It is common for emergency physicians (EPs) to care for patients who

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1 An Evidence-Based Approach To Severe Traumatic Brain Injury You have just started your shift and the charge nurse informs you that EMS has arrived with a 48-year-old man who was involved in a high-speed motorcycle collision. He was not wearing a helmet. He was initially awake and combative on-scene but became lethargic and unresponsive en route to the hospital. He was intubated by EMS prior to arrival. His pupils are unequal; the left is dilated and unreactive. His blood pressure is 136/78; heart rate is 88; oxygen saturation is 100%. He does not respond to verbal or painful stimuli. You suspect that the patient has a severe traumatic brain injury and realize that any hope for a meaningful recovery depends on your ability to mobilize resources, manage the intracranial pressure, and maintain the cerebral perfusion pressure. Before you even have time to finalize your plan, the EMS radio comes alive. The paramedics are bringing a 78-year-old woman with a history of dementia from a nursing home. The report notes that she suffered a minor fall yesterday, was lethargic this morning, and the staff could not arouse her from her nap this afternoon. According to the paramedics, she has a hematoma on her forehead and is protecting her airway but responds only to painful stimuli by withdrawing. Her vital signs are stable. EMS is requesting to use RSI to intubate her prior to transport and you are considering the wisdom of their request. It is common for emergency physicians (EPs) to care for patients who have suffered head injuries. Traumatic brain injuries (TBIs) remain a devastating consequence of accidents worldwide and are a leading cause of disability and death in all age groups. In addition to profound and permanent disability, these injuries often lead to diminished qual- Authors December 2008 Volume 10, Number 12 Rahul Bhat, MD Assistant Professor of Emergency Medicine, Georgetown University Hospital; Washington Hospital Center, Washington, DC Korin Hudson, MD, NREMT-P Attending Physician, Georgetown University, Washington, DC Tina Sabzevari, MD Resident Physician, The George Washington University Hospital, Washington, DC Peer Reviewers John J. Bruns, Jr, MD Clinical Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY Jeffrey J. Bazarian, MD, MPH Associate Professor of Emergency Medicine and Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY CME Objectives Upon completion of this article, you should be able to: 1. Identify a patient with a severe traumatic brain injury. 2. Initiate appropriate evaluation and treatment of patients with severe traumatic brain injury. 3. Recognize potentially confounding diagnoses. 4. Be familiar with the most up-to-date treatment modalities for the prevention of secondary brain injury. 5. Be aware of the controversies regarding various treatment options. Date of original release: December 1, 2008 Date of most recent review: November 10, 2008 Termination date: December 1, 2011 Medium: Print and Online Method of participation: Print or online answer form and evaluation Prior to beginning this activity, see Physician CME Information on the back page. Editor-in-Chief Andy Jagoda, MD, FACEP Professor and Vice-Chair of Academic Affairs, Department of Emergency Medicine, Mount Sinai School of Medicine; Medical Director, Mount Sinai Hospital, New York, NY Editorial Board William J. Brady, MD Professor of Emergency Medicine and Medicine Vice Chair of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA Peter DeBlieux, MD Professor of Clinical Medicine, LSU Health Science Center; Director of Emergency Medicine Services, University Hospital, New Orleans, LA Wyatt W. Decker, MD Chair and Associate Professor of Emergency Medicine, Mayo Clinic College of Medicine, Rochester, MN Francis M. Fesmire, MD, FACEP Director, Heart-Stroke Center, Erlanger Medical Center; Assistant Professor, UT College of Medicine, Chattanooga, TN Michael A. Gibbs, MD, FACEP Chief, Department of Emergency Medicine, Maine Medical Center, Portland, ME Steven A. Godwin, MD, FACEP Assistant Professor and Emergency Medicine Residency Director, University of Florida HSC, Jacksonville, FL Gregory L. Henry, MD, FACEP CEO, Medical Practice Risk Assessment, Inc.; Clinical Professor of Emergency Medicine, University of Michigan, Ann Arbor, MI John M. Howell, MD, FACEP Clinical Professor of Emergency Medicine, George Washington University, Washington, DC;Director of Academic Affairs, Best Practices, Inc, Inova Fairfax Hospital, Falls Church, VA Keith A. Marill, MD Assistant Professor, Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA Charles V. Pollack, Jr., MA, MD, FACEP Chairman, Department of Emergency Medicine, Pennsylvania Hospital, University of Pennsylvania Health System, Philadelphia, PA Michael S. Radeos, MD, MPH Research Director, Department of Emergency Medicine, New York Hospital Queens, Flushing, NY; Assistant Professor of Emergency Medicine, Weill Medical College of Cornell University, New York, NY. Robert L. Rogers, MD, FACEP, FAAEM, FACP Assistant Professor of Emergency Medicine and Medicine Director of Undergraduate Medical Education, Department of Emergency Medicine, The University of Maryland School of Medicine, Baltimore, MD Alfred Sacchetti, MD, FACEP Assistant Clinical Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA Scott Silvers, MD, FACEP Medical Director, Department of Emergency Medicine, Mayo Clinic, Jacksonville, FL Corey M. Slovis, MD, FACP, FACEP Professor and Chair, Department of Emergency Medicine, Vanderbilt University Medical Center, Nashville, TN Jenny Walker, MD, MPH, MSW Assistant Professor; Division Chief, Family Medicine, Department of Community and Preventive Medicine, Mount Sinai Medical Center, New York, NY Ron M. Walls, MD Professor and Chair, Department of Emergency Medicine, Brigham and Women s Hospital,Harvard Medical School, Boston, MA Scott Weingart, MD Assistant Professor of Emergency Medicine, Elmhurst Hospital Center, Mount Sinai School of Medicine, New York, NY Research Editors Nicholas Genes, MD, PhD Chief Resident, Mount Sinai Emergency Medicine Residency, New York, NY Lisa Jacobson, MD Mount Sinai School of Medicine, Emergency Medicine Residency, New York, NY International Editors Valerio Gai, MD Senior Editor, Professor and Chair, Department of Emergency Medicine, University of Turin, Turin, Italy Peter Cameron, MD Chair, Emergency Medicine, Monash University; Alfred Hospital, Melbourne, Australia Amin Antoine Kazzi, MD, FAAEM Associate Professor and Vice Chair, Department of Emergency Medicine, University of California, Irvine; American University, Beirut, Lebanon Hugo Peralta, MD Chair of Emergency Services, Hospital Italiano, Buenos Aires, Argentina Maarten Simons, MD, PhD Emergency Medicine Residency Director, OLVG Hospital, Amsterdam, The Netherlands Accreditation: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education (ACCME) through the sponsorship of EB Medicine. EB Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr. Bhat, Dr. Hudson, Dr. Sabzevari, Dr. Bruns, Dr. Bazarian and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Commercial Support: Emergency Medicine Practice does not accept any commercial support.

