16.3 Clinical Dermatology: Common, Inflammatory, Bullous, Malignant & Drug-Induced Dermatoses

Core Principles of Clinical Dermatology

Cutaneous disorders reflect both primary skin pathobiology and cutaneous manifestations of systemic disease. For the CAMC Registration Examination, candidates must be proficient in morphology recognition, histopathological correlation, differentiating intraepidermal from subepidermal blistering disorders, triaging life-threatening dermatological emergencies (such as Toxic Epidermal Necrolysis and Eczema Herpeticum), evaluating pigmented lesions for melanoma, and prescribing evidence-based topical and systemic dermatological therapeutics.

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Inflammatory Dermatoses

Atopic Dermatitis (Eczema)

Atopic dermatitis is a chronic, relapsing, highly pruritic inflammatory skin disorder resulting from a complex interaction between epidermal barrier breakdown, immune dysregulation, and environmental allergens.

• Pathophysiology: Loss-of-function mutations in the filaggrin (FLG) gene impair cornified envelope formation and reduce stratum corneum natural moisturizing factors, leading to excessive transepidermal water loss and allergen penetration. This incites a Th2-polarized immune response with hyperproduction of IL-4, IL-13, and IL-31 (the principal mediator of itch), resulting in intense pruritus and elevated serum IgE.
• Age-Specific Anatomical Distribution:
  • Infants (< 2 years): Involves the cheeks, forehead, scalp, and extensor surfaces of limbs; characteristically spares the diaper area (protected by hydration).
  • Children & Adults: Involves the flexural folds (antecubital and popliteal fossae, anterior neck, wrists, ankles), presenting with marked lichenification (epidermal thickening with exaggerated skin markings from chronic rubbing and scratching).
• Management Ladder:
  • Baseline Barrier Maintenance: Liberal, frequent application of bland, lipid-rich emollients (ointments or heavy creams applied immediately after bathing).
  • Topical Corticosteroids (TCS): First-line pharmacological therapy for acute flares. Match potency to site: low-potency (hydrocortisone 1%) for face, neck, and intertriginous flexures to avoid cutaneous atrophy and telangiectasias; moderate-to-high potency for trunk and lichenified limbs.
  • Topical Calcineurin Inhibitors (Tacrolimus, Pimecrolimus): Steroid-sparing agents particularly suitable for facial, eyelid, and intertriginous eczema without risking skin atrophy.
  • Systemic Therapy: For moderate-to-severe refractory disease: Dupilumab (monoclonal antibody targeting IL-4R alpha subunit, blocking IL-4 and IL-13 signaling).

Critical Dermatological Emergency: Eczema Herpeticum

Eczema Herpeticum (Kaposi varicelliform eruption) is a potentially fatal, disseminated cutaneous infection caused by Herpes Simplex Virus (HSV-1 or HSV-2) superimposed upon pre-existing atopic dermatitis or other barrier-disrupted skin.

• Clinical Presentation: Sudden eruption of crops of monomorphic, dome-shaped, umbilicated vesicles that rapidly evolve into punched-out, painful, hemorrhagic, crusted erosions. Accompanied by high fever, regional lymphadenopathy, and systemic toxicity.
• Complications: Secondary staphylococcal septicemia, herpes keratoconjunctivitis, and systemic viremia with multi-organ failure.
• Emergency Treatment: Immediate initiation of systemic antiviral therapy (intravenous Acyclovir for hospitalized or toxic children; high-dose oral acyclovir or valacyclovir for mild outpatient cases). Concomitant broad-spectrum anti-staphylococcal antibiotics (e.g., flucloxacillin) are added to treat secondary bacterial impetiginization. Treat underlying eczema with appropriate-potency topical steroids under dermatology guidance alongside systemic antiviral therapy; routine withdrawal is not required.

Psoriasis Vulgaris

Psoriasis is a chronic, immune-mediated systemic inflammatory disorder characterized by keratinocyte hyperproliferation and impaired epidermal differentiation.

