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Detailed answer according to weightage of marks based on standard surgical books

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Here are comprehensive answers to all questions based on standard surgical textbooks (Bailey & Love 28th Ed., Schwartz's Surgery 11th Ed., Current Surgical Therapy 14th Ed., Sabiston, Harrison's 22nd Ed.):

MS GENERAL SURGERY - YEAR 1 EXAMINATION ANSWERS

Total Marks: 100 | Time: 3 Hours

Q.1 — Long Answer (30 Marks)

Anatomy and Physiology of Spleen | Hypersplenism | Causes of Splenomegaly | Management

A. ANATOMY OF THE SPLEEN (6 marks)

Location and Size:

Lies in the left hypochondrium, behind the 9th-11th ribs
Weighs 75-150 g in adults; normally not palpable
Measures approximately 12 x 7 x 3 cm (the "1-3-5-7-9-11 rule": weighs 7 oz, 1×3×5 inches, lies under ribs 9-11)

Relations:

Anterior: stomach, tail of pancreas
Posterior: left kidney and adrenal
Inferior: splenic flexure of colon
Covered by peritoneum except at hilum

Ligaments:

Splenorenal (lienorenal) ligament - contains splenic vessels and tail of pancreas
Gastrosplenic ligament - contains short gastric and left gastroepiploic vessels
Phrenicosplenic and splenocolic ligaments (avascular)

Blood Supply:

Splenic artery - the largest branch of the coeliac axis (tortuous course along upper border of pancreas)
Splenic vein drains into portal vein

Histology:

Red pulp: sinusoids and splenic cords (of Billroth) - for filtration
White pulp: lymphoid tissue around central arterioles - Malpighian corpuscles (periarteriolar lymphoid sheaths + lymphoid follicles)
Marginal zone: between red and white pulp; site of antigen trapping

B. PHYSIOLOGY OF THE SPLEEN (5 marks)

Function	Details
Filtration	Removes aged/abnormal RBCs, cellular debris, particulate matter
Immunological	Produces IgM antibodies, opsonins (properdin, tuftsin), IgG; traps blood-borne antigens
Haematopoiesis	In fetal life (3rd-5th month); can resume in haematological disease (extramedullary haematopoiesis)
Reservoir	Stores ~30-40 mL blood; up to 1/3 of platelet pool held here
Culling	Removes RBCs with inclusions (Howell-Jolly bodies, Heinz bodies, siderocytes)
Pitting	Removes inclusions from RBCs without destroying the cell
Iron recycling	Macrophages break down haemoglobin; iron recycled

Post-splenectomy changes: Howell-Jolly bodies, target cells, thrombocytosis, leukocytosis; increased susceptibility to encapsulated organisms (Pneumococcus, Haemophilus, Meningococcus).

C. HYPERSPLENISM (5 marks)

Definition: A syndrome characterised by splenomegaly with sequestration and premature destruction of one or more blood cell lines (pancytopenia), compensatory marrow hyperplasia, and improvement after splenectomy.

Criteria (Doan's criteria):

Splenomegaly
Cytopenia in one or more cell lines (anaemia, leucopenia, thrombocytopenia)
Normal or hyperplastic bone marrow (compensatory)
Correction by splenectomy

Types:

Primary hypersplenism: No underlying cause identified; diagnosis of exclusion
Secondary hypersplenism: Due to an identifiable underlying disease (most common)

Pathophysiology: The enlarged spleen has an expanded blood pool and greater phagocytic activity. Increased splenic blood flow, pooling of cells, and enhanced destruction by hyperactive macrophages lead to peripheral cytopenia despite a reactive marrow.

Clinical Features: Anaemia (fatigue, pallor), thrombocytopenia (purpura, bleeding tendency), leucopenia (infections), splenomegaly, features of the underlying cause.