2 ity of life as well as major lifestyle and social changes. TBIs also have a significant economic impact given the intensive management, long-term consequences, and extensive rehabilitation that are involved. Whether working at a small community hospital or in a Level I trauma center, EPs play a critical role in the diagnosis and management of severe TBIs. This management begins as soon as the injury occurs with appropriate recognition of potentially severe injury, activation of EMS, and rapid transport or transfer to an appropriate facility. Once in the emergency department (ED), rapid diagnosis and proper treatment will have a significant impact on the patient s overall morbidity and mortality. The most commonly used method for grading the severity of brain injury is the Glasgow Coma Score (GCS) (see Table 1) and should only be scored after any required resuscitative measures. Developed by Teasdale and Jennett in 1974, the GCS uses 3 aspects of neurologic function: eye opening, verbal response, and motor response to permit serial evaluations of patients and facilitate communication between care providers. 1 The initial studies that used the GCS required the presence of coma for at least 6 hours. 2,3 The scale was not originally intended to replace a neurologic examination and was not designed for patients with mild or moderate TBIs. A single GCS is insufficient to determine the extent of injury after trauma and does not have prognostic value. 1 Serial GCSs are ultimately helpful in predicting clinical outcomes. A high GCS that decreases or a low GCS that remains low portends a poorer outcome than a persistently high GCS or a low GCS that improves gradually. 3-5 While a perfect GCS correlates with a low rate of intracranial pathology, a single high GCS does not eliminate the possibility of lesions requiring neurosurgical intervention, with up to 13% of patients with an initial GCS of 15 ultimately developing coma. 3,4 The GCS scale is used to grade the severity of TBIs and classify patients with mild, moderate, or severe head injuries. For patients with a history of head trauma, the classification is as follows: mild injury for a GCS of 13 to 15, moderate injury for a GCS of 9 to 12, and severe head injury for a GCS of 3 to 8. While there are several different TBI severity scales, overall Table 1. Glasgow Coma Score Eye Opening (E) Verbal Response (V) Motor Response (M) 4=opens spontaneously 3=opens to voice 2=opens to pain 1=none Adapted from ACS ATLS 6 5=normal conversation 4=disoriented conversation 3=words, incoherent 2=incomprehensible sounds 1=none 6=normal 5=localizes pain 4=withdraws from pain 3=decorticate posturing 2=decerebrate posturing 1=none severe TBIs account for approximately 10% of cases, moderate TBIs account for another 10%, and the remaining 80% of cases are categorized as mild. 7 Patients with severe TBI clearly benefit from prompt and effective emergency care, since most of the pathology that determines long-term outcome will be present in the first hours after TBI. 8 Therefore, a concise, clear, and practical approach to the evaluation and treatment of patients with severe traumatic brain injuries is necessary to avoid delays in management and minimize secondary brain injury. This issue of Emergency Medicine Practice is designed to provide an evidence-based approach to the evaluation and management of patients with blunt trauma to the head resulting in moderate to severe TBI. The scope of this discussion will be limited to adults as the evaluation and management of pediatric patients was recently reviewed in Pediatric Emergency Medicine Practice, December Critical Appraisal Of The Literature Current evidence regarding the management of severe TBI is mainly limited to consensus statements and Class II (moderate quality randomized controlled trials or good cohort or case controlled studies) and Class III (poor quality randomized controlled trials, moderate cohort or case controlled studies, or case series) studies. As with most areas of trauma research, there are few prospective randomized controlled trials specifically addressing any of the myriad management issues. The literature search was initiated using Ovid MEDLINE and PubMed to review articles from 1966 to Keywords used included traumatic brain injury and were limited to English articles only. A search of guidelines.gov, the National Guideline Clearinghouse, using the search term traumatic brain injury yielded 81 guidelines, 3 of which were pertinent to this article. 9 The Cochrane review was also searched using the same keywords and resulted in 88 results, 15 of which were relevant to emergency medicine and used for this review. As of the date of publication of this review, the American College of Emergency Physicians has no policy statement regarding management of severe traumatic brain injury, only a guideline for imaging in mild traumatic brain imaging. The most recent comprehensive review of the literature regarding management strategies in severe TBI was published in the Journal of Neurotrauma 2007 supplement. 10 The review was a joint collaboration between the Brain Trauma Foundation (BTF) and the Joint Section on Neurotrauma and Critical Care from the American Association of Neurological Surgeons (AANS) and Congress of Neurological Surgeons (CNS). The review looked at 15 areas of clinical controversy and resulted in one Level I (standard) recommendation and a mix of Level II Emergency Medicine Practice EBMedicine.net December 2008

3 (guidelines) and III (options) recommendations. In 2007, the BTF updated Guidelines for Prehospital Management of Traumatic Brain Injury. 11 These guidelines reviewed 7 key topics for the prehospital management of patients with TBI. Again, there was not sufficient data for Level I recommendations for prehospital treatment, but several Level II and Level III recommendations are discussed. Epidemiology and Etiology Traumatic brain injuries pose an important public health problem in the United States, with clinical manifestations ranging from mild concussion to coma and even to death. Severe TBI may not be well documented given that many of these critical patients may die at the scene or en route to the hospital. 12 Still, each year in the United States at least 1.4 million people sustain a TBI. 13 Of these, close to 50,000 die and 235,000 require hospitalization. The highest incidence of TBI occurs among males between the ages of 15 to 24 years and those 75 years of age and older. Falls, especially in children 0 to 4 years of age and in adults over the age of 75, are the leading cause of severe TBI. 13 This is followed by motor vehicle collisions, assaults, sports-related injuries, and other penetrating traumas. (See Figure 1.) TBIs may be described according to the primary or secondary injury. Primary injury occurs at the moment of insult and is caused by the initial mechanical forces generated by direct trauma to the head. During the primary injury, collision of the head with a surface or contact of the brain inside of the skull leads to epidural or subdural hematomas, subarachnoid or intraventricular hemorrhages, or cerebral contusions. Subdural hematomas are much more common and are present in between 12% and 29% of patients who have sustained a severe TBI. 14 Secondary injuries occur within hours to several days after the initial traumatic event and result from ongoing cellular damage from the release of calcium, excitatory amino acids, and other neurotoxins in response to impaired cerebral blood flow, edema, or increased intracranial pressure. 15 It is this hypoperfusion, in conjunction with increased metabolic demands, that makes the brain more susceptible to the hypotension, hypoxia, and neuronal damage involved in secondary injuries. Emergency intervention should be aimed at preventing or minimizing the ischemia and edema associated with secondary injury. 16 Traumatic intracranial hemorrhages can be epidural, subdural, subarachnoid, or intraparenchymal. Epidural hematomas most often result from a lateral skull fracture that lacerates the middle meningeal artery or vein and leads to the accumulation of blood between the skull and dura mater. (See Figure 2, page 4.) Usually the underlying brain parenchyma is minimally injured, and if rapid surgical decompression and repair are performed, patients have lower rates of mortality and a significant decrease in midline shift. 