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Burns, Plastic & Reconstructive Surgery

Bailey & Love's Short Practice of Surgery, 28th Edition - Chapter 46 & 47

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1. CLASSIFICATION OF BURNS

By Cause (Aetiology)

• Thermal: scalds (hot liquids/steam), flame, contact
• Chemical: acid or alkali
• Electrical: low voltage (<1000 V) or high voltage (>1000 V)
• Radiation: UV, ionising
• Cold (frostbite)

By Depth (The Two-Group Concept)

Detailed Depth Classification:

• Only epidermis involved
• Red, painful, no blisters (e.g., sunburn)
• Heals in 5-7 days, no scarring

• Epidermis + superficial dermis
• Blistered, moist, very painful, pink/red base
• Blanches on pressure, sensation intact
• Heals in 10-14 days with minimal scarring

• Epidermis + deeper dermis; adnexal structures partially preserved
• Pale/mottled, less painful (nerve endings damaged), does NOT blanch
• Heals slowly (>21 days) with significant scarring - often requires surgery

• Entire dermis destroyed; may involve fat, muscle, bone
• Leathery, white/brown/black, painless (nerves destroyed)
• Will NOT heal without skin grafting

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2. THE PATHOPHYSIOLOGY OF BURN INJURY

Local Effects - Jackson's Zones of Burn Injury

1. Zone of Coagulation - innermost; irreversible cell death
2. Zone of Stasis - surrounding; blood flow compromised but potentially salvageable - at risk of deepening with infection, hypoperfusion, or desiccation
3. Zone of Hyperaemia - outermost; increased blood flow, heals spontaneously

The goal of initial burn management is to prevent the zone of stasis from converting to coagulation.

Systemic Effects

• Burns >15% TBSA (adults) cause massive fluid shifts from the intravascular to extravascular compartment
• Massive capillary permeability increases (especially in the first 8 hours)
• Protein-rich oedema forms both locally and systemically
• Results in hypovolaemic shock ("burn shock")
• Fluid loss is maximum in the first 8 hours and slows by 24-36 hours

1. Upper airway injury - supraglottic thermal injury causing oedema and obstruction
2. Lower airway injury (smoke inhalation) - chemical pneumonitis from particles, loss of respiratory epithelium
3. Metabolic poisoning - CO and cyanide from incomplete combustion

• Burns to face and neck, blistering inside the mouth
• History of being trapped in an enclosed space
• Hoarseness/change of voice, stridor
• Singeing of facial and nasal hair

• Hypermetabolism, catabolism, immunosuppression, increased infection risk
• Thermoregulatory failure (loss of skin insulation)
• Hypothermia is part of the lethal triad: acidosis + coagulopathy + hypothermia

• Acute kidney injury (from hypovolaemia + myoglobinuria in electrical burns)
• Sepsis and multiorgan failure
• Stress ulceration (Curling's ulcer)
• Anaemia

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3. ASSESSMENT OF THE BURN WOUND (2008 SN)

Assessing Size - Rule of Nines (2005 SN, 2004 SN)

• Tends to overestimate burn size
• Inaccurate in obesity (torso proportion increases)
• Not suitable for children under 10 years (relatively larger head, smaller legs)

Assessing Depth

• Scalds: superficial partial-thickness
• Flame: mixed depth
• Chemical: variable, often deeper than appears
• Electrical: entry/exit point deep; internal damage unpredictable
• Contact: deep partial or full thickness

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4. FLUID THERAPY IN BURNS (2010 SN, 2007 SN, 2005 SN)

When to Start IV Resuscitation

• Adults with >15% TBSA burns
• Children with >10% TBSA burns
• Must start from time of burn (not time of arrival)

Modified Parkland Formula (Crystalloid - most widely used)

Volume (mL) = 4 × weight (kg) × % TBSA burned

• Fluid used: Hartmann's solution (Ringer's lactate) - most closely replicates plasma osmolality
• First half given in first 8 hours from time of burn
• Second half given over the next 16 hours
• Children also require additional maintenance fluid (dextrose-saline):
  • 100 mL/kg/24h for first 10 kg
  • 50 mL/kg for next 10 kg
  • 20 mL/kg for each kg >20 kg

Muir & Barclay Formula (Colloid - used in some UK burns units)

Volume per portion (mL) = % burn × weight (kg) ÷ 2

• Six portions given over 36 hours from time of burn:
  • 3 portions, one every 4 hours (12 hours total)
  • 2 portions, one every 6 hours (12 hours total)
  • 1 final portion over 12 hours
• Original fluid: fresh-frozen plasma or albumin

Worked Example

• First 3000 mL in 8 hours from time of burn
• Next 3000 mL over following 16 hours

• First 5000 mL in 8 hours
• Next 5000 mL over 16 hours

Monitoring of Resuscitation

• Target: 0.5-1.0 mL/kg/hour in adults
• <0.5 mL/kg/h: give a bolus of 10 mL/kg

• 2 mL/kg/h: reduce infusion rate (avoid over-resuscitation)

If oral resuscitation is necessary (resource-limited settings), salt must be added - plain water causes hyponatraemia and can be fatal.

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5. IMMEDIATE CARE OF THE BURN PATIENT

Primary Survey (ABCDE)

1. Airway: early intubation if airway burns suspected (progressive oedema can close airway)
2. Breathing: 100% high-flow oxygen (treats CO poisoning); escharotomy for circumferential chest burns
3. Circulation: two large-bore IV lines (through unburned or burned skin if necessary); commence fluids
4. Disability: analgesia, neurological assessment
5. Exposure/Environment: stop the burning process; maintain temperature (warm fluids, Bair Hugger, warm room)

Criteria for Admission to Burns Unit (Table 46.1)

• Burns >10% TBSA adults; >5% in extremes of age
• Full-thickness burns
• Burns to face, hands, feet, genitalia, perineum, major joints
• Circumferential burns
• Inhalation injury
• Chemical or electrical burns
• Burns + trauma
• Burns in vulnerable patients (frail elderly, children at risk of NAI)

Temperature Management

• Hypothermia is part of the lethal triad: acidosis + coagulopathy + hypothermia
• Infuse warmed fluids
• Warm the room/use external warmers (Bair Hugger)

Nutritional Support

• Early enteral feeding within 6 hours of burn
• Nasogastric tube in large burns
• Protein requirements dramatically increase

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6. TREATING THE BURN WOUND

Group A Burns (Superficial Partial-Thickness)