D. CAUSES OF SPLENOMEGALY (6 marks)

Massive Splenomegaly (crosses midline):

Chronic myeloid leukaemia (CML)
Myelofibrosis
Visceral leishmaniasis (Kala-azar)
Malaria (hyperreactive malarial splenomegaly)
Gaucher's disease

Classification by cause:

Category	Causes
Infections	Malaria, kala-azar, typhoid, infectious mononucleosis, TB, schistosomiasis, brucellosis
Haematological	CML, lymphoma (Hodgkin/NHL), haemolytic anaemias (hereditary spherocytosis, sickle cell, thalassaemia), polycythaemia vera, myelofibrosis, ITP
Congestive / Portal HTN	Liver cirrhosis, portal vein thrombosis, Budd-Chiari syndrome, right heart failure, splenic vein thrombosis
Infiltrative / Storage	Gaucher's disease, Niemann-Pick disease, amyloidosis, sarcoidosis
Autoimmune / Inflammatory	SLE, Felty's syndrome (RA + splenomegaly + neutropenia), haemolytic anaemia
Cysts / Tumours	Hydatid cyst, splenic abscess, primary splenic tumours (rare)

E. MANAGEMENT OF SPLENOMEGALY / HYPERSPLENISM (8 marks)

Investigations:

CBC with peripheral smear
LFTs, bone marrow biopsy
Ultrasound abdomen / CT scan
SAAG (serum-ascites albumin gradient) if ascites
Specific: Leishmania serology, Mantoux, haemoglobin electrophoresis, flow cytometry

Medical Management:

Treat the underlying cause: antimalarials, antivirals, treatment of portal hypertension
Propranolol (non-selective beta-blocker) for portal hypertension
Corticosteroids for autoimmune causes, ITP
Hydroxyurea for CML/myeloproliferative disease
Transfusion support as needed

Surgical Management - Splenectomy:

Indications:

Hypersplenism causing symptomatic cytopenia unresponsive to medical therapy
Hereditary spherocytosis, autoimmune haemolytic anaemia
ITP refractory to corticosteroids
Massive splenomegaly with pressure symptoms
Splenic rupture, splenic abscess, splenic cyst
Staging laparotomy (Hodgkin's lymphoma - historical)

Approaches: Open (midline or left subcostal/Kocher incision) or laparoscopic (preferred for elective cases, spleens <20 cm)

Pre-operative preparation:

Vaccinations: Pneumococcal, Meningococcal, Haemophilus influenzae type b (at least 2 weeks before)
Correct coagulation and cytopenia
Platelet transfusion if platelets < 50,000 (at time of splenic artery ligation)

Post-splenectomy complications:

Early: haemorrhage, left subphrenic collection, pancreatitis (tail of pancreas injury), portal/splenic vein thrombosis
Late: OPSI (Overwhelming Post-Splenectomy Infection) - septicaemia from encapsulated organisms; 0.5-1% lifetime risk but mortality ~50%

OPSI Prophylaxis:

Lifelong penicillin V prophylaxis (or amoxicillin) - especially children <16 yrs for minimum 2 years
Patient education: medical alert bracelet, fever protocols
Annual influenza vaccine

Partial Splenectomy / Splenic Conservation: Preferred in children (to preserve immune function), especially for trauma and benign cysts.

TIPS (Transjugular Intrahepatic Portosystemic Shunt): For portal hypertension-related congestive splenomegaly; reduces portal pressure and splenic engorgement. - Harrison's 22nd Ed., Ch. 355

Q.2 — Long Answer (30 Marks)

Gastric Outlet Obstruction - Aetiopathology, Presentation and Management

A. DEFINITION

Gastric outlet obstruction (GOO) is a clinical and pathophysiological syndrome caused by any disease process that produces a mechanical impediment to gastric emptying at the level of the pylorus, duodenum, or adjacent structures.

B. AETIOPATHOLOGY (10 marks)

Causes - Benign vs Malignant:

Benign	Malignant
Peptic ulcer disease (most common benign cause) - pyloric/duodenal ulcer	Carcinoma of the stomach (antrum/pylorus) - most common cause overall
Infantile hypertrophic pyloric stenosis	Carcinoma of the head of pancreas
Gastric polyps	Carcinoma of the duodenum
Adult hypertrophic pyloric stenosis	Extrinsic compression - lymphoma, metastases
Caustic ingestion stricture	Ampullary carcinoma
Crohn's disease
Tuberculosis
Annular pancreas
Duodenal atresia/web

Note: With decreasing incidence of peptic ulcer disease (H. pylori eradication, PPIs), malignancy now accounts for the majority of GOO in developed countries. GOO should be considered malignant until proven otherwise. - Bailey & Love 28th Ed.

Pathophysiology of peptic ulcer GOO: Repeated episodes of ulceration and healing lead to progressive fibrosis, scarring, and stricture of the pyloric canal. Acute oedema and spasm around an active ulcer may cause reversible obstruction, whereas chronic scarring causes irreversible mechanical obstruction.