17 Subdural hematomas occur in the setting of trauma as a result of shearing injury or rupture of the bridging cortical veins. This leads to an accumulation of rapidly clotting blood external to the brain and arachnoid mater and below the dura. Cerebral injury is due to the direct pressure from the collection of blood, increase in intracranial pressure, and cerebral vasoconstriction, which leads to ischemia and restriction of blood flow to the brain. (See Figure 3, page 4.) Rupture or damage to the arteries surrounding the subarachnoid space leads to buildup of blood in the space between the pia mater and arachnoid, also known as a subarachnoid hemorrhage. (See Figure 4, page 5.) The accumulation of blood in the subarachnoid space leads to an elevation in intracranial pressure, decreased cerebral perfusion, and an altered level of consciousness. The delayed effects of subarachnoid bleeding include vasospasm, hydrocephalus, and cerebral infarction. Death in patients with traumatic subarachnoid hemorrhages is often related to the severity of the initial mechanism of injury rather than to the effects of vasospasm and secondary brain damage. 18 Intraparenchymal hemorrhage refers to the accumulation of blood within the brain parenchyma or the surrounding meningeal spaces. (See Figure 5, on page 5.) Substantial growth of the hemorrhage in patients with intraparenchymal bleeding is common after trauma, and the associated edema and compression of the brain is more likely to lead to elevated intracranial pressures, neurologic dysfunction, and fatal herniation. 19 Diffuse axonal injury is the result of shearing or Figure 1 - Percentage Of Average Annual Traumatic Brain Injury-Related Emergency Department Visits, Hospitalizations, And Deaths Assault: 11% Motor vehicle collisions: 20% Struck by or against objects: 19% Falls: 28% Unknown: 9% Other: 13% Adapted from Langlois J, Rutland-Brown W, Thomas K, Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths, Centers for Disease Control and Prevention, national Center for Injury Prevention and Control, December 2008 EBMedicine.net 3 Emergency Medicine Practice 2008

4 rotational forces that occur when the head is rapidly accelerated or decelerated, as in the case of motor vehicle collisions, falls, or assaults. These injuries are a significant cause of morbidity in patients suffering from traumatic brain injuries. The pathology of diffuse axonal injury is most commonly characterized by widespread damage to the axons located in the gray-white matter junctions of the cerebral cortex. 20 The stretching of axons leads to a physical disruption and proteolytic degradation of the cytoskeleton, which leads to the opening of sodium and calcium channels. 21 The influx of ions along with secondary biochemical cascades leads to the degradation of intracellular products and eventual cell death. 22 These injuries are often difficult to detect with standard imaging techniques and thus should be suspected in patients with persistently altered levels of consciousness. Pathophysiology Many aspects of the pathophysiology of TBIs are crucial to shaping the clinical management of patients with brain injuries. TBI is a dynamic process with several contributing factors and cascading events, 23 as seen in Figure 6, page 6. Intracranial pressure (ICP) represents the pressure within the calvarium and is normally determined by the volume of the intracranial components consisting of brain, blood, and cerebrospinal fluid (CSF). Under abnormal conditions, such as in the case of TBI, these volumes may be Figure 2. Epidural Hematoma (CT Scan) supplemented with mass lesions and collections of blood. 24 Because the intracranial compartment is an enclosed space, any additional volume will lead to an increase in the ICP. ICP is useful for expressing the pressure within the intracranial compartment; it is also useful in following the cerebral perfusion pressure (CPP). CPP is defined as the difference between the mean arterial pressure (MAP) and the ICP (CPP = MAP - ICP). CPP serves as a rough estimate of cerebral blood flow (CBF) and correlates well with clinical outcomes following brain injuries. 24 Maintenance of adequate CPP is key in normal brain functioning. In the normal brain, when the MAP is between 60 and 150 mm Hg, cerebral vessels work to maintain desirable CBF through their ability to constrict and dilate. 25 This is termed autoregulation. When an injury occurs, this regulation is disrupted and leads to changes in the CBF. Because of these relationships, it is essential to avoid hypotension as well as prevent increases in ICP in patients with brain injuries so that the CPP can be maintained to sustain cerebral metabolic demands. Differential Diagnosis The most important step in evaluating a patient with a GCS of less than 9 is to maintain a broad differential and avoid premature closure on any one diagnosis. (See Table 2.) In addition, it is important to remember that the circumstances leading to a TBI may have been precipitated by a non-cns event (eg, hypoglycemia, myocardial infarction, seizure). A significant portion of the over 110 million ED visits in the United States each year is related to Figure 3. Subdural Hemtoma (CT Scan) Image is courtesy of Dr. Frank Berkowitz, MD, Department of Radiology, Georgetown University Hospital. Image is courtesy of Dr. Frank Berkowitz, MD, Department of Radiology, Georgetown University Hospital. Emergency Medicine Practice EBMedicine.net December 2008

5 unhealthy patterns of substance abuse, 26 with the role of alcohol and other substances well-documented as strong predisposing factors in traumatic brain injuries. In individuals with traumatic injuries, 1 study noted the prevalence of substance abuse within the last 12 months to be 12.3% for alcohol and 2.5% for other substances including marijuana, cocaine, and amphetamines. 27 More specifically, it has been estimated that more than 60% of TBIs are alcohol and substance related. 28 Clinical studies have shown that alcoholintoxicated patients with severe TBI were more likely Figure 4. Subarachnoid Hemorrhage (CT Scan) Image is courtesy of Dr. Frank Berkowitz, MD, Department of Radiology, Georgetown University Hospital. Figure 5. Intraparenchymal Hemorrhage (CT Scan) to require intubation and neurosurgical intervention and eventually had poorer neurological outcomes, increased complications, and higher death rates. 29,30 Hypoglycemia is a common metabolic emergency that results in mental status changes and can lead to permanent neurologic damage and death if left untreated. Classically, hypoglycemia in the ED occurs in the diabetic patient with altered mental status who is taking either insulin or oral agents. Less often, hypoglycemic patients may present with focal neurologic deficits or seizure activity. 31,32 Hypoglycemia can also masquerade as traumatic head injury in the setting of falls, motor vehicle collisions, or other traumatic events. The risk in clinical practice is to focus on the injuries and fail to check the blood glucose level. 33 Thus, the consideration and rapid recognition of hypoglycemia in the setting of traumatic events is essential, and a serum blood glucose level should be performed even when the clinical picture appears to be explained by other findings. 33 Nonconvulsive status epilepticus refers to a change in behavior or mental status without tonicclonic motor activity. It is definitively diagnosed through electroencephalographic recordings. 34 Clinical manifestations vary considerably and range from psychotic states to delirium and coma. Common signs and symptoms include lethargy, confusion, unresponsiveness, obtundation, or hallucinations. Nonconvulsive status epilepticus is often under-diagnosed, requires a high level of suspicion (eg, hyperreflexia, upgoing toes, incontinence, tachycardia), and in the setting of trauma or other injuries, can be a potentially treatable cause of altered awareness. 35 Prehospital Care The prehospital management of patients with severe TBI begins with bystander and emergency medical system (EMS) activation. EMS providers must quickly assess the patient and make an appropriate decision about whether the patient should be Image is courtesy of Dr. Frank Berkowitz, MD, Department of Radiology, Georgetown University Hospital. December 2008 EBMedicine.net Table 2. Differential Diagnosis Of Altered Mental Status In The Patient With TBI Epidural hematoma Subdural hematoma Subarachnoid hematoma Intraparenchymal hemorrhage Diffuse axonal injury Acute stroke Other non traumatic causes Drug or toxin exposures Infections Nonconvulsive status epilepticus Post-ictal state Metabolic causes hypoglycemia Psychogenic states 5 Emergency Medicine Practice 2008

