Impetigo, cellulitis and necrotising fasciitis

• Impetigo is a superficial, highly contagious bacterial infection of the epidermis: non-bullous impetigo forms golden-brown crusts, while bullous impetigo forms large blisters from toxins made by Staphylococcus aureus.
• Cellulitis is a deeper infection of the dermis and subcutaneous tissue, usually from streptococci or S. aureus; erysipelas is the superficial, well-demarcated form with a raised edge, usually streptococcal.
• Necrotising fasciitis is a surgical emergency: infection spreads along fascia, destroys tissue, and kills; pain out of proportion, rapid spread, warmth, bullae or skin colour change are red flags.
• The most common serious mimics of simple cellulitis are deep vein thrombosis, gout, contact dermatitis, stasis dermatitis and, for raised well-demarcated plaques, erysipelas itself.
• Many cases of uncomplicated impetigo and simple cellulitis can be treated in the community, but red flags such as hypotension, confusion, pain out of proportion or black skin demand urgent hospital care and surgery.

By the end of this page you should be able to:

1. Describe the differences between non-bullous impetigo, bullous impetigo, erysipelas and cellulitis, in words and in a table.
2. Plan treatment for impetigo and for cellulitis/erysipelas, including first-line drug, dose, route and duration, and when to change it.
3. Recognise the risk factors and triggers that lead to recurrence, and list the measures that reduce it.
4. Explain why necrotising fasciitis is so destructive, and list the red flags that should make you operate rather than keep watching.
5. Use the LRINEC laboratory score and understand its limits.
6. Distinguish cellulitis from necrotising fasciitis, from gout, from deep vein thrombosis and from stasis or contact dermatitis.
7. Describe the peri-operative care, including debridement timing, antibiotic strategy and reconstruction, for necrotising fasciitis.

Impetigo is most common in children, especially in warm, humid climates and in conditions of crowding, and it spreads by direct contact and by shared towels and linens. Bullous disease is almost always staphylococcal, while non-bullous disease can be streptococcal, staphylococcal or mixed.

A practical way to place any skin infection on the map is by depth: ^[3]

• Superficial: impetigo (epidermis), erysipelas (upper dermis, lymphatics), folliculitis, furuncles, carbuncles.
• Deep: cellulitis (dermis and subcutaneous fat), complex abscess, fasciitis, myonecrosis.
• Necrotising: necrotising fasciitis and myonecrosis, where infection destroys fascia and sometimes muscle.

Skin and soft tissue infections are also commonly split by severity and by whether they are purulent. The IDSA 2014 guidelines divide them into non-purulent and purulent disease, with mild, moderate and severe categories. ^[6]

The microbiological types are worth knowing because each has a different source and tempo, even though treatment is similar: ^[4]

• Type I: polymicrobial, often from bowel or perineal flora (mixed anaerobes and aerobes), more common in older or diabetic patients with perineal or trunk involvement.
• Type II: usually monomicrobial, most often group A beta-haemolytic streptococcus, occasionally S. aureus, including methicillin-resistant strains; often follows minor trauma in younger, previously healthy people.
• Type III: Gram-negative, often marine-related organisms such as Vibrio spp., with rapid systemic collapse, sometimes with little local skin change.
• Type IV: fungal, mainly in immunocompromised hosts.

Clostridial myonecrosis (gas gangrene) is a Type I subset with gas in tissues and rapid systemic toxicity.

Impetigo is a disease of childhood and of warm, humid, crowded settings. Non-bullous impetigo is the most common skin infection in children worldwide, and bullous impetigo is a staphylococcal disease of infants and young children. Outbreaks occur in schools, nurseries and households, and infection spreads quickly where hand washing and laundry are difficult.

Cellulitis most often affects the legs in adults. Recurrence is a real clinical problem: once someone has had an episode, the same area is prone to another, especially where there is oedema or damaged skin drainage. Risk factors repeatedly identified in reviews are: ^{[3] [4]}

• Skin barrier breakdown: tinea pedis, eczema, fissured heels, leg ulcers, insect bites, surgical wounds, injecting drug use.
• Oedema and poor drainage: chronic lymphoedema, venous insufficiency, heart failure, pregnancy, calcium channel blockers.
• Underlying disease: diabetes mellitus, obesity, immunosuppression, older age.
• Local trauma or a prior episode in the same area; athletes and travellers are also at risk.
• Recurrence is usually at the same site.

