Surgery

Key Facts

Peritonitis is a critical surgical condition requiring prompt recognition, resuscitation, and usually surgical intervention. The distinction between primary and secondary peritonitis guides management.

Epidemiology

Secondary peritonitis is the most common form. SBP occurs in ~10-30% of hospitalised patients with ascites from liver cirrhosis. Peritonitis carries overall mortality of ~10-20% (higher in elderly, immunocompromised, and delayed presentation).

Aetiology

Primary (SBP): Haematogenous/lymphatic bacterial translocation - usually E. coli, Klebsiella, Streptococcus pneumoniae. Secondary: Perforation (appendicitis, peptic ulcer, diverticulitis, trauma, anastomotic leak), post-operative. Tertiary: Failed source control - Enterococcus, Candida, coagulase-negative staphylococci.

Pathophysiology

• Peritoneal membrane has large surface area (~1.7m²) - inflammation causes massive fluid shifts and cytokine release
• Fibrin deposition may localise infection (abscess) or lead to adhesion formation

Clinical Features

• Pain: Severe, constant, worsened by movement or coughing
• Guarding: Involuntary muscular rigidity - board-like in generalised peritonitis
• Rebound tenderness: Pain on releasing palpation
• Absent bowel sounds: Paralytic ileus
• Fever, tachycardia, tachypnoea: Systemic sepsis
• Lying still: Movement exacerbates peritoneal irritation
• Distension: From ileus and fluid accumulation

SBP (Primary)

• Often insidious in cirrhotic patients - may present as worsening ascites, encephalopathy, or renal failure
• Fever, abdominal pain/tenderness, altered mental status
• May be clinically silent - maintain high index of suspicion

Red Flags

• Board-like rigidity - generalised peritonitis, likely perforation
• Haemodynamic instability - septic shock requiring immediate resuscitation
• Absent bowel sounds with fever - late presentation
• Free air on erect CXR - perforation confirmed

Bedside

• Observations: NEWS2 - likely high-scoring
• Erect CXR: Free air under diaphragm
• Urine dipstick, β-hCG: Exclude urological/gynaecological cause

Bloods

• FBC, CRP: Leucocytosis, raised inflammatory markers
• U&Es, LFTs: Organ function
• Amylase/lipase: Exclude pancreatitis
• Lactate: Severity marker for sepsis (>4 mmol/L = severe)
• Blood cultures: Before antibiotics
• Coagulation, G&S/crossmatch: Pre-operative
• ABG/VBG: Acid-base status

Imaging

• CT abdomen/pelvis with IV contrast: Investigation of choice - identifies source, free fluid, free air
• Erect CXR: Quick screen for pneumoperitoneum

Special Tests

• Ascitic tap (SBP): WCC >250 neutrophils/mm³ confirms SBP; send for culture, albumin, protein

Initial Resuscitation (Sepsis 6)

1. High-flow oxygen
2. Blood cultures
3. IV antibiotics: Co-amoxiclav 1.2g IV TDS + metronidazole 500mg IV TDS (or piperacillin-tazobactam 4.5g IV TDS per local protocol)
4. IV crystalloid fluid resuscitation
5. Lactate measurement
6. Urine output monitoring (catheter)

Surgical Management (Secondary Peritonitis)

• Source control is paramount - laparotomy or laparoscopy
• Repair perforation (e.g., omental patch for perforated peptic ulcer)
• Resection of diseased segment (e.g., perforated appendix, sigmoid colon)
• Peritoneal washout with warm saline
• May require temporary stoma (e.g., Hartmann's procedure for perforated diverticulitis)
• Planned relook laparotomy in severe cases

SBP Management

• IV cefotaxime 2g TDS (or co-amoxiclav) - 5-7 days
• IV albumin 1.5g/kg at diagnosis, 1g/kg at day 3 (reduces mortality - Sort & Levacher trial)
• Prophylaxis with ciprofloxacin 500mg OD or norfloxacin after SBP episode (secondary prophylaxis)

Referral Criteria

• All secondary peritonitis - urgent surgical team
• ICU referral for organ support
• SBP - hepatology/gastroenterology

• Secondary peritonitis: Mortality ~10-20% with timely surgery; increases to >50% if delayed
• SBP: In-hospital mortality ~20-30%; 1-year mortality ~50-70% (reflects underlying liver disease severity)
• Anastomotic leak: Mortality ~10-20%
• Elderly and immunocompromised patients have significantly higher mortality
• Post-operative adhesions are a common long-term complication

Causes of Pneumoperitoneum

Key Facts

Appendicitis remains the most common cause of an acute abdomen requiring surgery. Early recognition and surgery reduce the risk of perforation and its complications.

Epidemiology

Lifetime risk ~7-8%. Incidence ~100 per 100,000/year. Peak age 10-30 years. Slightly more common in males (M:F ~1.4:1). Perforation rate increases in children under 5 (~80-100%) and elderly (>50%).

Aetiology

• Luminal obstruction: Faecolith (~30-40%), lymphoid hyperplasia (children), tumour (elderly - caecal carcinoma), parasites

Pathophysiology

• Bacterial translocation (E. coli, Bacteroides) → transmural inflammation
• Periumbilical pain (visceral - T10 dermatome) → localises to RIF (somatic - parietal peritoneal irritation)

Classic Presentation

• Periumbilical pain (visceral) migrating to RIF over 12-24 hours
• Anorexia (almost universal - absence should raise doubt)
• Nausea ± vomiting (usually after pain onset)
• Low-grade fever (37.5-38.5°C)

Examination Findings

• RIF tenderness - maximal at McBurney's point
• Guarding: Voluntary initially → involuntary with peritonitis
• Rovsing's sign: LIF palpation → RIF pain
• Psoas sign: Pain on passive extension of right hip (retrocaecal appendix)
• Obturator sign: Pain on internal rotation of flexed right hip (pelvic appendix)

Atypical Presentations

• Retrocaecal: Back/flank pain, minimal anterior signs, positive psoas sign
• Pelvic: Suprapubic pain, diarrhoea, urinary frequency
• Pregnancy: RUQ pain (displaced appendix in third trimester)
• Elderly: Late presentation, vague pain, higher perforation rate

Red Flags

• Generalised peritonism - likely perforation
• Mass in RIF - appendix abscess or mass
• Elderly with appendicitis - exclude caecal carcinoma (colonoscopy at follow-up)

Bedside

• Observations: Temperature, HR, BP
• Urine dipstick: Exclude UTI; mild pyuria can occur with pelvic appendicitis
• β-hCG: All women of reproductive age

Bloods

• FBC: Leucocytosis (WCC 10-15 × 10⁹/L typical; >15 suggests perforation/abscess)
• CRP: Raised (>10 in most; >100 suggests complicated appendicitis)
• U&Es: Dehydration assessment
• LFTs, amylase: Exclude biliary/pancreatic pathology

Imaging

• CT abdomen/pelvis: Investigation of choice in adults (sensitivity ~98%, specificity ~95%)
  • Findings: Dilated appendix >6mm, periappendiceal fat stranding, faecolith, abscess
• Ultrasound: First-line in children and pregnant women (non-compressible appendix >6mm, target sign)
• MRI: Alternative in pregnancy if US non-diagnostic

Non-pharmacological

• NBM, IV fluids, analgesia
• VTE prophylaxis: LMWH

Surgical (Definitive)

• Laparoscopic appendicectomy: Gold standard
  • Lower wound infection rate, faster recovery, diagnostic advantage in women
  • Histology of all specimens - exclude carcinoid, adenocarcinoma
• Open appendicectomy: If laparoscopic not available; Lanz incision (cosmetic) or gridiron incision
• Appendix mass/abscess: Consider initial conservative management (IV antibiotics, percutaneous drainage) → interval appendicectomy at 6-8 weeks

Pharmacological

• Antibiotics: Co-amoxiclav 1.2g IV (pre-operative prophylaxis); continue if complicated appendicitis
• Analgesia: IV paracetamol 1g + IV morphine titrated to effect
• Antiemetics: IV ondansetron 4mg

Referral Criteria

• All suspected appendicitis - surgical team
• Elderly - ensure caecal carcinoma excluded (colonoscopy within 6 weeks if >40 years or atypical)

• Simple appendicitis: Mortality <0.1%; morbidity ~5% (wound infection)
• Perforated appendicitis: Mortality ~1-2%; morbidity ~20-30% (abscess, wound infection, adhesions)
• Perforation risk: Increases after 36-48 hours of symptoms
• Negative appendicectomy rate: ~10-15% (acceptable; balanced against missing diagnosis)
• Appendiceal carcinoid: Found in ~0.5% of specimens; >2cm → right hemicolectomy

Modified Alvarado Score (MANTRELS)

Key Facts

Bowel obstruction is a common surgical emergency. The key clinical decision is whether to manage conservatively or operatively, based on the cause and presence of complications.

Epidemiology

SBO accounts for ~20% of acute surgical admissions. LBO is less common but more frequently requires surgical intervention. Adhesional SBO has a high recurrence rate (~20-30%).

Aetiology

Small bowel obstruction:

• Adhesions (~60-75%) - from previous surgery
• Hernias (~15%) - inguinal, femoral (especially in elderly women)
• Crohn's disease strictures
• Malignancy
• Intussusception (children), gallstone ileus (elderly)

Large bowel obstruction:

• Colorectal cancer (~60%)
• Diverticular disease/stricture (~15%)
• Volvulus (~10%) - sigmoid (most common) or caecal

Pathophysiology

• Fluid sequestration into bowel lumen → dehydration, electrolyte imbalance

• Vomiting (early in proximal SBO, late in distal/LBO) → metabolic alkalosis with hypokalaemia

Small Bowel Obstruction

• Colicky central abdominal pain
• Early, profuse vomiting (may be bilious)
• Distension (moderate)
• Absolute constipation (may pass flatus/stool initially)
• Visible peristalsis (thin patients)
• High-pitched, tinkling bowel sounds

Large Bowel Obstruction

• Colicky lower abdominal pain
• Late vomiting (may become faeculent)
• Marked distension
• Early absolute constipation
• Resonant percussion

Sigmoid Volvulus

• Elderly, institutionalised, psychiatric patients, chronic constipation
• Massive distension ('coffee bean' sign on AXR)
• Treatment: Flexible sigmoidoscopic decompression → elective sigmoid colectomy

Red Flags (Strangulation)

• Constant (not colicky) pain - suggests ischaemia
• Peritonism (guarding, rebound)
• Fever, tachycardia
• Raised lactate
• Irreducible, tender hernia

Bedside

• Observations: NEWS2
• NG tube: Decompress stomach, monitor aspirate volume
• Fluid balance: Strict input/output

Bloods

• FBC: WCC (strangulation/perforation)
• U&Es: Dehydration, hypokalaemia, metabolic alkalosis (vomiting)
• LFTs: Exclude biliary pathology
• Lactate: Raised in strangulation/ischaemia (>2 mmol/L concerning)
• ABG/VBG: Acid-base, lactate
• G&S: Pre-operative

Imaging

• AXR: Small bowel >3cm dilated; large bowel >6cm; caecum >9cm (perforation risk)
• CT abdomen/pelvis with IV contrast: Investigation of choice - identifies level, cause, transition point, strangulation, perforation
• Water-soluble contrast follow-through (Gastrografin): Via NG tube in adhesional SBO - therapeutic (osmotic) and prognostic (if contrast reaches caecum by 24 hours → likely to resolve conservatively)

Conservative ('Drip and Suck')

• NG tube: Decompression - reduce vomiting, prevent aspiration
• IV fluids: Aggressive resuscitation (0.9% NaCl with KCl supplementation)
• NBM
• Urinary catheter: Monitor urine output
• VTE prophylaxis: LMWH
• Appropriate for adhesional SBO without signs of strangulation
• Reassess clinically and with AXR/CT at 24-48 hours

Gastrografin Challenge

• 100mL Gastrografin via NG tube
• AXR at 4-6 hours - if contrast in caecum, likely to resolve
• If no progress by 24 hours - consider surgery

Surgical

Indications for surgery:

• Strangulation (peritonism, raised lactate, constant pain)
• Closed-loop obstruction
• Hernia obstruction (irreducible)
• Failed conservative management (no improvement at 48-72 hours)
• LBO from cancer - resection ± stoma
• Sigmoid volvulus - sigmoidoscopic decompression → elective sigmoid colectomy

Procedures:

• Adhesiolysis (laparoscopic or open)
• Bowel resection if gangrenous
• Stoma if unsafe for primary anastomosis

Referral Criteria

• All suspected bowel obstruction - surgical team
• LBO - likely to need surgery; colorectal cancer pathway if appropriate
• Strangulation - emergency surgery

• Adhesional SBO: ~75% resolve with conservative management; recurrence ~20-30%
• Strangulated SBO: Mortality ~10-20% - increases with delayed surgery
• LBO from cancer: Depends on cancer stage - emergency surgery has higher morbidity than elective
• Sigmoid volvulus: Recurrence rate ~50-60% without definitive surgery; endoscopic decompression success ~80%
• Overall mortality: SBO ~3-5%; LBO ~10-15% (higher due to cancer and older population)

SBO vs LBO Comparison

Key Facts

Inguinal hernias are extremely common and represent a significant surgical workload. Understanding the anatomy of the inguinal canal is essential for diagnosis and surgical management.

Epidemiology

Lifetime risk ~27% in men, ~3% in women. ~70,000 inguinal hernia repairs performed annually in England. Peak incidence: Infants (indirect) and men aged 40-60 (direct). Indirect:direct ratio ~2:1.

Aetiology

Indirect: Patent processus vaginalis (congenital) or acquired; passes through deep ring lateral to inferior epigastric vessels. Direct: Weakness in posterior wall of inguinal canal (Hesselbach's triangle); acquired - chronic raised intra-abdominal pressure. Risk factors: Male sex, increasing age, chronic cough, constipation, prostatism (straining), heavy lifting, obesity, previous surgery, connective tissue disorders.