Metabolic consequences - Hypochloraemic Hypokalaemic Metabolic Alkalosis:

Vomiting of HCl-rich gastric juice → loss of H⁺ and Cl⁻ → primary metabolic alkalosis
Kidneys initially excrete HCO₃⁻ with Na⁺ and K⁺ to compensate
As volume depletion worsens: aldosterone activates → Na⁺ retention, K⁺ loss
Paradoxical aciduria occurs when H⁺ is exchanged for Na⁺ in tubules despite systemic alkalosis
Hyponatraemia, hypokalaemia, low Cl⁻, high serum HCO₃⁻, raised urea (pre-renal)
Lowered ionised calcium → tetany (Trousseau's and Chvostek's signs)

This metabolic triad is the hallmark of chronic, benign, high-grade pyloric obstruction.

C. CLINICAL PRESENTATION (8 marks)

Symptoms:

Projectile, non-bilious vomiting - contains undigested food (bile absent as obstruction is above ampulla of Vater)
Vomiting often occurs hours after eating; vomitus may have a "stale food" odour
Epigastric fullness and distension
Weight loss - from reduced caloric intake and vomiting
Constipation
Long history of peptic ulcer disease (in benign cases)
Anorexia, early satiety

Signs:

Patient appears wasted, dehydrated
Visible gastric peristalsis (waves moving left to right)
Distended stomach in the epigastrium
Succussion splash (audible 3+ hours after a meal/fluids) - pathognomonic of gastric outlet obstruction
Dehydration signs: sunken eyes, dry mucosa, reduced skin turgor
Tetany if severe hypocalcaemia

D. INVESTIGATIONS (4 marks)

Bloods: Urea, electrolytes, LFTs, glucose, serum calcium, ABG (metabolic alkalosis), CBC (anaemia)
Upper GI Endoscopy (OGD): Gold standard - identifies cause, site, mucosal biopsy mandatory to exclude malignancy; retained food in stomach
Barium meal: Shows dilated stomach, delayed emptying, narrowed pyloric channel ("rat-tail" or "hour-glass" deformity)
CT Abdomen/Pelvis: Identifies mass lesions, lymphadenopathy, metastases, periampullary pathology
Gastric emptying study: 4-hour nuclear medicine scan for subtotal obstruction
Salivagram / pH study: In selected cases

E. MANAGEMENT (8 marks)

Step 1 - Resuscitation and Metabolic Correction:

IV access; urine output monitoring (Foley catheter)
IV isotonic saline (0.9% NaCl) - replaces Na⁺ and Cl⁻, allows kidney to excrete excess HCO₃⁻
IV KCl supplementation (20-40 mmol/L until normokalamia)
Wide-bore nasogastric tube (or orogastric lavage) - gastric decompression and lavage
High-dose PPI infusion (omeprazole 40 mg IV BD)
Nutritional support (enteral or parenteral)
H. pylori testing and eradication therapy (if peptic cause)

Step 2 - Investigations (as above)

Step 3 - Definitive Treatment:

A. Benign GOO (Peptic Ulcer):

Conservative (acute/oedematous obstruction):

NGT decompression + IV fluids + PPIs
30-40% may resolve with medical treatment alone
Confirm resolution with barium study/endoscopy

Endoscopic Treatment:

Balloon dilatation (through-the-scope or wire-guided): Effective for benign strictures; may require repeated dilations; 50% avoid surgery for 1-2 years - Current Surgical Therapy 14th Ed.

Surgical Options:

Vagotomy and Antrectomy (V+A): Gold standard - lowest recurrence (~2%), reassures benign diagnosis; mortality 2%; reconstruction by Billroth I or II
Vagotomy and Gastrojejunostomy (V+GJ): Lower mortality; laparoscopic approach feasible; risk of marginal ulcer; preferred in high-risk patients
Truncal vagotomy and pyloroplasty (Heineke-Mikulicz): Simpler but higher recurrence
Note: all surgery must include tissue biopsy to exclude malignancy

B. Malignant GOO:

Resectable tumours: Radical surgery (Billroth II/total gastrectomy for gastric carcinoma; Whipple's procedure for periampullary carcinoma)

Unresectable/palliative:

Gastrojejunostomy (palliative bypass) - provides relief of obstruction
Endoscopic duodenal/pyloric stenting (expandable metal stent): Preferred for poor surgical candidates; immediate relief; useful for life expectancy <3 months
Chemotherapy and radiotherapy as appropriate

