乌鸦传媒

NASHVILLE, Tenn., Feb. 3 -- Elevated troponin I levels may identify trauma patients who have an increased risk of dying, according to a retrospective study reported here.

A troponin I level of more than 1.2 µg/L tripled the mortality risk compared with patients who had normal values for the cardiac enzyme, Matthew Eckert, M.D., of Madigan Army Medical Center in Seattle, said at the Society of Critical Care Medicine meeting.

Troponin elevations were not specific for heart or chest injuries, as penetrating injuries not involving the chest also triggered troponin production.

"Our data support the view that troponin I elevation following penetrating trauma is likely a marker for physiologic stress, not mechanical chest injury," said Dr. Eckert. "Elevated troponin levels do predict adverse outcomes, including mortality, in critically ill patients."

An exploratory analysis revealed a significantly higher survival in patients who had elevated troponin and were treated with beta-blockers. The observation raises the possibility that beta-blockade might be protective in that clinical setting, Dr. Eckert added.

The study grew out of a desire to explore a controversial association between elevated troponin levels and blunt cardiac injury. Moreover, the significance of elevated troponin levels after penetrating chest trauma was unclear.

In an effort to clarify troponin's association with trauma, investigators retrospectively reviewed records on all 601 patients with penetrating injuries admitted to a level I trauma center ICU. Patients whose ICU admission lasted less than 24 hours were excluded.

A normal troponin level was defined as 0 to 1.2 µg/L, and higher levels were considered elevated.

The study population was 323 patients with chest injuries and 278 with penetrating injuries involving other areas of the body. Gunshot wounds accounted for 76% of all cases.

Dr. Eckert reported that 28% of the patients had elevated troponin values while in the ICU, including 32% of patients with chest injuries and 23% of those without chest injury.

Among all patients with elevated troponin values, the median initial value was 2.8 µg/L, and the peak value was 3.6 µg/L. Patients with elevated troponin also had elevated lactate values and base deficit. Additionally, 27% of the patients were on vasopressor medication and 5.8% were treated with beta blockers.

Patients with cardiac injuries and elevated troponin levels had a median troponin value of 12.7 µg/L. In contrast, noncardiac chest injuries were associated with a median troponin value of 3.6 µg/L, which did not differ from the 3.5 µg/L median among patients with nonchest injuries.

In a multivariate analysis, predictors of elevated troponin levels were injury severity (OR 1.7, P=0.023), APACHE II score (OR 2.7, PP=0.006). Chest injury was not predictive, Dr. Eckert noted.

Comparing survivors and nonsurvivors, the investigators found that nonsurvivors had a significantly higher first troponin value (6.1 versus 1.8 µg/L, P=0.012) and peak troponin level (8.2 versus 2.4 µg/L, PPPP=0.001).

In a multivariate analysis controlling for age, sex, injury severity, and mechanism of injury, troponin I elevation increased mortality risk by threefold, compared with patients who had normal troponin I values (OR 3.0, P
The exploratory analysis of survival and beta-blocker treatment revealed similar survival in patients with normal troponin values who received beta-blockers (83%) or did not receive beta-blockers (87%). However, beta-blockade significantly improved the odds of survival in patients with elevated troponin (91% versus 59%, P