Clinical Surgery Notes PDF

1
The Podmedics’
Surgery Revision Notes
© Podmedics 2010
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Introduction
Welcome to these notes on the basics of surgery for undergraduates. Learning in an age where information,
both in the clinic and the library, is so accessible, the authors have often felt a little overwhelmed. While
many texts are excellent, we feel that none currently provide a good summary to get students started.
Often the hardest toil in studying medicine is figuring out how precisely to get started. In these notes we
outline some of the common processes that are used to break down both presentation of the disease and
the processes that drive it. Having done this, we then use these techniques as a schema for our notes.
The notes are based upon a series of podcasts written by Jonny and Ed during early 2008 (the podcasts are
available at the site). While they are clearly aimed at the level required for UK final MBBS, they should be
useful to students at any stage of their training. It is our belief that these notes, together with the supporting
podcasts, make up a definitive and useful revision tool for students.
A considerable amount of work has gone into preparing these notes. Please support us by telling you friends
and pointing them in our general direction.
Thank you and good luck.
The Podmedics Team
Contact us
The Podmedics constantly aim to improve the quality, accuracy and consistency of their content - please do
get in touch if you have any questions or comments.
Ed Wallitt: ed@podmedics.co.uk
Jonny Manley: jonny@podmedics.co.uk
Please do not reproduce these notes without prior permission. All images remain the property of their original
authors.
DISCLAIMER: No responsibility is taken for errors/omissions from these notes. They are written by students
for students.
© Podmedics 2010
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Podmedics’ Recommended Texts/Links/Courses
Websites
www.podmedics.com
Please forgive us the indulgence of being placed first.
www.onexamination.com
You must answer questions from this site!
Google images
Fantastic for practising presentations of just about anything you can think of.
Texts
Surgical Talk
Probably the only medical book ever written that is possible to read in bed.
Lecture Notes on Surgery
Harold Ellis was one of the finest surgeons and medical educators of his time. His book is
great (...if you want to be a surgeon)!
Courses
The 10-week Surgery Revision Course
Hosted by the MDU and the mighty Mr Barry Paraskevas
© Podmedics 2010
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Table of Contents
Key Principles ! 8
Surgical Fluids and Nutrition! 12

Fluids! 12
Nutrition! 15
Trauma Surgery! 18
Advanced Trauma Life Support (ATLS)! 18
Chest Trauma! 24
Head Trauma! 28
Burns! 32
Peri-operative Care ! 35
Pre-operative! 35
Post-operative! 38
Skin Disorders! 42
The Oesophagus ! 47
Clinical Anatomy! 47
Dysphagia! 48
Oesophageal Tumours! 50
Gastro-oesphageal reflux disease! 52
Hiatus Hernia and other conditions! 53
The Stomach! 57
Acute Upper GI Bleed! 59
Peptic ulcer! 61
Perforated Peptic Ulcer! 63
Gastric Cancer! 65
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Gallstone and Biliary Disease! 68

Introduction to Gallstones! 69
Gallbladder Complications! 70
Biliary Tree Complications! 73
Intestinal Complications! 75
The Spleen! 77
Hypersplenism & Hyposplenism! 78
Splenectomy! 79
Splenic Trauma! 80
The Pancreas! 83
Pancreatitis! 85
Pancreatic Tumours! 90
Basic Principles of the Lower Gastrointestinal Surgery ! 92

Important Clinical Anatomy! 92
Intestinal Obstruction! 95
Colon Cancer and Stomas! 100

Colorectal carcinoma! 100
Emergency bowel operations! 103
Stomas! 104
Inflammatory Conditions! 105

Appendicitis! 105
Diverticular Disease! 107
Surgical Ulcerative Colitis! 109
Crohn’s Disease! 111
Peri-Anal Disease! 113

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Haemmorrhoids! 114
Anal Fissures! 116
Anal abscess/Anal sepsis! 117
Anal Fistula! 118
Rectal Prolapse! 119
Anal Carcinoma! 120
Breast Disease ! 123

Diagnostic Principles in Breast Disease! 124
Benign Breast Disease! 125
Malignant Breast Disease! 127
Neck Lumps! 131

Lymphadenopathy! 134
Solitary Lumps in the Neck! 135
Thyroid Surgery! 139
Hernias ! 143
Vascular Surgery ! 149

Venous Disorders! 151
Arterial Disorders! 154
Orthopaedics! 167
Basic Fractures! 167
The Hip! 170
Important other fractures for finals! 175
The Knee! 179
Neurosurgery! 183
Spinal Cord Compression! 184
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Neurological Tumours! 186
Hydrocephalus! 187
Urology! 189
Common presentations! 190
Kidney and Bladder! 197
Prostate Disease! 202
The Scrotum! 206
Testicular Cancer! 210
Appendix! 212
Common abdominal scars! 212
Common drugs! 213
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Key Principles
Here we outline some of the different common techniques that can be applied throughout the field of surgery.
General approach to defining a disease
1. Definition (and classification)

2. Epidemiology (and risk factors)
3. Aetiology
4. Clinical features
a. Symptoms/Signs (further split each into general and specific)
5. Investigations
6. Management
7. Complications
Common techniques
Aetiology
When thinking about aetiology try to think in terms of...
1. Anatomy - i.e. what are the surrounding structures/associated pathologies that could be causing
the given problem.
2. ! Surgical sieve - what pathological processes could be occurring?
THE “VINTA MEDIC” SURGICAL SIEVE
Process Sub-split Process Sub-split
Vascular Heart Metabolic/Nutritional

Blood vessels
Infection Bacterial Electrolytic Anions

Viral Cations
Fungal Non-charged
Protozoal
Neoplastic Primary Degenerative

Secondary
Trauma Penetrating Iatrogenic Drugs

Non-penetrating Interventional
procedures
Autoimmune Gel and Coombs Congenital

classification
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Clinical features
This should be split into symptoms and signs and each of these should be sub-divided into general and
specific.
Have this table memorised in your head and go through it logically when you are thinking of investigations to
do.
Investigations
Modalities Tests + Findings
Cultures Blood
Urine MC & S, dipstick / pregnancy test
CSF
Joint aspirate
Pleural/peritoneal fluid
Bloods - ABG NB: usually justified if the patient is ill
Bloods - Venous For each test you must be able to justify why you are performing it
Imaging Plain X-ray e.g. chest, abdomen, bones

Plain X-ray series + contrast
USS
CT/MRI
PET/radio-isotope
Scopic/Biopsy -
Functional Specific tests for a given system that do not fit into the above.
e.g. ECG, lung function test, pH manometry
Treatment
If an emergency you must first talk about RESUSCITATION e.g. Airway, Breathing, Circulation etc.
Modalities Specifics
CONSERVATIVE Always think about:

1. Basic things e.g. analgesia, fluids,
2. Risk factor management
MEDICAL This is surgery..but we still use drugs
SURGICAL What techniques can be used, what do they involve and when are they
indicated
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Complications
These are split into general (applicable to any surgery) and specific (applicable to the described surgery).
GENERAL Think in terms of:
Airway e.g. difficulties with management

Breathing e.g. hypoxia
Circulation
Drugs e.g. allergies, anaesthetic reactions
Exposure to the theatre environment e.g. hypothermia, accidental
injury
Specific - Immediate At time of surgery
e.g. primary haemorrhage, visceral damage
Specific - Early 1-3 days post-surgery
e.g. pyrexia, SOB, reactionary haemorrhage, urinary retention,

oliguria
Specific - Late 3-10 days post-surgery
e.g. infection, DVT/PE, C. diff colitis
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Surgical Fluids and Nutrition
Fluids
Fluid and Electrolyte Distribution
Average 70kg man - 42L (60-70%)
! - ⅔ INTRACELLULAR
! - ⅓ EXTRACELLULAR (plasma, interstitial, transcellular e.g. ocular, fluid, pleural)
Osmolality (280-295 mosmol/l) - should be equal between IC and EC
CHARGED + UNCHARGED
∴ (Na++K++Cl-+HCO-) + (urea+glucose) = 2(Na++K+) + urea + glucose
INPUT OUTPUT
Oral 1.5L Urine 1.5L
Food 1L Stool 0.5L
Oxidative water 0.5L Skin 0.5L
Lungs 0.5L
TOTAL 3L 3L
Total insensible = skin loss + lung loss.
Daily Requirements
Water
• 40ml/kg/day ~ 3 L per day
Electrolytes
• Na+ = 100 mmol/day

• K+ = 60 mmol/day
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Indications for Intravenous Fluids
1. Pre-operative resuscitation
2. Replacement of normal loss
3. Replacement of additional loss
4. Postoperative resuscitation
5. Electrolyte disorders
Types of Fluids
Types Contents
CRYSTALLOIDS Normal saline 154 mmol Na+ in 1L

- “Electrolytes in water that form a true solution
and pass through semi-permeable membrane.”
Dextrose saline 30 mmol/l Na+ + 40g dextrose
5% dextrose 50g dextrose in IL
Hartmannʼs (lactated Anions + Cations + Ca + lactate

Ringerʼs solution)
COLLOIDS Natural
- “Fluid with high molecular weight molecules that e.g. blood, albumin
does not form a true solution and does not pass
through a semi-permeable membrane.”
Synthetic Dextran compounds

e.g. Gelofusin,
Haemaccel
Fluid Regimes
1L normal saline + 2L 5% dextrose
OR 3L dextrose saline
+ 20mmol/l of K+ per bag
Important caveats:
• Always replace ADDITIONAL LOSSES e.g. vomiting, diarrhoea, ileostomies, 3rd space
• If fever (20% extra/day or 500ml/degree above 37)
• No potassium 24-48 hours post surgery (non-cardiac)
Hartmannʼs is also known as LACTATED RINGERʼS SOLUTION and should be avoided in liver and renal
failure.
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Assessment of volume status
• Check fluid charts and other bedside charts, quick history.
• Observation: awake/orientated or confused, shortness of breath.
• Inspect for:
• Cap. refill (> 3 secs)
• Temperature of the hands Features of JVP:
• Increased skin turgor
• Tachycardia/tachypnoea • Falls on inspiration
• Blood pressure (late sign) • Falls on standing
• Low JVP • Non-pulsatile
• Sunken eyes • Lies between the 2 heads of the SCM
• Dry mucous membranes • Has a double waveform
• Examine chest and peripheries for oedema
URINE OUTPUT:
Should be 0.5 ml/kg/hr (= 30ml/hr for 70kg man)
If no output/anuria:
1. SIMPLE STUFF e.g. check catheter & bag, flush the catheter with 50 mL saline using a bladder
syringe
2. Fluid challange (250ml colloid - repeat a couple of times)
3. Senior review and consider CVP monitoring
A central venous pressure line is often

used in order to gauge the response to a
fluid challange.
• If the patient is UNDERFILLED the

CVP will not increase with the
challange or will increase the fall again
• If the patient FILLED then the CVP will

rise (> 10mmHg) and stay elevated
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Nutrition
Nutrition is important as it affects outcome
1. Impaired immune system

2. Delayed/poor wound healing
3. Longer rehabilitation (so increased cost, nosocomial infections, DVTs)
Assessment
HISTORY Eating habit, diet, recent changes in weight/appetite
EXAMINATION Regular weights

BMI
Waist circumference (>102 cm in men, > 88 cm in women)
ANTHROPOMETRIC Upper arm circumference

Ulnar length
Grip strength
Skin fold thickness
BLOOD TESTS Albumin

Pre-albumin
Phosphate
Transferrin
Lymphocyte count
BMI = weight (kg) / height (m)2
Normal 18.5 - 25
Overweight 25 - 30
Obese 30 - 40
Morbidly obese > 40
Waist circumference is a better representation of omental fat + better predicts development of metabolic
syndrome.
Daily Requirements
Calories:! 25-35 kcal/kg/2 hrs (usually ~ 2500 per day for men and ~ 2000 per day for women)
Protein:!! 1.5 kg/24
Nitrogen:! 12g per day
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Nutritional Therapy
Basic definitions:
• ENTERAL - “Nutrition that is delivered via the normal enteral route”
• PARENTERAL - “Nutrition that is delivered directly through the venous system.”
1. Enteral Nutrition
To use this form of nutrition it is necessary for patients to have some degree of functioning bowel.
There are 3 types of feed:
1. POLYMERIC
• Near to normal e.g. food-supplements (Nsure, Fortisip), OSMOLITE
2. DISEASE SPECIFIC
• Gluten-free diets in coeliac disease, liver disease feeds
3. ELEMENTAL
• Basic AA and saccharides e.g. chronic multiple fistulae in Crohns
This may be administered:
1. ORAL
2. Fine-bore NG tube (check for aspirate, CXR) [< 6 weeks]
3. Gastrostomy (surgical/PEG)
4. Jejunostomy
Complications of enteral nutrition:
Feed itself Too much feed/too little feed

Intolerance (nausea/vomiting and diarrhoea)
Electrolyte + glucose imbalance
Method of delivery Malposition of NG tube

Tube obstruction
Infection around gastrostomy/jejunostomy
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2. Total Parenteral Nutrition
This should be avoided if at all possible.
The main indication is NON-FUNCTIONING BOWEL

• e.g. short bowel syndrome, prolonged ileus, severe Crohnʼs disease
May be administered through:
1. Large peripheral line

2. Central line (tunnelled = Hickmann line)
Complications of parenteral nutrition:
Feed itself Reactive hypoglycaemia

Fatty liver
Vitamin deficiencies
Method of delivery Complications of inserting a central line e.g. pneumothorax, bleeding

Infection around site
Sepsis
Malposition
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Trauma Surgery
Advanced Trauma Life Support (ATLS)
Trauma is the leading cause of death due to injury worldwide, and may be defined as:
“A body wound or shock caused by a serious and life-threatening injury.”
The trimodal death distribution describes death due to injury in three peaks or periods. The first occurs within
seconds to minutes of injury and is due to severe injuries where only prevention can reduce deaths. The
second occurs within minutes to hours, where the golden hour of care with rapid assessment and
resuscitation can save lives. The third peak occurs after several days to weeks and is often due to sepsis
and multiple organ dysfunction.
When treating traumatised patients we use ATLS Principles:
1. Primary Survey/Resuscitation
• ABCDE
2. Secondary Survey
• AMPLE
• Top-to-toe examination
3. Definitive treatment
TRIAGE is the process of prioritising care based upon available resources and the extent of injuries
sustained.
The Primary Survey
This basically is RESUSCITATION and may be remembered using the Airway and C-spine
familiar mneumonic ABCDE.
Breathing
1. Airway and C-spine
The C-spine must be secured with in-line immobilisation. Unknown Circulation

trauma to this area could lead to severe spinal injury and breathing
compromise.
Disability
Initially this may require manual immobilisation, but eventually inline
support of the C-spine needs triple immobilisation with:
1. Hard collar
2. Blocks or sandbags Exposure
3. Tape over chin and forehead
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The airway must be assessed and treated.
ASSESSMENT 1. If orientated and speaking...AIRWAY IS SECURE.

2. If obtunded or gurgling/stridor...AIRWAY NEEDS SECURING.
3. If complete obstruction...OPEN and SECURE.
TREATMENT Chin lift or jaw thrust

Remove foreign bodies with fingers
Suction with a Yanker tube e.g. vomit, blood
Secure the airway

e.g. nasopharyngeal, oropharyngeal - Guedel, ET tube, surgical
Types of Airway
The best person to manage the compromised airway is an anaesthetist.
Airways may be divided into:
NON-SURGICAL and SURGICAL
and
NON-DEFINITIVE and DEFINITIVE
A definitive airway is an adequately secured, cuffed tube in the trachea. An ETT and tracheostomy are
definitive airways. Note that an LMA is not a definite airway, as patients are still at risk of aspiration. The
indications for a definitive airway are:
• Apnoea
• Inability to maintain a patent airway
• Risk of aspiration or obstruction
• GCS < 8
• Inadequate oxygenation via face mask oxygenation
NON-SURGICAL AIRWAYS
Nasopharyngeal Sizing - patientʼs little finger

For the conscious patient with an intact gag reflex
Contraindicated in basal skull fractures
Oropharyngeal (Guedel) Sizing - from the angle of the mouth to the tragus
For the unconscious patient with an absent gag reflex
Endotracheal tube (ETT) Sizing - 6-8 mm diameter, a general rule of thumb 7 mm for an adult
female and 8 mm for an adult male
This is a definitive airway
The correct positioning of an ETT can be confirmed with:
1. Bilateral air entry on auscultation
2. No borborygmi
3. C02 detector
4. CXR
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NON-SURGICAL AIRWAYS
SURGICAL AIRWAYS
Needle cricothyroidotomy These are required where attempted ETT has failed. A needle
cricothyroidotomy is a short-term measure. It can only oxygenate the
Surgical cricothyroidotomy patient for 30-45 minutes, as ventilation is limited with a wide-bore
cannulae. A surgical cricothyroidotomy is preferable to a tracheostomy in
an emergency situation.
Tracheostomy A tracheostomy is a definitive airway.
2. Breathing
Attach patients to a monitor for BP, HR, ECG tracing and oxygen saturations and do an ABG to assess
oxygenation. All patients should have high flow oxygen through a non-rebreathing mask.
Assessment:
INSPECTION PALPATION PERCUSSION AUSCULTATION
Signs Agitiation (hypoxia) Trachea for deviation Hyper-resonance Air entry (absent,
Obtundation (PNEUMOTHORAX) unilateral, bilateral)
(hypercarbia) Paradoxical breathing -
flail chest segments Hypo-resonance
Cyanosis (peripheral/ (HAEMOTHORAX)
central)
Respiratory rate and

oxygen saturations
Breathing pattern (in

cervical cord
transection involving
C3-5 supplying the
diaphragm there will be
abdominal breathing)
Snoring, gurgling,
stridor, hoarseness
Treat any life-threatening problems such as tension pneumothorax, massive haemothorax or flail chest. It is
important to maintain adequate oxygenation to prevent cerebral hypoxaemia and ischaemia.
3. Circulation
Secure IV access (2 large bore cannulae into ante-cubital fossae) and take trauma bloods (FBC, U&Es,
clotting) & CROSS-MATCH 6 units. Consider urinary catheterisation after PR to exclude a high-riding
prostate, which indicates urethral injury.
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Shock can be classified into:
1. HAEMORRHAGIC
2. NON-HAEMORRHAGIC
a. Cardiogenic
b. Neurogenic
c. Septic
The most common form of shock in the context of trauma is HAEMORRHAGIC shock.
Assess for hypovolaemia and SHOCK:
Observation: alert and orientated, confused, or unconscious.

Inspect for:
• Cap. refill (> 3 secs)

• Cold hands
• Tachycardia
• Tachypnoea
• Hypotension (late sign)
• Low JVP
• Low urine output
Haemorrhagic shock can be divided into four classes. The percentage blood loss parameters are easily
remembered using the tennis scoring system and blood loss volume is based on a 70 kg male, where total
blood volume is approximately 5 L (7 % of the circulating blood volume).
Class I Class II Class III Class IV
Blood loss (%) < 15 % 15 - 30 % 30 - 40 % > 40 %
Blood loss (mL) < 750 mL 750 - 1500 mL 1500 - 2000 mL > 2000 mL
HR < 100 100 - 120 120 - 140 > 140
BP Normal Normal Decreased Decreased
PP Normal Decreased Decreased Decreased
RR 14 - 20 20 - 30 30 - 40 > 35
UO (mL/hr) > 30 20 - 30 5 - 15 Anuric
CNS status Anxious Anxious Confused Lethargic
Simply put, patients with Class I shock have normal parameters but maybe anxious. Class II patients are
tachycardic and tachypnoeic but BP remains normal with a decreased PP. Class III patients have
tachycardia, tachypnoea, hypotension and confusion, and Class IV patients have all signs of shock with a
reduced GCS.
All patients with signs of shock are presumed to have haemorrhagic shock, as this is the most
common cause of shock in the context of trauma. 1-2 litres warm crystalloid (Hartmanns/normal saline)
should be administered STAT. Blood (type-specific, crossmatched or O. negative emergency blood) may
be required if the patient continues to haemorrhage.
There are four main sources of HAEMORRHAGIC SHOCK which can be remembered using the mneumonic
“Blood on the floor x four more”
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CHEST, RETROPERITONEUM, PELVIS, THIGH AND ON THE FLOOR
Response to initial fluid resuscitation (2 L crystalloid) determines subsequent therapy, and response can be
divided into rapid, transient and no response:
Rapid Response - Transient Response - No Response -

Minimal blood loss Ongoing blood loss or Exanguinating
inadequate haemorrhage
resuscitation
Vital signs Normal Transient improvement Remains shocked

but recurrence of
tachycardia and
hypotension
% Blood loss 10 - 20 % 20 - 40 % > 40 %
Need for more Low High High

crystalloid
Need for blood Low Moderate High
Blood preparation Type and crossmatch Type-specific O-negative
Need for operative Low Moderate High

intervention
4.Disability
Assess:
1. Coma scale (see head trauma)
• AVPU
• GCS
2. Limb Posture
3. Pupils! !
The Pupils
Assess for size, equality and responsiveness:
Appearance Cause
Bilateral fixed and dilated Death, hypovolaemia, drugs (ecstasy, adrenaline)
Unilateral fixed and dilated Orbital injury, oculomotor nerve compression, stroke
Bilateral pinpoint Opioid drugs
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Bilateral constriction Brainstem injury
Irregular Trauma, post eye operation
5.Exposure
Remove all clothes & prevent hypothermia (warmed IV fluids, warm resuscitation room, hot air).
Look for evidence of trauma:
• Front
• Back (log-roll to protect C-spine)
• PR for high-riding prostate
Imaging in Trauma
There are 3 important mobile tests:
1. C-spine XR (must include C7-T1)

2. Pelvis XR
3. Chest XR
[+ ultrasound abdomen] also known as a FAST scan.
Other tests may be performed but the patient should be stable first. Beware of the donut of death!
The Secondary Survey
This has 2 important components:
1. HISTORY - “AMPLE”
Age
Medication
Past medical history/pregnant
Last meal
Events
2. ! Top-to-toe examination
Note: if the patientʼs state changes at any time then you must return to the beginning of the primary survey.
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Chest Trauma
There a huge number of possible chest injuries that result from trauma. Here we consider the most
important:
1. Rib fractures, pulmonary contusion and flail segments

