12.1 Common Dermatoses & Dermatological Emergencies

Common Dermatoses & Dermatological Emergencies

Dermatological presentations in acute clinical practice range from chronic, relapsing inflammatory disorders requiring stepped outpatient therapy to life-threatening dermatological emergencies requiring immediate resuscitation, high-dependency organ support, and surgical debridement.

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Common Chronic Dermatoses

Atopic Eczema (Atopic Dermatitis)

Atopic eczema is a chronic, relapsing, highly pruritic inflammatory skin disorder resulting from a complex interplay between epidermal barrier disruption (characterised by loss-of-function mutations in the filaggrin gene [FLG]), environmental allergens, and immune dysregulation with predominantly Th2-skewed cytokine responses.

• Clinical Presentation: Intense pruritus is the hallmark symptom ("the itch that rashes"). Lesions appear as ill-defined, erythematous, xerotic patches and plaques accompanied by oedema, excoriations, and crusting. In chronic cases, repeated rubbing and scratching produce flexural lichenification (thickened, leathery skin with exaggerated markings). The anatomical distribution evolves characteristically with patient age:

  • Infants (<1 year): Typically involves the cheeks, forehead, scalp, and extensor surfaces of the limbs; the nappy/diaper area is characteristically spared due to ambient moisture.
  • Children & Adults: Predominantly localises to flexural creases, particularly the antecubital and popliteal fossae, anterior neck, wrists, hands, and periorbital regions.

• Maintenance Emollient Therapy: Liberal, frequent application of emollients forms the cornerstone of management. Emollients should be smoothed onto the skin in the direction of hair growth rather than vigorously rubbed, applied at least 2–3 times daily even when skin appears clear, and used as soap substitutes.

• Stepped Topical Corticosteroid (TCS) Ladder: During active inflammatory flares, topical corticosteroids are applied once daily in short courses (typically 7–14 days) to induce remission.

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Psoriasis Vulgaris (Chronic Plaque Psoriasis)

Psoriasis is an autoimmune, polygenic dermatosis driven by abnormal crosstalk between dendritic cells, T-helper 17 (Th17) lymphocytes, and epidermal keratinocytes. Hyperstimulation by interleukin-23 (IL-23) and interleukin-17 (IL-17) shortens the epidermal cell cycle transit time from the normal 28 days to merely 3–4 days, producing prominent hyperkeratosis and parakeratosis.

• Clinical Presentation: Chronic plaque psoriasis accounts for >80% of presentations, manifesting as symmetrical, well-demarcated, salmon-pink or erythematous plaques capped with thick, adherent, silvery-white micaceous scales on extensor surfaces (elbows, knees, scalp, lumbosacral spine, umbilicus).

• Diagnostic Examination Signs:

  • Auspitz Sign: Gentle scraping or mechanical removal of silvery scales reveals pinpoint capillary bleeding points, reflecting the thinning of the suprapapillary epidermis overlying dilated, tortuous dermal papillae capillaries.
  • Koebner Phenomenon (Isomorphic Response): Development of characteristic psoriatic lesions at sites of cutaneous mechanical trauma, surgical incisions, or excoriations 7–14 days following injury.

• Extracutaneous Manifestations: Nail changes occur in up to 50% of patients, including thimble-like nail pitting, onycholysis (separation of nail plate from bed), subungual hyperkeratosis, and pathognomonic "oil-drop" or "salmon patch" discoloration. Up to 30% develop psoriatic arthritis (dactylitis "sausage digits", enthesitis, asymmetrical oligoarthritis, or sacroiliitis).

• Stepped Management (NICE Guidelines):

  • First-Line Topical Therapy: Apply a potent topical corticosteroid (e.g. betamethasone valerate) combined with a vitamin D analogue (e.g. calcipotriol) once daily for up to 4 weeks (available as fixed-combination gel or foam).
  • Second-Line Topical Therapy: If improvement is insufficient after 4 weeks, switch to a vitamin D analogue applied twice daily, or a potent topical corticosteroid applied twice daily for 2–3 weeks, or a coal tar preparation.
  • Specialist Secondary Care: Extensive disease (>10% BSA) or refractory plaques warrant narrowband ultraviolet B (NB-UVB) phototherapy (2–3 times weekly), followed by oral systemic agents: oral methotrexate (first-line systemic; requires folic acid co-prescription and regular monitoring of FBC, LFTs, and renal function), ciclosporin, or acitretin. Severe refractory disease qualifies for biologic therapies targeting TNF-alpha (adalimumab), IL-17 (secukinumab), or IL-23 (guselkumab).

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Acne Vulgaris

Acne vulgaris is a chronic multifactorial disorder of the pilosebaceous unit involving follicular hyperkeratinisation, androgen-driven sebum hypersecretion, proliferation of Cutibacterium acnes, and host inflammatory responses.

