Citation

Pinto FC, Oliveira MF, Prist R, Silva MR, Silva LF, Capone Neto A. Arq. Neuropsiquiatr. 2015; 73(6): 499-505.

Affiliation

Unidade de Terapia Intensiva, Hospital Israelita Albert Einstein, Sao Paulo, SP, Brazil.

Copyright

(Copyright © 2015, Associacao Arquivos De Neuro-Psiquitria)

DOI

10.1590/0004-282X20150039

PMID

26083885

Abstract

Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI.

METHOD Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer's (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.

DISCUSSION and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.

Language: en