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Emergency And Acute Medicine – Impetigo
Basics
Description Impetigo is a common superficial bacterial skin infection. It may be a primary infection of minor skin breaks or a secondary infection of preexisting dermatoses (impetiginization). It is most prevalent in children aged 2–5 years and occurs more often in warm, humid climates and summer months. Predisposing factors include minor trauma (especially around the nose), insect bites, burns, diabetes mellitus, HIV infection, varicella, and chronic skin disease. Complications include acute poststreptococcal glomerulonephritis (1–5% of nonbullous cases), cellulitis, sepsis, endocarditis, toxic shock syndrome, and staphylococcal scalded skin syndrome.
Etiology
Classic (nonbullous) impetigo results from bacterial entry through disrupted skin and is caused by Staphylococcus aureus, group A β-hemolytic streptococci, or both. Bullous impetigo is caused exclusively by S. aureus producing exfoliative toxins (A, B, D) that cleave desmoglein 1, leading to intraepidermal blistering.
Diagnosis
Signs and symptoms Nonbullous impetigo begins as erythematous macules or papules that evolve into vesicles or pustules, which rupture and form characteristic honey-colored crusts. Lesions are highly contagious and often pruritic. Regional lymphadenopathy may occur; systemic symptoms are uncommon. Bullous impetigo presents with flaccid bullae containing clear or yellow fluid that rupture easily, leaving erythematous bases; Nikolsky sign is absent. Fever and systemic symptoms are rare.
Physical exam Lesions most commonly involve the face, extremities, and scalp. Diagnosis is clinical based on appearance and distribution.
Essential workup
Routine laboratory testing is not required. Consider bacterial culture of bullae or pustules for refractory disease, outbreak investigation, or suspected methicillin-resistant S. aureus.
Diagnosis tests and interpretation
Lab Anti–DNase B titers may be elevated in poststreptococcal glomerulonephritis. Urinalysis is indicated if hematuria or edema suggests nephritis.
Imaging and procedures Not routinely indicated; biopsy is rarely necessary.
Differential diagnosis
Herpes simplex, varicella zoster, atopic or contact dermatitis, dermatophytosis, candidiasis, scabies, folliculitis, erysipelas, bullous pemphigoid, pemphigus vulgaris, staphylococcal scalded skin syndrome, Stevens–Johnson syndrome, thermal burns, toxic epidermal necrolysis, and cutaneous anthrax.
Treatment
Prehospital Cover lesions and use universal precautions to prevent transmission.
Initial stabilization Impetigo is rarely life-threatening in otherwise healthy patients.
Emergency department management Local care includes gentle cleansing, removal of crusts, and wet dressings. Small, localized nonbullous lesions may be treated with topical antibiotics alone. Extensive disease, bullous impetigo, lymphadenopathy, systemic symptoms, or outbreak settings require systemic antibiotics. Empiric therapy should cover S. aureus and streptococci; adjust for MRSA based on local resistance patterns.
Medication
Topical (nonbullous only): mupirocin 2% TID for 10 days or retapamulin 1% BID for 5 days.
Oral options (10 days unless noted): amoxicillin–clavulanate, cephalexin, dicloxacillin, clindamycin, azithromycin (5-day course), or trimethoprim–sulfamethoxazole when MRSA suspected. Doxycycline may be used for MRSA in patients ≥8 years.
Follow-up and disposition
Admission criteria Rare; consider for widespread disease, extensive bullae or denuded skin, dehydration, treatment failure, toxic appearance, immunocompromise, or neonates.
Discharge criteria Nontoxic patients with reliable caregivers and ability to comply with therapy.
Follow-up recommendations Primary care follow-up to ensure resolution. Return for lack of improvement or signs of nephritis (hematuria, periorbital or leg edema).
Pearls and pitfalls
Use systemic antibiotics for bullous disease or lymphadenopathy. Rising antibiotic resistance limits older regimens; suspect mupirocin resistance with treatment failure and switch agents. Treat affected household contacts simultaneously to prevent reinfection.
