Significance of elevated pancreatic enzymes in intracranial bleeding

• Published in: Southern medical journal (Birmingham, Ala.) Vol. 87; no. 9; pp. 889 - 893
• Main Authors: Justice, A D, DiBenedetto, R J, Stanford, E
• Format: Journal Article
• Language: English
• Published: United States 01.09.1994
• Subjects: Amylases - metabolism; Cerebral Hemorrhage - enzymology; Craniocerebral Trauma - enzymology; Glasgow Coma Scale; Humans; Lipase - metabolism; Multivariate Analysis; Pancreas - enzymology
• ISSN: 0038-4348; 1541-8243
• DOI: 10.1097/00007611-199409000-00005

Hyperamylasemia of pancreatic origin has been noted in patients with severe head injury without abdominal trauma or evidence of pancreatitis. Thirty-eight patients with intracranial bleeding of various types were evaluated for elevated pancreatic amylase and lipase enzymes without associated pancreatitis. Twenty-five patients had elevated serum lipase; 17 of 25 also had elevated amylase without pancreatitis. Most lipase elevations occurred earlier than those of amylase. Six clinical variables--mannitol, ceftriaxone, nimodipine, steroids, Glasgow Coma Score, and total parenteral and enteral hyperalimentation--were evaluated to determine relationship to the enzyme elevations. A significant relationship exists between patients not treated with steroids and elevated lipase and amylase enzyme activities. Multivariate analysis revealed a significant interaction between lipase elevation and decreasing Glasgow Coma Score, indicative of increasing severity of intracranial bleeding. Proposed causes of enzyme elevations in intracranial bleeding include vagal stimulation, altered modulation of the central control of pancreatic enzyme release, and release of cholecystokinin from the brain. Physician awareness of the association of intracranial bleeding with the elevation of amylase and lipase without pancreatitis can save the patient needless cost and manipulation.