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Emergency and Acute Medicine – Cellulitis
Core Concepts
Cellulitis is an acute, spreading infection of the skin and subcutaneous tissues with erythema, warmth, pain, tenderness, and progressive expansion. Extension into deeper layers may evolve into necrotizing soft-tissue infection. Predisposing factors include lymphedema, tinea pedis, open wounds, pre-existing lesions such as furuncles, prior trauma or surgery, retained foreign body, vascular or immune compromise, and injection drug use.
Likely Causes
Uncomplicated cellulitis is most often due to group A streptococci or Staphylococcus aureus, including community-associated MRSA (CA-MRSA). CA-MRSA risk is higher with prior MRSA infection, close contact with MRSA cases, daycare exposure, children, soldiers, incarcerated persons, contact-sport athletes, IV drug users, and men who have sex with men; CA-MRSA prevalence is high enough that empiric coverage is often appropriate, especially in nonresponding cases. Hospital-acquired MRSA is associated with recent hospitalization or long-term care, surgery, vascular devices, dialysis, recent antibiotic exposure, and injection drug use and is resistant to many antibiotics. After lymphatic disruption, nongroup A β-hemolytic streptococci (groups C, B, G) are more common. Diabetic cellulitis may be polymicrobial with streptococci, S. aureus, gram-negatives, and anaerobes, especially with ulcers. Special patterns include periorbital cellulitis (staph and strep), buccal cellulitis (historically Hib, plus anaerobic oral flora with intraoral lacerations or dental abscess), and less common exposures such as Pasteurella (cat/dog bites), Eikenella (human bites), Pseudomonas (hot-tub folliculitis; puncture wounds), Aeromonas (freshwater), Vibrio (seawater/raw seafood), Erysipelothrix (raw fish/meat handlers), clostridia, and anthrax. Pediatric patterns include facial cellulitis (strep pneumo and Hib—declining with vaccination), perianal cellulitis (group A strep), and neonatal cases (group B strep).
Clinical Features
Typical findings include pain, warmth, erythema, edema/induration, fever/chills, tender regional nodes, lymphangitis, and sometimes superficial vesicles. A concurrent subcutaneous abscess can coexist, and a deep abscess should be suspected if there is treatment failure. Buccal/odontogenic cellulitis may progress with fever, neck swelling, dysphagia, and deep-space spread. Pediatric facial cellulitis can be rapidly progressive, usually unilateral with URTI symptoms, and carries risk of cavernous sinus thrombosis and optic nerve injury. Perianal cellulitis presents with pruritic erythema extending outward from the anus, pain with defecation, and sometimes blood-streaked stools. Bedside clues: staphylococcal infection tends to have focal pustule/abscess with fluctuance or drainage and a slower course, while streptococcal infection often has sharper borders, lymphangitis, lymphedema association, and may include nausea from toxin effects.
Key Assessment
Cellulitis is primarily a clinical diagnosis; the exam should look for a portal of entry or deeper infection and assess for airway risk in deep facial/neck involvement.
Testing Strategy
Routine WBC is usually unnecessary. Aspirate/punch biopsy for Gram stain and culture is most useful in treatment failures and in admitted patients to identify resistant organisms such as MRSA. Blood cultures are typically negative in uncomplicated disease but may help in lymphedema-associated infections, buccal or periorbital cellulitis, water-exposure cases, or systemic symptoms with fever/chills. Plain radiographs can detect foreign bodies, subcutaneous gas, or suggest abscess; early osteomyelitis is not reliably seen. Ultrasound helps identify abscess when exam is equivocal and may show “cobblestoning” of the subcutaneous tissue in cellulitis. CT/MRI can help evaluate for necrotizing fasciitis.
Conditions to Differentiate
Important alternatives include necrotizing fasciitis, lymphangitis/lymphadenitis, thrombophlebitis or DVT, insect bite/allergy, gout/pseudogout, ruptured Baker cyst, herpetic whitlow, neoplasm, phytophotodermatitis, erythema migrans, and for facial disease, angioedema, conjunctivitis, or contusion. Pediatric perianal differentials include Candida intertrigo, psoriasis, pinworms, abuse, behavioral causes, and inflammatory bowel disease.
Emergency Management
Airway compromise is a concern with deep facial or neck extension. General approach: account for local resistance patterns and include CA-MRSA coverage when appropriate (notably uncomplicated cellulitis in many settings, periorbital disease, and diabetics). Typical outpatient duration is 7–10 days, with cool compresses, analgesia, elevation, and treatment of tinea pedis when present.