6 transported by air or by ground. Further, they must decide whether the patient should be transported to the nearest ED, even if it is a community hospital, or whether the patient should be transported directly to a Level I trauma center, which may be farther away. Finally, EMS providers must provide appropriate treatment of the brain-injured patient while en route to the hospital. As mentioned previously, the Brain Trauma Foundation s Guidelines for Prehospital Management of Traumatic Brain Injury 36 reviews the literature on key topics related to the prehospital care of the patient with TBI and several recommendations are discussed here. Dispatch The prehospital course of the patient with severe TBI begins at the moment of injury. Bystanders should activate EMS via 911 or other appropriate emergency response system. Trained call takers should attempt to elicit key information from bystanders including mechanism of injury, loss of consciousness, and patient s current status (level of consciousness, pulse, respirations, etc). Though there are no data to indicate which questions yield information that may affect outcome, there are several studies that show the utility of EMS priority dispatch. 37,38 There are no Class I studies that evaluate the benefit of advanced life support (ALS) versus basic Figure 6. Contributing Events In The Pathophysiology Of Secondary Brain Injury Systemic Insults Head Injury Transient Neuronal Depolarization Intracranial Lesion life support (BLS) in trauma patients and there is no proven benefit for the use of ALS in patients with TBI. 39,40 EMS training and certification levels vary a great deal from state to state, and variations in training and in dispatch protocols may bias mortality data when more highly trained providers care for more seriously injured patients. Still, many EMS systems will dispatch the highest available level of ALS when severe trauma, including TBI, is suspected. Initial Assessment The first emergency providers on scene should first perform a rapid assessment of airway, breathing, and circulation and determine the patient s degree of disability (an A-B-C-D assessment). The degree of disability is generally defined by GCS as described previously. GCS is the most widely used clinical measure of the severity of TBI. 41 The GCS scale is widely known, recognized, and understood, and it has inter-rater reproducibility making serial examinations useful even when performed by different providers/practitioners. 42 A retrospective study by Davis et al of over 12,000 patients with moderate to severe TBI showed a high correlation between GCS measured by prehospital providers in the field and GCS measured upon arrival at the hospital. 43 After the initial evaluation, EMS providers should quickly evaluate the patient for other injuries. Assessment and treatment of other traumatic injuries should proceed according to regional EMS protocols. Care should be taken to maintain full spinal immobilization as spine injuries may accompany severe head injuries. 44 A full set of vital signs should be obtained, including oxygen saturation whenever possible. In addition, patients with altered mental status should have rapid assessment of blood glucose as severe hypoglycemic and hyperglycemic episodes may be the cause of the trauma and may contribute to altered mental status. Vital signs and the neurologic examination should be reassessed frequently. Cerebral Ischemia Metabolic Failure Neurotransmitter Release Neuronal Excitation Cell Energy Failure Membrane Disruption Cellular Edema Microanatomic Disruption Cerebral Edema Brain Swelling Adapted from Emerg Med Clinic North Am Impaired Autoregulation Altered CBF Transport Decision All areas should have an organized trauma system and should develop protocols that direct EMS providers regarding the treatment and transport of trauma patients. 11 Patients with severe TBI or patients with TBI and other traumatic injuries should be rapidly transported to the nearest Level I trauma center, even if another facility is closer. These centers have committed to having 24-hour availability of CT scanning, advanced monitoring capabilities, trauma surgeons, and neurosurgical services. 45,46 Patients transported first to a community hospital may have a delay in reaching definitive and/or specialist care. In a prospective study of 1123 patients with severe TBI, Härtl and colleagues found a 50% increase in mortality for patients who were transferred to a Level I trauma center from a non-trauma hospital compared to those Emergency Medicine Practice EBMedicine.net December 2008

7 who were transported to the trauma center directly. 47 Trauma centers have been shown to improve outcomes for all trauma patients, 48 and higher volume trauma centers have been found to have better patient outcomes than centers that treat fewer patients. 49 Several studies have evaluated the effectiveness of aeromedical transport vs. ground transport for patients with severe TBI. Aeromedical transport generally offers more highly trained medical providers with more critical care experience (nurseparamedic, nurse-nurse, or nurse-physician teams vs. paramedic-paramedic, or paramedic-emt teams on an ALS ground unit). Air crews may be able to provide advanced airway maneuvers, more advanced monitoring, and may be able to offer a greater range of pharmacotherapy than ground EMS units. Further, helicopters can transport patients rapidly over greater distances so that they reach definitive care more quickly. 50,51 Retrospective analysis of patients with moderate to severe TBI suggests improved outcomes in those transported by air. Those with the most severe injuries appear to derive the greatest benefit. 52 There are some situations, especially in urban EMS systems, where air transport is impractical or when the delay to wait for a helicopter may be longer than the transport time by ground. EMS providers must weigh these factors and must decide on a case-by-case basis which method of transport will provide patients with the best care and the fastest transport to an appropriate facility. Prehospital Treatment The most important aspect of prehospital treatment is avoidance of hypotension and hypoxemia as they are significant contributors to secondary injury and poorer outcomes. A single episode of hypotension (defined as systolic blood pressure less than 90 mm Hg) in a patient is associated with doubling of mortality and increased morbidity when compared to similar patients without hypotension. 53,54 While hypotension is independently associated with worse outcomes, no Class I study has directly evaluated the efficacy of preventing or correcting early hypotension or identifying an optimal blood pressure threshold in improving overall outcomes. Still, it is generally agreed that blood pressure should be frequently monitored and hypotension should be avoided when possible. A great deal of controversy surrounds what treatment modalities are best to achieve this goal. Isotonic crystalloid solutions are most commonly used in the prehospital setting, but there is scant data published to support its use. Wade and colleagues described a cohort study of 223 patients in which patients receiving a hypertonic saline and dextran-70 solution had a survival benefit over those who received standard fluid resuscitation (isotonic crystalloid). 55 However, in a prospective study of hypertonic saline versus lactated ringers as initial resuscitation fluid in hypotensive patients with traumatic brain injury, Cooper et al did not report a significant difference in outcomes between the 2 groups. 56 At this time there are insufficient data to support the use of one type of fluid resuscitation over another in the prehospital setting. Fluid resuscitation with both crystalloid solutions and colloid solutions has been studied and is discussed further in the ED Management section of this article. As with hypotension, a single episode of prehospital hypoxemia (defined as apnea, cyanosis, hemoglobin oxygen saturation less than 90% or PaO 2 less than 60 mm Hg by arterial blood gas analysis) also has an adverse impact on mortality from severe TBI. 57 Supplemental oxygen should be delivered to all patients with severe TBI in order to maintain adequate oxygen saturation. Patients with a GCS less than or equal to 8 who are unable to maintain their airway or oxygenation with supplemental oxygen should have their airways secured with an airway adjunct. 