RESUMO
Eisenmenger syndrome (ES) is a severe cardiac complication that arises from an untreated congenital cardiac defect, leading to the reversal of shunt flow, pulmonary hypertension, and cyanosis. This uncommon complication most frequently arises from small ventricular septal defects that are undiagnosed due to a lack of symptoms. However, it may arise from the reversal of any left-to-right cardiac shunt. In the following report, we present a case of acute-onset ES in a 52-year-old woman with no past cardiac history. The patient presented to the emergency department with a clinical presentation consistent with likely pulmonary embolism; however, after extensive work-up, this etiology of respiratory failure was deemed incorrect. After rapid respiratory decline requiring mechanical ventilation, the medical team performed two transthoracic echocardiograms (one with agitated saline study), one transesophageal echocardiogram, and a right cardiac catheterization on the patient. This work-up revealed pulmonary hypertension, right heart failure, and an atrial septal defect. Given these findings, the work-up was suggestive of ES secondary to an atrial septal defect shunt reversal. Because of the complexity of treatment, the patient was transferred via air to a university tertiary medical institution for extracorporeal membrane oxygenation along with other advanced treatments. This case provides a framework for the clinical presentation and treatment of this life-threatening disease. We hope that this information will help providers understand the clinical presentation, work-up, treatment, and prognosis of patients with Eisenmenger syndrome.
RESUMO
Patients presenting with immune thrombocytopenia (ITP) may have an associated underlying medical condition or medication exposure serving as the cause of their disease, but oftentimes, ITP is due to an idiopathic, autoimmune cause. While molecular mimicry is recognized as the pathogenesis behind infectious-related causes of ITP, drug-induced ITP is likely due to hapten formation, leading to an inappropriate immune-mediated response. Several drugs are associated with the development of ITP. Nitrofurantoin, a commonly prescribed antibiotic for the treatment of uncomplicated urinary tract infections (UTIs), is a medication not previously associated with the development of ITP, with only one case reporting the development of thrombotic thrombocytopenic purpura (TTP) after nitrofurantoin use. Herein, we report a case of a middle-aged Caucasian female with a history of anxiety and hypothyroidism who developed ITP following exposure to nitrofurantoin three weeks prior to presentation. The patient presented with signs and symptoms consistent with ITP: an isolated low platelet count of 1 x 109/L, petechia, fatigue, normal coagulation parameters, recurrent epistaxis, and melena. Subsequently, she was hospitalized for five days, receiving a total of four units of platelets during her stay. She was started on daily high-dose intravenous corticosteroids and received a one-time dose of intravenous immunoglobulin (IVIG). After achieving a platelet count greater than 30 x 109/L, she was discharged from inpatient care, having responded well to corticosteroid treatment. Upon follow-up with outpatient hematology, her platelet levels were maintained above 150 x 109/L, with full resolution of her acute illness. An autoimmune laboratory workup was negative except for an isolated, newly positive antinuclear antibody IgG with an elevated titer of 1:640, leading to the conclusion that an immunological response to nitrofurantoin had occurred. To our knowledge, this is the first report that describes an association between nitrofurantoin use and ITP. We hope this report aids clinicians in recognizing the various immune-mediated adverse reactions associated with nitrofurantoin.