Pathophysiology

• Inguinal canal: Runs from deep ring (midpoint of inguinal ligament) to superficial ring (above pubic tubercle)
• Contents: Spermatic cord (males) or round ligament (females)
• Hesselbach's triangle: Bounded by inferior epigastric artery (lateral), rectus sheath (medial), inguinal ligament (inferior)
• Direct hernias protrude through this triangle; indirect hernias pass lateral to it through the deep ring

Typical Presentation

• Groin lump: Increases with coughing, straining, standing; reduces when lying down
• May be asymptomatic or cause dragging/aching discomfort
• Lump above and medial to pubic tubercle (inguinal) - below and lateral = femoral
• Cough impulse: Palpable expansion on coughing

Indirect vs Direct

• Indirect: May descend into scrotum; controlled by pressure over deep ring; more common in young males
• Direct: Rarely enters scrotum; not controlled by deep ring pressure; bulge appears on standing, reduces on lying; older males

Complications

• Irreducibility: Cannot reduce contents - often omentum
• Incarceration: Contents trapped - risk of obstruction
• Obstruction: Bowel trapped → colicky abdominal pain, vomiting, constipation
• Strangulation: Blood supply compromised → bowel ischaemia/necrosis - surgical EMERGENCY (tenderness, erythema over hernia, systemic sepsis)

Red Flags

• Tender, irreducible hernia with vomiting - strangulation until proven otherwise
• Overlying skin erythema or peritonitis - bowel may be gangrenous
• Signs of bowel obstruction - emergency surgery required

Bedside

• Clinical diagnosis in most cases
• Examine standing and lying; cough impulse; attempt reduction; deep ring occlusion test
• Check contralateral groin

Imaging (if diagnostic uncertainty)

• Ultrasound: Useful for occult hernias (groin pain without obvious lump)
• CT abdomen/pelvis: If complicated hernia, incarceration, or obstruction
• MRI: Occasionally for complex or recurrent hernias

Conservative

• Watchful waiting: Option for asymptomatic/minimally symptomatic direct hernias in patients with significant comorbidities
• Trusses are NOT recommended - do not prevent complications and delay definitive treatment

Surgical (Definitive)

Open repair:

• Lichtenstein tension-free mesh repair: Gold standard; local/regional/GA; recurrence <2%
• Mesh placed to reinforce posterior wall of inguinal canal

Laparoscopic repair:

• TEP (Totally Extraperitoneal): Preperitoneal mesh placement without entering peritoneal cavity
• TAPP (Transabdominal Preperitoneal): Enters peritoneal cavity, mesh placed preperitoneally
• Advantages: Faster recovery, less chronic pain, better for bilateral/recurrent hernias
• NICE IPG252 supports laparoscopic repair

Emergency

• Strangulated/incarcerated hernia: Emergency surgery
• Resuscitate, IV antibiotics (co-amoxiclav 1.2g IV)
• Emergency repair with possible bowel resection if gangrenous

Referral Criteria

• All symptomatic inguinal hernias - surgical referral for repair
• Irreducible hernia - urgent referral
• Incarcerated/strangulated - emergency admission

• Mesh repair: Recurrence rate ~1-2%
• Laparoscopic: Slightly lower chronic pain rates than open (~5% vs ~10%)
• Chronic groin pain: Occurs in ~5-12% after repair - nerve entrapment (ilioinguinal, iliohypogastric, genital branch of genitofemoral)
• Mesh infection: ~1-2% - may require mesh removal
• Strangulated hernia: Mortality ~2-5% - higher in elderly and if bowel resection required
• Without repair: Annual risk of strangulation ~0.5-3%

Inguinal Canal Anatomy

Indirect vs Direct

Key Facts

Femoral hernias are less common than inguinal hernias but carry a much higher risk of strangulation. All femoral hernias should be repaired without delay.

Epidemiology

Femoral hernias account for ~5% of all groin hernias. More common in women (F:M ~4:1), elderly, multiparous women. However, inguinal hernias remain the commonest groin hernia in both sexes.

Aetiology

• Weakness at the femoral ring - below the inguinal ligament, medial to the femoral vein
• Risk factors: Female sex, multiparity, increased intra-abdominal pressure, previous inguinal hernia repair

Pathophysiology

• Abdominal contents (usually omentum or bowel) protrude through the femoral ring into the femoral canal
• Narrow, rigid boundaries of femoral canal (lacunar ligament medially) → high risk of incarceration and strangulation
• Richter's hernia: Only the antimesenteric border of bowel herniates → can strangulate and perforate without causing classic bowel obstruction

Typical Presentation

• Small, firm lump in the groin - below and lateral to the pubic tubercle
• May be difficult to detect clinically, especially in obese patients
• Often presents as an emergency with incarceration or strangulation

Examination

• Lump in femoral triangle below the inguinal ligament
• Non-reducible in many cases
• No cough impulse (if incarcerated)
• Distinguish from inguinal hernia by relationship to pubic tubercle

Red Flags

• Tender, irreducible femoral hernia - strangulation until proven otherwise
• Signs of bowel obstruction - colicky pain, vomiting, constipation
• Overlying skin changes (erythema, warmth) - bowel necrosis
• Richter's hernia - may present with localised peritonitis without frank obstruction

Bedside

• Clinical examination: Position relative to pubic tubercle is key
• Examine patient standing and lying

Bloods

• FBC, CRP, U&Es, lactate: If strangulation/obstruction suspected
• G&S: Pre-operative

Imaging

• CT abdomen/pelvis: If diagnostic uncertainty or suspected complication (obstruction, strangulation)
• Ultrasound: May identify hernia contents and vascularity

Surgical (All Femoral Hernias Should Be Repaired)

Elective:

• Low (Lockwood/crural) approach: Below inguinal ligament; simple, can be done under local
• High (McEvedy/preperitoneal) approach: Preferred for emergency; better access for bowel assessment and resection
• Laparoscopic (TEP/TAPP): Can be performed; offers advantage of bilateral repair
• Mesh repair where feasible (reduces recurrence)

Emergency:

• Strangulated femoral hernia = emergency surgery
• McEvedy approach preferred - allows assessment of bowel viability and resection if needed
• Do NOT attempt blind reduction - necrotic bowel may be returned to abdomen
• IV fluids, NG tube if obstructed, IV antibiotics (co-amoxiclav 1.2g)

Referral Criteria

• All femoral hernias - urgent surgical referral for repair (even if asymptomatic due to high strangulation risk)
• Suspected strangulation - emergency surgery

• Strangulation rate: ~30% - significantly higher than inguinal hernias (~1-3%)
• Emergency repair mortality: ~5-10% (much higher than elective <1%)
• Recurrence: ~2-5% after mesh repair
• Bowel resection required: In ~30-40% of emergency femoral hernia repairs
• Outcomes significantly better with elective repair → all femoral hernias should be repaired promptly

Inguinal vs Femoral Hernia

Key Facts

Incisional hernias are a common and significant complication of abdominal surgery. Prevention through optimal wound closure technique and post-operative care is paramount.

Epidemiology

Affects ~10-15% of all laparotomy wounds. Incidence is higher after emergency surgery (~23%), wound infection (~30%), and obesity. Most develop within 1-3 years of surgery but can present decades later.

Aetiology

Risk factors:

• Surgical: Wound infection (strongest modifiable factor), vertical midline incision, emergency surgery, re-operation, drain sites
• Patient: Obesity, malnutrition, diabetes, smoking, chronic cough/COPD, immunosuppression, connective tissue disorders, age >60
• Technical: Inadequate closure technique, inappropriate suture material

Pathophysiology

• Failure of fascial healing at the surgical incision site
• Increased intra-abdominal pressure (obesity, chronic cough, ascites) exacerbates defect
• Progressive enlargement over time as abdominal contents herniate through the defect

Typical Presentation

• Bulge at previous surgical incision, increasing with standing/straining
• Reducible in most cases
• May be asymptomatic or cause pain, dragging sensation
• Cosmetic concern, especially with large hernias

Complications

• Skin complications over large hernias (ulceration, dermatitis)
• Respiratory compromise with very large hernias (loss of domain)

Red Flags

• Tender, irreducible incisional hernia - strangulation
• Signs of bowel obstruction
• Overlying skin changes - compromise of contents

Bedside

• Clinical examination: Usually diagnostic; examine lying and standing

Imaging

• CT abdomen: Defines defect size, contents, complications, loss of domain
• Ultrasound: If clinical uncertainty
• CT is essential for surgical planning in large or complex hernias

Conservative

• Watchful waiting: For asymptomatic small hernias in high-risk surgical patients
• Abdominal binder: Symptomatic relief; does not prevent enlargement or complications
• Optimise risk factors: Weight loss, smoking cessation, glycaemic control, treat chronic cough

Surgical

• Mesh repair is superior to primary suture repair
  • Open mesh repair: Onlay, sublay (retromuscular - Rives-Stoppa), or underlay (intraperitoneal)
  • Sublay (retromuscular) placement has lowest recurrence rate
  • Laparoscopic repair (IPOM - intraperitoneal onlay mesh): Lower wound infection, faster recovery; NICE IPG134
• Component separation: For large hernias with loss of domain - allows tension-free closure
• Botulinum toxin A: Pre-operative injection to relax lateral abdominal wall muscles → aids closure of large defects (progressive pneumoperitoneum is an alternative)

Emergency

• Strangulated incisional hernia → emergency surgery, possible bowel resection

Referral Criteria

• Symptomatic incisional hernia - surgical referral
• Enlarging hernia - surgical referral
• Complicated hernia - emergency surgery

• Mesh repair recurrence: ~10-15% (vs ~30-50% for primary suture repair)
• Surgical site infection: ~5-10% (mesh-related)
• Chronic pain: ~5-10% post-repair
• Loss of domain: Complex surgical challenge; higher morbidity
• Prevention: Optimal primary wound closure technique is the most effective strategy

Jenkins Rule for Laparotomy Closure

Key Facts

Gallstone disease is extremely common and represents one of the largest surgical workloads in the UK. Understanding the spectrum from asymptomatic stones to life-threatening complications is essential.

Epidemiology

Prevalence ~10-15% in Western populations. Only ~20-30% become symptomatic over a lifetime. Annual risk of symptoms from asymptomatic stones: ~1-4%. Cholecystectomy is one of the most common elective operations (~70,000/year in England).

Aetiology

Cholesterol stones (~80%): Supersaturation of bile with cholesterol, reduced bile salt concentration, gallbladder stasis. Pigment stones: Black (haemolysis - sickle cell, hereditary spherocytosis); Brown (biliary infection/stasis - found in CBD). Risk factors: Obesity, female sex, age >40, multiparity, rapid weight loss, TPN, fibrates, OCP/HRT, Crohn's disease (terminal ileum - bile salt malabsorption).

Pathophysiology

• Stone impaction in cystic duct → biliary colic (obstruction without infection) or cholecystitis (obstruction + infection)

• Charcot's triad: RUQ pain + fever + jaundice (cholangitis)
• Reynold's pentad: Charcot's triad + confusion + hypotension (suppurative cholangitis - septic shock)

Biliary Colic

• RUQ/epigastric pain (constant, not truly colicky), often post-prandial (fatty food)
• Duration 30 minutes to 6 hours
• May radiate to right shoulder/interscapular region
• No fever, normal WCC/CRP
• Self-limiting once stone disimpacts from cystic duct

Acute Cholecystitis

• RUQ pain + fever + raised WCC/CRP
• Murphy's sign positive: Arrest of inspiration on RUQ palpation
• May have palpable gallbladder (not in chronic cholecystitis - fibrosed)
• Mild derangement of LFTs possible

Choledocholithiasis (CBD Stones)

• Obstructive jaundice (dark urine, pale stools, pruritis)
• Raised bilirubin, ALP, GGT; dilated CBD on US (>6mm)

Ascending Cholangitis

• Charcot's triad: RUQ pain, jaundice, fever/rigors
• Medical emergency - requires urgent ERCP and biliary drainage

Red Flags

• Reynold's pentad - suppurative cholangitis, septic shock
• Generalised peritonism - gallbladder perforation
• Gallstone pancreatitis - raised amylase/lipase

Bedside

• Observations: Temperature, HR, BP

Bloods

• FBC, CRP: Raised WCC/CRP in cholecystitis/cholangitis
• LFTs: Raised bilirubin/ALP/GGT suggests CBD stone; raised ALT in gallstone pancreatitis
• Amylase/lipase: >3× ULN suggests pancreatitis
• Blood cultures: If cholangitis suspected
• Coagulation: If jaundiced (vitamin K-dependent factors may be reduced)

Imaging

• Ultrasound abdomen (first-line): Gallstones, gallbladder wall thickening (>3mm = cholecystitis), CBD dilatation (>6mm)
• MRCP: Non-invasive imaging of biliary tree - for suspected CBD stones
• ERCP: Therapeutic - stone extraction, sphincterotomy, stenting
• CT abdomen: If complications suspected (perforation, abscess, pancreatitis)
• HIDA scan: If acalculous cholecystitis suspected (functional biliary disease)

Biliary Colic

• Analgesia: IM diclofenac 75mg (first-line - more effective than opioids for biliary colic) or IV paracetamol
• Elective laparoscopic cholecystectomy: Definitive treatment; within 6 weeks

Acute Cholecystitis

• IV antibiotics: Co-amoxiclav 1.2g TDS or piperacillin-tazobactam 4.5g TDS
• IV fluids, analgesia, NBM
• Laparoscopic cholecystectomy: Ideally within 1 week of presentation ('hot cholecystectomy') - reduces total hospital stays and complications (CholeS study)
• If unfit for surgery: Percutaneous cholecystostomy (drainage)

CBD Stones

• ERCP: Sphincterotomy and stone extraction → followed by cholecystectomy
• Laparoscopic bile duct exploration: Alternative in experienced centres

Cholangitis

• Sepsis 6 pathway: Antibiotics, fluids, cultures
• Urgent ERCP (within 24 hours) for biliary drainage

Referral Criteria

• Symptomatic gallstones - surgical referral for cholecystectomy
• CBD stones/cholangitis - urgent gastroenterology/surgery for ERCP
• Gallstone pancreatitis - cholecystectomy during same admission or within 2 weeks

• Cholecystectomy: Mortality <0.5%; bile duct injury ~0.3-0.5% (most feared complication)
• Biliary colic: ~70% will have recurrent episodes; ~1-3% annual risk of cholecystitis
• Acute cholecystitis: Mortality ~1% overall; higher in elderly and complicated cases
• Cholangitis: Mortality ~5-10% if treated promptly; higher if delayed
• Post-cholecystectomy syndrome: ~10-40% have persistent dyspepsia or diarrhoea

Complications of Gallstones

Key Facts

Acute pancreatitis has a wide spectrum of severity. Early aggressive fluid resuscitation and identification of aetiology are the cornerstones of management.

Epidemiology

Incidence ~30-40 per 100,000/year in UK. Increasing incidence due to rising rates of gallstones and alcohol consumption. Male predominance for alcohol-related cases. Overall mortality ~5%; severe necrotising pancreatitis mortality ~15-30%.