• Pathophysiology: Activated dendritic cells produce IL-23, which drives the differentiation and survival of Th17 cells. Th17 cells secrete IL-17A, IL-17F, and IL-22, which stimulate excessive keratinocyte proliferation, shortening epidermal transit time from normal 28 days to only 3 to 5 days. Neutrophils migrate into the stratum corneum, forming Munro microabscesses.
• Clinical Morphology:
  • Well-demarcated, erythematous, indurated plaques covered by thick, adherent, silvery-white (micaceous) scales.
  • Classic Predilection: Extensor surfaces of limbs (elbows, knees), presacral region, scalp, and umbilicus.
  • Auspitz Sign: Removal of adherent silvery scale reveals punctate, pinpoint bleeding points, caused by exposure of thinned suprapapillary epidermal plates over dilated dermal capillaries.
  • Koebner Phenomenon (Isomorphic Response): Development of classic psoriatic plaques at sites of cutaneous trauma or mechanical irritation (surgical scars, scratches, sunburn).
  • Nail Changes (in up to 50%): Coarse nail pitting, onycholysis (separation of nail plate from bed), subungual hyperkeratosis, and characteristic "oil-drop" (salmon) patches.
• Clinical Subtypes:
  • Guttate Psoriasis: Sudden eruption of numerous small (0.5 to 1.5 cm) teardrop-shaped papules on the trunk and limbs, characteristically triggered 1 to 2 weeks after an acute Group A beta-hemolytic streptococcal pharyngitis in children and young adults (elevated ASOT; often self-limiting or responsive to phototherapy).
  • Inverse Psoriasis: Involves intertriginous skin folds (axillae, groins, inframammary); appears smooth, red, and glistening without prominent silvery scale.
  • Pustular Psoriasis: Sterile pustules; localized (palmoplantar) or generalized (von Zumbusch).
• Pharmacotherapy:
  • Mild-to-Moderate: Topical corticosteroids combined synergistically with topical Vitamin D3 analogs (Calcipotriol); topical retinoids (Tazarotene); keratolytics (Salicylic acid).
  • Moderate-to-Severe: Narrowband UVB phototherapy; systemic conventional agents (oral Methotrexate, Cyclosporine, Acitretin); biologic therapies (anti-IL-17: Secukinumab, Ixekizumab; anti-IL-23: Guselkumab, Risankizumab; anti-TNF: Adalimumab).
• CRITICAL CONTRAINDICATION ALERT:
  • Systemic Corticosteroids (e.g., oral Prednisone, IV dexamethasone) are STRICTLY CONTRAINDICATED in the management of psoriasis! Although systemic steroids may induce temporary clearing, tapering or abrupt withdrawal of corticosteroids characteristically precipitates catastrophic, life-threatening Generalized Pustular Psoriasis (von Zumbusch) or generalized erythroderma, carrying high mortality from high-output cardiac failure, sepsis, and fluid loss.

Acne Vulgaris

Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit involving four key pathogenic factors: (1) follicular hyperkeratinization, (2) excess sebum production driven by androgens, (3) proliferation of Cutibacterium acnes, and (4) local inflammatory cytokine release.

• Lesion Spectrum: Non-inflammatory lesions (open comedones [blackheads] with melanin/lipid oxidation; closed comedones [whiteheads]) vs Inflammatory lesions (erythematous papules, pustules, nodules, and pseudocysts).
• Stepwise Management:
  • Mild Comedonal: Topical retinoid (Adapalene, Tretinoin) first-line.
  • Mild-to-Moderate Papulopustular: Topical Retinoid PLUS topical Benzoyl Peroxide (antimicrobial that does not induce bacterial resistance) with or without topical Clindamycin.
  • Moderate-to-Severe Papulopustular: Oral antibiotics (Doxycycline 100 mg daily or Lymecycline; limited to 3 to 4 months to prevent resistance) combined with topical retinoid and benzoyl peroxide.
  • Severe Nodulocystic or Scarring Acne: Oral Isotretinoin (synthetic 13-cis-retinoic acid).
    • Isotretinoin Rules: Absolute teratogen causing severe craniofacial, cardiac, and CNS malformations. For patients who could become pregnant, ensure effective pregnancy prevention for at least 1 month before, throughout, and 1 month after treatment, with contraception and pregnancy testing under the applicable local programme. Monitor liver enzymes and lipids (triglycerides).

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Autoimmune Blistering Diseases

Autoimmune blistering diseases are severe, potentially fatal disorders characterized by autoantibodies directed against structural adhesion proteins of the epidermis or basement membrane zone.