Necrotising fasciitis is uncommon but deadly. A review citing the Centers for Disease Control and Prevention puts incidence at 500 to 1500 cases per year in the United States. ^[4] Invasive group A streptococcal infection is reported at 2.4 to 3.1 per 100,000 person-years. Death occurs in roughly 20 to 30% of cases, and about half of survivors leave hospital needing further inpatient rehabilitation or with long-term functional loss. ^{[3] [4]}

Risk factors for necrotising infection mirror those for cellulitis but are more extreme: diabetes (22 to 59% of cases), obesity (17 to 31%), peripheral vascular disease, immunosuppression, chronic liver disease or alcohol misuse, injecting drug use, recent surgery or trauma, and malnutrition. ^[4] Staphylococci also show geographic variation: methicillin resistance in skin and soft tissue infections is reported at 35.9% in North America, 29.4% in Latin America and 22.8% in Europe. ^[3]

Staphylococcal scalded skin syndrome (SSSS) is chiefly a disease of infants and young children. The exfoliative toxins are produced by roughly 5% of S. aureus strains, and SSSS is more common in children under 2 years because renal clearance of toxin is immature and protective antibodies are low. ^[5]

Impetigo. Non-bullous impetigo is caused by group A streptococci and/or S. aureus (often both together): bacteria colonise broken skin, form a vesicle or pustule, and the released serum and cells dry to a crust. The bullous form is nearly always due to S. aureus alone. Its strains produce exfoliative toxins A and B (ETA, ETB), which are serine proteases that specifically cleave desmoglein 1, a protein that holds keratinocytes together in the upper epidermis. Loss of adhesion splits the superficial epidermis and creates the large flaccid blister. ^{[2] [5]}

Bullous impetigo can progress to SSSS if the toxin reaches the bloodstream, because the same cleavage of desmoglein 1 then happens over a wide area.

Cellulitis and erysipelas. Bacteria enter through a break in skin. Streptococci (usually group A beta-haemolytic Streptococcus) spread rapidly along lymphatics and produce spreading erythema with systemic upset; S. aureus is common where there is purulence or an abscess. Erysipelas is superficial, so its edge is sharp, raised and painful. Deeper cellulitis involves lymphatics in the dermis and fat, giving broader, less defined erythema. In MRSA, altered penicillin-binding protein (PBP-2a) and toxins complicate treatment; CA-MRSA strains often carry Panton-Valentine leukocidin. ^{[1] [3]}

Necrotising fasciitis. Infection starts in the subcutaneous tissue and fascia. Bacterial toxins and enzymes cause thrombosis of the small vessels that supply the skin and fascia, so tissue dies faster than it can be repaired. The process moves along fascial planes, often faster and further than the skin changes suggest. By the time skin turns purple, blue or black, the fascia underneath is already dead. Pain is severe early, when the nerves in the fascia are inflamed but the skin still looks almost normal, and the patient often has fever and systemic toxicity out of proportion to the visible lesion. ^[4]

SSSS, in contrast, is not tissue destruction but a toxin-mediated split at the level of the granular layer of the epidermis, with mucous membranes spared and a positive Nikolsky sign. ^[5]

Impetigo is confined to the epidermis: neutrophils, serum and bacteria dry to form the crust, and the surrounding dermis is essentially normal. ^[2] Bullous impetigo shows loss of adhesion between keratinocytes in the superficial epidermis where desmoglein 1 has been cleaved. ^[5]

Cellulitis and erysipelas show acute inflammation, oedema and bacteria within the dermal lymphatics and subcutaneous tissue; erysipelas is superficial with dense perivascular inflammation. ^[3]

Necrotising infection produces grey, oedematous, necrotic fascia, thrombosed vessels and loss of planes at operation; histology shows necrosis of fascia and subcutaneous fat with leucocyte infiltration and vascular thrombosis. ^[4]

SSSS shows a clean intra-epidermal split at the level of the granular layer with acantholysis, with no organisms in the blister. ^[5]

Figure 1Blackish discolouration with vesicle formation on the thigh NF

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Long description

A clinical photograph showing blackish discolouration with vesicle formation on the thigh in a case of necrotizing fasciitis.

Figure 2Facial erysipelas

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Clinical photograph of a person with a facial erysipelas infection.

Figure 3Impetigo Nase

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Long description

Clinical photograph labelled facial impetigo; the German description says it is the drying stage of a small-blister (vesicular) skin change on the nose, with Staphylococcus aureus grown on culture.

