Management of Traumatic Brain Injury

Traumatic brain injury (TBI) is a complex disease process that requires constant attention as one manages the associated body systems. Even though an “isolated” brain injury may be the cause for admission to the hospital, the injured brain cannot be thought of in isolation from the remainder of the body. All body systems, from cardiac to pulmonary, need to be addressed as one moves from the initial to the long-term management of the TBI. The multiple issues are best addressed with a dedicated neurocritical care team that is in continuous communication with the neurosurgical team throughout the course of treatment. To date, no pharmacologic treatment has led to improved outcomes after TBI, but it is becoming increasingly clear that advances in the critical care of TBI patients are contributing to better results.     

Models of Traumatic Brain Injury

We present a review of the currently popular preclinical models of non-penetrating traumatic brain injury (TBI). This article focuses on animal models that cause TBI by applying mechanical energy to the head, skull or dura. It attempts to provide a compendium of the main characteristics of each of these experimental models of TBI in respect to acute and chronic histological findings and behavioral impairment in neurologic motor and cognitive function. Finally, several limitations of the described models are discussed briefly.     

Extent of Cognitive Decline in Traumatic Brain Injury Based on Estimates of Premorbid Intelligence

Global cognitive impairment following traumatic brain injury (TBI) is common, with some abilities more significantly affected than others. However, due to difficulties in estimating premorbid intelligence, there has been no systematic evaluation of the extent of decline in different cognitive abilities following TBI. Recent studies indicate that the Wide Range Achievement Test-Revised (WRAT-R) Reading subtest is an accurate estimate of premorbid intelligence, suggesting that post-TBI cognitive test scores can be compared to the WRAT-R to estimate the extent of decline that occurs in specific cognitive abilities. The current study estimated the extent of deficit in intelligence, memory, attention, speed of processing, and cognitive flexibility for 97 outpatients with TBI. Extent of decline was calculated by subtracting WRAT-R z-scores from cognitive test 2-scores to determine a z-difference score (Z_Diff) for each cognitive ability. The results suggest that intelligence is least declined following TBI (WAIS-R 3-4-point decline; VIQ Z_Diff = -0.23: FIQ Z_Diff = -0.27), followed by attention (WMS-R 5-point decline; Z_Diff = -0.31), memory (WMS-R 6-9-point decline; Verbal Memory Z_Diff = -0.41; General Memory Z_Diff = -0.51; Delay Memory Z_Diff = -0.57), speed of processing (Trails A 15-16 second decline; Z_Diff = -1.90) and cognitive flexibility (Trails B 35-52 second decline; Z_Diff = -2.65). Implications for provision of feedback to individuals with TBI and their families are discussed.     

Vision Disturbances Following Traumatic Brain Injury

Opinion statement  

The Role of Neuroinflammation in Traumatic Brain Injury

Abstract In industrialized countries, traumatic brain injury (TBI) still represents the leading cause of death and persisting neurologic impairment among young individuals < 45 years of age. Patients who survive the initial injury are susceptible to sustaining secondary cerebral insults which are initiated by the release of neurotoxic and inflammatory endogenous mediators by resident cells of the central nervous system (CNS). The presence of hypoxia and hypotension in the early resuscitative period further aggravates the inflammatory response due to ischemia/reperfusion-mediated injuries. These are induced by the intrathecal generation of free radicals and activation of the complement cascade. Posttraumatic neuroinflammation is further exacerbated by the subsequent intracranial recruitment of blood-derived immunocompetent cells, leading to secondary cerebral edema and increased intracranial pressure. The profound endogenous neuroinflammatory response after TBI, which is phylogenetically aimed at defending the CNS from invading pathogens and repairing lesioned tissue, is, in large part, responsible for the development of secondary brain damage and adverse outcome. However, aside from these deleterious effects, posttraumatic inflammation mediates neuroreparative mechanisms after TBI as well. This dual effect of neuroinflammation has been the focus of extensive experimental and clinical research in the past years and has led to an expanded basic knowledge on the cellular and molecular mechanisms which regulate the intracranial inflammatory response after trauma. The present article provides an up-to-date overview on the pathophysiological mechanisms of neuroinflammation after TBI. New potential therapeutic strategies for reducing the extent of secondary brain damage after neurotrauma are discussed.     

颅脑创伤与麻醉管理

一、颅脑创伤：病理生理学 颅脑创伤初期的损伤是不可逆的。在初期的损伤之后，继发性损伤主要是由于低氧血症、低血压及颅内高压造成的。加强全身及中枢系统的监测可以用于早期发现和及时处理导致或加重继发性损伤的危险因素。在病人的院前处理、搬运、手术中，或是在ICU都应遵循这条原则。     

Impact of Secondary Insults in Brain Death After Traumatic Brain Injury

In addition to primary injury in severe head trauma, secondary systemic insults that aggravate the brain injury may result in fatal neurologic outcome. We aim to evaluate the correlation between brain death and secondary systemic insults in 100 patients with severe traumatic brain injury (TBI) admitted to the intensive care unit. We collected data on hypotension and hypoxemia at the time of admission to intensive care unit and data on hypotension, hypoxemia, hypocarbia, hypercarbia, shock, anemia, hyperglycemia, and hyperthermia within the first 24 hours. In addition, we recorded the category of TBI according to computed tomography findings. Twenty-six patients (26%) who developed brain death were significantly younger than survivors. Early hypotension (odds ratio [OR], 10.24; 95% confidence interval [CI], 3.64–28.78; P = .000) and early shock (OR, 8.31; 95% CI, 2.65–26.01; P = .000) were significantly more frequent among brain-death patients. The most featured factor that independently predicted the development of brain death in patients with severe TBI was the existence of hypotension (B–2.74; 95% CI, 0.016–0.252; P = .000). The most common type of injury among brain death patients was a surgically evacuated mass lesion. Although all critical care principles are applied to prevent secondary systemic brain insults, when brain death occurs, the prevention of hypotension will become significant in preserving organs in better condition for procurement.     

Extracellular Brain pH and Outcome following Severe Traumatic Brain Injury

The ability to measure brain tissue chemistry has led to valuable information regarding pathophysiological changes in patients with traumatic brain injury (TBI). Over the last few years, the focus has been on monitoring changes in brain tissue oxygen to determine thresholds of ischemia that affect outcome. However, the variability of this measurement suggests that it may not be a robust method. We have therefore investigated the relationship of brain tissue pH (pH(b)) and outcome in patients with TBI. We retrospectively analyzed prospectively collected data of 38 patients admitted to the Neurosciences Critical Care Unit with TBI between 1998 and 2003, and who had a multiparameter tissue gas sensor inserted into the brain. All patients were managed using an evidence-based protocol targeting CPP > 70 mm Hg. Physiological variables were averaged over 4 min and analyzed using a generalized least squares random effects model to determine the temporal profile of pH(b) and its association with outcome. Median (IQR) minimum pH(b) was 7.00 (6.89, 7.08), median (IQR) maximum pH(b) was 7.25 (7.18, 7.33), and median (IQR) patient averaged pH(b) was 7.13 (7.07, 7.17). pH(b) was significantly lower in those who did not survive their hospital stay compared to those that survived. In addition, those with unfavorable neurological outcome had lower pH(b) values than those with favorable neurological outcome. pH(b) differentiated between survivors and non-survivors. Measurement of pH(b) may be a useful indicator of outcome in patients with TBI.