• Two key goals: prevent infection (which can deepen the burn) and control pain
• Cleanse wound, remove devitalised tissue
• Apply appropriate dressings (silver-containing, biosynthetic, or moist wound dressings)
• Popular dressings: silver sulfadiazine (Flamazine), Mepitel, Mepilex, Acticoat, biosynthetic Biobrane
• Review at 48-72 hours; if healing well, conservative management continues

Group B Burns (Deep Partial-Thickness & Full-Thickness)

• Early tangential excision and skin grafting - ideally within 3-5 days of burn
• Benefits of early excision: reduces mortality, sepsis, hospital stay
• Anaesthetist must prepare for significant blood loss
• Tumescence fluid and topical adrenaline reduce bleeding
• Apply stable cover - split-skin graft (permanent) or dermal substitute (temporary)

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7. SKIN GRAFTING (2018 SN, 2016 SN)

Graft Failure Causes:

1. Shear forces disrupting graft from wound bed
2. Infection (especially group A β-haemolytic Streptococcus)
3. Haematoma or seroma lifting graft from bed

Types of Skin Grafts

1. Split-Thickness Skin Graft (STSG) / Thiersch Graft

• Contains epidermis + variable (partial) amount of dermis
• Thickness: typically 0.30-0.38 mm
• Harvested by dermatome (Humby knife) or graft knife, most commonly from the thigh
• Advantages:
  • Can cover large areas
  • Donor site heals by re-epithelialisation from adnexal structures (~10-14 days)
  • Can be meshed (expanded using rollers creating diamond-shaped cuts) to cover larger defects (1:1.5 to 1:9 ratio)
• Disadvantages:
  • More contraction than FTSG
  • Inferior cosmesis (dyspigmentation, abnormal texture)
  • Painful donor site
  • Meshed grafts leave a permanent mesh-pattern scar
  • Serial reharvesting thins the donor site

2. Full-Thickness Skin Graft (FTSG) / Wolfe Graft

• Contains epidermis + entire dermis
• Harvested from areas with skin laxity: groin, postauricular (behind ear), eyelid, inner arm
• Donor site must be closed primarily (direct suture)
• Advantages:
  • Less contraction
  • Better cosmetic result, better colour match
  • Better sensation
• Disadvantages:
  • Limited donor site availability
  • Cannot cover large areas

Graft Take and Survival

1. Plasmatic imbibition (0-48 h): graft absorbs fluid from wound bed passively
2. Inosculation (48-72 h): graft vessels align with wound bed vessels
3. Revascularisation/angiogenesis (days 3-5): new vessels grow into graft

Meshing

• Putting the STSG through rollers to create diamond-shaped perforations
• Expands coverage area
• Reduces haematoma/seroma risk
• Creates characteristic mesh-pattern scar post-healing

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8. PEDICLE GRAFT (2005 SN)

Types of Pedicle Flaps

• Cutaneous (skin only)
• Fasciocutaneous (skin + fascia)
• Musculocutaneous/myocutaneous (skin + muscle)
• Osseous/osteocutaneous (includes bone)

• Random pattern flap: blood supply from dermal/subdermal plexus; length-to-width ratio limited to ~1.5:1 (2:1 in face)
• Axial pattern flap: has a named arteriovenous pedicle running along its axis; can be much longer

• Local flaps: advancement (e.g. V-Y), rotation, transposition (e.g. Z-plasty, rhomboid flap), interpolation
• Regional/distant flaps: pedicled across body (e.g. cross-leg flap, groin flap to hand)

The Tubed Pedicle (Historical)

• Developed by Filatov and Gillies (1916-17) - the "waltzing" technique
• Skin rolled into a tube to carry blood supply across distances
• Largely replaced by free tissue transfer today

Delay Phenomenon

• Partial division of the pedicle prior to final transfer - conditions the flap to survive on the remaining pedicle blood supply, improving reliability

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9. MYOCUTANEOUS FLAP (1988 SN)

Blood Supply - Mathes & Nahai Classification (5 Types)

Advantages of Myocutaneous Flaps

• Carry reliable blood supply
• Fill dead space (muscle bulk)
• Bring healthy vascularised tissue to poorly vascularised/infected wounds
• Good for irradiated, infected, or avascular beds

Common Myocutaneous Flaps and Uses

Free Flap vs. Pedicled Flap

• Free flap: flap completely detached and revascularised at recipient site using microsurgical anastomosis - greater versatility, can reach any site
• Pedicled flap: remains attached - simpler, no microsurgery required, limited by pedicle reach

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10. POST-BURN CONTRACTURE (1992 SN, 1988 LQ)

Definition

Pathophysiology

• Deep dermal and full-thickness burns heal with dense fibrous scar tissue
• Myofibroblasts in healing wound contract the scar
• Contraction across joints causes progressive deformity (contracture)
• Immature scar continues to contract for up to 18 months

Common Sites

• Axilla (anterior axillary band)
• Neck (neck flexion deformity)
• Elbow/knee (flexion contracture)
• Hand (especially first web space - thumb adduction deformity)
• Eyelids (ectropion)
• Mouth (microstomia)

Prevention of Post-Burn Contracture

1. Early excision and grafting of deep burns - prevents prolonged secondary intention healing and wound contraction
2. Physiotherapy - early mobilisation during admission and rehabilitation
3. Splinting in position of function:
   • Hands: intrinsic-plus position (MCPs flexed, IPJs extended, thumb abducted)
   • Knees: extension
   • Axillae: abduction
   • Neck: extension
4. Pressure garments - custom-made elastic compression garments worn for 12-18 months; reduce scar hypertrophy and contracture
5. Silicone sheets - used in combination with pressure therapy
6. Patient education and compliance with therapy regimen

Treatment of Established Contracture

• Z-plasty: lengthens a linear contracture by transposing two triangular flaps - each limb at 60° doubles the length of the scar
• W-plasty: breaks up a linear scar
• Skin grafting (STSG or FTSG) after contracture release
• Local or free flaps for complex contractures or when grafted area likely to re-contract
• Severe contractures (neck, axilla) may require free tissue transfer

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11. COMPLICATIONS OF BURN INJURY (1988 LQ)

Immediate

• Airway obstruction and inhalation injury
• Hypovolaemic shock
• CO/cyanide poisoning

Early

• Acute respiratory distress syndrome (ARDS)
• Acute kidney injury (AKI)
• Sepsis - most common cause of late death
• Wound infection (Pseudomonas, Staphylococcus, Candida)
• GI complications: ileus, Curling's ulcer (stress ulcer - rare with modern prophylaxis)
• Hypothermia (lethal triad)

Late

• Hypertrophic scarring and keloids
• Post-burn contractures
• Heterotopic ossification
• Peripheral neuropathy
• Psychological sequelae (PTSD, depression, body image disorders)
• Anaemia (chronic)
• Growth disturbance in children
• Marjolin's ulcer: squamous cell carcinoma arising in chronic burn scar (long latency)

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Quick Summary Tables for Exam

Fluid Resuscitation Formulas

Split vs Full-Thickness Skin Graft

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4 × 50 × 30 = 6000 mL Hartmann's - first 3000 mL in 8h, next 3000 mL in 16h, target UO 0.5-1 mL/kg/h.

