Energy expenditure in acetaminophen-induced fulminant hepatic failure

Objective: To determine energy expenditure in critically ill patients suffe ring from acetaminophen-induced fulminant hepatic failure and compare it wi th values obtained in matched, healthy control subjects and in patients stu died during the anhepatic period of elective liver transplantation. Design: Prospective, controlled, observational study. Setting: A ten-bed intensive therapy unit and a liver transplant unit at a University teaching hospital. Patients and Subjects: Sixteen patients suffering from acetaminophen-induce d fulminant hepatic failure who were sedated, paralyzed, and mechanically v entilated; 16 age-, gender-, and weight-matched, awake, healthy control sub jects; and 16 patients with chronic liver disease, undergoing elective live r transplantation, who were studied during the anhepatic period of surgery. Interventions: None. Measurements and Main Results: The mean energy expenditure was calculated i n each case for a 30-min period, using indirect calorimetry, In the patient s undergoing liver transplantation, measurements were performed after cramp ing the hepatic veins and recipient hepatectomy. Energy expenditure was mar kedly increased in the fulminant hepatic failure group (mean energy expendi ture, 4.05 [SD 0.52] kJ.kg(-1) hr(-1)); in comparison with healthy control subjects (mean, 3.44 [0.27] kJ.kg(-1).hr(-1); mean difference, 18%; p < .00 1) and in comparison with patients during the anhepatic period of liver tra nsplantation (mean, 3.15 [0.61] kJ.kg(-1).hr(-1); mean difference, 29%; p < .001). These differences were even more pronounced when a correction facto r for differences in core temperature was included in the calculation. Harr is-Benedict predictions of energy expenditure were unreliable in the patien ts with acute liver failure. No correlations were found among energy expend iture and hemodynamic variables, the requirement for vasoconstrictors, or t he presence of renal failure. Conclusions: Despite the loss of functioning liver cell mass, the metabolic rate is substantially increased in patients with acetaminophen-induced ful minant hepatic failure. This finding is consistent with the marked systemic inflammatory response, which accompanies acute hepatic failure. The Harris -Benedict equation is unreliable when an estimation of energy expenditure i s required in patients with this condition.