Lucan · Conditions

Cellulitis

Australian guidance: eTG Antibiotic — Skin and Soft Tissue Infections

1. Definition and epidemiology

Cellulitis is an acute bacterial infection of the dermis and subcutaneous tissues, characterised by spreading erythema, warmth, oedema, and tenderness, without an identifiable purulent focus. It is one of the most common skin infections presenting to Australian emergency departments and general practitioners, with an estimated incidence of approximately 24 cases per 1,000 person-years in the community. Lower limb cellulitis accounts for the vast majority of presentations; recurrence affects roughly 30% of patients within three years, particularly those with chronic lymphoedema or tinea pedis as a portal of entry.

2. Pathophysiology

Per Robbins Ch 25, cellulitis arises when bacteria breach the epidermal barrier and proliferate in the poorly defended dermis and subcutaneous fat. The most common causative organisms are beta-haemolytic streptococci (predominantly Streptococcus pyogenes, group A streptococcus) and, less frequently, Staphylococcus aureus. Streptococcal exotoxins including streptolysin and hyaluronidase degrade extracellular matrix and facilitate lateral spread through tissue planes, explaining the rapidly advancing border that distinguishes cellulitis from a localised abscess. Bacterial products trigger pattern recognition receptors on keratinocytes and resident macrophages, driving local complement activation and neutrophil influx. The resulting acute inflammatory response produces the cardinal signs: vasodilation and increased permeability cause erythema and oedema; bradykinin and prostaglandins mediate pain; fever reflects systemic cytokine release. Pre-existing disruption of lymphatic drainage (from prior cellulitis, chronic venous insufficiency, or obesity) impairs local immune surveillance and bacterial clearance, creating a substrate for recurrent episodes. Portal-of-entry sites include tinea pedis, traumatic wounds, ulcers, and insect bites.

3. Clinical presentation and diagnostic criteria

Cellulitis presents with a warm, tender, erythematous, and swollen area of skin that typically lacks a defined purulent centre. Borders may be indistinct and spreading. The lower leg is the predominant site in adults. Constitutional symptoms including fever, rigors, and malaise indicate systemic involvement and influence decisions about hospital admission and intravenous therapy.

Erysipelas is a superficial variant involving the dermis and upper subcutaneous tissue, classically caused by S. pyogenes, and is distinguished by a sharply demarcated, raised, fiery-red border, most often on the face or lower leg.

Distinguishing cellulitis from non-infectious mimics is clinically important. Bilateral lower limb erythema and swelling is almost never bilateral cellulitis; it is far more likely to represent chronic venous insufficiency, lipodermatosclerosis, or contact dermatitis. Stasis dermatitis, deep vein thrombosis, and acute gout are the most common misdiagnoses. Assessment should include the Eron classification or a comparable scoring tool: Class I (no systemic toxicity, no significant comorbidities) is suitable for outpatient oral therapy; Class II (systemic toxicity or significant comorbidity); Class III (significant systemic toxicity or unstable comorbidities); Class IV (life-threatening infection such as necrotising fasciitis). Any rapidly spreading infection with severe pain, bullae, crepitus, or haemorrhage should prompt urgent surgical review to exclude necrotising fasciitis.

4. Investigations and AU-specific cutoffs

Investigations are guided by severity and clinical context.

Blood cultures: low yield in uncomplicated cellulitis (positive in approximately 2 to 4% of cases); not routinely recommended for Class I. Order for Class II to IV, immunocompromised patients, or any patient with haemodynamic instability.

Serum investigations: full blood count (FBC), C-reactive protein (CRP), and urea, electrolytes, and creatinine (UEC) are appropriate for Class II and above. Leucocytosis and elevated CRP support a bacterial aetiology and guide admission decisions. A CRP above 100 mg/L or a white cell count above 15 x 10^9/L suggests more severe infection.

Skin swabs from intact skin have no diagnostic value. Where there is a purulent component, wound swab or aspiration for microscopy and culture is appropriate.

Imaging: plain X-ray or computed tomography (CT) is indicated if gas-forming organisms or a deep space infection are suspected. Ultrasound can differentiate cellulitis from an abscess if a fluctuant component is present on examination.

The LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) score integrates CRP, white cell count, haemoglobin, sodium, creatinine, and glucose; a score of 6 or above warrants urgent surgical review.

5. Management

Management is stratified by severity using the Eron classification.

Class I (outpatient oral therapy): the preferred antibiotic per eTG Antibiotic — Skin and Soft Tissue Infections is cefalexin 500 mg orally four times daily (children: 12.5 mg/kg up to 500 mg, four times daily). Duration is typically 5 to 7 days, reviewed at day 2 to 3 for clinical response. The patient should be advised to mark the margin of erythema with a skin pen at the time of first assessment to monitor progression.

