1164

Abstract

Introduction: HGA is a potentially fatal disease if not treated appropriately. Because it often presents as a febrile illness with non-specific signs and symptoms, the diagnosis can be elusive. Patients may present with fevers, myalgia, nausea, vomiting, diarrhea, abdominal pain and respiratory complaints such as cough or shortness of breath. HGA presenting with myocardial dysfunction is uncommon and rare. This association is not well described, and hence the diagnosis may not be recognized and/or delayed. A 78-year-old man was brought to the ED due to extreme weakness and fatigue. He was fairly active until he developed non-bloody diarrhea for four days, associated with nausea and chills. He denied recent travel or outdoor exposure. His medical history is significant for HTN, atrial fibrillation, CKD s/p R nephrectomy for renal cell carcinoma, and interstitial lung disease. On presentation, he was alert and oriented, normotensive, afebrile, with adequate oxygenation, but in mild distress from rapid atrial fibrillation with ventricular rates in the 130-140s. Work-up revealed a WBC of 7,800/mm3 with 88.5% neutrophils, hemoglobin of 11.6 g/dl, platelets of 121,000/mm3, and a creatinine of 4.6 mg/dl (baseline of 3.0 mg/dl). His CXR and urinalysis were unrevealing. He received treatment for his tachyarrythmia and intravenous fluids for his acute (on chronic) renal failure. He then developed pulmonary edema and hypotension. An immediate echocardiogram done revealed new biventricular dysfunction and an EF of 30% - 35% (baseline EF 46%). BNP was markedly high at 70,930 pg/ml, troponin and CK were mildly elevated at 0.11 ng/ml and 348 units/L respectively. He was transferred to our hospital's cardiac care unit (CCU) the next day for acute decompensated heart failure with new biventricular dysfunction and cardiogenic shock, thought to be from tachycardia-induced cardiomyopathy. An underlying infection was in the differential and he was started on piperacillin/tazobactam and vancomycin. Upon transfer, the patient was hypoxic requiring intubation and mechanical ventilation. He was managed with diuresis and vasopressor. He was started on continuous veno-venous hemodialysis for worsening renal function. A Swan-Ganz catheter placed strongly suggested a septic component to the patient's shock, with a low systemic vascular resistance of 600 dynes*s/cm5. He was transferred to our medical ICU (MICU) on day four of initial presentation-- febrile, sedated, mechanically ventilated with ARDS picture, on norepinephrine and vasopressin for septic shock of unclear etiology. His exam was only significant for atrial fibrillation with ventricular rates in the 90s and basal crackles on chest auscultation. His WBC was down to 3,300/mm3, with platelets as low as 37,000/mm3. His AST was elevated at 145 units/L, ALT was normal, and direct bilirubin was slightly high at 1.6 mg/dl. His blood cultures remained negative. Doxycylcine was added to his regimen to cover atypical pulmonary pathogens and tick-borne diseases as well. He improved and was weaned off of vasopressors in two days after starting doxycycline. Repeat ECHO showed improvement of his EF to 40-50% (his baseline). His Ehrlichia PCR (anaplasma phagocytophila DNA) came back positive. He was extubated and later transferred to the floors after nine days in MICU. He did well and was discharged to rehab six days later. HGA, formerly human granulocytic ehrlichiosis, is a tick-borne disease caused by Anaplasma phagocytophilum. Typical lab findings are leukopenia, thrombocytopenia and elevated liver enzymes. Fulminant cases may lead to multi-organ failure. In the appropriate season and geographic area (our patient is a resident of MA and presented in the peak month of June), fever with few or no localizing symptoms should prompt suspicion for tick-borne disease. Myocardial dysfunction, although atypical, can be a presenting sign and may strongly warrant empiric therapy.