Provide essential fatty acids, fat – soluable vitamins
Vitamin/mineral supplementation
• Fat – soluble (ADEK)
• Vitamin B complex
• In supplementation blocks intentinal copper uptale
Rest and confinement
• Increase hepatic blood flow
• Reduced pain / tenderness associated with liver capsule stretching
TREATMENT OF HEPATIC CRISIS

105
Hepatic encephalopathy
• Identify and treat precipitating causes eg dehydration , GI bleeding Diet
• Alter intestinal flora
• Antibiotics
• Decreases urease – producing bacteria NH3 production
• Neomycin, metronidazole
• Lactulose syrup (15-30 ml QID PO – dose variable and empirical)
• Artificial disaccharide
• Modified by colonic bacteria – lactate and acetate – acidification – traps
NH3 as NH4 ( not absorbed)

Ascites and oedema
• Low sodium diet and Diuretics
• Paracentesis to remove ascetic fluid only for control of dyspnoea and

discomfort
*****

105
CLINICAL MANAGEMENT OF RENAL IMPAIREMENTS
M.VIJAYKUMAR
The kidneys have 3 basic types of function: 1) excretory, 2) regulatory, and 3)

biosynthetic. The excretory function involves elimination of toxins from the body by
way of glomerular filtration and tubular secretion. Elimination of urea, creatinine, and
other nitrogenous waste products of protein catabolism are excretory functions.
Excretory failure is often recognized as azotemia.
Loss of these renal functions results in a narrowing of the physiologic range over which
the kidneys are able to adapt. For example, loss of urine concentrating ability
(regulatory failure) leads to obligatory increases in water intake. The failing kidneys
have impaired ability to adapt to extremes (high or low) in electrolyte intake. This
limited ability of the failing kidneys to adapt to variations in intake directly relates to
therapeutic plans.
Acute Kidney Disease: Causes
Some of the common causes of acute kidney failure are as follows:
• Trauma such as a physical injury that leads to rapid fall in blood pressure. An
accident that causes significant amount of blood loss.
• Consumption of rat poison, turpentine or external toxins such as antifreeze,
pesticides and certain plants.
• Illnesses related to heart result in lack of, or inadequate supply of blood to the
dog's kidneys, which in turn can lead to accumulation of toxins in the
bloodstream.
• Chemotherapy drugs, anti-fungal medicines, and certain antibiotics.
• Urinary tract infections
• Bladder or urinary tract obstructions due to kidney stones.
Acute Kidney Disease: Symptoms

The most commonly observed symptoms of acute kidney failure are as follows:
• Dehydration
• Pain around kidneys
• Arched back and stiff legged gait
• Difficulty in urinating

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• Vomiting
• Dark tongue
• Little or no urine output
Chronic Kidney Disease: Causes

There are a number of factors responsible for causing chronic kidney disease. They are:
• Diabetes
• Physical trauma
• Abnormally developed kidneys.
• Cysts in kidneys.
• Autoimmune diseases
• An unbalanced or poor quality diet can cause chronic canine kidney disease.
Food that has high phosphorous content can be problematic for dogs. If the food
contains insufficient amount of calcium, then the kidneys are unable to remove
the phosphorous effectively. This leads to formation of kidney stones, which
eventually leads to kidney failure. Very high doses of vitamin D can also have
harmful effects on the dog's kidneys.
Chronic kindey disease symptoms:
• Increased thirst (the dog consumes greater amount of water than normal).
• Frequent urination, that is pale in color.
• Nausea and fatigue
• Depression
• Constipation
• Weight loss
• Weakness and inability to tolerate exercises
• Tendency to bruise or bleed easily
• Bad breath (smells like ammonia)
LABORATORY EXAMINATION
Urinalysis: In renal failure diagnosis,urinalysis is of prime importance.urine collection

may be made during the spontaneous micturition or manual compression of the bladder
or catheterization or by cystocentesis.fresh smaple of urine is always preferred for
analysis

105
Macroscopic urinalysis:
The first part of a urinalysis is direct visual observation. Normal, fresh urine is pale to
dark yellow or amber in color and clear. Normal urine volume is 750 to 2000 ml/24hr.
Turbidity or cloudiness may be caused by excessive cellular material or protein in the

urine or may develop from crystallization or precipitation of salts upon standing at
room temperature or in the refrigerator. Clearing of the specimen after addition of a
small amount of acid indicates that precipitation of salts is the probable cause of
turbidity.
A red or red-brown (abnormal) color could be from a food dye, eating fresh beets, a
drug, or the presence of either hemoglobin or myoglobin. If the sample contained many
red blood cells, it would be cloudy as well as red.
pH
The glomerular filtrate of blood plasma is usually acidified by renal tubules and
collecting ducts from a pH of 7.4 to about 6 in the final urine. However, depending on
the acid-base status, urinary pH may range from as low as 4.5 to as high as 8.0.
Specific Gravity (sp gr)
Specific gravity (which is directly proportional to urine osmolality(solute

concentration) measures urine density, or the ability of the kidney to concentrate or
dilute the urine over that of plasma. Specific gravity between 1.002 and 1.035 on a
random sample should be considered normal if kidney function is normal. If sp gr is not
> 1.022 after a 12 hour period without food or water, renal concentrating ability is
impaired and the patient either has generalized renal impairment or nephrogenic
diabetes insipidus. In end-stage renal disease, sp gr tends to become 1.007 to 1.010.
Protein
Normal total protein excretion does not usually exceed 150 mg/24 hours or 10 mg/100
ml in any single specimen. More than 150 mg/day is defined as proteinuria. Proteinuria
> 3.5 gm/24 hours is severe and known as nephrotic syndrome.
Glucose
Less than 0.1% of glucose normally filtered by the glomerulus appears in urine (< 130
mg/24 hr). Glycosuria (excess sugar in urine) generally means diabetes mellitus.

105
Ketones
Ketones (acetone, aceotacetic acid, beta-hydroxybutyric acid) resulting from either

diabetic ketosis or some other form of calorie deprivation (starvation), are easily
detected using either dipsticks or test tablets containing sodium nitroprusside.
Nitrite
A positive nitrite test indicates that bacteria may be present in significant numbers in
urine. Gram negative rods such as E. coli are more likely to give a positive test.
Leukocyte Esterase
A positive leukocyte esterase test results from the presence of white blood cells either
as whole cells or as lysed cells. Pyuria can be detected even if the urine sample contains
damaged or lysed WBC's.
MICROSCOPIC URINALYSIS
Red Blood Cells
Hematuria is the presence of abnormal numbers of red cells in urine due to: glomerular
damage, tumors which erode the urinary tract anywhere along its length, kidney
trauma, urinary tract stones, renal infarcts, acute tubular necrosis, upper and lower uri
urinary tract infections, nephrotoxins, and physical stress.
The presence of dysmorphic RBC's in urine suggests a glomerular disease such as a

glomerulonephritis.
White Blood Cells
Pyuria refers to the presence of abnormal numbers of leukocytes that may appear with
infection in either the upper or lower urinary tract or with acute glomerulonephritis.
Usually, the WBC's are granulocytes. If two or more leukocytes per each high power
field appear in non-contaminated urine, the specimen is probably abnormal.
Casts
Urinary casts are formed only in the distal convoluted tubule (DCT) or the collecting
duct (distal nephron). The proximal convoluted tubule (PCT) and loop of Henle are not
locations for cast formation. The factors which favor protein cast formation are low

105
flow rate, high salt concentration, and low pH, all of which favor protein denaturation
and precipitation, particularly that of the Tamm-Horsfall protein.
In end-stage kidney disease of any cause, the urinary sediment often becomes very
scant because few remaining nephrons produce dilute urine.
Bacteria
Generally, more than 100,000/ml of one organism reflects significant bacteriuria.

Multiple organisms reflect contamination. However, the presence of any organism in
catheterized or suprapubic tap specimens should be considered significant.
Crystals
Common crystals seen even in healthy patients include calcium oxalate, triple
phosphate crystals and amorphousphosphates
Type of Stone Frequency

Calcium oxalate (or phosphate) 75%
Magnesium ammonium phosphate (struvite, or "triple hosphate") 12%
Uric acid 6%
Summary of Diagnostic Tests Indicated for Renal Failure Patients
Evaluation Purpose
Blood urea nitrogen Assess degree of azotemia
Serum Creatinine To establish the diagnosis & measure intrinsic renal function
Urinalysis To establish diagnosis & identify renal complications
Urine culture To rule-out urinary tract infection
Complete blood count To detect anemia of renal failure & inflammatory
complications
Serum sodium To detect hyponatremia or hypernatremia
Serum potassium To detect hypokalemia or hyperkalemia
Serum total carbon dioxide To assess metabolic acid-base status
Serum chloride Useful in assessing serum tCO2 and Na concentrations
Serum phosphorus To detect hyperphosphatemia
Serum calcium To detect hypercalcemia or hypocalcemia
Serum albumin & total To assess nutritional status
protein concentrations
Body weight To assess nutritional status
Protein:creatinine ratio (if To assess magnitude of proteinuria
proteinuric)
Blood pressure To evaluate for hypertension
Fundic examination To evaluate for hypertensive retinopathy or other systemic

105
diseases
Survey abdominal To rule-out urolithiasis, structural lesions, or urinary
radiographs obstruction
Renal ultrasound To structurally evaluate the kidneys to establish a primary
diagnosis
Renal Biopsy To structurally evaluate the kidneys to establish a primary
diagnosis
CONSERVATIVE MEDICAL MANAGEMENT OF RENAL FAILURE:
Conservative medical management of CKD consists of supportive and

symptomatic therapy designed to correct deficits and excesses in fluid, electrolyte,
acid-base, endocrine, and nutritional balance and thereby minimize the clinical and
pathophysiological consequences of reduced renal function. Goals of conservative
medical management of patients with chronic primary renal failure are to: (1)
ameliorate clinical signs of uremia, (2) minimize disturbances associated with excesses
or losses of electrolytes, vitamins, and minerals, (3) support adequate nutrition by
supplying daily protein, calorie, and mineral requirements, and (4) modify progression
of renal failure. Conservative medical management is most beneficial when combined
with specific therapy directed at correcting the primary cause of renal disease.
Conservative Medical Management of Renal Failure in Dogs and Cats
Clinical or Laboratory Abnormality Treatment Options

Progression of CKD Diet therapy
Azotemia/uremia Diet therapy
Polyuria and polydipsia Free access to water
Consider diet therapy
Dehydration (prophylaxis) Free access to water
Avoid stress
Canned Food
Supplemental fluid therapy (?)
Metabolic acidosis Therapeutic alkalinization
Anemia of CKD Erythropoietin therapy
Supplemental Iron
Transfusion therapy
Androgen therapy
Hyperphosphatemia Diet therapy
Intestinal phosphate binding agents
Hypocalcemia Oral calcium supplements
Calcitriol therapy
Renal osteodystrophy Minimize hyperphosphatemia
(prophylaxis/ treatment)
Oral calcium supplements

105
Calcitriol therapy
Systemic hypertension Sodium restriction
Antihypertensive drug therapy
Drug reactions/overdosage Avoid nephrotoxic drugs
Adjust dosages according to renal function
Urinary tract infection Monitor for infection
Antibiotic therapy
Ameliorating clinical consequences of excretory failure:
Reducing protein intake:Controlled reduction of non-essential proteins wil result in

decreased production of nitrogenous wastes with consequent amelioration of clinical
signs of uremia
Indications of diet therapy:
Dietary Component Change from typical maintenance diets

Protein quantity Reduced
Protein quality Increased
Phosphorus Reduced
Sodium Reduced
Fatty acids Enhanced omega 3:omega 6 PUFA ratio
Caloric density Enhanced
Fiber Enhanced
Enhancing diet palatability:
Changes in the diet: changes in the diet should be made gradually over a period of one
– two weeks.Warming of food improves palatability.warm water should be added to
dry feed.fresh aromatic feed should be offered.
Food aversion : occurs if nauseated patients are force fed.If painful sample collection
or drug administration is associated with feeding unpalatable drugs should not be
mixed with regular feed or water.
Flavoring agents: agents like animal’s fat, butter,dehydrated cottage cheese,garlic

etc.enhance palatability
Modifying feeding patterns and environment: Animal should be fed frequently with
small quantities of food, placing palatable food in the patients mouth or paws may
stimulate a licking response
Pharmacological appetite stimulants

105
Anabolic steroids: even though these drugs are claimed to improve the appetite, no
data is available to support this in renal failure
Corticosteroids: there is no data to support longterm beneficial effect in ureamic dogs

and cats
Benzodiazepenes: diazepam stimulates appetite in various species.But only marginal

success in renal failure patients
Diazepam : 0.2mg/kg i.v with a maximum of 5mg/kg/patient,given twice a day,PO or

i.m can also be given
Oxazepam: used only for oral administration.2.5mg/patient,not suitable for longterm

usage
Modification of drug dosages: nephrotoxic drugs that require renal excretion should
be avoided in patients with renal failure
Avoiding clinical consequence of regulatory failure:
Hyperphosphatemia is managed by restricting dietary phosphorus intake , oral

administration of intenstinal phosphorous binding agents or a combination of these
methods . The ultimate aim is phosphoros restriction . Modified protein diets designed
for dogs with renal failure may contain as little as 0.13 to 0.28 % phosphorous on a dry
matter basis and provide about 0.3 to 0.5 mg/kg phosphorous (Typical commercial dog
food contain 1 to 2 % phosphorous on DM basis and 2.7 mg/Kcal phosphorous )
Modified protein diet for cats contains 0.5 % phosphorous on DM basis and 0.9
mg/Kcal of phosphorous ( Typical commercial food contains 1-4 % phosphorous on
DM basis and 2.9 mg/Kcal phosphorous).
Intestinal binding agents
These render ingested phosphorous contained in the saliva , bile and intestinal juices
unabsorable. These agents are administered by mixing food or just before meal.
Aluminium containing intestinal phosphorous binding agent include aluminum
hydroxide, aluminum carbonate and aluminum oxide, Dose 30 to 90 mg/kg/day .
Available as antacid preparation in liquid, tablet or capsule forms, Sucralfate, a
complex polyaluminium hydroxide salt of sulfate used primarily for gastro intestinal
ulceration is also effective than aluminum based agents, excess usage may lead to
hypercalcaemia Calcium acetate is the most effective and given at a dose rate of 60 –
90 mg/kg/day. Calcium carbonate is given at a dose rate of 90-250mg/kg, calcium
based agents must be administred with feed both to enhance phosphorous binding and
to minimize absorption of calcium.

105
Hypokalemia
Potassium replacement therapy is indicated for cats with hypokalemia (serum

potassium concentration less than 4 mEq/1r) even in the absence of clinical signs of
hypokalemia
Potassium gluconate 2-6 mEq/cat/day as powder , tablet , gel or elixir .Patassium citrate
can also be given.
Routine supplementation of low oral doses of potassium (2 meq/day ) has been

recommended for all cats with chronic renal disease. Diets that are acidifying and
restricted in magnesium content may promote hypokalemia and hence be avoided in
cats with chronic renal failure .
Fluid should be administred such as potassium is delivered intravenously at a rate less

than 0.5 meq/kg/hr
Metabolic acidosis : Alkalinization therapy designed to correct metabolic acidosis is

an important component in the management of patients with CRF. Oral alkalinization
therapy is indicated when serum bicarbonate concentration decline to or below 17
mEq/1r. Oral sodium bicarbonate 8-12 mg/kg 8-12 hrs is commonly used
Dehydration: Fresh clean unadulterated water should be available in adequate

quantities at all times. The composition of fluids selected for chronic parentral
administration should provide free water as well as electrolytes for maintenance
(Lactated ringers solution supplemented with KCL).
Arterial hypertension : Blood pressure may be measured directly by cannulation of an

artery or indirectly by doppler ultrasonography or oscillometry . Hypertension exists
when mean arterial blood pressure exceeds 152mm of Hg in dogs and 139mm in
cats.160/95 in dogs and 180/120 in cats warrant a diagnosis of hypertension. Therapy
should be directed at counteracting the effect of extracellular fluid volume and
vasoconstrictor effects of angiotension II and not epiephrine which is important in
arterial hypertension associated with CRF. There are non pharmacologic and
pharmacological therapies to reduce hypertension.
Non – Pharmacologic therapy:
Dietary sodium restriction: Daily sodium intake should be reduced to 0.1 to 0.3
percent of the diet on a dry matter basis ( 10-40 mg/kg/day) without reduction of
sodium intake administration of some anti – hypertensive drugs such as beta adrenergic
receptor antagonists and arteriolar vasodilators ; may lead to sodium retention extra
cellular fluid volume expansion attenuation of anti hypertensive effects .

