Vitale G C, Larson G M, Davidson P R, Bouwman D L, Weaver D W
J Surg Res. 1987 Sep;43(3):226-33. doi: 10.1016/0022-4804(87)90075-8.
To evaluate the influence of severe head injury (SHI) on amylase activity, we studied the amylase profile of 60 patients with SHIs and Glasgow Coma Scores less than 10. Fourteen additional multiple trauma patients without head injuries were studied as a control group. We excluded patients with pancreatic injury and abdominal trauma. Total serum amylase (TA), pancreatic isoamylase (PA), and nonpancreatic isoamylase (NPA) levels were measured on Days 0, 2, 4, 7, and 14 postinjury. Values greater than 2 SD above the normal mean were considered elevated. All SHI patients were comatose; 14 died. In the SHI group, TA increased in 23 patients, PA increased in 40, and NPA increased in 14. The source of hyperamylasemia was PA in 14, NPA in one, and mixed in 8 patients. While PA increases occurred throughout the study, NPA elevations occurred early. These increases did not correlate with shock (BP less than 80 mm Hg; 17 patients), facial trauma (24 patients), or associated injury (29 patients). On Day 7 postinjury, the mean TA (215 du%) and the mean PA (203.8 du%) were significantly elevated in the SHI patients compared to controls (122.1 du%, P less than 0.05, Wilcoxon's rank sum test). These data indicate that serum amylase is not a reliable index of pancreatic injury in patients with SHI. Severe head injury and multiple trauma activate pathways that increase amylase levels in the blood, suggesting a central nervous system regulation of serum amylase levels.