2. Pneumothorax
3. Haemothorax
4. Cardiac tamponade
5. Others: tracheobronchial tree injury, blunt cardiac injury, aortic disruption, diaphragmatic injury,
oesophageal rupture
Remember the mneumonic ATOM FC memorise life threatening chest injuries:
Airway obstruction
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Flail chest
Cardiac tamponade
1. Rib Fractures
• Fractures of ribs 1 - 3 imply severe injury to the head, neck and great vessels
• Fractures of ribs 4 - 9 are most common and can damage adjacent viscera leading to
haemopneumothorax and lung contusion
• Fractures of ribs 10 - 12 can damage the liver and spleen
Multiple fractures can lead to Flail segment
“ ≥ 2 consecutive ribs fractures in ≥ 2 places”
This causes HYPOXIA from
1. PARADOXICAL MOVEMENT ON INSPIRATION

2. Restricted chest wall movement due to pain
3. Underlying lung contusion
Treatment is with
• Analgesia
• Strapping of the segments
• Invasive positive pressure ventilation (if resistant hypoxia)
2. Pneumothorax
“Air in the pleural space.”
This is due to either blunt or penetrating trauma and there are 3 types:
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a. SIMPLE - “accumulation of air with no mediastinal displacement.”

b. TENSION - accumulation of air through a one-way valve leading to accumulation and mediastinal
displacement.”
c. OPEN - “opening in the chest wall (2/3 diameter of the trachea) resulting in a sucking chest wound.”
A tension pneumothorax is a MEDICAL EMERGENCY!
Important signs - Sudden - Reduced movement Hyper-resonant Absent breath sounds

cardiorespiratory on affected side on affected side
compromise - Tracheal displacement
- SOB away from affected
side
IMMEDIATE RX - “...large bore needle into 2nd intercostal space in mid-clavicular line.” (needle
thoracotomy)
Initial management of an open pneumothorax is placing a sterile dressing secured on three sides in order to
provide a flutter-type valve effect.
Definitive treatment for all pneumothoraces is the insertion of a chest drain on the affected side (draining
the apex) in the 5th intercostal space, just anterior to the mid-axillary line.
3. Haemothorax
“Blood in the pleural space”
These are due to penetration or decelerating injuries
Important signs - Distress - Decreased movement Stony dull Decreased breath

- Hypoxia on affected side sounds on affected side
- Distended neck veins - Tracheal deviation
away from the
affected side
Treatment depends on the size
• Small (< 1.5L)

• Fluid resuscitiation
• Chest drain
• Massive (> 1.5L or draining > 200ml/hr for 2 - 4 hrs) from damage to the great vessels, hilar and heart
• Fluid resuscitation (including blood)
• Chest drain
• Thoracotomy
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4. Cardiac Tamponade
“Blood from the great vessels/heart within the pericardial sac leading to restricted filling and contraction.”
Clinical features described in BECKʼS TRIAD
1. Elevated JVP (restricted filling)

2. Hypotension (restricted filling and contractility)
3. Muffled heart sounds (blood in pericardial sac)
Donʼt forget Kussmaulsʼ sign, a rising JVP with inspiration.
Investigation:
• Echocardiography
Management:
• Peri-cardiocentesis with ECG monitoring (to detect myocardium)

• Thoracotomy
5. Others
Tracheobronchial tree injury (high mortality)
Clinical features
• Haemoptysis
• Subcutaneous emphysema
• Tension pneumothorax with persistent air leak after tube thoracostomy
Investigation
• Bronchoscopy
Management
• Surgery
Blunt myocardial contusion
Clinical features
• Hypotension
• Dysrhythmias
• Wall motion abnormality on echocardiography
Management
• Monitor for dysrrhymias
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Aortic Disruption
Most common cause of death following rapid deceleration in an automobile collision or fall from a great
height. Usually , there is an incomplete laceration near the ligamentum arteriosum of the aorta and a
contained haematoma. Diagnosis requires a high index of suspicion.
Investigation
• CXR - widened mediastinum

• CT chest
Management
!
• Cardiothoracic surgery
Diaphragmatic injury
These are more common on the left side and maybe caused by blunt or penetrating trauma. Early diagnosis
requires a high index of suspicion.
Investigations
• CXR - elevation of the diaphragm
Management
• Surgery
Oesophageal rupture
This maybe due to blunt or penetrating trauma. Blunt oesophageal rupture is due to the forceful expulsion of
gastric contents into the oesophagus, after a severe trauma to the upper abdomen.
Clinical features
• Pain out of proportion to the injury

• Left pleural effusion or pneumomediastium
• Particulate matter in the chest drain
Investigations
• Oesophagosocpy
• Contrast studies
Management
• Chest drain
• Surgery
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Head Trauma
Basic anatomy
The scalp is made up of 5 layers of tissue which can be remembered using the mneumonic “SCALP”:
! Skin
! Connective tissue
! Aponeurosis
! Loose areolar tissue
! Pericranium
The skull is composed of:
1. Cranial vault - divided into three regions: anterior, middle and posterior cranial fossa and is thinnest
in the temporal regions (but protected by the temporalis muscle - note this is the area affected with
rupture of the middle meningeal artery and development of an extradural haematoma)
2. Base - irregular in nature and prone to injury from forceful movement
The meninges consists of three layers that cover the brain:
1. Dura
2. Arachnoid
3. Pia
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Classification
This is the commonest cause of trauma death.
Classification of brain injury
Mechanism
Blunt High or low velocity
Penetrating Gunshot or other penetrating injuries
Severity
Mild GCS 13 -15
Moderate GCS 9 - 12
Severe GCS < 8
Morphology
Vault Linear or stellate, depressed or non-depressed, open or closed
Basilar CSF leak or cranial nerve palsies
e.g. basal skull fracture - panda eyes, rhinorrhea, Battleʼs sign and
otorrhoea
Intracranial lesions
Focal Epidural, subdural, subarachnoid, intracerebral
Diffuse Concussion, contusion (coup and contracoup), hypoxic injury
Severity of injury should be assessed using: Observation Score
1. AVPU - a simplified version of the glasgow coma scale Eye opening

! Alert
! Voice - Spontaneous 4
! Pain (indicates GCS < 8)
- To speech 3
! Unresponsive
2. GCS (see table and assess using the best motor response) - To pain 2
! Mild - GCS 13 -15
! Moderate - GCS 9 - 12 - None 1
! Severe - GCS < 8
Best verbal response
The real problem with head injury is explained using the Monroe-Kelly
- Orientated 5
doctrine. It states that the total volume within the cranium must remain
constant, as the cranium is a rigid, non-expansile structure. A small - Confused 4
increase in volume can be compensated for but once the compensatory
mechanism is exhausted, there is an exponential increased in the ICP. If - Inappropriate words 3
this occurs then the pressure will rise leading eventually to BRAIN
HERNIATION, also known as coning. - Incomprehensible 2
- None 1
Features of raised intracranial pressure:
Best motor response
• Headache
• Vomiting - Obeys commands 6
• Seizures
- Localizes to pain 5
• Drowsiness
• Papilloedema - Withdraws from pain 4
•
Features of coning: - Abnormal flexion 3
• Ipsilateral pupil vasodilatation (CN III palsy) - Extension 2

• Contralateral hemiparesis
- None 1
• Cushingʼs response (rising BP and falling HR)
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• Coma
Investigations
• Skull XR (lateral is the most useful)

• C-spine XR
• Head CT (see NICE guidelines for head CT)
Main indications for head CT:

• GCS < 13
• Change in GCS 2 hours following injury
• Focal neurological deficit
• Open or depressed skull fracture
• Post-traumatic seizure
• Vomiting > 1
• LOC and > 65 years/coagulopathy/dangerous mechanism of injury/antegrade amnesia > 30 mins
Treatment of head injury
This depends on the severity:
MILD - discharge with written information and a responsible companion

MODERATE - admit for neurological observations
SEVERE - neurosurgical referral
CONSERVATIVE Airway - secure airway

Breathing - oxygen
Circulation - IV access, fluid resuscitation
MEDICAL Ventilation
Antiepileptics for seizures
SURGICAL Neurosurgical input
It is important to maintain good oxygenation to avoid cerebral hypoxia and ischaemic damage, and
normocapnia. Hypercapnia will cause cerebral vasoconstriction and lead to cerebral hypoxia and also
increased intracranial pressure.
Raised intra-cranial pressure is COMPLEX to treat.
CONSERVATIVE Try to correct complications e.g. hypoxia, hypercapnia, hypovolaemia
MEDICAL Ventilation
Steroids
Mannitol and fluid restriction
SURGICAL Neurosurgical input is very important
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Types of Cranial Bleeding
A quick revision of the different meningeal layers and blood supply in this region:
Pics from left to Location Injury Clinical Features Management

right
Extra-dural Outside the dura Disruption of arteries LOC CT

Pic: right grey lens mater from the middle Lucid period Lens shaped
shaped meningeal artery Deterioration (coning) haematoma
haematoma + Death
Rx: Neurosurgical
midline shift drainage
Sub-dural Between arachnoid Rupture of bridging vein Insidious onset CT
Pic: left and dura (alcoholics/elderly/ Cresenteric shaped
cresenteric epileptics/those on haematoma
haematoma + anticoagulants)
Rx: Surgical
midline shift Headache, sensory/ evacuation of
motor S/S haematoma
Subarachnoid Under arachnoid Trauma or ruptured Sudden onset occipital CT, cerebral
Pic: blood in the Berry aneurysm headache angiography
subarachnoid
basal cisterns Meningism Rx: Conservative
(nimodipine)/Surgery
(clipping/embolisation)
Intra-cerebral Within brain tissue Damage to brain Compressive and Surgical drainage
Pic: Intracerebral substance localising signs
and
intraventricular
haemorrhage
Remember on CT acute bleeding is high attenuation = white and older bleeding is low attenuation = black/
grey.
Always comment on ANY MIDLINE SHIFT!
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Burns
Burns tend to affect particular groups of people
• Age: Toddlers and elderly

• Disease states: epileptics, post-stroke, alcoholism
• Occupations: welders/chefs
There are 4 types of burn:

1. Thermal
2. Chemical
3. Electrical
4. Friction
The severity and management of a burn depends on its thickness:
Nomenclature Depth Clinical features
Superficial First degree burn Epidermis Erythema

Painful
Partial:
1. Superficial Second degree burn Papillary dermis Blistering
2. Deep Third degree burn Reticular dermis Painful
Deep Third degree burn Epidermis, dermis and Leathery

subcutaneous fat White to charred
Painless
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Assessment of a burn
This is done using a special assessment tool:
“WALLACE RULE OF NINES”
Management
Should be managed in a specialist burns unit (second/third degree burns > 10 % in children or > 20 % in
adults)
Requires a normal ATLS approach but with special considerations
AIRWAY
• Laryngeal oedema following inhalation injury may complicate intubation: low threshold for intubation,
surgical airways
BREATHING
• CO poisoning (carboxyhaemoglobin) and inhalational pneumonitis - oxygen and low threshold for
intubation and mechanical ventilation
• Escharotomy of chest wall
CIRCULATION
• Fluid losses can be huge and must assessed and replaced, best guide to adequate fluid replacement
is urine output
• Burns calculator
4 x weight (kg) x % burn = mL crystalloid in 24h, half given in 1st 8h then 2nd half given in the following
16h
or
[weight (kg) x % burn]/2 = mL colloid per 4h, 4h, 4h, 6h, 6h and 12h
Aim for urine output of 0.5 ml/kg/h
Additional adjuncts
• Partial thickness - flamazine cream/clingfilm/plastic bags/analgesia

• Escharotomy and fasciotomy
• Antibiotics
• Surgical skin grafting
• PPI (Curlingʼs ulcer - stress ulcer)
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Complications
Specific - Early Multiorgan failure

Pulmonary complications e.g. atelectasis, ARDS
Specific - Intermediate Infection

Constricting eschars
Specific - Late Contractures

Scarring
Curlingʼs ulcer
Psychological e.g. PTSD
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Peri-operative Care
May be split into:
- PRE-OPERATIVE
- OPERATIVE
- POST-OPERATIVE
Pre-operative
The main purpose is to identify RISK. Patients may be classified using the American Society of
Anaesthesiologists (ASA):
ASA Grade Definition Mortality
I Normal 0.05%
II Mild systemic disease 0.40%

No limit in activity
III Severe systemic disease 4.50%

Limits activity
Not incapacitating
IV Incapacitating systemic disease 25%
V Moribund > 50%

Not survive with or without
surgery for > 24h
Pre-Assessment of the Surgical Patient
“A SCREENING PROCEDURE for disease that may compromise the conduct or complications of surgery.”
Can follow a basic history structure:
PRESENTING COMPLAINT
• Review reasons for surgery and history surrounding problem.
PAST HISTORY AND SYSTEMATIC ENQUIRY

• Medical history
• Surgical history (previous operation and any adverse outcomes)
• Modified systematic enquiry looking for:
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1) CARDIOVASCULAR DISEASE (e.g. ischaemia, hypertension, arrhythmia)

2) RESPIRATORY DISEASE (e.g. COPD, asthma, lung fibrosis)
3) ENDOCRINE (e.g. DM, corticosteroids, thyroids)
DRUGS
• Allergy
• Current medication (steroids, anti-coagulant, contraception, immunosuppressants etc.)
• Anaesthetics
FAMILY HISTORY
• History of anaesthetic problems e.g. malignant hyperthermia, sickle cell
SOCIAL
• Habits and rehabilitation etc.
Then...move onto INVESTIGATIONS for specific problems.
Preparation for Surgery

FASTING/NBM Guidelines
This may be split into:

Fluids: none 2 hours before procedure
Food: none 6 hours before procedure
1) GENERAL
(usually patients are fasted from night
before)
• Consent
• Book theatre/anaesthetist
• Fasting or NBM
• Mark site of operation
• I.V. cannulation
• Urinary catheter
2) INVESTIGATIONS
• Bloods (FBC, U&Es, LFTs, clotting, G&S/CM, Hb electrophoresis)

• Imaging: CXR
• ECG
• MRSA swab
3) MEDICATIONS
• DVT prophylaxis (TEDS, LMWH)

• Prophylactic antibiotics e.g. abdominal surgery - cefuroxime and metronidazole, vascular surgery - co-
amoxiclav
• Bowel preparation
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Considerations for for specific conditions
CONDITIONS Consideration Pre-op Post-op
Type I DM Co-existing disease e.g. - “First on list” - Sliding scale until

renal/cardiovascular - Convert to sliding eating
scale
- Omit long-acting
insulin
Type II DM Co-existing disease e.g. - Omit oral - Sliding scale post-op

renal/cardiovascular hypoglycaemics on day - Restart oral when
of surgery eating
Steroid use Addisonian crisis - Continue steroid up - IV hydrocortisone until

until surgery normal oral intake
Obstructive jaundice Increased mortality: - Normalise clotting - Good hydration

- Coagulopathy - Prophylactic antibiotics
- Infections
- Hepato-renal
syndrome
Anti-coagulants Bleeding potential - Stop/convert to - Re-warfarinise once

heparin oral intake
- FFP lower INR in an
emergency
Chronic renal failure Hyperkalaemia/Fluids - Dialyses - IV naloxone

Drug clearance - Desmopressin for
impaired bleeding
function
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Post-operative
There are always many things to think about in the patient who has just returned from theatre:
1. Fluids (covered above in surgical fluids)

2. Pain relief
3. Complications (common ones include pyrexia)
Analgesia
The management of post-operative pain has 2 stages
a. Pre-operative: effective counselling about possibility of pain and patient choice
b. Post-operative: preventing and treating breakthrough pain
It is also important that pain and itʼs perception can have effects over and above psychological distress:
Organ system Effect
Psychological Anxiety
Fatigue
Cardiovascular Increased myocardial O2 consumption
Respiratory Reduced coughing ∴ sputum retention

Atelectasis
Gastrointestinal Decreased gastric emptying

Reduced gut motility
Genito-urinary Urinary retention
Musculoskeletal Reduced mobility (→ pressure sores

and DVTs)
Endocrine Hyperglycaemia
Protein catabolism
Sodium retention
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Assessment
Pain is subjective! Observer assessment is unreliable
Can be assessed by
1. Talking to patient
2. Looking at vital functions
3. Various scales
• Visual analogue scales
• Verbal numerical reporting scale
• Categorical rating scale
The Relief of Pain
This may be divided into:
1. NON-PHARMACOLOGICAL
• Basic things e.g. pre-op preparation, relaxation therapy, hypnosis, cold/heat, splinting, TENS
• Interventional e.g. local anaesthetic infiltration of wounds, nerve blocks.
2. PHARMACOLOGICAL
• This uses the WHO analgesic ladder
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Consider the following
• Regular administration
• Patient-controlled analgesia
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Post-operative Pyrexia
This is exceedingly common after surgery and is associated with different complications depending on when
it occurs.
All these complications are more serious in
Timeframe Complication Look for
< 24 h Systemic response to trauma Exclusion of others
Pre-operative infection -
24 - 72 hours Pulmonary atelectasis Tachycardia + tachypnoea

Reduced air entry to bases
CXR - consolidation and
collapse
Chest infection As above + more severe
3 to 10 days Chest infection As above + more severe
Wound infection Local erythema, discharge and

dehiscence
Urinary tract infection Symptoms

+ve. urine dipstick
Anastomotic leak
DVT/PE Calf pain and tenderness
Intraperitoneal sepsis Abdominal pain, distension and

ileus
Assessment
• Perform a good history and examination then do basic investigations and look bedside charts.
SEPTIC SCREEN
Cultures Blood
Urine MC & S
Bloods - ABG Yes
Bloods - Venous Routine bloods (infectious markers)
Imaging CXR
Abdominal ultrasound/CT
Scopic/Biopsy
Functional/Special ECG (? PE)
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Skin Disorders
This section is basically about lumps and bumps. We have chosen to put them at the start of
these notes as the principles outlined here are important for the rest of the course.
Basic Principles
Always think about lumps in terms of:
! SITE
! SIZE
! SHAPE (edge, surface)
!
! CONSISTENCY (transillumination, pulsation)
! COLOUR
! TENDERNESS
! TEMPERATURE
[+ always look for local lymph nodes]
The best way to approach lumps in an exam is to recognise what it is then real-off a ʻmodified definitionʼ.
In the rest of this section we shall consider these basic definitions.
Cystic swellings
“A fluid filled cavity lined by epithelium.”
1. Sebaceous cysts
• Mobile, firm swelling with a visible punctum.

• Fixed to skin + has a foul-smelling toothpaste-like discharge.
• Found in hair-bearing regions.
• If infected it is called an ABSCESS.
• Rx - excision
2. Dermoid cysts
There are 2 types
! 1. Inclusion dermoids
• Firm cystic swelling not attached to the overlying skin that occur at sites of embryological
fusion e.g. neck midline and outer angle of the orbit.
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• Rx - excision
2. Implantation dermoids
• Firm cystic swelling not attached to the overlying skin occurring most commonly in the hands
of gardeners due to penetration injury
• Rx - excision
Ganglions
• Tense cystic swellings on dorsum of hand, wrist not attached to overlying skin.
• Lined by fibrous tissue originating from the synovial lining of joint/tendon sheath.
• Rx - excision, traditionally hit with a bible
Lipomas
• Soft, non-tender, fluctuant lumps that have a definable edge and are not attached to the overlying skin
(particularly on trunk and limbs)
• If multiple and painful → Dercumʼs disease
• Rarely calcify or undergo sarcomatous change
Keloid scarring
• Irregular hypertrophy of collagen forming a raised edge that extends outside the scar
• [cf. hypertrophic scar - does not extend outside]
• More common in blacks
• Rx - corticosteroid injections/excision
Benign and Malignant skin tumours
1. Benign
Seborrhoeic keratoses
• “Brown/yellow oval lesion with a greasy and well demarcated border”

• Stuck-on appearance
• Very common in elderly patients
• Rx - nil
Keratoacanthoma (molloscum sebaceum)
• “Rounded swelling with rolled edges and a central keratin plug”

• Occurs on light-exposed skin
• Important differentials include BCC and SCC, however a keratoacanthoma will spontaneously regress
• Rx - watch and wait, or excision
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2. Malignant
Malignant cutaneous tumours are increasingly common in ageing skin exposed to prolonged UV radiation.
Those of fairer skin types are at higher risk.
Basal cell carcinoma (BCC)
• Lesion with a pearly rolled edge, telangiectasia and central depression

• Known as the “rodent ulcer” as the tumour rarely metastasises, but local invasion can be destructive
• Occurs on sun exposed areas
• Rx - excision
Actinic or solar keratoses
• Flat lesions with a red/scaly surface

• Sun-exposed areas (face, bald scalp, forearms, dorsum of hands) that progresses to become multiple
• Maybe pre-malignant to SCC
• Cryotherapy or topical 5-FU
Bowenʼs disease (squamous cell carcinoma in situ)
• Solitary patch of red, scaly skin often below the knees

• This is also known as Queyratʼs erythroplasia in the penis, or a Marjolinʼs ulcer when a SCC develops
in a chronic ulcer
• Maybe pre-malignant to SCC
• Rx - excision
Squamous cell carcinoma!
• A keratotic lump, polypoid mass or cutaneous ulcer in a sun-exposed area

• Rx - excision
Lentigo Maligna (Hutchinsonʼs freckle)
• Flat, brown are with irregular pigmentation usually on the face

• Rx - biopsy
Malignant melanomas
These are the most dangerous of the malignant skin tumours and may occur in pre-existing moles. With the
exception of lentigo maligna melanoma, they occur in a relatively younger age group than other skin cancers
and incidence is rising as a result of increased sun exposure.
Simplified diagnostic criteria:
Asymmetry
Border (iregular)
Colour (non-uniform)
Diameter > 7mm
Elevation
Look for neighbouring satellite lesions and localised lymphadenopathy.
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There are 4 types
1. Lentigo maligna melanoma - invasive nodular melanoma within a lentigo maligna

2. Superficial spreading melanoma - most common; irregularly pigmented patch with an irregular
edge usually on the leg or trunk
3. Nodular melanoma - rapidly growing lump
4. Acral melanoma - rare but more common in Asian or Afro-Carribean patients; pigmented patch on
the sole or palm, or subungual pigmentation
Prognosis is based on Breslowʼs thickness or Clarkeʼs level.
Rx - excision
Ulcers
“Interruption in the continuity of an epithelial surface.”
Necrotic material tends to accumulate as SLOUGH in the base of the ulcer.
Cause Sites Features Treatment
VENOUS Venous Medial side of the Sloping edge Conservative