Pemphigus Vulgaris vs Bullous Pemphigoid

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|                         AUTOIMMUNE BLISTERING DISEASES: COMPARISON MATRIX                         |
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| DIAGNOSTIC FEATURE      | PEMPHIGUS VULGARIS (PV)              | BULLOUS PEMPHIGOID (BP)          |
+-------------------------+--------------------------------------+----------------------------------+
| Target Autoantigens     | Desmoglein 3 (mucosa) &              | BP180 (Type XVII Collagen) &     |
|                         | Desmoglein 1 (skin)                  | BP230 in Hemidesmosomes          |
| Structural Junction     | Desmosomes (intercellular adhesion)  | Hemidesmosomes (basement membrane)|
| Level of Blister Split  | INTRAEPIDERMAL (Suprabasal)          | SUBEPIDERMAL (Dermal-epidermal)  |
| Histopathology          | Acantholysis; "tombstone" row of     | Subepidermal blister with dense  |
|                         | intact basal keratinocytes           | eosinophil & neutrophil infiltrate|
| Blister Characteristics | FLACCID, thin-walled, fragile;       | TENSE, thick-walled, firm;       |
|                         | rupture easily leaving raw erosions  | remain intact for days           |
| Oral Mucosal Involvement| PRESENT in > 90% (often first sign;  | RARE (< 10% to 20%);             |
|                         | painful erosions precede skin)       | transient when present           |
| Nikolsky Sign           | POSITIVE (shearing on normal skin)   | NEGATIVE                         |
| Direct Immunofluorescence| Intercellular IgG & C3 throughout    | Smooth, continuous LINEAR band   |
| (DIF) Pattern           | epidermis ("CHICKEN-WIRE" / "NET")  | of IgG & C3 along BASEMENT MEMBRANE|
| Typical Patient Age     | Young to middle-aged adults (40-60)  | ELDERLY individuals (age > 70)   |
| First-Line Therapy      | High-dose systemic corticosteroids   | High-potency TOPICAL steroid     |
|                         | (Prednisone 1 mg/kg) + RITUXIMAB     | (Clobetasol cream) or oral Pred  |
+---------------------------------------------------------------------------------------------------+

Clinical Insights: Acantholysis vs Subepidermal Cleavage

• Pemphigus Vulgaris: IgG autoantibodies bind the extracellular cadherin domains of desmoglein 3 and 1, disrupting intercellular desmosomal bridges. Keratinocytes uncouple and round up (acantholysis). Because the cleavage plane is intraepidermal (suprabasal), the blister roof consists of only a fragile single-to-few layer stratum spinosum/corneum, creating flaccid bullae that rupture easily from minor friction, leaving extensive, painful, weeping erosions that fail to heal. The positive Nikolsky sign (dislodgement of normal-appearing epidermis by light tangential sliding pressure) reflects this intercellular fragility.
• Bullous Pemphigoid: Autoantibodies bind BP180 (collagen XVII) and BP230 within hemidesmosomes anchoring basal cells to the basement membrane. Complement activation recruits eosinophils, which release major basic protein and elastases that cleave the entire dermal-epidermal junction. Because the blister roof consists of the entire full thickness of the intact epidermis, the bullae are tense, firm, and dome-shaped, often arising on an intensely pruritic, urticarial base. The Nikolsky sign is negative.
• Evidence-Based Therapy for Bullous Pemphigoid: Seminal clinical trials demonstrate that in elderly patients with bullous pemphigoid, high-potency topical corticosteroids (Clobetasol propionate 20 to 30 g daily applied to the whole body) are superior to high-dose oral prednisone, providing equivalent blister control with significantly lower 1-year mortality (preventing steroid-induced sepsis, diabetes decompensation, and cardiovascular death in frail elderly patients).

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Severe Cutaneous Adverse Reactions (SCAR)

Severe Cutaneous Adverse Reactions are life-threatening, immunologically mediated adverse drug reactions characterized by extensive epidermal necrosis, detachment, or severe multi-organ involvement.

Erythema Multiforme (EM)

• Pathophysiology: Cell-mediated immune response typically triggered by an infectious agent—predominantly Herpes Simplex Virus (HSV-1 and HSV-2 in > 70% of cases) or Mycoplasma pneumoniae; medications are a rare trigger.
• Pathognomonic Lesion: The Target (Iris) Lesion, defined by three distinct concentric zones:
  1. Central dark, dusky, purpuric disk or blister.
  2. Intermediate pale, edematous inflammatory ring.
  3. Outer, well-demarcated erythematous border.
• Distribution: Symmetrical, predominantly acral (dorsa of hands, palms, soles, forearms, extensor limbs, and face).
• Subtypes: EM Minor (skin lesions with minimal or no mucosal involvement); EM Major (target lesions with involvement of one or more mucous membranes [oral, ocular, genital], but total epidermal detachment is < 10% and lesions remain localized).
• Management: Symptomatic care, topical corticosteroids; treat underlying HSV with oral acyclovir; self-limiting over 2 to 4 weeks.