• Morphological Lesion Types: Non-inflammatory lesions include open comedones ("blackheads", oxidised melanin/lipids) and closed comedones ("whiteheads", obstructed follicles). Inflammatory lesions include erythematous papules, pustules, deep tender nodules, and pseudocysts, carrying a high risk of permanent atrophic "ice-pick" or hypertrophic scarring.
• NICE Stepped Treatment Algorithm (NG198):
  • Step 1 (Mild-to-Moderate Acne): First-line topical fixed-combination therapy for 12 weeks: topical retinoid plus benzoyl peroxide (BPO) (e.g. adapalene 0.1% + benzoyl peroxide 2.5% gel applied once daily at night), OR topical clindamycin 1% + tretinoin 0.025%, OR topical clindamycin 1% + BPO 5%. Topical antibiotic monotherapy is strictly contraindicated to prevent widespread antimicrobial resistance.
  • Step 2 (Moderate-to-Severe Acne): Oral tetracycline antibiotic (lymecycline 408 mg once daily or doxycycline 100 mg once daily) prescribed for a maximum duration of 12 weeks, ALWAYS co-prescribed with a topical retinoid or BPO to prevent resistant bacterial selection. In females, combined oral contraceptive pills containing anti-androgenic progestogens (e.g. co-cyprindiol / Dianette) provide a viable alternative.
  • Step 3 (Severe Nodulocystic or Scarring Acne): Urgent referral to a consultant dermatologist for oral isotretinoin (Roaccutane).

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Dermatological Emergencies

1. Eczema Herpeticum (Kaposi's Varicelliform Eruption)

Eczema herpeticum represents a life-threatening, disseminated cutaneous infection caused by Herpes Simplex Virus (predominantly HSV-1, less commonly HSV-2) superinfecting pre-existing dermatoses with an impaired stratum corneum barrier, most frequently atopic eczema.

• Clinical Presentation: The patient (often a young child with chronic atopic eczema) presents with an abrupt, acute deterioration characterised by high fever, malaise, chills, irritability, and tender regional lymphadenopathy. Examination reveals a widespread, explosive eruption of monomorphic, dome-shaped, umbilicated vesicles that rapidly rupture, coalesce, and evolve into punched-out circular erosions with overlying hemorrhagic or honey-coloured crusts. Commonest sites include the face, neck, and upper trunk.
• Emergency Management:
  • Immediate Systemic Antiviral Therapy: Commence oral aciclovir immediately (or IV aciclovir if the patient is systemically toxic, vomiting, neonate, or immunocompromised). Clinical administration must never be delayed to await diagnostic viral PCR swabs or electron microscopy results.
  • Ophthalmic Assessment: If vesicles are present in the peri-orbital region or eyelids, obtain an urgent emergency ophthalmology review to examine for herpes simplex dendritic keratitis, which risks corneal ulceration and permanent visual impairment.
  • Supportive & Antibacterial Care: Secondary bacterial superinfection with Staphylococcus aureus or Streptococcus pyogenes is common; add IV or oral flucloxacillin. Topical corticosteroids must be withheld during the initial acute phase.

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

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe, life-threatening, cell-mediated (CD8+ cytotoxic T-cell and natural killer cell-mediated release of granulysin and perforin) type IV hypersensitivity reactions that trigger widespread keratinocyte apoptosis and full-thickness epidermal necrolysis.

• Culprit Etiological Triggers: >80% of cases are drug-induced, typically manifesting 1–4 weeks following the initiation of therapy. Common culprits include: allopurinol, aromatic antiepileptics (carbamazepine, phenytoin, lamotrigine), sulfonamides (co-trimoxazole), NSAIDs (meloxicam, piroxicam), and nevirapine.
• Clinical Presentation: A prodromal influenza-like illness (high fever, malaise, cough, sore throat, stinging eyes) precedes cutaneous manifestations by 1–3 days. Skin lesions commence as tender, dusky, ill-defined erythematous macules that coalesce into atypical flat targetoid lesions (two concentric zones) spreading centrifugally from the face and trunk to the extremities.
• Nikolsky's Sign: Pathognomonic and positive: gentle lateral sliding pressure applied with a finger to erythematous skin elicits epidermal shearing and sheet-like detachment of the epidermis from the underlying dermis.
• Mucocutaneous Detachment Spectrum:

• Mucosal Manifestations: Involve ≥2 mucosal sites in >90% of patients: hemorrhagic, crusted, painful stomatitis of the vermilion border of the lips; purulent conjunctivitis with risk of pseudomembrane formation, symblepharon (adhesion of eyelid to globe), and corneal melting; and severe erosive genital/urethral ulceration.
• The SCORTEN Prognostic Score: Assessed within the first 24–48 hours of admission to calculate mortality risk (1 point per criterion: Age ≥40 years; Heart rate ≥120 bpm; Malignancy present; Initial BSA detachment >10%; Serum urea >10 mmol/L; Serum glucose >14 mmol/L; Serum bicarbonate <20 mmol/L). A score of 0–1 carries ~3% mortality, whereas a score of ≥5 predicts >90% mortality.
• Emergency Resuscitation & Management:
  1. Immediate Cessation of Culprit Drug: Stop all non-essential and suspected medications immediately; early drug withdrawal significantly reduces mortality.
  2. Transfer to Specialized Burns Centre or Intensive Care Unit: Environmental isolation in a thermoregulated room (warmed to 30–32°C) to prevent hypothermia due to loss of cutaneous thermoregulation.
  3. Fluid and Electrolyte Resuscitation: Denuded skin surfaces lead to massive evaporative fluid, protein, and electrolyte losses analogous to major thermal burns. Intravenous crystalloid infusion (Hartmann's solution) should be guided by urine output targets (0.5–1.0 mL/kg/h).
  4. Protective Wound Dressings: Avoid aggressive surgical debridement; apply non-adherent silicone or petrolatum-impregnated dressings under strict sterile conditions.
  5. Multidisciplinary Organ Protection: Emergency ophthalmology involvement (intensive preservative-free lubricants, daily release of symblepharon adhesions, topical antibiotics), urology/gynaecology consultation to prevent vaginal/urethral stenosis, and multimodal analgesia.

