S5549 Beyond Cirrhosis: Hepatic Encephalopathy Due to Acquired Portosystemic Shunt Following Billroth II Hemigastrectomy

Introduction: Hepatic encephalopathy (HE) is a neuropsychiatric disorder resulting from liver dysfunction and elevated ammonia levels. While typically associated with cirrhosis and portal hypertension, HE can also occur secondary to acquired portosystemic shunts (PSS). We present a rare case of HE that developed following the formation of an acquired portosystemic shunt after hemigastrectomy. Case Description/Methods: A 60-year-old woman with a medical history of coronary artery disease, and hemi-gastrectomy with Billroth II reconstruction in 2019 presented to the ED with acute confusion, noted by her husband. The patient had been experiencing nausea and vomiting since the previous evening. In the morning, her husband observed significant confusion, including behavior such as wearing mismatched footwear and expressing a desire to go out, which was atypical for her. Though she had occasional baseline confusion, that episode was much more pronounced. Her husband attributed it to a new medication she had taken earlier that morning (meclizine). On presentation, labs revealed an elevated total bilirubin 1.78 mg/dL, and ammonia of 166, but liver enzymes were within normal limits. A computed tomography (CT) scan of the head was unremarkable. Further evaluation with CT abdomen/pelvis revealed an intrahepatic portosystemic shunt, measuring up to 4 cm, connecting the right portal vein to the hepatic vein. Given the elevated ammonia level and suspicion of hyperammonemia-related encephalopathy, lactulose was started. Interventional radiology was consulted, and hepatic venous angiography performed which showed shunt originating from a central branch of the right hepatic vein with subsequent embolization performed. Following the procedure, the patient’s ammonia levels decreased significantly, and her mental status returned to baseline. Discussion: This case highlights a rare but important cause of hepatic encephalopathy: an acquired intrahepatic portosystemic shunt developing years after hemigastrectomy with Billroth II reconstruction. While hepatic encephalopathy is commonly linked to cirrhosis, clinicians should maintain a high index of suspicion for portosystemic shunting in non-cirrhotic patients presenting with unexplained hyperammonemia and altered mental status. For example, in cases similar to this one, where a history of gastrointestinal surgery may have altered intra-abdominal hemodynamics. Prompt recognition of this rare complication is crucial, as it can significantly impact patient management and outcomes.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001149656.31185.64
Primary Topic
Liver Disease and Transplantation
Type
article
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article

S5549 Beyond Cirrhosis: Hepatic Encephalopathy Due to Acquired Portosystemic Shunt Following Billroth II Hemigastrectomy

The American Journal of Gastroenterology
Liver Disease and Transplantation
article

S5549 Beyond Cirrhosis: Hepatic Encephalopathy Due to Acquired Portosystemic Shunt Following Billroth II Hemigastrectomy

article en

Abstract

Introduction: Hepatic encephalopathy (HE) is a neuropsychiatric disorder resulting from liver dysfunction and elevated ammonia levels. While typically associated with cirrhosis and portal hypertension, HE can also occur secondary to acquired portosystemic shunts (PSS). We present a rare case of HE that developed following the formation of an acquired portosystemic shunt after hemigastrectomy. Case Description/Methods: A 60-year-old woman with a medical history of coronary artery disease, and hemi-gastrectomy with Billroth II reconstruction in 2019 presented to the ED with acute confusion, noted by her husband. The patient had been experiencing nausea and vomiting since the previous evening. In the morning, her husband observed significant confusion, including behavior such as wearing mismatched footwear and expressing a desire to go out, which was atypical for her. Though she had occasional baseline confusion, that episode was much more pronounced. Her husband attributed it to a new medication she had taken earlier that morning (meclizine). On presentation, labs revealed an elevated total bilirubin 1.78 mg/dL, and ammonia of 166, but liver enzymes were within normal limits. A computed tomography (CT) scan of the head was unremarkable. Further evaluation with CT abdomen/pelvis revealed an intrahepatic portosystemic shunt, measuring up to 4 cm, connecting the right portal vein to the hepatic vein. Given the elevated ammonia level and suspicion of hyperammonemia-related encephalopathy, lactulose was started. Interventional radiology was consulted, and hepatic venous angiography performed which showed shunt originating from a central branch of the right hepatic vein with subsequent embolization performed. Following the procedure, the patient’s ammonia levels decreased significantly, and her mental status returned to baseline. Discussion: This case highlights a rare but important cause of hepatic encephalopathy: an acquired intrahepatic portosystemic shunt developing years after hemigastrectomy with Billroth II reconstruction. While hepatic encephalopathy is commonly linked to cirrhosis, clinicians should maintain a high index of suspicion for portosystemic shunting in non-cirrhotic patients presenting with unexplained hyperammonemia and altered mental status. For example, in cases similar to this one, where a history of gastrointestinal surgery may have altered intra-abdominal hemodynamics. Prompt recognition of this rare complication is crucial, as it can significantly impact patient management and outcomes.

The American Journal of GastroenterologyVol. 120(10S2)
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Liver Disease and Transplantation
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