C. Infantile Hypertrophic Pyloric Stenosis:

Ramstedt's pyloromyotomy (open or laparoscopic): definitive treatment after correction of metabolic alkalosis

Q.3 — Short Answer (20 Marks)

Q.3a - Meckel's Diverticulum (10 Marks)

DEFINITION AND EMBRYOLOGY

Meckel's diverticulum (MD) is a true diverticulum - it contains all three layers of the bowel wall (mucosa, muscularis, serosa). It results from failure of obliteration of the omphalomesenteric (vitelline) duct, which normally atrophies and disappears by the 5th-10th week of gestation. - Sleisenger & Fordtran's Gastroenterology

RULE OF 2s

2% of the population
2 feet (60 cm) from the ileocaecal junction
2 inches (5 cm) in length
2:1 male predominance
2 types of ectopic tissue (gastric and pancreatic - most common)
2 years: most symptomatic in children under 2 years

PATHOLOGY

Anti-mesenteric outpouching of the terminal ileum
50% contain ectopic mucosa; 80-85% of this is gastric mucosa (acid-secreting), 10-15% pancreatic
Ectopic gastric mucosa causes peptic ulceration at the junction of gastric-ileal mucosa ("marginal ulcer")

CLINICAL PRESENTATIONS

1. Painless Rectal Bleeding (most common - 50%):

Most common in children <2 years
Typically maroon-coloured blood (right-sided bleeding)
Caused by peptic ulceration from ectopic gastric mucosa
Can be massive, sometimes with hypovolemic shock
Melena may occur with slow bleeding
Management: Meckel's scan (99mTc-pertechnetate scintigraphy); angiography if negative; diverticulectomy at surgery

2. Intestinal Obstruction (20-30%):

More common in older children/adults
Mechanisms:
- Intussusception with MD as lead point (children >4 years)
- Volvulus around a fibrous vitelline cord
- Littre's hernia - MD in an inguinal/femoral hernia sac
- Adhesion formation
Presents: bilious vomiting, colicky abdominal pain, distension, obstipation

3. Diverticulitis (similar to appendicitis - 20%):

Indistinguishable from appendicitis clinically
May present with RLQ pain, fever, leucocytosis
MD diverticulitis occurs due to bacterial overgrowth or obstruction of the diverticulum
Complication: perforation, peritonitis

4. Umbilical Fistula / Umbilical Sinus:

Persistent patent vitelline duct → faecal discharge from umbilicus
Umbilical sinus if partially obliterated

5. Incidental Finding (50%):

Found at laparotomy/laparoscopy or imaging
Management of incidental MD remains controversial: resection recommended if <45 years age, male sex, MD length >2 cm, fibrous cord present, or palpably abnormal

INVESTIGATIONS

Meckel's scan (Tc-99m pertechnetate): Sensitivity 85%, specificity 95%; enhancement with pentagastrin, H2-blockers, or glucagon
CT abdomen: blind-ending tubular structure from anti-mesenteric ileum
CT enterography: better detection
Capsule endoscopy / double balloon enteroscopy
Angiography (for active bleeding)

MANAGEMENT (SURGERY)

Symptomatic MD: Surgical resection is always indicated
- Diverticulectomy: Wedge resection for narrow-neck MD without ileal involvement (via stapler or suture)
- Segmental ileal resection with primary anastomosis: For wide-neck MD, bleeding ulcer at base, inflamed or perforated MD

Q.3b - Volvulus / Sigmoid Volvulus (10 Marks)

DEFINITION OF VOLVULUS

A volvulus is a rotation or twisting of a loop of bowel about its mesentery, causing closed-loop obstruction with risk of strangulation and gangrene. It can affect the sigmoid colon (most common), caecum, small bowel, transverse colon, or stomach.

SIGMOID VOLVULUS

Epidemiology:

Most common form of colonic volvulus, accounting for 50-90% of all volvulus cases
2:1 male predominance
Patients typically present in the 7th decade or later
Mortality approaches 10%; up to 1 in 3 with recurrent volvulus
Common in Africa, Asia, Middle East (high-fibre/high-residue diet); institutionalised patients (psychiatric, neurologic conditions) - Current Surgical Therapy 14th Ed.

