Relationship of metabolic indexes to postoperative mortality in surgical infants

Abstract

Acute injury is known to evoke a metabolic stress response, characterized by cytokine release and reprioritization of hepatic protein synthesis to increase acute phase proteins at the expense of visceral proteins. The impact of these evolving, stress-induced, perioperative metabolic changes on clinical outcome in surgical infants has not yet been determined. The cytokine (tumor necrosis factor [TNF]), acute phase protein (C-reactive protein [CRP]), and visceral protein (prealbumin [PA]) responses to acute metabolic stress were evaluated in 41 infants (average age, 47 days) preoperatively and on postoperative days 1 through 7 (POD 1 to 7) following major surgery. Infants were retrospectively grouped according to whether they survived (group 1) or died within 30 days of surgery (group 2). Peak CRP values in the postoperative period were also included for both groups. Peak CRP levels (14.9 ± 5.5 v 8.1 ± 5.7 mg/dL) were significantly increased ( P = .0056) and preoperative prealbumin levels (6.0 ± 2.7 v 11.0 ± 5.2 mg/dL) were significantly decreased ( P = .0005) in group 2 (nonsurvivors) compared with group 1 (survivors). Though serum TNF levels were substantially increased in nonsurvivors compared with survivors, both preoperatively (16.5 ± 35.2 v 0.6 ± 2.6 pg/mL) and on POD 1 (3.6 ± 6.8 v 0.6 ± 2.7 pg/mL), these values did not reach statistical significance ( P > .05). The most significant difference ( P = .0001) was observed in persistently depressed late (POD 4 to 7) prealbumin levels in nonsurvivors relative to survivors (5.3 ± 3.1 v 10.5 ± 4.3 mg/dL), suggesting an increased risk of poor outcome if acute metabolic stress had not abated by this time. The metabolic response to acute injury is significantly related to clinical outcome (mortality) in surgical infants. Serial monitoring is necessary to delineate the course of the stress response. Such monitoring may be of particular clinical significance in identifying prolonged metabolic stress, which is associated with increased mortality.