105
Protein restriction : May limit or prevent renal hypertensive injury by reducing
intraglomerullar capillary pressures.
PHARMACOLOGIC CONSIDERATIONS
Renal insufficiency can markedly alter one or more of the pharmacokinetic parameters
of a drug including oral bioavailability, volume of distribution, drug binding to plasma
proteins, and most importantly the rates of metabolism and excretion, i.e., drug
clearance. To minimize drug toxicity and maximize therapeutic benefits, it is often
necessary to adjust drug dosage in proportion to the degree of renal efficiency
Dose adjustment may involve one or a combination of the following measures:
1. Extension of the dosing interval.

2. Reduction of the maintenance dose.
3. Administration of a loading dose.
4. Monitoring serum drug levels.
To maintain a therapeutic level and, at the same time, avoid drug accumulation and
toxicity in a patient with reduced renal function, the clinician must consider reducing
the size of the maintenance dose or the dosing frequency or both. In general, this
reduction should also be proportional to the degree of renal impairment but should also
take into account adaptive or compensatory changes in the metabolism and excretion of
the drug through non renal routes.
Commonly used drugs in the treatment of renal failure :
Class Generic name Dosage Indications

Angiotensin converting Enalapril 0.25mg/kg PO q 12-24 Systemic
enzyme inhibitor h (D) hypertension
Appetite stimulant Diazepam 0.2mg/kg PO,IV q 12- Appetite stimulant
24 h (D,C)
Oxazepam 0.2-0.4mg/kg PO,q12- Appetite stimulant
24 h (D,C)
Calcium channel blocker Amlodipine 0.625-1.25mg PO q 24 Systemic
h (C) hypertension
Dopamine antagonist Metaclopropa 0.2-0.4mg/kg q 6-8h Antiemetic/gastrokin
mide SQ,PO (D,C) etic
Gastric protectant Sucralfate 0.5-1.0g q 8-12 h PO Uremic
(D) gastropathy/phospha
te binding agent
H2 receptor antagonists Cimetidine 5mg/kg q 8-12 h Uremic gastropathy

PO,IV (D,C)
Ranitidine 2-2.5g/kg q 2 h PO Uremic gastropathy

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(D,C)
Famotidine 0.5mg/kg q 24h IV,PO Uremic gastropathy
(D,C)
Intestinal phosphate Aluminium 10-30mg/kg q 8h ,PO Phosphate binding
binders hydroxide (D,C) agents
gel,Al.carbona
te gel
Calcium 20-30mg/kg q 8h ,PO Phosphate binding
acetate (D,C) agents
Calcium 30-50mg/kg q 8h ,PO Phosphate binding
carbonate (D,C) agents
Iron supplements Ferrous 100-300mg/d PO,(D)
sulphate
Potassium supplements Potassium 2-6mEq/d PO,(C)
gluconate,pota
ssium citrate
Proton pump inhibitor Omeprazole 0.7mg/kg q 24h PO Ureic gastropathy
(D,C)
Recombinant human Erythropoietin 100U/kg 3times
erythropoietin weekly SQ (D,C)
Sertonergic agonist Cisapride 0.1-0.5mg/kg PO q 8- Antiemetic/Gastropr
12h (D,C) okinetic
Synthetic prostaglandin Misoprostol 2-5µg/kg q 8h PO(D) Uremic gastropathy
Vitamin D Calcitrol 2.5-3.5ng/kg q 24h PO
Antimicrobial Selection: Susceptibility testing should be performed on all urinary

bacterial isolates from patients with UTI. As a result of renal excretion, many
antimicrobial agents attain substantially higher concentrations in urine than in blood.
The drug selected should be administered frequently enough to maintain inhibitory
concentrations in urine and for sufficient time to eliminate the infecting agent from the
urinary tract. Decisions concerning treatment for superficial infections of the lower
urinary tract urothelium can be based on urine antimicrobial concentrations. However,
it is necessary to select agents that attain high concentrations in serum and urine to
eradicate deep seated infections such as pyelonephritis or prostatitis. Fluoroquinolones
are most likely to achieve therapeutic concentrations in renal tissue in patients with
pyelonephritis. Because of the blood prostatic fluid barrier is expected to be intact in
chronic prostatitis, an appropriate antimicrobial which will attain therapeutic
concentrations in prostatic secretions should be selected(e.g.quinolones,trimethoprim-
sulfonamidecombinations,chloramphenicol,clindamycin,erythromycin,oleandomycin).
Protocol for Therapy and Follow-up of UTI: Therapy is successful only if the urine
does not contain any pathogenic organisms. Treatment is ineffective and relapse will
occur if the bacterial colony count has only been reduced. It is recommended that acute,
uncomplicated UTIs and some reinfections be treated for a period of 10 to 14 days

105
whereas chronic or persistent UTI should be treated for at least 4 to 6 weeks.
Administration before bedtime (or other extended interval of confinement) assures that
the urinary bladder fills with urine containing a high concentration of the antimicrobial
agent.During long-term therapy, the effectiveness of prophylactic therapy should be
confirmed by urine cultures performed by cystocentesis about every 4 to 6 weeks. If
urine cultures are negative, therapy is continued.Anitmicrobials contraindicated in renal
failure include amphotericin B, carbenicillin, flucytosine, nalidixic acid, nitrofurantoin,
polymyxins etc.
Antimicrobials doses in renal ailments :

105
S.No Name of the drug Dosage (total dose) Dosing interval
Aminoglycosides
1 Amikacin 1.5–2.5 mg/kg q 24–48 h
2 Gentamicin 0.34–0.51 mg/kg q 24–48 h
3 Streptomycin 7.5 mg/kg (max. 1 g) q 72–96 h
4 Tobramycin 0.34–0.51 mg/kg q 24–48 h
β -lactams:cephalospoins (1st generation)
5 Cefadroxil 0.5 g q 36 h
6 Cefazolin 1–2 g q 24–48 h
7 Cephalexin 0.25–0.5 g q24–48 h
β -lactams:cephalospoins (2nd generation)
8 Cefotetan 1–3 g q 48 h
9 Cefoxitin 0.5–1.0 g IV q 24–48 h
10 Cefuroxime 0.25–0.5 g po q24 h
0.75 g IV q 24 h
β -lactams:cephalospoins (3rd generation)
11 Cefoperazone 1g q 12 h
2g q4h
12 Cefotaxime 1–2 g q 24 h
13 Ceftazidime 0.5 g q 24–48 h
14 Ceftizoxime 0.5 g q 24–48 h
15 Ceftriaxone 1–2 g q 24 h
β -lactams:cephalospoins (4th generation)
16 Cefepime 0.25–1 g q 24 h
β -lactams:penicillins
17 Amoxicillin 0.25–0.5 mg q24 h
18 Amoxicillin clavulanate 0.25–0.5 mg q24 h
19 Ampicillin 0.5-2.0 g q 12-24 h
20 Ampicillin-sulbactum 1.5–3.0 g q 24 h
21 Dicloxacillin 0.125–0.5 g q6h
22 Nafcillin 1–2 g q4h
23 Sponsored
KVC Oxacillin
CVE training programme 1–2 gon “Clinical Pharmacology
q 4 h& Forensic
24 Penicillin 24
College,Bidar,from G th -29th August,2009
0.5–2 million units q 4-6 h
105
25 Penicillin G benzathine 1.2 million units IM x 1 dose
26 Penicillin G procaine 0.6 million units q 12 h
27 Piperacillin 3–4 g q 12 h
*****
RATIONAL USE OF HORMONES IN ANIMAL PRODUCTION

MAHESH S.DODAMANI
Hormone(s), either alone or in combination with other therapeutic agents have

been employed by veterinarians, often with varying success. The clinical utility of
hormone(s) can be best harvested only if, its requirement is based upon perfect
clinical judgement of the case presented with uterine disorder or the endocrine
dysfunction. Judicious use of hormone(s) can be a substitute for conventional
antimicrobial therapy in most of the post-partum infections of the uterus.
Hormone(s) therapy alone or mostly as a adjuvant to antimicrobial therapy is
beneficial in retention of placental membrane (RFM), post-parturient
endometritis(PPE), pyometra and metritis
Prostaglandins (PGF2∝ ): Basically, PGF2∝ possess luteolytic and spasmogenic and
extra-uterine(pituitary) properties. The practicing veterinarian must understand
progesterone dependent and independent properties of prostaglandins before
exploiting prostaglandins(PGs) in post-partum cows/buffaloes. Prostaglandins are
found more effective in causing uterine evacuation, hence useful in metritis and
pyometra. However, uterine infections with systemic involvement must be treated
with suitable antibiotic in additions to PGs. Persistent of residue corpus-luteum is
one of the factors for unsuccessful treatment of post-partum infections of the uterus.
Further, fluid/pus within the uterine lumen are also responsible for preventing the
natural release of PGs from the endometrium. There is also possibility that
improper intra-uterine deposition of drug formulation or eve manipulation would
damage the endometrium and thereby prevents the release of PGF2α . Knocking
down the corpus-luteum (if present) by PGs would favor estrogenic environment in
the uterus, which would be a favorable for local defense (immune) mechanisms.
Generally, synthetic or semi-synthetic analogues of PGF2α are preferred over
natural by virtue of their luteolytic potency as well as minimal side effects (see
table for further details).
Oxytocin and Estrogens:
Exogenous administration of oxytocin (20 IU, i.v or more effectively as
continuous, slow intravenous infusion) can also be employed for its ecbolic actions,
but optimal response cannot be anticipated unless uterine microenvironment is
sensitized with estrogen. Therefore, the benefit of oxytocin is questionable when

105
used after 24-48 hour of calving for expulsion of RFM. Under normal
circumstances, oxytocin administration favors uterine involution, therefore
judicious use of estrogen and oxytocin is beneficial so as to prevent the possible
uterine infection and reduce the inter-calving period.
Estrogens have little or no effect on the rate of separation of fetal cotyledons and
maternal caruncles and therefore of little value if it is used for expulsion of RFM.
However, estrogens increase the uterine tone and muscular activity, relax cervix
and improves blood circulation to uterus. Therefore, they are quite useful either: (i)
- to augment the absorption of locally (intra-uterine) administered antimicrobial
agents or (ii) - to remove corpus-luteum(C.L) that exists during pyometra. Infact,
PGs or estrogen is preferred over manual removal of C.L, because there is less risk
to cows.
Estrogens (Oestradiol benzoate/-valerate/-cypionate) may be used intramuscularly
@ 5-10mg/cow to regress the C.L as well as to expel the uterine contents
(pyometra). If fails, the recommended dose may be repeated at 2 or 3 days interval.
Administration of Oestradiol benzoate/-valerate/-cypionate (3-5mg, i.m) in cyclic
cows increases the absorption of antibiotics like benzyl penicillin following
intrauterine deposition by virtue of increased blood flow or increases in capillary
permeability. Excessive use of estrogens must be avoided as this may lead to
extension of infection through the oviduct and may predispose ovarian adhesions.
Gonadotropin releasing hormone (GnRH): Often veterinarians succumb to
GnRH therapy in order to overcome extended long standing post-partum
anovulatory anestrous in cattle/ buffaloes, following one or the other method of
intra-uterine treatments without documenting the uterine infection. Metabolic
overload (eg.lactation), micronutrient deficiency, thermal stress,
lameness(corticosteroid), delayed involution of uterus, drug resistant pathogens in
the uterus are some of the important reasons for long standing cases of anovulatory
anestrous. GnRH administration in the intermediate period improves fertility in
cows with incomplete uterine involution, but not in normal cows.
The veterinarian must understand that the endocrine dysfunction is one among the
several cause of repeat breeding in animals, and therefore their utility in the clinics
without documenting the hormonal milieu becomes empirical treatment. Often
such clinical judgment would lead to more complicated situations rather than
clinical cure from the endocrine dysfunction.

105
Suggested antimicrobial/antifungal agents for intra-uterine administration
Drug Dose Remarks
Amikacin sulfate 2g Gm -ve
Amphotericin-B 50-200mg Dilute with sterile water, do not use
systemic -nephrotoxic
Amoxycillin 1-3g May irritate endometrium
trihydrate
Carbencillin 2-6g May irritate endometrium, against
Psedomonas sps.
Gentamicin SO4 0.5-3g Buffer with sodium bicarbonate, Gm-ve,
30ml, Streptococci infection
Kanamicin SO4 1-3g Spermatocidal, E.coli and not effective
against other Gm-ve organisms
Neomycin SO4 3-4g E.coli
Polymixin-B 10,000- Psedomonas, Do not use systemic
1x106 IU
Tricarcillin 1-6g Psedomonas, Klebsiella sps., Broad
spectrum
Clotrimazole 300-600g Every 2-3 days for 12 days, Candida sps.,
Miconzole 500mg Yeasts
Commercial preparations of hormone(s) and recommended dosage protocol in

cows
Trade name Dose and Route Remarks

Receptal  2.5ml; i.m, iv(0.01mg/cow) GnRH analogue, each ml contains
0. 004mg buserelin
Fertagyl 1.0ml; im;iv GnRH analogue

Cystorelin 2.0ml; im;iv GnRH analogue
Chorulon 1500-3000 I.U,im hCG

105
Coriogan 1500-3000 I.U,im hCG
Corion 1500-3000 I.U,im hCG
Luteinizing 25mg, slow iv Caution about adverse effects
hormone
Juramate 2.0ml;im;sc (500µ g) Synthetic PGF2∝ analogue
Tt. for luteal cysts
Synchromate 2.0ml; im (500µ g) Synthetic PGF2∝ analogue
Lutalyse 5.0ml; im (25mg) Natural PGF2∝
Tt.. for luteal cysts
Clostenol 2.0ml; im (500µ g) Synthetic PGF2∝ analogue
Prosolvin 2.0ml; im (15mg) Semi-synthetic PGF2∝ analogue
Ilirin 3.5ml (iv); 5.0ml(sc) Synthetic PGF2∝ analogue
(max: 0.75mg/cow) Tt. for luteal cysts
Duraprogen 40mg daily, im for 7days + 17-∝-hydroxy progesterone

Oestadiol benzoate (5mg,im) caproate
OR GnRH(250µ g,im) on
Note: Not a ideal method of
progesterone withdrawal
progesterone delivery for induction
of estrus
Proluton depot -do- -do-
Vetaprogen -do- -do-
Crestar 3mg norgestomet (a Management of anestrous
progestogen) & an injection
(2ml) containing 3mg
norgestomet & 5mg oestardiol
benzoate to be given on
removal of ear implant
Synchromate-B 6mg norgestomet + 5mg Management of anestrous
oestradiol valerate
CIDR Each onsert ccontains 1.38gm Management of nestrous

progesterone

105
Hormonally-active substances used in animal production :
Main use -
Substances Dose levels Form
Animals
Oestrogens alone: 10–20 mg/day feed additive steers, heifers
DES 30–60 mg/day implant steers
DES oil solution veal calves
steers, sheep,
DES 12–60 mg implant
calves, poultry
Hexoestrol 12–36 mg implant steers, sheep
Zeranol
Gestagens alone: 0.25–0.50 mg/day heifers
Melengestrol acetate
heifers, culled
Androgens alone: 300 mg implant
cows
TBA
Combined
25mg-120 mg
preparations: implant calves
DES+Testosterone feed additive swine
DES+Methyl-
30–45mg-300 mg
testosterone implant steers
Hexoestrol+TBA 36mg-300 mg
implant steers
bulls, steers
Zeranol+TBA 20mg-140 mg
implant calves, sheep
Oestradiol-17β+TBA 20mg-200 mg
implant heifers, calves
Oestradiol-17β benzoate
+ 20mg-200 mg
implant steers
Testosterone propionate
*****

105
THERAPEUTIC MANAGEMENT OF EPILEPSY AND
SEIZURES
SANTOSH .P. SARANGAMATH
Seizures are a clinical signs which occurs due to cerebral dysfunction, which
originates from structural (Trauma or Tumor) or functional (Physiological or
Metabolic) causes. Seizure, Convulsion, fits are all synonyms for abnormal electrical
discharge of brain cells which occurs all of a sudden and stops suddenly. Whereas,
epilepsy is somewhat confusing in the sense that, recurrent seizures will be there but
that occurs due to some other disease process or primarily it is unrelated to brain
disorder. Further epilepsy is classified into primary epilepsy also called as Idiopathic,
Genetic, True or inherited epilepsy where there is a genetic involvement is recognized.
Secondary epilepsy also called as acquired or symptomatic epilepsy, is due to residual
brain damage due to trauma, encephalitis, hydrocephalus...Etc.
STAGES OF SEIZURE:
A seizure has 4 stages, first prodrome stage which lasts for several hours to
days, second aura or preictal stage often it is not recognized in animals, Third actual
seizure or ictus stage which lasts for seconds to few minutes and Fourth postictal stage
which lasts for several minutes to hours or sometimes goes days together without
notice.
CLASSIFICATION OF SEIZURES:
Seizure can be classified into Generalized, Partial or Partial with secondary

generalization. Generalized seizures are most common type of seizures encountered in
dogs and cats. In generalized seizures neurons on both sides of the cerebral cortex
discharge simultaneously to produce symmetric involvement of the body. There are
several forms of generalized seizure; common form is tonic-clonic seizure where the
pet falls suddenly, losses consciousness, and manifests involuntary extension of limbs
followed by paddling, chewing motion, pupillary dilatation and salivation. Defecation
and urination may also occur during or after the seizure.
During Partial seizure, only one portion of the cerebral cortex is spontaneously
discharge electrical activity, therefore clinical appearance of seizure vary depending on
the function of the involved area. If the focus of the seizure is on the left motor cortex,
then involuntary muscle jerking is observed in the right side of the body. Partial with
secondary generalized seizure; some of the signs include at the beginning pet exhibits

105
turning of head towards at one side, lifting of one leg, unilateral facial twitching
followed by generalized seizures.
Neurological examination:
Soon after the seizure activity neurological examination will be abnormal.

