Case Presentation:
67‐year‐old woman with alcoholic Cirrhosis was admitted with 4 weeks of weakness, jaundice, gait disturbance and recurrent falls. She had no cough, pain, limb weakness, hematamesis or melena. Temperature was 103.2 degree F, and rest of the vital signs was normal. She was lethargic, icteric with an unremarkable cardio respiratory and abdominal exam. Labs revealed Sodium of 122, an anion gap metabolic acidosis, white blood cell count of 8.4 with no bandemia, hematocrit 34.7, thrombocytopenia to 78, INR 1.5, ammonia of 37. Liver function tests (LFT) were abnormal with a total bilirubin of 7.1, direct bilirubin 1.93 ALT 72. Chest xray and a non‐contrast Head CT scan were unremarkable. She subsequently developed worsening mental status and hypoxemia. Initial antibiotics were broadened to Vancomycin and Piperacillin‐Tazobactam. Echocardiogram, abdominal ultrasound and lower extremity dopplers were negative. Given the anemia and indirect hyperbilirubinemia, hemolysis was suspected and a peripheral smear was done. There was evidence of hemolysis along with erythrocytic parasites, diagnostic of Babesia. Ehrlichia was negative. All cultures were negative. She subsequently developed Septic shock and ARDS necessitating intubation and mechanical ventilation with no response to multiple pressors. Atovaquone and Azithromycin were later changed to Clindamycin and Quinine given the severity of Babesiosis. Doxycycline was added for possible co‐infection. Given the parasite load of 10% Exchange transfusion was begun. She received a total of ten exchanges but rapidly progressed to Acute Kidney Injury and acute bowel ischemia and subsequently expired.
Discussion:
Hospitalists and general internists commonly take care of patients with Cirrhosis. Infections commonly occur in this population. LFT abnormalities are also frequent during the course of the chronic liver disease and a careful analysis and recognition of the pattern of LFT abnormalities is essential. In this patient, the subacute elevation of indirect hyperbilirubin, generated the differential of hemolysis which along with features of sepsis led to the evaluation of the peripheral smear and the diagnosis of Babesiosis. The treatment options for severe Babesiosis, defined by high parasite load of 10% along with organ involvement should prompt therapy with exchange transfusion. Quinine with Clindamycin is preferred to Atovoaquone and Azithromycin in severe infection. Addition of Doxycycline is recommended for possible co‐infection from Lyme disease. There is additional evidence that Babesiosis in Cirrhotics carries a high mortality.
Conclusions:
Early recognition and evaluation of indirect hyperbilirubinemia in Cirrhotics with LFT abnormalities is vital. Babesiosis is endemic in the Northeast in summer . The high mortality from Babesiosis in Cirrhotics mandates early diagnosis and initiation of therapy.