Cellulitis, abscess and necrotising soft tissue infection

• Cellulitis is a deeper infection of the dermis and subcutaneous tissue, usually arising after a break in the skin; erysipelas is its superficial, fiery, sharply raised form.
• A cutaneous abscess is a localised collection of pus, most often due to Staphylococcus aureus, and is cured first by incision and drainage, not by antibiotics alone.
• Methicillin-resistant Staphylococcus aureus (MRSA) is a common cause of purulent infection but an uncommon cause of typical non-purulent cellulitis; cover it when risk factors are present and then tailor treatment.
• Necrotising soft tissue infection (NSTI) is a surgical emergency in which infection spreads along fascia and tissue dies; mortality is roughly 20 to 30% ^[3]. ^[2]
• Antibiotics are only an adjunct. In NSTI the aim is to drain or debride within hours, because mortality is lower when surgery happens early ^[2].

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

1. Distinguish cellulitis, erysipelas, abscess and NSTI by depth, margin and pace.
2. Name the usual pathogens for each, including when MRSA is likely, and why.
3. Plan treatment for simple abscess, cellulitis and erysipelas, including first-line drug, dose, route, duration and when to escalate.
4. Explain the principles of source control, and describe when and how to debride in NSTI.
5. Recognise NSTI red flags and interpret the LRINEC score and its limits.
6. Adjust management for penicillin allergy, children, pregnancy, immunocompromise and low-resource settings.
7. Describe measures that prevent recurrence.

Cellulitis is a deeper process. It sits in the dermis and subcutaneous tissue and usually follows contamination of a break in the skin. It produces spreading redness, warmth, pain, swelling and often lymphangitis, with fever and a raised white cell count. Erysipelas is a more superficial infection, still of the dermis and lymphatics, in which the involved skin is raised and separated from normal skin by a sharp line. A cutaneous abscess is a walled-off pocket of pus in the dermis and deeper tissues, most often staphylococcal. Necrotising soft tissue infection is an infection with progressive necrosis of skin, subcutaneous tissue, fascia or muscle, usually accompanied by sepsis and tissue breakdown.

Infections of the skin can be classified usefully in three independent ways:

1. By depth: superficial infections (impetigo, erysipelas, folliculitis, furuncle, carbuncle) versus deep infections (cellulitis, complex abscess, fasciitis, myositis).
2. By whether there is pus: non-purulent cellulitis and erysipelas versus purulent infection with an abscess.
3. By whether tissue is dying: non-necrotising versus necrotising infection.

Severities of systemic upset are often captured with the Eron classes, a bedside framework often used in emergency care ^[2].

Where the infection extends, and how purulent and necrotising it is, should be assessed separately rather than collapsed into a single category ^[2].

Skin and soft tissue infections are common and mostly uncomplicated, but the severe end matters greatly because it drives hospitalisation and death.

A population-based study of 376,262 people covered 471,550 episodes of skin and soft tissue infection. Cultures were taken in 23% of episodes and a pathogen was found in 54% of cultured episodes. Staphylococcus aureus was the most common pathogen in 81% of pathogen-positive specimens, and 46% of these S. aureus isolates were methicillin-resistant ^[2]. Methicillin resistance in S. aureus varies by continent, with the highest reported rate in North America at 35.9%, followed by Latin America at 29.4% and Europe at 22.8% ^[2].

Community-acquired MRSA (CA-MRSA) is genetically distinct from hospital-acquired MRSA. CA-MRSA carries SCCmec type IV or V and often produces Panton-Valentine leukocidin, a cytotoxin. It is resistant to fewer non-beta-lactam antibiotics. Its prevalence varies worldwide, from under 1% in some countries to over 50% in others, and it is more common in children than in adults ^[2].

Necrotising soft tissue infection is rare but lethal. The Centers for Disease Control and Prevention reports 500 to 1,500 cases per year in the United States ^[3]. For Group A streptococcal invasive infection, the reported incidence is 2.4 to 3.1 per 100,000 person-years ^[3]. Reported hospital mortality for NSTI is 20 to 30% ^[2]. About one-quarter to one-half of patients develop septic shock, roughly one-third develop acute kidney injury, and intensive care stay is typically 5 to 12 days ^[3].

Cellulitis has a tendency to recur, especially in the legs, and the new episode is usually in the same place as the last ^[2].