Weakness, blindness, behavioral changes, asymmetric neurological changes like,
circling to one side, weakness at one side of the body… etc will helps to localize the
lesion to one side of the brain.
OTHER LABORATORY TESTS :
CBC (complete Blood count) for e.g.: in lead poisoning, one can see nucleated RBC’s,
low/normal PCV, Basophilic stippling. In chronic disorders or in fungal diseases,
monocytosis may be observed and leucocytosis with shift to left indicate inflammatory
response and perhaps the infectious cause of seizure.
SERUM CHEMISTRY:
Elevated liver enzyme levels may be observed in liver disease as a potential

cause of seizure. Severe electrolyte abnormalities may indicate seizure activity. Also
severe hypoglycemia in a non diabetic patient may indicate hypoglycemia induced
seizure activity.
Urinalysis: calcium oxalate crystals may be observed in ethylene glycol toxicity

patients with seizure activity.
Cerebrospinal fluid analysis (CSF) analysis, skull radiography, EEG, CT, and MRI may
provide more information regarding the type and extent of intracranial lesion. Analysis
of CSF should include, RBC, WBC count, cytology, protein estimation and culture for
aerobic, non aerobic and mycotic infection. CSF analysis also includes measuring titers
for CD, Toxoplasmosis, Cryptococcosis. Specialized imaging techniques like CT and
MRI are becoming widely used and offer best means of diagnosing and locating brain
tumors and infracts.
MEDICAL MANAGEMENT OF SEIZURES OR EPILEPSY IN PETS:
Regardless of the cause, seizures ordinarily can be controlled by the available

anticonvulsants. Anticonvulsants are pharmacological agents which stabilize the
neuronal membranes and reduce the repetitive burst firing associated with clinical
seizures. This is achieved either directly by altering ion conductance and
hyperpolarizing the neuronal membrane, or indirectly by enhancing the actions of
inhibitory neurotransmitter at neurons, i.e. gamma amino butyric acid (GABA).

105
Anticonvulsant therapy is directed towards reducing the clinical signs of the disease
and not in treating the underlying etiology. These drugs may improve quality of life in
patients but in some cases fails to respond and such patients die due to complications.
The decision to begin therapy is based on several factors like, severity of seizures,
owner’s dedication and cost of the medicine. The best baseline for taking decision is
based on the severity of the problem. For e.g an animal with unacceptable preictal or
postictal behavior (aggression) or animal that end up developing status epilepticus or
repeated cluster seizures should receive aggressive therapy. Also, with some large
breeds of dogs like GSD, Irishsheter, spanials, it is difficult to control seizures with
standard anticonvulsants. So, more aggressive therapy is indicated in these breeds.
The goal of anticonvulsant therapy is to reduce the frequency, duration and

severity of the seizures while producing minimal side effects. The biological activity of
a drug depends on protein binding capacity, degree of ionization, lipid solubility at
physiological pH and its rate of elimination. A drug will develop appreciable serum
concentration only if it administered at least once every half life. Ideally, serum
concentrations should remain constant so that trough concentrations remain within the
therapeutic range while peak concentrations do not reach toxic levels. This typically
requires administration at least twice during the elimination of half life. Only those
drugs with half life greater than 24 hours are suitable for primary control of seizure
disorders. This limits the choice for Phenobarbital or primidone in dogs. Dugs with
shorter half life may be useful in refractory cases.
INITIAL THERAPY OF DOGS:
Phenobarbitol remains the mainstay of anticonvulsant therapy in dogs. The

recommended starting dose is 2.2 mg/kg administered twice daily. Negative side effects
include polyphagia, polydipsia, polyurea and sedation, vomiting. These things will
settle down after the initiation of treatment for 2 to 3 weeks. More serious
complications include bone marrow suppression, hepatotoxicosis and pancreatitis. In
dogs administration of phenobarbitol more than 10 mg/kg, twice daily is not
recommended because that may reach toxic levels of serum concentration.
Primidone is another analogue of phenobarbitol, administered at the rate of 5 to

10 mg/kg, which is rapidly metabolized into Phenylethylmalonic acid (PEMA) and
Phenobarbitol. These chemicals have anticonvulsant activity, but the primidone and
PEMA have shorter half lives so not so effective in management in seizures, but
sometimes in occasional cases where phenobarbitol failed to respond is well managed
with primidone.
In cats, phenobarbitol is administered at the dose of 1 to 2 mg/ kg , the side

effects are similar to that of dogs with more pronounced sedation initially.

105
Diazepam is another effective anticonvulsant in cats. A dose of 0.25 to 0.5
mg/kg b.i.d. is found be effective as per the literature. Some authors suggest a total
dose of 3 to 45 mg per cat.
Primidone in one study in cats reported to be safely used to control seizures at

the dosage of 20 mg/kg such drug can be used with caution in cases that have failed to
respond for the phenobarbitol.
Phenytoin half life of this drug in cat is reported to be varying from 24 to 108
hours. Because of this kind of variation in half life, dasage has to calculated on an
individual basis.
However, about 20 -30 % of epileptic dogs never attain satisfactory seizure

control with the above mentioned drugs and are considered refractory to that drug/s.
Recent literature reveals many of the common antiepileptic drugs used in people with
epilepsy are not acceptable alternatives in veterinary medicine because of lack of
efficacy (valproic acid, oral diazepam and lamotrigine- as a potential for causing
toxicosis). However, in the past decade several new drugs have promised to improve
seizure control and resulted in fewer side effects in people. Several recently published
reports describe the treatment of epileptic dogs with these new medicines, thus
veterinary medicine is seeing an increase in the options available for managing
refractory seizures in digs.
Different clinicians will stick to different protocol/guidelines for initiating therapy,

but most commonly, therapy is recommended in an animal that is experiencing more
than one seizure in a month or has cluster seizures irrespective of frequency, or has any
history of status eppilpticus. Even after giving the conventional epileptic drugs if
seizures are not getting controlled-means, in such animal one can include an additional
anti epileptic drug ( as a ADD-ON drug) along with routinely used antiepileptic drugs.
The following are some of the newer add on antiepileptic drugs.
• Felbamate: approved in human beings for use in US, as it has side effects of
causing aplastic anemia and hepatotoxicosis, its use is declined. The half life in
dogs is 5 to 8 hours, and recommended dosage is 15 to 60 mg/kg every 8 hours.
In combination with phenobarbitol it has potential to cause liver and kidney
damage, so such animals are to be routinely screened for liver enzyme activity
and kidney function tests.
• Gabapentin: The half life of the drug in dogs is 2 to 4 hours, so frequent
administration is must. It is primarily excreted by kidney in humans and dogs,
but in dogs it undergoes partial hepatic metabolism. Dosage is 10-15 mg/kg
t.i.d. liquid formulation is also available.

105
•Pregabalin: limited information is available for this drug as a use for
antiepileptic drug in dogs. Dosage is 2 to 4 mg/kg orally every 8 hours has been
recommended in dogs.
• Zonisamide: is a sulfonamide derived antiepileptic drug; half life is 15 to 20
hours which requires only twice administration. Most of the drug is excreted
through kidney and some of it undergoes hepatic metabolism, dosage is 5 to 10
mg/kg orally every 12 hours. It has teratogegic effect so its use in pregnant
bitches is to be avoided.
• Levetiracetam: It has minimal hepatic metabolism, half life is 3 to 4 hours and
recommended dosage is 20 mg/kg every eight hours. Very ideal in controlling
the seizures in refractory cases in combination with phenobarbitol or potassium
bromide. Desired serum concentration will be achieved with a short time, by
intra muscular injection peak concentration of the drug in the serum will be
noticed as early as 40 minutes. Thus this drug may be very useful in managing
cluster seizures or status epilepticus in dogs.
MANAGING PATIENTS WITH STATUS EPILEPTICUS
The WHO (World Health Organization) defines status epilepticus as “a

condition characterized by an epileptic seizure so sufficiently prolonged or repeated at
sufficiently brief intervals, so as to produce an unvarying and enduring epileptic
condition” from the clinical perspective, status epilepticus is one continuous seizure
lasting 30 minutes or more, or a series of multiple seizures within a short period
without intervening periods of normal consciousness.
Therapy:
Initially it should be directed towards stopping the seizure and correcting the
systemic consequences of seizure. The underlying cause should then be determined so
that a more definitive therapy can be instituted.
CONCLUSION:
Seizures should not be considered as a disease entity, but rather an undesirable

clinical sign of some other disease. Regardless of the cause, anticonvulsants have
provided clinicians with an effective means to control seizures in most patients. As our
understanding of the generation of a seizure discharge advances, more specific therapy
may become available. Until that time, careful monitoring and client education will
provide rewarding results in many cases.
*****

105
CLINICAL PROTOCOLS IN VETERINARY ANAESTHESIA
B. V. SHIVAPRAKASH
Surgery in wide range of species and for different organ disorders are being
attempted more commonly by field veterinarians. Anaesthesia cannot be same for all
surgeries and for all species of animals. This topic aims at discussion and
demonstration of anaesthetic protocols for surgery.
Before narrating different anaesthesia combination, an anaesthesian has to

follow following steps for successful anaesthesia and surgery.
1. Preoperative evaluation of anaesthetic patient and its preparation.

2. Selection of suitable preanaesthetic and anaesthetic agents, route of
administration and equipments.
3. Administration and intraoperative monitoring of anaesthesia.
4. Monitoring during recovery from anaesthesia.
Step 1: Preoperative evaluation of anaesthetic patient and its preparation.
Objective: To judge patient’s physical status and its ability to withstand stress of
anaesthesia and surgery.
Methods :
1. History
2. Physical examination
3. Palpation, percussion, auscultation
4. laboratory examination
 The history and physical examination are the best determination of the presence
of disease.
 Laboratory tests may be undertaken as per the history and signs of the patient.
Preanaesthetic history and signalment
A. signalment: i.Age ii.Breeds iii.Sex
B. Body weight
C. Duration of present complaint

105
D. Concurrent medication :Aminoglycosides, Chloromphenicol, NSAID’s, Calcium
channel blockers, Beta blockers, organophosphates
E. Signs of organs system disease
1. Vomition
2. Diarrhoea
3. Polyurea- Polydypsea
4. Seizures
5. Coughing
6. Exercise intolerance
7. Weight loss
F. Previous allergies and anaesthesia
G. Duration since last feeding
Protocol for Preanaesthetic physical examination in dogs
A. Body weight
1. Obesity
2. Cachexia
3. Dehydration
B. Cardiopulmonary evaluation
1. Heart rate and rhythm
2. Auscultation
3. Capillary refill time
4. Mucus membrane colour
5. Pulse character
C. CNS evaluation
1. Temperament
2. Seizers, coma
3. Vision, hearing
D. Gastrointestinal evaluation
1. Parasites
2. Abdominal palpation
E. Hepatic evaluation
1. Icterus
2. Abnormal bleeding
F. Renal evaluation
1. Palpate kidney and bladder
G. Integument
1. Tumour

105
2. Flea infestation
H. Musculoskeletal
1. Lameness
2. Fracture
Minimum laboratory screening in dogs before anaesthesia i.PCV ii.Adult dogs-BUN
iii.Other tests – based on symptoms
• List of conditions that should be treated prior to anaesthesia
• Severe dehydration
• Anaemia: PCV <20, Albumin: 2g/dl
• Acid base and electrolytes imbalance PH <7.2, K: < 2.5>6.0
• Pneumothorax
• Cyanosis
• Oliguria
• Congestive heart failure
Consideration for selecting an anaesthetic protocol in dogs
1 Procedure to be performed
. <15 min
15 min to 1 hr
> 1hr
Major/minor surgery
2 Available equipments, assistance
.
3 Temperament of the patient
.
4 Physical status
.
5 Breed
.
Based on history, physical examination and lab examination, patient has to be classified
under any one of the following category recommended by American society of
anaesthesiologists and anaesthetic agent and procedure has to be selected.
Category Physical status Disease

I A normal healthy patient Presented for ovario-
hysterectomy, castration

105
II A patient with mild systemic disease Skin tumour, simple fracture
III A patient with severe systemic disease Fever, anemia, dehydration
IV A patient with severe systemic disease that has Uremia,toxaemia, emaciation,
constant threat to life high fever
V A moribund patient not expected to survive for Extreme shock, infection,
24 hrs severe trauma
ANAESTHETIC PROTOCOLS IN DOGS:
Sedatives and tranquilisers :
Drug Dose (mg/Kg), route Use

1. Ketamine 2-10 IV, IM Not useful alone
2. Ketamine+Diazepam or 5.5 or 0.2 IV 5-10 minutes
Ketamine+midazolam poor muscle relaxation and
analgesia
3. Ketamine + Xylazine 10/0.7-1.0 20-40 minutes
Intravenous anaesthetics in dogs:
Drug Dose (mg/Kg), route Use

Thiopental 6-15 IV Short or intermediate
Propofol 4-6 IV 5-10 minutes, apnoea
Xylazine-Midazolam- 0.4/1.0/0.1 IV For several minutes
butorophanol
Anaesthetic protocols in dogs for less than 15 min surgery
1. Thiopental sodium
Disadvantage: Full recovery takes upto one hour.
I V route is difficult in ferocious dogs.
2. Propofol
3. Diazepam + Ketamine
4. Neurolept analgesia
15 minutes to one Hour (intermediate duration)
1. Thiopental sodium
2. Propofol
3. Diazepam + Ketamine
Above drugs can be used and redosed to effect by administering one third to
half of the original dose to prolong the effect more Halothane can also be used.
More than one hour (long duration): Inhalation anaesthesia – Best, Halothane,
Isoflurane: Rapid recovery, Even sick and debilitated dogs recover quickly.

105
INHALATION ANAESTHESIA FOR DOGS:
Inhalation anaesthesia can be initiated without premedication. However, premedication

aids in restraint. Induction is most easily accomplished by short acting Barbiturates
(Thiopental) or by Propofol.
Vaporizer settings :
Drug Induction out of circle Maintenance

Halothane 3 1-2
Isoflurane 3-4 1.5-3.0
Induction in circle
Halothane 2/3 open 1/2 open

Isoflurane 2/3 open 1/2 open
Intraoperative monitoring:
1. Endotracheal intubation soon after induction of anaesthesia

2. Monitoring of cardiovascular system -
Heart rate, blood pressure, capillary refill time
3. Respiratory system – respiratory rate

4. Muscle tone, palpebral reflex
Adjust vaporizer setting according depth.
Recovery in dogs
1.Monitoring of patient alert

2.Removal of endotracheal tube
3.Assessment of heart rate, respiratory rate
4.Never leave the animal if endotracheal tube in trachea
5. provide oxygen for sick or debilitated dogs or after N2O anaesthesia
HORSES
Standing chemical restraint
1. Chloral hydrate was widely used before the advent of other anaesthetics
2. Phenothiazine tranquilizers
Acepromazine and Promazine are two commonly used drugs.