58 However, controversy exists over what methods should be used to secure an airway in patients with severe TBI in the prehospital setting. Specifically, there is debate over whether prehospital endotracheal intubation with or without the use of neuromuscular blockade is beneficial or potentially harmful to patients with severe TBI who are maintaining their oxygenation. Winchell and Hoyt performed a retrospective study of 1092 patients that showed a decrease in mortality in patients with severe traumatic brain injury from 57% to 36% in the prehospital intubation group. 59 However, Wang and colleagues have suggested adverse outcomes for prehospital intubation in patients with severe TBI. In a retrospective study of 4098 patients, they described an increased adjusted odds ratio for death, poor neurologic outcome, and severe functional impairment after prehospital intubation compared to patients with similar injuries that were intubated in the ED. 60 Davis and colleagues suggested that perhaps the reason that severe TBI patients with early intubation have been shown to have worse outcomes is because they are inadvertently hyperventilated or because they have hypoxemic episodes during or after intubation attempts. 61,62 Davis et al suggested that the use of end-tidal capnometry monitoring decreases the adverse events seen with inadvertent hyperventilation. 63 Still others maintain that intubated TBI patients have worse outcomes because they are more critically ill than TBI patients who are not intubated. Most studies attempt to control for this by comparing patients with similar injury severity scores. Davis et al suggested that rapid sequence intubation using neuromuscular blockade improves the success rate of paramedic intubation. 64 In a retrospective study of 2012 patients with TBI, Bulger and colleagues showed that patients intubated with the December 2008 EBMedicine.net 7 Emergency Medicine Practice 2008

8 use of neuromuscular blockade were more likely to survive and have a good outcome than those who were intubated without the use of neuromuscular blockade. 65 However, in a prospective study of 114 patients, Ochs et al suggested that this technique may significantly increase on-scene time. 66 Regardless of the protocol used, the most highly trained and experienced provider available should always perform advanced airway skills and care should be taken to minimize the extent that advanced airway maneuvers delay on-scene time. The training and on-going assessment of all providers performing advanced airway skills should be frequently evaluated. Blood pressure, oxygenation, and when possible end-tidal CO 2 monitoring should be used in all patients with invasive airway adjuncts to confirm correct placement and to prevent hypoxemia or hyperventilation. Further prospective randomized studies are required to resolve the issue of when and how to intubate patients with severe TBI. ED Evaluation If the pre-arrival information suggests severe TBI, trauma systems including a neurosurgeon should be activated, when available. Upon arrival in the ED, the physician should perform a rapid initial assessment of the patient followed by a full trauma evaluation. Spinal injury should be assumed in any patient with severe TBI and spinal immobilization should be continued throughout the initial evaluation. Information from EMS, family members, or bystanders should be actively sought. A full set of vital signs including oxygen saturation, capnometry, and rapid blood glucose determination should be obtained. If continuous capnometry is not available, a blood gas will provide information regarding adequacy of oxygenation and ventilation. A secondary survey and head-to-toe examination and evaluation for other potential injuries should begin as soon as the initial examination (ABCs) is completed. Additional traumatic injuries should be addressed and treated according to local trauma protocol, with priority given to potentially life-threatening injuries first. History The AMPLE history framework can be used to help quickly guide the gathering of medical history and events of the injury. A- allergies, M- medications, P- past medical history, L- last meal, E- events/environment related to the injury. 67 Information from EMS, family members, or bystanders can be very valuable. While there are no Class I studies that validate the prognostic value of the history, understanding the mechanism of injury and circumstances surrounding the injury can help the practitioner understand the energy or speed involved and potential severity of trauma. If the patient was involved in a motor vehicle crash (MVC), how fast was the vehicle traveling? What caused the collision? Were restraints such as a seatbelt or airbags used? Was the patient ejected from the passenger compartment? Was the steering wheel deformed or windshield shattered? If the patient was involved in a bicycle, motorcycle, or all terrain vehicle (ATV) collision, was he or she wearing a helmet? How fast was the vehicle traveling? Was the patient struck by another vehicle? In sports-related trauma, what type of protective equipment was used (helmet, etc)? The EP should ask if the patient suffered a loss of consciousness, and if so, how long it lasted. Did the patient ever return to baseline mental status? Was alcohol or another intoxicating drug involved? Does the patient have any pertinent medical or surgical history? This includes a history of diabetes, seizures, stroke, intracranial lesions, or anticoagulant medication use. These questions can help guide the work-up and narrow the differential diagnosis in a patient with altered mental status. Many of the steps in the initial ED evaluation take place simultaneously, and additional staff may be used to help gather information while the EP is performing the initial physical examination and directing the diagnostic work-up. Physical Examination An analysis of outcome from severe TBI in the Trauma Coma Data Bank described by Chesnut and an Australian study described by Fearnside revealed 5 independent predictors for poorer outcome: age, head CT intracranial diagnosis, pupillary reactivity, post-resuscitation GCS, and presence or absence of hypotension. 68,69 While not all of these factors directly influence ED management, they may be of prognostic value. Age and hypotension have been discussed in previous sections, and the use of imaging for diagnosis will be discussed in the next section. Here, we will discuss further the implications for physical examination as well as pupillary response and GCS in the evaluation of the patient with severe TBI. Of particular interest is the arrival GCS. If the patient was not sedated and did not receive neuromuscular blockade prior to arrival, the GCS can give valuable information about the patient s degree of disability upon arrival and has prognostic value Specific attention should be paid to the motor examination in patients who have not been given sedative or neuromuscular paralytic medications. With the application of a painful stimulus, initially described by Teasdale et al as pressure to the nailbed, 73 patients may localize to the painful stimulus (motor score 5 points), withdraw from the stimulus (4 points), exhibit decorticate or flexor posturing (3 points), exhibit decerebrate or extensor posturing (2 points), or have no motor response at all (1 point). 74 While using this Emergency Medicine Practice EBMedicine.net December 2008