Stevens-Johnson Syndrome (SJS) & Toxic Epidermal Necrolysis (TEN)

SJS and TEN represent a severity spectrum of the same catastrophic, cell-mediated cytotoxic drug reaction characterized by widespread apoptosis and full-thickness necrolysis of keratinocytes.

• Pathophysiology: Drug metabolites bind to MHC Class I molecules, presenting foreign haptens to CD8+ cytotoxic T cells and natural killer (NK) cells. Massive release of Granulysin and Fas-Fas ligand (CD95) signaling triggers universal, caspase-mediated apoptosis of epidermal keratinocytes.
• High-Risk Culprit Medications (The Classic Mnemonic: S-A-T-A-N):
  • S — Sulfonamides (Trimethoprim-sulfamethoxazole, sulfadiazine)
  • A — Allopurinol
  • T — Anticonvulsants (Carbamazepine, Phenytoin, Lamotrigine, Phenobarbital)
  • A — Antibiotics (Aminopenicillins, Cephalosporins, Fluoroquinolones)
  • N — NSAIDs (Oxicam derivatives e.g., Piroxicam, Meloxicam) & Nevirapine

BSA Detachment Classification

Classification is defined strictly by the percentage of detached and detachable Body Surface Area (BSA):

• Stevens-Johnson Syndrome (SJS): < 10% BSA detachment.
• SJS/TEN Overlap: 10% to 30% BSA detachment.
• Toxic Epidermal Necrolysis (TEN): > 30% BSA detachment (frequently > 50-80%).

Clinical Course & Hallmarks

• Prodrome: 1 to 3 weeks after drug initiation; fever, malaise, sore throat, stinging eyes, and dysphagia.
• Cutaneous Eruption: Painful, dusky, poorly demarcated, purpuric macules that coalesce rapidly into flaccid, sheet-like bullae, leading to extensive epidermal sloughing (resembling severe scald burns). Positive Nikolsky sign and Asboe-Hansen sign (lateral extension of bulla under pressure).
• Severe Mucosal Involvement: Present in > 90% of cases, involving >= 2 mucosal sites (severe hemorrhagic, bloody crusting of lips and oral mucosa, pseudomembranous conjunctivitis with risk of symblepharon and blindness, erosive urethritis and vulvovaginitis).

SCORTEN: Mortality Prognostic Score

Calculated within the first 24 hours of admission; one point allocated for each independent risk factor (Score 0-1: < 4% mortality; Score >= 5: about 90% mortality):

1. Age > 40 years
2. Presence of underlying malignancy
3. Heart rate > 120 bpm
4. Initial detached BSA > 10%
5. Serum urea > 10 mmol/L (about 60 mg/dL urea or 28 mg/dL BUN)
6. Serum glucose > 14 mmol/L (> 250 mg/dL)
7. Serum bicarbonate < 20 mmol/L

Emergency Management Protocol for SJS/TEN

1. Immediate Withdrawal of ALL Culprit & Suspected Medications: The single most critical determinant of survival; delay in stopping the offending agent drastically increases mortality.
2. Urgent Specialist Inpatient Care: Discuss early with dermatology and a burn/ICU team. Extensive TEN (> 30% BSA) requires burn-centre care; organ failure requires intensive care. Stable limited adult SJS may be managed on an appropriate specialist ward.
3. Meticulous Fluid & Electrolyte Resuscitation: Use warmed balanced crystalloid, individualized to perfusion, electrolytes and adult urine output 0.5 to 1.0 mL/kg/h. SJS/TEN usually requires less fluid than thermal-burn formulas predict; avoid automatic Parkland dosing and over-resuscitation.
4. Gentle Wound Care: Biological dressings or non-adherent silicone dressings; Preserve epidermis with initial conservative care; avoid routine aggressive debridement. A specialist team may remove infected necrotic tissue or use surgical care when wounds deteriorate.
5. STRICT RULE ON ANTIBIOTICS: Prophylactic systemic antibiotics are STRICTLY CONTRAINDICATED! Routine prophylaxis does not prevent infection and selects for virulent, multi-drug resistant pathogens (Pseudomonas, MRSA, Candida); give systemic antibiotics when clinical findings suggest infection, obtaining cultures and using local microbiology advice; do not wait for culture proof or sepsis.
6. Adjuvant Immunomodulatory Therapy: Intravenous Immunoglobulin (IVIG), Cyclosporine, or Etanercept (TNF inhibitor) may halt apoptosis if initiated early.

