A role for epinephrine in post-traumatic hypokalemia.

We have previously described a high incidence of admission hypokalemia in trauma patients at our institution. We subsequently performed a prospective study of 112 trauma patients to examine the possible etiologies of post-traumatic hypokalemia. Trauma patients >or=5 years old were evaluated within 6 h of injury with a variety of studies including catecholamines, cortisol, and insulin levels, with studies repeated 24 to 36 h after admission. No potassium replacement was given during this time. Demographic factors such as age, types of injury, and severity of injuries were collected. We found that the mean age of those with post-traumatic hypokalemia (<or=3.5 mEq/L) was significantly younger (29 vs. 37 years old; P = 0.004) and epinephrine levels were significantly higher (863 vs. 406 pg/mL; P = 0.01) when compared with normokalemic patients on admission. At 24 to 36 h, the hypokalemia group compared with the normokalemic patients showed a significant rise in the mean potassium levels (17.2% vs. 4.1%; P < 0.001), a significant fall in mean epinephrine levels (-86.6% vs. -81.4%; P < 0.001), and a significant rise in insulin levels (161% vs. 24%; P < 0.005). Finally, because our previous study had shown that post-traumatic hypokalemia was predictive of injury severity score, 4 trauma admission groups were compared with regard to potassium levels and injury severity score. Those trauma patients with both high injury severity and hypokalemia had significantly higher admission epinephrine levels (1222 vs. 290 pg/mL; P = 0.005), glucose levels (174 vs. 126 mg/dL; P = 0.001), and lower carbon dioxide levels (21.3 vs. 24.6 mEq/L; P < 0.03) than those trauma patients with less severe injury and normokalemia. We conclude that post-traumatic hypokalemia seems to be related to a rise in epinephrine levels, that this rise in epinephrine levels seems to be blunted in older patients, and that post-traumatic hypokalemia is rapidly reversible without specific therapy.