Class II (may be managed in hospital or ambulatory care): dicloxacillin 500 mg orally four times daily or cefalexin 500 mg orally four times daily; consider intravenous therapy if there is rapid progression or failure of initial oral therapy.

Class III to IV (hospital intravenous therapy): flucloxacillin 2 g intravenously every 6 hours, or cephazolin 2 g intravenously every 8 hours, is the recommended empirical regimen. Cephazolin offers the advantage of less frequent dosing and equivalent efficacy against streptococci and methicillin-susceptible S. aureus (MSSA).

Penicillin allergy: for patients with a non-severe (immediate or delayed) penicillin hypersensitivity reaction, cefalexin or cephazolin can be used with caution. For patients with a severe penicillin hypersensitivity reaction, clindamycin 450 mg orally three times daily (or 450 mg intravenously every 8 hours) is the preferred alternative.

Methicillin-resistant S. aureus (MRSA): community-acquired MRSA is uncommon in uncomplicated cellulitis in Australia outside of specific risk groups (people who inject drugs, Aboriginal and Torres Strait Islander patients in some regions, patients with prior MRSA colonisation). If MRSA is suspected or confirmed, trimethoprim plus sulfamethoxazole 160 plus 800 mg orally twice daily or clindamycin are oral alternatives; vancomycin is used for severe MRSA cellulitis in the inpatient setting.

Adjunctive measures include elevation of the affected limb, analgesia, and treatment of the portal of entry (antifungal therapy for tinea pedis once the acute infection is controlled).

6. Pharmacology and AU PBS notes

First-line oral (Class I, no penicillin allergy): Cefalexin 500 mg orally four times daily. AU brands: Keflex, Ialex, and generics. PBS: listed on the Pharmaceutical Benefits Scheme (PBS) for bacterial skin infections (item 1883M for the standard 500 mg capsule, authority not required for uncomplicated cellulitis in general practice).

Alternative first-line oral: Dicloxacillin 500 mg orally four times daily. AU brand: Distaph. PBS listed. Must be taken on an empty stomach; absorption is significantly reduced by food. Flucloxacillin 500 mg orally four times daily. AU brands: Flopen, Staphylex. PBS listed. Administer 30 minutes before food.

First-line intravenous (Class III to IV, no penicillin allergy): Cephazolin 2 g intravenously every 8 hours. AU brand: Kefzol and generics. PBS: hospital formulary, Section 100 restricted benefit for severe skin and soft tissue infections. Flucloxacillin 2 g intravenously every 6 hours. AU brand: Flopen IV. PBS: restricted benefit inpatient.

Penicillin allergy, severe (oral): Clindamycin 450 mg orally three times daily. AU brand: Dalacin C. PBS: listed under restricted benefit; authority required for skin infections in some states.

Penicillin allergy, severe (intravenous): Vancomycin 25 to 30 mg/kg per day in two to three divided doses, targeting an area-under-the-curve to minimum inhibitory concentration (AUC/MIC) ratio of 400 to 600 (or trough 15 to 20 mg/L if AUC monitoring unavailable). Dose adjustment required in renal impairment. AU brand: Vancocin.

7. Complications and monitoring

The most immediately dangerous complication is necrotising fasciitis, which must be excluded in any patient with disproportionate pain, rapidly advancing borders, bullae, haemorrhagic changes, gas in the tissue, or haemodynamic instability. Necrotising fasciitis requires emergent surgical debridement.

Bacteraemia and sepsis occur in a minority of cases but carry significant mortality in immunocompromised patients, those with functional asplenia, and the elderly.

Recurrent cellulitis: patients with two or more episodes per year are candidates for prophylactic low-dose phenoxymethylpenicillin (penicillin V) 250 mg orally twice daily, or erythromycin 250 mg orally twice daily in patients with penicillin allergy. Prophylaxis should be continued for 6 to 12 months and is most effective when the portal of entry (e.g. tinea pedis, lymphoedema) is simultaneously managed.

Lymphoedema: repeated cellulitis of the lower limb causes progressive lymphatic damage, increasing oedema and susceptibility to further infection. Compression therapy and skin hygiene are essential long-term preventive measures.

Monitoring during active treatment: erythema margin should be reassessed at 48 to 72 hours. Failure to improve or clinical deterioration at 48 hours should prompt reassessment of the diagnosis, escalation to intravenous therapy, imaging to exclude abscess or necrotising fasciitis, and consideration of atypical organisms. Inflammatory markers (CRP, FBC) are useful to trend in hospitalised patients.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.