Aetiology

GET SMASHED:

• Gallstones (~50%)
• Ethanol (~25%)
• Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hyperlipidaemia/Hypothermia/Hypercalcaemia, ERCP, Drugs (azathioprine, valproate, mesalazine)
• Idiopathic ~10-20%

Pathophysiology

• Release of inflammatory mediators → local and systemic inflammatory response
• Severe cases: Pancreatic necrosis, peripancreatic fluid collections, organ failure (lung, kidney, cardiovascular)
• Fat necrosis → hypocalcaemia (calcium saponification)

Classic Presentation

• Epigastric pain radiating straight through to the back
• Constant, severe, worsened by lying flat, relieved by sitting forward
• Nausea and vomiting
• Abdominal tenderness with guarding

Examination Findings

• Epigastric tenderness ± generalised peritonism
• Reduced bowel sounds (paralytic ileus)
• Tachycardia, hypotension, fever (in severe cases)
• Grey Turner's sign: Flank bruising (retroperitoneal haemorrhage) - rare, late sign
• Cullen's sign: Periumbilical bruising - rare, late sign

Red Flags (Severe Pancreatitis)

• Persistent organ failure >48 hours (Revised Atlanta Classification: Severe)
• CRP >150 at 48 hours
• Modified Glasgow score ≥3
• Evidence of pancreatic necrosis on CT
• Respiratory failure (ARDS)
• Shock requiring vasopressors

Bedside

• Observations: NEWS2
• ABG/VBG: PaO₂, lactate, glucose, calcium
• ECG: Exclude MI

Bloods

• Amylase/lipase: >3× ULN diagnostic (lipase preferred - more specific and sustained)
• FBC, CRP: WCC, CRP >150 at 48h suggests severe
• U&Es: Renal function, dehydration
• LFTs: ALT >3× ULN suggests gallstone aetiology
• Calcium: May be low (fat saponification - poor prognostic sign)
• Glucose: May be elevated (endocrine dysfunction)
• Triglycerides: If >10 mmol/L, consider as cause
• G&S/crossmatch: If haemorrhagic pancreatitis suspected

Imaging

• US abdomen: First-line - assess for gallstones, CBD dilatation
• CT abdomen with IV contrast: At 72-96 hours if severe (assess necrosis - Balthazar score); or earlier if diagnostic uncertainty
• MRCP: If CBD stones suspected and not seen on US

Initial Management

• Aggressive IV fluid resuscitation: Goal-directed (Ringer's lactate preferred); target UO >0.5 mL/kg/hr
• Analgesia: IV paracetamol + opioids (morphine or PCA); avoid NSAIDs (renal risk)
• NBM initially → early enteral nutrition (within 24-48 hours via NG/NJ tube if not tolerating orally) - reduces infection and mortality vs TPN
• VTE prophylaxis: LMWH
• Catheter: Monitor urine output
• Avoid prophylactic antibiotics - only if confirmed/suspected infected necrosis

Specific Management

Gallstone pancreatitis:

• ERCP within 72 hours if concurrent cholangitis or persistent biliary obstruction
• Cholecystectomy during same admission or within 2 weeks (reduces recurrence)

Necrotising pancreatitis:

• If infected necrosis (gas in necrosis on CT, positive FNA culture, clinical deterioration):
  • Step-up approach (PANTER trial): Percutaneous/endoscopic drainage → video-assisted retroperitoneal debridement (VARD) or endoscopic necrosectomy if drainage insufficient
  • Antibiotics: Meropenem 1g IV TDS or piperacillin-tazobactam

Referral Criteria

• All acute pancreatitis - surgical/gastroenterology team
• Severe pancreatitis - HDU/ICU for organ support
• Necrotising pancreatitis with infection - specialist hepatobiliary/pancreatic unit

• Mild (no organ failure): Mortality <1%; most resolve within 1 week
• Moderate (transient organ failure <48h): Mortality ~5%
• Severe (persistent organ failure >48h): Mortality ~15-30%
• Infected necrosis: Mortality ~20-30% (doubles compared to sterile necrosis)
• Gallstone pancreatitis recurrence: ~30-50% without cholecystectomy
• Long-term: Risk of chronic pancreatitis (~10% after severe episode), diabetes, exocrine insufficiency

Modified Glasgow (Imrie) Score

Revised Atlanta Classification (2012)

Key Facts

Pancreatic cancer is the 10th most common cancer but the 5th leading cause of cancer death in the UK. Late presentation and aggressive biology contribute to its dismal prognosis.

Epidemiology

Incidence ~10,000 new cases/year in UK. Peak age 60-80 years. Slight male predominance (M:F ~1.3:1). Incidence is increasing. Lifetime risk ~1.5%.

Aetiology

• Smoking: Strongest modifiable risk factor (~2× increased risk)
• Chronic pancreatitis: ~5-10× increased risk (especially hereditary pancreatitis)
• Diabetes mellitus: Both risk factor and consequence (~50% of patients have new-onset DM at diagnosis)
• Obesity: ~20% increased risk
• Genetic: BRCA2 (~3-10× risk), Lynch syndrome, Peutz-Jeghers syndrome (~132× risk), familial atypical multiple mole melanoma (FAMMM)
• Alcohol: Indirect risk via chronic pancreatitis

Pathophysiology

• Pancreatic ductal adenocarcinoma: Arises from ductal epithelium; dense desmoplastic stroma limits drug penetration
• Key mutations: KRAS (~95%), TP53 (~75%), CDKN2A (~95%), SMAD4 (~55%)
• Precursor lesions: Pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), mucinous cystic neoplasm
• Head tumours obstruct CBD early → jaundice; body/tail tumours present late with pain and weight loss

Head of Pancreas (~60-70%)

• Painless obstructive jaundice: Dark urine, pale stools, pruritus
• Courvoisier's sign: Palpable, non-tender gallbladder in jaundiced patient
• Weight loss, anorexia
• New-onset diabetes mellitus
• Steatorrhoea (exocrine insufficiency)

Body/Tail (~30-40%)

• Back pain: Constant, dull, often worse lying down, better sitting forward
• Weight loss (marked)
• Presents late - often metastatic at diagnosis

Red Flags/Late Signs

• Trousseau's sign: Migratory thrombophlebitis - paraneoplastic
• Virchow's node (left supraclavicular lymphadenopathy)
• Sister Mary Joseph nodule (periumbilical metastasis)
• Ascites (peritoneal metastases)
• New-onset diabetes in patient >50 with weight loss - investigate for pancreatic cancer

Bloods

• LFTs: Obstructive pattern (raised bilirubin, ALP, GGT; mildly raised ALT/AST)
• CA 19-9: Elevated in ~80% (poor screening tool; useful for monitoring treatment response)
• FBC: Anaemia (chronic disease)
• HbA1c/glucose: New-onset diabetes
• Coagulation: May be deranged (vitamin K malabsorption from biliary obstruction)

Imaging

• CT pancreas (triple-phase): Investigation of choice - assessment of tumour size, vascular involvement (SMA, coeliac axis, portal vein/SMV), liver metastases, peritoneal disease
• MRCP: Biliary and pancreatic duct anatomy
• EUS (Endoscopic Ultrasound): FNA biopsy; best for small tumours; assesses vascular invasion
• PET-CT: If equivocal metastatic disease
• Staging laparoscopy: Before surgery - detects peritoneal metastases not visible on CT (~15-20%)

Special Tests

• ERCP: Therapeutic - biliary stenting for jaundice relief (if not proceeding to immediate surgery)
• Biopsy: EUS-FNA (tissue diagnosis for non-resectable disease before chemotherapy)

Surgical (Resectable Disease - ~10-20%)

• Head of pancreas: Whipple's procedure (pancreaticoduodenectomy) - resection of head of pancreas, duodenum, distal CBD, gallbladder, ± distal stomach
  • Perioperative mortality ~2-5% in specialist centres
  • Should be performed in high-volume centres
• Body/tail: Distal pancreatectomy ± splenectomy
• Adjuvant chemotherapy: Gemcitabine + capecitabine for 6 months (ESPAC-4 trial - median survival 28 months vs 25.5 months)

Non-Surgical

• Borderline resectable: Neoadjuvant chemotherapy (FOLFIRINOX) to downstage → reassess for surgery
• Locally advanced (unresectable): Chemotherapy (FOLFIRINOX or gemcitabine + nab-paclitaxel)
• Metastatic: Palliative chemotherapy - FOLFIRINOX (fit patients) or gemcitabine + nab-paclitaxel; median survival ~6-11 months
• Biliary stenting (ERCP): For jaundice palliation
• Palliative care: Early involvement - pain management (coeliac plexus block), nutrition (CREON for exocrine insufficiency), psychology

Referral Criteria

• Suspected pancreatic cancer - urgent 2WW referral (NICE NG12)
• MDT discussion at specialist HPB centre
• New-onset diabetes >50 with weight loss - urgent investigation

• Overall 5-year survival: ~7%
• Resected (Whipple's): Median survival ~20-28 months; 5-year survival ~15-20%
• Locally advanced: Median survival ~10-14 months
• Metastatic: Median survival ~3-6 months (without chemotherapy); ~6-11 months with FOLFIRINOX
• Adjuvant chemotherapy (ESPAC-4): Improves median survival by ~2.5 months
• 10-year survivors: Very rare - long-term cure is uncommon

Whipple's Procedure - What Is Resected

Key Trials

Key Facts

Colorectal cancer is a major public health challenge. The national bowel cancer screening programme has significantly improved early detection and outcomes.

Epidemiology

~42,000 new cases annually in UK. Lifetime risk ~5-6%. Peak age 60-80 years. Slight male predominance (M:F ~1.2:1). Incidence increasing in younger adults (<50).

Aetiology

• Microsatellite instability pathway: DNA mismatch repair deficiency (Lynch syndrome)

Risk factors:

• Age >50, family history (first-degree relative = 2-3× risk), IBD (UC > Crohn's)
• Lynch syndrome (HNPCC): Autosomal dominant; ~3-5% of CRC; MLH1, MSH2, MSH6, PMS2 mutations
• FAP: APC gene; >100 polyps; near 100% CRC risk by age 40 without prophylactic colectomy
• Modifiable: Red/processed meat, obesity, physical inactivity, alcohol, smoking

Pathophysiology

• Adenocarcinoma (~95%) arising from colonic epithelium

Left-Sided (Sigmoid, Descending)

• Change in bowel habit (increased frequency, looser stools)
• Rectal bleeding (bright red or dark, mixed with stool)
• Tenesmus (sensation of incomplete evacuation)
• Obstructive symptoms (narrow calibre stool, colicky pain)
• May present as emergency with LBO or perforation

Right-Sided (Caecum, Ascending)

• Iron-deficiency anaemia (occult blood loss) - often the presenting feature
• Weight loss, fatigue
• Palpable RIF mass
• Less likely to obstruct (wider lumen, liquid stool)

Red Flags/2WW Referral Criteria (NICE NG12)

• ≥40 with unexplained weight loss + abdominal pain
• ≥50 with unexplained rectal bleeding
• ≥60 with IDA or change in bowel habit
• Rectal or abdominal mass at any age
• FIT ≥10 μg Hb/g faeces in symptomatic patients

Bedside

• FIT (faecal immunochemical test): Quantitative; ≥10 μg Hb/g faeces in symptomatic patients → colonoscopy
• PR examination: Assess for rectal mass

Bloods

• FBC: Iron-deficiency anaemia (low MCV, low ferritin)
• LFTs: Liver metastases (raised ALP, GGT)
• CEA: Baseline pre-operative (for monitoring recurrence post-treatment)
• U&Es: Baseline

Imaging/Endoscopy

• Colonoscopy: Gold standard - allows visualisation, biopsy, polypectomy
• CT colonography: Alternative if colonoscopy incomplete or contraindicated
• CT chest/abdomen/pelvis: Staging (lung and liver metastases)
• MRI pelvis: Staging for rectal cancer (see separate topic)
• PET-CT: If surgical resection of metastases considered

Surgical (Curative Intent)

Colon cancer:

• Right hemicolectomy: Caecal/ascending colon tumours
• Extended right hemicolectomy: Hepatic flexure/transverse
• Left hemicolectomy: Descending colon
• Sigmoid colectomy: Sigmoid tumours
• Emergency: Hartmann's procedure if obstruction/perforation (resection + end colostomy)

Laparoscopic approach is standard where possible - faster recovery, fewer complications (CLASICC trial)

Adjuvant Chemotherapy

• Dukes' C (node-positive): 6 months adjuvant chemotherapy - FOLFOX (5-FU + oxaliplatin) or capecitabine + oxaliplatin
• Dukes' B: Consider if high-risk features (T4, perforation, <12 nodes sampled, poorly differentiated, lymphovascular invasion)

Metastatic Disease

• Liver metastases: Consider hepatic resection if suitable (5-year survival ~30-40% after resection)
• Lung metastases: Consider pulmonary metastasectomy if isolated
• Palliative chemotherapy: FOLFOX or FOLFIRI ± biological agents (cetuximab if KRAS wild-type; bevacizumab)
• Immunotherapy: Pembrolizumab for MSI-high/dMMR metastatic CRC

Referral Criteria

• 2WW referral as per NICE NG12 criteria
• MDT discussion for all confirmed cases
• Specialist HPB surgery for liver metastasis resection

• Overall 5-year survival: ~60%
• Stage-specific (Dukes'): A ~95%, B ~80%, C ~60%, D ~10%
• Screening-detected cancers: Earlier stage, better survival
• Adjuvant chemotherapy (Dukes' C): Improves 5-year survival by ~10-15%
• Liver metastasis resection: 5-year survival ~30-40% (vs ~5% without)
• Recurrence: ~30% within 5 years; most in first 2 years; CEA monitoring aids early detection
• Follow-up: CT at 1 and 3 years, colonoscopy at 1 year then 3-yearly (NICE NG151)

Dukes' Classification vs TNM

Hereditary CRC Syndromes

Key Facts

Rectal cancer management differs from colon cancer due to anatomical constraints of the pelvis, relationship to sphincter complex, and the role of neoadjuvant therapy. MRI pelvis is essential for treatment planning.

Epidemiology

Rectal cancer accounts for ~30-35% of all colorectal cancers. ~12,000-14,000 new cases annually in UK. Similar age and sex distribution to colon cancer.

Aetiology

Same as colorectal cancer - adenoma-carcinoma sequence, genetic syndromes, modifiable risk factors.

