Critical Care: Critical Care |

Staphylococcus-Associated Purpura Fulminans: Can We Expect a Better Outcome With Intravenous Immunoglobulin? FREE TO VIEW

Meenakshi Ghosh, MD; Abhisekh Sinha Ray, MD; Mingchen Song, MD; Jacob Varney, MD; Sreeparna Ghosh, MBBS; Janak Koirala, MD; Chad DeFrain, MD; Christopher Quarshie, MD
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Southern Illinois University School of Medicine, Springfield, IL

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A137. doi:10.1016/j.chest.2016.02.143
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SESSION TITLE: Critical Care

SESSION TYPE: Case Report Poster

PRESENTED ON: Sunday, April 17, 2016 at 11:45 AM - 12:45 PM

INTRODUCTION: Purpura fulminans (PF) is a rapidly progressive disease with large purpuric skin lesion evolving to hemorrhagic necrosis and bullae formation with fever, hypotension and DIC. Acute infectious PF is rare but often fatal. Although mostly related to meningococcal and streptococcal infection, it may also be caused by other bacterial or viral pathogens. We report a case of PF due to methicillin-sensitive Staphylococcus aureus (MSSA).

CASE PRESENTATION: 40 year old female with hepatitis C, polysubstance use admitted with malaise, nausea, vomiting for 3 days. On examination, she was restless, febrile (38.2°C), hypotensive (80/60) with tachycardia and tachyapnea. Laboratory analysis revealed leukocytosis (12,000/μL), thrombocytopenia (24000/μL), lactic acidosis (7mmol/L), elevated BUN (48mg/dL), creatinine (2mg/dL) and CK (15984U/L). Coagulation was abnormal (PT 23;PTT 48;INR 2.1). Procalcitonin was markedly elevated (14ng/mL). Pan-culture was obtained and empiric antibiotics (Vancomycin, Azetronam, Clindmycin) were initiated. She remained hypotensive despite fluid resuscitation requiring vasopressor support. Two days later diffuse erythematous macular and petechial skin rash developed over her lower extremities. Meanwhile she got intubated. Her skin lesions progressed rapidly with hemorrhagic bullae formation. She received FFP, platelet transfusions and underwent excisional biopsy of skin lesion. Tissue sample grew MSSA. Pathology showed septal panniculitis with small vessel leukocytoclastic vasculitis. She received intravenous immunoglobulin (IVIG) for 2 days following which skin lesions remained stable. Over the course she improved clinically and was extubated. She did undergo multiple extensive debridement of skin and soft tissue followed by Achilles tendon reconstruction but did not require amputation. She was discharged after 47 days of hospital stay.

DISCUSSION: Differenitials considered were Thrombotic thrombocytopenic purpura, levamisole induced vasculitis (h/o cocaine use), hepatitis C associated cryoglobulinemia but review of peripheral blood smear did not reveal schistocyte; pANCA and serum cryoglobulin level were negative. She received antibiotics for septic shock and hemodynamic support with aggressive fluid, vasopressors. As superantigens play significant role in pathogenesis, IVIG therapy was considered. Later she needed surgical debridement to decrease the risk of secondary contamination.

CONCLUSIONS: PF is a medical emergency with high mortality. We reaffirm that acute infectious PF should be treated with antibiotic promptly. As staphylococcal toxin production plays a significant role in pathogenesis of this disease, IVIG therapy has been used anecdotally to neutralize the exotoxins. Further studies are needed to clearly define the role of IVIG in treatment of infectious PF.

Reference #1: Kravitz G et al. Purpura Fulminans due to Staphyloccus aureus. Clin Infect Dis. (2005):40(7):941-947

Reference #2: Betrosian AP et al. PF in Sepsis. Am J Med Sci. 2006 Dec;332(6):339-45

DISCLOSURE: The following authors have nothing to disclose: Meenakshi Ghosh, Abhisekh Sinha Ray, Mingchen Song, Jacob Varney, Sreeparna Ghosh, Janak Koirala, Chad DeFrain, Christopher Quarshie

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