Effect of volume replacement during combined experimental hemorrhagic shock and traumatic brain injury in prostanoids, brain pathology and pupil status

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.

Outcomes after concomitant traumatic brain injury and hemorrhagic shock

“…26 Speed of resuscitation may also be imperative for protecting brain function; animal models using a stepwise ratio-guided protocol with FFP (compared to a bolus protocol) have demonstrated a neuroprotective effect. 27 Additional pharmacologic modalities, such as valproic acid 28,29 and hypertonic saline 30 continue to be studied for the prevention of cerebral metabolic derangements and excitotoxicity in patients with TBI + HS.…”

“…Whereas brain injury has been shown to cause altered vascular compensation in response to HS, 31 questions remain about the relationship between coagulopathy and the size of brain lesions. 15,22,30,32,33 Ratio-guided resuscitation with fresh frozen plasma (FFP) may have beneficial effects for patients with TBI + HS, 15 including fewer inflammatory complications. 5,6,9 In experimental large animal studies, early administration of FFP reduced the size of brain lesions, decreased cerebral edema, and substantially attenuated the degree of neurological impairment.…”

Traumatic Brain Injury—A Review of Intravenous Fluid Therapy

“…Animals resuscitated with HTS had higher CPP, lower ICP, higher serum sodium and osmolarity, less cerebral edema, and faster return of pupil responses compared to animals resuscitated with LRS. When animals were further resuscitated by returning their shed blood to maintain MAP >70 mmHg there was no difference in total volume infused between groups (64). In a rat model of TBI and hemorrhage, HTS (7.5%) resuscitation was associated with improved longterm neuronal survival as well as faster and more complete behavioral recovery compared to 0.9% sodium chloride or no resuscitation (65).…”

“…However, in patients with intracranial hypertension both HTS (3-23.4%) and mannitol effectively lower ICP (33,62). In two experimental dog models of TBI and hemorrhage the animals were resuscitated with either 3% HTS (8 mL/kg) or LRS (16 mL/kg) (63,64). Animals resuscitated with HTS had higher CPP, lower ICP, higher serum sodium and osmolarity, less cerebral edema, and faster return of pupil responses compared to animals resuscitated with LRS.…”