Pathophysiology

• The rectum lacks a serosal covering in the lower third → tumours can directly invade surrounding structures
• Mesorectum: Fatty tissue envelope surrounding the rectum containing lymph nodes and vessels - complete excision (TME) is critical to reduce local recurrence
• CRM (circumferential resection margin): <1mm = involved → high local recurrence risk; neoadjuvant therapy aims to achieve clear CRM

Typical Presentation

• Rectal bleeding (bright red, mixed with stool)
• Change in bowel habit (increased frequency, tenesmus)
• Mucus per rectum
• Sense of incomplete evacuation
• May present with obstruction or rarely perforation

Examination

• PR examination: Can palpate tumours in lower rectum - assess size, position, mobility, distance from anal verge
• Assess sphincter function pre-operatively

Red Flags

• Fixed tumour on PR - locally advanced, may be T4
• Obstructing tumour - may need emergency defunctioning stoma
• Weight loss and hepatomegaly - metastatic disease

Bedside

• PR examination: Distance from anal verge, mobility, size
• Rigid sigmoidoscopy: Confirms distance from anal verge; biopsy

Bloods

• FBC: Anaemia
• LFTs: Liver metastases
• CEA: Baseline

Imaging

• MRI pelvis: Essential for local staging
  • T stage: Depth of invasion
  • N stage: Mesorectal lymph nodes
  • CRM: Distance from mesorectal fascia (involved if <1mm)
  • EMVI (extramural vascular invasion): Poor prognostic factor
• CT chest/abdomen/pelvis: Distant staging (liver, lung)
• Colonoscopy: Full colonic assessment (synchronous tumours in ~3-5%)
• EUS (endorectal ultrasound): For early (T1/T2) tumours - assesses depth of invasion

Early Rectal Cancer (T1)

• Transanal endoscopic microsurgery (TEMS): Local excision for early, favourable T1 tumours (well-differentiated, no lymphovascular invasion, <3cm)
• If adverse histological features → completion TME surgery

Locally Advanced (T3/T4 or N+)

• Neoadjuvant chemoradiotherapy: Long-course 5-FU + radiotherapy (45-50.4 Gy over 5 weeks) → surgery at 6-10 weeks
• OR short-course radiotherapy (25 Gy in 5 fractions) → immediate surgery (if CRM clear on MRI)
• TME surgery: After neoadjuvant therapy

Surgery

• Anterior resection (AR): Upper/mid rectum; primary anastomosis ± defunctioning loop ileostomy
• Low anterior resection: Low rectum (preserving sphincter); almost always needs defunctioning ileostomy
• Abdominoperineal excision of rectum (APER): Very low tumours involving sphincter complex → permanent end colostomy
• Hartmann's: Emergency presentation with obstruction/perforation

Adjuvant

• Adjuvant chemotherapy (capecitabine/FOLFOX): If node-positive and no neoadjuvant chemoRT given
• Post-operative MRI/CT surveillance

Watch and Wait

• Emerging approach for patients with complete clinical response to chemoradiotherapy
• Regular surveillance (MRI, endoscopy, CEA)
• ~15-30% regrowth rate; salvage surgery usually feasible

Referral Criteria

• All rectal cancers - MDT discussion
• MRI staging before treatment decision
• Specialist colorectal surgeon for TME

• 5-year survival: Similar to colon cancer by stage
• Local recurrence: <5% with TME (vs ~30% historically without TME)
• Neoadjuvant chemoRT: Reduces local recurrence by ~50% in locally advanced disease
• LARS: Affects ~50-70% of patients after anterior resection - frequency, urgency, incontinence, clustering; may improve over 1-2 years
• Permanent stoma: ~10-20% of rectal cancer patients (APER or non-reversal of defunctioning stoma)
• Anastomotic leak: ~5-10% after anterior resection (reason for defunctioning ileostomy)

Rectal Cancer Surgery Decision

Key Trials

Key Facts

Breast cancer management has been revolutionised by screening, molecular subtyping, and targeted therapies. The multidisciplinary approach ensures individualised treatment.

Epidemiology

~55,000 new cases/year in UK (most common cancer overall). ~400 cases in men annually. Lifetime risk: ~1 in 7 (women). Peak incidence 55-65 years (second peak >70). 5-year survival: ~87% overall.

Aetiology

Risk factors:

• Non-modifiable: Female sex, age, family history, BRCA1/2 mutations (~5-10% of cases), early menarche, late menopause, nulliparity, previous breast cancer, atypical ductal hyperplasia, LCIS
• Modifiable: HRT (combined - increases risk), alcohol, obesity (post-menopausal), OCP (slight increase), physical inactivity
• BRCA1: ~60-80% lifetime risk of breast cancer; also ovarian cancer (~40%)
• BRCA2: ~45-55% lifetime risk of breast cancer; also ovarian, prostate, pancreatic

Pathophysiology

• Invasive ductal carcinoma (no special type - NST): ~70-80% of breast cancers
• Invasive lobular carcinoma: ~10-15%; diffuse growth pattern, often bilateral
• DCIS: Pre-invasive; ~25% progress to invasive cancer over 10 years if untreated
• Molecular subtypes: Luminal A (ER+/HER2−, low Ki-67), Luminal B (ER+/HER2+, high Ki-67), HER2-enriched, Basal-like (triple-negative)

Common Presentations

• Painless breast lump: Usually hard, irregular, fixed
• Screen-detected: Mammographic abnormality (microcalcifications, spiculated mass)
• Nipple changes: Retraction, Paget's disease (eczematous nipple - underlying DCIS/invasive cancer)
• Skin changes: Peau d'orange (lymphatic invasion), dimpling, tethering
• Axillary lymphadenopathy: May be the presenting feature
• Inflammatory breast cancer: Diffuse erythema, oedema, peau d'orange - rapidly progressive; poor prognosis

Red Flags (2WW Referral - NICE NG12)

• Unexplained breast lump in women ≥30
• Breast lump with other features (skin/nipple changes) at any age
• Unilateral nipple changes at ≥50 (discharge, retraction)
• Axillary lump in women ≥30
• Skin changes suggestive of breast cancer at any age

Triple Assessment (One-Stop Breast Clinic)

1. Clinical examination: Inspection and palpation of breast and axillae

2. Imaging:

• Mammography: Women ≥40 (microcalcifications, spiculated masses, architectural distortion)
• Ultrasound: Women <40 (dense breast tissue); also guides biopsy and assesses cysts
• MRI breast: BRCA carriers, lobular cancer (multifocality), pre-operative planning

3. Tissue diagnosis:

• Core biopsy (14G needle): Preferred - provides histological architecture
• FNA: Cytology only; used for lymph nodes

Staging

• CT chest/abdomen/pelvis: For locally advanced or suspected metastatic disease
• Bone scan/PET-CT: If bone/distant metastases suspected
• Sentinel lymph node biopsy (SLNB): Intraoperative staging - identifies first draining node(s)

Pathology

• Histological type, grade (Nottingham - tubule formation, nuclear pleomorphism, mitotic count)
• Receptor status: ER, PR, HER2 (IHC/FISH), Ki-67
• Oncotype DX: 21-gene recurrence score for ER+/HER2−/node-negative - guides adjuvant chemotherapy decision

Surgery

• Wide local excision (WLE/lumpectomy): Breast-conserving surgery + adjuvant radiotherapy - equivalent survival to mastectomy (NSABP B-06, EORTC trials)
• Mastectomy: If multifocal, large tumour:breast ratio, patient preference, BRCA carrier, inflammatory cancer
• Immediate or delayed reconstruction: Implant-based or autologous tissue (DIEP flap, LD flap)
• SLNB: Standard for clinically node-negative patients; if positive → axillary treatment (ANC or radiotherapy per AMAROS trial)
• Axillary node clearance (ANC): If >2 positive sentinel nodes or preoperative FNA-confirmed node involvement

Adjuvant Therapy

Radiotherapy:

• After WLE: Whole breast radiotherapy (reduces local recurrence from ~30% to ~10%)
• After mastectomy: If T3/T4, ≥4 positive nodes, positive margin

Endocrine therapy (ER+):

• Pre-menopausal: Tamoxifen 20mg OD for 5-10 years (± ovarian suppression)
• Post-menopausal: Aromatase inhibitor (anastrozole 1mg, letrozole 2.5mg) for 5-10 years
• Side effects: Tamoxifen - VTE, endometrial cancer; AIs - arthralgia, osteoporosis

Chemotherapy:

• ER−, HER2−, node-positive, high-risk: Anthracycline + taxane regimen (e.g., EC-T)
• Oncotype DX guides decision for ER+/HER2−/N0 patients

Targeted therapy:

• Trastuzumab (Herceptin): HER2+ disease - 1 year adjuvant; reduces recurrence ~50% (HERA trial)
• Pertuzumab: Added to trastuzumab for high-risk HER2+ (APHINITY trial)
• CDK4/6 inhibitors (ribociclib, abemaciclib): ER+/HER2− advanced disease

Referral Criteria

• Any breast lump meeting 2WW criteria - urgent referral to breast clinic
• BRCA carriers - specialist genetics and risk-reducing surgery discussion
• Metastatic disease - oncology

• Overall 5-year survival: ~87%
• Stage I: >95% 5-year survival
• Stage IV (metastatic): Median survival ~2-3 years; ~25% 5-year survival
• ER+ disease: Better prognosis than ER−; but late recurrence (>5 years) more common
• HER2+ with trastuzumab: Excellent outcomes; survival improved by ~30%
• Triple-negative: Poorer prognosis; higher recurrence rate but often occurs early (<3 years)
• Male breast cancer: Same stage-for-stage prognosis as female; often diagnosed later

Receptor Status and Treatment

Key Trials

Key Facts

Breast lumps are one of the commonest presentations to primary care and breast clinics. The systematic triple assessment approach ensures accurate diagnosis and timely detection of malignancy.

Epidemiology

Breast lumps are extremely common. ~90% of referrals to breast clinic are benign. Fibroadenoma is the most common benign tumour. Breast cysts are the most common cause of a discrete breast lump in women aged 35-50. Cancer accounts for ~10% of breast clinic referrals.

Aetiology

By age group:

• <25: Fibroadenoma most common; rarely cancer
• 25-40: Fibroadenoma, cyst; cancer less common but possible
• 40-55: Cyst, fibrocystic change, cancer becomes more common
• >55: Cancer must be excluded; cysts become less common post-menopause

Pathophysiology

• Fibroadenoma: Proliferation of both stromal and epithelial components; oestrogen-sensitive
• Breast cyst: Arise from terminal duct lobular units; apocrine metaplasia of epithelium
• Fibrocystic change: Spectrum of benign changes - cysts, fibrosis, epithelial hyperplasia, sclerosing adenosis

Fibroadenoma

• Firm, smooth, well-defined, mobile ('breast mouse')
• Usually 2-3cm; painless
• Peak age 20-30
• Giant fibroadenoma if >5cm
• May be multiple (~15%)

Breast Cyst

• Smooth, well-defined, fluctuant
• May be tender (especially pre-menstrually)
• Can appear suddenly
• Peri-menopausal (35-50 years)
• Simple cysts are benign; complex cysts require further assessment

Fibrocystic Change

• Cyclical breast pain and lumpiness
• Usually bilateral upper outer quadrant
• Improves after menopause
• Spectrum of histological changes

Fat Necrosis

• History of trauma or surgery
• Firm, irregular lump - can mimic carcinoma
• May have skin dimpling or retraction
• Mammography may show calcification

Red Flags (Refer 2WW)

• Hard, irregular, fixed lump
• Skin tethering, peau d'orange, nipple retraction
• Bloody nipple discharge
• Axillary lymphadenopathy
• Any breast lump in women ≥30
• Any lump with suspicious features at any age

Triple Assessment

1. Clinical examination:

• Inspection: Symmetry, skin changes, nipple changes
• Palpation: Location, size, consistency, mobility, fixity, axillary nodes

2. Imaging:

• Mammography: Women ≥40 (sensitivity increases with age due to less dense tissue)
• Ultrasound: Women <40 (dense breast tissue); also for cyst assessment and biopsy guidance
• MRI breast: Selected cases (BRCA carriers, lobular cancer, implants)

3. Tissue diagnosis:

• Core biopsy (14G needle): Preferred for solid lesions - histological architecture, receptor status
• FNA: Cytology only; useful for lymph nodes, cyst aspiration
• Vacuum-assisted biopsy: For microcalcifications or small lesions

Results Classified as:

• Imaging (U/M score): U1-5 (ultrasound) / M1-5 (mammography) - 5 = malignant
• Pathology (B score): B1-5 - B5 = malignant

Fibroadenoma

• <3cm, classic features, age <40: Conservative management with clinical/US follow-up
• >3cm, growing, atypical: Excision biopsy
• Vacuum-assisted excision: Alternative to surgical excision for confirmed fibroadenomas
• Observation is acceptable - many involute spontaneously

Breast Cyst

• Simple cyst: US-guided aspiration - fluid aspirated; if clear and lump resolves, no further action
• Bloodstained aspirate: Send for cytology - investigate further
• Complex cyst: Core biopsy - exclude intracystic carcinoma
• Recurrent cyst: Re-aspirate; consider excision if multiple recurrences

Fat Necrosis

• If benign on triple assessment: Reassurance and observation
• If any diagnostic uncertainty: Excision biopsy

Breast Abscess

• US-guided aspiration + antibiotics (flucloxacillin 500mg QDS)
• Incision and drainage: If aspiration fails or large abscess
• If non-lactational, exclude underlying malignancy

Referral Criteria

• 2WW criteria as per NICE NG12
• Any solid breast lump - referral to breast clinic for triple assessment
• Breast lump in male - exclude cancer

• Fibroadenoma: Benign; ~30% involute spontaneously; <0.3% risk of associated malignancy
• Breast cyst: Benign; slight increased risk of subsequent breast cancer (~1.5-2×)
• Fat necrosis: Benign; no malignant potential
• Phyllodes tumour: Borderline/malignant variants require wide excision; local recurrence risk ~15-25%
• Breast cancer: See Breast Cancer topic

Breast Lump Assessment by Age

Classification Scoring

Key Facts

Thyroid surgery requires detailed anatomical knowledge and meticulous technique. Understanding the complications and their management is essential for all surgical trainees.

Epidemiology

~10,000 thyroidectomies performed annually in England. Most common indication: Thyroid cancer (~30%), followed by multinodular goitre (~25%) and hyperthyroidism (~15%).

