Trimethoprim-Sulfamethoxazole-Induced Subcutaneous Sweet's Syndrome Masquerading as Septic Shock

Abstract

SESSION TITLE: Student/Resident Case Report Poster - Critical Care I SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Acute febrile neutrophilic dermatosis, or Sweet Syndrome (SS), is characterized by pyrexia, neutrophilia, and painful cutaneous erythematous papules or plaques associated with dense dermal neutrophilic infiltrate. SS may be idiopathic, malignancy-associated or drug-induced; the latter is usually self-limited1. We report a case of Trimethoprim-Sulfamethoxazole (TMP-SMX)-induced SS mimicking septic shock. CASE PRESENTATION: A 55 year-old healthy woman was admitted with fevers and rash. A week prior to admission, she started TMP-SMX for chronic, post-traumatic cellulitis on her left shin. The cellulitis rapidly improved, but five days later, she developed fevers and a new rash. On admission, she was febrile, hypotensive, and in rapid atrial fibrillation. Her extremities were warm and she had indurated erythematous nodules and plaques on her arms and legs (Fig 1A). Her left shin had an erythematous patch consistent with resolving cellulitis. She had leukocytosis with neutrophilia, no eosinophilia, and had elevated lactate (1.8 mmol/L), troponin (0.33 ng/ml), creatinine (1.4 mg/dL), and AST/ALT (340/314 U/L). CRP was 270 mg/L. TMP-SMX was discontinued. Fluids, vancomycin and cefepime were started for septic shock, and she required vasopressors for 24 hours. Infectious workup was negative. Echocardiogram was normal. Skin biopsy showed neutrophilic lobular infiltrate consistent with subcutaneous SS (Fig 1B). On day 3, she was hemodynamically stable, with improving labs and skin lesions. Follow-up in one week confirmed total resolution of the rash. DISCUSSION: We present a unique case of TMP-SMX-induced subcutaneous SS with multi-organ involvement and distributive shock. Symptom onset with TMP-SMX, the morphology of the skin lesions and biopsy support this diagnosis. Symptoms resolved with cessation of TMP-SMX. Subcutaneous SS is a rare variant characterized by neutrophilic infiltration in adipose tissue1. Multi-organ dysfunction and shock is uncommon in SS2. Pathogenesis of SS is not established, however elevated interleukins and G-CSF found in active SS suggest involvement of Th1 inflammatory cascade1. Thus, distributive shock with multi-organ dysfunction in SS is a logical manifestation. CONCLUSIONS: We present a case of TMP-SMX-induced subcutaneous Sweet syndrome with multi-organ dysfunction masquerading as distributive shock. SS should be considered in patients with rash, multi-organ dysfunction and distributive shock in the absence of infection. Reference #1: Cohen PR. Sweet syndrome - a comprehensive review of an acute febrile neutrophilic dermatosis. Orphanet J Rare Dis. 2007; 2:34. Reference #2: Matthews PC, Willatts SM. Sweet syndrome associated with systemic inflammatory response syndrome. Intensive Care Medicine. 1998 (10); 997-998. DISCLOSURE: The following authors have nothing to disclose: Johanna Hase, Helen Ma, Benjamin Wu, Mark Adelman, Joshua Farhadian, Alisa Femia, Shane Meehan, David Schwartz No Product/Research Disclosure Information