Most simple skin infections in healthy people are caused by aerobic Gram-positive cocci: S. aureus and the beta-haemolytic streptococci, above all Streptococcus pyogenes. Cellulitis associated with an abscess is usually staphylococcal, whereas typical non-purulent cellulitis is caused by both streptococci and S. aureus. MRSA is an unusual cause of typical non-purulent cellulitis but a common cause of purulent infection ^[2]. In neutropenic and immunocompromised hosts, Gram-negative organisms must also be considered ^[2].

Polymicrobial infection develops when aerobic Gram-negative organisms and anaerobes invade, usually in deep or necrotising infection or in patients with vascular disease or diabetes. Gas gangrene and clostridial infection, though rare, are a severe subgroup within this group.

Habits and diseases that break the skin barrier or weaken host defence raise the risk of serious infection:

• Any breach in skin integrity: trauma, bites, surgery, injection.
• Infection entering through minor trauma was found in 10 to 38% of NSTI cases ^[3].
• Diabetes mellitus, present in 22 to 59% of NSTI cases. ^[3]
• Obesity, affecting 17 to 31% of NSTI cases. ^[3]
• Cardiovascular disease in 9 to 45% of NSTI cases, peripheral vascular disease in 3 to 19%. ^[3]
• Intravenous drug use in 2 to 80% of NSTI cases, immunosuppression in 4 to 30%, and chronic alcohol abuse in 6 to 27% ^[3].
• Untreated perirectal abscess, cancer, smoking, autoimmune disease.
• Local factors for recurrence of cellulitis: leg oedema, especially lymphoedema, venous insufficiency, previous trauma or surgery to the area, and tinea pedis ^[2].

Erysipelas is caused mainly by Streptococcus species, most often S. pyogenes. S. aureus rarely causes erysipelas, and the role of MRSA remains controversial ^[2].

Healthy, well-vascularised skin resists bacterial invasion. Infection develops when organisms are pushed or pulled through a breach into the warm, nutrient-rich deeper layers, or when local defences fail.

Cellulitis travels along the dermal lymphatics and into subcutaneous tissue. The toxins and enzymes of streptococci and S. aureus allow spread through tissue planes and produce the classic heat, redness, swelling and pain. Erysipelas remains more superficial, which is why its border is sharp and raised above the skin.

An abscess forms when bacteria are walled off by the host inflammatory response. Pus accumulates in a cavity, pressure builds, and the centre becomes relatively avascular. Antibiotics penetrate poorly into this cavity, which is why drainage is the essential step.

Necrotising soft tissue infection is a different beast. Organisms and their toxins reach the fascia and then spread rapidly along fascial planes with little resistance. Tissue ischaemia develops, then necrosis, then systemic toxicity. Toxins produce the clinical picture long before the skin changes are obvious, which is why patients may have fever, pain and prostration with only subtle redness early on. A clinician who waits for black skin before diagnosing NSTI will operate too late. ^[3]

Cellulitis presents with spreading area of redness, heat, swelling and pain, often with a red streak up the limb (lymphangitis), regional lymph node tenderness and fever. The margins are not well defined. Erysipelas looks hotter and more sharply outlined, with a raised plaque and a clear demarcating line between involved and normal skin ^[2].

Recurrent cellulitis should raise the question of ongoing predisposing factors, especially lymphoedema and tinea pedis of the foot on the same side.

An abscess is a tender, fluctuant nodule with overlying redness, often with a central point. Furuncles (boils) arise from infected hair follicles and carbuncles are clusters of them. Recurrent abscess at a site should prompt a search for a local cause such as a foreign body, pilonidal disease or hidradenitis suppurativa ^[2].

Early NSTI can look deceptively like cellulitis. A systematic review of 1,463 patients found NSTI to be misdiagnosed at first presentation in 71% of cases, usually because pain and systemic illness were not recognised for what they were ^[3]. Patients often have severe prodromal symptoms such as malaise, myalgia, diarrhoea or anorexia before obvious skin changes ^[3].

The frequency of physical signs reported in NSTI cases is useful background, not a checklist ^[3].