Antibiotic Approach by Scenario
Simple cellulitis outpatient: oral cephalexin plus TMP-SMX for CA-MRSA coverage; alternatives for β-lactam include dicloxacillin, macrolide, or levofloxacin; alternatives to TMP-SMX include clindamycin or doxycycline. Inpatient: IV nafcillin (or equivalent) plus IV vancomycin. Post-lymphatic disruption cellulitis: treat like simple cellulitis. Diabetic cellulitis outpatient: amoxicillin/clavulanate plus TMP-SMX or clindamycin; inpatient: IV ampicillin/sulbactam or imipenem-cilastatin plus IV vancomycin. Adult periorbital cellulitis outpatient: dicloxacillin or azithromycin plus TMP-SMX; inpatient: IV vancomycin. Adult buccal cellulitis outpatient: amoxicillin/clavulanate; inpatient: IV ceftriaxone; odontogenic cases require drainage and anaerobe coverage such as clindamycin. Pediatric facial cellulitis: IV ceftriaxone. Perianal cellulitis: oral penicillin VK outpatient or IV penicillin G inpatient. Bite wounds: amoxicillin/clavulanate. Foot puncture wounds: ciprofloxacin or IV ceftazidime. MRSA: hospital-acquired—IV vancomycin or linezolid; CA-MRSA—TMP-SMX, clindamycin, or doxycycline orally, and vancomycin or clindamycin IV.
Medication Options
Common regimens include amoxicillin/clavulanate, ampicillin/sulbactam, azithromycin, ceftazidime, ceftriaxone, cephalexin, ciprofloxacin, clindamycin, dicloxacillin, doxycycline, imipenem-cilastatin, levofloxacin, linezolid, nafcillin, penicillin VK, aqueous penicillin G, TMP-SMX, and vancomycin with pediatric adjustments and therapeutic monitoring where appropriate.
Disposition Criteria
Admit patients who appear toxic, have tissue necrosis, immunosuppression, significant comorbid illness, inability to tolerate oral meds, unreliable follow-up, or high-risk anatomy. Discharge is reasonable for mild infection in a nontoxic patient who can take oral therapy, has no immunosuppression or major comorbidities, no hand/face involvement, and has reliable follow-up within 24–48 hours.
Follow-Up Guidance
Reassess within 24–48 hours, sooner if fever worsens, lymphangitis develops, or erythema expands. Mark the edge of erythema prior to discharge to track progression.
Clinical Traps
Strep and staph remain the most common causes, and CA-MRSA is common enough that empiric coverage is often required. Clinicians are not reliably accurate at identifying MRSA by appearance alone. Deep abscess can be mistaken for cellulitis; use clinical suspicion and ultrasound to avoid missed abscess.
Core Concepts
Cellulitis is an acute, spreading infection of the skin and subcutaneous tissues with erythema, warmth, pain, tenderness, and progressive expansion. Extension into deeper layers may evolve into necrotizing soft-tissue infection. Predisposing factors include lymphedema, tinea pedis, open wounds, pre-existing lesions such as furuncles, prior trauma or surgery, retained foreign body, vascular or immune compromise, and injection drug use.
Likely Causes
Uncomplicated cellulitis is most often due to group A streptococci or Staphylococcus aureus, including community-associated MRSA (CA-MRSA). CA-MRSA risk is higher with prior MRSA infection, close contact with MRSA cases, daycare exposure, children, soldiers, incarcerated persons, contact-sport athletes, IV drug users, and men who have sex with men; CA-MRSA prevalence is high enough that empiric coverage is often appropriate, especially in nonresponding cases. Hospital-acquired MRSA is associated with recent hospitalization or long-term care, surgery, vascular devices, dialysis, recent antibiotic exposure, and injection drug use and is resistant to many antibiotics. After lymphatic disruption, nongroup A β-hemolytic streptococci (groups C, B, G) are more common. Diabetic cellulitis may be polymicrobial with streptococci, S. aureus, gram-negatives, and anaerobes, especially with ulcers. Special patterns include periorbital cellulitis (staph and strep), buccal cellulitis (historically Hib, plus anaerobic oral flora with intraoral lacerations or dental abscess), and less common exposures such as Pasteurella (cat/dog bites), Eikenella (human bites), Pseudomonas (hot-tub folliculitis; puncture wounds), Aeromonas (freshwater), Vibrio (seawater/raw seafood), Erysipelothrix (raw fish/meat handlers), clostridia, and anthrax. Pediatric patterns include facial cellulitis (strep pneumo and Hib—declining with vaccination), perianal cellulitis (group A strep), and neonatal cases (group B strep).
Clinical Features
Typical findings include pain, warmth, erythema, edema/induration, fever/chills, tender regional nodes, lymphangitis, and sometimes superficial vesicles. A concurrent subcutaneous abscess can coexist, and a deep abscess should be suspected if there is treatment failure. Buccal/odontogenic cellulitis may progress with fever, neck swelling, dysphagia, and deep-space spread. Pediatric facial cellulitis can be rapidly progressive, usually unilateral with URTI symptoms, and carries risk of cavernous sinus thrombosis and optic nerve injury. Perianal cellulitis presents with pruritic erythema extending outward from the anus, pain with defecation, and sometimes blood-streaked stools. Bedside clues: staphylococcal infection tends to have focal pustule/abscess with fluctuance or drainage and a slower course, while streptococcal infection often has sharper borders, lymphangitis, lymphedema association, and may include nausea from toxin effects.
