Case Presentation: A hospitalized 71-year-old female became acutely encephalopathic after an esophagogastroduodenoscopy under conscious sedation which was performed to evaluate a chronic esophageal ulcer and other potential causes of dysphagia. Her past medical history was significant for obesity, hypothyroidism, chronic back pain, peripheral neuropathy, colorectal mucinous adenocarcinoma with carcinomatosis and metastases to the lung, chronic esophageal ulcer, hepatic steatosis and a chronic non-occlusive portal vein thrombus. Past surgical history was significant for right hemicolectomy and gastric bypass. She had been receiving ramucirumab, capecitabine, gabapentin, levothyroxine, low dose hydrocodone-acetaminophen and pantoprazole 40 mg BID.
Following her EGD, she was noted to be groggy and slightly confused. Confusion progressed overnight and she started confusing the sound of telemetry alarms for chirping birds. Her vital signs were normal and the remainder of her examination was unremarkable. She was noted to have an increase in her AST (247), ALT (103), and total bilirubin (3.1). The following day, her confusion worsened and she became difficult to awaken. Her low doses of hydrocodone-acetaminophen and gabapentin were discontinued. On hospital day four she became obtunded and non-responsive to sternal rub. She was given naltrexone without improvement and further workup was prompted.
A head CT was non-revealing for causes of her encephalopathy. CBC, electrolytes, ABG and TSH were normal. Renal function was reduced but stable. Chest x-ray, UA and blood cultures were non-revealing for signs of infection. In consideration of her gastric bypass anatomy, she was given IV thiamine. Abdominal ultrasound reveled new-onset complete occlusion of the portal vein with significant ascites. Paracentesis was performed which suggested portal hypertension as the etiology. She did not have spontaneous bacterial peritonitis. Serum ammonia was elevated at 141. She was started on lactulose with rifaxamin added the following day. Within two days of treatment for hepatic encephalopathy her cognition returned to baseline.
Discussion: Type B hepatic encephalopathy due to portal-systemic shunting in the absence of cirrhosis is a well described but less common cause of hepatic encephalopathy. Acute portal vein thrombosis is a known cause of type B hepatic encephalopathy and should be considered as a possible cause of metabolic encephalopathy, especially in patients with malignancy, chronic liver disease, inherited thrombophilia and processes localized to the epigastrium or hepatobiliary system. As is often the case, identification of the cause of this patient’s encephalopathy was particularly changeling due to the myriad of other potential etiologies. Though anticoagulation can be considered in the management of acute portal vein thrombosis, this patient was a particularly poor candidate due to her recently ablated esophageal ulcer.
Conclusions: Metabolic encephalopathy is a common problem encountered by the hospitalist. When working through a case of metabolic encephalopathy, it is important to consider a broad differential of potential etiologies. In the appropriate clinical context, the hospitalist would be wise to consider less common etiologies such as type B hepatic encephalopathy secondary to an acute portal vein thrombosis.