Fulminant pancreatic encephalopathy with brain edema and herniation in severe hypertriglyceridemia-induced pancreatitis: a case report
- 1Division of Pulmonary and Critical Care, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon
- 2Division of Gastroenterology and Hepatology, Department of Internal Medicine, American University of Beirut, Beirut, Lebanon
- 3Department of Internal Medicine, American University of Beirut, Beirut, Lebanon
Abstract
Pancreatic encephalopathy (PE) is a rare but potentially devastating neurological complication of severe acute pancreatitis. Its manifestations range from confusion and agitation to seizures, coma, and cerebral edema, often making the diagnosis challenging due to its overlap with other causes of encephalopathy. We report a 23-year-old woman with hypertriglyceridemia-induced acute pancreatitis who rapidly progressed to severe acute pancreatitis with multiorgan failure. Within 48 h of admission, she developed agitation, seizure-like activity, and coma. Neuroimaging demonstrated diffuse cerebral and cerebellar edema, features of elevated intracranial pressure, cerebellar tonsillar herniation, and extensive restricted diffusion. After evaluation of alternative etiologies, the neurological deterioration was attributed to PE. Despite aggressive medical management, including insulin therapy, renal replacement therapy, mechanical ventilation, and hyperosmolar therapy, she did not show any signs of neurological recovery. This case demonstrates that PE may rarely progress to malignant cerebral edema and tonsillar herniation. New neuropsychiatric manifestations in patients with severe acute pancreatitis should prompt urgent neurological assessment and early neuroimaging whenever clinically feasible.
Related
- Severe Hypertriglyceridemia Associated With Acute Pancreatitis in a Patient on Risankizumab.
- Transient pancreatic enlargement with peripancreatic inflammatory changes two days before clinical presentation and diagnosis of atezolizumab-related fulminant type 1 diabetes mellitus followed by pancreatic atrophy: a case report with review of literature
- Intrahepatic and Intrasplenic Pancreatic Pseudocysts Following Acute Pancreatitis: A Case Report
- Endoscopic management of pancreatic duct stones and stricture in chronic pancreatitis using a fully covered self-expandable metal stent.
- Spontaneous fistulization of a giant pancreatic pseudocyst into the duodenum following acute pancreatitis: a case report
BibTeX
@article{aboudargham2026fulminant,
title = {{Fulminant pancreatic encephalopathy with brain edema and herniation in severe hypertriglyceridemia-induced pancreatitis: a case report}},
author = {Nivine Aboudargham and Nour El Akach and Nada Hamieh and Aya Rammal and Kassem Barada and Imad Bouakl},
journal = {Frontiers in Medicine},
year = {2026},
month = oct,
doi = {10.3389/fmed.2026.1968843},
url = {https://doi.org/10.3389/fmed.2026.1968843},
note = {CC BY},
}
RIS
TY - JOUR
TI - Fulminant pancreatic encephalopathy with brain edema and herniation in severe hypertriglyceridemia-induced pancreatitis: a case report
AU - Nivine Aboudargham
AU - Nour El Akach
AU - Nada Hamieh
AU - Aya Rammal
AU - Kassem Barada
AU - Imad Bouakl
PY - 2026
DA - 2026/10/28
JO - Frontiers in Medicine
DO - 10.3389/fmed.2026.1968843
UR - https://doi.org/10.3389/fmed.2026.1968843
AB - Pancreatic encephalopathy (PE) is a rare but potentially devastating neurological complication of severe acute pancreatitis. Its manifestations range from confusion and agitation to seizures, coma, and cerebral edema, often making the diagnosis challenging due to its overlap with other causes of encephalopathy. We report a 23-year-old woman with hypertriglyceridemia-induced acute pancreatitis who rapidly progressed to severe acute pancreatitis with multiorgan failure. Within 48 h of admission, she developed agitation, seizure-like activity, and coma. Neuroimaging demonstrated diffuse cerebral and cerebellar edema, features of elevated intracranial pressure, cerebellar tonsillar herniation, and extensive restricted diffusion. After evaluation of alternative etiologies, the neurological deterioration was attributed to PE. Despite aggressive medical management, including insulin therapy, renal replacement therapy, mechanical ventilation, and hyperosmolar therapy, she did not show any signs of neurological recovery. This case demonstrates that PE may rarely progress to malignant cerebral edema and tonsillar herniation. New neuropsychiatric manifestations in patients with severe acute pancreatitis should prompt urgent neurological assessment and early neuroimaging whenever clinically feasible.
SN - 2296-858X
ER -