70 % hypertension leg, above the - 4 layered
medial malleolus bandage
Extravasation of (gaiterʼs region) technique (ABPI
blood → > 0.8)
lipodermatoscleros
is and poor blood Surgical
supply - Skin grafting
- Treat varicosities
ARTERIAL 1. Large vessel Pressure points Punched out edge Treat underlying
2% disease (e.g. cause e.g. poor
PVD) 1. Ball of the heel Erythematous halo perfusion
2. Small vessel 2. Malleoli
disease (e.g. 3. Between the Pale granulation Minimise risk
Buergerʼs toes tissue factors for
disease) arteriopathy e.g.
Cold skin smoking, HTN
NEUROPATHIC Repetitive Plantar aspect of Punched out edge Remove any callus
mechanical forces foot under
of gait metatarsal heads/ Sensory loss Proper shoes
toes
Metabolic control
Antibiotics
(pseudomonas in
diabetics)
• Neoplastic
• Malignant change in a pre-exisiting ulcer, with an everted/rolled edge = Marjolinʼs ulcer
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The Oesophagus
Clinical Anatomy
The oesophagus is a muscular tube about 25 cm in length (40 cm from mouth to stomach)
Important landmarks:
• Starts at C6 (cricoid)
• Passes behind thyroid and trachea.
• Important anterior relations: left bronchus, aortic arch, left atrium
• Pierces diaphragm at T8
• Forms gastro-oesophageal junction at T10.
May be divided into 3 parts:
1. UPPER THIRD (striated)

2. MIDDLE THIRD (mixed)
3. LOWER THIRD (smooth)
The oesophagus is lined by squamous non-keratinising epithelium.
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Dysphagia
The 3 important swallowing symptoms:
DYSPHAGIA - “conscious difficulty in swallowing”
APHAGIA - “inability to swallow”
ODYNOPHAGIA - “painful swallowing”
Divide these as follows:
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ORAL Painful Tonsillitis

Pharyngitis
Ulcers
Obstructive Quinsy
Pharyngeal pouch
Epiglottitis
NEUROLOGICAL Bulbar MND

GB-syndrome
Pseudobulbar CVA
MS
MND
Local CREST
Achalasia
MECHANICAL In the lumen Foreign body

Food
In the wall Carcinoma

Stricture
Outside the wall Retrosternal goitre

Lymphadenopathy
Bronchial carcinoma (left)
Thoracic aortic aneurysm
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Oesophageal Tumours
Divided into:
! PRIMARY
• Benign e.g. polyp, lipomas, haemangiomas, leiomyomas
• Malignant
! SECONDARY (rare)
There are 2 types of:
• 50% squamous cell carcinoma (upper half)

• 50% adenocarcinoma (lower half)
Adenocarcinomas are becoming more common as the incidence of GORD and Barrettʼs oesophagus
increases.
Note:
Epidemiology
10 % GORD Barrettʼs oesophagus
• Men (5:1)
• > 50y
• Iran/South Africa, China 1 % Barrettʼs Adenocarcinoma
Risk factors
• LIFESTYLE e.g. smoking, alcohol, diets rich in nitrosamines or vitamin C deficient

!
• OTHER DISEASE e.g. Barrettʼs (adenocarcinoma), achalasia (squamous), Plummer-Vinson
(squamous)
Clinical features
GENERAL
• Weight loss, anorexia, malaise
SPECIFIC
• Dysphagia (progressive, solids then liquids then saliva)

• Others e.g. haematemesis (bleeding), hoarseness (L. recurrent laryngeal nerve), aspiration
pneumonias, perforation (rare)
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Investigations
Cultures -
Bloods - ABG -
Bloods - Venous FBC (anaemia)

LFTS (mets)
U&Es (nutrition/dehydration)
Ca2+ (mets)
G&S + CXM
Imaging CXR
Barium swallow (apple-core appearance)
CT (staging)
Endoscopic ultrasound or mediastinoscopy (local staging)
Scopic/Biopsy Endoscopy & biopsy
Functional -
Metastases
• Local
• Mediastinum (trachea, aorta, pleura and lung)
• Lymphatic
• Paraoesophageal
• Blood
• Liver and lung
Prognosis
5 year survival < 5%
Management
CONSERVATIVE Analgesia
Reduce size of tumour (alcohol / lasers)
Relieve obstruction (stent, dilatation)
MEDICAL Chemoradiotherapy to shrink tumour (neo-adjuvant)
SURGICAL Oesophagectomy + lymph node removal

Only 1/3 are operable (approaches - thorax, abdomen or both)
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Gastro-oesphageal reflux disease
“Reflux of acidic contents into the oesophagus”
Problems due to:

!
! 1. Oesophagitis
! 2. Barrettʼs (pre-malignant transformation)
Risk factors
! LIFESTYLE e.g. alcohol, large meals, smoking (relaxes the LOS)
! RAISED IAP e.g. obesity, pregnancy
! STRUCTURAL PROBLEMS e.g. hernias
Clinical features
The main feature is retrosternal, burning chest pain that is worse when bending / lying down and is made
worse by meals (particularly spicy ones) and hot fluids. Other features include acid and water brash, and
aspiration pneumonia.
Investigations
As above - most important is ENDOSCOPY + / - barium swallow.
Manometry or 24h PH monitoring if endoscopy is normal.
Complications
Approximately 10% develop Barrettʼs oesophagus, which is metaplasia of squamous to columnar

epithelium in the lower oesophagus. This requires regular surveillance as it is pre-malignant for
adenocarcinoma.
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Hiatus Hernia and other conditions
Hernia may be defined as:
“Abnormal protrusion of a viscera and its coverings through a defect into a place where it should not be.”
(see later for more hernias)
3 types:
1. SLIDING (80%)
2. PARAOESOPHAGEAL or ROLLING (5%)
3. MIXED (15%)
Investigation
• Endoscopy
• Barium swallow
Management of hiatus hernia
Note: para-oesophageal hernias always require an operation due to risk of strangulation.
CONSERVATIVE Modify risk factors e.g. stop smoking, reduced alcohol, smaller meals,
eat > 3h before bed, avoid tight clothing
MEDICAL Antacids
Alginates e.g. Gaviscon
H2 antagonists e.g. ranitidine, cimetidine
PPI e.g. omeprazole, lansoprazole
SURGICAL Nissen fundoplication
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Other Oesophageal Conditions
Oesophageal rupture
This is rare and has a poor prognosis.
Aetiology
• TRAUMA (external or internal)

• INs/OUTs e.g. corrosives & violent emesis (Boerhaveʼs syndrome)
Clinical presentation
Severe, acute chest pain and collapse, with hydropneumothorax on chest radiograph.
Treatment
• Fluid resuscitiation
• Antibiotics to prevent medastinitis
• Surgery
Pharyngeal pouch
This is a pulsion diverticulae that occurs due to peristalsis against resistance resulting from un-coordinated
muscle spasm.
The diverticulae occurs in area of weakness between the thyro-pharyngeus and crico-pharyngeus inferior
constrictor muscles. This point of weakness is known as Killianʼs dehiscence. It is more common on the left
side.
Clinical features
Patients present with dysphagia, regurgitation and a palpable swelling in the neck which gurgles. The patient
may also complain of halitosis or present with an aspiration pneumonia.
Treatment
Excise the pouch or staple it endoscopically.
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Plummer-Vinson syndrome
This is the development of a oesophageal web due to hyperkeratinisation in the upper oesophagus. This
causes dysphagia and is associated with chronic iron deficiency anaemia.
Aetiology
• Middle-aged
• Men
It is a pre-malignant condition for SCC of the oesophagus in the cricopharyngeus. Other pre-malignant
conditions of the oesophagus include achalasia and Barrettʼs oesophagus.
Treatment includes ferrous sulphate tablets for iron deficiency anaemia and oesophageal dilatation.
Achalasia
“Degenerative of Auerbach plexus leading to loss of relaxation (lower 1/3rd)”
This can also occur with Chagaʼs disease (Trypanosome cruzii). Like Barrettʼs oesophagus and Plummer-
Vinson syndrome, this is a pre-malignant condition for squamous cell carcinoma.
Clinical features
Patients present with “intermittent” dysphagia.
Diagnosis is with barium swallow which shows the typical appearance of tapering birds beak or rats tail.
3 main treatments are available:
1. Endoscopic dilatation
2. Hellerʼs cardiomyotomy
3. Botulinum injection
Note features of barium swallow:
Feature Pathology
Birdʼs beak/ratʼs tail Achalasia
Apple core Oesophageal carcinoma
Corkscrew/nutcracker Oesophageal spasm
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The Stomach
Clinical Anatomy
The stomach is a J-shaped organ with 2 curvatures (GREATER and LESSER)
It has 4 parts:
• CARDIA (6)
• FUNDUS (2)
• BODY (1)
• PYLORIC ANTRUM (10)
Important glands of the stomach
• Parietal cells - secrete gastric acid and intrinsic factor; stimulated by gastrin; inhibited by somatostatin
of high PH
• Chief cells - secrete pepsinogen and renin
• APUD or enteroendocrine cells - secrete gastrin, histamine, serotonin, cholecystokinin and
somatostatin
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Blood supply
• Arterial
• Lesser curvature
• L. gastric (coeliac branch)
• R. gastric (R. hepatic branch)
• Greater curvature
• R. gastro-epiploic (gastroduodenal branch)
• L. gastro-epiploic (splenic branch)
• Venous
• Enters portal system of liver
• Lymphatics
• Perigastric
• Coeliac nodes
• Nervous supply
• Vagus nerve has a posterior and anterior branch. It has motor (emptying) and secretory (acid
production) functions.
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Acute Upper GI Bleed
This is a MEDICAL EMERGENCY
Aetiology
• ULCERATION (duodenal 40%, gastric)!

• INFLAMMATION (gastritis, oesophagitis)
• OTHERS e.g. Mallory-Weiss, carcinoma, varices, angiodysplasia, HHT, Peutz-Jegherʼs, aortoenteric
fistula
Clinical features
These are due to:
1. DISPLACED BLOOD leading to malaena (black/tarry) or haematemsis (coffee-ground vomit)
2. LOSS OF BLOOD leading to hypovolaemia
Management
“I would make sure the patient was in a safe place, attached to monitoring equipment and inform a senior
colleague...
...I would then resuscitate with respect to
Airway
• Secure
Breathing
• High flow oxygen
Circulation
• 2 x large bore IV cannulae

• Take bloods (Normal bloods + amylase + group and save and crossmatch 4 units)
• Assess volume status, catheterise
• Give fluids
• 2L normal saline STAT
• Then... colloid or blood
Direct patient towards OGD with therapeutic adjuncts
1. Omeprazole
2. Antibiotics e.g. cephalosporin
3. Terlipressin (if varices are likely)
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ROCKALL SCORING SYSTEM - a prognostic indicator.
It has 2 components
1. Pre-OGD (age, co-morbidity and shock)
2. At OGD (diagnosis and risk of re-bleed)
[< 3 = good, > 8 = bad]
Purpose of OGD:
• DIAGNOSTIC
• THERAPEUTIC
• Banding
• Sclerotherapy
• Adrenaline injection
After the OGD...classify as STABLE or UNSTABLE
STABLE UNSTABLE
= uncontrollable haemorrage/
significant risk of re-bleed
CONSERVATIVE Treat cause Stabilise
MEDICAL PPI -
H.pylori eradication
SURGICAL DU - Underunning
GU - Excision of gastrectomy
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Peptic ulcer
Epidemiology
• M > F, elderly
Sites
• Duodenum - often in the 1st part of the duodenum, 2cm from the pylorus
• Stomach
• Oesophagus
• Jejunum (Zollinger-Ellison syndrome)
• Meckelʼs diverticulum (in the presence of gastric mucosa)
Risk factors
1. Lifestyle: smoking, alcohol
2. Other disease: H.pylori & drugs (NSAIDS, steroids), burns (Curling ulcer), head injury (Cushingʼs
ulcer), Zollinger-Ellison Syndrome
Clinical features
Patients maybe assymptomatic or present with symptoms of dyspepsia, indigestion, retrosternal pain. In a
DU pain is relieved by eating (or drinking milk) and is worst at night or before meals. In PU pain is worst
when eating.
There are two important complications of a PU

!
1. Perforation
2. Bleeding - this usually occurs in a posterior duodenal ulcer that erodes into the gastroduodenal artery
(see acute GI bleed)
A PU can also lead to gastric outlet obstruction and malignancy. We will discuss a perforated PU in further
detail later on.
Investigation
Endoscopy and CLO test, urease test, urea breath test or serology for H.pylori.
Treatment
Modalities Treatment
Conservative Avoid NSAIDS, steroids, alcohol and stop smoking
Medical H.pylori eradication

PPI
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Modalities Treatment
Surgical Vagotomy - CN X normally stimulates gastric acid secretion and

relaxation of the pyloric sphincter, therefore a highly selective
This is rarely required now since vagotomy to the nerves of Latarjet can be performed. However a
the success of PPIs in PU pyloroplasty or gastroenterostomy is required as this causes pyloric
disease sphincter contraction and bilious vomiting.
Antrectomy and vagotomy

• Billroth I (gastroduodenostomy)
• Billroth II (gastrojejunostomy)
Subtotal gastrectomy and roux-en-Y formation for refractory disease

or Zollinger-Ellison syndrome
Zollinger-Ellison syndrome
This is a gastrinoma of the pancreas which causes hypersecretion of gastrin, and therefore HCl from the
parietal cells of the stomach.
These may be sporadic or inherited (MEN) and 60 % are malignant.
Clinical features
• Abdominal pain
• Dyspepsia
• Diarrhoea and steatorrhoea
• Haematemesis
Treatment
• High dose PPI

• Excision
• Chemotherapy
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Perforated Peptic Ulcer
This is a MEDICAL EMERGENCY
1. Symptoms
• Sudden onset abdominal pain (epigastric then generalised)
2. Signs
General Unwell patient Rigid abdomen Tender Absent (paralytic)
Generalised
tenderness with
guarding +
rebound
i.e. peritonitic
Investigations
Cultures -
Bloods - ABG Yes
Bloods - Venous As above
Imaging Erect CXR (will show 70%) - “free air under the diaphragm”
CT for location of perforation
Scopic/Biopsy -
Functional -
Management
First… RESUSCITATION
If patient is very unwell and ∴ unsuitable for surgery, manage conservatively as perforation may self-seal
IV Fluids and catheterisation
NBM + NG tube
MEDICAL Antibiotics
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MOST COMMON PERFORATIONS
1. Duodenal (1st part anterior)

2. Gastric
3. Ulcerative gastric cancer
SURGICAL DU - Laparotomy + washout + omental repair

GU/cancer - excision or gastrectomy
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Gastric Cancer
Epidemiology
• M>F
• Common in Japan, China
Risk factors
! Lifestyle: smoking, alcohol, diet
! Other diseases: Blood group A, atrophic gastritis, pernicious anaemia, previous partial gastrectomy
Pathology
Most are ADENOCARCINOMAS (others - MALT, lymphoma)
2 classification systems:
1. MACROSCOPIC - Bormann Classification

• Fungating
• Excavating
• Ulcerating and raised
• Linitis plastica
2. MICROSCOPIC
• INTESTINAL (53%)
• DIFFUSE (30%)
Clinical features
Patients may present with general features of malignancy (weight loss, anorexia, fatigue) or specific to
the stomach e.g. upper abdominal mass, haemorrhage or rarely, gastric outflow obstruction
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous FBC (anaemia due to chronic disease/blood loss)

LFTs (mets)
Clotting (pre-surgical & as an LFT)
Imaging Barium meal

CT for staging
Scopic/Biopsy Gastroscopy + biopsy
Functional -
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Management
Antiemetics
Anti-secretion e.g. hyoscine
MEDICAL Palliative therapy

Chemotherapy
SURGICAL Only possible in early disease
Total (proximal lesion) or partial (distal lesion) gastrectomy
2 types of partial gastrectomy

1. Billrothʼs I - gastroduodenostomy; direct anastomosis of stomach to
duodenum
2. Billrothʼs II - gastrojejunosotmy; anastomosis of stomach to jejunum
leaving a duodenal stump
Lymph clearance
D1 = + perigastric nodes
D2 = + coeliac nodes
Or palliative interventions for gastric outlet obstruction e.g bypass,

resection or stenting
Complications of gastrectomy
Complication
Early Haemorrhage
Infection
Duodenal stump leak
Failure of gastric emptying and bilious vomiting
Intermediate D - Dumping syndrome presents with abdominal distension, flushing

and sweating
• Early dumping syndrome: immediately after a mearl, food has an
osmotic effect casuing nausea, fluid shift and hypotension
• Late dumping syndrome: ~ 2 hours after a meal, reactive
hypoglycaemia occurs due to fast transit of food through the small
bowel and insulin production
D - Diarrhoea
Late D - Deficiency of B12 (IF is produced by the stomach), Fe (HCl is

required for the absorption of iron), vitamin D (osteomalacia)
Alkaline gastritis
Blind-loop syndrome - bacterial proliferation in the duodenal stump of
Billroth II
Recurrent ulceration
Malignancy
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Complications of Gastrectomy can be remembered using the 3 Ds.
D - Dumping syndrome
D - Diarrhoea
D - Deficiency of vitamin B12
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Gallstone and Biliary Disease
Clinical Anatomy
Gallbladder lies between R and quadrate lobes of the liver. MCL at R. costal margin.
There are 3 parts:
1. Fundus
2. Body
3. Neck (Hartmannʼs pouch)
It open into CYSTIC duct (joins common hepatic to form the common bile duct) and holds around 50 ml of
bile.
The blood supply is:
• ARTERIAL - cystic artery from R. hepatic artery
• VENOUS - direct to liver sinusoids
The epithelium is composed of COLUMNAR CELLS + mucus glands
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Introduction to Gallstones
“Stones that form within the biliary system.”
There are 3 types:
1. MIXED (80%)
2. CHOLESTEROL (15%) - large stones - known as SOLITAIRES (fasceted when you cut through
them)
3. PIGMENT (5%) - haemolytic states such as HS and SS
Epidemiology
5 Fʼs:
• Incidence increasing
• F>M Fatty
• Most asymptomatic (15% over 60y)
Fertile
• More common in blacks and Asians
Forty
Female
Aetiology Fair
Largely unknown but common theories include
1. BILE SUPERSATURATED WITH CHOLESTEROL (Amirandʼs triangle)

2. Biliary tree sepsis
3. Lithogenic bile secretion
4. Anatomical abnormalities
Risk factors
Traditional classification is 5 Fs - Fat, Forty, Female, Fertile, Fair.
New classification
• Lifestyle: e.g. high fat/cholesterol

!
• Other conditions e.g. haemolytic states (pigment states), loss of terminal ileum (Crohnʼs)
• Drugs e.g. COC
Complications depend on the site of impaction:
1. GALLBLADDER
e.g. biliary colic, acute and chronic cholecystitis, mucocoele, empyema, perforation, carcinoma of
the gallbladder
2. IN BILIARY TRACT
e.g. obstructive jaundice, ascending cholangitis, pancreatitis
3. OUTSIDE BILIARY TRACT

e.g. gallstone ileus and small bowel obstruction
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Gallbladder Complications
1. Biliary Colic
“Blockage in the cystic duct”
Clinical features
Symptoms:
• RUQ pain after fatty meal (radiates to epigatrium and tip of R scapula)
• Associated with sweating/nausea/flatulent dyspepsia
Signs:
• Mild RUQ tenderness
Note: classically biliary colic IS NOT A COLIC. Pain rises to plateau and remains there for many hours!
Management
FBC, LFTs, CRP are normal, however USS reveals gallstones.
RESUSCITATION and exclude emergency (e.g. perforation, pancreatitis).
CONSERVATIVE Fluids
Analgesia (pethidine 50mg/4h IM/PO)
NBM
MEDICAL
SURGICAL Urgent cholecystectomy
Elective cholecystectomy (6-12 weeks later)
2. Acute Cholecystitis
“Obstructed gallbladder + infection.”
This can be divided into acalculous (10%) and calculous (90%).
Clinical features - “patient is more unwell”
Symptoms:
• Systemically unwell
• Severe, constant RUQ pain, greater radiation
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Signs:
• More severe RUQ tenderness

• Positive Murphyʼs sign (cessation of inspiration with pressure on gallbladder - must be negative on
the left) [present in 75%]
• Low-grade temperature
Investigations
Cultures Blood, urine dipstick (bilirubin)
Bloods - ABG Lactate
Bloods - Venous FBC (infection)

CRP (infection)
U&Es (dehydration)
Amylase (exclude pancreatitis)
LFTs (obstruction)
Clotting (pre-surgical & as an LFT)
Imaging AXR (10-15% radio-opaque)

CXR (exclude perforation)
USS (distended thickened gallbladder, gallstones, pericholecystic fluid)
Scopic/Biopsy -
Functional -
Management
CONSERVATIVE Fluids
NBM
MEDICAL Cefuroxime and metronidazole
SURGICAL Urgent cholecystectomy (< 72h and severe)
Elective cholecystectomy (6-12 weeks later)
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Complications of acute cholecystits
• Recurrence
• Gangrene leading to perforation
• Mucocoele
• Empyema (drained with cholecystostomy)
• Mirriziʼs syndrome - large gallstone compressing the bile duct causing obstructive jaundice
A cholecystectomy maybe performed open or laparoscopically. An open incision is known as a Kocherʼs

incision.
Specific complications of laparoscopic cholecystectomy
Specific Complication
Immediate Trocar related vessel or visceral damage

CBD injury and bile leak
Conversion to open cholecystectomy/laparotomy
Stone spillage
Early Acute pancreatitis
Late Incisional hernia
Laparoscopic vs. open cholecystectomy
Advantages Disadvantages
Small incisions have better cosmesis Special equipment and training required
Less post-op pain More difficult to control complications
Earlier mobilisation Loss of tactile feedback
Reduced risk of DVT and hospital acquired CI in bleeding disorders, shock and adhesions
infection
Earlier return to work
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Biliary Tree Complications
There are 3 important sequelae to impaction of gallstones within the biliary tree:
1. Obstructive jaundice
2. Ascending cholangitis
3. Pancreatitis (considered later)
1. Obstructive jaundice
“Small stone blocks distal biliary ductsʼ
Patient will therefore have features of an elevated conjugated bilirubin
• Jaundice (late)
• Pale stools (like houmous)
• Dark urine (like coca-cola)
It is always important to investigate these patients for cancer e.g. pancreatic, cholangiocarcinoma.
First line investigation is an ultrasound to assess for the presence of gallstones, pancreatic mass, level of
obstruction, degree of dilatation of the CBD +- intrahepatic biliary tree.
2. Ascending Cholangitis
“Infection upon a background of obstruction of distal biliary ducts”
CHARCOT’s TRIAD is classical
Symptoms
I. FEVER (+rigors)
II. PAIN
III. JAUNDICE
Signs
Remember Courvoisierʼs law:
“In the presence of obstructive jaundice if there is a palpable gallbladder it is unlikely to be stone.”
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Investigations
As above
Consider 3 SCOPIC INVESTIGATIONS:
1) Endoscopic retrograde cholangio-pancreatography (ERCP)
• Endoscope passed into 2nd part of duodenum and papilla is cannulated. Dye is injected an image
taken of the biliary tree.
• Biopsies can be performed
• Can also be therapeutic (stone removal, stent insertion)
2) Percuaneous transhepatic cholangiography
• This performed 2nd line (after ERCP failure or if not possible)

