EFFECT OF ELEVATED TROPONIN-I ON IN-HOSPITAL MORBIDITY AND MORTALITY IN POSTOPERATIVE NONCARDIAC-SURGICAL PATIENTS

L. A. Wibbenmeyer; T. G. Buchman; T. E. Saak; M. J. Sharafuddin; J. H. Landeson; P. R. Eisenberg

doi:10.1097/00003246-199801001-00429

Introduction: Perioperative cardiac morbidity remains the leading cause of death following anesthesia and surgery. The serum marker troponin-l (TNI) is sensitive and specific for perioperative cardiac ischemia. We postulated that elevations in TNI would correlate with perioperative in-hospital cardiac morbidity and mortality. Methods: We retrospectively reviewed medical records of 38 patients (mean age 70±11 yrs, M/F: 22/16) with serum TNI >0.4 ng/mL following noncardiac surgery (mean 10.1 ±11.8). A variety of "risk variables" were analyzed including the presence of preoperative cardiac disease, anemia, systemic disease, and American Society of Anesthesiologists (ASA) score. Also evaluated were the type of surgery, and the degree of perioperative stress as estimated by the stress sum score (1 for each of: general anesthesia, blood loss, total blood administered, total fluids administered, hypotension, tachycardia, length of surgery; range 0-7). "Outcome variables" included in-hospital postoperative cardiac morbidity and mortality events [CHF, arrhythmia, unstable angina, and death), alteration in the medication regimen, length of hospitalization (LOS), acute physiology score (APS), vasopressor dependence, and organ failure). Risk factors for elevated TNI were evaluated using stepwise forward multiple regression analysis. TNI levels were compared to all outcome-related variables using non-parametric statistics. Results: Only intraoperative blood loss correlated significantly with an elevated TNI (r = 44, p > .01). A cutoff TNI level > 20 ng/ml was a significant determinant of mortality (80% for TNI >20 versus 27% for TNI < 20, p < .05 ), although only one death in the TNI > 20 group was attributed to cardiac causes while the remainder were from multiple system organ failure (MSOF). Although there were more cardiac interventions in patients with higher TNI values, this did not reach significance (mean 11.5 ±3.8 versus 9.9 ±12.4, p=.08). Elevated TNI was not associated adversely with any of the above outcome variables. Conclusion: Elevated TNI does not appear to significantly adversely impact any of the evaluated in-hospital postoperative morbidity and mortality variables. However, a large prospective study is needed to verify our results and to determine the impact on long-term cardiac morbidity. The results of this retrospective study do not justify the added cost of evaluating all elevated TNI levels in post-operative patients.

EFFECT OF ELEVATED TROPONIN-I ON IN-HOSPITAL MORBIDITY AND MORTALITY IN POSTOPERATIVE NONCARDIAC-SURGICAL PATIENTS

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