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3. Necrotising Fasciitis

Necrotising fasciitis is a fulminant, rapidly progressive soft tissue infection tracking along the deep fascial planes, leading to microvascular thrombosis, liquefactive necrosis of subcutaneous fat and fascia, and overwhelming septic shock.

• Microbiology:
  • Type 1 (Polymicrobial, ~70%): Synergistic mixture of obligate anaerobes (Bacteroides, Peptostreptococcus) and facultative aerobes (Enterobacteriaceae, Streptococcus species); classically seen in elderly, diabetic, or immunocompromised patients following abdominal surgery, perianal sepsis, or perineal trauma (Fournier's gangrene).
  • Type 2 (Monomicrobial, ~30%): Caused by Group A Streptococcus (Streptococcus pyogenes), alone or co-infecting with Staphylococcus aureus; typically occurs in previously healthy individuals following minor cutaneous trauma, insect bites, or surgical procedures.
• Clinical Presentation: The hallmark early diagnostic sign is excruciating, severe pain entirely out of proportion to the subtle overlying physical skin changes (which may show only mild erythema and soft tissue swelling). The infection spreads with alarming velocity. Late findings include dusky purple or violaceous skin discoloration, cutaneous blistering with hemorrhagic bullae, subcutaneous crepitus (gas in tissues, predominantly in Type 1), focal skin anaesthesia (caused by ischaemic thrombosis of cutaneous nerves running through the necrotic fascia), and rapid progression to septic shock (hypotension, tachycardia, refractory lactic acidosis, multiorgan failure).
• Emergency Management Protocol:
  1. Immediate Radical Surgical Debridement: Necrotising fasciitis is a surgical emergency; emergency surgical exploration and wide radical excision of all non-viable, necrotic tissue and fascia is the definitive life-saving intervention. Medical management alone carries a 100% mortality rate; delays in surgical debridement increase mortality exponentially.
  2. Empirical Broad-Spectrum Intravenous Antimicrobials: Immediately administer high-dose IV broad-spectrum antibiotics: e.g. IV meropenem (or piperacillin-tazobactam) PLUS IV clindamycin PLUS IV vancomycin (or teicoplanin for MRSA coverage). Clindamycin is specifically included because its inhibition of bacterial ribosomal 50S protein synthesis arrests the transcription and release of streptococcal pyrogenic exotoxins and toxic shock syndrome toxin (TSST-1), blunting cytokine storm.
  3. Hemodynamic Resuscitation: High-volume IV crystalloids, early invasive arterial monitoring, central venous access, and vasopressor support in an intensive care setting.

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4. Malignant Melanoma

Malignant melanoma arises from the neoplastic transformation of melanocytes, representing the deadliest form of cutaneous malignancy due to its propensity for early lymphovascular invasion and distant metastasis. Primary risk factors include intermittent intense ultraviolet (UV) radiation exposure (particularly blistering sunburns in childhood/adolescence), fair skin (Fitzpatrick skin phototypes I and II), multiple atypical dysplastic naevi (>50), family history, and genetic mutations in CDKN2A and BRAF (V600E).

• Clinical Detection: The ABCDE Diagnostic Rule:

• Histopathological Prognosis: Breslow thickness—the vertical microscopic measurement in millimetres from the top of the epidermal granular layer (or base of ulceration) to the deepest invasive malignant melanocyte in the dermis—is the single most significant independent prognostic determinant of overall survival and nodal metastasis.
• Management Pathway: Any pigmented lesion suspicious for melanoma (NICE NG12: a weighted 7-point checklist score of 3 or more, or dermoscopy suggesting melanoma) needs a suspected cancer pathway referral to a specialist dermatology service. The diagnostic procedure of choice is a complete excisional biopsy with a 2 mm clinical margin and an intact cuff of subcutaneous fat. Partial biopsies (incisional, shave, or punch biopsies) are strictly contraindicated because they risk sampling error, incomplete assessment of maximum Breslow thickness, and inaccurate pathological staging. Once melanoma is histologically confirmed, formal wide local excision (WLE) with safety margins determined by Breslow thickness (1 cm margin for Breslow <1 mm; 2 cm margin for Breslow ≥2 mm) is performed, alongside consideration of sentinel lymph node biopsy (SLNB).