Brain Injury review

This abstract is from Pinto et al from the University of Sao Paulo. It is available in full from the Journal of Trauma, issue number 60, starting on on page number 758.
BACKGROUND

The devastating effects of hypotension on head-trauma-related mortality are well known. This study evaluates the systemic and cerebral hemodynamic responses to volume replacement with 3% hypertonic saline (HSS) or lactated Ringer’s solution (LR), during the acute phase of hemorrhagic shock (HS) associated with traumatic brain injury.

 METHODS

Fifteen dogs were assigned to one of three groups (n = 5, each) according to the volume replacement protocol, infused after traumatic brain injury  (brain fluid percussion, 4 atm) and epidural balloon to an intracranial pressure (ICP) higher than 20 mm Hg and HS, induced by blood removal to a mean arterial pressure (MAP) of 40 mm Hg in 5 minutes: Group HS+traumatic brain injury +HSS (8 mL/kg of 3% HSS), HS+TBI+LR (16 mL/kg LR), and Group HS+TBI (controls, no fluids).

We simulated treatment during prehospital and early hospital admission. Groups HS+ traumatic brain injury  and HS+TBI+LR received shed blood infusion to a target hematocrit of 30%. Measurements included shed blood volume, fluid volume infused to restore MAP, MAP, cardiac output, cerebral perfusion pressure, cerebral and systemic lactate, and oxygen extraction ratios.

RESULTS

Fluid replacement with HSS 3% or LR promoted major hemodynamic benefits over control animals without luids. Cerebral perfusion pressure was higher than controls and similar between treated groups; however, HSS 3% infusion was associated with lower ICP during the “early hospital phase” and a higher serum sodium and osmolarity. CONCLUSION:: In the event of severe head trauma and hemorrhagic shock, the use of HSS 3% and larger volumes of LR promote similar systemic and cerebral hemodynamic benefits. However, a lower ICP was observed after HSS 3% than after LR.

The pubmed number of this article is 16612295

This abstract is taken from the Edwards and Tan paper in Current opinion in pediatrics.

PURPOSE OF REVIEW: The association between perinatal infection and brain injury is widely accepted but a cause-and-effect relationship has not yet been proven. This article summarizes available evidence and current primary publications for debate.

RECENT FINDINGS: Work completed during the review period has reinforced current understanding of perinatal infection, prematurity and brain injury. In animal experiments: lipopolysaccharides have been further implicated in brain injury, not only as a cause of brain injury but also as mediators of preconditioning and protection. Recent studies suggest that cerebral injury following low-dose lipopolysaccharide administration may become compensated in adulthood. Other studies have emphasized the complexity of the response by showing that plasma cytokine levels may not reflect those in the central nervous system or inflammatory events in the brain.

SUMMARY: Perinatal infection and maternofetal inflammation is strongly associated with preterm birth. Inflammation probably represents an important mechanism for cerebral damage, and both overt lesions and maldevelopment can result. Epidemiological data and multiple animal models to link infection, inflammation and brain damage exist, but proof of causation is elusive.

If you are intersted in the full article it can be found under the pubmed ID 16601489

This Abstract is taken from the Journal of International Medical Reserch (2006 Jan-Feb;34(1):58-64.) and is by Liu et al, in the Wang group at the Department of Neurosurgery at Zhejiang University, China.

The Abstract is as follows

We prospectively investigated non-invasive selective brain cooling (SBC) in patients with severe traumatic brain injury. Sixty-six in-patients were randomized into three groups. In one group, brain temperature was maintained at 33 - 35 degrees C by cooling the head and neck (SBC); in a second group, mild systemic hypothermia (MSH; rectal temperature 33 - 35 degrees C) was produced with a cooling blanket; and a control group was not exposed to hypothermia. Natural rewarming began after 3 days. Mean intracranial pressure 24, 48 or 72 h after injury was significantly lower in the SBC group than in the control group. Mean serum superoxide dismutase levels on Days 3 and 7 after injury in the SBC and MSH groups were significantly higher than in the control group. The percentage of patients with a good neurological outcome 2 years after injury was 72.7%, 57.1% and 34.8% in the SBC, MSH and control groups, respectively. Complications were managed without severe sequelae. Non-invasive SBC was safe and effective.

If you are interested in the full article the Pubmed Identification is 16604824