• Percutaneous cannulation of intrahepatic bile duct and injection of dye.
3) Magnetic resonance cholangiopancreatography
• Non-invasive technique that does not require the use of contrast

• Produces images similar to ERCP
Management
CONSERVATIVE Fluids
NBM
MEDICAL Cefuroxime and gentamicin (for pseudomonas cover)
SURGICAL 1. EMERGENCY - remove stone and insert a T-tube (open or ERCP)
2. ELECTIVE - cholecystectomy
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Intestinal Complications
There is only 1 important complication here and it is rare.
GALLSTONE ILEUS
Occurs as large gallstone (e.g. solitaire) fistulates into first part of the duodenum then becomes stuck in the
small intestine.
See later for notes on small bowel obstruction.
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The Spleen
Clinical Anatomy
• Largest organ of the

lymphoreticular system
• Situated in LUQ (9,10,11th ribs)
note: spleen is not palpable in health
Important relations:
• Anterior: stomach
• Posterior: ribs, diaphragm
• Medial: L. kidney
• Lateral: splenic colonic flexure
Blood supply via SPLENIC ARTERY

(coeliac axis) and SPLENIC VEIN
Functions (reflects pathology nicely)
1. Immunological e.g. a large

lymph node
2. Haematology e.g.
sequestration and removal of
old cells
Clinical characteristics of the spleen
• Enlarges INFERO-MEDIALLY (start RIF and move toward LUQ)

• Dull to percussion
• Cannot get above it
• Notched
• Cannot ballot (cf. kidney)
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Hypersplenism & Hyposplenism
1. Splenomegaly
There are 3 types:
1. MASSIVE (> 8cm)
2. MODERATE (4-8cm)
3. TIP (<4cm)
Types Causes
MASSIVE 1. Myeloproliferative disorders e.g. CML

2. Myelofibrosis
3. Tropical disease e.g. malaria, leishmaniasis, kala-azar
MODERATE 1. Myeloproliferative disorders

2. Infiltration (Gaucherʼs/amyloid)
TIP 1. Myeloproliferative
2. Congestion
3. Excessive usage e.g. haemolytic states
4. Infection (EBV, IE)
MYELOPROLIFERATIVE/LYMPHOPROLIFERATIVE disorders are a cause of all of them
HYPOSPLENISM
May be either:
1. IATROGENIC (asplenism)
• e.g. post-trauma or surgery
1. AUTOSPLENECTOMY (hypospenism)
• Haemolytic e.g. sickle-cell
• Inflammatory process e.g. SLE, coeliac, UC
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Investigations
Cultures Blood cultures (infection)
Bloods - ABG -
Bloods - Venous FBC (leukocytosis)

U&Es (dehydration, electrolyte disturbance)
LFTS (liver disease)
CLOTTING (liver disease)
G&S + CXM (for surgery)
Imaging AXR
Ultrasound
Abdominal CT
Scopic/Biopsy Bone marrow biopsy (haematological disorder)
Functional Cr51 red cell scan to show ectopic splenic tissue
Splenectomy
Indications
There are 2 important indications for splenectomy:
1) TRAUMA (see later)
2) HAEMATOLOGICAL COMPLICATIONS
• e.g. ITP, hereditary spherocytosis
Others: part of another procedure (e.g. radical gastrectomy), primary splenic lesion (tumours, abscess, cysts,
aneursyms)
Surgical Approaches
Surgery may be either:
1. OPEN (emergency - laparotomy, elective - upper middle

and L. subcostal incision)
2. LAPARASCOPIC
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Complications
GENERAL Think in terms of ABCDE
Specific - Early L. lower lobe atelectasis

Sepsis
Specific - Intermediate Pancreatitis

Sub-phrenic abscess
Specific - Late Encapsulated infections
ALL PATIENTS REQUIRE INFECTION

PROPHYLAXIS
1. Pneumococcus (Pneumovax)
2. Meningococcus (Men C)
3. Haemophilus (Hib)
+ Prophylactic penicillin
Splenic Trauma
This is relatively common and an

important cause of spleen removal.
The key problem is vascularity of the

organ that leads to large internal blood
losses.
Mechanism of injury
• Penetration/non-penetrating trauma
• Iatrogenic trauma (e.g. surgery to
colon/stomach)
• Spontaneous rupture e.g. EBV
infection
Remember: small degrees of trauma may lead to SUB-CAPSULAR HAEMATOMA
Classification - based on CT scan
I - Capsular Tear
II - Capsular Tear + Parenchymal injury
III - Tear up to the hilum
IV - Complete fracture
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Clinical features
There will be a history together with LUQ pain and tenderness or generalised peritonitis. Features of shock
will also be present.
2 important eponymous signs:
1. Kehrʼs sign: L. shoulder tip pain

2. Ballanceʼs sign: new onset shifting dullness in R. flank
Management
CONSERVATIVE: for Type I & II!

• Analgesia and fluid resuscitiaion: IV fluids (blood), monitoring!
SURGICAL: For Type III & IV

• Laparotomy (suture, salvage, splenectomy - partial or total)!
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The Pancreas
Clinical Anatomy
The pancreas is a retro-peritoneal organ (level of L1 in transpyloric plane)
It is contained within the C-curve of the duodenum
It has 3 parts:
1. Head (+/- uncinate process)

2. Body
3. Tail
Relations
• POSTERIOR: IVC, aorta, mesenteric vessels, diaphragm crura

• ANTERIOR: stomach
• TAIL: splenic hilum
Blood supply
• ARTERIAL: superior and inferior pancreatico-duodenal, splenic

• Corresponding VEINS (to portal system)
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Lymphatics
• Upper border nodes

• Superior mesenteric nodes
Structure/Function
Pancreas has 2 broad functions
1) ENDOCRINE - insulin, glucagon, stomatostatin

2) EXOCRINE - trypsinogen (protease) and chymotrypsinogen (lipase)
Microstructure is composed of alveoli of secretory cells. Formed into ductules. These then join into 2 main
ductal systems:
1) Main duct (Wirsung) - joined by the common bile duct to form Ampulla of Vater.
2) Accessory duct (Santorini) - drain superior to main duct directly into D2.
ISLETS OF LANGERHANS - found between alveoli (most are in the tail)
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Pancreatitis
There are 2 types of pancreatitis:
1) Acute
2) Chronic (+ acute-on-chronic)
Acute Pancreatitis
“Inflammatory condition of the pancreas”
This should be regarded as both a local and systemic disorder.
Epidemiology
• Common - 1:100 general surgical admissions

• Middle age
• M=F
• Mortality is ~ 12%
Aetiology
Gallstones (45%)
Ethanol (25%)
Trauma
Steroids
Mumps + other infections e.g. Coxsackie B
Autoimmune e.g. PAN
Scorpion venom
Hyperlipidaemia (+ hypercalcaemia, hypotension, hypothermia)
ERCP
Drugs e.g. thiazides, HIV drugs
IDIOPATHIC (20%)
Clinical Features
Symptoms:
• Epigastric/perigastric pain radiating to the back

• Relieved by sitting forwards/Associated with vomiting
Signs:
• General: unwell patients with fever, tachycardia, jaundice

• Specific: Localised/Generalised peritonitis +/- shock/ileus
• Cullenʼs sign - peri-umbilical echymosses!

• Grey-Turners - flank echymosses
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Investigations
Cultures urine dipstick (bilirubin, glucose)
Bloods - ABG Yes
Bloods - Venous FBC (leukocytosis and low haematocrit)

U&Es (dehydration, renal function)
LFTs (obstructive)
Amylase
Lipids (hyperlipidaemia)
Serum lipase
Calcium (hypo- and hypercalcaemia)
Glucose
Albumin
Imaging Erect CXR (exclude perforation)

AXR (paralytic ileus)
Ultrasound (inflammation around pancreas, gallstones)
CT abdomen (define anatomy + Balthazar score)
Scopic/Biopsy ERCP
Functional -
Notes on amylase
• 80% raised in acute pancreatitis within 2-12 hours (return normal within week)
• NON-SPECIFIC
• If > 1000 pancreatitis over other causes
RANSON/GLASGOW (UK) CRITERIA (PANCREAS mneumonic)
• Predictive of severity and mortality

• RANSON is better for alcohol-induced and only applied after 48 hours
PaO2 < 8 kPa

Age > 55
Neutrophilia > 15x109
Calcium < 2.0 mmol/l
Renal function impaired
Enzymes e.g. LDH > 600 IU, AST > 200 IU
Albumin < 32 g/dl
Sugar > 10 mmol
1 = MILD
2 = MODERATE
> 3 within 48 hours = SEVERE
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Management
CONSERVATIVE Fluids
Analgesia (pethidine and morphine)
NBM + NG tube
Oxygen (keep Pa02 > 8 KPa
Correct abnormal metabolities e.g. calcium
Insulin sliding scale if elevated glucose
? Alcohol withdrawal - chlordiazepoxide and vitamins
MEDICAL Moderate/severe - Antibiotics (meripenem, imipenem)
SURGICAL Indicated for severe complications e.g. necrosis, pseudocyst, abscess, failure
of resolution
1. Laporotomy and debridement/lavage
2. Laparostomy (pack and leave open in ITU)
Complications
Specific - Early ARDS

Atelectasis
Pleural effusion (transudate)
Organ failure (cardiac, renal)
DIC

Necrosis
Pseudocyst formation
Specific - Late Chronic pancreatities

Pancreatic tumour
Pancreatic Pseudocyst
“Collection of fluid in lesser sac that occurs in around 20% cases. “
• Suspect with persistently raised amylase.

• If < 6cm it may resolve spontaneously
• If > 6cm it requires surgery e.g. percutaneous drainage, laparoscopic, laparotomy
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Chronic Pancreatitis
“Repeated episodes of pancreatic inflammation leading to structural damage and fibrosis.”
Leading to complications of:
1. Exocrine dysfunction e.g. malabsorption

2. Endocrine dysfunction e.g. diabetes mellitus
Epidemiology
• Uncommon ~ 30/100,000
• Most due to ALCOHOL
• Other causes are cystic fibrosis, congenital causes e.g. pancreas divisum, hyperlipaemia and
idiopathic)
Clinical Features
Symptoms:
• General: weight loss, poor appetite

• Specific:
• Pain
• Exocrine deficiency e.g. steatorrhoea
• Endocrine deficiency e.g. polyuria, poldipsia etc.
Signs:
• General: thin patient

• Specific: erythema ab igne (from hot water bottles), epigastric tenderness
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous FBC (leukocytosis and low haematocrit)

U&Es (dehydration, renal function)
LFTs (obstructive)
Amylase
Lipids (hyperlipidaemia)
Serum lipase
Calcium (hypo- and hypercalcaemia)
Glucose
Albumin
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Imaging AXR (speckled pancreatic calcification)

CT scan (structural changes and inflammation)
MRCP (gallstones)
MRI (structural changes)
Scopic/Biopsy ERCP (gallstones)
Functional Pancreolauryl test (for endocrine function)
Management
CONSERVATIVE Analgesia (can be problematic and require strong opiods/coeliac plexus block)
Treat exocrine dysfunction (Pancreatin, Creon)
Treat endocrine dysfunction (insulin)
MEDICAL Moderate/severe - Antibiotics (meripenem, imipenem)
SURGICAL Indicated for complications e.g. uncontrolled pain
1. REMOVE OBSTRUCTION e.g. stenting, cholecystectomy

2. DRAIN DUCTS/CYSTS e.g. pancreaticojejunostomy
3. RESECT - Distal (distal pancreatectomy), Proximal (Whippleʼs procedure =
pancreatoduodenectomy)
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Pancreatic Tumours
May be either:
1) BENIGN - uncommon. Occur as part of the MEN syndromes.

2) MALIGNANT
Pancreatic Carcinoma
Most pancreatic carcinomas are DUCTAL ADENOCARCINOMAS and occur in the HEAD.
Others: ampullary tumour, insulinomas, gastrinomas, glucagonomas, VIPomas
Epidemiology
• Increasing incidence
• M>F
• Elderly
• Western Countries
Risk factors
1. LIFESTYLE: smoking and alcohol

2. DYE EXPOSURE: naphthylamine, benzidine
3. DISEASE STATES: chronic pancreatities, diabetes
4. CONGENITAL: pancreas divisum
Clinical Features
Symptoms:
• General: anorexia, malaise, weight loss

• Specific: Chronic epigastric pain radiating to the back (relieved by sitting forwards), steatorrhoea i.e.
disturbed exocrine function, symptoms of diabetes i.e. disturbed endocrine function.
Signs:
• General: cachexia, lymphadenopathy, signs of chronic EtOH use, jaundice

• Specific: palpable gallbladder (courvoisierʼs law), hepatosplenomegaly, ascites
Rare features are thrombophlebitis migrans and marantic endocarditis
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Investigations
Cultures Urine dipstick (glucose, bilirubin)
Bloods - ABG -
Bloods - Venous FBC (anaemia of chronic disease)

U&E (illness and dehydration)
LFTs (obstructive jaundice, mets)
Glucose (endocrine dysfunction)
CA 19.9 [sensitivity of 90%]
Imaging USS abdomen (mass, dilatation and gallstones)

Triple phase CT (mass and staging)
MRCP
Scopic/Biopsy ERCP + biopsy

Ultrsound-guided biopsy
Laparoscopy
Functional Pancreolauryl test (for endocrine function)
Management
CONSERVATIVE Analgesia (strong opiod or coeliac plexus block)

Relieve obstruction
Palliative radiotherapy
MEDICAL -
SURGICAL 20% of tumour are resectable
1. Whippleʼs procedure
2. Chemotherapy post-op
The prognosis is dismal with a mean survival of around 6 months
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Basic Principles of the Lower Gastrointestinal

Surgery
Important Clinical Anatomy
The Duodenum
• C-shaped (~ 25cm in length)

• 4 sections: D1-D4
Important relations:
D1 - Gastroduodenal and CBD posterior

D2 - Duodenal papilla receives CBD and pancreatic duct
at sphincter of Oddi and accessory pancreatic duct
D3 - Mesenteric vessel anteriorly 9SMA and SMV)
D4 - Suspensory ligament of Treitz distinguishes this
part from ileocaecal junction
Blood supply
• D1-D2: superior pancreaticoduodenal artery
(gastroduodenal a. from coeliac axis)
• D3-D4: inferior pancreaticoduodenal artery (sup.
mesenteric a.)
Small Intestine
• ~ 6.5m in length
• Split into
• 50% JEJUNUM
• 50% ILEUM
JEJUNUM ILEUM
Location Umbilical Hypogastric/pelvic
Diameter Wide Narrow
Wall Thick Thin
Arcades Few Many
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Large Intestine
• ~ 1.5m in length
• Distinguished from the small
bowel as it is
1. Wider
2. Taenia coli which end
at the appendix
3. Haustra
4. Appendiced
epiploicae
Divided into:
1. Caecum
2. Vermiform appendix
3. Ascending colon
4. Hepatic flexure
5. Transverse colon
6. Splenic flexure
7. Descending colon
8. Sigmoid colon
9. Rectum
10. Anus
Peritoneal attachments
• PERITONEUM: transverse
and sigmoid
• NO PERITONEUM:
ascending and descending
• VARIABLE: caecum, rectum
Arterial Blood Supply
Divide structures into:
A. FOREGUT (mouth to D2)

• Coeliac axis (T12)
B. MIDGUT (D2 to distal transverse colon)
• Superior mesenteric artery (L1)
C. HINDGUT (distal transverse colon to anus)
• Inferior mesenteric artery (L3)
Venous supply
A. SUPERIOR MESENTERIC VEIN (→ portal vein)

B. INFERIOR MESENTERIC VEIN (→ splenic vein)
Lymphatic drainage
• Corresponds with the blood supply

• Small nodes on bowel drain to large mesenteric nodes… then to mesenteric vessel nodes then to
cisterna chyli.
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Peritoneal cavity
2 layers:
! Parietal - outer
! Visceral - inner
Between these layers are serous fluid.
The peritoneum has two main regions which is connected by the epiploic foramen (foramen of Winslow)
• Greater sac
• Lesser sac - which is further subdivided into the lesser and greater omentum
The peritoneum acts to protect the organs and hold them in place. There are areas in which there are double
folds of peritoneum, which are known as:
1. Mesentery contains nerves and blood vessels to supply organs. The mesentery connects organs to the
posterior abdominal wall, for example mesoappendix, transverse and sigmoid mesocolon.
2. Ligaments which connect one organ with another or another part of the body.
3. Omentum which is divided into the lesser and greater omentum.
The lesser omentum extends from the liver to the lesser curvature of the stomach. The greater omentum
extends from the the greater curve of the stomach, descends infront of the small intestine and turns up
towards the transverse colon, forming an apron. The greater omentum has a cribiform appearance, which
contains adipose tissue.
Sometimes a loop of intestine can become strangulated in the foramen of Winslow. Also the hepatic artery
can be compressed in the foramen of Winslow if the cystic artery is damaged during cholecystectomy.
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Intestinal Obstruction
There are 3 important types of intestinal obstruction
1. SIMPLE - 1 obstructing point & no vascular compromise

2. STRANGULATED - vascular compromise
3. CLOSED LOOP - 2 obstructing points and danger of perforation
• LBO in the presence of a competent ileocaecal valve
• Caecal volvulus
• Sigmoid volvulous
The most useful classification is based upon AETIOLOGY
1. MECHANICAL
In the lumen In the wall Outside the wall
MECHANICAL Faeces CONGENITAL ADHESIONS

Foreign bodies e.g. atresia, imperforate Hernia
Gallstones anus, stenosis Volvulus
Intussusception
ACQUIRED
• Neoplasia
• Inflammation e.g.
IBD, diverticulitis
2. NON-MECHANICAL - the bowel is “shock”
• SURGICAL SHOCK e.g. post-operative, peritonitis, ischaemia

• MEDICAL SHOCK e.g. electrolyte aberrations, drugs e.g. anticholinergics
Ogilivieʼs syndrome: features of obstruction on AXR but no obvious obstructing point
In practice remember:
Small bowel - ADHESIONS and HERNIAS

Large bowel - NEOPLASIA, DIVERTICULITIS and VOLVULUS
Clinical features
There are 4 cardinal symptoms:
1. PAIN (usually central - SBO, lower - LBO and colicky, if constant think of strangulation/impending
perforation)
2. CONSTIPATION (absolute - no faeces or flatus)
3. VOMITING (early in SBO)
4. DISTENSION (prominent in low obstruction)
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Signs
General Unwell patient Tender + rebound/ Percussion Small bowel

Distended guarding in tenderness if • Tinkling
abdomen strangulation/ strangulation/ Paralytic
perforation perforation • None
Masses
Specific Surgical scars

Hernia (inguinal/
femoral)
Investigations
Cultures Bloods (if septic), Urine dipstick
Bloods - ABG Metabolic acidosis in ischaemia

U&Es (dehydration, electrolyte disturbance)
Amylase (any acute abdomen)
G&S + CXM
Imaging Erect CXR (exclude perforation) & AXR (look for obstruction)
Gastrograffin enema
CT
Scopic/Biopsy -
Functional -
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Basic Interpretation of the Related Chest and Abdominal Radiograph
Erect chest radiograph
Causes of air under the diaphragm:
Perforated viscus e.g. bowel/PU

Iatrogenic e.g. laparotomy/scopy
Gas forming bacteria
Water-skiers
Abdominal radiograph
The 3,6,9 rule: if SB > 3cm, LB > 6cm and caecum > 9cm, the bowel is dilated
Look at the rectal area for gas - if there is no gas this is an indication for bowel obstruction
Comparison of large and small bowel obstruction features
Feature SBO (left) LBO (right)
Bowel diameter (cm) 3-5 >5
Position of loops Central Peripheral
Fluid levels (erect) Many Few
Bowel markings Valvulae conniventes (all the way Haustra (partially across)
across)
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Management
1. Mechanical
These are mostly managed if a conservative fashion (unless there are signs of strangulation)
Look for signs of resolution for around 24 hours:

• Reduced pain
• Reduced NGT aspirate
• Passage of flatus
• Resolution of AXR findings
CONSERVATIVE NBM & NG tube (“drip and suck”)

Analgesia
Gastrograffin (oral/NG tube)
Flatus tube for sigmoid volvulus
MEDICAL -
SURGICAL There are 3 important indications:

1. Simple obstruction (neoplasms or failure of conservative approach)
2. Closed loop obstructions
3. STRANGULATION/PERFORATION
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2. Non-Mechanical
CONSERVATIVE Prevention
e.g reduced bowel handling, peritoneal lavage
Analgesia
NBM & NG tube (“drip and suck”)
MEDICAL Treat cause (e.g. electrolytes)
SURGICAL -
As a general rule:
Virgin abdomens will probably end up requiring an operation to relieve the obstruction
Non-virgin abdomens will probably only require conservative management
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Colon Cancer and Stomas
Colorectal carcinoma
“A malignant neoplasm of the colon or rectum.”
Epidemiology
• 3rd commonest cancer

• M=F
• Elderly
• Western
Aetiology
• Lifestyle: Western diet (red meat, low fibre), smoking

• Familial
1. Familial adenomatous polyposis (AD)

2. Gardinerʼs syndrome (AD)
3. Hereditary non-polyposis coli
4. Peutz-Jeghers syndrome
5. Family history
• Previous disease states: IBD - 10 % risk/10 years in those with UC

• Previous therapies: radiation, gastrectomy
Pathology
May be classified with 2 classification systems:
! 1. MACROSCOPIC
• 30% recto-sigmoid junction
• 25% sigmoid colon
• L. sided tumours → annular stenosing

• R. sided tumours → sessile/polypoid
2. MICROSCOPIC (Dukeʼs criteria)
A. Confined to bowel wall

B. Through bowel node but no nodal involvement
C. In lymph nodes
! ! ! C1
! ! ! C2 involved apical node
D. Distant mets
Note that Dukeʼs B with perforation requires adjuvant chemotherapy.
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Clinical features
Symptoms:
• General: weight loss, anorexia, malaise