Aetiology

Indications for thyroid surgery:

• Confirmed or suspected thyroid malignancy (Thy4/Thy5 on cytology)
• Compressive goitre (dysphagia, dyspnoea, stridor)
• Retrosternal goitre
• Toxic multinodular goitre or Graves' disease (failed medical/radioiodine)
• Cosmesis

Pathophysiology

Anatomical considerations:

• Recurrent laryngeal nerve: Runs in tracheo-oesophageal groove; left hooks under aortic arch; right hooks under subclavian artery; enters larynx behind cricothyroid joint
• External branch of SLN: Runs with superior thyroid artery; injury → weak, monotonous voice (difficulty projecting)
• Parathyroid glands: Usually 4 glands; superior (from 4th pharyngeal pouch) more constant position; inferior (from 3rd pouch) more variable
• Berry's ligament: Posterior suspensory ligament - RLN at highest risk at this point

Pre-operative Assessment

• TFTs: Ensure euthyroid (especially in hyperthyroidism - carbimazole/propranolol pre-operatively)
• Vocal cord assessment: Flexible nasendoscopy - document pre-operative function
• Imaging: US neck, CT if retrosternal extension suspected
• Cytology/histology: FNA result (Thy1-5 classification)
• Calcium/PTH: Baseline

Post-operative Complications

Early:

• Hypocalcaemia: Usually within 24-48 hours; perioral tingling, tetany
• RLN injury: Hoarseness (unilateral); stridor (bilateral)
• SLN injury: Weak voice, difficulty projecting
• Wound infection: Uncommon

Late:

• Permanent hypoparathyroidism (~1-2%): Lifelong calcium/alfacalcidol
• Hypothyroidism: After total thyroidectomy - requires lifelong levothyroxine
• Keloid scar

Red Flags

• Expanding neck swelling post-op - haematoma, open at bedside
• Stridor post-op - bilateral RLN injury or oedema; assess airway urgently
• Symptomatic hypocalcaemia - IV calcium gluconate 10mL 10% over 10 minutes

Pre-operative

• TFTs: Confirm euthyroid status
• Calcium, PTH: Baseline
• US neck: Nodule characteristics, lymph nodes
• FNA cytology: Thy classification (1-5)
• CT neck/thorax: If retrosternal extension
• Flexible nasendoscopy: Vocal cord assessment

Post-operative

• Serial calcium: Every 6 hours for 24-48 hours; corrected calcium
• PTH: Measured at 4-6 hours post-op; predicts hypocalcaemia
• Vocal assessment: Voice quality; formal laryngoscopy if concerns
• Histology: Final pathology for cancer staging

Haematoma (Emergency)

• Expanding neck haematoma = airway emergency
• At the bedside: Remove clips/sutures, evacuate clot, call for help
• Return to theatre: Definitive haemostasis
• Keep skin closure trolley at bedside for all thyroid patients

Hypocalcaemia

• Symptomatic: IV calcium gluconate 10mL 10% over 10 minutes (can repeat)
• Ongoing replacement: Oral calcium carbonate 1-2g TDS + alfacalcidol 0.25-1mcg OD
• Monitor calcium daily until stable
• Most transient cases resolve within 1-6 months
• Permanent: Lifelong calcium + vitamin D analogues

RLN Injury

• Unilateral: Hoarse voice; ENT review; speech therapy; most recover within 6-12 months
• Bilateral: Stridor - may need re-intubation or tracheostomy; ENT urgent review
• Medicolegal: Pre-op laryngoscopy documentation is essential

Post-thyroidectomy Thyroid Replacement

• Total thyroidectomy: Levothyroxine started immediately (1.6 mcg/kg/day)
• TSH suppression: For differentiated thyroid cancer - TSH target <0.1 mU/L (initial)
• Hemithyroidectomy: ~30% will need levothyroxine; monitor TFTs at 6 weeks

Referral Criteria

• Suspected thyroid malignancy - MDT
• Compressive goitre - surgical referral
• Failed medical management of hyperthyroidism - endocrine surgeon

• Overall mortality of thyroid surgery: <0.1%
• RLN injury: Temporary ~5-8%; permanent ~1-2%
• Hypoparathyroidism: Temporary ~20-30%; permanent ~1-2%
• Haematoma: ~1-2% - potentially life-threatening if unrecognised
• Thyroid cancer: Excellent prognosis for differentiated cancer (papillary/follicular) - >95% 10-year survival
• Higher-volume surgeons have lower complication rates

Thy Classification (FNA Cytology)

Key Facts

Thyroid nodules are one of the most common endocrine findings. The challenge is identifying the ~5% that harbour malignancy while avoiding unnecessary surgery for the majority.

Epidemiology

Palpable nodules in ~5% of adults. Incidental nodules on US in ~50% of adults >50 years. Thyroid cancer incidence: ~3,500/year in UK. Female predominance for benign nodules (F:M ~4:1); malignancy ratio less pronounced.

Aetiology

Benign:

• Colloid/hyperplastic nodule (~60-70%)
• Follicular adenoma (~15-20%)
• Thyroiditis (Hashimoto's, subacute)
• Cyst

Malignant (~5%):

• Papillary carcinoma (~80% of thyroid cancers)
• Follicular carcinoma (~10-15%)
• Medullary carcinoma (~5-8%)
• Anaplastic carcinoma (~1-2%)
• Lymphoma (rare, associated with Hashimoto's)

Pathophysiology

• Papillary: Spread via lymphatics; multifocal in ~30%; Orphan Annie nuclei, psammoma bodies on histology
• Follicular: Spread via blood (haematogenous - lung, bone); needs capsular/vascular invasion for malignancy diagnosis
• Medullary: C-cell origin; calcitonin production; amyloid stroma; RET proto-oncogene (MEN2)
• Anaplastic: Undifferentiated; extremely aggressive; no iodine uptake; rapid local invasion

Assessment of Thyroid Nodule

History:

• Duration and rate of growth
• Compressive symptoms (dysphagia, dyspnoea, hoarseness)
• Hyper/hypothyroid symptoms
• Radiation history (childhood neck irradiation)
• Family history of thyroid cancer, MEN, FMTC

Examination:

• Size, consistency (hard → concerning), mobility
• Fixation to surrounding structures
• Cervical lymphadenopathy
• Signs of thyroid dysfunction

Features Suggesting Malignancy (Red Flags)

• Rapid growth
• Hard, irregular, fixed nodule
• Cervical lymphadenopathy
• Vocal cord palsy (hoarseness)
• Male sex; age <20 or >60
• History of radiation exposure
• Family history of thyroid cancer/MEN

Bedside

• TFTs: If suppressed TSH → radionuclide scan (hot/cold nodule); hyperfunctioning nodules rarely malignant

Bloods

• TFTs: TSH, FT4
• Calcitonin: If medullary carcinoma suspected or family history of MEN2
• Thyroid antibodies: If thyroiditis suspected

Imaging

• Ultrasound neck: First-line - classify using U classification (BTA/RCR)
  • U1: Normal
  • U2: Benign (isoechoic, halo, egg-shell calcification)
  • U3: Indeterminate (solid, hypoechoic, mixed solid/cystic)
  • U4: Suspicious (irregular margins, microcalcifications, tall > wide)
  • U5: Malignant (features of U4 + invasion/nodes)
• FNA: Guided by U classification (U3-U5)
• Radionuclide scan (Tc99m): If TSH suppressed - hot nodule (autonomous, rarely malignant) vs cold (requires FNA)
• CT neck: If compressive symptoms or staging for malignancy

Cytology (Thy Classification)

• Thy1: Non-diagnostic → repeat
• Thy2: Benign → observation
• Thy3a: Atypical → repeat FNA or lobectomy
• Thy3f: Follicular neoplasm → diagnostic lobectomy
• Thy4: Suspicious → surgery
• Thy5: Malignant → surgery

Benign (Thy2)

• Observation: Clinical and US follow-up
• Repeat US at 3-6 months then annually for 3-5 years
• If growing or changing → repeat FNA

Indeterminate (Thy3)

• Thy3a: Repeat FNA; if persistent → diagnostic lobectomy
• Thy3f: Diagnostic lobectomy - histology determines if benign adenoma or follicular carcinoma

Malignant (Thy4/5)

Papillary/follicular (differentiated thyroid cancer):

• Total thyroidectomy (if >4cm, bilateral, or high-risk features) or hemithyroidectomy (if low-risk, <4cm, unifocal)
• Radioactive iodine (RAI) ablation: Post-operatively for intermediate/high-risk disease
• TSH suppression: Levothyroxine to suppress TSH (reduces recurrence in differentiated cancer)
• Surveillance: Thyroglobulin (tumour marker), neck US

Medullary thyroid cancer:

• Total thyroidectomy + central neck dissection
• RAI NOT effective (C cells do not take up iodine)
• Screen for RET mutation; screen family members for MEN2

Anaplastic carcinoma:

• Palliative approach in most cases - surgery rarely curative
• External beam radiotherapy ± chemotherapy
• Tracheostomy may be needed for airway compromise

Referral Criteria

• 2WW referral (NICE NG12) if unexplained thyroid lump

• Papillary carcinoma: 10-year survival >95%; 20-year survival >90%
• Follicular carcinoma: 10-year survival ~85-90%
• Medullary carcinoma: 10-year survival ~70-80%; worse with MEN2B
• Anaplastic carcinoma: Median survival ~6 months; near 100% mortality at 1 year
• Benign nodules: Excellent prognosis; ~5% annual growth rate; malignant transformation very rare

Thyroid Cancer Comparison

Key Facts

AAA is a common and potentially fatal condition. The NHS screening programme has reduced AAA-related mortality. Understanding the indications for surveillance and repair is essential.

Epidemiology

~6,500 new AAA diagnoses/year in UK. Rupture accounts for ~4,000 deaths/year. Prevalence decreasing due to declining smoking rates. The NHS AAA screening programme (since 2013) has reduced AAA-related mortality in screened populations.

Aetiology

• Atherosclerosis: Degenerative process in aortic wall - most common cause
• Smoking: Strongest modifiable risk factor (~5× increased risk)
• Genetic: Family history (first-degree relative = 4× risk); connective tissue disorders (Marfan, Ehlers-Danlos type IV)
• Inflammatory: Mycotic (infected) aneurysm - rare but important
• Other risk factors: Male sex, age >65, hypertension, COPD, hyperlipidaemia

Pathophysiology

• Chronic inflammation of aortic wall → destruction of elastin and collagen in media and adventitia
• Matrix metalloproteinase (MMP) activity breaks down structural proteins
• Wall tension increases with diameter (Laplace's law: Wall tension = Pressure × Radius)
• Risk of rupture increases exponentially with size: <5.5cm ~1%/year; 5.5-6cm ~10%/year; >7cm ~30%/year
• Most AAAs are infrarenal (~95%); may extend to involve iliac arteries

Asymptomatic (Most Common)

• Incidental finding on screening USS or imaging for other indications
• Pulsatile, expansile abdominal mass above umbilicus

Symptomatic (Unruptured)

• Abdominal or back pain (expansion or inflammation)
• Peripheral embolisation (blue toe syndrome, trash foot)
• Compression of adjacent structures

Ruptured AAA (Surgical Emergency)

• Classic triad: Sudden-onset abdominal/back pain + haemodynamic instability + pulsatile abdominal mass
• Only ~50% present with all three features
• May present with syncope, flank pain mimicking renal colic, groin pain
• Retroperitoneal rupture (more common): Tamponaded; patient may initially be stable
• Intraperitoneal rupture: Rapidly fatal - free blood in peritoneum

Red Flags

• Sudden abdominal/back pain + known AAA = ruptured until proven otherwise
• Hypotension in patient >50 with abdominal pain - consider ruptured AAA
• Do NOT delay transfer to theatre for CT if patient is haemodynamically unstable

Screening/Surveillance

• USS abdomen: Measure AP diameter (accurate ± 2mm)

Elective Pre-operative

• CT angiography: Gold standard for surgical planning - anatomy, size, relation to renals, iliac involvement
• Cardiac assessment: CPET (cardiopulmonary exercise testing) to assess fitness
• Renal function: U&Es (contrast nephropathy risk)
• FBC, G&S/crossmatch: Pre-operative

Emergency (Suspected Rupture)

• CT aortogram: If haemodynamically STABLE → confirms diagnosis, guides management
• If UNSTABLE: Direct to theatre - do NOT delay for imaging
• Crossmatch 6-10 units: Major haemorrhage protocol

Surveillance (Small AAA)

• <5.5cm: Conservative management with surveillance USS
• Optimise cardiovascular risk factors: Smoking cessation (most important), statin, antihypertensive, antiplatelet
• No evidence that beta-blockers slow AAA growth

Elective Repair (≥5.5cm or Symptomatic or Growing >1cm/year)

EVAR (Endovascular Aneurysm Repair):

• Stent graft deployed via femoral arteries under fluoroscopic guidance
• Lower 30-day mortality (~1.5% vs ~4.5% open)
• Requires suitable anatomy (adequate neck length/angulation, iliac access)
• Requires lifelong CT surveillance for endoleaks
• No long-term survival advantage over open repair (EVAR-1 trial)

Open Surgical Repair:

• Laparotomy, cross-clamp aorta, synthetic graft (Dacron)
• Higher initial mortality but more durable - fewer re-interventions
• No need for lifelong surveillance CT

Emergency Repair (Ruptured AAA)

• Permissive hypotension: Target systolic ~80-100 mmHg (prevents further bleeding)
• Major haemorrhage protocol: O-negative blood initially, then crossmatched
• EVAR (if anatomy suitable and expertise available) or open repair
• Even with emergency surgery, mortality ~50%

Referral Criteria

• AAA ≥5.5cm - vascular surgery MDT
• Rapid growth (>1cm/year) - vascular surgery
• Symptomatic AAA - urgent vascular referral
• Suspected rupture - 999, immediate vascular surgery

• Elective EVAR: 30-day mortality ~1.5%
• Elective open: 30-day mortality ~4-5%
• Ruptured AAA: Overall mortality ~80%; ~50% reach hospital alive; operative mortality ~50%
• EVAR-1 trial: Lower early mortality but no difference in long-term survival; higher re-intervention rate for EVAR
• Screening: Reduces AAA-related mortality by ~45% (MASS trial)
• Small AAA (<5.5cm): Annual rupture risk <1%; surveillance is safe

AAA Surveillance Programme

Key Trials

Key Facts

PAD is a marker of systemic atherosclerosis. Management focuses on cardiovascular risk reduction and limb-specific treatment.

Epidemiology

Prevalence ~5-10% of adults >50 years; increases to ~15-20% in >70 years. Only ~25% of PAD patients are symptomatic. ~100,000 people have CLI in the UK.

