Abstract

Purpose: Fulminant Hepatic Failure (FHF) often affects young people and has a very high mortality. Incidence approaches around 2,000 cases annually in the United States. Drug toxicity comprises more than 50% of acute liver failure cases. Nearly 15% of cases remain of indeterminate etiology. A 64 yr-old male with history of hypertension presented to emergency room with fever, chills, and right flank pain. Physical exam was unremarkable. Labs revealed AST: 337 u/l, ALT: 215 u/l, Alkphos: 431 u/l. CT scan of the abdomen revealed consolidation of left lung bases with bilateral small calcified lung nodules, hepatomegaly and non-specific abdominal lymphadenopathy. Patient refused hospital admission, thus sent home on levofloxacin and prevacid and asked to follow up with the primary care physician for further evaluation. Ten days later he was admitted to hospital with progressive confusion, dyspnea, lethargy, and abdominal pain. Abdomen was soft, slightly distended, and mildly tender in the right upper quadrant. Bowel sounds were positive. Liver was palpable with a span of 18 cms. Admission labs revealed worsening of liver function. Chest X-ray showed persisting left lower lobe infiltrate. He was started on unasyn and azithromycin. CT of abdomen displayed massive hepatomegaly 30.4 cm along with extensive abdominal lymphadenopathy. On day two, patient became encephalopathic with profound liver and renal failure necessitating ICU transfer and was started on lactulose. Non-contrast CT scan of chest showed a 2.2 cm mass in the left upper lobe with extensive mediastinal lymphadenopathy and airbronchograms involving the left base. Liver biopsy unmasked massive infiltration of hepatic parenchyma with poorly differentiated Small cell Lung Cancer (SCLC) with intrasinusoidal involvement. He was started on high dose steroids, fractionated cytoxan and, transferred to a transplant center but died on the fourth day with advanced Multiorgan dysfunction syndrome. FHF from liver metastases is relatively rare (0.44%). Only 20 cases of FHF from SCLC were reported in literature. The most striking features at presentation of FHF secondary to metastatic disease are massive hepatomegaly, elevated serum LDH, uric acid, and increased serum LDH to ALT ratio. LDH levels are often used as a marker of tumor growth and predictor for impending liver failure in patients with SCLC. Imaging of the liver often fails to demonstrate a well defined lesion. Diffuse involvement of the liver is the norm. Liver biopsy is warranted to eliminate other causes of liver failure. After the onset of FHF prognosis is dismal and, these patients rapidly progress to MODS. Death invariably follows in days.

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