Low-Volume Plasma Exchange for Fulminant Hepatic Failure Secondary to Hepatitis A in a Young Adult: A Case Report.

Acute liver failure accounts for a very fatal and severe complication. It is defined as acute liver injury with hepatic encephalopathy (HE) and an elevated international normalized ratio (INR above 1.5). There are multiple factors that can lead to acute liver failure. These different etiologies can vary depending on certain geographical areas where they are more prevalent than other factors in the area. Hepatitis caused by the Hepatitis A virus (HAV) is one of the leading causes of acute liver failure worldwide, especially in developing countries. Artificial Liver Support System (ALSS), on the other hand, consists of certain techniques by which the function of the liver is maintained artificially outside the body. These techniques try to filter out harmful substances and detoxify the blood. We report a 20-year-old male, with no known comorbidities, who presented to the medical outdoor with a history of high-grade fever for 5 days. On examination, the patient had mucocutaneous jaundice, moderate epigastric tenderness. His initial laboratory investigation showed Hb = 13.5, TLC = 6.8, PLT = 236, Pt = 22 (13 control), INR 1.7, Bilirubin total = 17.9, Bilirubin direct = 11.6, Bilirubin indirect = 6.3, AST = 5868, ALT = 5368, ALP = 160. His HbsAg and HCV by ELISA were negative, hepatitis E virus IgM was negative, and Hepatitis A IgM was positive. He was preliminarily diagnosed as a case of acute viral hepatitis A. He was shifted to the medical HDU for optimization. Over the next 12 h, the patient gradually deteriorated. He developed high-grade fever, 102°F, total bilirubin worsened, and hepatic encephalopathy grade II developed, with flapping tremors appreciated. The patient was shifted to the Medical Intensive Care Unit for monitoring and probable need for ventilatory support. Over the next 24 h, due to worsening clinical and biochemical parameters, it was decided to proceed with plasma exchange. Three sessions of plasma exchange were carried out, using eight units of fresh frozen plasma (approximately 1.6 L) as the replacement solution, over a period of 1.5 h for each session. The patient showed a marvelous improvement in clinical and biochemical parameters. He was admitted to the medical ICU for 7 days. He was stepped down to medical HDU for a further 2 days before being discharged. Low-volume plasma exchange therapy is a relatively safe option for young adult patients with fulminant hepatic failure secondary to hepatitis A infection. The therapy can be used early in the disease course when neurological signs/haptic encephalopathy start to develop. This can lead to a better prognosis and survival in selected patients.