• Specific
• R. sided tumours → present late with diarrhoea and anaemia
• L. sided tumours → commonly cause obstruction
• Rectal tumours → obstruction/rectal symptoms (tenesmus)
Signs:
• General: anaemia & cachexia

• Specific
• Mass
• Signs of obstruction
• Hepatomegaly
• PR - mass or fistulae
Investigations
Cultures FAECAL OCCULT BLOOD suggested as screening programme
Bloods - ABG -
Bloods - Venous FBC (anaemia of chronic disease, iron deficiency anaemia)

U&Es (diarrhoea)
LFTs (mets)
CEA (better at monitoring course)
Clotting
G&S/CXM (pre-surgical)
Imaging CXR (mets)

Barium/gastrograffin enema - apple core lesion
CT/MRI (staging) - liver, lung and bone metastases
CT for virtual colonoscopy
Scopic/Biopsy Sigmoidoscopy + biopsy (flexible sigmoidoscopy can reach the splenic

flexure)
Colonoscopy + biopsy (colonoscopy can reach the ileocaecal valve)
Functional -
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Management
CONSERVATIVE/PALLIATIVE By-pass, diversion or decompression
MEDICAL Adjuvant chemotherapy in Dukeʼs C or B (perforated) or for colon

tumours and neoadjuvant radiotherapy for rectal tumours
SURGICAL RESECTION (see below)
R hemicolectomy for R sided

tumours
Extended R hemicolectomy for

distal R sided tumour/
transverse colon tumour
L hemicolectomy for left sided

tumours
Sigmoid colectomy for sigmoid

tumours
Anterior resection for tumours > 4cm from the

anal verge. The colon is anastomosed to the
remaining rectal stump, and a defunctioning loop
ileostomy may be performed.
Abdomino-perineal resection for tumours < 4cm

from the anal verge. There is complete removal
of the anus and a permanent end colostomy is
formed.
Neoadjuvant radiotherapy maybe used to shrink

the rectal tumour prior to resection. Adjuvant
chemotherapy is used for types B and C
colorectal carcinomas.
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Emergency bowel operations
In large bowel obstruction due to colorectal carcinoma or stricture, for example diverticulitis, a Hartmannʼs
procedure is performed. The obstruction is removed, the rectal stump is closed and left in the pelvis whilst a
temporary colostomy is formed. Often, a direct anastomosis is not undertaken as this affects healing in the
presence of inflammation.
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Stomas
“A stoma (mouth) is a surgical created communication between the bowel and the skin.”
They may either temporary or permanent
Types:
1. Colostomy
2. Ileostomy
3. Urostomy (ileal conduit)
When inspecting a stoma ask yourself:
• Where is it?
• What is in it?
• How is the communication created?
+ look for scars and ALWAYS CHECK THE PERINEUM.
Colostomy Ileostomy Urostomy
Site L. iliac fossa (usually) R. iliac fossa (usually) R. iliac fossa (usually)
Bag Contents Solid Liquid Urine
Opening Flush with skin Spouted Flush with skin
Complications of stoma formation
Specific Complication
Immediate Haemorrhage
Early High output stoma

Hypokalaemia
Retraction
Ischaemia
Late Prolapse
SBO
Parastomal hernia
Fistulae
Dermatitis
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Inﬂammatory Conditions
In this section we talk about
A. Appendicitis
B. Diverticular disease
C. Crohnʼs disease
D. Ulcerative colitis
Appendicitis
“Inflammation of the vermiform appendix”
Epidemiology
• Very common (up to 12% of population)

• Can occur at any age
• Rare < 2
• Peaks in childhood years
Pathology
The main processes occuring are
1. Obstruction - usually due to a feacolith

2. Lymphoid hyperplasia
The main worry is PERFORATION
• Localised → appendix mass

• Systemic → peritonitis
Clinical features
Symptoms:
• General: Pyrexia, malaise and anorexia

• Specific
• Central colicky abdominal pain (hindgut colic)
• Vomiting
• Pain localized to R. iliac fossa
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Signs:
• General: patient still with flexed hips and knees. Pyrexia, fetor oris + coated tongue
• Specific
• Localised - garding and rebound over McBurneyʼs point (⅔ distance between umbilicus and ASIS)
• Generalised - rigid and tender over all abdomen + an ileus
Investigations
Cultures Urine MC & S + dipstick + βHCG
Bloods - ABG -
Bloods - Venous FBC (neutrophil leucocytosis)

CRP (infectious marker)
amylase
Imaging Ultrasound (exclude gynae cause, appendix inflammation indicated by

free fluid and diameter > 6mm)
CT for atypical cases
Scopic/Biopsy Laparoscopy
Functional -
Management
Fluids
NBM
SURGICAL OPEN
LAPAROSCOPIC - particularly good for girls
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3 important complications to be aware of:
1. PERFORATION (young and the old)
2. MASS (may resolve with antibiotics)
3. ABSCESS (may require antibiotics and drainage)
Diverticular Disease
“An acquired condition of mucosal lined out-pouchings through the wall of the colon.”
Epidemiology DIVERTICULUM Single out-pouching
• Very common DIVERTICULOSIS Many out-pouchings

• F>M
DIVERTICULAR Symptomatic out-
DISEASE pouchings
Risk factors
• Lifestyle: low fibre diet and obesity

• Other conditions: hiatus hernia & cholelithiasis
(SAINTʼS triad) Complication Features
Diverticulitis L. sided appendicitis

Clinical features
Haemorrhage Sudden painless, large
PR bleed
Most patients and asymptomatic (∴ do not have diverticular
disease) Perforation Peritonitis
Symptomatic patients may have Abscess formation Swinging fever and boggy
rectal mass
• Mild alteration in bowel habit with L. sided colic
relieved on defecation Fistulae Enterocolic
• A complication Colovaginal
Colovesical
Investigations Strictures Large bowel obstruction
Will depend on the situation. For acute diverticulitis…
Cultures -
Bloods - ABG If unwell

CRP (infectious marker)
U&E (dehydration)
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Imaging Erect CXR (perforation)

AXR (fluid level, air in the wall)
Gastrograffin enema
Ultrasound
Angiography
CT scan
Scopic/Biopsy Sigmoidoscopy/colonoscopy
Functional -
Treatment
This will depend on the severity and the specific complication.
If mild symptomatic disease:
• Treat conservatively with! risk factor modification e.g. increase fibre/fluids and lose weight
• Antisposmodic may help e.g. mebeverine
For acute diverticulitis:
Fluids
NBM
SURGICAL This is indicated for PERFORATION, HAEMORRHAGE and

OBSTRUCTION
1. Harmannʼs procedure
2. Elective sigmoid colectomy and anastomosis
For less severe PR bleeding an angiography and embolisation can be

performed
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Surgical Ulcerative Colitis
“A chronic relapsing inflammatory condition of the colonic mucosa”
It ALWAYS starts at the rectum and spreads proximally (20% develop a PAN-COLITIS)
Epidemiology
• Most common between 20 - 35 years

• F>M
• Non-smokers
Clinical features
Symptoms:
• General: weight loss, fever, anorexia and malaise

• Specific
• Crampy abdominal pains
• Diarrhoea (blood/mucus)
• Rectal symptoms (urgency or tenesmus)
• Extra-intestinal manifestations e.g. uveitis, ank. spondylitis, erythema nodosum
Signs:
• General: clubbing. Systemically unwell in acute disease

• Specific (if acute disease)
• Tender abdomen
• PR bleeding on glove
Complications include
• Toxic megacolon
• Perforation
• Strictures
• Perianal disease
• Colorectal carcinoma
Investigations:
Cultures Stool (exclude infection), blood
Bloods - ABG In unwell
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CRP and ESR (infectious marker)
U&E (dehydration)
LFT (albumin)
G&S/CXM if for surgery

AXR (toxic megacolon, thickened walls, thumb printing, strictures)
Gastrograffin enema (lead-piping, loss of haustra, granular mucosa)
CT scan
Scopic/Biopsy Sigmoidoscopy/colonoscopy (no serosal involvement and crypt abscess)
Functional -
Severity may be graded using the Truelove and Witts Criteria
Management
If chronic/intermittent the MEDICAL MANAGEMENT
• Surgery may be reserved for chronic symptoms or high grade dysplasia.
If acute… SURGICAL MANAGEMENT
• Toxic megacolon
• Perforation
• Massive PR haemorrhage
• Colitis not responding to medical management
Fluids
NBM
MEDICAL IV hydrocortisone
Rectal steroids e.g. prednisolone foam enemas
Blood transfusion if Hb low
If improves...prednisolone + sulphasalazine
SURGICAL If no improvement..
Panproctocolectomy, total or subtotal colectomy with ileostomy
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Crohn’s Disease
“An inflammatory condition of unknown aetiology that can affects the entire length of the GI tract.”
It is characterised by:
• Patchy transmural inflammation

• Non-caseating granulomas
Epidemiology
• Most common between 20-35 years

• Smokers
• M=F
Clinical features
Symptoms:
• General: weight loss, fever, malaise and anorexia

• Specific
• Diarrhoea (blood/mucus)
• Crampy abdominal pain
• Bowel obstruction
• Extraintestinal: anl. spond, erythema nodosum
Signs:
• General: thin, clubbing, aphthous ulcers

• Specific
• Tender abdomen
• Look for RIF mass
• PR - perianal disease e.g. fistulas, fissures, perianal abscess
Investigations
Cultures Stool (exclude infection), blood
Bloods - ABG In unwell

CRP, ESR (infectious marker)
U&E (dehydration)
LFT (albumin)
G&S/CXM if for surgery
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AXR (toxic megacolon, strictures)
Gastrograffin enema + FOLLOW -THROUGH (cobblestone mucosa,
rosethorn ulcer, string sign)
CT scan
MRI (perianal disease)
Scopic/Biopsy Colonoscopy (cobblestones appearance, fissuring, serosal involvement)
Functional -
Management
Usually this is managed medically with steroids + immunosuppressants
Surgery is reserved for 2 setting:
1. Emergency (complications)
2. Elective (chronic problems)
Surgical options include
• Stricturoplasty
• Limited resections
• Ileo-caecal resection
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Peri-Anal Disease
Clinical Anatomy
Rectal Anatomy
The rectum is ~ 15cm and curved
It starts at 3rd segment of sacrum and ends at prostate/lower ¼ of the vagina
Important relations
• POSTERIOR: Sacrum, midle sacral artery and coccyx

• ANTERIOR: Prostate, bladder, vagina
Note: the muscle layer are completely fused ∴ no haustrae.
Anal Canal
The anal canal is ~ 5cm and straight
It is divided into two ½s by the DENTATE LINE
! LOWER HALF - squamous epithelium and inferior rectal artery

!
! UPPER HALF - columnar epithelium and superior rectal artery (branch of inferior mesenteric)
Continence is maintained by two sphincters
INTERNAL SPHINCTER
• Involuntary circular muscle of rectum
EXTERNAL SPHINCTER
• Made up 3 striated rings (external, superficial and subcutaneous)

• Supplies by pudendal nerve (S 2,3,4)
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Haemmorrhoids
“Dilated and disrupted vascular anal cushions”
These are most commonly found at the 3,7 and 11 oʼclock positions
May be classified according to anatomical severity:
• 1st degree - never prolapse

• 2nd degree - prolapse on straining
• 3rd degree - constantly prolapsed
A “strangulated haemorrhoid” occurs when the sphincter cuts off the blood supply
Epidemiology
• 50% of Western population affected
Risk factors
• Lifestyle: low fibre diet

• Impaired venous return e.g. pregnancy, portal hypertension and pelvic malignancy
• Rectal carcinoma
Clinical Features
Symptoms:
• Fresh PR bleeding
• A lump
• Pain
• Itching
Signs:
• May be seen, ellicited or felt on PR

• Abdominal exam may reveal abnormality
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Management
CONSERVATIVE Increase fibre and fluid intake

Toilet habit (limit time)
MEDICAL Topical steroid/anaesthetic e.g. Anusol

Laxative e.g. lactulose
SURGICAL 1. 5% phenol in almond oil

2. Endoscopic banding/cryotherapy
3. Haemorrhoidectomy (final resort)
Note: Peri-anal haematomas
These are haematomas that are caused by burst peri-anal venules. Usually due to straining
Compared to haemorrhoids they appear blue. Most will resolve spontaneously but may need surgical
drainage
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Anal Fissures
“A tear in the anal mucocutaneous epithelium.”
These are most common at the 6 and 12 oʼclock positions.
Aetiology is usually either hard stool or trauma. However may be associated with Crohnʼs, syphilis and anal
carcinoma.
Clinical features
Symptoms:
• Pain on defaecation
• Fresh PR bleeding
Signs:
• Pain on cheek spreading

• PR usually impossible
• May be a “sentinal pile.”
Treatment
CONSERVATIVE Increase fibre and fluid intake

Toilet habit (limit time)
MEDICAL Stool softeners

Reduce anal spasm e.g. 0.2% GTN cream, diltiazen cream, botulinum
injection
SURGICAL Lateral spincterotomy at 3 o'clock
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Anal abscess/Anal sepsis
Anal sepsis either originated from ABOVE (e.g. pelvic abscess) or is due to a LOCAL problem (e.g. infection
of the anal glands)
Common organisms include
• Staph.
• Strep.
• E. coli
The most important compliation is the

formation of a FISTULA.
Types:
a. Perianal
b. Ischiorectal
c. Pelvirectal
d. Inter-sphincteric
Clinical features
Symptoms:
• General: Swing fevers and malaise

• Local
• Mass
• Throbbing pain + surround tenderness
• Purulent discharge
Signs
• General: systemic infection

• Perianal erythema
• Discharge
• Bulging mass
• PR - a boggy and fluctuant painful mass
Treatment
MEDICAL Flucloxacillin + penicillin
SURGICAL If above fails…
Incision, drainage and packing

...leave to heal.
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Anal Fistula
“An abnormal connection between the ano-rectal passage and the skin.”
There are many types:
• INTER-SPINCTERIC
• TRANS-SPINCTERIC
• SUPRA-SPHINCTERIC
• EXTRA-SPHINCTERIC
Clinical features
Symptoms
• Pain and discharge of purulent fluid/faeces

• Perianal irritation
Signs
• “Dot” and associated discharge and skin changes

• PR - indurated area around the fistula
Treatment
MEDICAL Antibiotics if associated infection
SURGICAL 1. EUA to determine extent

2. Lay open tract and heal by secondary intent
If low… division of spincters

Ih high...Seton suture to stimulate fibrosis of tract
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Rectal Prolapse
“Protrusion of rectal tissue through the anal canal.”
There are 2 types:
a. PARTIAL - mucosa only (common in children)

b. COMPLETE - full thickness of rectum
Clinical features
Symptoms:
• Mass
• Associated bleeding and ulceration
• Incontinence of urine or faeces
Signs:
• View the prolapse on straining

• PR - tone
Investigations
These must be investigated as there may be an underlying lesion e.g. carcinoma
• Imaging - endoanal ultrasound/MRI

• Scopic - Sigmoidoscopy
• Functional - anorectal manometry
Treatment
CONSERVATIVE Pelvic floor exercise
MEDICAL Stool softeners
SURGICAL 2 approaches
1. Delormʼs procedure: perineal approach to resection of excess rectal

mucosa
2. Rectopexy: the rectum is fixed to the sacrum
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Anal Carcinoma
Epidemiology
• Uncommon
• Most occur in male homosexuals due to associated with High Grade HPV (16, 18, 31, 33)
Pathology
Can be broken down by histology
• 80% squamous
• 20% others e.g. adenocarcinoma, lymphoma, melanoma
..or location
• Anal margin: below the dentate line (men with a good prognosis) - spreads to pelvic nodes
• Anal canal: above the dentate line (women with a poor prognosis) - spread to inguinal nodes
Clinical features
Symptoms:
• General: malaise, weight loss, anorexia

• Specific
• Rectal bleeding
• Pain
• Incontinence
Signs:
• Mass + lymph nodes +/- fistula
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous FBC (anaemia of chronic disease/blood loss)

LFTs (mets)
Ca (mets)
Imaging CT (spread)
Scopic/Biopsy Rectal EUA + biopsy
Functional/Special -
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Treatment
CONSERVATIVE Analgsia
Palliative radiotherapy
MEDICAL Chemo + radiotherapy (if inguinal nodes involves)
SURGICAL Resection
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Breast Disease
Clinical Anatomy
The breast are modified sweat-glands that are located between 2-6th ribs on the anterior chest wall
Underlying muscles are:
• ⅔ PECTORALIS MAJOR
• ⅓ SERRATUR ANTERIOR
The basic structure is composed of
1. ADIPOSE TISSUE
2.15-20 LOBULES arranged in a hierarchical duct system

(TLDU, extra-lobular duct, major duct)!
Arterial Blood Supply
•Axillary artery
•Internal thoracic arteries
•Intercostal arteries
Lymphatic Drainage
There are 3 basic lymphatic channel draining the

breast and these are very important:
1. AXILLARY
2. INTERNAL MAMMARY
3. SUPRACLAICULAR
The axillary nodes are split into 5 distinct groups
• Anterior
• Posterior
• Lateral
• Central
• Apical
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Diagnostic Principles in Breast Disease
“Triple Assessment” are the key words here:
Modality Specific
1. Clinical Assessment History

• Particularly lumps, pain, nipple discharge
• PMH/FH/DH
Examination
• Breast
• Nodes/back
2. Radiology Ultrasound (if < 35 years)
Mammography
• Oblique and cranio-caudal views
• 10% false negative rate
3. Biopsy Fine needle aspiration cytology

• Easy to do
• 95% sensitivity
Core biopsy/Tru-cut
• Histology
• Oestrogen receptor status
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Benign Breast Disease
These should be divided into:
a. Congenital
These are rare conditions such as amastia (absence of breast), hypoplasia and accessory nipples.
Accessory nipples represent failure of the milk line to regress and can be excised if problematic.
b. Acquired
You can divide these further into:
1. Hormonal/cyclical
• ANDI, cystic breast disease, fibroadenomas
2. Infective
3. Inflammatory
• Fat necrosis, duct ectasia
4. Neoplastic
• Duct papilloma, lipomas, cysts
1. Hormonal/cyclical
ANDI = Abnormalities of Normal Development and Involution
Benign Mammary Dysplasia/ANDI
Abnormality of cycles - Fibrocystic disease
• Common in pre-menopausal women (25-45) with painful and nodular lump in second half of cycle
• Investigation - triple assesment if lump
• Treatment
• 1st line - Analgesia/evening primrose oil
• 2nd line - Tamoxifen/bromocriptine
• 3rd line - excision
Abnormality of Development - Fibroadenoma
• Overgrowth of single breast lobule

• Young women with smooth, firm, mobile mass (“breast mouse”)
• Investigate with TRIPLE ASSESSMENT
• If < 30 - observe, if > 30 excise
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2. Infective breast disease
They are all treated with analgesia and antibiotics (e.g. flucloxacillin)
There are 2 important types:
1. Lactational
• Cracked nipple from breast ffeding allows stap. entry

• Most important compication is breast abscess formation
• No need to stop breast feeding
2. Non-lactational
• Staph. aureus
• Most important complication is periductal mastitis (suggested by chronicity e.g. mastalgia, discharge
and fibrosis that lead to nipple retraction)
3. Inflammatory breast disease
1. Duct ectasia
• Dilated sub-areolar ducts that become filled with cellular debris → periductal inflamatory response
• Present with subareolar lump and green discharge
2. Fat necrosis
• Trauma (postive history in 50%) followed by fibrosis and calcification

• Increased incidence of cancer
4. Benign Neoplasms
• Can be from the skin
• e.g. lipoma, cysts
• From the breast itself
• Duct papilloma (present with blood stained discharge and treated with microdochectomy)
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Malignant Breast Disease
Epidemiology
• Very common (1:11) in the Western world.

• Risk increased with age
Risk factors
• 1% occur in men
• Lifestyle: alcohol intake, high saturated fat diet
• Prolonged exposure to oestrogens: early menarche, late menopause, exogenous hormones
• Family history: Ca in first degree relative. BRCA 1 & 2
• 1st child over 30 years
Pathology
The most important types of tumour are:
1. DUCTAL
2. LOCULAR
Both of these tumours go through an IN SITU phase (ductal is much more common).
• Carcinoma that has not penetrated the basement membrane
• Low- to high- grade
Other include:
• Medullary - younger patients
• Colloid/mucinous - older patients and tend to look benign on the mammogram
• Papillary
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Investigation
1. Triple assessment (histological grading and oestrogen receptor status)

2. Staging
• CLINICAL
• TNM
Clinical staging system
Stage 1 Early disease

Tumour confined to breast
Stage 2 Early disease

Tumour spread to movable ipsilateral axillary nodes
Stage 3 Local advanced disease

Tumour spread to superficial chest wall + involvement of ipsilateral internal
mammary
Stage 4 Advanced
Metastases present at distant sites e.g. liver, lungs, brain
TNM Staging System
0 1 2 3 4
Tumour CIS/Pagetʼs < 2cm 2-5cm 5-10cm > 10cm

No skin fixation Skin distortion Ulceration Chest wall
Fixed to pectoral extension
muscle
Nodes No nodes Ipsilateral Ipsilateral Internal Mammary

Mobile Fixed
Mets No mets Liver, bone, lung
Management
This should be in a specialist breast centre and is multi-modality e.g. surgery, radiotherapy and
chemotherapy.
Divide treatments into:
1. Early disease
2. Advanced disease
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1. Early disease
There are 4 aims:
1. Local treatment of the tumour
• Wide local excision + radiotherapy

• Mastectomy (large tumours or patient choice)
2. Axillary clearance
• Assessment with axillary sampling/Sentinal mode mapping

• Treatment with axillary clearance
3. Prevention of recurrence
• Radiotherapy after WLE

• Chemotherapy if young, large tumour or high risk of recurrence
• Hormonal e.g. Tamoxifen/Arimidex
4. Reconstruction
• TRAM flap
• Latissimus dorsi flap
Sentinal Node Mapping
Involves identification of the first node draining the tumour through injecting radioactive isotope and
a dye.
Sampling of this node then determines whether axillary clearance is necessary
2. Advanced disease
The first line is usually TAMOXIFEN
Other important adjuncts include
• Local recurrence - re-excision, radiotherapy

• Metastatic disease - bisphosphonates and steroids
• Palliation - package of care, analgesia
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Complications of breast surgery
Specific - Early Pneumothorax

Haematoma
Seroma
Specific - Late Frozen shoulder

Lymphoedema
Nerve damage e.g. brachial numbness
Breast Screening
This is a programme introduced after publication of the Forest Report (1988)
Involves:
1. Self-examination
2. 2-view mammography every 3 years between 50-64 year old (> 64y can self-refer)
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Neck Lumps
Clinical Anatomy
The neck may be subdivided into:
• ANTERIOR TRIANGLE
• Submandibular (under chin)

• Submental (under chin in midline)
• Carotid (pulsatile)
• Muscular (midline)
• POSTERIOR TRIANGLE
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It is important to be aware of the different lymphatic drainage areas of the neck:
Submental/
1
submandibular
II Jugulo-digastric
III Middle jugular nodes
IV Inferior jugular nodes
V Posterior triangle
Ant. compartment
VI
group
The Thyroid
• Endocrine organ that lies in the pre-tracheal fascia over the 2-4th tracheal rings
• Relations:
ANTERIOR: strap. muscles

POSTERIOR: parathyroid glands, larynx, trachea, superior and recurrent laryngeal nerves
There are 3 parts to the gland
1. Isthmus
2. Lateral lobes
3. Pyramidal lobes (inconsistent)
Blood supply
• Arterial
• SUPERIOR THYROID A. (branch of external carotid)
• INFERIOR THYROID A. (branch of subclavian)
• Venous
• SUPERIOR THYROID V. (internal jugular)
• MIDDLE THYROID V. (internal jugular)
• INFERIOR THYROID V. (brachiocephalic)
• Lymphatic
• Mostly towards the middle jugular nodes
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The Salivary Glands
There are 3 sets
1. Sublingual
2. Submaxillary
3. Parotid (largest)
The Parotid Gland
This is the largest of the 3 glands
Shape/Location
• It resembles a three-sided pyramid with the apex directed downwards.