Predisposing Factors:

Long sigmoid mesentery with narrow base (congenital predisposition)
High-residue diet (Africa, Eastern Europe)
Chronic constipation and dysmotility
Institutionalisation (psychiatric hospitals, nursing homes)
Neurological disorders (Parkinson's, multiple sclerosis)
Pharmacological: anticholinergics, opioids
Diabetes mellitus, pregnancy

PATHOPHYSIOLOGY

The sigmoid colon, when excessively redundant with a narrow mesenteric base, can twist upon itself, producing a closed-loop obstruction. The proximal colon continues to fill with gas; the obstructed loop distends enormously. Venous obstruction occurs first, followed by arterial compromise, ischaemia, and ultimately perforation and faecal peritonitis if untreated.

CLINICAL FEATURES

Obstipation (no flatus or stool - often most prominent symptom)
Abdominal distension - massive, disproportionate (whole abdomen)
Colicky abdominal pain
Nausea and vomiting (late feature compared to small bowel obstruction)
Tachycardia, hypotension, fever with progressive disease
Peritonitis and sepsis if strangulation/perforation occurs

INVESTIGATIONS

1. Plain X-Ray Abdomen (erect + supine):

"Bent inner tube" / "Omega loop" sign or "coffee bean" sign in 60-75% of cases
Massively dilated sigmoid loop extending from pelvis to right upper quadrant
Absence of rectal gas
Two fluid levels in the volvulus loop

2. CT Abdomen (near 100% accuracy):

"Whirl sign" - twisting of mesenteric vessels
Paucity of rectal gas
Delineates ischaemia, perforation
Preferred when plain films non-diagnostic

3. Water-Soluble Contrast Enema:

"Bird's beak" or "ace of spades" deformity at site of torsion
Not always necessary if CT available

MANAGEMENT

Decision point: Is there peritonitis/ischaemia?

A. Stable patient without peritonitis/strangulation:

1. Endoscopic Detorsion (First line):

Flexible sigmoidoscopy preferred (rigid proctoscopy if flexible unavailable - higher perforation risk)
A "pinwheel" sign is seen at the point of torsion on endoscopy
Pass scope gently through torsed segment with insufflation
Success rate: 55-94%
Leave a flatus tube (soft red-rubber rectal tube) after detorsion for continued decompression and to prevent early recurrence

Note: Endoscopic detorsion is NOT definitive therapy. Recurrence occurs in 85-90% of cases without subsequent surgery.

2. Elective Surgery (after detorsion):

Performed 48-72 hours after detorsion once patient is optimised
Gold standard: Sigmoid colectomy with primary anastomosis (Hartmann's procedure or single-stage resection)
Colonic fixation (sigmopexy) historically used but high recurrence rate; not recommended routinely

B. Patient with peritonitis / strangulation / failure of endoscopic detorsion:

Emergency surgery required:

Hartmann's procedure: Sigmoid resection with end colostomy and rectal stump closure - safest in emergency; avoids anastomosis in contaminated/ischaemic field
Primary resection with anastomosis + covering ileostomy (in selected cases with acceptable risk)
Laparoscopic approach feasible in experienced hands

Post-operative care:

Reversal of Hartmann's procedure at 3-6 months if patient fit
Long-term: High-fibre diet, laxatives, treatment of underlying neurological/psychiatric conditions

Q.4 — Short Answer (20 Marks)

Q.4a - Tuberculosis of the Small Intestine (10 Marks)

INTRODUCTION

Intestinal tuberculosis is caused by Mycobacterium tuberculosis (or rarely M. bovis). It predominantly affects the ileocaecal region (terminal ileum + caecum) due to the abundance of lymphoid tissue (Peyer's patches) and relative stasis, which promotes bacterial lodgement. In the developing world (India, Africa) it is a common cause of intestinal obstruction. - Bailey & Love 28th Ed.

Route of Infection:

Swallowing of infected sputum in pulmonary TB (primary route)
Haematogenous spread from pulmonary focus
Ingestion of M. bovis in unpasteurised milk (rare now)

PATHOLOGICAL TYPES

Type	Features
Ulcerative	Multiple transverse ulcers in terminal ileum; risk of perforation and haemorrhage
Hyperplastic (hypertrophic)	Thickening of bowel wall, fibrosis, stricture formation; mass in RIF - may mimic Crohn's or carcinoma
Ulcerohypertrophic	Mixed pattern; most common overall
Miliary / Peritoneal	Tubercles on peritoneal surface; ascites

CLINICAL FEATURES

Chronic presentation:

Gradual onset over weeks to months
Constitutional symptoms: weight loss, malaise, evening/low-grade fever, night sweats, cough
GI symptoms: alternating constipation and diarrhoea, recurrent abdominal pain (periumbilical/right iliac fossa), distension
Examination: Doughy feel of the abdomen (characteristic), palpable mass in RIF (hyperplastic type), signs of malnutrition

Acute / Emergency presentation:

Subacute intestinal obstruction (most common surgical emergency): bilious vomiting, abdominal distension, absolute constipation - Bailey & Love 28th Ed.
Perforation of tuberculous ulcer: Peritonitis (rare, carries high mortality)
Fistula formation (entero-enteric, enterocutaneous)

INVESTIGATIONS

Blood:

Raised ESR, CRP
Anaemia (normocytic/normochromic)
Leucocytosis
Low albumin (nutritional)

Microbiological:

Sputum AFB smear and culture (30-50% have concurrent pulmonary TB)
Ascitic fluid culture (if ascites present)
Tissue culture from biopsy (gold standard - takes 6-8 weeks)
Interferon-gamma release assays (IGRAs) - QuantiFERON, T-SPOT.TB

Imaging:

Chest X-ray: Pulmonary infiltrates, cavities (essential investigation)
Barium meal and follow-through / Small bowel enema: Multiple small bowel strictures especially in ileum; subhepatic caecum pulled up; narrow ileum entering caecum from below upwards in a straight line (Stierlin's sign); shortened and rigid caecum
Ultrasound abdomen: Localised ascites, lymphadenopathy, bowel wall thickening, RIF mass
CT abdomen: Bowel wall thickening, lymphadenopathy (with central hypodense necrosis), mesenteric fat stranding
Colonoscopy + biopsy: Ileocaecal ulcers, nodularity; histology shows caseating granulomas (pathognomonic)
Laparoscopy: Tubercles on bowel serosa, multiple strictures, high caecum, caseating nodes, ascites (most definitive)

TREATMENT

Medical Treatment (Primary):

Anti-tubercular therapy (ATT): Standard 4-drug regimen (HRZE - Isoniazid, Rifampicin, Ethambutol, Pyrazinamide) for 2 months intensive phase, followed by 2-drug continuation phase (HR) for 4 months = 6 months total
Nutritional rehabilitation
Monitor for drug hepatotoxicity (especially INH, Rifampicin)

Surgical Treatment:

Elective (after completion of ATT):

Reimaging after treatment: residual strictures may need surgery
Ileocolic resection with anastomosis for ileocaecal hyperplastic disease
Strictureplasty for single ileal stricture (preserves bowel length)
Bowel resection for multiple closely placed strictures
Right hemicolectomy for extensive ileocolic disease
Principles: same as Crohn's disease - conservative resections, preserve bowel

Emergency surgery:

Patient often extremely ill: dehydration, malnutrition, anaemia, active pulmonary TB
Vigorous resuscitation precedes surgery
Minimum life-saving procedure: Resection of diseased segment + proximal ileostomy + distal mucus fistula (avoid primary anastomosis in contaminated, malnourished field)
One-stage resection and anastomosis only if general condition excellent
ATT started post-operatively; reversal of stoma at 3-6 months after disease control - Bailey & Love 28th Ed.

Q.4b - Classification of Wounds (10 Marks)

INTRODUCTION

Wounds are diverse and no single classification covers all clinical contexts. Multiple classification systems are used, and descriptors from more than one may be required to accurately characterise a wound. - Bailey & Love 28th Ed.

1. CLASSIFICATION BY MECHANISM / AETIOLOGY

Type	Description
Incised wound	Clean cut by a sharp instrument (knife, glass); minimal tissue destruction; heals well
Laceration	Tear caused by blunt force; irregular edges; more contamination
Contusion / Bruise	Blunt trauma without skin breach; haematoma formation
Abrasion / Graze	Superficial scraping of epidermis
Puncture / Stab wound	Small entry with deep penetration; risk of internal organ injury
Crush wound	Heavy force; extensive tissue damage; poor blood supply; high risk of infection
Degloving / Avulsion	Skin and subcutaneous tissue sheared from underlying fascia
Blast/Gunshot wounds	High-energy transfer; cavitation effect; extensive tissue damage
Burns	Thermal, chemical, electrical, radiation
Bite wounds	Human, animal; high contamination risk