Aetiology

• Atherosclerosis is the cause in >95% of cases
• Risk factors: Smoking (strongest - 4× risk), diabetes, hypertension, hyperlipidaemia, age, male sex, CKD, family history
• Other causes: Buerger's disease (thromboangiitis obliterans - young male smokers), popliteal entrapment, fibromuscular dysplasia

Pathophysiology

• CLI: Insufficient perfusion at rest → rest pain (worse at night, improved by hanging leg down - gravity-dependent), tissue loss
• Common sites: Superficial femoral artery (most common), iliac arteries, tibial arteries (especially in diabetics)

Intermittent Claudication (Fontaine II)

• Cramping pain in calf (SFA disease), thigh (iliac disease), or buttock (aortoiliac) on walking
• Consistent claudication distance
• Relieved within minutes of rest
• No pain at rest

Leriche Syndrome (Aortoiliac Occlusion)

• Buttock/thigh claudication + absent femoral pulses + erectile dysfunction

Critical Limb Ischaemia (Fontaine III-IV)

• Rest pain: Severe, usually forefoot; worse at night; relieved by dependency (hanging foot over bed)
• Tissue loss: Ulceration (typically painful, punched-out, distal) or gangrene
• 6 Ps: Pain, Pallor, Pulselessness, Perishing cold, Paraesthesia, Paralysis (acute ischaemia)

Acute Limb Ischaemia

• Sudden onset of the 6 Ps
• Causes: Embolism (AF, mural thrombus), thrombosis in situ, graft occlusion
• Surgical/interventional EMERGENCY - limb has ~6 hours before irreversible damage

Red Flags

• Rest pain - CLI, urgent referral
• Tissue loss (ulceration/gangrene) - limb-threatening
• Acute onset 6 Ps - emergency, consider embolectomy

Bedside

• ABPI: <0.9 = PAD; 0.5-0.9 = moderate; <0.5 = severe/CLI; >1.3 = calcified (unreliable)
• Pulse examination: Femoral, popliteal, dorsalis pedis, posterior tibial

• Handheld Doppler: Assess arterial signals

Bloods

• FBC, U&Es, HbA1c, lipids: Cardiovascular risk assessment
• Coagulation: If revascularisation planned

Imaging

• Duplex ultrasound: First-line - non-invasive, identifies stenosis/occlusion
• CT angiography: Pre-operative planning for revascularisation
• MR angiography: Alternative to CTA (avoids contrast nephropathy risk)
• Digital subtraction angiography (DSA): Gold standard (but invasive); used during endovascular intervention

Conservative (First-Line for Claudication)

• Supervised exercise programme: 2 hours/week for ≥3 months (NICE CG147) - improves walking distance by ~100-200%
• Smoking cessation: Most important modifiable intervention
• Statin: Atorvastatin 80mg OD (regardless of lipid levels)
• Antiplatelet: Clopidogrel 75mg OD (preferred over aspirin - CAPRIE trial)
• Antihypertensive: Target <140/90 (or <130/80 if diabetic)
• Diabetes optimisation: HbA1c target
• Foot care: Chiropody, appropriate footwear (especially diabetics)

Revascularisation (CLI or Lifestyle-Limiting Claudication Failing Conservative)

Endovascular (angioplasty ± stenting):

• First-line for short-segment stenosis/occlusion
• Iliac angioplasty has best long-term patency (~70-80% at 5 years)

Surgical bypass:

• Autologous vein graft (long saphenous) preferred - better patency than synthetic
• Femoral-popliteal bypass; femoral-tibial bypass for distal disease
• Consider for long-segment occlusion or failed endovascular

Amputation:

• If revascularisation not possible and CLI/unreconstructable - below-knee (BKA) preferred over above-knee (AKA)
• Rehabilitation with prosthesis

Referral Criteria

• CLI (rest pain, tissue loss) - urgent vascular referral (within 24 hours for tissue loss)
• Acute limb ischaemia - emergency vascular surgery
• Lifestyle-limiting claudication despite 3 months supervised exercise - vascular referral

• Claudication: ~75% remain stable or improve with exercise; ~25% worsen; ~5% proceed to CLI over 5 years
• CLI: 1-year mortality ~25%; 1-year amputation rate ~30%
• Cardiovascular mortality: PAD patients have ~3× increased risk of MI, stroke, CV death
• 5-year mortality: ~20% for claudicants; ~50% for CLI patients (from cardiovascular events)
• Post-bypass patency: Vein graft ~70-80% at 5 years; synthetic ~50-60% at 5 years
• Post-amputation: 30-day mortality ~10-15% (major amputation); 50% mortality at 2 years

Fontaine Classification

ABPI Interpretation

Key Facts

Carotid artery disease is a significant and treatable cause of stroke. Timely intervention with CEA in symptomatic patients reduces stroke risk substantially.

Epidemiology

~100,000 strokes/year in UK; ~20-30% caused by carotid disease. Asymptomatic carotid stenosis >50% found in ~5-10% of adults >65.

Aetiology

• Atherosclerosis: ~95% of carotid disease
• Plaque at carotid bifurcation: Low shear stress promotes plaque formation
• Mechanism of stroke: Plaque rupture → thromboembolism to cerebral circulation (artery-to-artery embolism) - more common than haemodynamic compromise from stenosis

Pathophysiology

• Atherosclerotic plaque most commonly at carotid bifurcation where ICA originates
• Plaque vulnerability (lipid-rich core, thin fibrous cap, intraplaque haemorrhage) determines stroke risk
• Emboli travel to MCA territory → cerebral ischaemia
• CEA removes the plaque surgically → eliminates embolic source

Symptomatic Carotid Disease

TIA (resolves within 24 hours):

• Amaurosis fugax (transient monocular blindness - 'curtain descending over eye')
• Hemiparesis, hemisensory loss (contralateral)
• Dysphasia (dominant hemisphere)

Stroke (persistent deficit >24 hours):

• Same territory as TIA but persistent
• MCA territory most common

Asymptomatic

• Bruit on auscultation over carotid bifurcation (not reliable - absent bruit doesn't exclude stenosis; bruit without stenosis possible)
• Incidental finding on imaging

Red Flags

• TIA or crescendo TIA - urgent assessment within 24 hours (ABCD2 score)
• Acute stroke - thrombolysis/thrombectomy if eligible; CEA only after stabilisation

Bedside

• ABCD2 score: Risk stratify TIA (Age, BP, Clinical features, Duration, Diabetes)
• Neurological examination: Document deficits

Bloods

• FBC, U&Es, lipids, HbA1c, glucose: Cardiovascular risk
• Coagulation: Pre-operative

Imaging

• Carotid duplex USS: First-line - non-invasive; assesses stenosis degree and plaque morphology
• CT angiography (CTA): Confirms stenosis degree; pre-operative planning
• MR angiography (MRA): Alternative if CTA contraindicated
• CT/MRI brain: Assess infarction territory
• ECG/echocardiography: Exclude cardiac source

Stenosis Grading (NASCET)

• Percentage = (1 − narrowest ICA diameter / normal distal ICA diameter) × 100

Symptomatic Carotid Stenosis

70-99% stenosis:

• CEA within 14 days of symptoms (NICE CG68) - NNT ~6 to prevent 1 stroke over 5 years
• Delay beyond 14 days significantly reduces benefit

50-69% stenosis:

• CEA offers modest benefit (NNT ~22) - consider based on patient factors
• Greater benefit in men, older patients, cortical (vs retinal) events

<50% stenosis:

• Best medical therapy only - CEA not beneficial

Near-occlusion (99%) or occlusion:

• CEA not indicated for complete occlusion
• Near-occlusion: Individual decision; benefit unclear

Asymptomatic Stenosis

• Best medical therapy: First-line in most cases
  • Atorvastatin 80mg, clopidogrel 75mg, antihypertensive, smoking cessation
• CEA: Consider only in specialist centres for patients with ≥60% stenosis AND additional high-risk features AND expected perioperative risk <3%
• ACST-2 trial results suggest medical therapy may be comparable to surgery in asymptomatic patients

Carotid Artery Stenting (CAS)

• Alternative to CEA in selected patients (high surgical risk, post-radiotherapy neck, recurrent stenosis)
• Similar long-term outcomes to CEA but higher perioperative stroke risk (ICSS, CREST trials)

Referral Criteria

• Symptomatic carotid stenosis ≥50% - urgent vascular surgery referral
• TIA/stroke with carotid territory symptoms - rapid access TIA clinic/stroke team

• CEA for 70-99% symptomatic: Reduces 5-year stroke risk from ~26% to ~9%
• Perioperative stroke/death risk: ~2-3% in experienced centres (audit requirement)
• Benefit diminishes with delay - maximal if done within 14 days; minimal after 12 weeks
• Asymptomatic stenosis: Annual stroke risk ~1-2% with modern medical therapy (much lower than in original trials)
• Long-term: Re-stenosis ~5-10% at 5 years after CEA; higher after CAS

Key Trials in Carotid Surgery

Key Facts

ATLS provides the universal framework for initial trauma management. A structured approach saves lives by ensuring life-threatening injuries are identified and treated in order of priority.

Epidemiology

Trauma is the leading cause of death in people aged 1-44 in the UK. ~16,000 major trauma patients/year in England. Road traffic collisions, falls, and assaults are the most common mechanisms. Major trauma networks centralise care to specialist trauma centres.

Aetiology

• Blunt trauma: RTCs (~40%), falls (~30%), assaults, sports injuries
• Penetrating trauma: Stabbings, GSWs (less common in UK than US)
• Blast injuries: Primary (pressure wave), secondary (debris), tertiary (displacement), quaternary (burns/inhalation)
• Polytrauma: Injury Severity Score (ISS) >15 = major trauma

Pathophysiology

• Trimodal death distribution: Immediate (seconds-minutes - massive injury), early (minutes-hours - haemorrhage, airway), late (days-weeks - sepsis, organ failure)

• Damage control resuscitation: Aims to break the lethal triad - permissive hypotension, minimise crystalloid, blood products 1:1:1, prevent hypothermia

Primary Survey (ABCDE)

A - Airway with C-spine control:

• Can the patient talk? → Airway patent
• Stridor, gurgling, snoring → airway compromise
• Jaw thrust, chin lift, suction, oropharyngeal/nasopharyngeal airway
• Definitive airway (intubation) if GCS ≤8 or unable to maintain airway
• In-line C-spine immobilisation until cleared

B - Breathing:

• Life-threatening conditions: Tension pneumothorax, massive haemothorax, open pneumothorax, flail chest
• Assess: RR, chest expansion, tracheal position, percussion, auscultation
• Tension pneumothorax: Needle decompression (2nd ICS MCL or 4th/5th ICS MAL) → chest drain

C - Circulation with haemorrhage control:

• Identify sources of haemorrhage: Chest, abdomen, pelvis, long bones, external ('blood on the floor and four more')
• 2× large bore IV access, IV fluids/blood products
• Pelvic binder if pelvic fracture suspected
• FAST scan (Focused Assessment with Sonography in Trauma)

D - Disability:

• GCS, pupil size and reactivity
• Blood glucose
• Lateralising signs

E - Exposure:

• Full exposure, log roll, prevent hypothermia
• Temperature management

Red Flags (Immediately Life-Threatening)

• Airway obstruction
• Tension pneumothorax
• Massive haemothorax (>1500mL)
• Cardiac tamponade
• Catastrophic external haemorrhage

Bedside

• Primary survey: Clinical assessment
• FAST scan: Free fluid in abdomen/pericardium
• Blood gas (ABG/VBG): pH, lactate, base deficit, Hb
• Point-of-care testing: TEG/ROTEM for coagulopathy

Bloods

• Group and crossmatch: Immediate (O-negative if type not available)
• FBC, coagulation, U&Es, LFTs: Baseline
• Lactate: Marker of tissue perfusion
• Ethanol level, urine drug screen: If indicated

Imaging

• CXR and pelvic X-ray: In primary survey if unstable
• CT traumagram (whole-body CT): Head, C-spine, chest, abdomen/pelvis - gold standard in haemodynamically stable patients
• CT angiography: If vascular injury suspected
• X-rays of long bones: As indicated in secondary survey

Damage Control Resuscitation

• Permissive hypotension: Target SBP ~80-90 mmHg until surgical haemorrhage control (avoid in head injury)
• 1:1:1 ratio: pRBCs:FFP:platelets
• TXA (tranexamic acid): 1g IV within 3 hours of injury (CRASH-2 trial - reduces mortality by ~10%)
• Prevent hypothermia: Warm fluids, forced-air warming, warm environment
• Minimise crystalloid: Avoid dilutional coagulopathy
• Calcium: Replace (citrate in blood products chelates calcium)

Damage Control Surgery

• Abbreviated surgery: Control haemorrhage (packing, ligation), control contamination (staple bowel ends)
• Transfer to ICU for resuscitation (correct lethal triad)
• Return to theatre for definitive surgery at 24-48 hours

Specific Interventions

• Chest drain: Haemo/pneumothorax - triangle of safety (4th/5th ICS, anterior axillary line)
• Thoracotomy: Massive haemothorax (>1500mL initial or >200mL/hr), cardiac tamponade, cardiac arrest in penetrating chest trauma
• Laparotomy: Haemodynamically unstable with positive FAST, peritonism, evisceration
• Pelvic binder: Pelvic fracture with haemodynamic instability

Referral Criteria

• All major trauma (ISS >15) - major trauma centre
• Activation criteria defined by local trauma network

• UK major trauma: Overall mortality ~15-20% (has improved with trauma networks)
• TXA within 3 hours: Reduces all-cause mortality by ~10% (CRASH-2)
• Golden hour: First 60 minutes critical for trauma outcomes
• Damage control resuscitation: Has significantly reduced mortality in massive haemorrhage
• Trauma network implementation: 19% reduction in mortality since 2012 (TARN data)

ATLS Primary Survey Summary

Haemorrhage Classification (ATLS)

Key Facts

Head injury is extremely common (~1.4 million ED attendances/year in England). Most are minor, but identifying patients who need CT imaging and neurosurgical intervention is critical.

Epidemiology

~1.4 million head injury presentations to ED annually. ~200,000 admissions/year. Leading cause of death in under-40s. Most common mechanism: Falls (~40-50%), assaults (~20-30%), RTCs (~20%).