• Lies over the MANDIBULAR RAMUS (anterior and inferior to the ear)
Important relations
! FACIAL NERVE
! EXTERNAL CAROTID ARTERY (bifurcated beneath to form the maxillary and superficial temporal a.
Drains into Stensonʼs duct → upper 2nd molar at the parotid papilla.
The Submandibular duct
Lies above the digastric muscle
Separated into SUPERFICIAL and DEEP portions by mylohyoid.
Drains into Whartonʼs duct → sublingual caruncles (either side of sublingual frenulum)
The Sublingual Gland
This is the smallest of the 3 glands and lies ANTERIOR to the submandibular gland.
Drains via Bartholinʼs duct to join the submandibular duct → sublingual caruncles.
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Lymphadenopathy
“Enlarged lymph nodes”
This is the COMMONEST CAUSE of a lump in the neck.
Divide them into:
• LOCALISED
• GENERALISED
Infection Neoplasia Autoimmune
LOCALISED Primary e.g. Primary e.g. lymphoma

lymphadenitis
Secondary
GENERALISED Infections Lymphoma Sarcoid
1. Acute e.g. EBV CLL

2. Chronic e.g. HIV
The history/examination should be fairly definitive and is the most important diagnostic tool.
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous FBC, CRP, TFTs, LFTs, blood film, serological test
Imaging CXR
Scopic/Biopsy FNAC, core biopsy
Treatment
• Obviously directed at cause
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Solitary Lumps in the Neck
[Note: these will still usually be lymph nodes]
Divide up as follows
• ANTERIOR TRIANGLE
• POSTERIOR TRIANGLE
Anterior Triangle lumps
This may be subdivided into
1. Pulsatile
2. Non-pulsatile
3. Submandibular
Pulsatile lumps
These occur in 3 settings:
• Tortuos carotid artery (normal)

• Carotid artery aneurysm
• Carotid body tumour (chemodactoma)
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Non-pulsatile lumps
Classify these according to whether they are in the midline or not
MIDLINE
• Thyroglossal cyst
• Dermoid cyst
• Ectopic thyroid tissue
NON-MIDLINE
• Branchial cyst
• Pharyngeal pouch
• Laryngocele (wind instrument players)
2 important ones are:
Branchial cysts
• These are “embryological remnants of the 2nd pharyngeal cleft.”

!
• Present in early adulthood with SOFT-SWELLING and transilluminated (often post-URTI)
• Occur at upper ⅔ of anterior sternomastoid.
• Need aspiration shows cholesterol crystals
• Treatment is excision
Pharyngeal pouch
• This is a “mucosal protrusion between the 2 parts of the inferior laryngeal constrictor”
• Present on the left in elderly patients
• It is a lump that INCREASES IN SIZE ON SWALLOWING
• Treatment is excision + cricopharygeal myotomy.
Submandibular lumps
These are usually secondary to infection e.g. jugulo-digastric with tonsillitis.
Rarely you may have
• Tumours
• Impacted salivary stones (post-parandial pain and swelling). Do a plain XR or sialogram to detect as
80% are radio-opaque.
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Posterior Triangle lumps
Common lumps here include
1. Cervical rib
2. Cystic hygroma
3. Subclavian artery aneurysm
Cervical rib
“Enlarged costal element from the C7 vertebra.”
This is fairly common (1:150) but only 10% are symptomatic
Causes a variety of syndromes
1. VASCULAR - compression of subclavian

• Thrombosis
• Raynauds
• Arm claudication
2. NEUROLOGICAL - pressure on the brachial plexus

• Paraesthesia
• Weakness
Cystic hygroma
“Collection of lymphatic cysts behind the clavicle.”
Often notices AT BIRTH
Treatment with either with injection of sclerosing hypertonic saline or excision.
Parotid Lumps
Lumps in the parotid can either be due to
• Swelling of the WHOLE gland e.g. mumps, bacterial infection, sarcoid (uveoparotid syndrome), chronic
liver disease
• LOCALISED swelling (usually neoplastic)
Pathology
This really concerns the neoplasic processes:
PRIMARY - benign (pleiomorphic adenoma), malignant (pleiomorhic adenosarcoma, adenocarcinoma)
SECONDARY - from lymphoma/mets
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Clinical Features
• There will be a LUMP/swelling +/- a facial palsy (LMN type)
Investigations
• 2 investigations are important: FNA and CT scan
Treatment
• Superficial/radical parotidectomy
• Radiotherapy
The most important complication post-op is a FACIAL PALSY
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Thyroid Surgery
Surgeons are usually concerned about GOITRES
“Any enlargement of the thyroid gland.”
Causes may be divided as follows:
! 1. CONGENITAL
!
! 2. ACQUIRED
• Simple
• Toxic
• Inflammatory! !
1. Congenital
2 most common are:
1. Lingual thyroids
• Residual tissues at the base of the tongue
2. Thyroglossal cysts
• Remnant thyroid tissue
• Midline, smooth and cystic mass that moves upwards on swallowing
2. Acquired
Smooth Nodular
Simple Simple goitre Multinodular goitre
Toxic multinodular
Toxic Grave’s disease
goitre
Acute suppurative
DeQuervain’s
Inflammatory Riedel’s
Hashimoto’s
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1. Acute suppurative thyroditis

• Staph/strep infection of the thyroid
2. DeQuervainʼs thyroiditis
• Viral infection. non-suppurative
3. Riedelʼs thyroditis
• Woody fibrosis and infiltration with scar tissue
• Associated with retro-peritoneal fibrosis
4. Autoimmune/Hashimotoʼs thyroditis
• Lymphatic infiltration of gland due to antibodies against thyroglobulin
• Hyperthyroidism followed by hypothyroidism
• Associated with LYMPHOMA
Thyroid Neoplasms
May be:
• Benign - follicular adenoma

• Malignant:
Occurrence Age Associations Prognosis
Papillary 70% Young Multi-focal and OK

poor response to
radio-iodine
surgery
Follicular 15% Older Good response to Excellent

radio-iodine
Medullary 10% Any MEN Type II Good if no nodes
Anaplastic 5% Older Aggressive V. poor

Possible to shrink
with radiotherapy
!
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous Thyroid function (T4, TSH, thyroid auto-antibodies)

All other bloods
Imaging CXR (thoracic inlet view)

Ultrasound (solid vs. cystic)
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Scopic/Biopsy FNA & Tru-Cut

Radio-isotope scan (hot vs. cold areas)
Laryngoscopy pre-op (determine if laryngeal nerves involves)
Thyroid Surgery
This is indicated for 3 reasons
A. Problem goitres e.g. pressure symptoms

B. Relapsing hyper-function
C. Malignancy e.g. medullary
The operation is a subtotal thyroidectomy and involves removing ⅞ of the gland via a collar incision.
Complications
Specific - Immediate Haemorrhage (beware tension haematoma)

Laryngeal oedema
Nerve damage
Specific - Early Hypocalcaemia
Specific - Late Hypothyroidism

Keloid scaring
Recurrence
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Hernias
A hernia may be defined as -
“Protrusion of a viscus and itʼs covering through a defect into an abnormal position.”
It essentially has 3 components:
1. Sac (neck, body and fundus)

2. Contents (bowel, omentum)
3. Defect
There are a number of important terms used to describe them:
• REDUCIBLE - “sac may be returned to original cavity”

• IRREDUCIBLE - “sac unable to be returned to original cavity”
• OBSTRUCTED - “contains obstructed bowel”
• STRANGULATED - “contains bowel whose blood supply has become compromised.”
There are many types depending on location/defect e.g. inguinal (direct and indirect), femoral, incisional,
umbilical/paraumbilical, epigastric, Spigelian, obturator, lumbar and parastomal
Inguinal Hernias
The inguinal canal is the oblique passage taken through the abdominal wall by the testis/round
ligament.
It is ~ 4cm in length and moves from:
• INTERNAL/DEEP RING - pierces the transversalis fascia (1-2 cm

above mid-inguinal point)
• EXTERNAL/SUPERFICIAL RING - piereces external defect in external
oblique aponerosis (just above pubic tubercle)
Relations:
• ANTERIOR - muscle, superficial fascia and skin

• POSTERIOR - transversalis fascia (lateral ½) and conjoint tendon
(medial ½)
• SUPERIOR - internal oblique and transversus abdominis
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• INFERIOIR - inguinal ligament
In an inguinal hernia
1. SAC - peritoneum
2. CONTENTS - nothing, bowel, omentum, bladder
3. DEFECT
• DIRECT INGUINAL HERNIA - posterior wall

• INDIRECT INGUINAL HERNIA - along the canal!
Epidemiology
• Very common (R > L)

• M:F = 9:1
• All ages at risk
Risk factors
1. Congenital e.g. patent processus vaginalis
2. Acquired
• Increased IAP e.g. obesity, chronic cough, straining
• Weakness in wall e.g. previous incision
Clinical features
Symptoms:
• In an emergency - pain +/- features of obstruction

• History of lump
• Dull dragging pain in the groin/scrotum
Signs:
• Is it reducible?
• Can it be controlled by pressure over the internal ring?
Note: important differential for a lump in the groin:
• Femoral hernia
• Lymphadenopathy
• Vascular e.g. saphena varix or femoral aneurysm
• Psoas abscess
• Undescended/ectopic testes
• Lipoma
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Investigation
This is not usually necessary. USS, MRI and herniography may be used
Management
CONSERVATIVE Decrease intra-abdominal pressure e.g. loose weight, treat cough,

laxatives
Rarely - hernial truss
MEDICAL -
SURGICAL 1. Open
2. Laparoscopic
In this operation you must

1. Define, inspect and excise the sac
2. Close defect and tension-free repair
e.g. suture (herniorrhaphy), mest (hernioplasty)
Complications
Specific - Immediate Bleeding

Viscus perforation
Specific - Early Infection

Haematoma
Specific - Late Recurrence

Chronic groin pain
Ischaemic orchitis
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Femora Hernia
The important anatomy to be aware of here is that of the FEMORAL CANAL.
Important points here:
• Canal is ~ 1.5 cm
• Part of femoral sheath together with femoral artery and nerve
• Boundaries:
ANTERIOR: inguinal ligament

POSTERIOR: pectineal ligament
MEDIAL: lacunar ligament
LATERAL: femoral vein
Femoral hernias are much more common in women (female pelvis) and are commonly acquired in old age.
Importantly they like to obstruct.
Aetiology
! All are acquired (same risk factors as above)!
Clinical features
Symptoms
• Emergency - features of obstruction

• Non-emergency - history of lump in the groin
Femoral vs. Inguinal
Femoral: INFERIOR AND LATERAL TO PUBIC TUBERCLE
Inguinal: MEDIAL AND SUPERIOR TO PUBIC TUBERCLE
Management
CONSERVATIVE -
MEDICAL -
SURGICAL Emergency - HIGH APPROACH

Elective - LOW APPROACH
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Incisional Hernias
ʻThis a hernia through a previously acquired defect.”
Risk factors for their development
1. PRE-OPERATIVE e.g. high pre-op risk factor profile
2. OPERATIVE e.g. sutures used, midline incisions, skill
3. POST-OPERATIVE e.g. increased IAP due to haematoma or prolonged ileus
Clinical features
There will be a history of previous injury/procedure +/- complications.
On examination look for
• Scar
• Mass protruding through the scar on cough/head tilt
Management
CONSERVATIVE Reduce intra-abdominal pressure

Corset
MEDICAL -
SURGICAL Normal principles
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Umbilical/Para-umbilical
CONGENITAL INFANTILE ADULT
Defect Abdominal wall Incomplete fusion of Linea alba

umbilicus to abdominal
wall
Types Exomphalos Umbilical Paraumbilical

Gastroschisis
Epidemiology Prematurity is biggest Afro-Caribbean Obesity

risk factor Downʼs syndrome Multiparity
Congenital Middle age
hypothyroidism
Features Obvious at delivery Asymptomatic Above/below umbilicus

Often self-resolve Frequenctly obstructs
Treatment Resuscitation Reassurance Surgical repair (Mayo)

Surgical repair Surgical repair if not
closed by 3 years
Rare Types of Hernia
Epigastric hernia
• Pea-sized swelling caused by a defect in linea alba

• ABOVE umbilicus
• Treatment is surgical
Spigelian hernia
• Protrusion through linea semilunaris (rare cause of a mass in right lower quatrant)
• Usually tender
• Treatment is surgical.
Obturator
• Protrusion through obturator canal (felt in femoral canal or vagina)

• Cause pain over the medial knee
• Commonly obstructs
Lumbar
• Following loin incisions
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Vascular Surgery
Clinical Anatomy
To understand and talk about vascular disease you need a passable knowledge of vascular anatomy. Here
we will basically cover:
1. Venous drainage of the lower limb

2. Arterial supply to the lower limb
1. Venous drainage of the lower limb
Blood drains from the lower limb in 2 systems:
1. DEEP
2. SUPERFICIAL
a. Great/long saphenous
b. Small/short saphenous
c. Tributaries
The long saphenous vein
Pathway:
• Dorsum of foot (venous arch)
• Anterior to medial malleolus
• Up medial calf and thigh
• Drain into sapheno-femoral junction
• Important peforators
• 3 calf-perforators
• 1 mid-thigh perforator (Hunterian)
The short saphenous vein
Pathway:
• Dorsum of foot
• Posterior to malleolus
• Up back of calf
• Drain inconsistently into deep veins at
politeal fossa
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The sapheno-femoral junction
Landmark: 4cm lateral and below the pubic tubercle.
2. Arterial supply to the lower limb
The basic arterial tree is shown below
abdominal aorta
L2
internal iliac
external iliac
5cm distal to inguinal ligament
common femoral
deep femoral
superficial femoral
posterior tibial
anterior tibial
lateral plantar
medial plantar
dorsalis pedis
Anterior tibial artery → anterior compartment

Peroneal artery → lateral compartment
Posterior tibial artery → posterior 2 compartments
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Venous Disorders
The basic conditions to cover here are:
1. Varcose veins
2. Lymphoedema
Varicose veins
“Long, tortuous and dilated veins of the superficial venous system”
Most common site is LOWER LIMB (may also occur in abdominal wall, anus, vulva and pampiniform plexus)
Epidemiology
• Very common
• F>M
Aetiology
This may be divided into 3 sets of risk factors:
Specific
Proximal venous obstruction Abdominal/pelvic malignancy

Ascites
Pregnancy
Destruction of valves Thrombosis

Overactive muscle pump
Increased flow AV malformation

e.g. Kippel-Trenaunay
The most common sites of incompetence are
• Sapheno-femoral junction
• Mid-thigh perforators
• Sapheno-popliteal junction
• Calf perforators
Varicose veins must be described in terms of their distribution e.g. long saphenous, short saphenous, medial
calf, mixed
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Clinical Features
Patients most often complain about cosmetic problem.
Some get mild pain and ankle swelling.
Important skin changes most commonly occur in the GAITER REGION (lower medial ⅓ of leg)
• Lipodermatosclerosis (induration and thickening)

• Eczema
• Haemosiderosis
• Ulceration
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous Pre-surgical set (FBC, U&E)
Imaging Colour duplex scanning (shows valvular and perforator incompetence)

Venography (obstructions)
Ultrasound (demonstrates reflux into superficial veins)
Scopic/Biopsy -
Functional/Special Cough test

Tredelenburg/Tourniquet test
Management
Surgery is required for patients with sapheno-femoral incompetence or major perforator damage.
CONSERVATIVE Treat underlying cause e.g. relieve constipation, lose weight

Graded support stockings
Injection sclerotherapy (small veins as an outpatient)
MEDICAL -
SURGICAL 1. Ligation operation (long saphenous → Trendelenburg procedure,

short saphenous, perforators)
2. Stripping
3. Multiple avulsion
4. Endoscopic divison (SEPS)
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Complications of varicose vein surgery
Most are performed as DAY CASE SURGERY.
Specific - Early Haematoma

Nerve damage e.g. saphenous in stripping
Specific - Late Recurrence
Lymphoedema
This may be split into:
! PRIMARY (congenital < 1y, praecox < 35y, tarda > 35y)
! SECONDARY
• Previous surgery e.g. axillary clearance
• Malignant obstructing disease
• Radiotherapy
• Infection (parasites/multiple previous episodes of cellulitis)
There is usually as history of limb swelling that is worse on standing.
The oedema is NON-PITTING and usually unilateral. Consider primary type if bilateral.
• Associated skin changes: secondary infection, fissuring, hyperkeratosis.
Aims of management are:
a. Allow function
• e.g. skin care, physiotherapy, prevention of infection
b. Decrease swelling
• e.g. compression, debulking operations, bypass operations
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Arterial Disorders
In this section we shall cover:
1. Limb ischaemia
2. Carotid artery disease
3. Aneursyms
4. Aortic dissection
5. AV fistulas
6. Vasospastic conditions
Limb Ischaemia
“A spectrum of ischaemic changes resulting from atherosclerotic process.”
These changes may lead to:
1. Narrowing → CHRONIC ISCHAEMIA
2. Thrombosis secondary to rupture → ACUTE ISCHAEMIA/ACUTE-ON-CHRONIC ISCHAEMIA
This changes are formally classified using the Fontaine STAGE Symptoms
Classification
Stage 1 Asymptomatic
Stage 2 Intermittent
claudication
Stage 2: Intermittent claudication
Stage 3 Ischaemic rest pain
Stage 4 Ulceration/
Symptoms:
gangrene
This is a muscular, cramp-like pain experienced on walking and
relieved by rest.
There also be rest pain at night that is relieved by walking or hanging the leg.
Site
• Calf (femoral disease)

• Buttock (iliac disease)
Signs:
INSPECTION Special PALPATION AUSCULTATION
Signs Loss of hair Vascular angle/ Temperature Bruits in:

Pale, discoloured skin Buergerʼs angle Capillary refill - aorta
Muscle wasting Pulses - iliac
Venous guttering Buergerʼs test/venous - adductor canal
ULCERS filling time
Necrotic toes
Nail changes
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Note:
• Ulcers are typically described as “punched out with pale granulation tissue and an erythematous
halo.”
• Inspect all pressure areas (heel, malleoli, in between toes)
• Dorsalis pedis is non-palpable in 10% people.
• Walk test = treadmill for 5 mins and stop when maximal claudication. Mearure ABPI ( > 20% drop
significant)
Investigations
Cultures Urine dipstick (renal disease)
Bloods - ABG -
Bloods - Venous FBC (baseline), U&Es (renal function), clotting, lipids, G&S
Imaging Dopplex (triphasic vs. biphasic vs. monophasic)

ABPI
MRA / spiral CT
Scopic/Biopsy Angiography (advance guide wire to aorta then inject to visualise arterial
tree) - look for 1. Level of blockage 2. Collateral blood supply
Functional/Special ECG
Management
CONSERVATIVE Treat underlying risk factors
MEDICAL Aspirin 75mg O.D. (clopiodgrel if contra-indicated)
SURGICAL 1. ENDOVASCULAR e.g. PTA - best for iliac and superficial femorals,
stents and PTFE/Dacron grafts
2. BYPASS SURGERY (autologous veins below inguinal ligament or
synthetic above)
Types 1. Anatomical e.g. fem-pop 2. Extra-anatomical e.g. axiloo-

femoral
3. Endarterectomy
4. Amputation
5. Sympathectomy (chronic pain in small vessel disease)
Amputations is indicated for
1. Lethal limb (ischaemia, tumour)

2. Dead limb (PVD, extensive loss)
3. Useless limb (fixed flexion deformity, vestigial fingers)
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Acute Limb Ischaemic
This is a SURGICAL EMERGENCY
Aetiology
• Thrombosis 60% e.g. previously stenosed vessel
• Embolism 30% e.g. from LA thrombus, air, cholesterol
• Others e.g. trauma, vasospastic disorders, aortic dissection, popliteal aneurysm
It is important to tell the difference between thrombosis and embolism
Thrombotic Embolic
Hx of claudication/rest pain Recent MI, atrial fibrillation,

aneurysm
Onset over hours Onset over seconds
Signs of chronic vascular No evidence of previous disease

insufficiency
Hard arteries. No bruits Soft artery. Bruits
Clinical features
The 6 Pʼs
1. Pallor (marble white → mottled with branching → mottled and non-blanching → fixed staining)
2. Pain
3. Pulselessness
4. Perishing with cold
5. Paraesthesia (severe sign)
6. Paralysis (severe sign)
Management
First...Resuscitate the patient
Fluids
NBM
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MEDICAL Antibiotics
Heparinisation
Thrombolysis (tPA or streptkinase)
SURGICAL 1. Endovascular e.g. angioplasty, stenting, embolectomy

2. Emergency reconstruction + fasciotomy
3. Amputation
The precise first line guidelines depend on whether the event is EMBOLIC or THROMBOTIC.
1. Thrombotic
• Thrombolysis
2. Embolic
• Embolectomy with Fogarty catheter

• Then..thrombolysis (in unsuccessful)!
Post-operative care
All patients require heparin for 48 hours then long-term anticoagulation.
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Carotid Artery Disease
Patients with significant carotid stenosis are at increased risk of
1) Stroke - “Sudden neurological deficit of vascular origin > 24h.”