The red flags that should push you from "watch and treat with antibiotics" to "operate now" are:

• Pain out of proportion to the visible skin changes, or pain that continues to worsen despite treatment.
• Tense swelling with skin that has turned violaceous, purple or black.
• Bullae, especially haemorrhagic bullae.
• Crepitus under the skin.
• Systemic toxicity: fever, tachycardia, tachypnoea, hypotension, confusion.
• Rapid spread of redness despite appropriate antibiotics.

Pain is often the earliest sign. The skin can still look almost normal when deeper tissue is already dead, so a patient with severe pain and systemic upset needs examination of the fascial plane, not reassurance.

Cellulitis is famous for being overdiagnosed. Several common conditions mimic it and many are treated very differently.

NSTI must be separated from necrotising myositis and from pyomyositis, which penetrate into muscle rather than fascia. It also needs separating from straightforward abscess, which is localised and non-progressive.

Erysipelas can be confused with cellulitis; the raised, sharp margin is the key bedside sign ^[2].

The diagnosis of most skin infections is clinical, and testing should not delay treatment in the ill patient.

NICE advises taking a swab for microbiological testing only when the skin is broken and there has been a penetrating injury, exposure to water-borne organisms, or an infection acquired outside the UK ^[1]. Blood cultures have low yield in uncomplicated erysipelas and are not routinely helpful, though they are worth sending in severe disease ^[2]. In NSTI, blood cultures are positive in about 60% of type II (group A streptococcal) infections and are routinely positive in necrotising myositis ^[3].

Send a swab and a deep tissue sample, with Gram stain, in NSTI during debridement. Culture includes fungi in immunocompromised hosts ^[3].

No blood test diagnoses cellulitis. In early NSTI the results are nonspecific: leukocytosis with left shift, acidosis, coagulopathy, hyponatraemia, raised C-reactive protein and erythrocyte sedimentation rate. Creatine kinase and aspartate aminotransferase may be raised when deeper tissue or muscle is involved, suggesting something deeper than cellulitis ^[3].

Two bedside laboratory pointers are useful:

• Wall's model: a white cell count over 15,400 per microlitre or serum sodium under 135 mmol per litre favours NSTI over non-necrotising infection ^[3].
• The necrotising soft tissue infection clinical risk index NECROSIS: systolic blood pressure 120 mmHg or under, violaceous skin, and a white cell count over 15,000 per microlitre. When all three are present, they were 100% specific and had 100% positive predictive value for NSTI ^[3].

Imaging can support the diagnosis of NSTI but must never delay surgery when suspicion is high ^[3].

The Laboratory Risk Indicator for Necrotising Fasciitis score (LRINEC) combines white cell count, haemoglobin, sodium, glucose, creatinine and C-reactive protein into a score ^[3].

Interpretation ^[3]:

• Under 6 points: low risk, with under 50% risk of necrotising fasciitis. ^[3]
• 6 to 7 points: intermediate risk, 50 to 75% risk. ^[3]
• 8 or more points: high risk, greater than 75% risk. ^[3]

The LRINEC score is useful but limited: sensitivity ranges from 36 to 77%, specificity from 72 to 93%. Its weak sensitivity means a low score does not exclude NSTI, and it should never be used to delay surgical exploration. Its specificity is its strength: a high score supports the diagnosis ^[3].

Every skin infection is managed in layers:

1. Source control (drain the pus, cut out the dead tissue, remove any foreign body) is the decisive step for abscess and NSTI.
2. Antibiotics support source control, treat surrounding cellulitis, and cover systemic sepsis.
3. Resuscitation and supportive care for the toxic patient: oxygen, fluids, analgesia, monitoring.
4. Multidisciplinary care: surgery, infectious diseases, intensive care, and where relevant urology or plastics.

For a simple abscess, incision and evacuation of pus and debris, with probing of the cavity to break loculations, is effective treatment. The wound should be left open and lightly packed with antiseptic-soaked packing ^[2].

Antibiotics are added only in selected patients for 5 days, extendable to 7 to 10 days if symptoms have not resolved ^[2]. Antibiotics are indicated when:

• the abscess is larger than 5 cm; ^[2]
• it lies in a difficult area to drain, such as the face, hand or genitalia;
• there is no response to incision and drainage alone;
• there are multiple localisations; or
• the patient is immunosuppressed ^[2].