9 scoring system, it is important to remember that decorticate or decerebrate posturing may indicate severe increased ICP and imminent herniation and thus require the initiation of immediate aggressive measures to decrease ICP. These methods will be discussed in more detail later in this article. Special attention should be paid to the pupillary examination as well as the pupillary light reflex because it may be an indirect measure of cerebral herniation or brainstem injury. Increased intracranial pressure may result in uncal herniation and compression of the third cranial nerve, which reduces the parasympathetic tone to the pupillary constrictor fibers and results in a dilated pupil. Destruction of the parasympathetic brainstem pathway of the third cranial nerve also results in a fixed and dilated pupil. The size of each pupil should be recorded as well as the reaction of each pupil to direct bright light. Specific notation should be made of any direct ocular or orbital trauma, which could result in a dilated or nonreactive pupil in the absence of intracranial injury. The pupil examination has been shown to be a prognostic indicator in patients who have not received sedatives or neuromuscular blockade prior to their initial ED evaluation. In several large studies, patients who had bilaterally absent pupillary light reflexes had poor outcomes (death or vegetative state) However, the outcome is influenced by the underlying pathology and timing of neurosurgical intervention in amenable lesions. 78 Thus, while initial ED evaluation of pupil response is important, repeat examinations after resuscitation and surgical interventions are also valuable. Laboratory Tests Bedside evaluation of blood glucose should be performed rapidly to rule out hypoglycemia as a cause of altered mental status (low GCS). 79 Evaluation of blood alcohol level and urine or blood drug screen may also be performed but should not guide clinical care. These results are often not readily available, and in the setting where there is a clinical suspicion of TBI these values should not be used to explain altered mental status without further evaluation for potential injury. 80,81 Other laboratory tests are not useful in the initial ED evaluation of the patient with severe traumatic brain injury. However, the admitting trauma or neurosurgical team may request baseline labs to guide further evaluation, trauma resuscitation, and treatment. These may include a complete blood count, complete metabolic panel, coagulation studies, arterial blood gas, serum lactic acid, and blood typing in case future transfusions or coagulopathy correction are required. Electrocardiogram (ECG) ECG evaluation is not routinely helpful in the initial evaluation and treatment of the patient with severe TBI. Though there are no studies which show that it improves outcomes, cardiac monitoring is generally recommended. 82 If indicated for evaluation of other medical emergencies (such as TBI caused by MVC after the patient had a myocardial infarction) or trauma evaluation (severe chest trauma), then a 12-lead ECG is indicated. However, in the patient with isolated severe TBI who is hemodynamically stable, obtaining an ECG should not delay the further evaluation or treatment of the head injury. Patients with severe TBI may have ECG changes that are concerning to the EP. 83,84 ECG changes are most common in patients with subarachnoid hemorrhage but may occur with other CNS injuries as well. These changes include large T-waves that may be inverted, U-waves, prolonged QT segments, and ST segment elevation or depression, which may mimic a myocardial infarction. Dysrhythmias may also occur, including bradycardia or tachycardia, sinus arrhythmia, atrial fibrillation, premature ventricular contractions, or ventricular tachycardia. Though the exact mechanism for these ECG changes is not known, they may stem from CNS-mediated derangement of the autonomic nervous system. The classic Cushing response of sinus bradycardia with increased systolic blood pressure and widened pulse pressure may also be seen and is related to increased intracranial pressure. Imaging The mainstay of evaluation and characterization of TBI is radiographic imaging. The American College of Radiology convened an expert committee to develop appropriateness criteria for radiographic imaging in patients with TBI. 85 Their consensus guidelines are available at and were most recently updated in In their recommendations, they discuss imaging of mild, moderate, and severe traumatic brain injuries, and their guidelines focus on identifying intracranial injuries while minimizing unnecessary imaging. Their recommendations also focus on imaging modalities rather than the clinical care or prognostic value of findings. In patients with a GCS less than or equal to 8 and in whom TBI is suspected, a rapid non-contrast CT scan is the study of choice and is considered essential for the evaluation of lesions that may require immediate neurosurgical interventions. CT scans offer high sensitivity for any type of acute hemorrhage, mass effect, mid-line shift, ventricle size, and bony injuries. CT scans have the benefit of being widely and rapidly available even at community hospitals and non-trauma centers. 86 CT scan has also been found to have prognostic value. In a prospective study of 121 patients with TBI and presenting GCS of less than or equal to 8, Van Dongen and colleagues reported a positive predictive value of 78% for poor outcome in patients with an abnormal initial CT scan. 87 Further, more December 2008 EBMedicine.net 9 Emergency Medicine Practice 2008

10 favorable outcomes are reported in patients with normal CT scans on admission, especially in the absence of extracranial injuries. 88,89 Multiple studies have been published that attempt to assign prognostic value to specific CT findings, 90,91 but this discussion is beyond the scope of this article. CT does have limitations. For example, in the acute setting, CT cannot reliably evaluate increased intracranial pressure or cerebral edema that may result from secondary injury. In addition, small non-hemorrhagic lesions and lesions that are adjacent to bony structures may not be well evaluated on CT scan. MRI may depict pathology not visible on CT and is superior for evaluating non-hemorrhagic lesions and secondary effects of trauma such as hypoxic or ischemic injury as well as for identifying diffuse axonal injuries. 92,93 However, several factors (including the length of time required to obtain images, the lack of availability of imaging centers, and the limited capacity for intensive monitoring of the patient during imaging) make MRI a poor choice for the ED evaluation of unstable patients or patients with severe TBI. 94 Other imaging modalities exist but have limited use in the ED evaluation of TBIs. Plain radiographs of the skull are not routinely recommended because though they can identify fractures, they cannot assess for intracranial pathology. Routine vascular evaluation, CT-angiography, or MR-angiography are not recommended in most patients with TBI, though they may be required in patients with penetrating trauma to the head and neck. PET scans and cerebral ultrasound have little to no role in the acute evaluation of adults with TBI. 95 Imaging of the cervical spine should be performed in all patients with moderate or severe TBI, as clinical clearance of the spine is difficult or impossible in patients with altered mental status. Plain radiographs and CT have been used for initial evaluation of the cervical spine, though several studies have found that the use of CT or CT in conjunction with plain films is superior in identifying bony cervical injuries Though CT can identify bony cervical spine injury, it does not identify ligamentous or soft tissue injuries, and debate exists over how to fully clear the cervical spine in patients with altered mental status. There has also been a great deal of discussion regarding the use of MRI, dynamic fluoroscopy, or flexion/extension films in these patients EPs should work with their local trauma team and neurosurgical service to develop protocols for their hospitals. During the initial evaluation, most EPs agree that patients with suspected moderate or severe TBI should remain in cervical immobilization until the cervical spine has been completely cleared. ED Management When a patient with a severe traumatic brain injury arrives in the ED, there are often several other concomitant injuries that must first be addressed. As with all trauma patients, management of the ABC s takes first priority. The goal of resuscitation, as it relates to TBI, is to reduce the secondary injury to the brain caused by hypotension and hypoxemia. Airway By definition, a patient with a severe TBI has a GCS of less than 9 and warrants definitive protection of the airway. One must be careful to ensure as little increase in ICP during laryngoscopy as possible, and a variety of agents can be used with this goal in mind. In addition, one must assume that the cervical spine and cord may be concomitantly injured, and care must be taken to ensure immobilization of the spine with in-line stabilization while securing the airway. Lidocaine Endotracheal intubation can lead to an increase in ICP via 2 major pathways. The first is a reflex sympathetic response to laryngoscopy, which increases the heart rate and blood pressure causing intracranial hypertension with the loss of cerebral autoregulation. The second is a direct cough reflex from airway manipulation. The routine use of lidocaine pretreatment prior to endotracheal intubation to prevent these reflexes remains controversial. A recent review of the literature cited several studies in which the reflex sympathetic effects of endotracheal intubation were described. 