!
2) Transient Ischaemic Attack (TIA) - “Sudden neurological deficit of vascular origin < 24h.”
Clinical Features
Most are asymptomatic and picked up on cardiovascular examination (bruit or thrill)
If they do present with a neurological event it will be of the ANTERIOR CIRCULATION (unilateral weakness,
dysphasia/dysarthria, visual defects)
Investigations
• Duplex doppler scan is most important
Others - intravenous/arterial DSA, MRA
Management
• Based upon trial data from NASCET and ECST.
CONSERVATIVE Control risk factors for all patients
MEDICAL Aspirin (clopidogrel) for all patients
SURGICAL ENDARTERECTOMY if stenosis > 70%

Transluminal angioplasty is alternative
Note
• Risk of stroke with stenosis > 70% = 5% per year
• Never operate if < 30% stenosis
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Aneurysmal Disease
“An aneurysm is an abnormal dilatation of a blood vessel.”
It may be classfied as:
a. TRUE aneurysm - involves ALL layers and > 50% diameter.
b. FALSE aneurysm - dilated blood vessel representing a haematoma around an area of damage.
c. DISSECTING aneurysm - blood tracking into layers of vessel wall.
Process Examples
CONGENITAL - Berry aneurysms in

Circle of Willis
ACQUIRED Degenerative Atheroscerotic

(infrarenal AAA)
Infective Syphilis (thoracic)
Mycotic Bacterial endocarditis
Inflammatory
Traumatic Trauma
Connective tissue Ehlers-Danlos

disease Marfanʼs
Pseudoxanthoma
elasticum
Specific types covered here include
1. AAA
2. Others e.g. thoracic, popliteal, femoral
3. Dissecting aneurysms
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Abdominal aortic aneurysms
These are the most common type of aneurysms and occur just below the renal arteries.
Epidemiology
• Elderly
• Male > female
Clinical features
Symptoms:
• 75% are asymptomatic

• Patients may complain of
• Bloating
• Pulse/mass in abdomen
• Emergency presentation
• Epigastri/umbilical pain radiating to the back, flank or into the groin
• Acute limb ischaemia
• “Blue-toe syndome”
• Aortointestinal fistula
Signs:
This obviously depends on the situation
General: patient may have known vasculopathy. Present hypotensive and shocked
Specific
• Abdominal tenderness
• Left midline expansile and pulsatile mass
• Bruits over aneurysm
Investigations
Cultures
Bloods - Venous If unwell: EMERGENCY e.g. FBC, U&Es, clotting, LFTs, CXM - 10 units
Imaging CT scan/MRI
Ultrasound
Plain abdominal xray (poor but may be signs of calcification)
Scopic/Biopsy Arteriography may be used to describe relations of vessel
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Management
Obviously in the case of rupture this is an EMERGENCY with a very poor survival. Aim to keep systolic less
than 80 mmHg
CONSERVATIVE < 5cm should have serial ultrasounds/CT

Treat co-exisiting risk factors
MEDICAL -
SURGICAL This may be either to PREVENT complications or deal with rupture
1. Conventional grafts (aorta clamped above and below then disease

portion replaced with dacron graft). Mortality ~ 5%
2. Endovascular repair (EVAR) - endoprosthesis introduce through a
femoral arteriotomy
Guideline for surgery based upon ʻUK small aneurysm trialʼ. Indications include
1. Symptomatic
2. Asymptomatic
• > 5.5cm in diameter
• Expanding > 1cm per year
• Complicated e.g. emboli
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Aortic Dissection
“Split of the intima and internal media such that blood is able to enter and track up and down the vessel
wall.”
Leading to
1. Double lumen formation that may occlude vital branches e.g. coronaries, carotids, renal
2. Haemorrhage
3. Undermining of attachments e.g. aortic valve → aortic incompetence
Classification
There are 2 types:! Type A (70%): ascending aorta and arch

! ! ! Type B (30%): discending aorta affected distal to left subclavian
Clinical features
Symptoms
• Sudden severe chest pain that is tearing in nature and radiaed to back
• Features of hypotension due to haemorhage
• Features of other vessel involvement e.g. hemiplegia (carotids), paraplegia (spinal arteries), renal
(anuria and haematuria)
Signs
• General: shocked patient

• Specific: differening BP between each arm
Investigations
Cultures
Bloods - Venous If unwell: EMERGENCY e.g. FBC, U&Es, clotting, LFTs, CXM - 10 units
Imaging CXR (mediastinal widening + L. pleural effusion)

Echo (aortic regurgitation)
CT scan - investigation of choice but patient must be stable
Scopic/Biopsy
Functional/Special ECG (signs of infarct)
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Management
This is a SURGICAL EMERGENCY and the patient may very well require resuscitation.
Ultimately management will depend on the type of dissection:
! Type A: require surgical management e.g. replacement of aortic root.
! Type B: Conservative treatment e.g. β-blockers to prevent further extension. + revascularisation of

secondary ischeamia
Other types of aneurysm
Locations Presentation Treatment
Ascending thoracic aorta

1. Chest pain
2. SVC obstruction
3. Aortic regurgitation
4. Obstruction to R main bronchus
Arch of aorta Classically caused by syphilis - now

atherosclerosis and Marfansʼs
1. Hoarse voice
2. Compression of trachea
3. Ulceration into trachea
4. Compression of L bronchus
Descending thoracic aorta 1. Back pain

2. Compression of oesophagus
3. Erosion into oesophagus
Popliteal ACUTE LIMB ISCHAEMIA Saphenous vein bypasss graft
Femoral ACUTEL LIMB ISCHAEMIA
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AV fistulae
“An abnormal connection between the arterial and the venous system.”
They may be either large (macrofistulae) or small (microfistulae)
Aetiology
1. Congenital - rare
• Localised e.g. in head and neck
• Multiple e.g. Kippel-Trenaunay syndrome
2. Acquired
• Trauma
• Renal fistula
Clinical features/Investigations
1. Superficial
• These are palpable as soft, pulsatile swelling that have a machinery bruit on auscultation.
2. Deep
• Detected on CT/angiography.
Management
CONSERVATIVE Left to resolve spontaneously
MEDICAL
SURGICAL Embolisation
Occlusion of feeding vessel and excison
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Vasospastic disorders
“A group of conditions that affect the small arteries of the distal extremities.”
1. Raynaudʼs disease - idiopathic disease and normal arterioles.
A bilateral process (usually of women) that involves episodes of vasospasm leading to colour changes in the
digits
1. Digital pallor (vasoconstriction)

2. Cyanosis (arterioles have relaxed but no venules)
3. Reactive hyperaemia (complete reversal)
2. Raynaudʼs phenomenon - underlying disease of the arterioles.
Associated with
• Vibrating tools
• Connective tissue disease (SLE, RA, scleroderma)
• Haematological conditions - polycythaemia, cryoglobulinaemia
• Cervical rib
• Drugs e.g. beta blockers and ergot alkaloids
Management
CONSERVATIVE Remove cause

Heated gloves/socks
Avoidance of cold
MEDICAL Nifedipine
5HT antagonists
SURGICAL Sympathectomy (symptoms usually return within 6 months)
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Orthopaedics
Basic Fractures
Definition and Classifications
“A fracture is a break in the continuity of the bone.”
Further classified as:
1. Simple fracture - skin is intact

2. Open/compound fracture - skin broken with bone out
3. Complicated fracture - neurovascular compromise
When talking about a fracture talk about:
1. FRACTURE LINE e.g. transverse, oblique,

spiral, crush, comminuted, greenstick,
avulsion
2. SHIFT or DISPLACEMENT e.g. lateral,

medial
3. TILT or ANGULATION e.g. degree of lateral

or medial
4. TWIST or ROATIONS
Fracture Aetiology
There are 3 important mechanisms
1. Trauma (direct, indirect, avulsion)

2. Stress e.g. continual pressure on 1 area
3. Pathological i.e. low energy that normal would not fracture bone. Indicated underlying pathology e.g.
osteoporosis, malignancy
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Clinical Features
These are fairly obvious but it is important to always do a NEURO-VASCULAR examination.
Investigations
Most of the time this is an X-ray. But…
• Obtain 2 views (lateral and AP)

• Joint above and below
If pathological fracture or scaphoid you may need CT or bone scan.
Management
First… RESUSCITATE THE PATIENT (see ATLS chapter)
1. REDUCE Alignment is more important than opposition
1. Manipulation e.g. Collesʼ

2. Traction (skin or skeletal)
3. Open (if intra-articular or complicated)
2. FIX CONSERVATIVE e.g. slings/plaster/collar&cuff
SURGICAL
1. Internal fixation
2. External fixation
3. WAIT FOR UNION This depends on good bone healing
1. Haematoma formation
2. Organisation of haematoma and fibroblastic infiltration
3. Callus formation
4. Consolidation of lamellar bone
5. Remodeling
4. REHABILITATE Basically involves graded-exercise therapy and physio.
Rules of thumb for bone healing
Upper limb: 6-8 weeks

Lower limb: 12 weeks
Children: ½ the time
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Complication of fractures
GENERAL Blood loss

Fat embolus
Specific - Immediate Visceral damage e.g. rib fractures

Nerve damage
Vascular damage
Specific - Early Infection
Compartment syndrome
- always suspect with pain on passive stretching or if poor perfusion
Rx - remove bandaging or fasciotomy
If not treated may result in Volkmannʼs ischaemic contracture
Specific - Late Joint stiffness and later osteo-arthritis
Problems with union e.g. mal-union, delayed union, non-union
Avascular necrosis e.g. NOF, scaphoid, talus
Reflex sympathetic dystrophy/Sudekʼs atrophy
Myositis ossificans (elbow)
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The Hip
SI joint
Iliac crest
ASIS
Superior
pubic rami
Obturator
foramen
Inferior
Pubic pubic rami
tubercle Pubic
symphysis
Greater
trochanter
Lesser
trochanter
Muscles acting on the hip

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Type Muscles
FLEXORS Psoas major

Rectus femoris
Sartorius
Pectineus
EXTENSORS Gluteus maximus

Hamstrings
ABDUCTORS Gluteus medius

Gluteus minimus
ADDUCTORS Adductor longus

Adductor brevis
Adductor magnus
LATERAL ROTATORS Gluteus maximus assisted by

obturators
MEDIAL ROTATORS Anterior fibres of gluteus medius

and minimus
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Fractured Neck of Femur
Very common fracture - particularly in elderly, osteoporotic individuals. Mortality is approx. 30% in 6 months
following a fracture.
Classification
These may be
1. INTRACAPSULAR
• Subcapital
• Trans-cervical
1. EXTRACAPSULAR
• Basicervical
• Inter-trochanteric
• Sub-trochanteric
The intracapsular fractures are then further classified using GARDENʼS CLASSIFICATION
I II
III IV
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Clinical features
Symptoms
• Hip pain
• Unable to weight bear
Signs
• Shortened (pulled up by ileo-psoas)

• Externally rotated (gluteus maximus)
Remember to consider cause and effect of the fall
• Cause e.g. UTI, pneumonia, MI, arrhythmias

• Effects e.g. aspiration, dehydration, head injury
Investigations
Cultures -
Bloods - ABG -
Bloods - Venous FBC (infection)

U&E (electrolytes disturbance, dehydration)
G&S/CXM - 2 units
Imaging AP pelvic xray + lateral of affected side

CXR (cause)
Scopic/Biopsy -
Functional/Special ECG (signs of infarct)
Management
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CONSERVATIVE Analgesia (consider 5lb skin traction)

Fluids
NBM
Post-operative - physiotherapy + OT assessment
MEDICAL Treat cause
SURGICAL 1. INTRACAPSULAR
“I, II - screw, III, IV - Austin-Moore”
I/II - Cannulated screw or dynamic

III/IV - Hemiarthroplasty (Austin-Moore - uncemented, Thompson -
cemented)
2. EXTRACAPSULAR
Dynamic hip screw
Complications
Specific - Early Deep vein thrombosis
Specific - Late Avascular necrosis

Mal-union
Acetabular wear from hemiarthroplasty (so THR if severe

OA)
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Important other fractures for finals
Fractures at the Wrist
1. Collesʼ fracture
• Fracture of distal radius with shortening, dorsal displacement and angulation of the distal fragment.
• M.O.A. - fall on outstreched hand
• Rx:
• Closed reduction followed by immobilisation in forearm cast for 6 weeks
• Check position with XRay 1 week after.
2. Smithʼs fracture
• Fracture of distal radius with shortening, anterior displacement and

angulation of the distal fragment
• Rx
• Try closed reduction
• Often requires open reduction and fixation with a butress plate.
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3 uncommen intra-articular fractures are:
• Bartonʼs fracture: fracture subluxation of the distal radius

• Galeazzi fracture: distal radial fracture + dislocation of the radio-ulnar joint
• Monteggia fracture: proximal ulnar fracture with dislocattion of the
radial head
3. Scaphoid fracture
• Fracture of scaphoid bone

• M.O.A. - fall on outstretched hand
• Clinical features: Pain and swelling in the wrist + tenderness in the

anatomical snuffbox/telescoping of the tumb.
• Most important complication: avascular necrosis of proximal
portion
• Investigations: AP and lateral X-rays of wrist. Diagnosis often

uncertain ∴ repeat after 10 days.
• Rx
• Immobilise in scaphoid plaster (if displaced/non-union -
internal fixation with a Herbet screw)
4. Bennettʼs fracture
• Intra-articular fracture dislocation of the first metacarpal bone

• Very common thumb injury
• Rx
• Usually requires fixation with K-wire/screw
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Upper limb fractures/dislocations
1. Shoulder dislocation
• Most common is an anterior and inferior dislocation.

• Posterior dislocations in association with epileptic fit/electric
shock
• Clinical features of pain and decreased movement, together with

a loss of deltoid contour and the arm being held internally rotated
and abducted
• Most important complications - axillary nerve damage
• Investigation: AP and axial (Y-view) X-rays
• Treatment
• Reduction e.g. modified Kocherʼs method
• Immobilize with broad sling
2. Proximal humeral fracture
• Often occurs in elderly

• M.O.A - RTA, fall from standing height
• Treatment is usually CONSERVATIVE - collar-and-cuff

+ physiotherapy
• If comminuted then needs ORIF
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Lower limb fractures
Tibial Plateau Fracture
• Often complex fractures caused by high-impact injuries
• May be classified using the Schatzker system (Type I-IV)
• Requires ORIF due to possible articular consequences
Tibial Fracture
• High energy fractures that are associated with large amounts of soft tissue injury.
• The most important complications are:
• COMPARTMENT SYNDROME
• Common peroneal injury (proximal)!

• Test sensation to first toe web space and
dorsiflexion movement of the great toe.
• Treatment is with:
• Plaster
• Intramedullary nail
• External fixation e.g. Ilizarov frame
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The Knee
The structures that are most often affected by pathology in the knee are:
• BONES e.g. arthritis!

• KNEE CAP e.g. recurrent dislocation
• MENISCI e.g. meniscal injuries
• CRUCIATE LIGAMENTS e.g. ACL and PCL injuries
Osteoarthritis of the Knee
Epidemiology
• Very common
• Older people
• May be related to trauma
Clinical features
Symptoms:
• Pain, stiffness and swelling made worse by use of the joint. ʻJoint locking + painful give-wayʼ due to
loose bodies.
Signs
• LOOK: varus/valgus deformity, swelling
• FEEL: effusion, tenderness over joint lines, crepitus
• MOVE: movement-fixed flexion deformity
Management
CONSERVATIVE Weight loss

Analgesia
Walking stick + foam heel wedges
Physiotherapy
MEDICAL -
SURGICAL Variety of procedures possible

1. Arthroscopy (determine extent + wash-out - may provide up to 1 year
of relief)
2. Osteotomy (particularly good for younger patients where medial only
side is affected - last 8-10 years)
3. Total knee replacement
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Recurrent patellar dislocations
Patella is a mobile sesamoid bone within the quadriceps tendon
There are 2 types:
1.! Full dislocation: always lateral following direct trauma to medial side. Knee locked in 30-40 degree
flexion + pain + swelling
2.! Subluxation: patella felt to ʻpopʼ out turning. Momentary pain and swelling 24h later
Important to due a SKYLINE x-ray to reveal a OSTEOCHONDRAL fracture.
Meniscal injuries
These occur when the meniscus becomes

ʻtrapped between joint surfaces.ʼ
The distribution is:
• Medial meniscus 70% (less mobile

than lateral)
• Lateral meniscus 25%
• Both 5%
Clinical features
Symptoms:
• History of twisting injury
• Pop/click or tearing sensation
• Swelling
Signs
• LOOK: swelling, wasted quadriceps
• FEEL: effusion, tenderness at joint line
• MOVE: springy feel in a locked knee. McMurrayʼs test
Management
CONSERVATIVE Analgesia/anti-inflammatories (creams etc)

Physiotherapy
MEDICAL -
SURGICAL Indicated for failure of conservative

1. Arthroscopy (diagnostic and therapeutic to excise the tear)
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Cruciate Ligament Injury
1. ACL Injury
Common. Occur following twisting and valgus strain e.g. men - football, women - skiing.
• There is often co-existant damage to medial collateral ligament and medial meniscus
Clinical features
• Only diagnoses 70%
Management
CONSERVATIVE Intensive rehabilitation

Brace
MEDICAL -
SURGICAL Arthroscopy (diagnosis and reconstruction)

1. Extra-articular strengthening - strength lateral side of knee
with fascia
2. Intra-articular strengthening - ACL replaced with variety of
materials e.g. bovine collagen, autologous patellar
2. PCL Injury
Not common. Usually occurs in RTA when tibia is forced posteriorly on femoral condyles.
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Neurosurgery
In this section we shall be looking at:
a. Spinal cord compression

b. Neurological tumours
c. Hydrocephalus
For information on intracranial bleeds please see trauma section
Clinical Anatomy
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Spinal Cord Compression
THIS IS A MEDICAL EMERGENCY
“Compression of the spinal cord”
Clinical features
Structure Pathology
Symptoms
Vertebral body Malignancy (primary/secondary)
• Sudden onset back pain Osteoporosis
Abscess e.g. Pottʼs
• Neurological phenomena:
Vertebral disc Acute intervertebral disc rupture
1. Leg weakness Chronic degenerative disease
2. Sensory loss
3. Painless urinary retention Spinal cord Tumour
Blood vessels Haematoma (e.g. warfarin therapy)
Signs
This will usually be an upper motor neurone pattern.
• Increased tone
• Weakness in a pyramidal distribution
• Hyper-reflexia
• Up-going plantars
+ a SENSORY LEVEL.
Note: with sudden onset spinal compression there may be spinal shock (LMN pattern)
Investigations
Cultures Urine dipstick (? BJP)
Bloods - ABG -
Bloods - Venous FBC (anaemia), U&Es, clotting (coagulopathy), Calcium (malignancy)
Imaging MRI (to look at presence/degree of spinal compression)

CT for bone injuries
Scopic/Biopsy -
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Management
The management depends on the cause. The key is EARLY INTERVENTION - this offers the best chance of
recovery.
CONSERVATIVE Neurological observations

Analgesia
Fluids
NBM if for surgery
MEDICAL Metastases - steroids, bisphosphonates, radiotherapy

Abscess - antibiotics
SURGICAL 1. Disc prolapse - decompression

2. Abscess - drainage
3. Metastases - surgical decompression
Cauda Equina Syndrome
This is a particular form of compression where the problem is with the cauda equina.
As the cauda equina is made up of nerves that have come from the spinal cord the signs may be different:
• LMN signs e.g. weakness with absent reflexes

• Bladder and bowel dysfunction
Treatment is as for above.
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Neurological Tumours
There are lots of different tumours that affect the brain and spinal cord. They are rare but may be divided
into:
1. PRIMARY
• Benign
• Malignant
2. SECONDARY (most common)
Table of the most common tumours and their features
Origin Characteristics Treatment
Glioma Primary from glial cells Surgery where

possible
1. Astrocytomas
2. Medulloblastomas Palliation
3. Ependymomas
4. Oligodendromas
Meningioma Primary from arachnoid Benign and slow growing Surgery where
cells possible
Palliation
Acoustic Neuroma Primary from schwann Press on Surgery but risk of

cells of CN VIII. nerve damage.
1. 8th nerve (deafness)
Note: usually unilateral. 2. 5th/7th nerve (facial
Bilateral if with NF numbness and weakness)
Pituitary Tumours Adenomas 1. Endocrine abnormalities Medical hormonal

e.g. hypopituitarism, manipulation
Cushingʼs syndrome
Surgical - removal
2. Visual abnormalities e.g.
biltemporal hemianopia
Lymphoma B cell Association with AIDS Radiotherapy

T cell
Poor survival
Metastases Breast, lung, kidney and V. common Palliative

malignant melanoma
e.g. steroids
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Hydrocephalus
“Raised CSF pressure within the ventricular system that is characterised by dilated cerebral ventricles.”
Note: the intraventricular pressure may either be NORMAL or RAISED
Types:
1. Communicating hydrocephalus
• Obstruction within subarachnoid space → dilatation in entire system

• e.g. meningitis, subarachnoid haemorrhage,
congenital abnormality in arachnoid villi.
2. Non-communicating hydrocephalus
• Obstruction within the ventricular system

• E.g. aqueduct stenosis, intraventricular
tumours.
Acute hydrocephalus present with features of a

raised ICP e.g. headache, visual disturbance
Signs would be
• Loss of physiological cupping

• Blurring of disc margins
• Engorged pulsatile veins
Chronic hydrocephalus present with characteristic

features
• Enlarging head circumference

• Sun-set eyes
• Tense fontanelle
• Cranial nerve palsies
Investigation
The most important study here is MRI
Management
Established hydrocephalus required drainage. This may be
1. Temporary e.g. to an extraventricular dran

2. Permanent e.g. peritoneum, right atrium, pleural cavity
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Urology
Clinical Anatomy
The Kidney
• These are retroperitoneal organs
• Contains a hilum into which goes the renal artery, renal vein, pelvis of ureter, nerves and lymphatics.
• Contains adrenal glands on superior aspect.
• Structure:
1. Pelvis
2. Major calyces
3. Minor calyces (collecting ducts discharge here)
Blood supply
• Renal artery from aorta

• Renal vein into IVC
• Para-aortic lymph nodes
The Ureter
• 25 cm in length and split into 3 parts:
1. Abdominal
2. Pelvic
3. Intravesical
Blood supply:
• Segmental blood supply from all arteries along itʼs course
There are 3 important sites of narrowing
1. Pelvis of kidney (PUJ)