DRESS Syndrome (Drug Reaction with Eosinophilia & Systemic Symptoms)

• Definition: Severe, idiosyncratic, multi-organ adverse drug reaction characterized by a prolonged latency period (typically 2 to 8 weeks after starting the drug) and strong association with reactivation of latent herpesviruses (HHV-6, HHV-7, EBV, CMV).
• Clinical Diagnostic Triad:
  1. Fever & Severe Skin Eruption: High spiking fever (> 38.5°C), widespread confluent morbilliform maculopapular eruption, and pathognomonic facial and periorbital edema.
  2. Hematologic Abnormalities: Marked peripheral blood eosinophilia (absolute eosinophil count >= 0.7 to 1.5 x 10⁹/L) or atypical lymphocytosis.
  3. Internal Visceral Organ Involvement:
     • Liver (most common, > 80%): Severe acute hepatitis with transaminitis (ALT > 2-5x normal).
     • Kidneys (second most common): Acute interstitial nephritis with elevated creatinine and proteinuria.
     • Heart (acute hypersensitivity myocarditis), lungs (interstitial pneumonitis).
• Common Culprits: Allopurinol, aromatic antiepileptics (Carbamazepine, Phenytoin), Minocycline, Dapsone, Sulfonamides, Vancomycin.
• Management: Immediate culprit drug discontinuation; systemic corticosteroids (oral Prednisone 0.5 to 1.0 mg/kg/day) with a very slow, gradual taper over 2 to 3 months to prevent rebound visceral relapse.

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Cutaneous Malignancies

Cutaneous malignancies represent the most common human cancers. Early clinical recognition and accurate histological staging are paramount.

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|                         CUTANEOUS MALIGNANCIES: COMPARISON MATRIX                                 |
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| FEATURE                 | BASAL CELL CARCINOMA (BCC)           | SQUAMOUS CELL CARCINOMA (SCC)    |
+-------------------------+--------------------------------------+----------------------------------+
| Cell of Origin          | Basal cells of interfollicular basal | Malignant epidermal keratinocytes|
|                         | layer or hair follicle outer sheath  | of stratum spinosum              |
| Primary Etiology        | Intermittent intense UV radiation;   | Cumulative lifetime UV radiation;|
|                         | PTCH1 / Hedgehog pathway mutations   | chronic ulcers (Marjolin), HPV   |
| High-Risk Population    | Fair-skinned individuals (types I-II)| Organ transplant recipients      |
|                         |                                      | (65x to 100x increased risk!)    |
| Precursor Lesion        | None (arises de novo)                | Actinic Keratosis; Bowen disease |
| Classic Morphology      | Pearly, translucent pink papule with | Indurated, hyperkeratotic, firm  |
|                         | rolled border & telangiectasias      | crusted nodule or non-healing    |
|                         | ("Rodent ulcer" with central crater)| ulcer with everted borders       |
| Anatomical Sites        | Sun-exposed face (nose, forehead),   | Lower lip, ears, bald scalp,     |
|                         | neck, upper trunk                    | dorsa of hands; scars            |
| Metastatic Potential    | EXCEPTIONALLY RARE (< 0.05%);        | MODERATE (2% to 5% overall; up to|
|                         | locally invasive & destructive       | 20% in lip/ear or transplant pts)|
| Surgical Treatment      | Excision with 4-5 mm margins;        | Wide local excision (4-6 mm for  |
|                         | Mohs surgery for face / H-zone       | low risk; >= 10 mm for high risk)|
+---------------------------------------------------------------------------------------------------+

Malignant Melanoma

Malignant melanoma arises from the neoplastic transformation of melanocytes. Although accounting for only ~1% of all skin cancers, it is responsible for > 75% of skin cancer deaths.

The Clinical ABCDE Diagnostic Rule

• A — Asymmetry: One half of the pigmented lesion does not match the other half.
• B — Border Irregularity: Scalloped, notched, ragged, or poorly circumscribed borders.
• C — Color Variation: Multiple variegated colors within the same lesion (shades of dark brown, jet black, red, white [regression], and slate blue).
• D — Diameter: Diameter > 6 mm (approximately the size of a standard pencil eraser); however, melanomas can be smaller.
• E — Evolving: Changes in size, shape, surface elevation, color, or new symptoms (pruritus, tenderness, bleeding, crusting). The single most important clinical historical indicator of malignancy.