Basics
Description Impetigo is a common superficial bacterial skin infection. It may be a primary infection of minor skin breaks or a secondary infection of preexisting dermatoses (impetiginization). It is most prevalent in children aged 2–5 years and occurs more often in warm, humid climates and summer months. Predisposing factors include minor trauma (especially around the nose), insect bites, burns, diabetes mellitus, HIV infection, varicella, and chronic skin disease. Complications include acute poststreptococcal glomerulonephritis (1–5% of nonbullous cases), cellulitis, sepsis, endocarditis, toxic shock syndrome, and staphylococcal scalded skin syndrome.
Etiology
Classic (nonbullous) impetigo results from bacterial entry through disrupted skin and is caused by Staphylococcus aureus, group A β-hemolytic streptococci, or both. Bullous impetigo is caused exclusively by S. aureus producing exfoliative toxins (A, B, D) that cleave desmoglein 1, leading to intraepidermal blistering.
Diagnosis
Signs and symptoms Nonbullous impetigo begins as erythematous macules or papules that evolve into vesicles or pustules, which rupture and form characteristic honey-colored crusts. Lesions are highly contagious and often pruritic. Regional lymphadenopathy may occur; systemic symptoms are uncommon. Bullous impetigo presents with flaccid bullae containing clear or yellow fluid that rupture easily, leaving erythematous bases; Nikolsky sign is absent. Fever and systemic symptoms are rare.
Physical exam Lesions most commonly involve the face, extremities, and scalp. Diagnosis is clinical based on appearance and distribution.
Essential workup
Routine laboratory testing is not required. Consider bacterial culture of bullae or pustules for refractory disease, outbreak investigation, or suspected methicillin-resistant S. aureus.
Diagnosis tests and interpretation
Lab Anti–DNase B titers may be elevated in poststreptococcal glomerulonephritis. Urinalysis is indicated if hematuria or edema suggests nephritis.
Imaging and procedures Not routinely indicated; biopsy is rarely necessary.
Differential diagnosis
Herpes simplex, varicella zoster, atopic or contact dermatitis, dermatophytosis, candidiasis, scabies, folliculitis, erysipelas, bullous pemphigoid, pemphigus vulgaris, staphylococcal scalded skin syndrome, Stevens–Johnson syndrome, thermal burns, toxic epidermal necrolysis, and cutaneous anthrax.
Treatment
Prehospital Cover lesions and use universal precautions to prevent transmission.
Initial stabilization Impetigo is rarely life-threatening in otherwise healthy patients.
Emergency department management Local care includes gentle cleansing, removal of crusts, and wet dressings. Small, localized nonbullous lesions may be treated with topical antibiotics alone. Extensive disease, bullous impetigo, lymphadenopathy, systemic symptoms, or outbreak settings require systemic antibiotics. Empiric therapy should cover S. aureus and streptococci; adjust for MRSA based on local resistance patterns.
Medication
Topical (nonbullous only): mupirocin 2% TID for 10 days or retapamulin 1% BID for 5 days.
Oral options (10 days unless noted): amoxicillin–clavulanate, cephalexin, dicloxacillin, clindamycin, azithromycin (5-day course), or trimethoprim–sulfamethoxazole when MRSA suspected. Doxycycline may be used for MRSA in patients ≥8 years.
Follow-up and disposition
Admission criteria Rare; consider for widespread disease, extensive bullae or denuded skin, dehydration, treatment failure, toxic appearance, immunocompromise, or neonates.
Discharge criteria Nontoxic patients with reliable caregivers and ability to comply with therapy.
Follow-up recommendations Primary care follow-up to ensure resolution. Return for lack of improvement or signs of nephritis (hematuria, periorbital or leg edema).
Pearls and pitfalls
Use systemic antibiotics for bullous disease or lymphadenopathy. Rising antibiotic resistance limits older regimens; suspect mupirocin resistance with treatment failure and switch agents. Treat affected household contacts simultaneously to prevent reinfection.
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