• Non-bullous: a red macule becomes a vesicle or pustule that rapidly crusts into a golden-brown or honey-coloured scab; new lesions appear as old ones heal. Itch and mild soreness are common; children are otherwise well.
• Bullous: thin-roofed blisters filled with clear fluid on otherwise normal skin, often in moist areas such as the axillae, neck and groin. They rupture easily and leave a thin, flat, yellow-brown crust. Patients may be systemically unwell if SSSS develops.

Look for the primary site, count lesions, and exclude scabies or head lice, which may have introduced the infection. Check for secondary spread by scratching.

History in the patient's words: pain, tightness, warmth, redness spreading, fever or rigors, a recent cut, bite, blister, athlete's foot, surgery or injection. Ask about diabetes, swelling, varicose veins, heart failure and previous episodes.

Examination:

• Erysipelas: raised, brightly erythematous, shiny plaque with a sharp margin; fever and malaise are common.
• Cellulitis: spreading erythema, warmth, swelling and tenderness, often with lymphangitis and tender regional nodes; the margin is indistinct.
• Both are usually unilateral. Mark the edge with a pen to judge spread. ^[1]

Be aware that redness may be harder to see on darker skin; rely on warmth, tenderness and swelling. ^[1]

Early on, this looks like mild cellulitis. Clues that it is much worse: ^[4]

• Pain out of proportion to the skin appearance.
• Rapid spread despite appropriate antibiotics, or redness far beyond what was first seen.
• Skin colour change: erythema progressing to dusky purple, blue, green or black.
• Bullae, haemorrhagic blisters, or skin that feels wooden or tense.
• Crepitus or gas in the tissues (a late and unreliable sign).
• Systemic toxicity: fever, tachycardia, hypotension, confusion, or organ dysfunction.
• Induration far beyond the visible erythema (tenderness or hardening deep to skin).
• Pain on passive stretch of the limb or joint (suggests deep tissue or fascial involvement).

A useful bedside picture: a patient with "cellulitis" of the leg who looks septic and has severe pain when the foot is passively moved probably has necrotising infection until proven otherwise.

SSSS presents with sudden erythema, often perioral or in flexures and friction sites, followed by superficial desquamation like "scalded" skin; Nikolsky sign is positive (gentle lateral pressure makes the skin slip). Mucous membranes are spared. It occurs mainly in neonates and young children, and in adults with renal failure. Blood cultures are usually negative (about 3% positive); the exotoxin is produced at a distant colonised site such as the nose or throat. ^[5]

For simple impetigo and simple cellulitis, diagnosis is clinical and no test is needed. Tests are used when infection is severe, recurrent, atypical or not responding. ^{[1] [3]}

The LRINEC (Laboratory Risk Indicator for Necrotising Fasciitis) score combines C-reactive protein, white cell count, haemoglobin, sodium, creatinine and glucose as above. A score of 6 or more is the cut-off used for necrotising fasciitis. ^[4]

Blood tests are normal in many people with simple cellulitis. If you are genuinely worried that "cellulitis" is necrotising, the important test is surgical exploration, not imaging. ^[4]

There is no universally agreed score for cellulitis itself. Severity is judged clinically: systemic upset (fever, tachycardia, hypotension), rapid spread, pain out of proportion, or a site near the eye or nose. ^{[1] [3]}

For necrotising infection, use red-flag assessment plus LRINEC. The WSES global pathways classify skin and soft tissue infections into three treatment groups: surgical site infections, non-necrotising infections (including erysipelas, impetigo, simple abscess) and necrotising infections. ^[3] Severity and necrosis should be assessed independently of anatomical site. ^[3]

The NICE guidance on cellulitis itself reminds clinicians to exclude other causes of redness, such as an inflammatory reaction to an immunisation or insect bite, and non-infectious causes such as chronic venous insufficiency. ^[1]

• Treat impetigo topically first in most localised cases; use oral flucloxacillin for bullous or widespread or systemically unwell patients.
• Treat non-purulent cellulitis/erysipelas with oral flucloxacillin first line, 5 to 7 days, up to 14 days; use co-amoxiclav when infection is near the eyes or nose; add MRSA cover only when needed; reassess at 48 hours if intravenous. ^[3]
• Drain every abscess properly.
• Treat necrotising infection as a surgical emergency: resuscitate, give broad-spectrum intravenous antibiotics with clindamycin, and take the patient to theatre without delay; aim for debridement within 6 hours.
• Prevent recurrence by fixing predisposing factors: treat tinea pedis, control oedema and diabetes, and consider long-term prophylactic phenoxymethylpenicillin for adults with 2 or more episodes a year.