Major Melanoma Subtypes

1. Superficial Spreading Melanoma (70%): Most common subtype; characterized by a prolonged horizontal (radial) intraepidermal growth phase before entering vertical invasion. Classically on the back in men and lower legs in women.
2. Nodular Melanoma (15-20%): Aggressive subtype with rapid onset and early vertical growth phase; presents as a dark blue-black or amelanotic firm dome-shaped polypoid nodule with early ulceration.
3. Lentigo Maligna Melanoma (5-10%): Arises on sun-damaged, atrophic facial skin of elderly patients from a pre-existing lentigo maligna (melanoma in situ).
4. Acral Lentiginous Melanoma (ALM):
   • Critical CAMC Clinical Pearl: Occurs on palms, soles (plantar surface), and subungual nail beds.
   • Predominant Subtype in Dark-Skinned Populations: Represents the most common form of melanoma in individuals of African, Caribbean, and Asian descent (accounting for up to 60-70% of melanomas in Black patients).
   • UV Independence: Completely unrelated to ultraviolet radiation exposure or sun exposure.
   • Hutchinson Sign: Extension of brown-black pigmentation from the subungual nail matrix onto the adjacent proximal or lateral nail fold and cuticle, raising concern for nail-unit melanoma and requiring specialist biopsy.

Breslow Thickness & Surgical Margin Guidelines

Breslow Microscopic Thickness (measured in millimeters with an ocular micrometer from the top of the granular cell layer of the epidermis to the deepest invading malignant melanocyte) is the single most powerful prognostic factor for localized melanoma and dictates definitive surgical excision margins.

CRITICAL BIOPSY SAFETY RULE FOR SUSPECTED MELANOMA

• Preferred Procedure: Complete narrow-margin biopsy (1 to 2 mm) deep enough to avoid transecting the lesion and permit accurate Breslow measurement.
• Avoid superficial shave biopsy, which may transect an invasive lesion and underestimate Breslow depth. Complete elliptical excision, punch excision or sufficiently deep saucerization can be appropriate. Specialist-selected partial biopsy is acceptable when complete removal is impractical, including some acral or large lesions.

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Cutaneous Infections & Infestations

Superficial cutaneous infections and parasitic infestations are high-volume primary care presentations in tropical and temperate climates alike. Differentiating superficial epidermal infections from deep dermal and soft-tissue emergencies is essential for antimicrobial stewardship and infection control.

Impetigo: Non-Bullous vs Bullous

Impetigo is a highly contagious superficial bacterial skin infection predominantly affecting children aged 2 to 5 years, characterized by intraepidermal pustules and crusting.

• Complications: Post-streptococcal glomerulonephritis (PSGN) can follow streptococcal impetigo (note: antibiotic therapy reduces transmission but does not prevent PSGN; acute rheumatic fever can also follow group A streptococcal skin infection).

Erysipelas vs Cellulitis: Comparative Differentiation

Differentiating between erysipelas and cellulitis is a frequent CAMC examination checkpoint, guiding pathogen identification and antimicrobial selection.

Dermatophytosis (Tinea Infections)

Dermatophytoses are superficial fungal infections of keratinized tissues (stratum corneum, hair, and nails) caused by dermatophyte genera: Trichophyton, Microsporum, and Epidermophyton.

• Clinical Variants:
  • Tinea Corporis ("Ringworm"): Annular, pruritic, erythematous scaling plaques with an active, elevated, advancing papulovesicular border and characteristic central clearing.
  • Tinea Cruris ("Jock Itch"): Symmetrical, sharply marginated, erythematous scaling rash in the groin folds and inner upper thighs; characteristically spares the scrotum and penis (distinguishing it from cutaneous Candida intertrigo, which involves the scrotum and displays satellite pustules).
  • Tinea Pedis ("Athlete's Foot"): Interdigital maceration, scaling, and fissuring (especially between 4th and 5th toes) or "moccasin-type" hyperkeratosis of the soles.
  • Tinea Unguium (Onychomycosis): Subungual hyperkeratosis, yellow-brown nail dystrophy, and onycholysis; confirmed by fungal nail clippings before initiating oral terbinafine.
• Diagnostic Confirmation: Direct microscopic examination of skin scrapings mounted in 10% to 20% Potassium Hydroxide (KOH) reveals diagnostic translucent, branching, septate hyphae and arthrospores.
• CRITICAL CLINICAL & THERAPEUTIC RULE — Tinea Capitis:
  • Tinea Capitis (Scalp Ringworm): Common in children; presents with scaling scalp patches, patchy alopecia, broken "black dot" stubbled hairs, and painful boggy inflammatory nodules (kerion).
  • MANDATORY SYSTEMIC PHARMACOTHERAPY: Topical antifungal creams, lotions, and shampoos CANNOT penetrate the hair follicles or hair shaft and are strictly ineffective for eradication! Tinea capitis ALWAYS requires SYSTEMIC ORAL ANTIFUNGAL THERAPY: Oral Griseofulvin (20 to 25 mg/kg/day for 6 to 8 weeks, taken with fatty meals to maximize absorption) or oral Terbinafine (weight-adjusted for 4 to 6 weeks).

