PMID: 11009009
Issn Print: 0090-3493
Publication Date: 2000/09/01
Hyperventilation in severe brain injury revisited
Excerpt
During the past four decades, management of traumatic brain injury has advanced on several fronts. The development of prevention programs, improved safety equipment, and safety legislation has positively impacted the epidemiology of head injury. Implementation of rapid transport systems and the advent of trauma centers coinciding with advances in emergency medicine, critical care medicine, and trauma neurosurgery have improved the outcome of the head-injured patient (1). Despite these general technological advances, medical management of the brain-injured patient remains somewhat erratic among centers. A survey of centers treating brain-injured patients showed tremendous variability in treatment protocols (2). This variability is largely because of a poor understanding of the basic pathophysiologic changes in the injured brain. Subsequently, severe brain injury remains one of the most challenging clinical problems facing the critical care physician today. It is particularly important to identify and implement uniform treatment strategies because as much as 40% of the morbidity and mortality of severe brain injury occurs in a delayed setting while the patient is admitted to a critical care unit. Recent advances in neuromonitoring technology have provided us with a better understanding of brain physiology and reaction to injury. This new insight may help us develop cogent strategies that will ameliorate some of this delayed injury and enhance head injury outcome. A major advance in the approach to the management of the head-injured patient was an increased emphasis on cerebral perfusion pressure (CPP) and cerebral blood flow (CBF). Many of the traditional strategies for lowering intracranial pressure (ICP) in the treatment of brain injury actually impair CPP and, thereby, impede CBF with potentially deleterious effects. The Joint Committee on Trauma and Critical Care of the American Association of Neurologic Surgeons and the Congress of Neurologic Surgeons supported by the Brain Trauma Foundation compiled a set of guidelines (1) for the management of patients with severe brain injury. This effort evaluated the existing world literature and made recommendations based on the validity of available clinical data. Through this extensive literature search, only two treatment recommendations, both negative, were well enough supported to be defined as treatment standards. The committee determined that chronic, prolonged hyperventilation therapy (Paco2, <25 torr [3.33 kPa]) should be avoided in the absence of elevated ICP. In addition, although the scientific evidence was not as strong, prophylactic hyperventilation (Paco2, <35 torr [4.67 kPa]) should be avoided in the first 24 hrs after brain injury. The role of brief periods of hyperventilation treating ICP spikes and the use of hyperventilation therapy in the presence of ICP that remains elevated despite conventional ICP lowering therapies remain poorly defined. Hyperventilation had been a mainstay of therapy for increased ICP in traumatic brain injury for decades. The hypocapnea-induced vasoconstriction and subsequent reduction in CBF and cerebral blood volume can rapidly decrease ICP (3, 4). The use of aggressive hyperventilation (Paco2, <25 torr [3.33 kPa]) in an attempt to achieve lower ICP did not, however, translate into improved patient outcome. CBF is already reduced as much as 50% in the immediate postinjury period (5). Further reduction in CBF associated with the induced vasospasm caused by hyperventilation carries the risk of brain tissue ischemia that aggravates the preexisting brain injury. When the use of hyperventilation was studied in a prospective, randomized clinical study, improved outcomes were noted when prophylactic hyperventilation was avoided (6). The role of mild or episodic hyperventilation needs to be further evaluated and clarified.
With new methods of monitoring brain oxygenation now available, several studies have directly measured the effect of artificially lowered Pco2 on brain tissue (7–9). In this issue of Critical Care Medicine, Dr.
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