Aetiology

• Primary injury: Direct impact → contusion, laceration, diffuse axonal injury, skull fracture
• Secondary injury: Develops hours-days later - cerebral oedema, intracranial haematoma, raised ICP, hypoxia, hypotension
• Prevention of secondary injury is the primary goal of management

Pathophysiology

• Subdural haematoma: Bridging veins torn → blood between dura and arachnoid; acute (high-energy trauma) or chronic (minor trauma in elderly/atrophic brain)
• Diffuse axonal injury: Rotational acceleration → widespread axonal shearing; CT may be normal; poor prognosis

GCS Assessment

• Eye opening: Spontaneous (4), to voice (3), to pain (2), none (1)
• Verbal: Oriented (5), confused (4), inappropriate words (3), incomprehensible sounds (2), none (1)
• Motor: Obeys commands (6), localises pain (5), withdraws (4), abnormal flexion (3), extension (2), none (1)
• Total: 15 maximum; ≤8 = severe (intubate); 9-12 = moderate; 13-15 = mild

Signs of Basal Skull Fracture

• Battle's sign: Bruising over mastoid (posterior fossa fracture)
• Raccoon eyes: Periorbital bruising (anterior fossa fracture)
• CSF otorrhoea/rhinorrhoea: Clear fluid from ear/nose
• Haemotympanum: Blood behind tympanic membrane
• Cranial nerve palsies: CN VII (facial) most common

Red Flags

• GCS drop ≥2 points - urgent CT
• Lucid interval followed by rapid deterioration - EDH
• Unilateral fixed dilated pupil - uncal herniation
• Cushing's reflex - impending brainstem herniation

CT Head Indications (NICE NG232)

Within 1 hour:

• GCS <13 on initial assessment
• GCS <15 at 2 hours post-injury
• Suspected open or depressed skull fracture
• Signs of basal skull fracture
• Post-traumatic seizure
• Focal neurological deficit

• 1 episode of vomiting

Within 8 hours:

• Loss of consciousness or amnesia + age ≥65
• Loss of consciousness or amnesia + coagulopathy (including anticoagulants)
• Dangerous mechanism (pedestrian vs vehicle, fall >1m, >5 stairs)

Other Investigations

• C-spine CT: If unable to clear clinically (Canadian C-spine rules)
• ABG/VBG: Identify hypoxia, acidosis
• FBC, coagulation: Baseline; correct coagulopathy urgently
• Blood glucose: Exclude hypoglycaemia
• CT angiography: If vascular injury suspected

Initial Management (ABCDE)

• Airway: Intubate if GCS ≤8; avoid nasal adjuncts if basal skull fracture suspected
• Breathing: Aim SpO₂ >96%, PaO₂ >13 kPa, PaCO₂ 4.5-5.0 kPa
• Circulation: Maintain MAP >80 mmHg (cerebral perfusion pressure = MAP − ICP; target CPP >60-70 mmHg)
• Disability: GCS, pupils, glucose
• C-spine: Immobilise until cleared

Raised ICP Management

• Head elevation: 30° with head in midline (optimise venous drainage)
• Osmotherapy: IV mannitol 20% (0.25-1g/kg) or hypertonic saline 3-5%
• Hyperventilation: Only as temporary bridge (target PaCO₂ 4.0-4.5 kPa) - NOT routine
• Sedation: Propofol, midazolam - reduce cerebral metabolic demand
• Decompressive craniectomy: Considered for refractory raised ICP (RESCUEicp trial)

Surgical Intervention

• Extradural haematoma: Craniotomy for evacuation - time-critical emergency
• Acute subdural: Craniotomy if >10mm, midline shift >5mm, or GCS drop
• Chronic subdural: Burr holes and drainage
• Depressed skull fracture: Elevation if depressed > skull thickness or compound

Referral Criteria

• All abnormal CT heads - discuss with neurosurgery
• GCS ≤8 - neurosurgical centre
• Skull fracture, intracranial haemorrhage - neurosurgical opinion

• Mild head injury (GCS 13-15): >95% good outcome
• Extradural haematoma: Excellent prognosis if operated before herniation; mortality <5% if treated early
• Acute subdural haematoma: Mortality ~40-60%; functional outcome often poor
• Diffuse axonal injury: Mortality ~30-40%; survivors often have significant disability
• Chronic subdural: Good prognosis with drainage; recurrence ~10-20%
• Overall head injury mortality: ~1% of all head injuries; ~30% of severe head injuries

NICE CT Head Criteria Summary (NG232)

Key Facts

Burns management requires systematic assessment of depth, area, and associated injuries. Appropriate fluid resuscitation and timely referral to specialist services are critical.

Epidemiology

~175,000 burn injuries/year in UK (most minor). ~13,000 ED attendances for burns. ~4,500 hospital admissions. ~300 deaths annually. Peak populations: Children <5 (scalds) and young adult males (flame burns).

Aetiology

• Thermal: Flame (~35%), scald (~30%), contact (~10%)
• Chemical: Acid, alkali (alkali typically causes deeper injury - liquefactive necrosis)
• Electrical: Low voltage (household), high voltage (>1000V - deep tissue injury, cardiac arrest risk)
• Radiation: Sunburn, industrial
• Non-accidental injury: Consider in children - symmetrical burns, clear demarcation, inconsistent history

Pathophysiology

Jackson's burn model (zones of injury):

• Zone of coagulation: Central; irreversible tissue necrosis
• Zone of stasis: Surrounding; potentially salvageable tissue (at risk of ischaemia in first 48 hours)
• Zone of hyperaemia: Peripheral; will recover

Adequate resuscitation protects the zone of stasis from converting to necrosis.

Burn Depth Assessment

Red Flags

• Airway: Stridor, hoarseness, carbonaceous sputum, facial burns, singed nasal hairs → EARLY intubation (airway oedema progresses rapidly)
• Circumferential burns: Limb - vascular compromise; chest - respiratory compromise → escharotomy
• Electrical burns: May have minimal skin injury but deep tissue/organ damage; risk of cardiac arrhythmias, compartment syndrome, rhabdomyolysis
• Non-accidental injury: Child with glove/stocking pattern burn, clear tide marks, inconsistent history

Bedside

• TBSA assessment: Rule of Nines (adults) or Lund and Browder chart (more accurate, especially children)
• Patient's palm: ~1% TBSA (useful for small or scattered burns)
• Airway assessment: Flexible nasendoscopy if inhalation injury suspected
• ECG: Electrical burns (arrhythmia risk)

Bloods

• FBC, U&Es, LFTs: Baseline
• CK: Rhabdomyolysis (electrical burns, major burns)
• ABG/VBG: CO level (carboxyhaemoglobin) if inhalation injury - co-oximetry
• Lactate: Perfusion marker
• G&S/crossmatch: Major burns
• Clotting: DIC in severe burns

Imaging

• CXR: Inhalation injury, ARDS
• CT: If associated trauma

Immediate (Pre-Hospital and ED)

1. Safety: Remove from source of burn; stop the burning process
2. Cool: Running tepid water for 20 minutes (effective up to 3 hours post-injury); avoid ice (causes vasoconstriction)
3. Cover: Cling film (single layer, loosely) - reduces pain, prevents contamination
4. ABCDE: Especially airway - intubate early if inhalation injury suspected
5. 100% O₂: If CO poisoning suspected (SpO₂ unreliable - CO gives falsely normal SpO₂)

Fluid Resuscitation (Burns >15% TBSA adults, >10% children)

• Parkland formula: 4mL × weight (kg) × %TBSA burns
• Give 50% in first 8 hours from time of burn (NOT from time of arrival), remaining 50% over next 16 hours
• Use Hartmann's solution (Ringer's lactate)
• Titrate to urine output: Adults 0.5-1 mL/kg/hr; children 1 mL/kg/hr

Wound Management

• Superficial: Simple dressings, analgesia
• Partial thickness: Non-adherent dressings (e.g., Mepitel), silver-based antimicrobials if needed
• Full thickness: Will require surgical debridement and skin grafting
• Escharotomy: Circumferential full-thickness burns causing vascular/respiratory compromise

Referral to Burns Centre

• 10% TBSA (adults), >5% (children), >5% (elderly >60)

• Full-thickness burns >5%
• Circumferential burns
• Face, hands, feet, genitalia, perineum, major joints
• Inhalation injury
• Chemical or electrical burns
• Non-accidental injury
• Pre-existing medical conditions complicating management

Surgical

• Debridement and grafting: Full-thickness and deep partial-thickness burns
• Split-thickness skin graft (SSG): Most common; donor site (thigh) heals spontaneously
• Negative pressure wound therapy: Aids graft take

• Baux score: Mortality estimate = Age + %TBSA (modified Baux adds 17 for inhalation injury)
• Minor burns (<10% TBSA, partial thickness): Excellent prognosis
• Major burns (>40% TBSA): Significant mortality; modern burn centres have improved survival
• Inhalation injury: Doubles mortality for any given TBSA
• Hypertrophic scarring: Common in deep partial and full-thickness burns; managed with pressure garments, silicone, physiotherapy
• Psychological morbidity: PTSD, depression, body image issues - psychological support essential

Rule of Nines (Adults)

Parkland Formula

Key Facts

Understanding wound healing physiology is fundamental to surgical practice. Identifying and addressing factors that impair healing optimises patient outcomes.

Epidemiology

Chronic wounds affect ~2-4% of the population. NHS spends ~£5 billion/year on wound management. ~200,000 patients have chronic leg ulcers. Surgical site infections affect ~3-5% of surgical wounds.

Aetiology

Types of wound:

• Incisional (surgical), laceration, abrasion, contusion, puncture, avulsion, burn
• Acute wounds: Expected to heal through normal phases
• Chronic wounds: Fail to progress through normal healing - stuck in inflammatory phase (e.g., venous ulcers, diabetic ulcers, pressure ulcers)

Pathophysiology

Phase 1 - Haemostasis (minutes):

Phase 2 - Inflammation (days 1-5):

• Neutrophils (first 24-48 hours) → macrophages (day 2-5; KEY orchestrating cell)
• Phagocytosis, debridement, cytokine release (TGF-β, PDGF, VEGF)

Phase 3 - Proliferation (days 5-21):

• Angiogenesis → granulation tissue formation
• Epithelialisation from wound edges/adnexal structures
• Wound contraction (myofibroblasts)

Phase 4 - Remodelling (weeks to ≥1 year):

• Type III collagen replaced by type I collagen
• Cross-linking increases tensile strength
• Maximum strength ~80% of normal skin at 3 months

Normal Healing

• Progressive wound closure, decreasing inflammation
• Clean, pink granulation tissue
• Contracting wound edges (secondary intention)
• Decreasing pain and exudate

Impaired Healing

• Wound dehiscence (partial or complete)
• Chronic non-healing wound (>6 weeks without healing)
• Excessive exudate, necrotic tissue, biofilm
• Surrounding cellulitis (infection)

Abnormal Scarring

• Hypertrophic scar: Raised, red, stays within wound boundaries; may improve over 1-2 years
• Keloid scar: Extends beyond original wound; does not regress spontaneously; more common in darker skin, earlobes, sternum, shoulders
• Contracture: Excessive wound contraction → functional limitation (especially over joints)

Red Flags

• Wound dehiscence post-laparotomy with pink serous discharge ('pink fluid') - may herald evisceration
• Non-healing wound in elderly or diabetic - exclude malignancy (Marjolin's ulcer - SCC arising in chronic wound)
• Rapidly spreading cellulitis around wound - consider necrotising fasciitis

Bedside

• Wound assessment: Size, depth, tissue type (granulation, slough, necrotic), exudate, edges, surrounding skin
• Wound swab: If clinical infection suspected (not routine - treat clinically)
• ABPI: For leg ulcers - venous (>0.8) vs arterial (<0.5)

Bloods

• FBC: Infection, anaemia
• CRP: Infection
• HbA1c, glucose: Diabetes optimisation
• Albumin, pre-albumin: Nutritional status
• U&Es: Renal function

Imaging

• Duplex US: Venous ulcers (assess venous insufficiency)
• X-ray: Osteomyelitis, foreign body
• MRI: Deep infection, osteomyelitis
• Biopsy: Non-healing wound >6 weeks - exclude malignancy

Optimise Healing Factors

• Nutrition: Adequate protein, calories, vitamin C (collagen synthesis), zinc
• Glycaemic control: HbA1c <58 mmol/mol
• Smoking cessation: Nicotine causes vasoconstriction, reduces oxygen delivery
• Remove/reduce: Steroids, immunosuppressants where possible
• Offloading: Pressure ulcers and diabetic foot ulcers
• Treat infection: Antibiotics only for clinical infection (cellulitis, systemic sepsis)

Wound Management

• Debridement: Sharp, autolytic (hydrogels), mechanical, enzymatic, biological (larval)
• Dressings: Match to wound type - alginate (exudative), foam (moderate exudate), hydrocolloid (low exudate), hydrogel (dry/necrotic)
• Negative pressure wound therapy (NPWT/VAC): Promotes granulation, reduces oedema; useful for complex wounds
• Compression: For venous ulcers (only if ABPI >0.8)

Surgical

• Skin grafting: Split-thickness (SSG) or full-thickness (FTSG) for wounds unable to close
• Flap reconstruction: For complex wounds requiring tissue bulk
• Fasciotomy: Compartment syndrome

Referral Criteria

• Non-healing wound >6 weeks - tissue viability/wound specialist
• Suspected malignancy - biopsy and 2WW
• Complex wounds - plastic surgery
• Diabetic foot - MDT diabetic foot team

• Primary intention wounds: Heal within 1-2 weeks
• Secondary intention: Variable - weeks to months depending on size, depth, patient factors
• Venous ulcers: ~70% heal within 6 months with compression; recurrence common
• Diabetic foot ulcers: ~50% heal within 20 weeks; ~15% lead to amputation
• Pressure ulcers: Prevention is more effective than treatment; mortality ~25-33% in hospitalised patients with Grade IV
• Wound strength: Never exceeds ~80% of original tissue

Phases of Wound Healing

Factors Impairing Wound Healing

Key Facts

Compartment syndrome is a time-critical emergency. Clinical suspicion must lead to urgent action - delays result in irreversible muscle necrosis, contracture, and potential amputation.

Epidemiology

Incidence ~3.1 per 100,000/year. Most common in young males (higher muscle mass). Tibial fractures account for ~40% of cases. Also occurs in forearm (supracondylar fractures in children), thigh, hand, foot, buttock.