Scabies Infestation

Scabies is a highly contagious parasitic dermatosis caused by the microscopic obligate human itch mite Sarcoptes scabiei var. hominis.

• Transmission: Acquired through prolonged, direct skin-to-skin contact (sexual partners, household contacts, institutional facilities) or contaminated bed linen/fomites.
• Pathophysiology: Fertilized female mites (0.3 to 0.5 mm) burrow into the stratum corneum at a rate of 1 to 5 mm per day, depositing 2 to 3 eggs daily and scybala (feces). The eggs hatch into larvae in 3 to 4 days. The hallmark itching represents a Type IV delayed-type hypersensitivity reaction to mite proteins, saliva, and feces, which develops 2 to 6 weeks after primary infestation (or within 24 to 48 hours upon re-infestation).
• Clinical Hallmarks:
  • Severe, intractable pruritus, classically worsening dramatically at night (when the skin is warm under bed covers).
  • Pathognomonic Cutaneous Burrows: Fine, wavy, thread-like, serpiginous, whitish-grey or skin-colored elevated ridges (2 to 10 mm in length), frequently terminating in a tiny vesicle containing the female mite ("maggot-like" microscopic appearance).
  • Predilection Sites: Interdigital web spaces of the hands, flexor surfaces of the wrists, elbows, anterior axillary folds, periumbilical area, belt line, buttocks, and the male genitalia (pathognomonic, exquisitely pruritic, indurated erythematous nodules on the penile glans, shaft, and scrotum).
  • Infantile Scabies: Unlike older children and adults, infants frequently have involvement of the face, scalp, palms, and soles, with diffuse vesiculopustules.
• Diagnostic Confirmation: Dermoscopy (demonstrating the "delta-wing jet plane" or triangular head-and-claw sign) or microscopic examination of mineral oil skin scrapings of a burrow showing live mites, oval eggs, or feces.
• Definitive Treatment Protocol:
  1. Topical Permethrin 5% Cream (Drug of Choice): Applied meticulously to every square centimeter of the body from the jawline/neck down to the soles of the feet and tips of the toes (including under fingernails, between fingers and toes, and genital folds; in infants and elderly, include the scalp, neck, and face). Leave on the skin for 8 to 14 hours (typically overnight) before thoroughly washing off with cool water.
  2. MANDATORY REPEAT APPLICATION: The application MUST BE REPEATED EXACTLY 7 TO 10 DAYS LATER to eradicate newly hatched nymphs that were resistant to treatment in the egg stage.
  3. TREAT ALL CLOSE CONTACTS SIMULTANEOUSLY: All household members, family contacts, and sexual partners must be treated concurrently on the exact same schedule, regardless of whether they have pruritus or symptoms (as asymptomatic carriers incubate the infestation for weeks).
  4. Environmental Decontamination: Wash all clothing, bed linen, and towels used within the prior 4 days in hot water (> 60°C) followed by a hot drying cycle, or seal in airtight plastic bags for at least 72 hours (as mites die within 48 to 72 hours away from human skin).
  5. Post-Scabetic Itch: Reassure patients that itching and rash may persist for 2 to 4 weeks after successful mite eradication due to persistent delayed hypersensitivity; treat with oral antihistamines, mild topical steroids, and emollients.
  6. Crusted (Norwegian) Scabies: Highly contagious variant in immunocompromised individuals (HIV, leprosy, elderly debility) with millions of mites presenting as thick, hyperkeratotic, fissured, non-pruritic plaques. Treated aggressively with combination oral Ivermectin (200 µg/kg on days 1, 2, 8, 9, and 15) plus daily topical Permethrin 5% cream.

