Protecting the Brain During Severe Hemorrhagic Shock

Peter Safar, Samuel Tisherman, Peter Carrillo, Akira Takasu, Gretchen Stolz, C. Edward Dixon, Gad Bar-Joseph, Ann Radovsky, Gutti Rao, S. William Stezoski
1997 Prehospital and Disaster Medicine  
Some patients who have survived severe hemorrhagic shock (HS) without brain trauma seem to have some persistent neurobehavioral deficits. This report, relevant for traumatology, concerns unpublished data in monkeys and rats on studies which advance the hypothesis that cerebral vasodilation protects the brain during HS as long as mean arterial blood pressure (MAP) is maintained at or above 40 mmHg. Monkey studies: Under normothermia throughout, lightly anesthetized cynomolgus monkeys were
more » ... d with hemorrhage by volume-controlled blood withdrawal followed by pressure controlled maintenance of HS at MAP 30 mmHg over 2 hours (h). All-out fluid resuscitation and controlled ventilation to 20 h were followed by intensive care to 72 h with evaluation of overall performance categories (OPC 1-5) and neurologic deficit scores (NDS 0-100%). At 72 h after perfusion fixation, brain histologic damage (HD) was scored in 20 brain regions. All 72 h survivors had OPC 1 (normal), NDS 0-10% (normal), and histologically "clean" brains, with no ischemic (pink, shrunken, pyknotic) neurons. Rat studies: Under normothermia throughout, 10 lightly anesthetized rats (in comparison with 10 sham experiments and 5 normal controls were insulted with hemorrhage of 2 ml/lOOg over 10 minutes (min.), followed by further withdrawal or reinfusion of blood to maintain MAP at 40 mmHg to 60 min. without heparinization. Then, all-out fluid resuscitation to normotension and Hct of 30% were followed by MAP controlled to 1 h and observation to 10 days, for the determination of OPC, NDS, and HD scoring; and special motor and cognitive function tests. The 10 HS rats with 10 day survival had, from 72 h on, OPC 1 (normal), NDS 0-10% (normal), and under light microscopy, histologically "clean" brains, when 6 coronal sections were scored and hippocampal neurons counted (compared with shams). Motor and cognitive water-maze learning tests showed no difference between HS and sham rats. Acute (<4 h) abnormal motor function in beam balance and beam walking tests, was attributed to femoral artery ligation. An additional 10 rats were subjected to MAP 30 mmHg for 45 min. MAP of 30 mmHg frequently led to cardiac arrest before 60 min. Brain outcome results after MAP of 30 mmHg are in progress and also will be reported. Conclusions: We conclude that clinical guidelines for hypotensive fluid resuscitation during severe HS to maintain MAP at about 40 mmHg seem reasonable to prevent even subtle brain damage.
doi:10.1017/s1049023x00046318 fatcat:5zwra5bzp5dpzowadp4zndmmmu