Key Assessment
Cellulitis is primarily a clinical diagnosis; the exam should look for a portal of entry or deeper infection and assess for airway risk in deep facial/neck involvement.
Testing Strategy
Routine WBC is usually unnecessary. Aspirate/punch biopsy for Gram stain and culture is most useful in treatment failures and in admitted patients to identify resistant organisms such as MRSA. Blood cultures are typically negative in uncomplicated disease but may help in lymphedema-associated infections, buccal or periorbital cellulitis, water-exposure cases, or systemic symptoms with fever/chills. Plain radiographs can detect foreign bodies, subcutaneous gas, or suggest abscess; early osteomyelitis is not reliably seen. Ultrasound helps identify abscess when exam is equivocal and may show “cobblestoning” of the subcutaneous tissue in cellulitis. CT/MRI can help evaluate for necrotizing fasciitis.
Conditions to Differentiate
Important alternatives include necrotizing fasciitis, lymphangitis/lymphadenitis, thrombophlebitis or DVT, insect bite/allergy, gout/pseudogout, ruptured Baker cyst, herpetic whitlow, neoplasm, phytophotodermatitis, erythema migrans, and for facial disease, angioedema, conjunctivitis, or contusion. Pediatric perianal differentials include Candida intertrigo, psoriasis, pinworms, abuse, behavioral causes, and inflammatory bowel disease.
Emergency Management
Airway compromise is a concern with deep facial or neck extension. General approach: account for local resistance patterns and include CA-MRSA coverage when appropriate (notably uncomplicated cellulitis in many settings, periorbital disease, and diabetics). Typical outpatient duration is 7–10 days, with cool compresses, analgesia, elevation, and treatment of tinea pedis when present.
Antibiotic Approach by Scenario
Simple cellulitis outpatient: oral cephalexin plus TMP-SMX for CA-MRSA coverage; alternatives for β-lactam include dicloxacillin, macrolide, or levofloxacin; alternatives to TMP-SMX include clindamycin or doxycycline. Inpatient: IV nafcillin (or equivalent) plus IV vancomycin. Post-lymphatic disruption cellulitis: treat like simple cellulitis. Diabetic cellulitis outpatient: amoxicillin/clavulanate plus TMP-SMX or clindamycin; inpatient: IV ampicillin/sulbactam or imipenem-cilastatin plus IV vancomycin. Adult periorbital cellulitis outpatient: dicloxacillin or azithromycin plus TMP-SMX; inpatient: IV vancomycin. Adult buccal cellulitis outpatient: amoxicillin/clavulanate; inpatient: IV ceftriaxone; odontogenic cases require drainage and anaerobe coverage such as clindamycin. Pediatric facial cellulitis: IV ceftriaxone. Perianal cellulitis: oral penicillin VK outpatient or IV penicillin G inpatient. Bite wounds: amoxicillin/clavulanate. Foot puncture wounds: ciprofloxacin or IV ceftazidime. MRSA: hospital-acquired—IV vancomycin or linezolid; CA-MRSA—TMP-SMX, clindamycin, or doxycycline orally, and vancomycin or clindamycin IV.
Medication Options
Common regimens include amoxicillin/clavulanate, ampicillin/sulbactam, azithromycin, ceftazidime, ceftriaxone, cephalexin, ciprofloxacin, clindamycin, dicloxacillin, doxycycline, imipenem-cilastatin, levofloxacin, linezolid, nafcillin, penicillin VK, aqueous penicillin G, TMP-SMX, and vancomycin with pediatric adjustments and therapeutic monitoring where appropriate.
Disposition Criteria
Admit patients who appear toxic, have tissue necrosis, immunosuppression, significant comorbid illness, inability to tolerate oral meds, unreliable follow-up, or high-risk anatomy. Discharge is reasonable for mild infection in a nontoxic patient who can take oral therapy, has no immunosuppression or major comorbidities, no hand/face involvement, and has reliable follow-up within 24–48 hours.
Follow-Up Guidance
Reassess within 24–48 hours, sooner if fever worsens, lymphangitis develops, or erythema expands. Mark the edge of erythema prior to discharge to track progression.
Clinical Traps
Strep and staph remain the most common causes, and CA-MRSA is common enough that empiric coverage is often required. Clinicians are not reliably accurate at identifying MRSA by appearance alone. Deep abscess can be mistaken for cellulitis; use clinical suspicion and ultrasound to avoid missed abscess.
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