Follow NICE NG153. ^[2]

For localised non-bullous impetigo in someone well, consider hydrogen peroxide 1% cream applied two or three times a day for 5 days. If that is unsuitable or has failed, offer a short course of a topical antibiotic: fusidic acid 2% applied three times a day for 5 days as first choice (or mupirocin 2% three times a day for 5 days if fusidic acid resistance is suspected). ^[2]

For widespread non-bullous impetigo, offer a short course of a topical or oral antibiotic, taking into account practicality of applying cream over large areas, earlier topical use, and rapid development of resistance to topical agents (so avoid extended or repeated use). ^[2]

For bullous impetigo, or for non-bullous impetigo in someone systemically unwell or at high risk of complications, offer a short course of an oral antibiotic: flucloxacillin 500 mg four times a day for 5 days in adults, or weight and age-appropriate doses in children. Alternatives for penicillin allergy are clarithromycin (250 mg twice a day for 5 days in adults, increased to 500 mg twice a day for severe disease) or, in pregnancy, erythromycin 250 to 500 mg four times a day for 5 days. ^{[2] [1]}

Do not combine topical and oral antibiotics for impetigo. If impetigo persists after topical treatment, step up to an oral antibiotic and consider a skin swab; if it recurs frequently, send swabs and consider nasal decolonisation. ^[2]

A 5-day course is usually enough, but may be extended to 7 days based on clinical judgement. ^[2] Very low birth-weight or preterm infants with SSSS-type disease need admission and intravenous therapy (see below).

Follow NICE NG141. ^[1]

Offer an antibiotic for both conditions; take account of severity, site (especially near the eyes or nose), risk of unusual organisms, prior swab results and known MRSA status. ^[1]

• First-line (give orally unless unable): flucloxacillin 500 mg to 1 g four times a day by mouth, or 1 g to 2 g four times a day intravenously, for 5 to 7 days. ^[1]
• Penicillin allergy or flucloxacillin unsuitable: clarithromycin 500 mg twice a day (oral or IV), or erythromycin 500 mg four times a day in pregnancy, or doxycycline 200 mg on day one then 100 mg once daily, all for 5 to 7 days. ^[1]
• Near the eyes or nose (higher risk of serious intracranial complication): co-amoxiclav 500/125 mg three times a day by mouth or 1.2 g three times a day IV for 7 days; if allergic or unsuitable, clarithromycin plus metronidazole. ^[1]
• Severe infection (hospital): co-amoxiclav, cefuroxime, clindamycin or ceftriaxone are the alternatives listed in NG141. ^[1]
• Confirmed or suspected MRSA: add vancomycin, teicoplanin or specialist-use linezolid, with combination therapy. ^[1]

Give oral antibiotics first line if the person can take them and does not need intravenous therapy. If intravenous antibiotics are used, review by 48 hours and step down to oral when possible. ^[1] A longer course, up to 14 days in total, may be needed, but the skin takes time to return to normal and full resolution at 5 to 7 days is not expected. ^[1]

Reassess patients if symptoms worsen rapidly or significantly, do not improve within 2 to 3 days, or if there is systemic illness, severe pain out of proportion, or spreading redness. ^[1] Other diagnoses to remember are an inflammatory reaction to an insect bite or vaccination, gout, thrombophlebitis, eczema, allergic dermatitis and deep vein thrombosis. ^[1]

Refer to hospital for orbital, osteomyelitis, septic arthritis, necrotising fasciitis or sepsis. ^[1]

A simple abscess is best treated by incision and drainage, not antibiotics alone. Incise, evacuate pus and debris, break loculations and lightly pack; antibiotics for 5 days are added for abscesses over 5 cm, in difficult sites such as the face, hand or genitalia, multiple lesions, immunosuppression, or lack of response to drainage. ^[3]

Furuncles and carbuncles often drain spontaneously with warm compresses; larger ones need incision and drainage. Carbuncles are deeper and often need packing. A recurrent abscess demands a search for a foreign body, fistula or underlying disease such as hidradenitis suppurativa. ^[3]

Purulent cellulitis (cellulitis with an abscess) is managed primarily with drainage, with antibiotics added when there is surrounding cellulitis. ^[3]