105
Hypotension and priapism are noticed
Acepromazine(1%)- 10 mg/ml, used for standing restraint prior to
transportation
Because it is long acting, inexpensive and does not produce severe ataxia.
3. Xylazine more commonly used in India can also be administered epidurally.

4. Detomidine : 80-100 times more potent than xylazine and duration of action is
twice longer than xylazine.
Acepromazine – Xylazine
Combination of acepromazine (0.02-0.03 mg/kg) and xylazine (0.2-0.5 mg/kg) has

been used to produce improved tranquilization with some reduction of deleterious
side effects. The combination produces faster onset and longer duration of action
and horse stands more squarely on all four feet. This produces less of a “head-
down” posture.
Intravenous anaesthesia in horses:
• Preanaesthetics are always given before intravenous anaesthetics.

• Never anaesthetize an excited horse
• Intravenous anaesthetics can be safely used for 60 minutes without usin
oxygen.
1. Thiopental: (sedation is must before induction) single bolus produces 15 to 20

minutes anaesthesia. Recovery is acceptable with ataxia dose. Recovery is
acceptable if total dose is less than 7 mg/kg.
2. Ketamine :
Always used with xylazine
Xylazine - 1.0 mg/kg IV
Ketamine – 2.2 mg/kg IV
Xylazine is given 3 to 5 minutes prior to ketamine. Horse becomes recumbent

in 90-120 seconds, is anaesthetised for 15-20 minutes and stands within 30-45
minutes. Recovery is generally smooth.The duration of action can be increased by
re-administering half of the original doses of each agent.Diazepam can be
combined with xylazine-ketamine for better muscle relaxation.
3. Guaifenesin: It is a centrally acting skeletal muscle relaxant that produces mild

sedation and analgesia. It is given intravenously at 5, 10, and 15% at 50-100

105
mg/kg BW. It should not be given as single anaesthetic as the analgesia is not
adequate. It is combined with thiopental or with xylazine-ketamine.
4. Guaifenesin-thiopental: they may be given together intravenously (2-3g of

thiopental in 1 lit of guaifenesin 5 to10%). Alternatively, induction is first
achieved by Guaifenesin followed by thiopental (0.2-0.3%. 3-4mg/kg IV) or
ketamine. Anaesthetics are repeated if longer duration is required. After single
bolus, anaesthesia lasts for 15-25 min.
5. Guaifenesin- xylazine-ketamine: All the above drugs may be given together or
separately xylazine (500 mg), ketamine (2000 mg) and guaifenesin (50 mg) are
mixed in 1 lit solution and given at 1-2 ml/kg for induction and 2 ml/kg/hr for
maintenance. Bradycardia and respiratory depression are major concern.
Inhalant anaesthesia in horses:
• A specific large animal anaesthetic apparatus is required

• Inhalant method is preferred if surgery is longer than 45 min
• Halothane and isoflurane are commonly used inhalant anaesthetics.
• Recovery is faster with isoflurane than halothane
• Cardiovascular and respiratory depressions are present with both
anaesthetics.
• Induction should not be attempted with inhalant drugs in adult horses.
Unlike foals induction is achieved using thiopental or xylazine-
ketamine.
Intraoperative monitoring in horses:
Physical methods of monitoring are usually adequate. Eye examination is

important. In surgical plane, there is dull palpebral reflex, strong corneal reflex and
slow nystagmus. Rapid nystagmus and blinking will indicate lighter anaesthesia. Blood
pressure monitoring becomes important if anaesthesia and surgery exceeds 45 min.
Recovery: Horses need extreme care during recovery due to fractures and injuries
during that period. Xylazine (0.2mg/kg) can be given to calm down the horse during
recovery. Head rope and tail rope may be applied and tied to the rings in the recovery
room.
Clinical protocol of anaesthesia in ruminants:
Ruminants accept physical restraint well and can be operated under sedation and local
analgesia. General anaesthesia is used for thoracic surgery or for Diaphragmatic
hernia.

105
Sedation: Xylazine is the most commonly used sedative in cattle (0.05-0.1mg/kg).
Higher doses will lead to recumbancy and lighter general anaesthesia.Sheep and goats:
require 0.1mg/kg BW of xylazine. Acepromazine is a commonly used phenothiazine
derivative in cattle. However, it is not commonly used in cattle like horse’s, dose of
0.01-0.03mg/kg IM is sufficient. Sedation with acepromazine is associated with
protrusion of penis and regurgitation if rumen is full.
General anaesthesia: sedatives are not usually used before induction in cattle as they
may prolong recovery. IV anaesthetics recommended for ruminants are thiamylal (6-
10mg/kg), propofol (6mg/kg), guaifenesin. Propofol produces anaesthesia for 5-10
minutes, induction and recovery is smooth. Xylazine (0.05mg/kg) and ketamine
(2mg/kg) can also be used.
Local analgesia: Most of the operations in ruminants are done under local analgesia
with sedatives. Various local anaesthetic techniques such as linear infiltration, regional
nerve blocks are used. Lignocaine hydrochloride is the most commonly used agent. The
dose is 2mg/kg BW.
Anaesthetic protocols for caesarean
Dogs: Reduce dose of general anaesthetics to one third, Lumbosacral epidural

analgesia. (Thiopental/propofol/ketamine)
Horse: General anaesthetics (reduced dose); thiopental + halothane
Ruminants:Local analgesia (sedative may be avoided),Reduce dose of analgesia
Conclusions
Necessity of anaesthetic combination and techniques are increasing
 Not a single protocol is suitable for all species and for all surgeries
 Dogs and horses are operated under general anaesthesia
 Mostly cattle, sheep and goats are operated under local analgesia
 Success of general anaesthesia depends on type of species, weather canine,
equine, ruminant or wildlife.
*****

105
RATIONAL MEANS OF ANTIMICROBIAL SELECTION IN
VETERINARY PRACTICE
M.VIJAY KUMAR
The choice of antimicrobial agent in the clinical practice should be based upon
susceptibility of the infecting organism to the drug concentrations achieved in the tissue
and pharmacokinetic characteristics of the drug and its dosing protocol. Although,
several class of antimicrobials are readily available, the clinical cure may not be always
successful and its partially attributable to lack of culture and sensitivity tests under field
conditions. Therefore, atleast, one can bank upon certain pharmacokinetic principles in
the routine clinical practice as well as in serious infections like meningitis, endocarditis
and in immuno-compromised hosts.
Why Pharmacokinetics ?
Pharmacokinetics deals with absorption, distribution, metabolism and excretory pattern
of a given therapeutic agent. Selection of antimicrobial agent based on its
pharmacokinetic characteristics aid in achieving optimal concentration at the desired
site. For example, the location of infection can have a major influence on the drug
concentration achieved there, as some sites (eg: CNS) are protected by barriers to drug
penetration, while others (eg. mammary gland, urinary tract) local pH may favour drug
accumulation. Knowledge of pharmacokinetic data is also useful to avoid possible
toxicity in a given species as well to take necessary precautions during physiological
stress (eg. pregnancy, lactation) or pathological conditions (eg: hepatic failure, renal
dysfunction). The probable antimicrobial agent that can be employed in the clinical
practice should be selected after giving due considerations to following issues:
 What organ/s is/are involved?
 What pathogen is most likely?
 What antibiotic in most likely to be effective?
 What drug concentrations at the site of infection?
 What drug/route are most likely to achieve that concentration?

105
ANTIMICROBIAL
PHARMACOKINETCS
Absorption Distribution Metabolism Excretion
Species Plasma protein binding Species Species

Dosage forms Physiological barrier Hepatic dysfunction Urinary pH
Pka/pH Dehydration Enterohepatic cycling Diuretics
Chemistry Blood buffer Nutrition Renal path.
Route of adm. Inflammation
First-pass-effect Pregnancy/Lactation
Neonates Drug interaction
Diet
Concomitant medication
G.I motility modifiers
Fig: Factors affecting antimicrobial concentration in blood/tissue & its action
Clinical Pharmacokinetics
Absorption: The absorption and disposition of antimicrobial agents in the body are
largely governed by their chemistry and certain physiochemical properties as well
as status of the animal (Fig.1). The various antimicrobials are basically grouped
into weak organic electrolytes (acids/bases), amphoteric or neutral compounds.
The absorption is primarily dependent on extent of lipid solubility and degree of
ionization, which are determined by pKa of the drug and pH of the biological fluid
in question. These factors also determine the extent of distribution and elimination
process for antimicrobials. Only non-ionized forms of drugs are passively diffuses
across GIT or can pass across blood-brain or blood-milk barrier. For acidic drugs, a
fall in 1 pH unit results in a 10 fold increase in the concentration of the non-ionized
form and converse applies for organic bases.
Distribution and elimination: Some of the lipophilic antimicrobials listed below
enter most tissues of the body and penetrate cellular barriers and can generally
reach infection foci.

105
 Chloramphenicol
 Trimethoprim
 Erythromycin
 Metronidazole
 3rd generation cephalosporins like moxalactam
 Fluoroquinolones: Enrofloxacin, Pefloxacin, Ofloxacin, Norfloxacin
These antimicrobials are eliminated mainly by hepatic metabolism and/or
carrier mediated biliary exertion. This rate of elimination varies with species, but
obeys first order kinetics when therapeutic doses are administered.
Tetracyclins: The lipid solubility of tetracyclins varies with the compound but
enter most tissues and body fluids except CSF. The more lipophilic number,
minocycline attain effective concentration at relatively inaccessible infection site,
such as the prostate. As a result of chelation with calcium, tetracyclins become
bound at active sites of ossification and in developing teeth. Long acting
tetracyclins (doxycyline, minocycline) undergo biliary excretion and may adversely
affect indigenous microbes in the caecum/colon of horses. However, they are
suited for biliary and upper intestinal tract infection in farm animals.
Oxytretracyclin in 2-PVP base (IM only) exert long duration of action over
propylene glycol base. Because of poor water solubility, oxytetracyclin dihydrade
must be given in much higher dose (50 mg/kg) than the hydrochloride salt to
produce equivalent tissue concentration.
Sulfonamides: Most of the sulfonamides predominantly non-ionized in biological
fluid of pH below their pKa value (sulfisoxzole = 5; sulfonilamide = 10.4).
Commonly used compounds like sulfamethazine (pka = 7.4) and sulfadimethoxin
(pKa = 6.1) enter most tissues of the body and eliminated by a combination of
metabolic reactions (acetylation) and renal exertion (filteration and pH - dependent
passive tubular reabsorption). Cats are poor acetylators and therefore sulfonamides
are contraindicated. Sulfisoxazole (pKa = 5.0) is more ionized in the plasma and
widely distributed and eliminated mainly by glomerular filtration (best suited for
UTI), but their exerction is dependent on urinary pH.
Penicillins: Distributions of penicillin are limited due to high ionization and they
attain low concentration in cells and do not penetrate well into transcellular fluids.
Protein binding varies among penicillin over a wide range (80%-cloxacillin, 22%-
ampicillin) and this is responsible for low extra-vascular distribution. However,
penicillin and/or in combination with streptomycin is best suited for lower
respiratory tract infection (unknown pathogen) with exudation. Penicillins are
rapidly eliminated by kidney. Probencid compete with their excretion (for tubular
excretion) and delays penicillins excretion.

105
Antibiotic Desired environment for optimal action
Penicillins
Hexamine(only UTI) Acidic pH
Nitrofurazones
Cephalosporins
Tetracyclins
Fluoroquinalones Alkaline pH
Aminoglycosides
Ampicillin, amoxicillin and naficillin undergoes enterohepatic circulation and

therefore their half-lives are longer than penicillin-G. Penicillins and
cephalosporins (beta- lactams) are highly active during logarithmic phase of
bacterial growth (time dependent action). Dosing of beta-lactams should be aimed
to keep serum concentration over MIC to prevent regrowth. Penicillins retains their
activity even in the presence of fibrin and abscess formation.
Antibiotic Factors decrease their action
Sulfonamides Pus, blood clot
Penicillin,Cephalosporins Intracellular organisms
Aminoglycosides (Leukocyte, Macrophage)
Gentamicin,Polymyxin Pus
Aminoglycosides Decreased pH, anaerobiasis, hyperosmalarity
Cephalosporins:
Wide variation in pharmacokinetic properties is observed among cephalosporins.
Generally cephalosporins possess widespread distribution in ECF in the body, but
their penetration across biological membranes/barriers varies with the compound.
Many cephalosporins (II & III generations) diffuse across biological
membranes/barriers and attain high concentration in synovial fluid, occular fluid,
prostate or CSF.
Group I (eg: cephalothin, cefaloridine) does not pass across blood : milk or
blood : CSF barrier. However, Group II (eg: cefataxime, cefamandole) can pass
across inflamed meningeal layers and therefore, drug of choice for meningitis
caused by enterobacteriaceae. Group III (eg: cefoperazone) and Group IV
(moxalactam) are highly active against P.aeruginosa. Third generation

105
cephlosporins are also lipid soluble. Cefoperazone undergoes hepatic metabolism
and disturb large bowel (horse) activity but it is suitable for intramammary
administration (250 mg in oily base) in bovine mastitis. Its milk concentration
exceeding MIC of common pathogens stays upto 48 h following single infusion.
Aminoglycosides :
Aminoglycosides does not attain therapeutic levels in CSF and ocular fluid. Poor
diffusibility is attributed to this low degree of lipid solubility. Hafl-lives are short
(1-2 hr) in domestic animals. Inspite of limited distribution, selective binding to
renal tissue (cortex) occurs. Their bacteriocidal action is rapid but killing of Gm-ve
aerobes is concentration dependent and produce a prolonged post-antibiotic effect.
Due to this biphasic mode of action, serum concentration continuously exceeding
MIC are not required unlike penicillins. Loop diuretics and impaired renal function
delays their renal excretion and it is necessary to adjust maintenance dosage to
prevent ototoxicity and nephrotoxicity. One should not administer large IV dose or
multiple injections in dehydration or ureamic conditions. Intravenous eg:
neomycin) must be restricted to one or two occasions only. Systemic
administration does not give satisfactory levels in milk and therefore local
(intramammary) route should be employed in mastitis cows.
Chloramphenicol:
In pre-ruminant calves, chloromphenicol is well absorbed from GIT following
systemic administration. The drug readily pass through cellular barriers and attain
sustained concentration in CSF and aqueous humor. The drug can readily cross
placenta. Penetration of the blood: prostate barrier is relatively poor. Due to
lipophilic nature, the apparent volume of distribution is large (> 1L/kg) in all
species and its distribution is independent of pH. It possess short half-lives in most
species except cat (poor in conjugation with glucoronic acid). Due to short of half-
life chloromphenicol (sodium succinate) at the rate of 50 mg/kg (priming dose)
followed by maintenance doses of 25 mg/kg at 8-12 interval is suggested in
ruminants.
Fluoroquinolones:
These are amphoteric compounds and having low degree of ionization. Therefore,
their distribution is widespread and even penetrate well into CSF (>50% serum
levels in meningitis), bronchial secretions, bone and cartilage and prostatic tissue.
Partially metabolised in liver and bile concentrations are 2-10 times the serum
levels and even enterohepatic circulation may occur. Plasma half-lives varies with
species and urinary concentration exceed serum concentration by several hundred
times and remain high for 24 hr after administration. Clearance of certain drugs
like theophylline get reduced leading to adverse effects and one should not

105
administer concurrently. They have affinity for weight bearing cartilages and
therefore do not administer to puppies (before 8 months of age) or foals (below 1
year of age). Reduction of dosage is required in animals with impaired renal
function.
Antimicrobial combinations and their effect
Bacteriostatic (systemic) + bacteriocidal (systemic) Antagonistic
Bacteriostatic (local) + bacteriocidal (systemic) Antagonistic
Bacteriocidal (local) + bacteriostatic (systemic) Antagonistic
Chloramphenicol + Aminoglycosides Antagonistic
Macrolid + Chloramphenicol Antagonistic
β -lactum (old) + III - Gen. of cephalosporins Depression of
resistance enzymes
Trimethoprim + Sulfonamide Synergistic
Ampicillin + Cloxacillin Synergistic
Penicillin-G + Streptomycin Agonistic.
Conclusion:
The antimicrobial chemotherapy particularly in the absence of antibiotic sensitivity
testing facility under field conditions is a difficult task. In the routine clinical
practice as well as in the absence of microbial sensitivity pattern, one can adopt
certain pharmacological principles discussed here so as to obtain clinical and/or
bacterological cure. To ensure this, the veterinarian must update their knowledge
pertaing toclinical pharmacology of newer antimicrobials released in to market.
*****

