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Hepatic encephalopathy secondary to hyperammonaemia is a known complication of chronic liver disease. In contrast, non-cirrhotic hyperammonaemia is a lesser-known entity that should be considered in a patient with acute encephalopathy as part of the diagnostic workup as prompt identification can help to avoid complications such as seizures and cerebral oedema. We present a case of a middle-aged woman who presented electively for a total pancreatectomy-duodenectomy with splenectomy, hepatico-jejunostomy, gastro-jejunostomy and developed encephalopathy on postoperative day 10 due to non-cirrhotic hyperammonaemia.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167428 | PMC |
http://dx.doi.org/10.1136/bcr-2019-233218 | DOI Listing |
Cureus
November 2024
Department of Internal Medicine, Wrexham Maelor Hospital, Wrexham, GBR.
Hyperammonemia is a serious metabolic condition marked by elevated ammonia levels in the blood, leading to neurological damage and systemic complications if untreated. While often associated with liver dysfunction, inborn metabolic errors such as fatty acid oxidation defects, pyruvate metabolism disorders, urea cycle disorders (UCDs), urea splitting bacterial infections, hemato-oncological disorders, and portosystemic shunts are less commonly recognized but significant causes, particularly outside neonatal populations. These metabolic errors, due to partial enzyme deficiencies, may present later in life with atypical symptoms.
View Article and Find Full Text PDFPathology
October 2024
The University of Western Australia, Perth, WA, Australia; Inborn Errors of Metabolism Service, Department of Endocrinology, Royal Perth Hospital, Perth, WA, Australia; PathWest Laboratory Medicine, Department of Biochemistry, Fiona Stanley Hospital Network, Perth, WA, Australia. Electronic address:
Acute hyperammonaemia is a medical emergency as it can progress to cerebral oedema, seizures, coma and death. Hepatic encephalopathy secondary to cirrhotic disease or portosystemic shunting are relatively well-known causes, but non-cirrhotic aetiologies of acute hyperammonaemia are less well-known, especially in the emergency department. However, an elevated ammonia is not required to make the diagnosis of hepatic encephalopathy.
View Article and Find Full Text PDFCureus
July 2024
Internal Medicine, Howard University Hospital, Washington, D.C., USA.
Hyperammonemia is a metabolic disorder characterized by supraphysiologic ammonia (NH) concentrations in the blood. Although usually seen in adults with liver disease, hyperammonemia is a notable complication in 4.1% of lung transplants.
View Article and Find Full Text PDFJ Investig Med High Impact Case Rep
June 2024
Hepatic encephalopathy is uncommon in the absence of cirrhosis. We report a 71-year-old woman who presented with altered mental status in the setting of hyperammonemia for the second time in 6 months. Magnetic resonance imaging of the abdomen revealed an uncommon portosystemic shunt involving an enlarged posterior branch of the right portal vein and an accessory right hepatic vein, with no features of cirrhosis.
View Article and Find Full Text PDFCureus
April 2024
Internal Medicine, University of Central Florida College of Medicine, Gainesville, USA.
Hepatic encephalopathy is typically seen in advanced liver disease and in patients with a transjugular intrahepatic portosystemic shunt. Common triggers include infections, gastrointestinal bleeding, electrolyte disturbances, dehydration, and drug/toxin use such as benzodiazepines and alcohol. In rare instances, other metabolic abnormalities such as hypothyroidism may also exacerbate hyperammonemia in patients with underlying liver disease due to hypothyroidism-induced myopathy, which increases urea production and decreases clearance through reduced glutamine synthetase activity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!