2. CLASSIFICATION BY DEPTH

Depth	Layers Involved
Epidermal	Epidermis only (abrasions)
Dermal - superficial	Epidermis + superficial dermis
Dermal - deep	Deep dermis involved
Full thickness	All layers of skin and may include deeper structures

3. CLASSIFICATION BY CONTAMINATION (CDC / NRC Surgical Wound Classification)

(Most widely used in surgical practice; introduced by US National Research Council 1964, adapted by CDC)

Class	Category	Description
Class I	Clean	Uninfected operative wound; no respiratory/alimentary/urinary tract entered; primarily closed; no inflammation
Class II	Clean-contaminated	Respiratory/alimentary/genital/urinary tract entered under controlled conditions; no unusual contamination; no evidence of infection
Class III	Contaminated	Open fresh traumatic wounds; major breaks in sterile technique; gross GI spillage; acute non-purulent inflammation
Class IV	Dirty	Old traumatic wounds with devitalised tissue; existing clinical infection; perforated viscera

SSI risk: Class I: <2%, Class II: 3-11%, Class III: 10-17%, Class IV: >27%

4. CLASSIFICATION BY DURATION (Healing)

Acute wounds: Heal in a predictable manner and timeframe; by primary/secondary/tertiary intention. Become chronic if not healed after 4 weeks of treatment.
Chronic wounds: Vascular ulcers (venous, arterial), pressure ulcers, diabetic ulcers; impaired healing

5. CLASSIFICATION BY MECHANISM OF HEALING (Schwartz's Principles of Surgery)

Type	Definition	Example
Primary intention (1° closure)	Wound edges approximated immediately with sutures/staples/clips; minimal granulation	Clean surgical incision
Secondary intention	Wound left open to heal by granulation tissue, contraction, epithelialisation	Abscess cavity, wound infection
Tertiary intention (delayed primary closure)	Wound kept open for 3-5 days, then closed when clean; combines 1° and 2°	Contaminated traumatic wound, open abdominal wound

A fully healed wound achieves only 75-80% of normal tensile strength; maximum strength is reached at about 6 weeks. - Schwartz's Surgery 11th Ed.

6. CLASSIFICATION BY COMPLEXITY (Summary Box - Bailey & Love)

Simple: Uncomplicated, involving only skin
Complex: Significant soft-tissue loss, open fracture/joint, visceral involvement
Complicated: Infected, necrotic, haematoma, gas gangrene, compartment syndrome

NNIS RISK SCORE (National Nosocomial Infections Surveillance)

Predicts SSI risk - scored 0-3, one point each for:

Contaminated or dirty wound (Class III/IV)
ASA score ≥3
Operative time >75th percentile for procedure

References:

Bailey & Love's Short Practice of Surgery, 28th Edition
Schwartz's Principles of Surgery, 11th Edition
Current Surgical Therapy, 14th Edition (Cameron & Cameron)
Sabiston Textbook of Surgery, 21st Edition
Harrison's Principles of Internal Medicine, 22nd Edition
Sleisenger & Fordtran's Gastrointestinal & Liver DiseaseAll 6 questions are answered. Here is a quick guide to mark allocation so you can write proportionately in the exam:

Quick Mark Allocation Guide

Question	Sub-parts	Suggested word-count
Q1 (30 marks)	Anatomy 6 + Physiology 5 + Hypersplenism 5 + Causes 6 + Management 8	~2500 words + diagrams
Q2 (30 marks)	Aetiopathology 10 + Presentation 8 + Investigations 4 + Management 8	~2500 words + diagram of metabolic alkalosis
Q3a (10 marks)	Embryology+Rule of 2s 3 + Clinical presentations 4 + Investigations+Surgery 3	~800 words
Q3b (10 marks)	Definition+Causes 2 + Pathophysiology 2 + Features 2 + Investigations 2 + Management 2	~800 words
Q4a (10 marks)	Pathology types 2 + Clinical features 3 + Investigations 2 + Treatment 3	~800 words
Q4b (10 marks)	Mechanism classification 2 + CDC surgical classification (table) 4 + Depth 1 + Healing types 2 + NNIS 1	~700 words + table

Key diagrams to draw (as the paper instructs):

Q1: Anatomy of spleen, White/Red pulp histology
Q2: Metabolic alkalosis cycle; Billroth reconstructions
Q3a: Meckel's diverticulum anatomy (Rule of 2s labelled)
Q3b: Plain X-ray "omega loop" / "coffee bean" sign
Q4b: Table of CDC wound classification (Classes I-IV)

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