LIVER & OESOPHAGUS - Surgery Past Papers

Bailey & Love's Short Practice of Surgery, 28th Edition - Chapters 6, 66, 69

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PART A: LIVER

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1. HYDATID CYST OF THE LIVER

Pathogenesis & Life Cycle

• Definitive host: Dog (adult worm lives in small intestine)
• Intermediate hosts: Humans, sheep, cattle
• The dog passes eggs in faeces - highly resistant to temperature extremes
• Humans are infected by the oral route through close contact with infected dogs (contaminated hands, food, water)
• Eggs hatch in the human duodenum; the oncosphere (hexacanth embryo) penetrates the intestinal wall and enters the portal circulation
• Carried to the liver (first filter) - the liver is the most commonly affected organ (75%)
• If it escapes the liver - the lung is next most common (second filter, ~15%)
• Any organ can be affected (brain, bone, kidney, spleen)
• In colder climates, E. multilocularis causes alveolar echinococcosis - spreads by actual invasion rather than expansion (behaves like a malignancy)

Structure of the Hydatid Cyst

1. Pericyst (outer layer): Derived from compressed host liver tissue - thick, fibrous, may calcify
2. Ectocyst (laminated/hyaline layer): Acellular, white, non-infective, allows nutrient transfer - like the white of a hard-boiled egg
3. Endocyst (germinal/inner layer): The living parasite layer - secretes the ectocyst fluid and produces brood capsules, scolices (protoscolices) and daughter cysts (invaginations of the germinal layer)

WHO Classification of Hepatic Hydatid Cyst (Table 6.1, Bailey & Love)

Clinical Features

• Gradual right upper quadrant pain/heaviness
• Palpable liver swelling - smooth, rounded
• A sheep farmer with a growing RUQ mass should be suspected
• Asymptomatic - incidental finding on imaging

1. Rupture into the peritoneum - anaphylactic shock (most dangerous, can be fatal), peritonitis, secondary peritoneal hydatidosis
2. Rupture into bile ducts - jaundice, cholangitis, biliary colic (daughter cysts/membrane in CBD)
3. Rupture into pleural cavity / bronchus - expectoration of salty fluid ("salty water with grape skins"), haemoptysis
4. Secondary infection - becomes pyogenic abscess
5. Pressure effects - on portal vein (portal hypertension), bile ducts (obstructive jaundice), IVC

Investigations

Never aspirate a hydatid cyst blindly (risk of anaphylaxis and dissemination) - except under strict conditions with PAIR.

Treatment

• Albendazole 400 mg BD (cycles of 28 days on, 14 days off) - before and after intervention
• Praziquantel - scolicidal, used adjunctively
• Used in Group 3 (inactive/calcified) - conservative/watch and wait

• Puncture (ultrasound-guided)
• Aspiration of cyst contents
• Injection of scolicidal agent (20% hypertonic saline, 95% ethanol)
• Re-aspiration after 5-15 minutes
• Pre-treatment with albendazole mandatory (at least 4 hours before)
• Performed in a tertiary centre with hepatobiliary surgeon, physician, and interventional radiologist

• Indicated when PAIR fails, cysts unsuitable for PAIR (superficial, CE3b with solid matrix, biliary communication, infected cysts), or complications
• Precautions during surgery:
  • Continue albendazole perioperatively
  • Pack peritoneal cavity with 20% hypertonic saline-soaked packs
  • Instil 20% hypertonic saline into cyst before opening (scolicidal)
  • Avoid spillage
• Options:
  • Radical: Pericystectomy (complete excision of pericyst) or liver resection - no risk of recurrence
  • Conservative (open/partial cystectomy): Deroofing, evacuation, capitonnage (suturing cyst wall to obliterate cavity), or marsupialization
  • A biliary communication must be actively sought and sutured
  • Omentoplasty (packing with pedicled omentum) reduces bile leak and residual cavity

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2. AMOEBIC LIVER ABSCESS

Aetiology & Pathogenesis

• Caused by Entamoeba histolytica (protozoan)
• Spread via faeco-oral route (contaminated food/water in endemic areas)
• Trophozoites from amoebic dysentery in colon enter portal bloodstream → liver
• Right lobe predominantly affected (receives most portal flow)
• Typically solitary, large abscess ("anchovy sauce" pus - chocolate-brown, odourless, sterile)

Clinical Features

• Pain - right hypochondrium (may refer to right shoulder tip)
• Fever - high, swinging, with rigors
• Tender hepatomegaly - intercostal tenderness
• Diaphragmatic irritation - right basal pleural effusion, raised right hemidiaphragm
• History of dysentery (present in only 30%)
• Travel to/residence in endemic area

Investigations

• Ultrasound: Hypoechoic cystic lesion in right lobe
• CT scan: Peripheral enhancement, wall enhancement
• Serology: Amoebic complement fixation test, ELISA - positive in >95%
• Aspiration: "Anchovy sauce" pus (no organisms seen on microscopy - amoebae are in wall)
• FBC: Leucocytosis, raised ESR; anaemia in chronic cases
• LFTs: Raised ALP and bilirubin

Treatment

• Metronidazole 800 mg TDS for 10 days - highly effective (90-95% success with medical treatment alone)
• Follow up with diloxanide furoate (luminal amoebicide) to eradicate intestinal cysts
• Aspiration indicated if:
  • Failure to respond to metronidazole within 48-72 hours
  • Large abscess (>5 cm) - risk of rupture
  • Left lobe abscess (risk of pericardial rupture)
  • Imminent rupture
• Surgery: Rarely needed - laparoscopic drainage if repeated aspiration fails or rupture occurs

Amoebic vs Pyogenic Liver Abscess

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3. HEPATOMA (HEPATOCELLULAR CARCINOMA)

Definition & Epidemiology

• HCC = malignant tumour arising from hepatocytes - most common primary liver cancer
• Fifth most common cancer in men, seventh in women
• Responsible for a third of all cancer-related deaths globally
• Over 80% of cases in Asia and sub-Saharan Africa (incidence 99/100,000 vs 5/100,000 in Europe)
• Three times more common in men than women
• HCC is the leading cause of death in cirrhotic patients

