Abstract:
We present the case of a 64-year-old female with a complex medical history who developed severe thrombocytopenia shortly after receiving vancomycin treatment. The patient`s platelet count dropped precipitously from 552 to 27 within 24 hours of initiating vancomycin therapy. The patient`s thrombocytopenia was attributed to vancomycin use, and the drug was promptly discontinued. This case highlights the importance of vigilance in monitoring for adverse drug reactions in patients with multiple comorbidities and underscores the need for prompt recognition and management of drug-induced thrombocytopenia.
Introduction:
Thrombocytopenia, defined as a platelet count less than 150,000/μL, can be attributed to various causes including medications. Vancomycin, a commonly used antibiotic for the treatment of serious gram-positive bacterial infections, is known to be associated with various adverse reactions including hypersensitivity reactions, nephrotoxicity, and thrombocytopenia. Here, we present a case of vancomycin-induced thrombocytopenia in a patient with a complex medical history.
Case Presentation:
A 64-year-old female with a past medical history of hypertension, GERD, type 2 diabetes mellitus, depression, obesity, anemia, overactive bladder, asthma, peripheral arterial disease, liver disease, atrial fibrillation, and anxiety presented to the emergency department with hypoglycemia. The patient had experienced a fall recently, resulting in minor injuries to her left arm and leg. During her hospitalization, vancomycin was initiated for suspected infection.
Clinical Course:
Upon initiation of vancomycin therapy, the patient`s platelet count exhibited a rapid decline from 552 to 27 within 24 hours. The patient`s hemoglobin level also decreased from 9.6 to 7.8, potentially due to the dilutional effect of intravenous fluids. No active bleeding was observed, and the patient remained conscious and conversant. Physical examination revealed no signs of bleeding, bruising, or petechiae. The decision was made to discontinue vancomycin therapy due to suspected drug-induced thrombocytopenia.
Management and Outcome:
Following discontinuation of vancomycin, the patient was closely monitored. Her platelet count improved gradually over the subsequent days, and no further signs of bleeding or hematological abnormalities were observed. The patient`s symptoms of fatigue and somnolence were likely related to her multiple chronic conditions and the recent hypoglycemic episode. The patient was stabilized and transferred to a Skilled Nursing Facility for ongoing management of her chronic medical conditions.
Discussion:
Vancomycin-induced thrombocytopenia is a rare but serious adverse effect that should be considered in patients receiving vancomycin therapy, especially in those with rapid and significant decreases in platelet counts. The mechanism underlying vancomycin-induced thrombocytopenia is not fully understood, but it is believed to involve an immune-mediated process. Prompt recognition and discontinuation of the offending agent are crucial in preventing further complications.
Conclusion:
This case illustrates the potential for vancomycin-induced thrombocytopenia in patients with complex medical histories. Clinicians should maintain a high index of suspicion for adverse drug reactions and promptly intervene by discontinuing the offending medication. Monitoring platelet counts in patients receiving vancomycin, especially when used in conjunction with other potentially myelosuppressive agents, can aid in early detection and management of thrombocytopenia, ultimately leading to improved patient outcomes.