105
POST-MORTEM EXAMINATION IN VETEROLEGAL
POISONING CASE
B.KALA KUMAR
The veterinarian will be encountered with diagnosing and treating the animals
exposed to toxicant /poison which may be either accidental or malicious in origin.
History, clinical signs and necropsy of the animals will assist in rapid tentative
diagnosis which will help in the treatment of other affected animals in case of
accidental poisoning. In case of malicious poisoning, which may turn up into
veterolegal case, the identification of the toxin/poison is a must to establish the cause of
death. In all poisonous/toxicological cases, chemical analysis of the biological
specimens is essential to know the cause of death or illness., for which proper
collection and despatch of toxicological specimens to the laboratory is necessary.
History of the case is of great importance in the diagnosis of poisoning. This

includes the number of animals in the farm, number of animals affected, method of
feeding, regularity of feeding, recent changes in the rations or attendants, spraying of
pastures with pesticides or fertilizers, rodenticides, presence of poisonous plants in the
farm environment, the possibility of industrial effluents coming in contact with
grazing/watering sources etc.
 Post-mortem examination
Necropsy by routine procedure is to be performed as soon as possible
after the death of animal. The animal should be examined externally for the presence
of any incisions (for sui poisoning, snake bite etc.,) on the skin or mucous membranes.
The oral cavity is examined for corrosive lesions (acids/alkali) or changes in colour of
mucous membrane (nitrate, co, cyanide poisoning). As most of the toxins gain entry
through gut, examination of gut mucosa, the contents, their smell, colour and pH (acids,
alkali, urea) is a valuable guide in diagnosing toxicoses. Poisoning by salts of heavy
metals results in significant post mortem lesions but poisoning by alkaloids like
strychnine produces very feeble lesions.
The natural orifices, sub-cutaneous fat tissue, muscles, bones and teeth (in
fluorine poisoning), body cavities, and internal organs should be examined. The
stomach should be punctured rather than cut open for examination to note the character
of smell. Puncture ensures greater accuracy and a longer time smell. Some of the
poisons emit characteristic smell like bitter almond in hydrogen cyanide poisoning,

105
garlic odour in phosphorus poisoning, rotten garlic or horse radish smell in selenium,
tobacco odour in nicotine, acetylene odour in zinc phosphide and ammoniacal odour in
urea poiosoning.
The colour of stomach contents also to be examined as copper salts impart a

greenish blue colour whereas picric and nitric acid impart yellow colour to the contents.
The contents of the stomach ,small intestine and large intestine vary from
traces to flakes of paints or lead objects, grains or baits, seeds etc. Blood should be
examined for its colour and clotting characters. Cyanide poisoning imparts cherry red
colour, arsenic imparts rose red colour and nitrate poisoning turns the blood to brown
colour.
Examination of other visceral organs should be done in relation to their size,

colour etc. Spleen size is decreased and colour is changed to dark brown or black in
copper poisoning and spleen size is increased in mycotoxicoses. The description of
morphological changes should be noted clearly and absence of changes should be
notified.
 Collection of samples
A successful toxicological investigation requires appropriate specimens, history
and clinical signs, necropsy lesions and circumstantial evidences. Sample for analysis
should include a suspected source material; often gut contents, so that ingestion of
suspected material can be proved. Secondly, a sample of tissue (depending on tissue
affinity of the suspected poison) must be included, to prove that absorption of the
poison has occurred. It is always advisable to include a sample of liver to confirm
absorption of orally ingested poison. In survival cases the following materials may be
sent for analysis:
• Stomach wash / Ruminal contents.

• Vomitus
• Blood
• Urine
• Saliva / dung
• Water and feed
Most xenobiotics are ingested. Therefore one of the unique advantages of
analyzing gastrointestinal contents is that qualitative tests can be easily carried out in
order to determine the animal has oral access or not. Guidelines for submitting
specimen for toxicological examination is listed in Table 1. In cases where the poison
is suspected to be absorbed per-cutaneously or consumed by inhalation, appropriate
tissue specimens (skin or lung, brain, heart) must be collected. In case of abortion

105
following ingestion of poisonous material, uterus and fetus may also be helpful during
investigation. If there is a strong suspicion of criminal poisoning or if litigation appears
possible in accidental poisoning, specimens should be collected in duplicate and placed
in sealed containers in the presence of witness. In such medico-legal cases, the
veterinarian should record clinical, pathological and epidemiological findings in detail.
Further photographing of the affected animals and the surrounding environment is also
indicated for documentation, if required to be produced in the court. The skeleton or
the remnant bones are the important material for analysis in cases of exhumed bodies
while burnt bones and ashes should be preserved for analysis in cases cremated bodies.
 Sampling containers
Specimens for toxicological examination must be collected preferably in wide
mouth glass bottles of about 2L capacity having air tight stoppers. Alternatively,
plastic containers can be used in place of metallic containers or old cans to avoid
contamination by lead or other metals. The sampling bottles should be numbered,
labeled properly, indicating details of the case, nature of content, place and date of
preservation. Do not forget to put your signature (i.e. veterinarian who has conducted
necropsy). Specimens should be packed individually and necessary measures should
be taken to avoid loss of some poisons by escape of gas or by bacterial fermentation.
 Preservation of materials
 For visceral organs like pieces of liver, kidney, stomach, intestine, contents of a
stomach and intestine saturated solution of sodium chloride can be used.
 Suspected plants or food can be sent to the laboratory without adding any
preservative
 Ice pack/ waterproof frozen sachets, are used in case of the samples being
transported in refrigerated or frozen state
 Rectified spirit (95% ethyl alcohol) 1 ml/g of tissue is the ideal preservative for
toxicological specimens. ( except in alcohol, phosphorous and carbolic acid
poisoning conditions)
 Formaline should never be used for toxicological analysis of specimen samples as
it hardens the tissue without giving scope for scraping and interferes in with the the
analysis by making the extraction of poison much more difficult. .
 Blood ,urine and serum should be refrigerated and never be frozen.
 The materials for histopathological examination can be kept in a fixative preferably
10 percent formalin in a wide mouthed glass container with proper labelling and
well protected by cotton padding/ covering.
 Adequate refrigeration is of special importance when submitting body fluids and
materials for nitrate/nitrite analysis

105
 Preservation of blood samples can be done either by using sodium fluoride (20
mg/ml of blood) or mixture of sodium citrate and HgCl2 (10 g + 0.2g, dissolved in
100 ml of distilled water, add 0.5ml / 10 ml of blood).
 Packing
Samples submitted to the laboratory should be individually packed and labelled
so as to avoid any confusion about specimen identification. Sample should be -wrapped
in foil to protect light sensitive compounds from degrading or frozen to prevent volatile
compounds from escaping o. All specimens should be double bagged ans submitted in
appropriate shipping containers to prevent leaking.
Following points to be taken in to consideration during packing the sample to be sent

for the investigation .
• Samples must be placed in strong waterproof plastic bags or wide mouthed

glass container without adding any preservatives/fixative to the sample
• The container tightly stoppered, properly sealed with paraffin sealing wax
should be kept kept in a larger wooden box which is sealed in cloth
• All the specimens are to be taken in separate containers (polythene jars/covers),
securely tied, properly labelled with particulars of date, case number., organs
collected, species, name of preservative used etc.
• A sample of the preservative used, brief history of the case along with treatment
given particulars should be sent
• Details of the addresses of the sender and the address of the laboratory is
written on outside the box which can be sent either through a messenger or by
post
• The sample should not come in direct contact with any absorbent material like
cotton wool, gauze which will dry out the sample.
• Empty used medicinal bottles, plastic mineral water bottles should not be used
• Glass containers if used , must be well protected to prevent breakage in transit ,
by packing with sufficient absorbent material like sawdust, newspaper etc
• The containers should never be filled completely as fermentation may occur
particularly with stomach/ ruminal contents
• The samples transported at ambient temperature or higher must be provided
heat seal, screw caps must be reinforced with tape.
• In case of the samples being transported in refrigerated or frozen state using
ice pack/ waterproof frozen sachets, screw caps should not be used.
• Rumen contents/vomitus is preferred to be sent to establish that the toxin has
been ingested.
• Liver, spleen and blood are preferred to establish toxin/ poison absorption.
• Kidney, urine and milk are preferred be sent for detecting toxin excretion.

105
• A sample of preservative in a separate sealed container to be sent particularly
in veterolegal cases
• The container with indelible pen / marker labelling must be sealed properly to
ensure that the original contents are not being tampered or so as to to provide
proof for being tampered especially in vetero legal cases .
In case of small animals (poultry, small dogs, lab animals) the cadavers are sent as
it is, in case of large animals the gastrointestinal contents are collected from the
vicinity of changes in the gastric/intestinal mucosa. If there are no changes, a
representative sample is collected, but in medium sized animals the stomach tied at
oesophageal and duodenal end, intestine tied at both ends and bladder with tied
ends is sent separately.
♦ It is always preferable to send the specimens through a special

messenger.
♦ In veterolegal cases, the specimens should be sealed in the presence
of a witness
♦ A sample of the preservative used should be sent.
It is always better to have a duplicate
 Labelling information
The samples being sent to the laboratory must be accompanied by proper
protected labelling with all the details regarding the case, including the following
information
 Name and address of the doctor and the owner of the animal
 Animal identification characteristics-species, colour, age, sex, breed etc.
 Number of animals affected and number of animals dead
 Date of onset of symptoms and the death
 Clinical signs recorded by the doctor and symptoms noticed by the owner
 Type and the quantity of samples sending
 Postmortem findings
 Suspected poison/toxicant
 Any other circumstantial fact or information which may assist the laboratory in
identifying the causative agent
In veterolegal cases , the label containing the details is placed inside the
specimen container and another label is pasted on the wooden box/cloth covering
the container. The sample is then sent to the forensic laboratory , with the

105
forwarding letter ,a copy of request letter from the police and a copy of the
postmortem report
Toxicological specimens for laboratory examination

Sl.No. Suspected Specimen required Amount Remarks
Xenobiotic for required
Analysis
1. Ammonia/Urea Whole Blood or 5ml Frozen or add 1-2
serum drops of saturated
5ml
mercuric chloride.
Urine
100 g
Rumen contents
2. Arsenic Liver, kidney 100g
Whole blood 15ml
Urine 50ml --
Ingesta 100 g
Feed 1-2 kg
3. Chlorinated Cerebrum ½ Use only glass
hydrocarbons containers
Fat 100g
Avoid aluminum
Liver, Kidney, 100g
foil for wrapping
Ingesta
specimens
5. Cyanide/HCN Forage /Ingesta 1-2kg Rush sample to
laboratory
Whole blood 10ml
Frozen in air tight
Liver 100g
bottle. Stomach
contents in 1%
mercuric chloride
6. Fluoride Bone 20g Ideal sample will
be lesion seen in
Water 100ml
organal bone
Forage 100g
Urine 50ml
7. Herbicides Treated weedy 1-2kg
Urine 50ml --
Ingesta 500g
Liver, Kidney 100g
8. Lead, Mercury Kidney 100g Heparinized, do not
use EDTA
Whole blood 10ml

105
Liver 100g
Urine 15ml
9. Mycotoxins Forages, Feed 100g Airtight containers
sample, or plastic bags.
100g
Cloth bags for dry
Liver, Kidney,
feeds
Brain.
10. Nitrate/Nitrite Forage/Ingesta 1kg Ingesta in
chloroform or
Water 100ml
formalin filled air
Body fluids 10-20ml tight container
11. Organophosphates Feed 100g

and Ingesta 100g --
Organocarbamates Liver 100g
Urine 50ml
12. Oxalates Fresh forage 100g Fixed in formalin
Kidneys 100g
13. Sodium (NaCl) Brain 100g
Serum 5ml --
CSF 1ml
Feed 1-2kg
14. Znic phosphide Liver, Kidney 100g --
Gastric contents 100g
*****

105
GENERAL LINE OF TREATMENT OF POISONING IN
ANIMALS
M.VIJAY KUMAR
For the majority of cases of poisoning treatment with an antidote is not possible,
instead prompt medical intervention to improve the condition of the animal can
ensure its survival. These practices focus on promoting the removal of the poison
or neutralizing it, whilst maintaining the vital functions of the animal.
 Removal of the poison
1. Decontamination of the skin:
Some substance (hydrocarbons, acids, alkalis, agrochemicals, etc.) may,
as a result of an accident or a spillage, contaminate the feathers or fur of animals.
In general it is important that in such circumstances the following are undertaken:
• Epidermal structures (wings, nails, claws, feathers, fur) should all be cleaned with
the greatest care, paying particular attention to areas such as the ears, between toes,
etc.
• The cleaning should be undertaken quickly to avoid licking and ingestion of the
poison, and to limit cutaneous absorption.
• Use soapy water (preferably a soap with a low pH), rinsing with copious tap water;
repeat as often as necessary
• Dry carefully and thoroughly (e.g. with a hair dryer)
• The following must never be used: organic solvents (alcohol, white spirit, etc.) or
oily substances which may actually increase percutaneous absorption of the toxin.
• Do not rub the area vigorously; cleaning and drying must be gentle but thorough
• The animal could well be in a state of shock and must be handled accordingly.
• Move to a quiet place with additional heating (e.g. a heat pad, if necessary)
2. Gastric emptying:
a. Emetics:
Use emetics if ingestion has taken place within the preceding 2-3 hours. Never
induce vomiting in following circumstances:

105
• If caustics or hydrocarbons have been ingested
• If the condition of the animal does not allow such treatment, specifically if the
patient is presenting with convulsions (unless controlled), coma or severe
respiratory difficulties; this avoids any secondary complications due to aspiration.
• In pregnancy? And ingestion of slow releasing drug formulations.
Recommended emetics for use in dogs and cats (if necessary, in pigs):
• Apomorphine for dogs: Prompt effect, thorough, but does have a central depressive
effect and the possibility of cardio-toxicity (arrhythmias)
Dogs: 0.05-0.1 mg/kg s.c or im; contraindicated in cats or pigs
• Xylazine, for dogs and cats: Acts within 10-20 minutes; 0.25-0.5 ml of a 2%
sol.,s.c.
• Ipecachuana (10% syrup) for dogs and cats: Acts in 20-30 minutes; orally, 10-20 ml
for a dog, 2-5 ml for a cat administered in a phased manner
If none of the above compounds are available, possible alternatives include:
• Sodium chloride (salt), p.o, 1-3 teaspoons in warm water
• Hydrogen peroxide, by mouth, 1 ml/kg
• Copper sulphate is not recommended as it is an irritant and facilitates the absorption
of poisons. Preferred in pigs (4% solution, max: 60ml,p.o)
b. Gastric lavage:
Currently used in dogs. It is indicated:
• If ingestion has taken place in the preceding 2-4 hours
• On anaesthetized animals with endotracheal intubation
Use 10 ml/kg of an isotonic solution of sodium chloride (occasionally sodium
bicarbonate); repeat the procedure until the washout fluids is clear.
Manual gastric emptying is used in ruminants. Emergency gastrotomy with manual
emptying may be necessary in some cases of plant poisoning or for indigestible
materials (such as plastic, polyurethane foam).
2. Purgatives:
• Never use irritant purgatives and
• Oil-based purgatives as they facilitate absorption
Recommended purgatives:
Sodium sulphate, magnesium sulphate, by mouth or as enema, using solutions
of various strengths (make up to 20%):
• Small animals : 2-25 g, Large animals: 100-200 g (max: 300 – 400g)
• Liquid paraffin (mineral oil), by mouth:Dogs: 5-15ml, Cats: 2-6ml