Aetiology & Risk Factors

1. Chronic Hepatitis B (HBV) - accounts for >50% of worldwide cases; HBV vaccination reduces incidence
2. Chronic Hepatitis C (HCV) - increases risk 17-fold by promoting end-stage liver disease
3. Cirrhosis (any cause) - alcoholic, NASH, metabolic
4. Alcohol - lifetime exposure, independent risk factor
5. Aflatoxin (Aspergillus flavus contamination of rice/grain) - seasonal variation in high-risk areas
6. Obesity and diabetes mellitus - independent risk factors
7. Haemochromatosis, primary biliary cirrhosis, alpha-1 antitrypsin deficiency

Clinical Features

• Often asymptomatic until advanced
• Right upper quadrant pain, weight loss, anorexia, malaise
• Features of underlying cirrhosis (jaundice, ascites, splenomegaly)
• Hepatic decompensation in previously compensated cirrhosis
• Raised alpha-fetoprotein (AFP) - marker for HCC
• Rarely: Paraneoplastic syndromes (hypoglycaemia, erythrocytosis, hypercalcaemia)
• Budd-Chiari syndrome from hepatic vein invasion; portal hypertension from portal vein invasion

Investigations

1. AFP (alpha-fetoprotein) - raised in >70% of HCC; >400 ng/mL strongly suggestive
2. Ultrasound - initial screening; hypoechoic mass
3. CT with contrast (triphasic) - arterial enhancement ("washout" pattern) - characteristic
4. MRI - excellent for characterisation; gadolinium-enhanced
5. Biopsy - avoided if resection planned (risk of seeding); used if diagnosis uncertain
6. Staging by BCLC (Barcelona Clinic Liver Cancer) system - most widely used:
   • Accounts for tumour characteristics, liver function (Child-Pugh), and performance status

Staging - BCLC System

Treatment

• Only 20-40% of patients are candidates
• Best outcomes: solitary tumour, no vascular invasion, no extrahepatic spread, preserved liver function
• Anatomical resection preferred (especially for HCC)
• Contraindications: extrahepatic metastases, bilobar/multiple tumours, main portal vein/IVC thrombus, main bile duct involvement

• Tumour ≤5 cm (single), or up to 3 nodules each ≤3 cm, no vascular invasion, no extrahepatic disease
• 4-year overall survival 75%, recurrence-free survival 83% (Mazzaferro, 1996)
• Treats both tumour AND underlying cirrhosis

• RFA (radiofrequency ablation): For small (<3 cm) unresectable lesions - comparable to surgery for small HCC
• TACE (transarterial chemoembolisation): Intermediate stage; chemotherapy + embolisation via hepatic artery
• SIRT (Selective Internal Radiation Therapy): Yttrium-90 microspheres

• Sorafenib (multikinase inhibitor) - first-line for advanced HCC (BCLC C)
• Atezolizumab + bevacizumab - now preferred first-line in many centres

Prognosis

• Median survival following diagnosis: 6-20 months
• Overall 5-year survival: <10%
• 60% of deaths from cancer, 40% from underlying liver disease

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PART B: OESOPHAGUS

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4. ACHALASIA CARDIA

Note: "Kardiospasm" is the old term for achalasia - same condition.

Definition & Pathology

1. Failure of the Lower Oesophageal Sphincter (LOS) to relax on swallowing
2. Absent or disordered peristalsis in the oesophageal body

Aetiology

• Exact aetiology uncertain
• Loss/degeneration of inhibitory ganglion cells in Auerbach's (myenteric) plexus at the LOS
• Postulated mechanism: virus-induced autoimmune destruction of inhibitory neurons (VIP and NO-releasing neurons)
• Histology: Reduction in ganglion cells, variable chronic inflammation
• Result: Loss of inhibitory neurotransmission (VIP/NO) → LOS fails to relax; excitatory neurones predominate

• Idiopathic (primary) - most common
• Chagas disease (South America) - Trypanosoma cruzi destroys myenteric plexus; clinically identical
• Allgrove syndrome (rare genetic) - achalasia + adrenal insufficiency + alacrimia (triple-A syndrome)
• Pseudo-achalasia: Secondary to malignancy (gastric cardia cancer, lung, lymphoma) - must be excluded

Pathophysiology

1. Normal swallowing triggers sequential peristalsis + LOS relaxation
2. In achalasia: Absent inhibitory neurons → LOS does not relax + peristalsis absent/disordered
3. Progressive dilation of oesophageal body (retained food + fluid)
4. Oesophagus becomes progressively tortuous and dilated (megaoesophagus, "sigmoid oesophagus")
5. Persistent retention oesophagitis due to fermentation → increased risk of squamous cell carcinoma of oesophagus

Chicago Classification of Achalasia (HRM-based)

Clinical Features

• Age: 30-60 years; equal sex distribution
• Dysphagia: To both solids AND liquids (distinguishes from mechanical obstruction which is solids first) - paradoxical dysphagia (fluids may be worse initially)
• Regurgitation: Of undigested food eaten hours/days ago (no acid taste - non-acid contents)
• Heartburn: Present (from fermentation, not acid) - often misdiagnosed as GORD
• Chest pain / odynophagia: Especially in early and Type III achalasia
• Weight loss: Variable; patients adapt diet, may maintain weight
• Aspiration / nocturnal cough: From retained food
• Halitosis: From fermentation of retained food
• Eckardt score used to quantify symptom severity (dysphagia, regurgitation, chest pain, weight loss; each 0-3; total 0-12)

Diagnosis

• "Bird's beak" or "rat's tail" deformity at the LOS - smooth, symmetrical tapering
• Hold-up of contrast at the distal oesophagus
• Dilated oesophageal body; absent peristalsis
• Absent gastric air bubble (no air swallowed through closed LOS)
• Advanced: "Sigmoid oesophagus"

• Frothy saliva pool in oesophagus
• Resistance at the OGJ (but scope can pass with gentle pressure - unlike cancer)
• Dilated oesophagus with retained food
• Important to exclude pseudo-achalasia (malignancy at OGJ)

• Elevated integrated relaxation pressure (IRP >15 mmHg)
• Absent peristalsis / spastic contractions
• Classifies into Types I, II, III (Chicago classification)

• Measures distensibility of LOS
• Distensibility index (DI) reduced in achalasia