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Worked Clinical Scenarios

Scenario 1: Eczema Herpeticum in an Atopic Child

• Presentation: A 3-year-old boy with a known history of severe flexural atopic dermatitis is brought to the pediatric emergency center with acute lethargy, a temperature of 39.4°C, and a rapid flare of his skin lesions over the past 24 hours. Examination reveals extensive atopic eczema on his face, neck, and antecubital fossae, but superimposed across his cheeks, forehead, and neck are numerous crops of distinct, uniform, monomorphic, punched-out, umbilicated vesicles and small hemorrhagic crusts. Several lesions have ruptured, leaving painful circular erosions. The cervical lymph nodes are tender and markedly enlarged.
• Diagnostic Assessment: This child has developed Eczema Herpeticum (Kaposi varicelliform eruption), a life-threatening dermatological emergency caused by secondary Herpes Simplex Virus-1 (HSV-1) infection on barrier-defective atopic skin.
• Management Action: The patient requires immediate hospital admission and emergency intravenous Acyclovir (5 to 10 mg/kg every 8 hours) without waiting for viral swab PCR results. Concomitant intravenous Flucloxacillin is started to treat secondary Staphylococcus aureus infection. Continue appropriate topical eczema treatment, including topical corticosteroids as directed by dermatology, alongside systemic acyclovir. An urgent ophthalmology consult is obtained to rule out corneal involvement (herpes dendritic keratitis).

Scenario 2: Toxic Epidermal Necrolysis in a Gout Patient Started on Allopurinol

• Presentation: A 54-year-old man was diagnosed with gout and started on Allopurinol 300 mg daily 16 days ago. He presents to the acute medical unit with a 2-day prodrome of fever, conjunctival burning, and painful throat, followed by a generalized eruption of tender, dusky red, coalescent macules over his face, trunk, and extremities. Within 24 hours, the epidermis begins peeling off in massive sheets, exposing raw, weeping dermis. Approximately 35% of his total body surface area displays detached or detachable epidermis. Severe hemorrhagic, blood-crusted erosions cover his lips, tongue, and buccal mucosa, and his eyes show purulent conjunctivitis. Tangential sliding pressure on intact perilesional skin readily shears the epidermis (Nikolsky sign positive).
• Diagnostic Assessment: The clinical presentation of acute widespread epidermal detachment involving > 30% BSA with severe mucositis and positive Nikolsky sign 2 to 3 weeks after allopurinol initiation confirms Toxic Epidermal Necrolysis (TEN). Age > 40 and BSA > 10% supply two SCORTEN points. Obtain heart rate, malignancy history, urea, glucose and bicarbonate before calculating the full score and predicted mortality.
• Management Action: Allopurinol is immediately discontinued. The patient is transferred urgently to a specialized Burn Intensive Care Unit. Emergency resuscitation includes warmed intravenous Ringer's lactate titrated to urine output, strict barrier isolation in an ambient room temperature of 30-32°C, and placement of non-adherent silicone wound dressings. Surgical debridement of sloughed skin is avoided. Prophylactic systemic antibiotics are strictly withheld, starting antibiotics promptly if clinical infection is suspected, then targeting treatment to culture results; culture-proven sepsis is not a prerequisite. Ophthalmology provides hourly lubricating eye drops and glass rod lysis of conjunctival adhesions to prevent symblepharon and permanent corneal blindness.

Scenario 3: Pigmented Plantar Lesion in an Afro-Caribbean Patient

• Presentation: A 62-year-old Afro-Caribbean woman notices a dark spot on the heel of her left foot that has gradually enlarged over the past year. She had attributed it to a callous or blood blister from a tight shoe. On examination, the plantar heel displays an asymmetrical, deeply pigmented, dark brown-to-black macule measuring 14 mm x 9 mm with scalloped, irregular borders and variegation in pigmentation (including black and slate-grey hues). There is no regional inguinal lymphadenopathy.
• Diagnostic Assessment: This lesion exhibits classic ABCDE criteria for Acral Lentiginous Melanoma (ALM), the predominant melanoma subtype in patients of African and Caribbean descent. Because ALM is unrelated to sun exposure and frequently painless, patients frequently present with advanced, thick lesions.
• Management Action: The preferred immediate procedure is a complete narrow-margin biopsy (1 to 2 mm) deep enough for accurate Breslow measurement. Avoid superficial shaves. Suitable deep saucerization or punch techniques are not categorically prohibited; specialist-selected partial sampling may be appropriate if complete acral excision is impractical. Histopathology confirms invasive acral lentiginous melanoma with a Breslow depth of 1.8 mm (T2a). Guided by the Breslow thickness, the patient undergoes definitive wide local excision with a 1.0 to 2.0 cm surgical margin down to the plantar fascia, combined with Sentinel Lymph Node Biopsy (SLNB) for nodal staging.