Empiric oral therapy when needed ^[2]:

• Amoxicillin-clavulanate 1 g every 8 hours, or cephalexin 500 mg every 6 hours. ^[2]
• If there is risk of CA-MRSA (immunocompromise, prior personal or household MRSA infection or colonisation in the past 12 months, antibiotic use for 5 days within the last 90 days, or failure of first-line therapy), add an anti-MRSA oral agent: minocycline 100 mg every 12 hours, doxycycline 100 mg every 12 hours, or trimethoprim-sulfamethoxazole 160/800 every 12 hours. ^[2]
• For penicillin allergy, use clindamycin 300 mg every 8 hours. ^[2]

An abscess treated with prolonged antibiotics but never drained can form a sterile collection walled by thick fibrous tissue, a hard lump that may mimic malignancy. Surgical drainage with excision of the fibrous wall is then needed ^[2].

Recurrent abscess always warrants a search for local causes, including a foreign body. A culture should be taken to define the organism and susceptibility ^[2].

Treatment is usually 5 days of antibiotics, extendable to 7 to 10 days if symptoms have not resolved ^[2]. Give oral first-line therapy when the patient can take oral medicines and is not severely unwell; review intravenous therapy by 48 hours and switch to oral when possible ^[1].

International empiric options ^[2]:

• Outpatient or step-down: amoxicillin-clavulanate 1 g every 8 hours, or cephalexin 500 mg every 6 hours.
• Add anti-MRSA coverage for patients at risk of CA-MRSA: trimethoprim-sulfamethoxazole 160/800 to 320/1600 every 12 hours, or minocycline 100 mg every 12 hours, or doxycycline 100 mg every 12 hours. ^[2]
• Penicillin allergy: clindamycin 300 mg every 8 hours.
• Inpatient: cefazolin 2 g every 8 hours, or amoxicillin-clavulanate 1.2/2.2 g every 8 hours; and, for CA-MRSA risk or failure, vancomycin 25 to 30 mg per kg loading then 15 to 20 mg per kg every 12 hours, or linezolid 600 mg every 12 hours. ^[2][3]
• For Gram-negative risk or severe infection that is not responding, consider piperacillin-tazobactam 4.5 g every 6 hours. ^[2]

In the United Kingdom, NICE NG141 recommends a different first-line choice for adults 18 years and over with cellulitis or erysipelas ^[1]: flucloxacillin 500 mg to 1 g four times a day orally, or 1 g to 2 g four times a day intravenously, for 5 to 7 days, with alternatives for penicillin allergy (clarithromycin or doxycycline) and longer courses up to 14 days when needed. Both approaches are guideline-concordant; the choice depends on local resistance patterns and national guidance.

When an abscess accompanies cellulitis, incision and drainage is the primary treatment and antibiotics are generally added ^[2].

• Outpatient oral therapy: amoxicillin-clavulanate 1 g every 8 hours, or cephalexin 500 mg every 6 hours.
• Where CA-MRSA prevalence exceeds 10% of clinical S. aureus isolates, or in high-risk patients, use one of trimethoprim-sulfamethoxazole 160/800 to 320/1600 every 12 hours, minocycline 100 mg every 12 hours, or doxycycline 100 mg every 12 hours.
• Inpatient IV therapy: vancomycin 25 to 30 mg per kg loading then 15 to 20 mg per kg every 12 hours, or linezolid 600 mg every 12 hours.
• Severe or non-responding cases: piperacillin-tazobactam 4.5 g every 6 hours, with Gram-negative and anti-anaerobe cover ^[2].

Treatment is antibiotics for 5 days, extendable to 10 days ^[2]. Use intravenous antibiotics if there are signs of systemic inflammation.

• Outpatient: amoxicillin-clavulanate 1 g every 8 hours, or cephalexin 500 mg every 6 hours.
• For MRSA risk: add trimethoprim-sulfamethoxazole, minocycline or doxycycline, or use vancomycin or linezolid if inpatient.
• Penicillin allergy: clindamycin 300 mg every 8 hours.
• Inpatient: cefazolin 2 g every 8 hours, or amoxicillin-clavulanate 1.2/2.2 g every 8 hours, with vancomycin or linezolid added for CA-MRSA risk ^[2].

Unless the case is severe, neither blood cultures nor punch biopsy cultures are recommended, because their yield is low in typical erysipelas ^[2].

MRSA should be treated as a cause, not a label. The right move is to decide whether MRSA cover is needed and then to use agents that are active against it.