105
1. Diuretics:
A. Increase glomerular filtration by instituting a forced diuresis or osmotic diuresis
• 5% glucose solution, by slow intravenous infusion:
Large animals: 2-5 ml/kg per 24h, Small animals: 5-20 ml/kg per 24hr
• 10% glucose solution, by slow intravenous infusion:
Large animals: 0.5-1 ml/kg per 24 h, Small animals: 1-2 ml/kg per 24 hr
• 10% mannitol solution, by intravenous infusion:
Large animals: 1-2 ml/kg per 24 h, Small animals: 2 ml/kg per 24 hr
B. With diuretics (Note: strong diuretics are contraindicated):
• Frusemide (im or iv), Large animals: 0.5-1 mg/kg, Small animals: 2.5-5 mg/kg
C. Reduce tubular reabsorption by modifying urinary pH
Forced acid diuresis to eliminate weak bases can be done by:
• Ammonium chloride, PO:
Large animals: 20-40 g, Small animals: 2-5 g
• Arginine chloride, im, or iv
Large animals: 7-10 g, Small animals: 0.1-0.2 g/kg
• Ascorbic acid, iv, all species: 40 mg/kg
Forced alkaline diuresis to eliminate weak acids:
Sodium bicarbonate, 1.4%w/v, iv infusion, Large animals: 2-4 ml/kg per 24 hr
Small animals: by regular monitoring of the acid – base balance (number of ml to
perfuse = base deficit (in mmol) x 0.6 x body weight in (kg)
• Ringer’s lactate, by iv infusion: all species: 5-10 ml/kg per hr
• Trometamol, 3.66% solution by iv infusion:
Dogs: 1-4 ml/kg per 24 hr
• Use a diuretic such as acetazolamide
Dialysis:
In cats and dogs peritoneal dialysis with an appropriate dialysate* 20-25 ml/kg is
suggested. Repeat the procedure several Times as necessary. Very effective in case
of renal failure/renotoxicity.* Commercial preparations meant for human use can be
employed

105
Neutralization of poisons with in the gastrointestinal tract
1. Adsorbents
Activated vegetable charcoal (fine medicinal charcoal or BCK granules).
These are the most effective and most highly polyvalent adsorbents. They can be
administered preferably as a suspension in water, several minutes to 24 hours after
ingestion, if possible before any emetic.
• Large animals: 250-500 g, Small animals: 5-50 g
Other adsorbents: All other adsorbents are less effective than activated charcoal
and are of academic interest only:
• Magnesium oxide (magnesia), Kaolin, Universal antidote (vegetable charcoal
10g+ magnesia 5g + kaolin 5g + tannin 5g with water added up to 200 ml)
2. General chemical antidotes
Substances which form a complex or insoluble precipitate with poisons and
neutralize them in the gastrointestinal tract. The effects are often limited and
debatable. This category includes:
• Water-containing albumens (proteins which are capable of forming insoluble
complexes with heavy metals and which neutralize acids and bases).
• Tannins (these precipitate heavy metals aluminum, lead, silver and some
alkaloids)
Less useful against copper, mercury and nicotine), Lugol’s iodine can partially
precipitate heavy metals like Pb, Hg, Ag and Strychnine.
• Ferric hydrate (action as above).
Milk is commonly believed to act as the best general antidote; in fact, milk
promotes the absorption of liposoluble poisons. A cardinal rule, therefore, is “never
administer milk”.
C. Additional treatment measures
These vary widely according to the symptoms observed, but one of the main
preoccupations of the practitioner will be to support vital functions (respiration and
circulation). The most frequently used agents are:
• Doxapram: A respiratory stimulant, Dog/Cat: 2 mg/kg, iv, repeat as required
• Caffeine and theophylline: Cardiovascular and respiratory stimulants, which
also have a diuretic action. Dosage: 100-250 mg iv, im, hypodermally or as
required
• Nikethamide: A respiratory stimulant. Dog: 22-44 mg/kg, im, iv,

105
• Heptaminol: A cardiac stimulant
Rational Use of Charcoal
Activated charcoal is useful in following circumstance. Charcoal is ineffective
against cyanide. It can also adsorb vitamins/minerals and therefore continued use
may prove to be harmful.
Aconite Antimony Antipyrene Parathion
Alcohol Arsenic Atropine Nicotine
Camphor Iodine Barbiturates Phenolpthaline
Cocaine Oxalates Morphine Phenothiazine
Digitalis Selenium Mercuric chloride Sulfonamides
Glutethimide Silver Strychnine Penicillin
Methylene blue Phosphorus Salicylates Ethylene glycol
Copper sulphate Stramonium Muscarine Ipecacuana
Quinine Penicillin
Note: This is not an exhaustive list
Method of administration:
Make slurry of the activated charcoal using lukewarm water. The rate of 2-8 g/kg
should be given in a concentration of 1g/5-10ml water. Administration can be done
by a stomach tube using either a funnel or a large syringe. Administer a cathartic
(sodium sulphate or magnesium sulphate) 30 minutes after the administration of
charcoal.
In pet animals this technique can be modified if the charcoal is used in conjunction
with an emetic or gastric lavage (Normal saline: 10 ml/kg) with endotracheal
intubation.
*****

105
THERAPEUTIC MANAGEMENT OF CRITICALLY ILL
PATIENTS
VIVEK .R. KASARALIKAR
Critically ill patient is a special challenge to the clinician because the underline
problem is not evident for about 24 to 48 hrs after initial presentation. Expeditious
therapy in right time can be life saving, whereas delayed adequate therapy may be
ineffective therapeutic failure. Most common clinical conditions in ambulatory patients
are trauma with internal/ external hemorrhage, poisoning and post surgical
complication. In fact, specialized care of emergent patient begins with initial phone call
from the owner and instructions to be given regarding first aid and transport
procedures. Level of consciousness, breathing pattern and external hemorrhage should
be enquired on priority.
Few important tips for first aid are:
• Immobility and transport on firm flat surface
• Mouth to nose resuscitation in critical patient which is unconscious and

not breathing (Ten to twelve times per minute)
• Pulsating arterial bleeding should be controlled by digital pressure and

pressure bandage
• Penetrating foreign objects should be left in place till specialized help is

available
• Head should be elevated by 20o in altered mental status after head or

spinal injury
Evaluation and initial treatment:
Triage is the art of assigning the priority to emergency patients and to their
problems by evaluating certain parameters. Three important assessment criterion are A,
B and C.
A – Airway:
Airway patency should be evaluated on priority. Noisy breathing without need

of stethoscope suggests Large airway problem e.g. trachea and bronchus, whereas

105
inspiratory dyspnoea implies extra-thoracic airway compromise. Loud expiratory
sounds reflect towards pathology of intra-thoracic airway including bronchioles and
lung parenchyma.
B – Breathing:
Sequence of respiratory compromise is increased in respiratory rate initially,

followed by change in respiratory pattern. Laboured open mouth breathing with
development of cyanosis suggests significant compromised pulmonary function.
In both the above conditions, immediate Oxygen administration is the priority.

Intra-nasal catheter is the best choice for compromised breathing patients, whereas
slash tracheotomy with endotracheal intubation is preferred in unconscious and apneic
patients (Nasal Oxygen flow rate should be kept at 50 – 100 ml/kg/min).
C – Circulation:
Hemodynamic and cellular changes that occur as a result of abnormality in

circulation is referred as shock or peripheral circulatory failure. It is clinically classified
in to four main categories.
 Hypovolemic shock: It occurs due to at least 15-25 percent deficit in

circulatory blood volume
 Cardiogenic shock: it occurs due to failure of heart to pump requisite quantity

of blood in to circulation
 Distributive shock: It is due to impaired distribution of circulatory blood

volume as a result of peripheral vasodialatation
 Septic shock: This is endotoxin mediated shock
THERAPEUTIC MANAGEMENT OF CRITICALLY ILL PATIENT:
1. Cardio-pulmonary Resuscitation (CPR):
Hallmarks of Cardio-pulmonary arrest
• Stage of apnea with cyanosis of visible mucous membranes
• Absence of palpable pulse
• Absence of heart sounds
• Dilatation of pupils

105
Guidelines for Cardio-pulmonary resuscitation
a) Positioning of animal:
Lateral recumbency on small animal examination table is optimal position

in small sized dogs (< 7 kgs), whereas dorsal recumbency is preferred for
large sized dogs.
b) Resuscitation:
Chest compression coupled with mouth to nose ventilation should be

performed in patients in apneic stage.
Compression rate should be 60 to 120 per minute and the compression –

ventilation ratio should be 15:2. It means for every 15 compressions 2
cycles of ventilation should be performed.
2. Management of shock:
Assessment of shock:
• Pale to cyanotic mucous membranes
• Tachycardia with weak pulse
• Significant fall in Systolic blood pressure (Below 60 mm of Hg)
• Central Venous Pressure (CVP) less than 5 mm of H2O
• Elevated level of Blood lactate (> 80 mg/dl)
• Significant increase in Capillary Refill Time (CRT)
Therapeutic management:
Emphasis should be given to
 Fluid therapy:
The main aim of fluid therapy is to restore circulation and improve the
tissue perfusion. Choice between crystalloid and colloidal solutions
should be determined. Crystalloid supplements fluid along with
electrolytes, whereas colloidal solutions expand the plasma volume.

105
Commonly used colloidal solutions are
• Dextran 70
• Hexastarch
• Gelatin polymers
• Frozen plasma
• Packed cell component
Commonly used crystalloids are
• Normal Saline
• Lactated Ringer’s solution
• Dextrose Normal Saline
• 7.5 % Normal saline
• Hypertonic dextrose solution
Corticosteroids:Stabilization of cell membrane, blocking of arachidonic acid

metabolism and gluconeogenesis are few important roles of corticosteroids in
the treatment of shock
Cyclo-oxygenase inhibitors:These drugs decrease the prostaglandin synthesis

and other vaso-active amines. Flunixin Meglumin@ 0.25 mg/kg, Ketoprofen @
0.5 - 2.2 mg/kg
Antibiotic therapy in septic shock: Broad spectrum antibiotic therapy has

additional advantage in endotoxin related shock. Anti-bacterials with synergistic
action are also preferred in septic shock. III to IV generation ceophalosporin
like cefoperazone, ceftrioxone and cefixim are frequently used in small animal
practice.
Control of hemorrhage and blood transfusion: Antifibrinolytic drugs are

preferred to counteract extensive hemorrhage. PAMBA (Para amino methyl
benzoic acid), EACA (Epsilon amino caproic acid) and Botropase have fast
styptic activity.
Alpha Adrenergic agonist: These drugs help in improving cardiac output and
thereby improve tissue perfusion. Dopamine used @ 5 – 10 µg/kg/min as

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constant infusion has positive ionotropic effect and increase the systolic
pressure.
*****
TOXICOLOGY OF POISONINGS OF VETERINARY

INTEREST AND THEIR CLINICAL MANAGEMENT
N.PRAKASH
Poisoning in most occasions is accidental in farm animals, but it may

occasionally be deliberate or what we call ‘criminal poisoning’. In the veterinary field
(farm animals) toxicities are often found as a result of ingestion of poisonous
substances while grazing or through water. Suspicion of poisoning is also aroused when
illness occurs in a number of previously healthy animals, all affected at a same time,
sharing the same signs, necropsy findings, to the same degree of severity.
SOURCE OF POISONINGS
Agrochemicals (viz: insecticides, fungicides, herbicides, defoliants, rodenticides

etc.), HCN containing fodder crops/plants/seeds, nitrate/nitrite rich plants or water
source, industrial effluents, lead based paints, mycotoxins, water contaminated with
blue-green algae and regional specific poisonous plants (also seasonal) are some of the
common source of accidental poisonings in farm animals.
1. Insecticides:
Insecticides are the major source of poisonings in livestock.. Most of the

insecticides are basically ‘neurotoxic’, hence they may share some of the clinical signs,
but their mechanism of action differs. Therefore, their chemical classification is helpful
in early diagnosis of poisoning and to initiate suitable therapeutic measures in poisoned
animals.
Insecticides can be classified in to following categories:
Chemical class Examples
 Organochlorines: Aldrin, Endosulfan, Lindane, Dicofol etc.
 Oraganophosphates: Acephate, Malathion, Parathion, Methyl parathion,

Dimethoate, Phosphamidon,, Chlorpyriphos, Chlorfenvinphos,

105
Monocrotophos etc.,
 Carbamates: Carbaryl, Metacil, Dimetan, Pyramat etc.
 Pyrethroids (Synthetic): Deltamethrin, Cypermethrin,Permethrin, Allerthrin etc.
Miscellaneous: Chloro-nicotinic acid (nicotine), Arsenic compounds,Captan
Organochlorines: By virtue of their high lipid solubility these agents can enter the
neuronal membrane with ease and therefore interfere with normal functioning of the
nerve membrane sodium channel. The clinical signs of toxicity can be broadly
categorized in to:
Behavioural signs - Anxiety, aggressiveness, abnormal posturing, maniac

symptoms like jumping over inanimate objects, wall climbing etc.
Neurological signs – Hypersensitive to external stimuli, spasm and twitching of

fre-and hind quarter muscles, fascicualtions of facial and eye lid muscles and variations
in body temperature (subnormal temperature to hyperthermia, up to 116°F).
Autonomic effects: Marked salivation (normally thick/ sticky saliva), Mydriasis,

frequent urination, defecation and lacrimation.
Organophosphates: Clinical essentially appears as a result of irreversible inhibition of

AChE, causing accumulation of acetylcholine in the neuro-muscular junction leading to
‘spastic paralyses. The cause of death is due to respiratory collapse. Muscaranic signs
(miosis, watery, drooling saliva, urination, colic and /or defecation, lacrimation are the
common signs followed by nicotinic effects (muscle fasciculations, tremors) and
C.N.S effects( ataxia, convulsions and later depression of respiratory and circulatory
centers). Hypotension, bradycardia and dyspnoea are observed in poisoned animals.
Carbamates: The inhibition of AChE enzyme by carbamates is ‘reversible’, therefore,

on most occasions animals recovers on own unless ingested large quantity of pesticide.
Synthetic pyrethroids: Although these compound process low insect: mammalian

toxicity ratio, treatment of poisoned animals may be a difficult task probably because
of multiple mechanisms involved in toxicity and variations among pyrethroid class
(type-I & type-II). Hypersalivation, lacrimation, mucoid nasal discharge, excitement,
in-coordination, extension of limbs are observed in deltamethrin toxicity in buffalo
calves. Few pyrethroids also cause contact dermatitis.
Studies (experimental) have indicated that Type-I pyrethroids (allerthrin,

permethrin,cismethrin etc.,) cause ‘T-syndrome’- characterized by tremors. On the

105
other hand type-II pyrethroids cause burrowing behaviour, clonic seizures and profuse
salivation.
2. Rodenticides:
Commonly used among farming community to control animal pests like rats,
mice and wild species. These include Warfarin and second generation warfarin like
compounds, Zinc-and aluminum phosphide, ANTU, Flouroacetate and outdated
methods like bait made up of Arsenicals or Strychnine (seed powder).
Anticoagulant rodenticides: These include warfarin (less used now a days) and second
generation anticoagulant rodenticides viz: Bromadiolone (Mortin), brodifucoum. The
main source of poisoning is the ingestion of residues of the rodenticides or baits
intended for killing rodents. These rodenticides interferes with normal function of
vitamin-K and causes coagulation defects by inhibiting clotting factors II,VII,IX and X.
The poor coagulation mechanism cause massive internal haemorrhages over aperiod of
time. Normally after period of about 2-5 days clinical signs appears and these include
anorexia, pulmonary coughing (epitaxis, dyspnoea),hypothermia, haematuria, stiffness
of hind quarters and sudden death. Internal haemorrhage, blood in the
GIT(gastroenteritis), haemopericardium and menigeal/cerebral bleeding and
haemorrhages in joints are the pathological lesions one can observe during necropsy.
The affected animals should be shifted to quiet and warm place and the line of
treatment include Vitamin-K1 in physiological saline (Vitamin-K3 not recommended)
and cardio-vascular support.
Zinc phosphide/ Aluminium phosphide: It is one of the cheapest and quite effective
rodenticide. Commonly used in fruit market, horticultural farming, and almost every
grocery shops/ APMC yard to destroy rats, mice, squirrels etc. Often it is also used in
malicious poisonings to kill dogs, cats and even wild animals. Monogastric species
are more sensitive rather than ruminants. Acute zinc phosphide toxicities is due to
conversion of Zinc-phosphide → phosphine (PH3) gas in the stomach following
hydrolytic reaction with water in the GIT under acidic pH. Absorption od phosphine is
responsible for wide spread cellular toxicity with necrosis of GIT and other vital organs
like liver and kidneys. Clinical signs include anorexia, lethargy, abdominal pain, bloat
(in ruminants), deep respiration, ataxia, prostration and dyspnoea, gasping, convulsions
and death. Post-mortum lesions include pulmonary congestion, edema, sub-pleural
haemorrhages, congestion of liver and kidneys. Acetylene odour may be detected in
stomach. No specific treatment is possible, however symptomatic and supportive care
maybe given. Gastric lavage with 5% Sodium bicarbonate, Calcium boro-gluconate
injection, anticonvulsants and measures to prevent shock can be undertaken as a life
saving measure.