Treatment

• Calcium channel blockers (nifedipine), nitrates, 5'-phosphodiesterase inhibitors (sildenafil)
• Reduce LOS pressure temporarily
• Significant side effects; reserved for poor operative candidates

• Injected into LOS endoscopically; inhibits acetylcholine release from excitatory neurones
• Effect lasts only 6-12 months (needs repeated injections)
• Suitable for elderly/frail patients unfit for surgery
• Efficacy decreases with repeat injections; may make subsequent surgery more difficult

• Graded dilatation of LOS using balloons (30mm, 35mm, 40mm)
• Effective in 70-85% at 1 year; 50% at 5 years
• Best results for Type II achalasia
• Main risk: Perforation (~2-3%)
• Preferred in elderly or those unfit for surgery; can be repeated

• Gold standard surgical treatment
• Anterior longitudinal myotomy through LOS, extending 6 cm up oesophagus and 2 cm onto gastric cardia
• Must include partial fundoplication (Dor anterior or Toupet posterior) to prevent GORD (45% incidence without it)
• Effective in ~90% at 1-5 years
• Comparable to pneumatic dilatation (RCTs)

• Submucosal tunnel created endoscopically; circular muscle fibres divided from inside
• Myotomy: minimum 6 cm in oesophagus + 2 cm into gastric cardia
• Particularly advantageous for Type III achalasia (long myotomy)
• RCTs show similar efficacy to PD and Heller's
• Disadvantage: Higher incidence of post-procedure GORD (~57% oesophagitis at 3 months)

• Reserved for "end-stage" achalasia - massively dilated sigmoid oesophagus not responding to other treatments
• Significant morbidity; used only in surgically fit patients

Summary Box (Bailey & Love)

• HRM is the gold standard for diagnosis
• A normal endoscopy does NOT exclude achalasia
• Always exclude pseudo-achalasia (malignancy at OGJ)
• Laparoscopic myotomy, pneumatic dilatation, and POEM are all effective treatments
• Type III achalasia may be better treated with long myotomy by POEM

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5. CARCINOMA OF THE OESOPHAGUS

Epidemiology

• 8th most common cancer worldwide, 6th most common cause of cancer death
• Presents in 6th-7th decades
• Two main types: Squamous cell carcinoma (SCC) and Adenocarcinoma (ADC)
• Worldwide: SCC predominates; in Western countries, incidence of ADC has overtaken SCC since 1990s

Aetiology (Bailey & Love Table 66.3)

Pathology

• Upper/middle third oesophagus
• Arises from squamous epithelium
• Macroscopic: Proliferative (exophytic), ulcerative, or infiltrative

• Lower third and OGJ (gastro-oesophageal junction)
• Arises from Barrett's metaplasia (intestinal metaplasia)
• GORD → Barrett's → Low-grade dysplasia → High-grade dysplasia → Adenocarcinoma

Clinical Features

• Progressive dysphagia - first to solids, then liquids (mechanical obstruction - opposite to achalasia)
• Weight loss (significant, often >10% body weight)
• Odynophagia (pain on swallowing)
• Regurgitation
• Cough, hoarseness (recurrent laryngeal nerve involvement)
• Aspiration pneumonia
• Haematemesis (uncommon)
• Bone pain, lymphadenopathy - metastatic disease

• Left supraclavicular lymphadenopathy (Virchow's node)
• Hepatomegaly
• Horner's syndrome (T1 involvement)
• Stridor (tracheal invasion)
• Oesophagorespiratory fistula - coughing when swallowing

Investigations

1. Barium swallow: Mucosal irregularity, rat-tail narrowing, shouldering; apple-core deformity
2. OGD + biopsy (essential for histological diagnosis)
3. CT chest/abdomen/pelvis (staging - mediastinal invasion, distant metastases)
4. EUS (Endoscopic Ultrasound): Best for T-staging and local nodal staging
5. PET-CT: Identifies distant metastases, changes management in ~20%
6. Bronchoscopy: Mid/upper oesophageal tumours - exclude airway invasion (contraindication to surgery)
7. Laparoscopy: Lower oesophageal/OGJ tumours - exclude peritoneal metastases
8. FBC, LFTs, nutritional assessment

Staging (TNM - AJCC 8th Edition)

Management

• Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) for T1a (limited to mucosa, no lymphovascular invasion)
• Radiofrequency ablation (RFA) for high-grade dysplasia in Barrett's

• Oesophagectomy remains the primary surgical option
• For ≥T3 or N+: Neoadjuvant chemoradiotherapy (CROSS protocol: carboplatin + paclitaxel + RT) → surgery
• Surgical techniques:
  • Ivor Lewis oesophagectomy (right thoracotomy + laparotomy, intrathoracic anastomosis) - most common
  • McKeown (three-stage) oesophagectomy - cervical anastomosis
  • Transhiatal oesophagectomy - avoids thoracotomy; cervical anastomosis
  • Minimally invasive approaches (thoracoscopic/laparoscopic)
• Conduit: Gastric pull-up (most common); alternatively, colonic interposition
• Pre-operative optimisation: Stop smoking and alcohol; chest physiotherapy; nutritional support (nasogastric/jejunostomy)

• Self-expanding metal stent (SEMS): Relieves dysphagia rapidly
• Palliative chemoradiotherapy: Improves survival and swallowing
• Chemotherapy alone (cisplatin + 5-FU or carboplatin-based)
• Radiotherapy: SCC more radiosensitive than ADC
• Laser endotherapy / APC: Tumour debulking
• Feeding jejunostomy / nasogastric tube: Nutritional support

Prognosis

• Overall 5-year survival ~20%
• Surgical series: 30-40% at 5 years in selected patients
• T1 disease treated endoscopically: >90% cure

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6. GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD) & REFLUX OESOPHAGITIS

Definition

Pathophysiology

• Reflux barrier = Lower oesophageal sphincter (LOS) + crural diaphragm
• Impaired by: Transient LOS relaxations (TLOSRs), LOS hypotension, hiatus hernia
• TLOSRs (transient lower oesophageal sphincter relaxations) are the main mechanism - physiological venting of gastric fundus after meals; abnormally frequent in GORD
• Acid and bile reflux cause mucosal injury

Symptoms

• Heartburn (pyrosis) - retrosternal burning, post-prandial, worse lying flat
• Regurgitation - effortless return of acid/food to mouth
• Extra-oesophageal: Asthma, chronic cough, laryngitis, dental erosion, globus

Complications

1. Oesophagitis - erosive or non-erosive
2. Oesophageal stricture (peptic/Schatzki's ring)
3. Barrett's oesophagus - columnar metaplasia replacing squamous epithelium; premalignant
4. Adenocarcinoma of oesophagus