When to add MRSA cover (risk criteria from WSES 2022 ^[2]): immunocompromised status; personal or household contact with MRSA infection or colonisation in the past 12 months; antibiotic use for 5 days in the previous 90 days; penetrating trauma, particularly from illicit drug use (cellulitis); multiple, recurrent or purulent disease; lack of response to first-line therapy; and regions or populations where more than 10% of clinical S. aureus isolates are MRSA.

Oral anti-MRSA options ^[2]:

• Minocycline 100 mg every 12 hours.
• Doxycycline 100 mg every 12 hours.
• Trimethoprim-sulfamethoxazole 160/800 or 320/1600 every 12 hours.
• Clindamycin 300 to 450 mg every 8 hours (resistance is now common, so use with caution). ^[2]
• Linezolid 600 mg every 12 hours.
• Tedizolid 200 mg every 24 hours. ^[2]

Intravenous anti-MRSA options ^[2]:

• Vancomycin 25 to 30 mg per kg as a loading dose, then 15 to 20 mg per kg per dose every 12 hours.
• Linezolid 600 mg every 12 hours.
• Daptomycin 6 mg per kg every 24 hours. ^[2]
• Ceftaroline 600 mg every 12 hours. ^[2]
• Dalbavancin 1000 mg once, then 500 mg one week later, or 1500 mg as a single dose. ^[2]
• Clindamycin 600 to 900 mg every 8 hours. ^[2][3]
• Tigecycline as a single dose of 100 mg then 50 mg every 12 hours. ^[2]
• Telavancin 10 mg per kg every 24 hours. ^[2][3]

NICE NG141 uses a different IV recommendation for adults when MRSA is suspected or confirmed: vancomycin 15 to 20 mg per kg two or three times a day IV, maximum 2 g per dose, adjusted to serum vancomycin concentration; teicoplanin with a loading phase then 6 mg per kg once a day; or linezolid 600 mg twice a day if vancomycin cannot be used ^[1]. That difference (15 to 20 mg per kg two or three times a day versus 25 to 30 mg per kg loading plus 15 to 20 mg per kg every 12 hours) is a genuine disagreement between bodies; follow the guideline used in your setting and the local microbiologist.

Both WSES and NICE agree that oral MRSA agents should usually be combined with a beta-lactam when streptococcal cover is also needed, because trimethoprim-sulfamethoxazole, minocycline and doxycycline are not active against beta-haemolytic streptococci ^[2].

CA-MRSA skin infections, particularly those caused by PVL-producing strains, more often produce boils, abscesses and severe necrotising infection than simple cellulitis.

Surgery is the treatment. Broad-spectrum antibiotics alone do not substitute for it ^[3].

• Perform the initial debridement as soon as possible, ideally within 6 hours of suspected diagnosis. A systematic review and meta-analysis showed mortality of 19% when surgery occurred within 6 hours versus 32% when surgery was delayed beyond 6 hours (odds ratio 0.43, 95% confidence interval 0.26 to 0.70) ^[2]. ^[3]
• Where safe, the first debridement is carried out at the presenting hospital rather than waiting for transfer; transferred patients may have up to twice the mortality of those treated locally ^[3].
• A surgical exploration will often be needed even when the diagnosis is uncertain, looking for grey necrotic fascia, loss of soft tissue planes, "dishwater" fluid, absence of bleeding and non-contracting muscle. In one retrospective series, exploration was negative in 20% of suspected cases ^[3].
• Debride until healthy, bleeding tissue is seen, and go beyond the visible skin change because infection travels further along fascia.
• Culture and Gram stain deep tissue during debridement, including fungal culture in immunocompromised patients ^[3].
• Re-explore at 12 to 24-hour intervals, or sooner if the patient worsens, until little or no further debridement is needed. Re-exploration at 24 hours rather than 48 hours has been associated with lower mortality (7% versus 33%) and less acute kidney injury (9% versus 33%) ^[3].
• The Eastern Association for the Surgery of Trauma advocates debridement within 12 hours, and an evaluation of six studies found 14% mortality with early debridement against 26% when it was delayed ^[3].
• Limb amputation may be necessary in up to 25% of patients with extremity NSTI, when source control cannot be achieved or functional outcome is better with amputation ^[3].
• Skin-sparing debridement, using counter-incisions to preserve viable skin, is an option in fascial-only disease but should be used with caution while the evidence base is small ^[3].

