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.