DermatologyTier 1Disease (DEADMAN)

Bacterial infections - cellulitis

Description

Acute spreading infection of the dermis/subcutaneous tissue - ill-defined, non-raised border (contrast with erysipelas)
Erysipelas - more superficial (upper dermis/lymphatics), sharply demarcated, raised border, more likely to cause systemic symptoms/high fever at onset - a variant on the same spectrum, same overall approach
Usually unilateral - bilateral leg "cellulitis" is a common misdiagnosis (usually venous stasis dermatitis/lipodermatosclerosis instead)

Very common - one of the commonest reasons for hospital admission for a skin infection
Risk factors: lower limb (commonest site), obesity, lymphoedema, chronic venous insufficiency, tinea pedis (portal of entry), diabetes, immunosuppression, prior cellulitis (recurrence risk)

Streptococcus pyogenes (group A strep) and Staphylococcus aureus - the two dominant pathogens for non-purulent cellulitis; usually not identified microbiologically (blood/skin cultures low yield in uncomplicated cases)
Purulent cellulitis (associated abscess/purulent drainage) - more likely staphylococcal, consider MRSA cover
Entry via a breach in skin barrier - tinea pedis (interdigital) is a classic recurrent portal of entry, toe web maceration, minor trauma, IV drug injection sites
Lymphoedema/chronic venous disease - impairs lymphatic clearance of bacteria, predisposes to recurrence in the same limb

Clinical - diagnosis is clinical

Erythema, warmth, swelling, tenderness with an ill-defined, spreading margin; +/- fever, malaise, lymphangitis (red streaking), regional lymphadenopathy
Mark the leading edge to monitor progression/response to treatment

Investigations - selective, not routine

Blood cultures/skin swabs - low yield, reserve for severe/systemically unwell, immunosuppressed, or atypical/non-responding cases
Consider imaging (ultrasound) if abscess suspected, or if diagnosis uncertain (e.g. excluding DVT as a differential for unilateral leg swelling)
Assess for a portal of entry - check interdigital toe web spaces for tinea in every lower-limb cellulitis, and treat it to reduce recurrence

A. Mild-moderate, no systemic upset - oral therapy

Flucloxacillin or cephalexin (covers strep + meth-sensitive staph) - first-line
Purulent/MRSA risk - add/switch to cover MRSA (e.g. trimethoprim-sulfamethoxazole, clindamycin) per local resistance patterns

B. Systemic upset, rapidly spreading, or failure of oral therapy - IV therapy

IV flucloxacillin or cefazolin; benzylpenicillin added if severe streptococcal disease suspected
Step down to oral once improving and afebrile

C. Adjuncts

Elevate the affected limb - reduces oedema, aids resolution
Mark and monitor the margin; expect initial erythema to lag behind clinical improvement (do not escalate antibiotics purely because redness hasn't fully receded within 24-48h if the patient is otherwise improving)
Treat the portal of entry (e.g. topical antifungal for tinea pedis) to reduce recurrence risk

D. Severe/atypical - escalate concern for necrotising fasciitis

Pain out of proportion to examination findings, rapidly progressive, crepitus, bullae, systemic toxicity - urgent surgical review, do not treat as simple cellulitis

E. Recurrent cellulitis (same site, >=2 episodes/year)

Address predisposing factors (lymphoedema management, compression, tinea treatment, weight management)
Consider prophylactic antibiotics (e.g. low-dose penicillin) if recurrent despite addressing risk factors

Lymphoedema, chronic venous insufficiency, obesity
Tinea pedis - recurrent portal of entry
Diabetes, immunosuppression - risk of more severe/atypical disease
Prior cellulitis in the same limb - strongest risk factor for recurrence (lymphatic damage from prior episode)

Uncomplicated cellulitis - resolves with appropriate antibiotics over 5-10 days; oedema/erythema can take longer to fully settle than symptoms
Complications: abscess formation, bacteraemia/sepsis, lymphangitis progressing to systemic infection, and rarely necrotising fasciitis
Recurrent cellulitis progressively damages lymphatics -> chronic lymphoedema -> further recurrence risk (a self-perpetuating cycle without addressing the portal of entry/underlying venous-lymphatic disease)

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