Start broad-spectrum, bactericidal therapy immediately on suspicion. Tailor it once the microbiology is known ^[3].

Empiric regimens by clinical state, normal renal function ^[3]:

• Stable, non-shocked patient: amoxicillin-clavulanate 1.2 to 2.2 g every 8 hours; or ceftriaxone 2 g every 24 hours plus metronidazole 500 mg every 8 hours; or cefotaxime 2 g every 8 hours plus metronidazole 500 mg every 8 hours. ^[3]
• Shocked patient: piperacillin-tazobactam 4.5 g every 6 hours; or meropenem 1 g every 8 hours; or imipenem-cilastatin 500 mg every 6 hours. ^[3]
• Gram-positive cover in both: vancomycin 25 to 30 mg per kg loading then 15 to 20 mg per kg every 8 hours; or daptomycin 6 to 8 mg per kg every 24 hours; or telavancin 10 mg per kg every 24 hours. ^[3]
• Adjuvant toxin suppression: clindamycin 600 to 900 mg every 8 hours; linezolid 600 mg every 12 hours or tedizolid 200 mg every 24 hours can be substituted ^[3].

Duration is not fixed by guidelines. Antibiotics are usually continued until source control is achieved and there is no further evidence of systemic infection ^[3], and recent studies show no significant difference in mortality or amputation between courses shorter than 7 days and longer courses ^[3]. Empirical antifungal therapy is added only for immunocompromised patients ^[3].

Hyperbaric oxygen and intravenous immunoglobulin have been proposed, but evidence is low quality or conflicting. Intravenous immunoglobulin reduced mortality from 33.7% to 15.7% in clindamycin-treated streptococcal toxic shock syndrome in one meta-analysis, but the effect is not firmly established ^[3].

Negative pressure wound therapy can be used after debridement but is best delayed until the wound is stable and repeat debridement is no longer needed; its effect on mortality, length of stay and complications is limited and uncertain ^[3].

For extensive perineal or Fournier's gangrene, a temporary diverting colostomy may reduce faecal contamination and help wound healing ^[3].

Reconstruction with skin grafts or, more rarely, flaps follows once the wound is clean.

• Manage underlying triggers: oedema and lymphoedema, venous insufficiency, cellulitis-prone skin, tinea pedis.
• Do not routinely offer antibiotic prophylaxis. It should only be considered by a specialist for an adult with at least two separate episodes of cellulitis or erysipelas treated in hospital, or under specialist advice, in the previous 12 months ^[1].
• Where prophylaxis is used, NICE lists phenoxymethylpenicillin 250 mg orally twice a day as first choice in adults, with erythromycin 250 mg orally twice a day for penicillin allergy. Choose the antibiotic with regard to recent microbiology and avoid using the same agent for treatment and prophylaxis ^[1].
• Review prophylaxis at least every 6 months, assessing success and the risk of resistance ^[1].

This topic draws on three open-access sources. NICE NG141 (2019) is the newest available prescribing guidance for community and hospital cellulitis and erysipelas in adults and children. WSES and its partner societies published their global clinical pathways in 2022, the newest general SSTI guidance used here. Tedesco and colleagues' 2025 review is the newest source for NSTI surgical and intensive care management. IDSA last published SSTI guidance in 2014 and MRSA guidance in 2011; those editions are not open access and were not used as independent sources.

For MRSA, NICE NG141 and WSES 2022 differ in vancomycin dosing, as described above. For empiric community therapy, NICE favours flucloxacillin in the United Kingdom while WSES favours amoxicillin-clavulanate or cephalexin with added MRSA agents where appropriate. Responsible clinician practice is to use the national guideline in force locally.

Cellulitis, erysipelas and abscess:

• Recurrent infection, usually at the same anatomical site.
• Local spread to tendon sheath, joint, bone (osteomyelitis, septic arthritis).
• Bacteraemia and sepsis.
• Scarring, lymphatic damage and chronic oedema after repeated episodes.
• In perianal and perirectal disease, complex fistula formation if inadequately drained.

Necrotising soft tissue infection:

• Septic shock in one-quarter to one-half of patients.
• Acute kidney injury in about one-third.
• Limb loss in up to 25% of extremity infections.
• Long-term functional disability: only about half of survivors return home directly, the rest needing further hospital or rehabilitation care ^[3].
• Death in roughly 20 to 30% of patients ^[2].