105
3. Herbicides & Fungicides:
Dinitro-compounds: Dinitrophenol, DNP; dinitro-orthro cresol, DNOC); are some of

the commonly used as herbicides. Accidental ingestion foliage sprayed with these
compounds may lead to acute toxicity in ruminants. These compounds are reduced by
ruminal microflora in to diamine metabolites which induce methaemoglobinemia. They
uncouple oxidative phosphorylation and convert all the cellular energy in the form of
heat. In ruminanats, but not in non-ruminants intravascular haemolysis is observed.
Hyperthermia, dark coloured blood and gastroenteritis are observed in poisoned
animals. Rapid onset of rigor mortis, yellowish-green coloured tissues/urine may be
recorded during post mortem examination.
Organic mercurials: These compounds include ethyl mercuric chloride and –

hydroxide, methyl mercuric dicyandiamide and methoxy ethyl mercuric silicate used as
fungicides for seed dressing. Organic mercurials are neurotoxic unlike inorganic
mercurials which are corrosive and nephrotoxic.
Zeneb & Thiram: Zeneb (Zinc-ethylene dithiocarbonate) and Thiram (Tetra-methyl

thiuron sulfide) are the two most commonly used fungicides in agricultural practice.
Although acute poisonings is less likely to observe in field, chronic toxicities may get
unnoticed. Zeneb can induce thyroid hyperplasia, hypothyroidism, degenerative
changes in myocardial, skeletal tissues and depletion of testicular germ cells. Thiram
exposure may cause conjunctivitis, rhinitis, bronchitis, abortion (ewes) and teratogenic
effects.
4. Hydrocyanic acid (HCN) /Cyanide:
The most prevalent for m of HCN poisoning in livestock is caused by various

cyanogeneetc plants capable of producing hydrocyanic acid. Such plants (see
poisonous plants discussed below) contain cyanogenetic glucocides (dhurrin in
sorghum, amygdalin in bitter almond etc.) which hydrolyzed in to HCN in ruminants.
Wilted, drought affected, injured (chopping, rinsing etc.) plants are more dangerous
than fresh plants because of their preformed HCN. Any plants possessing 20mg HCN
per 100gm (wet wt.) may serve as potential source of HCN poisoning. Other source of
cyanide poisonings are: industrial grade Na/K and calcium cyanide (also fertilizer) and
effluents from vicinity of electroplating/metal coating industries workshop.
The lethal effects of cyanide is due the its binding with Fe+3 component of
cytochrome oxidase a3, a key enzyme involved in cellular respiration. Thus,
hyperoxygention of blood would lead to cherry red/ bright red colour of venous blood .
Intoxicated animals shows salivation (frothy), bradypnoea, mydriasis, ataxia,tremors,
epileptiform scizure, cardiac arrhythmia and clonic-tonic convulsions. Invariably loss

105
of conscious, coma and death with several jerky and convulsive movements if poisoned
animals are not attended with in a with in 1-11/2 hours after the appearance of clinical
initial signs. Odour of the breath is ammonical/ bitter almond due to benzaldehyde
production (often bloating, regurgitation is observed). Opening of rumen during post-
mortem examination impart similar odour. Animals suspected for HCN poisoning
must be differentiated from nitrite and other sr milar agents before initiating antidote
therapy (see table 2). In addition to antidotes, per oral administration of Cobalt
chloride(10 mg/kg)and glucose is also indicated.
5. Nitrate/Nitrite:
Drought is one of the root causes of nitrite toxicity in cattle/buffaloes. Nitrates

are reduced to nitrite in ruminates. Otherwise, pigs are most sensitive species for nitrate
toxicity. Contamination of drinking water with sewage, several plants species
(Amarantus sps,Palak etc.), plants grown in highly acidic soil, water logging and rich
nitrated fields / effluents zone, deep well water or pond water originated from
leaching of top soil (after -nitrate fertilizer application) are some of the common source
of nitrite poisonings. Water soaked/entry of moisture may also render paddy hays/ corn
in to nitrite rich within 18-22 hours. Frequent application of fields with non-toxic weed
killer 2,4-D and nitratic fertilizer favour accumulation of nitrtes in plants. Any forage
that contains over 1.5% nitrate (expressed as pot. nitrite) is considered relatively unsafe
for livestock and should be fed with extreme caution. Nitrite ions induce meth-
haemoglobenaemia as well as marked vasodilatation. Clinical signs include cyanosis,
staggering gait, muscular tremors, rapid pulse, dyspnoea and dilated pupil.
Opisthotonus, polyurea, chocolate brown colour of the blood and cyanotic mucous
membranes are the characteristic features of nitrite toxicity. Untreated animals die with
out a struggle. Reducing agents like Methylene blue or Ascorbic acid are the antidotes
(see table 2 for details). Mineral oil or mucilaginous substances and diluted vinegar
(4-5 lt. in cold water, per os) must be administered to counter GI irritation and further
reduction of nitrates in the rumen respectively. Cardiovascular support
(vasoconstrictor); and stimulants to counter prostration.
Systemic antidotes-Dosage and method of treatment (Large Animals)
Poisoning Antidote/ treatment Dosage and method of treatment

105
Hydrocyanic Sodium nitrite Administer 1% sodium nitrite @
acid/Cyanide followed by Sodium 15-25mg/kg,i.v followed by 25%
thiosulfate sodium thiosulphate @ 1.25g,i.v
In emergency:
Na nitrite + Na
thiosulfate
Cattle: 20%, 10ml + 20% ,50
ml
Horse: 20%, 10ml +
20%,50ml
Sheep: 10%,10ml +
10%,20ml
• Administer 4L of vinegar in 10-

20Lcold water; give a large dose of
vitamin B12
• Administer anticonvulsants if
necessary
Nitrate/nitrite Methylene blue 1% methylene blue @ 8.8mg/kg,

i.v
Administer 8-10L cold water and
or Ascorbic acid
saline purgatives; Broad spectrum
antibiotics intra-ruminally
Heavy metals British anti- BAL: 3mg/kg as 5% mixture of

Lewisite(BAL) 10% benzyl benzoate in mineral oil.
(Arsenic,antimony
Give deep i.m injection every
, mercury, etc.)
4hr.on first two days, every 6 hr on
third day and then b.i.d for next 10
days.
• In cattle and horse sodium
thiosulfate can also be used @ 8-
10gram in the form of 10-
or 20%solution (i.v) or 20-30gram
per-orally in 300ml water.
• Fluid therapy and other supportive
treatment as required
Administer @ 30-40mg ,i..v + 60-
d-penicillamine 80mg/kg ,p.o, b.i.d or t.i.d for 3-4
Arsenic poisoning (Expensive) days
Urea Reduce the rumen pH Administer 20-30L cold water and
drench 4-6L of 5 % acetic acid

105
Strychnine Phenobarbital sodium @ 30mg/kg,i.v or
(Strychnous- nux or Chloral hydrate 5g/45 kg body weight, i.v
-vomica)
• Drench tannic acid and then
cathartic
• Anticonvulsants, Leave the animal
in calm, noise free and dark room
Lead Calcium disodium Make 6% solution and administer
EDTA @ 73 mg/kg,i.v(repeat, if required).
After two days gap start therapy
again for next 5days
• Anticonvulsants
Copper Ammonium tetra 1.7 mg/kg,i.v drip daily for 3-5
molybdate days.Allow 2days gap and then start
therapy for next5days
or Ammonium
molybdate + Sodium Give ammonium molybdate 50-
thiosulphate 500mg p.o, s.i.d and sodium
thiosulfate 300-1000mg,p.o,s.i.d for
three weeks
or
• Supportive treatment
d-penicillamine
• 26mg/kg,p.o,b.i.d for 6 days
(Expensive)
Warfarine Vitamin K1 300-500mg,s.c,every 4-6hour
• Blood transfusion and supportive
care
Ethylene glycol Ethyl alcohol 20% ethanol @ 5ml/kg for every 4-
8 hours interval
Carbamate Atropine sulphate 0.25mg-0.5mg/kg,give ¼
insecticides intravenously and remaining ¾ by
intramuscular or subcutaneous route
Organophosphates Atropine sulphate + Atropinization: 0.25mg-
0.5mg/kg,give ¼ i.v,remaining ¾
2-PAM
by i.m or s.c for every 3-6 hours.
Observe for papillary dilatation and
recovery symptoms and continue
treatment as required .
2-PAM: 20%solution @ 25-
50mg/kg,i.v
• Fluid therapy and supportive care

105
Organochorines Pentobarbitone sodium 30mg/kg,i.v and supportive care
( D.D.T;, B.H.C or 5g/45 kg ,i.v and supportive care
& endosulphan
Chloral hydrate
etc.,)
Dinitro- In ruminants only: Methylene blue: 2-4%,8-
compounds Treat for 10mg/kg,i.v every 8hr. or Ascorbic
(Herbicides like methaemoglobinemia acid: 5-10mg/kg,
DNOC,
with methylene blue i.v every 8hr. for first 24-48hr.
dinitrophenol)
or ascorbic acid
• Do not give antipyretics to control
hyperthermia. Use cold water or
ice packs. Administer saline
purgatives. Fluid therapy with
dextrose saline
Systemic antidotes-Dosage and method of treatment (Small Animals)
Toxic agent Systemic antidote Dosage and method of treatment

Acetaminophen N-acetylcysteine 150 mg/kg loading dose PO or IV,
then 50 mg/kg q 4h for 17-20
additional doses.
Arsenic, mercury Dimercaprol (BAL) 10% solution in oil:give small
and other heavy animals 2.5-5.0 mg/kg IM q6h for
[Knoll Pharma]
metals except 2 days then q12h for the next 10
cadmium, lead days or until recovery (Note: With
silver, selenium and severe acute poisoning, 5 mg/kg
thallium. should be given only on the first
day).
D-penicillamine Developed for chronic mercury
(Artamin)® - VHB poisoning and now seems most
promising drug. No reports on
(Cilamin)® - IVIL
dosage in animals but give 3-4
mg/kg q6h.
Atropine, Physostigmine salicylate 0.1-0.6 mg/kg (do not use
belladonna neostigmine)
alkaloids
Barbiturates Doxapram 2% solution: give small animals 3-
5 mg/kg, IV only (0.14-0.25
ml/kg). Repeat as necessary. (Note:
The above is reliable only when
depression is mild; in animals with
deeper levels of depression
ventilatory support (and oxygen) is
preferable).

105
Cholinergic agents Pralidoxime chloride 5% solution 20-50 mg/kg IM or by
and cholinesterase slow IV (0.2-1.0 mg/kg) injection
(2-PAM)
inhibitors (maximum dose is 500 mg per
minute). Repeat as needed. 2-PAM
Organophosphates,
alleviates nicotinic effect and
some Carbamates
regenerates cholinesterase.
but not carbaryl,
Morphine, succinylcholine and
dimethan or carbam
phenothiazine tranquilizers are
piloxime)
contraindicated.
Copper d-penicilamine See arsenic
(Artamin)
Coumarin- Vitamin K (K1) Give 3-5 mg/kg SC or PO per day
derivative with canned food. Treat 7 days for
1% emulsion or capsule
anticoagulants. warfarin-type. Treat 21-30 days for
second generation anticoagulant
rodenticides, oral therapy is more
effective than parenteral route
Fresh whole blood. Blood transfusion 10-25 ml/kg; as
required.
Fresh plasma or fresh
frozen plasma
Edrophonium chloride 1% solution give 0.05-1.0 mg/kg
IV.
Ventilatory support
Cyanide Methemoglobin (sodium 1% solution of sodium nitrite,
nitrite is used to form dosage is 16 mg/kg IV (1.6 ml/kg)
methemoglobin) and
Sodium thiosulfate Follow with 20% solution of
sodium thiosulfate at dosage of 30-
40 mg/kg (0.15-0.2 ml/kg) IV. If
treatment is repeated, use only
sodium thiosulfate (Note: both of
the above may be given
simultaneously as follows:- 0.5
ml/kg of combination consisting of
10g sodium nitrite and 15 g
sodium thiosulfate in distrilled
water QS. to 250 ml. Dosage may
be repeated once and if further
treatment is required give only
20% solution thiosulfate at 0.2
ml/kg.)
Digitalis glycosides Potassium chloride Dogs : 0.5-2.0 g PO in divided
Oleander and Bufo doses or in serious cases as diluted
toads solution given IV by slow drip
(ECG monitoring is essential)

105
Diphenylthydantoin 25 mg per minute IV, until
ventricular arrhythmias are
controlled.
0.5-1.0 mg/kg IV or IM. Give as
Propranolol (β - needed to control cardiac
Blocker) arrhythmias (ECG monitoring is
essential)
0.02-0.04 mg/kg as needed for
cholinergic and arrhythmia control.
Atropine sulfate
Fluoride Calcium borogluconate 3-10 ml of 5-10% solution.
Pentobarbital May protect against lethal dose
(experimental) (Note: all
treatments are generally
unrewarding).
Heparin Protamine sulfate 1% solution give 1.0-1.5 mg by
slow IV injection to antagonize
each 1 mg of heparin. Reduce dose
as time increases between heparin
injection and start of treatment
(after 30 minutes give only 0.5 mg)
Iron salts (Iron Deferoxamine mesylate Dosage for animals not yet
tonics) (Desferal, Ciba) established. Dosage for humans is
5 g of 5% solution PO, then 20
mg/kg IM q4h-q6h. In case of
shock, the dosage is 40 mg/kg by
IV drip over 4-hour period. May be
repeated in 6 hours then 15 mg/kg
by drip q8h.
Lead Calcium disodium Maximum safe dosage is 75 mg/kg
EDTA (CaEDTA) per 24 hours (only for severe case);
EDTA is available in 20% solution
for IV drip, dilute in 5% glucose to
0.5%; For IM, add procaine to 20%
solution to give 0.5% concentration
of procaine.
EDTA and BAL BAL is given as 10% solution in
oil.
(a) In severe cases (CNS
involvement with > 100 µ g lead
per 100 µ g whole blood) give
4 mg/kg BAL only as initial dose:
follow after 4 hours and q4h for
3-4 days with BAL and EDTA

105
(12.5 mg/kg) at separate IM sites:
skip 2 to 3 days and then treat
again for 3-4 days:
(b) In subacute cases with < 100 g
lead per 100 µ g whole blood give
only 50 mg EDTA/kg per 24 hours
for 3-5 days:
Penicillamine (c) May use after either treatment
(Cuprimine, Merck, (a) or (b) with 100 mg/kg per day
Artamin® VHB) PO for 1-4 weeks.
Thiamine hydrochloride Experimental to treat CNS signs: 5
mg/kg IV q12h for 1-2 weeks: give
slowly and watch for untoward
reactions.
Methanol Ethanol Give 1.1 g/kg (4.4 ml/kg) of 25%
solution IV: then give 0.5 g/kg (2.0
ml/kg) q4h for 4 days. Prevent or
correct acidosis with sodium
bicarbonate 0.4 g/kg IV. Activated
charcoal, 5 g/kg PO if within 4
hours of ingestion.
Oxalates Calcium 10% solution of calcium gluconate
IV; give 3-20 ml (to control
hypocalcemia)
Phenothiazine Methamphetamine 0.1-0.2 mg/kg. Treatment for
hydrochloride hypovolemic shock may be
required.
For CNS depression, 2.5 mg/kg IV
Diphenhydramine
to treat extrapyramidal sings.
hydrochloride
Strychnine and Pentobarbital Give IV to effect: higher dose is
brucine (Nux- usually required than that required
vomica) for anesthesia. Place animal in
warm and quiet room.
Amobarbital Give slowly IV to effect: duration
of sedation is usually 4-6 hours.
Dog/cat : 60-70 mg/kg IP.
Thiobarbiturates
Glyceryl guaiacolate 110 mg/kg IV 5% solution; repeat
as necessary
2.5 mg/kg; controls convulsions
Diazepam (Valium®,
Roche)
Prussian blue 0.2 mg/kg PO in 3 divided doses
daily.

