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Prehospital Management of Traumatic Brain Injury

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Prehospital Management of Traumatic Brain Injury Neurosurg Focus 25 (4):E5, 2008 Prehospital management of traumatic brain injury SHIRLEY I. STIVER , M.D., PH.D., AN D GEOFFREY T. MANLEY , M.D., PH.D. Department of Neurosurgery, School of Medicine, University of California San Francisco, California The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and long- term outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are ad- dressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommenda- tions are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury. (DOI: 10.3171/FOC.2008.25.10.E5) KEY WOR ds • hypotension • hypoxia • intracranial hypertension • outcome assessment • traumatic brain injury REA T MEN T of patients with TBI begins at the time reach definitive treatment. The key goals of the emergen- of impact. By its nature, trauma demands focused cy response team are to stabilize and treat damage from attention on the most paramount life-threatening the primary injury, to abrogate or minimize secondary Tproblems. Less urgent problems are relegated to a lesser injury, and to prevent secondary insults at all costs. With priority. However, less urgent does not necessarily equate comparatively few available resources, care in the field with less important. We performed a literature search of (prehospital setting) is a critical determinant of outcome the National Library of Medicine encompassing the years for patients with TBI. 1980 to May 2008 using search terms pertinent to prehos- pital care, emergency triage, trauma system organization, and brain injury. The goal of this review was to evalu- Epidemiology ate the critical role that prehospital management plays in In the US every year, 1.4 million people sustain a the pathophysiology and outcome of TBI. By the time TBI. Trauma is the leading cause of death and disability the patient is in the emergency department, the damage in children and young adults, and TBI accounts for ap- of primary injury has made its mark and the processes proximately 52,000 (or one-third) of all deaths.148 Rough- of secondary injury have been set in motion. The qual- ly twice this number suffer permanent neurological defi- ity of the care rendered in the prehospital setting is as cits. The severity of TBI is categorized based on the GCS important, if not more important, than the time taken to score. Severe TBI (GCS Scores from 3 to 8) comprises approximately 10% of TBI, moderate head injury (GCS scores from 9 to 12) comprise approximately another 10%, and the vast majority of TBI (~ 80%) is classified as mild head injury, presenting with a GCS Score rang- Abbreviations used in this paper: CBF = cerebral blood flow; 78 CPP = cerebral perfusion pressure; GCS = Glasgow Coma Scale; ing from 13 to 15. In the last 30 years, dedicated trauma ICP = intracranial pressure; OR = odds ratio; RSI = rapid sequence programs have demonstrated that aggressive prehospital intubation; TBI = traumatic brain injury. programs reduce morbidity and death from TBI.1,7,9,61,82 Neurosurg. Focus / Volume 25 / October 2008 1 Unauthenticated | Downloaded 09/26/21 04:45 PM UTC S. I. Stiver and G. T. Manley Mechanisms of Injury to hypoxia, a compensatory increase in CBF occurs, but not until the partial pressure of O2 drops to < 50 mm An understanding of the pathophysiological mecha- Hg.50,86,101 Results from the Trauma Coma Data Bank nisms of primary and secondary injury are crucial to set- showed that a low PaO2 (≤ 60 mm Hg) occurred in 46% ting optimal protocols of care to enable further advances of 717 admissions to the emergency department.26 Arte- in the outcome of patients with TBI. Primary injury oc- rial desaturations to this degree, even for a short time, curs at the time of impact and is not reversible. Direct were associated with a 50% mortality rate and 50% se- damage involves contact energy transfer and inertia en- vere disability among survivors.143 Multiple studies have ergy transfer. In addition to these mechanical forces to confirmed that a low PaO2 (< 60 mm Hg) correlates with the brain itself, primary injury also occurs to the cerebral worsened patient outcomes.23,28,104,156 vasculature leading to vessel shear and disruption. Sec- Although airway control is intuitively important, ondary injury evolves as a cascade of cellular events that a few studies have unexpectedly reported worse out- are set in motion at the time of the primary impact. With- comes for patients with TBI who were intubated in the in the first hours after injury a complex array of inflam- field.14,33,37,41,53,110,158 In the field, hypoxia is defined as ap- matory, excitotoxic, oxidative stress, metabolic, vascular, nea, cyanosis, an O2 saturation < 90%, or a PaO2 < 60 mm and mitochondrial mechanisms have been activated and Hg. Marked degrees of hypoxia to saturations < 70% are each has progressed to initiate further injury. The various common during intubation with 57% of patients experi- components of secondary injury interact with each other encing transient hypoxia lasting a mean of 2.3 minutes.51 in a multiplicative rather than additive fashion. Second- The risk of desaturation associated with intubation is de- ary injury is a direct consequence of the primary impact, pendent on the starting O saturation and occurs 100% whereas secondary insults are discrete processes, often 2 of the time if the O2 saturation is ≤ 93%, versus 6% if it iatrogenic, that occur independently of the primary im- is > 93% (p < 0.01).38 A comparison of 1797 patients with pact. Improved outcomes following aggressive treatment severe TBI who were intubated in the prehospital setting of mass lesions, hypoxia, hypotension, and fluid and elec- with 2301 patients who were intubated in the emergency trolyte abnormalities have shown that secondary events 160 department demonstrated a 4-fold increase in death and following TBI are preventable and treatable. a significantly higher risk of poor neurological and func- tional outcome in the group of patients who were intu- Prevention of Secondary Injury in the bated in the field.158 Prehospital and Emergency Setting Endotracheal intubation is associated with risks of increased ICP, aspiration, and hypoxia. The detrimen- Increased ICP, cerebral edema, cerebral dysautoreg- tal effects of aspiration or hypoxia before arrival of the ulation, and alterations in brain metabolism are inherent emergency response team may not be reversible.38 Posi- sequelae of the primary brain injury. Exogenous or iatro- tive pressure ventilation can increase intrathoracic pres- genic events exacerbate these secondary injury processes. sure, which may decrease venous return, and in a hy- Patients with multiple traumas frequently incur injuries povolemic patient this can impair CPP. Furthermore, that compromise cardiopulmonary status, and they are sedative agents used during RSI can cause hypotension.39 therefore particularly vulnerable to secondary injury. Prehospital intubation may also delay transport. Impor- Secondary insults are common and are independent 28,47,102 tantly, endotracheal intubation in the field predisposes predictors of poor outcome in patients with TBI. the patient to an increased incidence of overly aggressive Depth and duration of hypotension, but not hypoxia, has hyperventilation that has been shown to adversely affect been shown to trend in a dose-response manner with the outcome34,36,110 A series of 851 patients with TBI, prehos- 3-month functional Glasgow Outcome Scale score.6 In pital intubation, and a range of PCO2 levels on arrival to contrast, hypoxia and hypotension do not have nearly as the emergency department (17%, PCO2 < 30; 47%, PCO2 profound an effect on outcome in patients with extracra- 30–39; and 26%, PCO2 > 40) were divided into 2 groups. nial trauma. The prehospital guidelines were developed Those within the target PCO2 range of 30–39 had a mor- by the Brain Trauma Foundation (www.braintrauma.org) tality rate of 21%, whereas those whose PCO2 persistently to standardize acute TBI care and prevent secondary inju- 19,59,146 remained outside the target range experienced a mortality ries and insults. Implementation of these guidelines rate of 34%.159 With increasing head severity, there was an with prevention and treatment of
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