Resting energy expenditure in brain death

Citation
M. Bitzani et al., Resting energy expenditure in brain death, INTEN CAR M, 25(9), 1999, pp. 970-976
Citations number
28
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
INTENSIVE CARE MEDICINE
ISSN journal
03424642 → ACNP
Volume
25
Issue
9
Year of publication
1999
Pages
970 - 976
Database
ISI
SICI code
0342-4642(199909)25:9<970:REEIBD>2.0.ZU;2-J
Abstract
Objective: To evaluate resting energy expenditure (REE) in brain dead patie nts and to investigate the hypothesis that the reduction in REE results fro m a decrease in cerebral blood flow. Design: Prospective, open labeled, control study. Setting: General intensive care unit of a tertiary referral teaching hospit al. Patients: 30 critically ill patients with isolated head injury divided in t wo 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 brai n death (GCS = 3). Group 2 patients were divided into two subgroups: Group 2a (n = 11) were admitted as brain dead (GCS = -3) and group 2b (n = 9) wer e admitted with a GCS > 3 and progressed to brain death. Interventions: Clinical and instrumental, using transcranial Doppler sonogr aphy (TCD), diagnosis of brain death. Cerebral blood flow studies of the mi ddle cerebral artery bilaterally by bidimensional TCD and measurement of RE E using indirect calorimetry. Measurements and results: Measurements of REE and TCD studies were performe d simultaneously on admission and after hemodynamic and neurologic stabiliz ation. In cases with progressive neurologic deterioration, serial measureme nts were performed REE values were expressed as percentage of basal metabol ic rate (% BMR), which were estimated according to each patient's gender, a ge, height, and weight. Group 1. patients, had normal TCD patterns througho ut their hospitalization and their REE value was 21 +/- 11% higher than BMR . Group 2 patients demonstrated TCD patterns compatible with brain death an d their REE value was 24.5 +/- 11% lower than BMR (p < 0.01). Group 2 a pat ients, who were admitted as brain dead and remained brain dead, had REE val ues 30 +/- 11% lower than BMR (p < 0.01). Group 2b patients, who were not b rain dead on admission but progressed to brain death, in serial measurement s revealed a significant relationship between REE and TCD findings (R = -0. 77, p < 0.0001). In this subgroup of patients, with multiple regression ana lysis a significant relationship was found only between REE and the TCD pat tern, but not with body temperature. Conclusions: In brain dead patients, REE decreases to values lower than BMR . This can be attributed to the cessation of cerebral blood flow and conseq uently cerebral metabolism and not to hypothermia.