Treatment

• Lifestyle: Weight loss, head of bed elevation, avoid late meals, reduce alcohol, coffee
• PPI (proton pump inhibitor) - first-line; >90% mucosal healing at 8 weeks; "step-down" after initial 8 weeks
• H2-receptor antagonists, antacid-alginate preparations

• Indications: Failed medical therapy, young patients requiring lifelong PPI, GORD with large hiatus hernia, regurgitation not controlled by PPI
• Laparoscopic Nissen fundoplication (360° wrap) - gold standard
• Partial fundoplication alternatives: Dor (anterior 180°), Toupet (posterior 270°)

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7. HIATUS HERNIA

Definition

Types (4 types)

• Sliding hernia closely associated with GORD
• Giant paraoesophageal hernia: >50% of stomach in thorax; risk of gastric volvulus
• Gastric volvulus: Organoaxial (most common - rotates on longitudinal axis) or mesentericoaxial
  • Emergency presentation: Obstruction, strangulation, ischaemia, perforation

Clinical Features

• Type I: Heartburn, regurgitation (GORD symptoms)
• Type II/III: Obstructive symptoms, dysphagia, postprandial fullness
• Incidental finding on CXR (retrocardiac gas bubble)

Investigations

• CXR: Intrathoracic gas bubble/fluid level behind heart
• Barium swallow: Confirms type and extent
• OGD: Assesses oesophagitis, Barrett's, OGJ position
• CT: For large hernia, assess other visceral involvement

Management

• Asymptomatic sliding: Conservative
• Symptomatic: Medical (PPI) for GORD component
• Surgical indications: All symptomatic paraoesophageal hernias (risk of volvulus/strangulation), type II/III/IV, failure of medical therapy
• Laparoscopic hiatal repair + fundoplication (most common)

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8. MALLORY-WEISS SYNDROME

Definition

Pathophysiology

• Sudden increase in intra-abdominal/intragastric pressure from retching/vomiting
• Longitudinal mucosal tear through mucosa ± submucosa (not full thickness - if full thickness = Boerhaave's syndrome)
• Tear is almost always on the gastric side of the OGJ

Causes/Associations

• Alcoholic retching (most common)
• Severe vomiting (any cause)
• Vigorous coughing, stridor
• Cardiopulmonary resuscitation (CPR)
• Endoscopy, weightlifting

Clinical Features

• Haematemesis following an episode of forceful vomiting/retching - characteristically the patient vomits first (non-bloody), then the next vomit contains blood
• Bleeding is rarely severe and usually self-limiting
• Melaena may follow
• Rarely haemodynamic compromise

Investigations

• OGD (upper GI endoscopy) - diagnosis confirmed; shows longitudinal tear at OGJ
• FBC, coagulation studies, cross-match

Treatment

• Majority: Conservative - bleeding stops spontaneously in 80-90%
• Endoscopic treatment if active bleeding: Adrenaline (epinephrine) injection OR endoscopic clips
• Haemostasis: Very rarely angiographic embolisation or surgery required

Distinction from Boerhaave's Syndrome

• Mallory-Weiss: Mucosal tear only; haematemesis; managed endoscopically
• Boerhaave's: Full-thickness oesophageal rupture; severe chest pain; mediastinitis; surgical emergency

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Quick Reference Summary Tables

Liver Topics

Oesophageal Topics

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SKIN TUMOURS

Bailey & Love's Short Practice of Surgery, 28th Edition - Chapter 45

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1. BASAL CELL CARCINOMA (BCC) / RODENT ULCER

Definition

Epidemiology

• Strongest predisposing factor: Ultraviolet radiation (UVR)
• 95% occur between ages 40-80 years
• Incidence rises with proximity to equator
• 33% arise in areas NOT usually exposed to sun
• White-skinned people almost exclusively affected
• More common in men than women
• Other risk factors: arsenical compounds, coal tar, aromatic hydrocarbons, infrared radiation, immunosuppression, genetic syndromes (Gorlin's)

Pathogenesis

• No apparent precursor lesions
• Development proportional to initial carcinogen dose (not duration of exposure)
• Metastasises extremely rarely (distinguishing feature from SCC)
• Locally invasive - hence the name "rodent ulcer" (gnaws/erodes locally)

Types / Macroscopic Classification

1. Nodular - most common; smooth, pearly, translucent papule; telangiectasia on surface; raised rolled edge
2. Nodulocystic - as above with cystic component; 90% of BCCs are nodular or nodulocystic
3. Pigmented - heavily pigmented variant; blue/brown/black; may mimic melanoma
4. Naevoid - associated with Gorlin's syndrome

Microscopic

• 26 histological subtypes described
• Characteristic: Ovoid cells in nests with a single "palisading" outer layer
• Only the outer layer of cells actively divides - explains slow growth rate
• Incompletely excised lesions are more aggressive

Clinical Features - The Rodent Ulcer

• Starts as a pearly, translucent nodule with telangiectatic vessels on the surface
• Central ulceration with a characteristic rolled, pearly edge (everted/raised border)
• Slow progressive enlargement with central crusting/ulceration
• Painless in early stages
• "Rodent ulcer" - the ulcer appears to be gnawed, advancing edge slowly invades and destroys local tissue
• Most common on sun-exposed face - particularly nose, nasolabial folds, inner canthus of eye, pre-auricular areas, and scalp (the "H-zone" of the face carries highest risk)

Sites

• Face - 80% of BCCs (especially nose, periorbital, cheeks, temples)
• Ear, scalp, neck
• Trunk (superficial type)
• Lower limb (rare)

Prognosis - High-Risk vs Low-Risk BCC

• Size >2 cm
• Sites giving access to cranium: near eye, nose, ear
• Recurrent tumours
• Immunosuppressed patients
• Morphoeic or micronodular/infiltrating histological subtypes

• Small, well-defined
• Nodular histology
• Easily accessible sites

Management

• Tumour and margins assessed and marked under loupe magnification
• Surgical margins: 2-15 mm depending on macroscopic variant
• Standard excision with histological margin assessment
• Two-stage approach: For ill-defined margins or where tissue is at a premium (nose, eyelid) - excise, wait for histology confirming clear margins, then reconstruct
• Mohs' micrographic surgery: Excision under real-time microscopic control; gold standard for high-risk BCCs, recurrent tumours, or sites where tissue conservation is critical (eyelid, nose, lip); achieves highest cure rates

