Hypoxia and hypotension, the “lethal duo” in traumatic brain injury: implications for prehospital care

Excerpt

Sir: Traumatic brain injury (TBI) remains a leading health problem worldwide [1, 2]. In the United States alone, about 1.5 million people sustain a TBI each year, of which approximately 500,000 are admitted to hospital care and 50,000 patients die [2, 3]. It has been estimated that 2.5–6.5 million people currently live with physical, cognitive, or psychological impairment as long-term sequelae of TBI in the United States. One of the central aspects of our current understanding of the pathophysiology of TBI is that the extent of neurological injury is not solely determined by the traumatic impact itself, but rather evolves over time. This “secondary brain injury” occurs as a consequence of complicating processes initiated by the primary injury and is characterized by neuroinflammation, ischemia/reperfusion injuries, cerebral edema, intracranial hemorrhage, and intracranial hypertension [4‐6]. In addition, iatrogenic factors, such as prophylactic hyperventilation and overzealous crystalloid infusion, may contribute to the extent of secondary brain injuries. Those patients who survive the initial trauma are highly susceptible to secondary insults to the injured brain, mainly due to hypoxia and hypotension during the early resuscitative period [7, 8]. A myriad of data from retrospective studies and prospective clinical trials in the past three decades have unequivocally determined these two parameters as independent early predictors of adverse outcome after TBI [9‐15]. …