Abstract
Background
Stevens-Johnson Syndrome (SJS) is a rare and potentially life-threatening condition causing blistering and epithelial sloughing of the skin and mucous membranes. It is most commonly caused by infective pathogens or drugs.
Case presentation
A 14-year-old male patient presented with reduced oral intake following painful oral ulcerations secondary to a diagnosis of Mycoplasma pneumoniae -induced SJS. Treatment involved intravenous fluids, antimicrobials and analgesia, alongside atraumatic conservative management of the oral mucosa.
Conclusion
While there are no evidence-based treatment guidelines for Mycoplasma pneumoniae -induced SJS, conservative care is the cornerstone of management of paediatric presentations.
1
Introduction
Stevens-Johnson Syndrome (SJS) is a rare and potentially life-threatening disease within a spectrum of severe cutaneous adverse reactions (SCAR) involving blistering and epithelial sloughing of the skin and mucous membranes. This spectrum also includes erythema multiforme (EM) and toxic epidermal necrolysis (TEN) as the least and most extensive phenotypes respectively [ , ]. The incidence of SJS in children is approximately 5.3–6.3 cases per million per year [ ]. The mortality rate for children (7.5 %) is lower than for adults (20–25 %). In SJS, vesiculobullous lesions involve multiple mucosal surfaces and epithelial detachment affects less than 10 % body surface area (BSA). By contrast, EM presents with concentric target and raised papule skin lesions with a predominantly acral distribution and less severe mucosal involvement. TEN affects more than 30 % BSA with skin lesions resembling second-degree burns and carries a higher mortality rate (30–50 %). Intermediate BSA involvement (10–30 %) is termed SJS/TEN overlap [ ].
1.1
Case description
A 14-year-old male patient presented to the Emergency Department at the Children’s Hospital Westmead, Australia with painful oral ulcerations. He had developed purulent cough and fevers twelve days prior, which resolved by day five. Lip blisters developed on day seven and progressed to increasingly painful oral and penile lesions. On day 10, the patient was commenced on oral acyclovir by his general medical practitioner for presumed herpetic gingivostomatitis. Our patient had no contributory past medical history, was not on medications and had no known allergies. There was no history of family members or close contacts having developed similar signs or symptoms.
On initial examination, the patient was afebrile and fully alert with a temperature of 36.8 <SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='°C’>°C°C
°C
, a heart rate of 74 beats/minute, blood pressure of 105/54 mmHg, respiratory rate of 18 breaths/minute and oxygen saturation of 98 % while breathing room air. He had a height of 174.8cm and weighed 77.9kg, with his mother reporting weight loss of 12 kgs over the last two weeks due to reduced oral intake. The patient was hospitalised on intravenous (IV) fluids and acyclovir and topical application of xylocaine viscous 2 % gel. Acyclovir was chosen for its antiviral activity against herpes simplex virus (HSV) until otherwise excluded as a causative agent. Blood and oral swabs were sent for serology, culture and polymerase chain reaction (PCR) investigations. Dermatological assessment confirmed ulceration of the lips and urethral meatus. A SCORTEN [ ] score of 0 was assigned. A chest radiograph showed bilateral streaky changes but no focal consolidation.
The following day, dental assessment demonstrated haemorrhagic lip crusting, generalised gingival sloughing ( Fig. 1 ) and an oral malodour. Extraoral examination excluded any cutaneous lesions involving the face and neck ( Fig. 2 ). Ophthalmological assessment noted mild eyelid involvement with bilateral non-exudative conjunctivitis. On day three, small white papules emerged on the tongue, and the soft palate displayed more widespread purpuric erythema extending into the oropharynx ( Fig. 3 ).
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