A 56‐year‐old white man was admitted with 3 days of worsening mentation refractory to increasing doses of lactulose. History included remote alcohol abuse, alcohol‐induced cirrhosis diagnosed after a sentinel variceal bleed, and chronic encephalopathy. The patient was compliant with lactulose, rifaximin, and spironolactone. He denied fevers, chills, abdominal pain, or abdominal girth. Over the past year, the patient had increasing episodes of hospitalization for ence‐phalopathy, with the time interval between periods of lucidity and encephalopathy decreasing significantly. During prior hospitalizations, the patient was treated with antibiotics for suspected cellulitis and lactulose, with improvement in symptoms. Current examination revealed an obese man oriented only to self, nonagitated, and cooperative. Patient was afebrile with stable vital signs. Abdomen was soft, nontender, and without signs of ascites. There was lymphedema of the left lower extremity with areas of black discoloration and erythema. He displayed poor concentration, poor short‐term memory, and asterixis. Laboratory analysis was significant for hyponatremia and elevated ammonia level with normal white blood cell count. The patient was given piperacillintazobactam to treat cellulitis and high‐dose lactulose for encephalopathy. Despite this, the patient remained confused. Repeat labs revealed further elevations in ammonia level. Prompted by the refractory nature of his encephalopathy despite improved cellulitis, another cause of encephalopathy was sought. Liver ultrasound with Doppler flow study revealed hepatic parenchymal disease and a small portal vein with complete reversal of blood flow. Based on this data, lack of ascites, and no further variceal bleeds, a CT of the abdomen/pelvis with contrast was obtained, which was consistent with spontaneous mesocaval shunt (a type of portal‐systemic shunt).
The estimated prevalence of chronic liver disease/cirrhosis in the United States is approximately 5.5 million cases. Hepatic encephalopathy occurs in 30%–45% of patients with cirrhosis and 10%– 50% of patients who have undergone transjugular intrahepatic portosystemic shunt. Recurrent/refractory encephalopathy is defined by 2 episodes of hepatic encephalopathy occurring within 1 year. Hepatic encephalopathy is commonly seen and often attributed to poor medication compliance, bleed, or infection. However, in patients who present with little to no ascites/ varices but with chronic refractory encephalopathy; spontaneous portal‐systemic shunt should be sought as a cause. If found, there are treatment options such as shunt reduction/embolization procedures by interventional radiology. Without identification, these patients often have frequent hospitalizations and significant deterioration in their quality of life.
The purpose of reporting this case is to increase awareness of spontaneous portal‐systemic shunts as a cause of chronic/refractory hepatic encephalopathy.
R. Gibbons ‐ none; K. Pedram ‐ none
To cite this abstract:Gibbons R, Pedram K. Spontaneous Portal‐Systemic Shunt As Cause of Refractory Encephalopathy. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 286. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/spontaneous-portalsystemic-shunt-as-cause-of-refractory-encephalopathy/. Accessed September 19, 2019.