• Radiotherapy: For elderly/infirm patients; similar recurrence rates to surgery but risks secondary malignancy after 1-2 decades
• Topical 5-fluorouracil (5-FU): For biopsy-proven superficial BCCs
• Topical imiquimod (immune response modifier): For superficial BCCs
• Photodynamic therapy (PDT): For superficial BCCs
• Vismodegib (hedgehog pathway inhibitor): For advanced/metastatic BCC or Gorlin's syndrome

• 67% recurrence if margins grossly involved
• 33% recurrence within 2 years with microscopic involvement or "close" margins

• Patients with completely excised uncomplicated lesions: Can be discharged
• Follow-up required for: High-risk sites, globally sun-damaged skin, genetic syndromes, those declining re-excision after incomplete margins

Important Feature: Local Invasion without Metastasis

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2. SQUAMOUS CELL CARCINOMA (SCC) / EPITHELIOMA

Definition

Epidemiology

• Second most common skin cancer (4 BCCs for every 1 SCC)
• Strongly related to cumulative sun exposure
• More common in men than women
• More common with proximity to equator

Aetiology / Predisposing Factors

1. Ultraviolet radiation (UVR) - most important; cumulative exposure
2. Infrared radiation (IR) - occupational
3. Chemical carcinogens: Arsenicals, coal tar (chimney sweeps - Sir Percivall Pott's scrotal SCC, 1775)
4. Viral: HPV subtypes 5 and 16 (ano-genital SCC especially)
5. Tobacco: Current/previous use doubles relative risk
6. Immunosuppression (transplant recipients at especially high risk)
7. Chronic inflammation and scarring:
   • Chronic sinus tracts
   • Pre-existing scars (burn scars - Marjolin's ulcer)
   • Osteomyelitis sinuses
   • Chronic venous ulcers
   • Vaccination points
   • Chronic radiation dermatitis
8. Pre-malignant conditions:
   • Actinic (solar) keratosis - most common precursor; up to 20% form SCC
   • Cutaneous horn (keratin horn) - 10% have underlying SCC
   • Bowen's disease - SCC in situ (full-thickness epidermal dysplasia)
   • Erythroplasia of Queyrat - SCC in situ on the glans penis
   • Leukoplakia (oral/mucosal)
   • Xeroderma pigmentosum

Pathology

• Initially a raised, firm, indurated papule/nodule
• Develops into an ulcer with raised, everted, indurated edge and surrounding inflammation (cf. BCC: rolled/pearly edge; cf. Marjolin's: flat, painless)
• Can be proliferative (exophytic, cauliflower-like) or ulcerative

• Irregular masses of squamous epithelium proliferating from the basal layer and invading the dermis
• Broders' grading - describes proportion of dedifferentiated cells:
  • Grade 1: >75% differentiated (well differentiated)
  • Grade 2: 50-75% differentiated
  • Grade 3: 25-50% differentiated
  • Grade 4: <25% differentiated (poorly differentiated/anaplastic)
• Keratin pearls (whorls of keratin) - feature of well-differentiated SCC
• Positive for cytokeratins 1 and 10

Clinical Features

• Raised, firm nodule that ulcerates
• Ulcer with everted edges, indurated base, surrounding inflammation
• May present as a proliferative mass
• Bleeds easily, crusting
• Tender (unlike BCC which is painless)
• Regional lymphadenopathy if metastasised

Sites

• Sun-exposed areas: Face, scalp, ears, dorsum of hand, lower lip
• Mucocutaneous junctions: Lip, anal margin, genitalia
• Areas of chronic scarring/inflammation (Marjolin's ulcer)

Prognostic Variables

1. Depth: SCC <2 mm - metastasis highly unlikely; SCC >6 mm - 15% metastasised
2. Size: >2 cm - high risk
3. Site: Ear, lip, genitalia, scar-related SCC - higher metastatic risk
4. Histological grade: Poorly differentiated - worse prognosis
5. Perineural/vascular invasion: Poor prognosis
6. Immune status: Immunosuppressed patients fare worse

• Low-risk SCC: ~2%
• High-risk SCC: Up to 30%
• Route: Regional lymph nodes first, then distant

TNM Staging (Table 45.1 - Bailey & Love)

Management

1. Surgical excision (treatment of choice):
   • Wide local excision with adequate margins (minimum 4-6 mm for low-risk; 10+ mm for high-risk)
   • Mohs' micrographic surgery for high-risk/recurrent SCC
2. Lymph node management:
   • Clinically involved nodes: Therapeutic lymph node dissection
   • Sentinel node biopsy for high-risk cases
3. Radiotherapy: Primary treatment in elderly/inoperable; adjuvant post-surgery for high-risk
4. Topical/destructive methods: Only for in-situ (Bowen's) disease - 5-FU, imiquimod, PDT, cryotherapy
5. Systemic therapy: Cetuximab or platinum-based chemotherapy for advanced/metastatic disease

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3. MARJOLIN'S ULCER

Definition

Aetiology / Causes of Underlying Scar

1. Burn scars - most common
2. Chronic venous ulcers (varicose)
3. Osteomyelitis sinuses
4. Pilonidal sinus tracts
5. Radionecrosis scars
6. Old vaccination scars
7. Lupus vulgaris (tuberculosis of skin)
8. Pressure sores

Pathogenesis

• Chronic inflammation/scarring leads to loss of normal immune surveillance in the scar tissue (scar is relatively avascular/immunologically inert)
• Repetitive trauma, irritation and chronic infection cause mutagenic changes
• SCC arises from the edges of the non-healing ulcer or unstable scar
• Long latency period (average 25-40 years between original injury and malignant transformation for burn scars; shorter for other causes)

Features

Clinical Features

• Ulcer or growth in a chronic non-healing scar or wound
• Raised, irregular, proliferative edges
• Painless - important distinguishing feature (scar has no sensation)
• May bleed
• Lymph node spread is delayed but once it occurs, prognosis is poor

Investigations

• Biopsy (essential for diagnosis) - wedge biopsy from edge of ulcer
• CT/MRI for staging
• Regional lymph node assessment

Management

• Wide local excision with adequate margins
• Lymph node dissection if clinically involved
• Reconstructive surgery (split-skin graft or flap) after excision
• Radiotherapy for high-risk or inoperable cases
• Poor prognosis overall: 5-year survival ~30%

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4. MALIGNANT MELANOMA

Definition & Epidemiology

• Cancer of melanocytes - can arise in skin, mucosa, retina, or leptomeninges
• Accounts for <5% of skin malignancy but responsible for >75% of skin malignancy deaths
• Rising incidence globally
• Commonest cancer in young adults (20-39 years)
• Australia and New Zealand: highest incidence (33.6/100,000)
• 5% of all melanoma patients develop a second primary melanoma
• 7% of melanomas present as occult metastasis from an unknown primary