103 Lidocaine prior to endotracheal intubation was associated with a significant reduction in catecholamine release; however, none of the studies specifically addressed ICP. Two notable studies addressed the utility of lidocaine prior to endotracheal suctioning and found a significant treatment effect in lowering ICP by blocking the cough reflex. 104,105 One study directly examined the efficacy of lidocaine in blunting the increase in ICP that occurs during laryngoscopy. The study was limited to 20 patients with brain tumors undergoing elective intubation prior to surgery. 106 It concluded that lidocaine reduced the ICP increase during laryngoscopy by 12 mm Hg. There is minimal evidence that lidocaine may cause harm; in 1 study, thiopental/lidocaine caused greater incidence of hypotension compared with thiopental/placebo. 107 A caveat to this study is that the use of thiopental alone can lead to significant hypotension and may have played the larger role in causing worsening hypotension with the addition of lidocaine. There is no study to date specifically addressing the effect of lidocaine pretreatment on mortality or neurologic outcome. The best available evidence suggests a treatment benefit for reduction of ICP during intubation with no clear evidence of harm, leading to a recommendation to routinely pretreat prior to intubation. The dose is 1.5 mg/kg as an IV bolus, with a maximum dose of 100 mg. Lidocaine Emergency Medicine Practice EBMedicine.net December 2008

11 must be administered at least 3 minutes prior to laryngoscopy for its maximal benefit. 108 Other Pretreatment Agents Other agents used to blunt the hemodynamic and neurologic effects of intubation include opiates, beta-blockers, and nondepolarizing neuromuscular blocking agents. Fentanyl (3 mg/kg IV) clearly alleviates the pain (as measured by diminished rise in heart rate and blood pressure) involved with laryngoscopy and intubation. 109,110 Esmolol (2 mg/kg IV) has also been well studied in the anesthesia literature for its use in reducing the sympathetic response to laryngoscopy in patients with cardiac disease. One study in the emergency medicine literature also examined the hemodynamic effects of lidocaine versus esmolol pretreatment in 30 patients with isolated head injuries. 111 The study found that both agents had similar hemodynamic effects during and immediately after laryngoscopy. No well-designed studies have been conducted using fentanyl, esmolol, and lidocaine in combination. The available studies suggest that there is a pretreatment benefit with either esmolol or fentanyl and that either agent should routinely be used in the hemodynamically stable head trauma patient 3 minutes prior to intubation. The last class of pretreatment agents used for intubation is nondepolarizing neuromuscular blocking drugs, such as vecuronium. The theoretical benefit of a defasciculating dose of vecuronium (0.01 mg/kg IV) prior to administration of succinylcholine is to blunt the fasciculation-induced increase in ICP. This beneficial effect has been observed in elective neurosurgical intubation 112 but has not been studied in the TBI population; therefore, its use is an option based on local practice. Sedation, Paralysis, And Intubation Once pretreatment has been given, sedation agents such as thiopental, benzodiazepines, and etomidate can be used to facilitate endotracheal intubation in trauma patients. Thiopental (3-6 mg/kg IV) and benzodiazepines, such as midazolam ( mg/kg IV), have a rapid onset of action and amnestic properties but often cause or exacerbate hypotension; this limits their use in the unstable trauma patient, so they are often not the initial induction agent of choice. 113,114 Etomidate (0.3 mg/kg) is a cardiacneutral drug from the standpoint of blood pressure and heart rate and also has a rapid onset of action with amnestic properties. Although even single intravenous dose induction with etomidate has been associated with relative adrenal insufficiency, 115 the resulting hypotension can readily be treated with steroid replacement. Neuromuscular blockade with succinylcholine (1.5 mg/kg IV) provides a rapid muscular relaxation with a short duration of action. Intubating conditions with succinylcholine have been shown to be more favorable than with rocuronium. 116 Breathing Supplemental oxygen should be provided as needed to prevent hypoxemia because hypoxemia may lead to significantly worse outcomes. 117,118 Pulse oximetry should supplement arterial blood gas analysis to monitor oxygenation as it provides continuous information regarding oxygenation rather than a single static measurement. The use of brain oximetry and/ or jugular venous oxygen monitoring is controversial and is outside the scope of practice of most EPs. Ventilation should target an arterial PaCO 2 of 35 to 40 mm Hg. Hyperventilation, once a standard of care, 119 has been associated with increased morbidity and mortality and thus must be avoided. 120,121 The proposed mechanism of harm is through alkalemiainduced vasoconstriction caused by the low PaCO 2 in the brain. Short-term hyperventilation to reduce ICP in the setting of imminent herniation of the brain stem has not been well studied; consequently, there are no Level I or II recommendations regarding its use. A Level III recommendation was made in the most recent BTF guidelines to use hyperventilation only as a temporizing measure for the reduction of ICP based on consensus. 122 Fluid Resuscitation After the airway is secured and adequate oxygenation and ventilation have been achieved, resuscitation should proceed with non-hypotonic fluid administration in the hypotensive patient. There are a variety of agents available, including normal saline, hypertonic saline, colloid solutions such as albumin, and blood components. Crystalloid vs. Colloid Saline has long been the standard fluid of choice for resuscitation of all critically ill patients, including those with traumatic brain injury. Recent studies have compared saline with alternative fluid therapies. The SAFE trial (Saline versus Albumin Fluid Evaluation) concluded that in a heterogeneous critically ill population there was no difference between the saline resuscitation and albumin resuscitation groups in measures of organ injury, mortality, or days in the ICU. 123 However, a post-hoc analysis reviewing TBI patients only found that at 2 years patients resuscitated with albumin (146 patients) had an all-cause mortality rate of 41.8% compared with the saline group (144 patients), which had a mortality rate of 22.2%. 124 There are no human trials to date showing a survival advantage for patients with severe TBI using albumin over saline. In addition, there are no human trials to date showing an advantage using synthetic colloid solutions over saline. December 2008 EBMedicine.net 11 Emergency Medicine Practice 2008

12 Blood Products The administration of blood products should be in keeping with ATLS protocols, 6 as there are no studies to date specifically addressing transfusion thresholds for patients with isolated severe TBI. Hyperosmolar Therapy The current standard treatment with hyperosmolar therapy is mannitol administered at a dose of 0.25 to 1 mg/kg. It is a one-time intravenous bolus dose, and there is limited evidence to support multiple doses or infusion dosing of the medication Mannitol works to reduce ICP by 2 mechanisms. 128 The first, which begins within minutes of infusion, is by expanding plasma volume, thereby reducing the hematocrit and blood viscosity, leading to increased cerebral blood flow and oxygen delivery. The second, which takes 15 to 30 minutes, is through an osmotic effect from a gradient between the plasma and neuronal cells, causing net movement of water out of the cells. As an osmotic agent, diuresis will ensue and hypotension can result if the patient is not kept euvolemic. 129 Hypertonic saline (HTS) has gained recent attention as a potential therapy for the management of both hypotension and elevated ICP. Based on animal models, the theoretical advantage of HTS (usually 3% or higher) over standard concentrations of saline (0.9%) is that cerebral edema is less likely to result from aggressive resuscitation. 130,131 This effect is due to a shift of free water out of the CNS due to the higher osmolality of the surrounding vasculature. The same effect is also present in the rest of the body, leading to fluid shift out of the interstitium and into the vasculature, improving blood pressure and cardiac output. 