Resting energy expenditure in brain death

To evaluate resting energy expenditure (REE) in brain dead patients and to investigate the hypothesis that the reduction in REE results from a decrease in cerebral blood flow.

Prospective, open labeled, control study.

General intensive care unit of a tertiary referral teaching hospital.

30 critically ill patients with isolated head injury divided in two groups: group 1 patients (n = 10) with a Glasgow Coma Scale (GCS) score of 4 to 8 and group 2 patients (n = 20), in whom the final outcome was brain death (GCS = 3). Group 2 patients were divided into two subgroups: Group 2 a (n = 11) were admitted as brain dead (GCS = 3) and group 2 b (n = 9) were admitted with a GCS > 3 and progressed to brain death.

Clinical and instrumental, using transcranial Doppler sonography (TCD), diagnosis of brain death. Cerebral blood flow studies of the middle cerebral artery bilaterally by bidimensional TCD and measurement of REE using indirect calorimetry.

Measurements of REE and TCD studies were performed simultaneously on admission and after hemodynamic and neurologic stabilization. In cases with progressive neurologic deterioration, serial measurements were performed REE values were expressed as percentage of basal metabolic rate (%BMR), which were estimated according to each patient's gender, age, height, and weight. Group 1 patients, had normal TCD patterns throughout their hospitalization and their REE value was 21 +/- 11 % higher than BMR. Group 2 patients demonstrated TCD patterns compatible with brain death and their REE value was 24.5 +/- 11 % lower than BMR (p < 0.01). Group 2 a patients, who were admitted as brain dead and remained brain dead, had REE values 30 +/- 11 % lower than BMR (p < 0.01). Group 2 b patients, who were not brain dead on admission but progressed to brain death, in serial measurements revealed a significant relationship between REE and TCD findings (R = -0.77, p < 0.0001). In this subgroup of patients, with multiple regression analysis a significant relationship was found only between REE and the TCD pattern, but not with body temperature.

In brain dead patients, REE decreases to values lower than BMR. This can be attributed to the cessation of cerebral blood flow and consequently cerebral metabolism and not to hypothermia.