Risk Factors

• UVR exposure (especially "flash fry" intense/intermittent exposure - sunburn)
• Personal history of melanoma
• First-degree relative with melanoma

• 30 sun-acquired naevi

• History of >5 severe sunburns before age 16
• Fair-skinned, red-haired individuals
• Giant pigmented congenital naevi
• Atypical naevi (dysplastic naevus syndrome)
• Immunosuppression (increases risk 20-30 fold)
• Male gender and solitary living (associated with thicker melanomas at diagnosis)

Classification - Macroscopic Types

• Amelanotic melanoma: Flesh-coloured; may mimic other lesions; also presents as GI metastasis
• Desmoplastic melanoma: Head and neck; propensity for perineural infiltration; often amelanotic; high local recurrence
• Subungual melanoma: Usually SSM under fingernail; Hutchinson's sign (see below)

Hutchinson's Sign (Subungual Melanoma)

• Pigmentation extends from the nail bed into the nail fold and surrounding skin
• Widens progressively to produce a triangular pigmented macule with nail dystrophy
• Differential: Benign racial melanonychia (linear dark streak under nail in dark-skinned individual; NO nail fold involvement)

ABCDE Features (Warning Signs of Malignant Change in Naevus)

Growth Phases

1. Horizontal (radial) growth phase: Cells spread along dermoepidermal junction; predominantly radial; may breach dermis but no true invasion
2. Vertical growth phase: Dermis invaded; metastatic potential correlates with depth of vertical invasion; nodularity clinically heralds vertical phase

Microscopic & Staging

• Measures depth from the granular cell layer of the epidermis to the deepest tumour cell
• The greater the Breslow thickness, the worse the prognosis

• I: Epidermis only (in situ)
• II: Papillary dermis
• III: Fills papillary dermis
• IV: Reticular dermis
• V: Subcutaneous fat

• Stage I-II: Localised primary tumour
• Stage III: Regional nodal/in-transit metastases
• Stage IV: Distant metastases

Investigations

1. Excision biopsy - gold standard; provides full histological depth assessment; do NOT do incision or shave biopsy (inadequate for Breslow measurement)
2. Sentinel node biopsy (SNB): For tumours >1 mm Breslow thickness (or <1 mm with high-risk features); maps lymphatic drainage; first node in regional basin biopsied
3. CT chest/abdomen/pelvis: Staging - lymph nodes, distant metastases
4. MRI brain: If neurological symptoms
5. PET-CT: Staging of advanced disease
6. LDH: Elevated in metastatic disease (M1 staging)
7. BRAF mutation testing: For advanced disease (guides targeted therapy)

Management

Margins are measured clinically from the visible tumour edge.

• SNB (sentinel node biopsy): Staging tool; maps which node to remove for pathological assessment
• Completion lymphadenectomy after positive SNB: Remains optimum for regional control despite no proven overall survival benefit from MSLT-II trial; patients must accept morbidity
• Therapeutic lymphadenectomy: For clinically palpable/imaging-detected lymph node metastasis

• Vemurafenib or Dabrafenib (BRAF inhibitors): Block BRAF V600 mutation signalling - affects MAPK pathway in 50% of melanomas
• Trametinib (MEK inhibitor): Combined with dabrafenib to counter acquired resistance
• Used in Stage III-IV disease

• Ipilimumab (anti-CTLA-4): First approved immunotherapy; prolonged survival in metastatic melanoma
• Pembrolizumab / Nivolumab (anti-PD-1): Superior to ipilimumab for first-line metastatic melanoma; also used adjuvant in Stage III
• Selective immune checkpoint blockade removes "brakes" on anti-tumour T-cell response

• Not primary treatment for melanoma
• For palliation of brain/bone metastases, or after lymph node dissection in high-risk nodal disease

• For multiple in-transit metastases of the limb
• Hyperthermic perfusion with melphalan ± TNF-alpha

• Excision of distant metastases where feasible
• Radiotherapy for brain/bone metastases
• Systemic targeted therapy/immunotherapy

Prognosis

• Breslow thickness is the single most important prognostic indicator
• Stage I (T1a): >95% 5-year survival
• Stage II: 45-80% 5-year survival
• Stage III: 30-60% 5-year survival
• Stage IV: 5-20% 5-year survival (historically; improved with immunotherapy)
• Ulceration and mitotic rate are additional adverse prognostic features

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5. HUTCHINSON'S FRECKLE / LENTIGO MALIGNA

Definition

Clinical Features

• Site: Face, neck, dorsum of hands - chronically sun-exposed areas
• Age: Elderly patients (>60 years)
• Sex: Women > men
• Appearance: Slow-growing, variegated (mixed) brown/tan macule with irregular borders; may show areas of darker pigmentation (regression areas appear pale)
• Grows over years to decades
• Eventually (in ~5-10%) progresses to lentigo maligna melanoma when vertical growth phase begins (develops a palpable nodular component)

Pathology

• Atypical melanocytes proliferating along the dermoepidermal junction
• Chronically sun-damaged skin: Solar elastosis, atrophic epidermis
• In situ: Confined to epidermis
• LMM: Invasion into dermis

Management

• Excision with 5 mm margins for lentigo maligna (in situ)
• Wider margins once invasive (as per Breslow thickness)
• Mohs' micrographic surgery or staged excision - useful given large size and ill-defined borders
• Radiotherapy: For cases where surgery not feasible (very large or elderly patients)
• Imiquimod 5% cream: Topical immunotherapy for lentigo maligna not amenable to surgery (non-licensed use but evidence base growing)

Key Points for Exam

• "Hutchinson's freckle" = lentigo maligna = in-situ stage of LMM
• Not all lentigo malignas become invasive - estimated 5-10% lifetime risk of invasion
• Distinguished from a simple solar lentigo (benign "liver spot" / "age spot") by the presence of melanocytic atypia histologically
• Hutchinson's sign (different from Hutchinson's freckle): Pigmentation extending from subungual melanoma into the nail fold

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Summary Tables for Exam Revision

BCC vs SCC vs Melanoma

Breslow Thickness & Excision Margins

Types of Melanoma - Exam Mnemonic: SNLA

• Superficial spreading - 70% - most common
• Nodular - 15% - most aggressive, de novo
• Lentigo maligna - 5-10% - elderly, face, Hutchinson's freckle
• Acral lentiginous - rare in white; common in non-white; soles/palms/subungual

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