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SAEM Clinical Image Series: Pediatric Rash

Drew Birrenkott, Ph.D. |

pediatric rash

A 17-month-old girl with a history of eczema presents to the pediatric emergency department for evaluation of a rash. The rash is different from her usual eczema, developed three days prior to presentation, and is described as red with yellow crusting. Her mother also noticed blistering in her groin and under her axilla. She has associated fussiness and decreased feeding, but no fever.

Vitals: T 37.7°C; HR 161; BP 115/75; RR 24; O2 sat 100% on room air

General: Fussy but consolable

Eyes: No conjunctival erythema or discharge

Mouth: Yellow crusting and fissuring surrounding mouth; no intra-oral lesions

Neck: No nuchal rigidity

Cardiovascular: Tachycardic with regular rhythm; no murmurs

Respiratory: Normal rate; normal breath sounds

Abdomen: Non-tender to palpation; non-distended; normal bowel sounds

Neurologic: Alert

Skin: Diffusely erythematous; scaling rash over the face with areas of yellow crusting; erythematous areas with blistering/desquamation to the anterior trunk, axilla, and inguinal regions

Complete blood count (CBC) and comprehensive metabolic panel (CMP) unremarkable.

Staphylococcal scalded skin syndrome caused by impetigo.

This case describes a patient with a rash, blistering/desquamation of axilla and groin, and systemic symptoms consistent with staphylococcal scalded skin syndrome (SSSS). Clinical features of SSSS include erythema to intertriginous areas, rapid progression of erythema, and systemic symptoms such as fever, irritability, and poor oral intake. Mucous membranes are not typically involved. Physical exam findings include perioral crusting and fissuring (seen in photo), blanching erythema, desquamation, shallow skin erosions, and a positive Nikolsky sign. SSSS is caused by exfoliative toxin A (ETA) and exfoliative toxin B (ETB), two exotoxins produced by certain strains of S. aureus. ETA and ETB cause the breakdown of keratinocyte adhesions within the epidermis, leading to desquamation. Infection with S. aureus at any site can cause SSSS, including bacterial conjunctivitis, wound/skin infection, staphylococcal pneumonia, pyomyositis, septic arthritis, and endocarditis. SSSS is more common in children, a phenomenon thought to be due to a lack of protective antibodies against staphylococcal antigens. The diagnosis of SSSS is clinical but can be confirmed with histopathology. In this case, the extensive yellow, crusting lesions of the face suggest impetigo, a superficial skin infection predominantly caused by S. aureus, as the etiology of SSSS. Children with eczema are at increased risk of impetigo due to disruption of the normal skin barrier. Complications of SSSS include fluid losses due to extensive skin breakdown, electrolyte abnormalities, sepsis, and death.

Penicillinase-resistant penicillins (oxacillin, nafcillin) or first- or second-generation cephalosporins. Clindamycin monotherapy should be avoided due to high rates of resistance. Management of SSSS in most cases also includes hospitalization for IV antibiotics and supportive care. In patients with significant skin involvement, admission to either an ICU or burn unit is warranted for close monitoring and wound care.

Take-Home Points

  • Staphylococcal scalded skin syndrome (SSSS) is caused by the release of S. aureus exfoliative toxins A and B into the bloodstream, thus SSSS can be caused by any infection caused by S. aureus.
  • Penicillinase-resistant penicillins are the first-line therapy in patients with SSSS. First- and second-generation cephalosporins, as well as vancomycin, can also be considered.
  • Treatment with clindamycin monotherapy should be avoided in patients with SSSS due to high levels of resistance among strains of S. aureus which cause SSSS.

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Author information

Drew Birrenkott, Ph.D.

Drew Birrenkott, Ph.D.

Medical Student
Stanford University

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