2. Pelvic brim
3. Ureteric orifice (VUJ)
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The testicles/scotum
Common presentations
Renal tract stones
Also known as nephrolithiasis/renal calculi
Epidemiology
• Very common to see

• Any age
• M:F = 2:1
Aetiology
Can form anywhere in the system (kidney to urethra)
Aetiology can be linked to 3 basic factors:
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1. Increased solute Hypercalcaemia

concentration Hyperoxaluria (tea, spinach, rhubarb)
Hyperuricaemia
Cystinuria
Thiazides decreasing calcium excretion
2. Increased urine Dehydration

concentration Increased dietary protein
Diuretics
3. Stasis UTIs
Congenital tract abnormalities e.g. pelvic-ureteric junction obstruction/

horse-shoe kidney
Types of stone
1. Calcium oxalate (75%) - spikey and radio-opaque [metabolic/idiopathic]

2. Triple phosphate (17%) - large, radio-opaque may form staghorn calculus [proteus UTIs]
3. Uric acid (5%) - smooth, brown, radio-lucent [hyperuricaemia]
4. Hydroxyapatite (1%)
5. Cysteine (1%) - yellow, crystalline, semi-opaqe [renal tubular defects, cystinuria]
Clinical Features
NOTE: a febrile patient with renal obstructed is a SURGICAL EMERGENCY
Symptoms:
• Asymptomatic
• Ureteric colic: severe pain from loin to groin

• Associated with pyrexia, vomiting, rigors +/- blood in urine
• Features of infection: polyuria, dysuria
Signs:
• General: moving around on the bed, febrile,

• Specific: loin tenderness is a feature of infection above the stone
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Investigations
Cultures Urine: MC & S, dipstick (haematuria, infection), 24h collection for ions
Bloods - ABG -
Bloods - Venous FBC (leucocystosis)

U&Es (dehydration)
Specific levels of Ca2+, Mg2+, urate, phoshate
Imaging Plain KUB (85% are radio-opaque)

IVU (control, immediate, 20 min
Scopic/Biopsy -
Management
Definitive management will depend on the size of the stone
• If stone < 5mm in lower ⅓ then will pass - send pt. home
• If stone > 5mm - operative intervention
CONSERVATIVE Analgesia (e.g. diclofenac/pethidine/morphine)

Encourage oral intake/I.V. fluids
Home if pain resolved and stone < 5mm
MEDICAL If infection - cefuroxime and metronidazole
INTERVENTIONAL If stone > 5mm or pain not resolved

1. Kidney - ESWL, percutaneous nephrolithotomy, open removal
2. Ureter - Ureteroscopic removal, ultrasound/laser
3. Bladder - lithotripsy or open
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Haematuria
“The passage of blood in the urine.”
2 types:
• Microscopic
• Macroscopic
Or may be divided according to aetiology:
1. FALSE
e.g. beetroot, rifampicin, porphyria, PV/PR bleed
2. TRUE
1. General
• Coagulopathy, HSP, anticoagulants
2. Kidney
• Stones, tumours, infections
3. Ureter
4. Bladder
5. Prostate
• Stones, tumours, BPH
6. Urethra
• Stones, tumours, infections, trauma
Clinical features
It is important to determine the following in the history
1. Timing (beginning, end or throughout)

2. Painful vs. painful
3. Clots?
4. Other obstructive symptoms
5. Drug history and clotting defects
Investigations
Cultures Urine: MC & S, dipstick, urine cytology
Bloods - ABG -
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Bloods - Venous FBC (leucocytosis)

U&Es (renal function)
Clotting (? coagulopathy)
Imaging IVU
Renal USS
Scopic/Biopsy Flexible cystoscopy and biopsy

CT scan
Management
• Treat the cause
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Acute Urinary Retention
This is a common - particularly in the post-operative setting.
The aetiology may be:

IN THE LUMEN Stones
1. ACUTE Cots (with clot retention)
2. CHRONIC
3. Acute-on chronic
IN THE WALL Tumours (bladder, prostate,
urethra)
Infection
Clinical Features Trauma
OUTSIDE THE WALL Constipation

Symptoms: Fibroids
SYSTEMIC Cauda equina syndrome

• Progressive reduction in ability to pass water
Drugs (e.g. EtOH,
• Suprapubic pain
anticholinergics)
Signs:
• General: patient agitated and in pain

• Specific: Palpable bladder that may extend up to umbilicus
• Always do a PR for constipation, prostate and rectal tone
• Neurological examination as well.
Investigations
Cultures Urine MC & S, dipstick

U&E (renal function)
G&S
PSA
Imaging CXR & KUB (? stones)

USS (residual volume, size of bladder and hydronephrosis)
Scopic/Biopsy -
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Management
CONSERVATIVE Mobilise + run tap

Treat underlying cause
IV fluids for secondary diuresis
MEDICAL Catheterise (+ shot of gentamicin)

TWOC only > 24 hrs
INTERVENTIONAL 1. Suprapubic catheter

2. Emergency TURP
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Kidney and Bladder
Topics covered here
1. Renal transplantation
2. Renal cell carcinoma
3. Bladder carcinoma
Renal Transplantation
Kidneys may be obtained from:
1. Live related donor

2. Cadaveric donor (brainstem death or non-heart beating donor)
The most important indication is END STAGE RENAL FAILURE (GFR < 10ml/min).
Suitable candidates should be
• Young
• Fit for anaesthesia
• Suitable anatomy
• Compliant with post-op immunosuppression
• Suitable anatomy
Recipient Donor
Normal pre-op Normal pre-op
Specific bloods - ABO screen, HLA matching (A, B, Specific bloods - ABO screen, HLA matching (A, B,
DR), cross-match with donor lymphocytes DR), cross-match
Infectious screen - HIV, CMV, HTLV-1, hepatitis,
syphilis
Imaging - USS, KUB, Imaging - IVU, USS, MRA
Procedure
The operation occurs in 2 parts.
1. Remove donor kindey

2. Anatastomosis in recipient with:
• Renal vein → external iliac vein
• Renal artery → external iliac artery
Note: may be palpated in the abdomen.
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There will be 2 scars:
1. Loin scar for a nephrectomy

2. Rutherford-Morrison incision for anastamosis
Post-operatively
• Immunosupression using steroids, azothioprine and cyclosporine.
Specific - Immediate Hyperacute rejection
Specific - Early Accelerated rejection
Specific - Late Acute rejection - “flu-like symptoms and graft tenderness.”

Chronic rejection
Tumours (skin cancers/lymphomas)

Complications of immunosuppressive treatment (steroids, infection
and malignancy)
UTIʼs
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Renal Tumours
Renal tumours may be:
a. BENIGN (e.g. cysts)

b. MALIGNANT
Epidemiology
• They are uncommon

• Present late middle age
• M>F = 2:1
Aetiology
• Carcinogens → TCC
• Stones → SCC
• Hypernephroma in Von Hippel-Lindau Syndrome
LOCATION TYPES CHARACTERISTICS
PELVIS Transitional cell carcinoma Associated with carcinogens

Highly malignant
Squamous cell carcinoma Associated with chronic stones
Papilloma
KIDNEY Hypernephroma (Grawitz tumour) Most common types (80%)

Adenocarcinoma
Large & aggressive
Nephroblastoma (Wilmʼs tumour) Large tumours in children
Clinical features
Symptoms:
• General: weight loss, PUO

• Specific
• Microscopic haematuria
• Rarely - loin pain, loin mass and haematuria
• Metastatic symptoms
Signs:
• General: anaemia
• Specific
• Mass in loin
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• Varicocele (tumour spreads along renal vein obstructing left testicular vein)
• Hypertension
• Polycythaemia
• Hypercalcaemia
Investigations
Cultures Urine dipstick (haematuria)
Bloods - Venous FBC (anaemia of chronic disease, polycythaemia)

U&Es (renal function)
LFTs (mets)
Ca2+
Clotting
Imaging CXR (mets - cannonball)

IVU (filling defect, hydronephrosis, renal mass)
Renal USS (demonstrate mass and look at IVC)
CT (staging)
Scopic/Biopsy -
Management
CONSERVATIVE Palliation with radiotherapy and chemotherapy
MEDICAL Radio/chemo are never curative
INTERVENTIONAL 2 operations
1. Nephro-uretectomy (TCC - removal of entire 1 side, one scar in loin

and second in groin)
2. Nephrectomy (other tumours - may require chest apporach!)
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Bladder Carcinoma
Epidemiology
• Common in middle aged and elderly

• M:F = 4:1
Aetiology
Important predisposing factors are smoking, dye exposure and chronic irritation say with schistosomiasis.
Pathology
1. Transitional cell carcinoma (90%) - solid or papillary

2. Squamous (7%) - associated with chronic irritation
3. Adenocarcinoma (2%)
4. Sarcoma
There is a detailed staging system that it is not necessary to know - most are pT1 (invasion of sub-epithelial
tussie) or pT2 (involvement of superficial muscle)
They may also be classified according to differentiation eg. G1 (well), G2 (intermediate), G3 (poor)
Clinical features
Symptoms:
• General: Weight loss, anorexia

• Specific
• Painless haematuria
• Urinary retention (clots or bladder neck obstruction)
• Uraemic symptoms
Signs:
Usually there are NONE.
• General: anaemia
• Specific:
• Bladder mass
• Lymphadenopathy
• Features of metastases e.g. papable liver, abnormal chest examination
Management
This depends on the stage
1. Trans Urethral Resection of Bladder Tumour (TURBT) - Tis, T1, T2

• Adjuvants - Intravesical chemotherapy, immunotherapy using Montreal strain of BCG
2. Cystectomy with re-implantation of ureters through an ileal conduits
• Adjuvants - Radiotherapy
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Prostate Disease
In this section we shall talk about
1. Prostatitis
2. Benign Prostatic Hyperplasia
3. Carcinoma of the prostate
Prostatitis
“Infection and inflammation of the prostate.”
May be ACUTE or CHRONIC
Most common organisms are
• Strep. feacalis
• E. coli
• Chlamydia
Clinical features
Symptoms:
• General: malaise, fever/rigors

• Specific
• Pain (prostadynia)
• Haetospermia
• Retention
• Features of urinary tract infection e.g. dysuria, discharge
Signs
• General: pyrexia
• Specific
• Tender prostate on PR
• Tender testicles in epididymo-orchitis
Investigation as you might expect e.g. FBC, CRP and MSU
Definitive treatment is antibiotics e.g. ciprofloxacin
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Benign Prostatic Hyperplasia (BPH)#
“Benign and profuse nodular proliferation of the musculofibrous and glandular layers of the prostate”
Epidemiology
• Very common and get worse with advancing years
Aetiology
There are 2 theories behind itʼs development
a. HORMONE THEORY - reduced testosterone and proportional increase in oestrogen → hyperplasia

b. NEOPLASTIC THEORY - benign neoplastic enlargement
Clinical features
Symptoms:
• Obstructive symptoms e.g. poor stream, hesitancy, post micturation dribbling

• Symptoms due to bladder retention e.g. frequency, nocturia, overflow incontinence, infection, stones
Signs:
• Smoothly enlarged prostate with definable median sulcus.
Invesigations
Cultures Urine dipstick & MC & S
Bloods - ABG -
Bloods - Venous FBC (Hb low if uraemia)

PSA
Imaging KUB & IVU

USS of kidneys and bladder (residual volume, hydronephrosis)
Transrectal ultrasound
Scopic/Biopsy -
Functional/Special Urodynamics (pressure/flow cystometry)
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Management
CONSERVATIVE Address drinking habits
MEDICAL 1. Alpha blockers e.g. Tamsulosin α1c

2. 5α reductase inhibitors e.g. Finasteride
INTERVENTIONAL Indicated if severely affecting QOL.
1. Trans Urethral Resection of Prostate (excise lateral and middle lobes

with diathermy cutting loop) Send chipping to histology
2. Trans Urethral Incision of Prostate - youger patients
3. Trans Urethral ElectroVaporisation of Prostate
4. Laser Prostatectomy (Nd: YAG - lower risk of impotence and
retrograde ejaculation)
5. Open - if very large
6. Transurethral Microwave Thermotherapy
Carcinoma of Prostate
Epidemiology
• Most common cancer in men

• 60% over 80 have it at autopsy
Aetiology
Involves age-dependent alteration in oestrogen and androgens
Pathology
• These are always ADENOCARCINOMAS and affect the outer zone of the gland.
! ! Note: malignant spread causes osteosclerotic lesions on XR)
• It is staged using the GLEASON SYSTEM (based upon two worsed affected areas)
Clinical features
Many pts. are asymptomatic
Symptoms:
• General: many
• Specific:
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• Obstructive symptoms
• Sympoms of spread e.g. back pain, SOB, pathlogical fracture
Signs:
• Prominent nodule on PR
Investigations
Cultures Urine dipstick & MC & S
Bloods - ABG -

Alk phosphate
PSA
Imaging CXR, spine/skull/pelvic radiographs

USS of prostate/liver
CT scan
Bone scan
Scopic/Biopsy Transrectal biopsy
Quick notes on the PSA
• A proteolytic enzyme that is part of the ejaculate

• Values increased with: age, infection (UTI, prostatitis), TURP, post-ejaculation
Treatment
CONSERVATIVE “Watch and wait” stategy (PSA & PR)
For palliation DXT used
MEDICAL 1. LHRH analogue e.g. Goserelin (Zoladex)

2. Anti-androgens e.g. cyproterone acetate
3. Radiotherapy for spinal mets
INTERVENTIONAL 1. TURP
2. Radical prostatecctomy and lymph clearance
3. Brachytherapy
Note: old treatment is bilateral or orchidectomy
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The Scrotum
In this section we look at:
a. Torison of the testicle

b. Undescended testicles
c. Lumps in the scrotum
Testicular Torsion
“A twisting of the spermatic cord that cuts off the blood supply to the testicle and surrounding structures
within the scrotum.”
This is a SURGICAL EMERGENCY! 4-6 hours window in which testicle is salvageable
Usually affects affects children and young adults.
Aetiology
• Trauma
• Lack of a bare area attaching testicle to scrotum predisposed to torsion. This is know as a CLAPPER
BELL TESTICLE
Clincal features
Symptoms:
• Extreme pain in scrotum (unilateral)

• Lower abdominal pain (T10 innervation_
Signs:
• Hot and swollen testicle

• Extreme tenderness
• HIGH RIDING and TRANSVERS in lie
Managment
• Direct patient to theater ASAP (do not perform US)

• Procedures
i. Untwisting of testicle with salvage

ii. Orchidectomy
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Undescended Testicles
The testicles should normally be present in scrotum at birth
Epidemiology
• 3% are undescended at birth

• 1% after 1 year
• Prematurity increases the risk hugely.
There are a number of possible results
1. Crytoorchidism - “complete lack of testicles from the scrotum”

!
2. Retractile testes - “norma genitalia but overactive cremasteric reflex.”
• Testes may be persuaded in scrotum with warm hand

• No treatment except reassurance
3. Maldescended testes - “testicles stopped descending down normal path.”
• Scrotum is underdeveloped and flat

• Testicle will be small
• There will a patent processus vaginalisis (+/- a hernia)
• Always require repair
4. Ectopic testicles - “testes in an abnormal site.”
• Common sites: abdomen, superficial inguinal pouch, root of penis
Complications
• Infertility
• Prone to trauma/torsion (superficial site)
• Hernias
• Malignancy (replacing it does not help this)
Management
• ORCHIDOPLEXY (< 2y) - Dantos pouch procedure
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Lumps in the Scrotum
This is v. common for exams.
Always ask yourself 4 questions:
a. Can you get above it?

• If not then it must be from above → inguinal hernia
b. Is the testis separate from the lump?

• What structure is it from? - testis or epididymis/cord
c. Is the lump tender?

• Epidido-orchitis is most common
!
d. Does the lump transilluminate?
• Cystic things transulluminate e.g. hydrocele/varicole
• Tumours/spermatoceles/haematocele do not
Brief notes on each conditions
Hydrocele
“A collection of serous fluid within the tunica vaginalis.”
May be PRIMARY (congenital and associated with patent processus, large) or SECONDARY (reaction to
other pathology in testis, small)
Rx
• Infants - leave until 1y as most will resolve spontaneously

• Adults - should resolve spontaneously if not aspirate and send for cytology
• Drainage and excision in theatre
Varicocele
“Dilated veins of the pampiniform plexus.”
May be PRIMARY (idiopathic) or SECONDARY (left sided renal tumour).
Present with bag of worms scrotum and a dull ache (L > R)
Rx
• Conservative
• Surgical
• Clip the testicular vein
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Haematocele
“Blood within the tunica vaginalis”
Rx
• Conservative
• Surgical - drain
Epididimo-orchitis
“Infection and inflammation of the testis and surrounding structures.”
Occurs in association with
• Mumps (usually 1 week post-parotitis)

• Ascending infection e.g. UTI, prostatitis
• STD e.g. Chluamydia
Present in a similar fashion to testicular tumours:
• Importat differences are systemic features (fever, unwell), features of UTI/STD, secondary hydrocele
Definitive treatment
• Analgiesia, bed rest, scrotal support

• Ciprofloxacin
Sperm granuloma
• Painful lump post-vasectomy
Epididymal cyst
• Tender cystic lump coomon in middle-aged and elderly. May be bilateral
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Testicular Cancer
Epidemiology
• Tumour of young men
Aetiology
• Increased risk with undescended testicles and infertility
Pathology
“Teratomas for Troops (young), Seminomas for Sergeants (older)”
1. Seminomas
• Solid and slow growing tumours

• Radiosensitive
2. Teratomas
• Solid or cystic
• Secrete α-fetoprotein
Rare types
• Choriocarcinomas (HCG producing)

• Leydig cell tumours (secrete androgen)
• Sertoli adenomas (secrete oestrogens)
• Lymphomas (elderly with poor prognosis)
Clinical features
Symptoms:
• Asymptomatic
• Lump
Signs:
• Heavy, irregular lump

• Non-tender
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Investigations
Staging is via the Royal Marsden Classification
Cultures -
Bloods - ABG -

2 tumour markers
1. α-fetoprotein
2. β-HCG
Imaging CXR (mets)

USS scrotum
CT abdomen (staging)
Scopic/Biopsy Never perform a percutaneous biopsy (seeding)
Treatment
CONSERVATIVE Important adjuncts

- Conservation of other testicle for fertility
- Cryopreservation of semen
- Prosthesis
MEDICAL Chemotherapy and radio-therapy may be offered to para-aortic nodes
INTERVENTIONAL 1. Inguinal orchidectomy +/- lymph node dissection
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Appendix
Common abdominal scars

+ Roof-top =
Mercedes-benz
Roof-top Roof-top
Loin
Roof-top
Subcostal/
Kocherʼs
Midline
Loin
R.
paramedian Loin
Lanz L.
paramedian
Grid-iron
Pfannenstiel
Inguinal
+ always look for lapaoscopy scars!
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Common drugs
Drug Dose Drug Dose
ANALGESIA HYPNOTICS
Paracetamol 1g Q.D.S. Zopiclone 3.75-7mg nocte
Aspirin 300mg Q.D.S. Temazepam 10-20mg nocte
Diclofenac 50mg T.D.S.
Codeine phosphate 30mg Q.D.S. ANTI-HISTAMINES
Morphine 5-10mg / 4h Chlorphenamine 10mg IV/4mg PO
Tramadol 50mg / 4h Cetirizine 5-10mg/24h PO
Pethidine 50mg / 4h
ANTI-ACIDS
ANTI-EMETICS Cimetidine 800mg nocte
Cyclizine 50mg T.D.S. Ranitidine 300mg nocte
Metaclopramide 10mg T.D.S. Omeprazole 20mg
Ondansetron 4mg T.D.S. Lansoprazole 30mg
ANTIBIOTICS ANTI-DIARRHOEALS
Amoxicillin 500mg T.D.S. Loperamide 4mg stat then 2mg with

each motion
Flucloxacillin 500mg Q.D.S. Codeine phosphate 30mg Q.D.S.
Erythromycin 500mg Q.D.S.
Ciprofloxacin 500mg B.D.
Cefuroxime 1.5 g I.V.
Metronidazole 500mg I.V.
ANTI-COAGULANTS
Unfractionated heparin 5000U B.D. s.c.
Enoxaparin DVT prophylaxis

20-40mg/24 s.c.
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© Podmedics 2010

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Surgery Revision Notes

Thank you and good luck.

The Podmedics Team

Jonny Manley: jonny@podmedics.co.uk

Podmedics’ Recommended Texts/Links/Courses

Please forgive us the indulgence of being placed first.

You must answer questions from this site!

Lecture Notes on Surgery

The 10-week Surgery Revision Course

Hosted by the MDU and the mighty Mr Barry Paraskevas

Surgical Fluids and Nutrition! 12

Gastro-oesphageal reflux disease! 52

Hiatus Hernia and other conditions! 53

Acute Upper GI Bleed! 59

Perforated Peptic Ulcer! 63

Gallstone and Biliary Disease! 68

Biliary Tree Complications! 73

Hypersplenism & Hyposplenism! 78

Basic Principles of the Lower Gastrointestinal Surgery ! 92

Colon Cancer and Stomas! 100

Emergency bowel operations! 103

Inflammatory Conditions! 105

Diverticular Disease! 107

Surgical Ulcerative Colitis! 109

Crohn’s Disease! 111

Peri-Anal Disease! 113

Anal Fissures! 116

Anal abscess/Anal sepsis! 117

Anal Fistula! 118

Rectal Prolapse! 119

Anal Carcinoma! 120

Breast Disease ! 123

Diagnostic Principles in Breast Disease! 124

Benign Breast Disease! 125

Malignant Breast Disease! 127

Neck Lumps! 131

Solitary Lumps in the Neck! 135

Thyroid Surgery! 139

Vascular Surgery ! 149

Venous Disorders! 151

Arterial Disorders! 154

The Hip! 170

Important other fractures for finals! 175

The Knee! 179

Spinal Cord Compression! 184

Neurological Tumours! 186

Common presentations! 190

Kidney and Bladder! 197

Prostate Disease! 202

The Scrotum! 206

Testicular Cancer! 210

Common drugs! 213

General approach to defining a disease

1. Definition (and classification)

When thinking about aetiology try to think in terms of...

2. ! Surgical sieve - what pathological processes could be occurring?

THE “VINTA MEDIC” SURGICAL SIEVE

Process Sub-split Process Sub-split

Vascular Heart Metabolic/Nutritional

Infection Bacterial Electrolytic Anions

Neoplastic Primary Degenerative

Trauma Penetrating Iatrogenic Drugs