105
Potassium chloride Give simultaneously with
thiocarbazone or Prussian blue;
2-6 g PO daily in divided doses.
*****

105
MYCO AND ZOO TOXINS OF VETERINARY
IMPORTANCE: MANAGERIAL METHODS
M.VIJAY KUMAR
Mycotoxins are defined as toxic metabolites released by moulds under certain

conditions conducive for their growth. Acute or chronic toxicoses can result from
exposure to feed or bedding contaminated with toxins that may be produced during
growth of various saprophytic or phytopathogenic fungi or molds on cereals, hay,
straw, pastures, or any other fodder. A few principles characterize mycotoxic diseases:
1) The cause may not be immediately identified
2) They are not transmissible from one animal to another
3) Treatment with drugs or antibiotics has little effect on the course of the disease
4) Outbreaks are usually seasonal because particular climatic sequences may favor
fungal growth and toxin production
5) Study indicates specific association with a particular feed
There are various types of mycotoxins and are classified as follows:
Classification:
i)Based on the causative organism:
Aflatoxins - Aspergillus flavus, A. parasiticus.
Rubratoxins - Penicillium rubrum, P.purpurogenum.
T-2 toxins - Fusarium sp. F.gramaenareum and F. roseum.
Ergotoxins – Claviceps purpurea and C. paspali.
Among these most common are aflatoxins. Aspergillus moulds grow rapidly
when the moisture is <15%and the temperature is 24-25ºC.They commonly affect
GNC, CSC, coconut cake, sunflower cake, wheat, sorghum, millets, soybean, peas and
almonds.

105
Susceptibility: -Ducks, rabbits, dogs, pigs, calves, chicken, cows, quail and sheep are
susceptible in the order of preference. Broilers are more susceptible than layers. Calves
are more susceptible than adult dairy cattle. Maximum allowable conc. in dairy cattle is
20 ppb (0.02 ppm) for the fear of M1 metabolite. In India the practicable limit is up to
50 ppb (0.05ppm) that can be fed to beef cattle, poultry and swine.
Depending on fluorescence aflatoxins are classified into B1, B2, and G1, G2. B1 is most
toxic and need to be converted into its active metabolites.
Toxicity is through ingestion of aflatoxin-contaminated feed. Aflatoxins are not

accumulated to any appreciable extent by animal tissues with the exception of milk.
Signs: i)Acute - sudden death or anorexia, depression, dyspnoea, coughing, nasal

discharge, anaemia, epistaxis, bloody faeces, possible convulsions and death.
ii)Sub- acute - jaundice, hypoprothrombinemia, haematomas and haemorrhagic

enteritis.
iii)Chronic - decreased feed efficiency, decreased productivity and weight gain, rough
hair coat, anaemia, enlarged abdomen, mild jaundice, depression and anorexia.
Abortions may occur.
Postmortem Lesions:
 Wide spread heamorhages,Icterus,Gastroenteritis,Hepatic necrosis,Massive
centrilobular necrosis,fibrosis of bile duct,Enlarged liver,Hydrothorax,
Ascites,Oedema of Gall bladder wall,Pericellular cirrhosis
Microscopically
 Typical hyperplasia of bile duct,Neoplastic growth of
hepatocytes,Hyperchromasia
Diagnosis: based on
 History,Clinical signs,PM findings,Detection of Aflatoxin M1 in milk &
urine,liver, kidney,Serum liver enzymes SGOT,SGPT,ALP elevated,Reduced
prothrombin activity,Hyperbilerubinemia,Tlc,Hplc,RIA,ELISA
Differentiate diagnosis:
Warfarin (haemorrhages), coal tar (mottling of liver) Copper poisoning

(haemoglobinuria, hemolysis); Pyrrozolidine alkaloids (present in plants),
CCl4, blue-green algae, crotalaria are hepatotoxic.
Rx: -
1. Avoidance of contaminated feed

105
2. Hydrated sodium calcium alumino silicate (HSCAS) adsorb aflatoxins @5kg
/ton
3. Stanozolol (2 mg / kg) I/M decreases hepatic necrosis
4. Oxytetracycline (10mg / kg) I/M decreases hepatic necrosis.
**Never administer oxytetracycline and stanzolol combination,
they are mutually antagonistic.
5. Activated charcoal 6.7 mg / Kg I/R as 30% W/V slurry in M/15, PH7 Phosphate
buffer
**Along with charcoal,stanzolol/oxytetracycline(any one)
6. GSH Precursors Cysteine,methionine @2.2mg/kgi/p

7. Multi vitamins Like E,K & Selenium
8. Treatment of grains with anhydrous NH3,H2o2,Chlorine,O3 but efficacy not
been established
9. Feeding easily digestible and low fat diet containing adequate protein
Sample collection :
Much of the error in detecting mycotoxins in feed results from sampling (or
subsampling) rather than from analytical methodology. Samples can be taken at various
stages—from growing crops or during transport or storage. Whenever possible,
samples should be taken after particulate size has been reduced (Ex: by shelling or
grinding) and soon after blending has occurred (as in harvesting, loading, or grinding).
Sampling is most effective if small samples are taken at periodic, predetermined
intervals from a moving stream of grain or feed. These individual stream samples
should be combined and mixed thoroughly, after which a subsample of 10 lb (4.5 kg)
should be taken.
Probe sampling is acceptable when grain has been recently blended but is less reliable
because different microenvironments within the storage facility may cause areas of
mold or mycotoxin concentration. A suggested method of probe sampling is to sample
at 5 locations, each 1 ft (30 cm) from the periphery of a bin, plus once in the center.
This should be done for each 6 ft (2 m) of bin depth. Thus, taller bins would require
more samples, and the total weight should be >10kg.
Dry samples are preferable for transport and storage. Samples should be dried at 176-
194°F (80-90°C) for > 3 hr to reduce moisture to 12-13%. If mold studies are to be
done, drying at 140°F (60°C) for 6-12 hr should preserve fungal activity.
Containers should be appropriate for the nature of the sample. For dried samples, paper
or cloth bags are recommended. Plastic bags should be avoided unless grain is dried
thoroughly. Plastic bags are useful for high-moisture samples only if refrigeration,

105
freezing, or chemicals are used to retard mold growth during transport and storage.
Once a sample has been cooled or frozen, warming may induce condensation and allow
mold growth.
Zootoxins- care and management of envenomed patients:
There are about 236 species of snakes in India but only 50 of these are
venomous, However, the common poisonous snakes of India that man and animal come
into contact, which are those we call the ‘Beg Four’: Cobra, Krait, Russel’s viper and
Sea scaled viper, Apart from these, the other venomous snakes found in India includes
Sea snakes, Pit viper and King cobra. However, Occurrence of venomous bite from
these snakes are less common. In animals, many a time incidence of snakes bite is near
leg region and nostrils.
Sensitivity: Horse>Man>Sheep>Cattle>Goat>Dog>Pig>Cat
Venom composition: The venom compositions vary significantly among various class
of poisonous snakes. Therefore, the course of toxicity as well as well as cause of death
will be different, and obviously therapeutic approach will also vary. On most occasions,
the identification of snake is not available or doubtful.
Table 1: Nature of toxicity of poisonous snakes

Family Elapidae Viparidae Crotalidae
Poisonous snakes Cobra Russel viper * Pit Viper

King Cobra
Krait
Toxic Nature Neurotioxic Haemotoxic Neutrotoxic
Haemotoxic
Table 2: Venom discharge and lethal dose of various snake venom
Snakes Discharge/bite (approx) Lethal dose
Cobra 200 mg 12-15 mg
Krait 20 mg 6-8 mg
Russel viper 150 mg 15-18 mg
Echis 3.8 mg 8-10 mg

105
All the bites from venomous snakes do not lead to death due to “dry bites”
which means that no venom was injected. But, since some snake venoms (like that of
the krait) do not have immediate effect even in a bad bite, it is wise to give
veterinary/medical care.
Cobra: Cobras are widespread group of snakes. In India, we have three kinds: the
monocled, spectacled and black. Cobras can be easily identified by their “defence
display” by spreading their long bones to their famous hood. Cobras are most active at
dust, having along the wedges of agricultural fields in search of rats/mice. For this
reason they live mostly in cultivated area. They lay eggs (10-30) between June &
August and female stays with them until they hatch two months later. The cobra venom
is rich in 10 or more macromolecular substances. These includes enzymes, cardiotoxic,
neurotoxic factors. The cobra venom is rich in enzyme acetylcholinesterase. Therefore,
rapid depletion of acetylcholine (ACh) at neuromuscular junction occurs following
envenomation. This leads to “muscular paralysis” (flacid paralysis). In addition to it,
the alpha-neurotoxin is a powerful cholinoceptor blocker (nicotinic receptors). These
factors hinder the function of muscles involved in respiration and consequently death
occurs due to “respiratory paralysis”. It is important to identify the “big four”
dangerous snakes. At first sight cobra looks like a non-venomous rat snake, but,
remember that the rat snake has a pointed head and larger eyes and it can run faster.
Krait: The common krait is easy to recognise. It has bluish-bluck body with white
cross bands and the head is short and blunt. Kraits venom is 10 times as powerful as
that of the cobra and of all the Asian snakes its venom is the most toxic (neurotoxic).
Kraits are noctoural. They are active at night and rest during the day. They are
found throughout India and live mostly in sandy soil in rat burrows. Their favarite
hiding places are piles of wood (on bricks which provide many pray to shelter in. They
are canibalistic- eat snakes, rats, lizards and birds. Famale lays eggs (10-15) and stays
with them until hatch. The krait is often confused with smaller harmless wolf-snake.
Russel viper: Is a fat and bulky snake, but it can move with surprising speed when in
danger. Its regular chain-like pattern and flat arrow shaped head make it easy to
recognise. Its fangs are along and curved. They give birth to youngones directly,
usually 20-40 at a time and equipped-with venom and fangs birth, viper venom is rich
in proteolytic enzymes, hemolytic and spreading factors.
Saw scaled viper: It is the smallest member of “big four” and usually confused with
long and thinner cat snake. In South India it grows to only 30 cm. length and it is the
causes of many bites as it is widely distributed. The body has brownish and white zig-
zag pattern and the head, as in all vipes, is flat, Usually they hide under rocks and
bouldersor/in low shrub bushes.Like kraits, saw scaled vipers are noctoral but

105
sometime can be seen in sun after a wet night. They have living young. usually 4-8 at a
time, which are just 8 cm. at birth.
Pit vipers:These are forest snakes and feed on frogs and lizards. Commonly found in
coffee and tea plantations in India. Pit vipes have a small “pits” between nostrils and
eyes. They are heat sensitive and can detect change in temperature when warm blooded
animal comes near. There are 15 species of pit vipers and bites are fairly common.
Venon is not powerful and seldom results in death. Young pit vipers aften lift their
“colourful tail” to attract frogs.
First-Aid treatment:
The first and foremost aim, in case of cobra/krait bite is to retard the absorption
of venon from the site of bite. This can be done by applying a torniquet, provided site
of bite is suitable for that. Do not disturb/ or/excite the animal with little care incise the
area (1/4) and bleed. It is always better to avoid KMnO 4 solution for wound wash and
instead use 5% soap wash in 30 min. after bite. It is not advisible to apply torniquet in
case of vipers bite as this venom is rich in spreading factors (local tissue necrosis). In
such case, freezing of tissue is ideal to reduce enzyme activity.
Hospital treatment:
The nature of hospital treatment practically depends on identity of the poisonous snake.
Polyvalent antivenin (Haffkine Institute, Mumbai) is the drug of choce in the absence
of identity. It is better to avoid administration of anti-histaminic as they are found to
increase toxic potential of certain viper’s venom. Popularly, hopital treatment can be
remembered as “AAA”:
∗ A = Antivenin.
∗ A = Antibiotic (broad spectrum)
∗ A = Antitetanus / Gas gnagrene antitoxins.
The antivenin (monovalent/polyvalent) should be administered IV at the rate of
100 ml. (small animals) or 10-50ml. (large animals). Administer antivenom with 1:00
epinephrine (0.5-1 ml. s/c) to avoid shock. Apply 1-2ml. of antivenin over the wound
(site of bite in case of viper bite. Monitor the cardio vascular activity constantly.
Narcotic analeptic is recommended in case of cobra bite to counteract intense pain.
Epinephrine and corticosteroid to overcome hypotension and shock. Employ plasma
volume expander (6% dextran-40) and calcium gluconate to reduce hemolysis. In case
of viper bite, even if the patient survive, amputation may be performed to avoid spread
of local tissued necrosis or gangrene formation.

105
Note: - Anitivenom should be stored at 40C. Do not administer if they are discoloured
or after the date of expiry.
*****

105

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PHYSIOLOGY OF VITAL ORGANS: A REVIEW

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The heart is effectively a syncytium, a meshwork of cardiac muscle cells

The lung or pulmonary system is the essential respiration organ in air-breathing

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• alter the pH of blood by facilitating alterations in the partial pressure of carbon

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summary of physiologic activities in nephrons and collecting ducts during

Component of Nephron Physiologic Process

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Ocular antimicrobial therapy differs from treating infections in other tissues

Routes of drug administration :

The 3 primary methods of delivery of ocular medications to the eye are :

1. Topical-most common route of administration:

Degree of penetration of topically applied medications depends on integrity of

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2. Sub conjunctival (bulbar conjunctiva):

Antibiotics and antifungal drugs have been effectively used in microgram

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5. Systemic-P.O., I.V. or I.M:

Systemic administration is required for treatment of diseases of the retina,

Ocular dosage forms:

Topical ophthalmic drugs are formulated as ointments, suspensions and

Antibacterial ocular drug therapy:

1. Chloramphenicol: Broad spectrum, bacteriostatic. Soluble in both water and fat so

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a. Neomycin: Usually found in combination with other antibiotics. Broad spectrum-

b. Gentamicin: Broad spectrum bactericidal activity including Streptococcus,

a. Bacitracin: Bactericidal, active against gram positive microorganisms. Used in

b. Polymyxin B: Poor penetration. Bactericidal. Effective mainly against gram-negative

The combination of neomycin,bacitracin and polymixin B is known as “triple

a.Cefazolin: Broad spectrum, first generation cephalosporin.Topical use for gram +

5. Fluoroquinolones: Eg: Ciprofloxacin HCl ,Levofloxacin, Ofloxacin etc. Broad

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Antiviral ocular drug therapy:

1. Idoxuridine: 0.5% ointment and 0.1% solution. Frequency of administration is 1

2. Vidarabine: 3%Ointment-it is poorly lipid soluble, so corneal penetration is

3.Trifluridine: 1%Solution-Current drug of choice for feline herpetic keratitis.

4. Others: Lysine, Acyclovir, Interferons

Antifungal ocular drug therapy :

Ocular antifungal agents belong to one of three classifications: polyenes,

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b. Amphotericin B: Fungistatic, generally used systemically for fungal endophthalmitis,

b.Fluconazole: Synthetic triazole, fungistatic. Strength 2 mg/ml IV preparation.

Anti-inflammatory ocular drug therapy:

1. Corticosteroids: Subconjunctival injection of corticosteroids provide a greater local

2. Nonsteroidal anti-inflammatory ocular drugs : They include salicylic acids

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4. Flunixin meglumine: Effective anti-inflammatory agent in the Horse and Dog ,

5. Flurbiprofen: Used topically preoperatively to stabilize the blood-aqueous barrier in

Ocular topical Anesthetics:

Most topical anesthetics are effective within 30 seconds to 3 minutes to facilitate

c.Lacrimogenics: These are drugs potentially capable of stimulating tear secretion.

1. Pilocarpine: Prescribed as 2 drops of 2% Pilocarpine per 4.5kg body weight added

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2. Cyclosporine A 0.2% ointment : Cyclosporine is a potent suppressor of T-cell

3. Tacrolimus 0.02%, 0.03% ointment or solution:Effective alternative to

Anticollagenase/Mucolytic Agents:Collagenase inhibitors are indicated for the

1. Acetylcysteine : Anticollagenase (i.e,. Pseudomonas aeruginosa infection). Diluted

2. Autogenous serum – anticollagenase: Use topically. Must be refrigerated and each

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Cardiology is an interesting subject in recent times not only in human medicine