This is a surgical emergency. Delays are the main cause of death. ^{[3] [4]}

1. Resuscitate: oxygen, fluids, analgesia, and manage septic shock if present. ^[4]
2. Give broad-spectrum intravenous antibiotics immediately after blood cultures and before surgery. A suggested regimen is a broad-spectrum backbone (piperacillin-tazobactam, a carbapenem or ceftriaxone plus metronidazole according to condition) plus clindamycin for its toxin-suppressing effect, plus MRSA cover where suspected; Gram-positive deep infection may need vancomycin, linezolid or daptomycin. ^{[3] [4]}
3. Take to theatre without delay for surgical exploration and debridement. Joint WSES/GAIS/WSIS/SIS-E/AAST guidance advises debridement within 6 hours of admission, because surgery within 6 hours has been associated with a 19% mortality versus 32% when delayed beyond 6 hours (odds ratio 0.43, 95% confidence interval 0.26 to 0.70, from ten studies). ^{[3] [4]} Older guidance from EAST recommended within 12 hours, and delays beyond 12 to 14 hours have also been linked with much higher mortality. ^{[4] [5]}
4. Explore widely. Remove all necrotic fascia and tissue until healthy, bleeding tissue is seen; dishwater fluid, grey dead fascia, loss of tissue planes and lack of bleeding are the operative clues. ^[4]
5. Take cultures and Gram stain of deep tissue, including fungal cultures, during debridement. ^[4]
6. Re-explore every 12 to 24 hours until the wound is clean; patients commonly need 3 to 4 operations. ^{[3] [4]}
7. Continue antibiotics until source control is achieved and systemic infection has resolved; the exact duration is not settled, and shorter (less than 7 days) and longer courses have shown similar mortality and amputation rates in retrospective studies. ^[4]
8. Adjuvant options: negative pressure wound therapy helps wound management after the wound is stable; IVIG has mixed evidence; hyperbaric oxygen is not supported by good evidence. Amputation is sometimes required (up to 25% of extremity cases) when source control is impossible. ^[4]

Skin-sparing debridement can leave viable skin in place when only fascia is necrotic, but it should not compromise source control. ^[4] Reconstructive surgery and rehabilitation follow once infection is controlled.

Treat as a toxin-mediated staphylococcal disease, usually in children: ^[5]

• Empirical antibiotic for a penicillinase-resistant penicillin (flucloxacillin or nafcillin) in areas of low MRSA prevalence; use a first- or second-generation cephalosporin such as cefazolin for penicillin allergy. Add vancomycin where MRSA is highly prevalent or if first-line therapy fails.
• Evidence does not support clindamycin as adjunct anti-toxin treatment (no faster recovery).
• Start intravenously; switch to oral once improved and there is no bacteraemia.
• Duration 5 to 14 days, depending on recovery and susceptibility results. ^[5]
• Supportive care is vital: intravenous fluids, meticulous skin care with non-adherent dressings, and pain control. Topical antibiotics are useful in superficial disease but much less so in SSSS, where the skin is not the primary source.

• Pregnancy: erysipelas at or near the nose or eyes can be serious. Avoid doxycycline; macrolides in true penicillin allergy must be weighed as in the guideline label. ^{[1] [2]}
• Children: NICE age bands apply; babies under 1 month need specialist advice for cellulitis. Impetigo in infants is usually managed topically where possible, with oral flucloxacillin when widespread or bullous. ^{[1] [2]}
• Older adults: higher MRSA risk, more recurrence, slower healing; review for venous insufficiency, oedema and foot care.
• Immunosuppressed or neutropenic patients: Gram-negative organisms must be covered; cultures have higher yield; low threshold for intravenous broad-spectrum therapy and imaging. ^[3]
• Neonates with SSSS: preterm and immunocompromised infants are at highest risk; recurrence is confined largely to these groups. ^[5]

Cellulitis recurs because the predisposing factor remains. Treat the portal: eradicate tinea pedis, eczema, leg ulcers, fissures and ingrown nails; manage venous insufficiency and oedema; reduce weight; stop smoking; use well-fitting footwear. ^{[1] [3]}

NICE NG141 does not recommend routine antibiotic prophylaxis for recurrent cellulitis. For adults who have had at least two episodes treated in hospital or under specialist advice in the past year, specialists may consider a trial of prophylaxis after shared discussion, with review every 6 months: phenoxymethylpenicillin 250 mg twice daily, or erythromycin 250 mg twice daily for true penicillin allergy. ^[1]

For impetigo, stop transmission: cover lesions, hand-washing, separate towels and bedding, and keep children from school until crusts have gone. Recurrent nasal carriage may justify decolonisation; swab if recurrence is frequent. ^[2]

Necrotising infection prevention is general good care: control diabetes, avoid injection of non-prescribed drugs, and fast surgical debridement of any skin or soft-tissue infection that is not settling.

