Severe steatohepatitis with hepatic decompensation resulting from malnutrition after pancreaticoduodenectomy
A 68-year-old female patient presented with abdominal distension of one month duration and slurred speech for one day. She had been diagnosed with pancreatic cancer 5 months previously, and had subsequently undergone pancreaticoduodenectomy. In the operation field, the pancreatic consistency was intermediate and pancreatic resection line was conducted on, but not including, the portal vein. During operation, no hypotension or massive bleeding was encountered. The surgical pathologic finding was ductal adenocarcinoma and complete tumor resection (safety margins of 2 and 3 cm from the duodenum and common bile duct, respectively). However, since pancreaticoduodenectomy, she suffered a loss of appetite and consequently her body weight reduced from 51 kg to 44 kg over 3 months (body mass index from 22.1 to 19.0 kg/m2), even though she had experienced no postoperative diarrhea or obstructive gastrointestinal symptoms. A routine check of pancreas by dynamic CT at three months after surgery revealed severe fatty liver but no tumor recurrence (). At that time, the CT value of liver parenchyma had decreased from 50 Hounsfield units (HU) by preoperative CT to -30 HU.\nThe patient began to develop abdominal distension one month before presentation, and as a result, her body weight increased from 44 to 55 kg at presentation. At admission, vital signs were as follows; blood pressure 110/60 mmHg, heart rate 90/min, and body temperature 36.0℃. In addition, she complained of cold sensation. Pertinent physical findings included shifting dullness with abdominal distension, anemic conjunctivae, pretibial pitting edema, and flapping tremor with slurred speech. summarizes laboratory findings, which showed anemia with a chronic illness pattern, prolonged prothrombin time, hypoalbuminemia, markedly depressed lipid profiles, and slight decreases in level of calcium and phosphorus. To evaluate the presence of steatorrhea, a stool study was performed, and did not show stool fat. Hemoglobin A1c was 6.0% without anti-diabetics, although she had been diagnosed with diabetes two years prior to the pancreaticoduodenectomy. Viral markers for hepatitis B and C were negative. Carbohydrate antigen (CA) 19-9 had been maintained within the normal range post-pancreaticoduodenectomy. Infectious and autoimmune causes of liver disease and functional abnormalities of the thyroid and adrenal glands were excluded by laboratory testing. She denied alcohol intake and taking any other medicine, including herbal medicine, except supportive pancreatic enzyme. Follow-up liver dynamic CT at this presentation also revealed marked fatty liver and newly developed moderate amounts of ascites (). There was no evidence of local tumor recurrence or lymph node enlargement. The ascites was tapped and proved to be transudate (serum-ascites albumin gradient 1.5) free of malignant cells. It was then controlled with diuretic agents. Her slurred speech, disorientation, and flapping tremor improved within 1-2 days of frequent laxative administration (lactulose). Although her laboratory findings showed mild metabolic alkalosis (pH 7.52, PCO2 33 mmHg, PO2 66 mmHg, HCO3 26.9 mmol/L, O2 saturation 95.0%) in blood gas analysis, mild electrolyte imbalances and no electroencephalographic study was performed, the neurologist checked our patient and there was no organic problem explaining her mental state except hepatic encephalopathy. A liver biopsy was performed to exclude other causes of liver parenchymal disease, and its findings were consistent with severe steatohepatitis which of NAFLD activity score 7 (NAS; macrovesicular steatosis (3), lobular inflammation (2) and hepatocellular ballooning (2)) and a fibrosis score of 1 (). In addition, a Mallory's body was observed in the high power field ().\nThe patient was hydrated with saline at 20-30 mL/kg/day and then parenteral and enteral feeding was started at 10 kcal/kg/day for 3 days and then increased to 20-25 kcal/kg/day, in view of the risk of refeeding syndrome. In addition, she was administered multi-vitamins including folic acid, thiamine, and zinc and selenium. Her electrolyte levels, body weight, and urine output were checked daily. After 3 months of nutritional support, follow-up CT showed some regression of fatty liver (CT value 10 HU) and near complete regression of the ascites (no diuretic was administered; ). After 7 months of controlled oral nutritional intake, she was free of symptoms of ascites and encephalopathy and her liver function tests and lipid profiles were improved without evidence of tumor recurrence ().