Aetiology

Increased compartment contents:

• Fractures (especially tibial shaft)
• Crush injuries
• Post-ischaemic swelling (after revascularisation)
• Burns
• Haemorrhage (anticoagulants)
• Snake bite

Decreased compartment size:

• Tight casts/dressings/bandages
• Circumferential burns with eschar
• Closure of fascial defects

Pathophysiology

• Raised pressure within closed fascial compartment → exceeds capillary perfusion pressure (~25-30 mmHg)

• Irreversible muscle necrosis begins after ~6 hours of ischaemia
• Volkmann's ischaemic contracture: End result of untreated forearm compartment syndrome - fibrosis and contracture of flexor muscles

Five Ps (but early signs are most important)

1. Pain: Out of proportion, not relieved by analgesia, worsened by passive stretch of affected muscles (EARLIEST and MOST IMPORTANT)
2. Pressure: Tense, swollen compartment
3. Paraesthesia: Numbness in distribution of nerve traversing compartment
4. Paralysis: LATE sign - indicates irreversible damage
5. Pulselessness: Very LATE sign - pulses are usually present as compartment pressure rarely exceeds arterial pressure

By Location

• Leg (anterior compartment): Pain on passive plantarflexion; numbness in 1st web space (deep peroneal nerve); weakness of dorsiflexion
• Forearm (volar compartment): Pain on passive extension of fingers; weakness of finger flexion
• Thigh: Less common; massive swelling post-fracture

Red Flags

• Increasing analgesic requirement despite adequate fracture immobilisation
• Pain on passive stretch of the involved muscles
• Paraesthesia - nerve ischaemia has begun
• Tense, swollen limb segment
• Remember: Compartment syndrome can occur WITH intact distal pulses

Clinical (Most Important)

• Clinical diagnosis is paramount - do NOT delay for measurements if suspicion is high
• Pain on passive stretch: Most sensitive clinical sign

Compartment Pressure Measurement

• Stryker needle/manometer: Measure directly
• Absolute pressure >30 mmHg: Diagnostic
• Delta pressure (diastolic BP − compartment pressure) <30 mmHg: Indicates compartment syndrome
• Only measure if diagnosis uncertain and patient cannot reliably report symptoms (e.g., obtunded, sedated)

Bloods

• CK: Elevated from muscle necrosis (rhabdomyolysis)
• U&Es: Myoglobin → AKI; hyperkalaemia from cell death
• Myoglobin: In urine
• FBC, coagulation: Baseline

Emergency Treatment

1. Remove all constricting material: Split casts/dressings/bandages to skin immediately
2. Keep limb at heart level: NOT elevated (elevation reduces perfusion pressure)
3. Emergency fasciotomy: Within 6 hours of symptom onset - definitive treatment

Fasciotomy

Leg (4 compartments):

• Two-incision technique: Lateral incision (anterior and lateral compartments) + medial incision (superficial and deep posterior compartments)
• All 4 compartments MUST be released
• Leave wounds open → delayed primary closure or skin grafting at 48-72 hours

Forearm:

• Volar incision from proximal to distal; carpal tunnel also released

Post-Fasciotomy

• Wound left open: Temporary coverage with VAC/dressings
• Second look at 48-72 hours: Assess muscle viability; debride necrotic tissue
• Delayed closure: Primary closure, split-skin graft, or secondary intention
• Aggressive IV fluids: Prevent rhabdomyolysis-related AKI (target UO >1 mL/kg/hr)

Referral Criteria

• ALL suspected compartment syndrome - immediate orthopaedic/surgical review
• Do NOT delay for investigations

• Fasciotomy within 6 hours: Good functional outcome in most cases
• Fasciotomy after 6 hours: Increasing risk of irreversible muscle necrosis, nerve damage
• Delayed/missed diagnosis: Volkmann's contracture (forearm), muscle necrosis, amputation, rhabdomyolysis, AKI, hyperkalaemia, cardiac arrest
• Mortality: From complications (rhabdomyolysis, AKI, sepsis) - overall low if treated promptly
• Medicolegal significance: Missed compartment syndrome is a common source of litigation in orthopaedics

Compartments of the Leg

Key Facts

Necrotising fasciitis is one of the most feared surgical emergencies. Recognition and immediate surgical intervention are paramount - delays of even hours significantly increase mortality.

Epidemiology

Incidence ~0.4-1 per 100,000/year in UK. Type I more common than Type II. Fournier's gangrene (perineal necrotising fasciitis): M:F ~10:1. Mortality ~20-40% overall; >60% if surgery delayed >24 hours.

Aetiology

Type I (Polymicrobial - 70-80%):

• Mixed aerobic and anaerobic organisms (Bacteroides, Clostridium, E. coli, Streptococcus, Staphylococcus)
• Risk factors: Diabetes, immunosuppression, obesity, peripheral vascular disease, alcohol, chronic renal failure
• Often follows surgery, trauma, or spreads from perianal/genitourinary infection

Type II (Monomicrobial - 20-30%):

• Usually Group A Streptococcus (GAS) ± Staphylococcus aureus
• Can affect young, previously healthy individuals
• May follow minor trauma, varicella, NSAID use (controversial)

Pathophysiology

• Skin initially appears normal because disease spreads beneath it - skin necrosis is a LATE sign

Early Signs (Critical to Recognise)

• Pain out of proportion to clinical findings - most important early sign
• Erythema spreading rapidly (mark the boundary to track progression)
• Swelling, warmth, tenderness out of keeping with apparent cellulitis
• Systemic toxicity: Fever, tachycardia, hypotension disproportionate to apparent infection

Late Signs

• Skin necrosis: Dusky, purple-black discolouration
• Bullae/blisters: Haemorrhagic or serous
• Crepitus: Subcutaneous gas (especially Type I) - may be palpable or visible on imaging
• Anaesthesia: Loss of sensation over involved skin (cutaneous nerve destruction)
• Dishwater grey discharge: Thin, grey, foul-smelling fluid on surgical exploration

Red Flags

• Rapidly spreading cellulitis not responding to IV antibiotics
• Pain out of proportion
• Systemic sepsis with soft tissue infection
• Crepitus or subcutaneous gas on imaging
• Skin necrosis, bullae
• LRINEC score ≥6

Bloods

• FBC: WCC (often >15 × 10⁹/L or <4 × 10⁹/L in severe sepsis)
• CRP: Markedly elevated (often >150)
• U&Es: AKI, raised creatinine
• Glucose: Often elevated (diabetes, stress response)
• Sodium: Often low (<135)
• Lactate: Elevated (tissue hypoperfusion)
• CK: May be elevated (muscle involvement)
• Blood cultures: Before antibiotics
• Clotting: DIC screen

LRINEC Score

Imaging (Do NOT Delay Surgery)

• CT: May show fascial thickening, gas tracking, fluid collections
• MRI: Most sensitive (hyperintense fascial planes on T2) - but time-consuming
• Plain X-ray: May show subcutaneous gas
• Imaging is supportive only - clinical diagnosis and early surgery are paramount

Immediate (Emergency)

1. Resuscitation: Sepsis 6 pathway - O₂, cultures, antibiotics, fluids, lactate, urine output
2. IV antibiotics: Empirical broad-spectrum:
   • Meropenem 1g IV TDS + clindamycin 600mg IV QDS (anti-toxin effect) + flucloxacillin 2g IV QDS (if MRSA not suspected)
   • Adjust based on cultures
3. Emergency surgical debridement: ALL necrotic tissue must be excised; extent often far greater than skin changes suggest
   • 'Finger test': If tissue separates easily from fascia with finger dissection, it confirms necrotising fasciitis
4. ICU referral: Organ support (ventilation, vasopressors, renal replacement)

Post-Operative

• Planned re-look at 24-48 hours: Further debridement until tissue is healthy
• Multiple returns to theatre may be needed
• IVIG: Consider for streptococcal toxic shock syndrome (controversial)
• Wound management: NPWT (VAC) → eventual reconstruction (skin grafting, flaps)
• HDU/ICU care: Multi-organ support

Referral Criteria

• Any suspected necrotising fasciitis - immediate senior surgical review
• Do NOT delay for imaging or score calculation if clinical suspicion is high

• Overall mortality: ~20-40%
• Mortality if surgery delayed >24 hours: >60%
• Fournier's gangrene: Mortality ~20-40% (higher in elderly and diabetics)
• Type II (GAS): Can be rapidly fatal in previously healthy individuals
• Survivors: May require extensive reconstruction; significant functional and psychological morbidity
• Amputation: May be necessary for limb involvement
• Long-term: Chronic wounds, disfigurement, PTSD

Type I vs Type II Necrotising Fasciitis

Key Facts

SSI is a significant cause of post-operative morbidity, prolonged hospital stay, increased cost, and mortality. Prevention through best practice ('care bundles') is more effective than treatment.

Epidemiology

~3-5% of all surgical procedures; higher in emergency surgery (~10%). Accounts for ~16% of all healthcare-associated infections in UK. Increases hospital stay by ~7-10 days. Estimated cost: ~£10,000 per SSI episode.

Aetiology

Patient factors: Obesity, diabetes, smoking, malnutrition, immunosuppression, extremes of age, chronic disease Surgical factors: Wound classification, surgical duration, technique, emergency surgery, foreign body/implant, drains, hypothermia, hyperglycaemia Microbial factors: MRSA carriage, pre-existing infection, wound contamination

Pathophysiology

• 10⁵ organisms per gram of tissue generally required for infection (lower threshold with foreign body/implant)

• Biofilm formation on implants → chronic infection resistant to antibiotics

Superficial SSI (Most Common)

• Within 30 days of surgery
• Involves skin and subcutaneous tissue only
• Erythema, warmth, swelling, tenderness around wound
• Purulent discharge
• Wound dehiscence may occur

Deep SSI

• Involves fascia and/or muscle layers
• May present with deep wound abscess
• Fever, pain, systemic sepsis possible

Organ/Space SSI

• Infection in any part of the body opened/manipulated during surgery (excluding the incision)
• e.g., Intra-abdominal abscess after laparotomy, empyema after thoracotomy
• May present days-weeks post-operatively with fever, pain, or sepsis

Red Flags

• Systemic sepsis (fever, tachycardia, hypotension) with wound signs
• Rapidly spreading wound infection - consider necrotising fasciitis
• Prosthetic joint infection - orthopaedic emergency
• Sternal wound infection post-cardiac surgery - high mortality

Bedside

• Wound assessment: Signs of infection (rubor, calor, tumor, dolor, pus)
• Wound swab: If purulent discharge - send for MC&S (not routine for surveillance)
• Observations: NEWS2

Bloods

• FBC, CRP: Raised WCC and CRP
• Blood cultures: If systemic sepsis
• Procalcitonin: May help guide antibiotic duration

Imaging

• USS: Wound collection/abscess
• CT: Deep/organ-space SSI (e.g., intra-abdominal abscess)
• MRI: Prosthetic joint infection, osteomyelitis

Prevention (NICE NG125 - SSI Care Bundle)

• Pre-operative: MRSA screening and decolonisation, smoking cessation, glucose optimisation, nutritional optimisation, hair removal with clippers (not razor), skin preparation (2% chlorhexidine in 70% isopropyl alcohol)
• Intraoperative: Prophylactic antibiotics at induction (within 60 minutes before incision), maintain normothermia (>36°C), meticulous surgical technique, minimise tissue handling
• Post-operative: Sterile dressing for 48 hours, hand hygiene, appropriate wound care

Prophylactic Antibiotics

• Clean surgery without implant: Not routinely indicated
• Clean with implant: Single dose at induction (e.g., cefazolin 2g IV)
• Clean-contaminated: Single dose at induction (e.g., co-amoxiclav 1.2g IV)
• Contaminated/dirty: Therapeutic course of antibiotics (not just prophylaxis)

Treatment of Established SSI

• Superficial: Open wound, drain pus, irrigate; may not need systemic antibiotics if localised
• Deep/organ-space: IV antibiotics (guided by cultures); drainage of collections (percutaneous or surgical)
• Implant-related infection: Often requires implant removal, debridement, prolonged antibiotics
• MRSA SSI: Vancomycin 15-20mg/kg IV BD or linezolid 600mg IV/PO BD

Referral Criteria

• Deep/organ-space SSI - surgical team
• Prosthetic joint infection - orthopaedic specialist
• MRSA infection - microbiology advice

• Superficial SSI: Usually resolves with local wound care; minimal morbidity
• Deep/organ-space SSI: Significant morbidity; may require reoperation; mortality ~5-10% in severe cases
• Prosthetic joint infection: Complex; may require implant removal; long-term functional impact
• Increased hospital stay: ~7-10 days per SSI episode
• Financial cost: ~£10,000 per SSI episode
• Prevention: Care bundles reduce SSI rates by 30-50%

Wound Classification (CDC)

Key Facts

Perioperative care is a multidisciplinary process. Systematic assessment, optimisation, and evidence-based care pathways significantly improve surgical outcomes.

Epidemiology

~4.7 million surgical procedures performed annually in England. ~1 in 4 surgical patients has significant comorbidities. Emergency surgery carries ~10× the mortality of elective surgery. Post-operative complications occur in ~10-20% of cases.

Aetiology

Perioperative complications arise from the interaction of patient factors (comorbidities, functional capacity), surgical factors (complexity, duration, emergency vs elective), and anaesthetic factors.

Pathophysiology

Surgical stress response:

• Tissue injury → neuroendocrine response (cortisol, catecholamines, ADH, aldosterone)
• Catabolic state → protein breakdown, insulin resistance, sodium/water retention
• Inflammatory response → risk of organ dysfunction, wound healing impairment
• ERAS pathways aim to minimise the stress response

Pre-operative Assessment

History:

• Comorbidities: Cardiac, respiratory, renal, hepatic, diabetes
• Functional capacity: Can the patient climb 2 flights of stairs? (≥4 METs)
• Previous surgery and anaesthetic history: MH, difficult intubation
• Medications: Anticoagulants, antiplatelets, antihypertensives, insulin, steroids
• Allergies, smoking, alcohol
• Airway assessment: Mallampati score

ASA Classification:

Post-operative Complications

Immediate (0-24 hours):

• Haemorrhage (reactionary), anaesthetic complications (PONV, hypothermia)

Early (1-7 days):

• Surgical site infection, DVT/PE, pneumonia, AKI, urinary retention, paralytic ileus, anastomotic leak

Late (>7 days):

• Wound dehiscence, incisional hernia, adhesions, chronic pain

Pre-operative

• Bloods: FBC, U&Es, LFTs, coagulation, G&S/crossmatch, HbA1c (diabetics)
• ECG: If cardiac risk factors, age >65, ASA ≥III
• CXR: Not routine; only if clinical indication (NICE NG45)
• Echocardiography: If suspected valvular disease, HF symptoms
• CPET: For major surgery in patients with limited functional capacity
• Lung function tests: If COPD/asthma for major thoracic/abdominal surgery