Vancomycin-Induced Thrombotic Microangiopathy: A Rare Association
- Glomerular Diseases: The Excitement of Clinical Cases
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1202 Glomerular Diseases: Immunology and Inflammation
- Rajashekar, Gaurav, Washington University in St Louis, St Louis, Missouri, United States
- Java, Anuja, Washington University in St Louis, St Louis, Missouri, United States
Group or Team Name
- Washington University in St. Louis
Thrombotic microangiopathies (TMAs) are life-threatening conditions characterized by hemolytic anemia, thrombocytopenia and AKI. Drug-induced TMA (DITMA) is a diagnostic challenge because specific tests to identify a drug etiology are not available.
A 40 yr-old female with history of neurofibromatosis type 2 underwent resection of a T10-11 schwannoma. The surgery was complicated by wound dehiscence which was treated with incision and drainage followed by intravenous vancomycin and cefazolin. The next day, she developed fever, altered mental status and a diffuse purpuric rash (Fig 1). Labs showed anemia (Hgb, 6.2 g/dl), thrombocytopenia (PLT, 15 k/µl), elevated LDH and anuric AKI requiring dialysis. C3 and C4 were low. Coombs test was negative. She subsequently developed disseminated intravascular coagulation and elevated liver enzymes. Skin biopsy revealed a leukocytoclastic vasculitis with IgG and complement deposition within vessel walls. Given the concern for DITMA versus thrombotic thrombocytopenic purpura, vancomycin was discontinued. Treatment with prednisone and plasmapheresis was initiated which led to improvement of renal function, mental status and hematologic parameters within 48 hrs. Renal biopsy confirmed TMA. ADAMTS-13 activity and complement genetic testing came back normal. Unfortunately, later during the hospitalization, she developed acute respiratory failure leading to cardiac arrest.
This is a rare case of vancomycin-induced TMA. We speculate the mechanism is immune-mediated given the presence of low complement levels (although we did not test for vancomycin-dependent antibodies). Patients with immune-mediated DITMA present with sudden onset of severe systemic symptoms after a short exposure to the implicated drug. Greater awareness with improved methodology for diagnosis of DITMA is critical for clinicians evaluating such patients. Recognition of DITMA and documentation of the drug etiology are essential for patient safety.
Diffuse purpuric rash