Case Presentation: A 68 year-old male with past medical history of alcohol use presented after a motor vehicle accident. Labs showed a hemoglobin (Hb) of 12.4 mmol/L and platelet (plt) count 235 x 10^9/L. He received four units of whole blood in the emergency department and underwent repair of left lower extremity fractures. He was given vancomycin for broad coverage on Day 1. Hospital course was complicated by ventilator-dependent respiratory failure secondary to aspiration pneumonia, right pleural effusion requiring a chest tube, and Staphylococcus epidermidis bacteremia. Thus he was started on vancomycin and cefepime along with subcutaneous heparin for deep vein thrombus prophylaxis. Plts were initially stable post-operatively; however, they steadily began to decline three days post-operatively to 132×10^9/L on hospital day 11, and continued to decrease rapidly to 11×10^9/L on day 16. International normalized ratio (INR) was 1.3 and activated partial thromboplastin time (aPTT) was 32 seconds. The patient had stable anemia with Hb 7.0-9.0 mmol/L throughout admission. 4T score for heparin-induced thrombocytopenia (HIT) was three, and anti-PF4 antibody was 0.19 ruling out HIT. He received four units of plts over the following two days with no improvement. PLASMIC score was four points therefore there was a low probability for thrombotic thrombocytopenic purpura in the given clinical setting. Other causes including nutritional deficiencies (B12 and folate), splenomegaly, liver dysfunction secondary to alcohol use were ruled out. Thus, immune thrombocytopenia (ITP) was suspected. Causes of drug-induced immune thrombocytopenia (DITP) were evaluated and an abrupt drop in plt counts upon re-introduction of vancomycin on hospital day 11 (Fig. 1) was noted. It was promptly discontinued and two doses of intravenous immune globulin (IVIG) 1000mg/kg were given. Plt counts increased from 11 to 84×10^9/L over the next four days, eventually recovering to 386×10^9/Lby discharge.
Discussion: ITP is caused by autoantibodies against plts and has an incidence of 12/100,000 in adults; however, DITP is even less commonly reported (1). Vancomycin is one of the few antibiotics associated with DITP. Typical presentations of DITP include petechiae, bruising, and epistaxis with an accompanying acute drop in plts (commonly < 20x10^9/L ). In this case, strong evidence favoring DITP or vancomycin induced immune thrombocytopenia (VIIT) includes exposure to a previously identified causative drug, normalized plt counts after discontinuation of drug (Day 7), and re-exposure to drug resulting in recurrent thrombocytopenia (Day 10)(2). Other causes including HIT as mentioned in case presentation were ruled out. Treatment for DITP includes stopping the offending agent primarily. Additionally, plts are transfused to increase critically low counts, even if transiently. Glucocorticoids and IVIG can also be used. Glucocorticoids lead to apoptotic death of autoantibody-producing lymphocytes and IVIG interferes with macrophage consumption of autoantibody-coated plts (2,3). Our patient was given IVIG for rapid increase in plt counts as his thrombocytopenia was refractory to previous transfusions. Steroids were avoided as the patient was acutely bacteremic. After treatment with IVIG, plt counts improved and stabilized to 386x10^9/L.
Conclusions: This case highlights the importance of keeping secondary causes of ITP in mind, as early detection and removal of offending agents can allow for better recovery (4).