Uncomplicated cellulitis and abscess resolve with source control and a short antibiotic course. Recurrence risk depends on how well predisposing factors are controlled.

For NSTI, prognosis is strongly tied to speed of diagnosis and surgery. Mortality is 19% with surgery within 6 hours against 32% with delay, and early debridement is consistently associated with better survival. Among survivors, half need further institutional care and many have lasting pain, scarring and reduced movement. Each point rise on the APACHE II score increases the odds of death by 16 to 18% ^[3].

• Protect and promptly clean breaks in the skin.
• Treat and prevent tinea pedis, intertrigo and eczema.
• Reduce oedema with compression, limb elevation and treatment of the underlying cause; manage venous insufficiency and lymphoedema.
• Weight reduction and smoking cessation reduce risk and recurrence.
• Control MRSA at population and household level with hand hygiene, decolonisation where local policy supports it, and appropriate wound care.
• Educate patients to seek help early if skin redness spreads, pain escalates or systemic symptoms begin.

Children. CA-MRSA is more common in children than adults. NICE NG141 gives paediatric dosing bands for cellulitis and erysipelas, and the dosing differs from adult regimens; follow that structure rather than scaling adult doses ^[1]. Surgical drainage principles are the same.

Pregnancy. If a macrolide is needed in pregnancy, for example in true penicillin allergy where benefit outweighs harm, erythromycin is preferred. Follow local pregnancy prescribing guidance. Many beta-lactams are safe, but always check ^[1].

Immunocompromised and neutropenic patients. Consider Gram-negative pathogens, take cultures, and be more aggressive with imaging and debridement. In NSTI, add empirical antifungal therapy only when immunocompromised ^[3].

Older adults. Comorbidity, vascular disease and reduced skin integrity raise both risk and mortality. Early assessment and low threshold for inpatient care.

• Clinical diagnosis remains the basis. LRINEC, bedside ultrasound looking for fascial fluid and subcutaneous gas, plain radiographs and common sense are practical.
• CT scanning is often unavailable and should not delay surgery if clinical suspicion of NSTI is high.
• Source control is the step that saves lives and can be carried out with basic surgical equipment. Debride at the first hospital capable of doing so and transfer afterwards if needed.
• Where IV vancomycin or linezolid is not available, oral step-down options and local formulary alternatives exist; discuss with the local microbiologist.
• Save at least the wound and blood Gram stains and basic cultures where possible.
• Referral should follow the same red-flag criteria as in better-resourced settings; delay anywhere makes the outcome worse.

• Cellulitis is deep and erysipelas is superficial; the sharp, raised border of erysipelas is the clinical signature of the latter.
• S. aureus is the dominant pathogen in cultured skin infection; MRSA makes up a large and variable fraction, especially in purulent infection.
• Simple abscess is treated by incision and drainage; antibiotics are adjuncts reserved for selected patients.
• MRSA cover is decided by risk, not by habit, and combines with beta-lactams when streptococci must also be treated.
• Non-purulent cellulitis and erysipelas are usually treated with short courses of oral antibiotics, with mandatory reassessment if there is no improvement in 2 to 3 days.
• Purulent cellulitis is primarily a drainage problem; MRSA or broad-spectrum IV regimens are stepped up for severe or non-responding cases.
• NSTI kills 20 to 30% of patients; operation within 6 hours almost halves mortality compared with later surgery.
• The diagnosis of NSTI is made at operation; pain out of proportion and systemic toxicity out-rank skin appearance.
• The LRINEC score is specific but not sensitive; it supports rather than excludes the diagnosis.
• Antibiotics for NSTI are broad-spectrum and bactericidal, with clindamycin or linezolid as adjuncts for toxin suppression.
• Recurrence prevention is mechanical and behavioural: lymphoedema control, treating tinea, and trigger management.
• Long-term antibiotic prophylaxis is not routine; reserve it for frequent, severe recurrences in selected adults.

• Bacterial skin infections: impetigo, cellulitis and necrotising fasciitis (dermatology topic, impetigo and erysipelas prescribing overlap).
• Sepsis and septic shock.
• Diabetic foot infection.
• Antimicrobial resistance and MRSA.
• Lymphoedema and chronic oedema management.