• A careful bedside examination usually makes the diagnosis of impetigo and cellulitis; no imaging is needed in uncomplicated disease.
• Reserve antibiotics for clearly bacterial disease; treat impetigo topically where possible.
• Mark the edge of cellulitis with a pen or skin pencil and review in 48 hours.
• If an antibiotic is given by mouth, flucloxacillin is cheap and effective where resistance allows; macrolides substitute in true allergy.
• Abscesses need safe incision and drainage; use simple dressings.
• Necrotising infection can be recognised by pain out of proportion, rapid spread and systemic illness. Do not wait for imaging or laboratories. Start broad-spectrum antibiotics and transfer or operate as early as possible; irrigation and debridement with basic instruments saves lives.
• For SSSS in neonates, intravenous access and supportive care are the priorities; where vancomycin is unavailable, a penicillinase-resistant penicillin or cephalosporin remains appropriate in a low-MRSA area.
• Skin and soft tissue outcomes worsen with delay; refer early when the general condition is not good.

The management above is based on NICE NG141 and NG153, with severity and source-control concepts from the WSES/GAIS/WSIS/SIS-E/AAST global pathways (2022) and the WSES/GAIS source-control review for necrotising infection. ^{[1] [2] [3] [4]} The recommendations agree on flucloxacillin first line for simple cellulitis in the UK, but use of MRSA cover, drug choice and duration differ worldwide (for example co-trimoxazole or doxycycline are used more in some countries). ^[3] The Infectious Diseases Society of America 2014 guidance classifies these infections as purulent versus non-purulent with severity classes, and supports prompt surgical exploration for necrotising disease; as with other guidance, antibiotic choice should follow local resistance data and formulary. ^[6] British dermatology practice and NICE Clinical Knowledge Summaries (CKS) cover impetigo and cellulitis management in the UK; StatPearls reviews SSSS and necrotising infection and is a useful background text.

Bacterial skin infection, soft tissue infection, and infection topics relevant to this page include atopic dermatitis, anorectal disease, foot infection and osteomyelitis, lymphoedema, surgical sepsis, postpartum infection, toxic shock syndrome, primary immunodeficiency, Staphylococcus aureus infections and infectious disease skin and soft tissue infections.

• Impetigo is a superficial, crusted or blistered infection of the epidermis; bullous impetigo is caused by S. aureus exfoliative toxins and can progress to SSSS.
• Non-bullous impetigo is golden-brown crusted; bullous impetigo forms large flaccid blisters with a thin yellow-brown crust. ^[2]
• Erysipelas is superficial with a raised, sharp edge; cellulitis is deeper with an ill-defined border. ^[3]
• Simple impetigo and cellulitis are usually treated in the community with short oral courses (typically 5 to 7 days, extendable to 14 for cellulitis). ^{[1] [2]}
• First-line drug for simple cellulitis is flucloxacillin; alternative for penicillin allergy is clarithromycin, erythromycin in pregnancy, or doxycycline. ^[1]
• To reduce cellulitis recurrence, treat tinea pedis, venous disease and oedema; routine long-term antibiotic prophylaxis is not recommended. ^{[1] [3]}
• Necrotising fasciitis presents with pain out of proportion, rapid spread and systemic illness; skin colour change, bullae and crepitus appear late. ^[4]
• LRINEC (CRP, white cells, haemoglobin, sodium, creatinine, glucose) supports diagnosis but has poor sensitivity; a score of 6 or more is the standard cut-off. ^[4]
• Surgical exploration and debridement within about 6 hours, with broad-spectrum antibiotics, are the life-saving steps. ^{[3] [4]}
• Abscesses need incision and drainage; antibiotics are adjuncts. ^[3]
• SSSS is a toxin-mediated desquamation, spares mucous membranes, has positive Nikolsky sign, and is treated with penicillinase-resistant penicillin plus supportive care. ^[5]
• SSSS and bullous impetigo share exfoliative toxins and pathophysiology; the difference is localised versus widespread toxin. ^[5]