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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.

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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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