132 The reality of HTS in clinical use is that there have been few well-designed human trials addressing HTS with outcomes of mortality and neurologic injury. As noted in a 2006 review of HTS literature, there have been fewer than 300 patients enrolled in all hospital based clinical trials to date, and many of these patients were children. 133 Two recent small randomized controlled trials with a total of 34 patients suggested improved ICP control using HTS compared with mannitol. 134,135 A subsequent trial, mentioned earlier in the prehospital literature, failed to show any survival or neurologic outcome benefit with HTS. 56 Currently, there are no Class I or II studies showing a benefit of HTS for the resuscitation of patients with severe TBI, and the most recent BTF guidelines continue to support mannitol as the first line hyperosmotic agent. Intracranial Pressure Monitoring After completion of appropriate resuscitation and imaging, including CT scan of the brain, ICP monitoring is needed to guide optimization of cerebral perfusion pressure (CPP). The Brain Trauma Foundation guidelines support routine ICP monitoring (preferably with a ventriculostomy device) in all severe TBI patients based on Class II evidence of benefit The recommended treatment strategies for increased ICP (greater than 20 mm Hg) include CSF drainage, hyperosmolar therapy, and sedation. These patients are all best managed in an ICU setting, but as boarding times have grown in EDs across the country, the initial management of ICP increasingly rests with the EP. Medical Therapy For Increased ICP The indication for treatment of elevated ICP with hyperosmolar therapy is for short-term treatment while further diagnostic procedures (CT scan of the brain) and interventions (such as treatment of mass lesion found on CT scan) are performed. As discussed previously, hypertonic saline has shown some promise in the reduction of ICP through a hyperosmolar effect, but there are as yet insufficient well-designed studies to support its routine use over mannitol which has more established efficacy. Therefore, mannitol remains the first-line treatment for reducing intracranial hypertension. 128 Sedation has been shown to decrease ICP and thereby optimize CPP when used as part of a monitoring/treatment protocol. The goal of treatment is to bring ICP below 20 mm Hg through a combination of sedative agents such as benzodiazepines along with opiates. 140,141 Paralytic agents may help reduce ICP by preventing shivering and posturing and improving ventilator synchrony, thereby reducing intrathoracic pressure and improving cerebral venous return. 142 The use of paralytic agents should be weighed against the potential complications including prolonged ICU stay and myopathy. Barbiturates have also long been used for refractory intracranial hypertension; however, a recent review by the Cochrane Injuries Group concluded that barbiturates do not improve outcomes and may exacerbate hypotension, thereby reducing CPP. 143 Propofol ( mcg/kg/min) is another option that has been shown to reduce ICP when used along with an opiate 144 or when used alone. 145 However, long-term and high-dose (> 83 mcg/kg/min) use of propofol in the severe TBI population has been linked with increased rates of propofol infusion syndrome (lactic acidosis, arrhythmias, rhabdomyolysis) and ultimately cardiovascular collapse. 146 Early neurosurgical consultation is essential, as refractory elevation of ICP may require decompressive craniotomy in cases of diffuse injury or drainage in cases of mass lesions such as epidural or subdural hematomas. The evidence supporting decompression for diffuse injury is limited to case reports, as there are no randomized adult trials evaluating the morbidity or mortality advantage of this procedure. 147, 148 Positioning of the ventilated patient should Emergency Medicine Practice EBMedicine.net December 2008

13 optimally be with the head of the bed at 30 degrees (after radiographic exclusion of spinal injuries). There are several small studies showing that ICP is significantly lower in this position, although CPP is not consistently altered Additional Therapies Anticonvulsants Common complications of severe TBI include both early (less than 1 week post injury) and late (greater than 1 week post injury) posttraumatic seizures (PTS). 153 The proportion of severe TBI cases without prophylactic anticonvulsant administration with early PTS ranges from 4% to 25% and late PTS from 9% to 42%. 154 The use of phenytoin or fosphenytoin (20 mg/ kg or 20 phenytoin equivalents/kg respectively) has been shown to be beneficial in a double blind RCT of 404 patients in preventing early PTS but not late PTS. 155 Phenytoin and fosphenytoin carry the potential side effects of rash and, less commonly, arrhythmia. Hypotension is also an uncommon side effect usually related to rapid infusion, and in the non-seizing trauma patient, the infusion rate should be slow, usually over 1 hour. One randomized controlled trial with 380 patients comparing valproic acid with phenytoin demonstrated equal efficacy in the prevention of early PTS and no difference in late PTS. This trial also demonstrated a trend towards increased mortality in the valproate group (7% in the phenytoin group and 13% in the valproate group). 156 The reason for this increased mortality was not clear but leaves valproate as a less attractive alternative to phenytoin for the prevention of PTS. There are no trials to date demonstrating a benefit of an anticonvulsant in preventing the development of late PTS, and the reduction of early PTS has not been shown to improve outcomes of neurologic recovery or survival. 157 The BTF guidelines have a Level II recommendation to use anticonvulsants to decrease the incidence of early PTS, with the caveat that early PTS are not associated with worse outcomes or a higher proportion of posttraumatic epilepsy. Steroids Prior to 2004, there were conflicting studies regarding the efficacy of steroids for the lowering of ICP and reduction of cerebral edema. The vast majority of trials showed no difference between patients treated with steroids at any dose when compared with placebo In 2004, an international collaboration known as the CRASH trial (Corticosteroid Randomization After Significant Head Injury) found a significant deleterious effect of methylprednisolone when compared to placebo in a study of 10,008 patients with traumatic brain injury. 164 The current recommendation from the Brain Trauma Foundation based on this trial is a Class I recommendation to not give steroid therapy. 165 December 2008 EBMedicine.net Special Circumstances The Alcohol-Intoxicated Patient The acutely alcohol-intoxicated patient presents a confounding challenge to the EP. Alcohol-intoxicated patients with severe TBI are more likely to have delayed care 166 as well as poorer outcomes. 167 In a retrospective review of 57 patients, alcohol intoxicated patients received intracranial pressure monitoring an average of 151 minutes later than non-intoxicated patients. 166 In a separate retrospective review of 520 patients, intoxicated patients were more likely to be intubated in the field, to later develop respiratory distress requiring ventilatory assistance, and to develop pneumonia. 167 It is also important to note that alcohol intoxication should not be used as the sole explanation of a patient s low GCS. 168 The Geriatric Patient Geriatric patients more frequently suffer from TBI, with rates of 272 hospitalizations per 100,000 people over the age of 75 compared with a rate of 85.2 hospitalizations per 100,000 people in the general population. 169 Older patients with severe TBI are far more likely to have a poor outcome, with death rates of 50.6 per 100,000 per year compared with 18.1 per 100,000 per year in the general population. 170,171 There are more often pre-existing medical problems such as coronary disease, congestive heart failure, renal failure, and reduced physiological reserve that makes resuscitation more problematic. The prognosis and co-morbidities should be considered when discussing with family members the level of aggressiveness in the resuscitation of elderly patients with severe TBI. The Anticoagulated Patient Patients on oral anticoagulation therapy are yet another challenging subset of patients with traumatic brain injury. These patients have worse outcomes with higher INR levels than patients not on anticoagulation, as demonstrated in several studies. 172,173 There are few trials to date that have examined the mortality benefit of reversing anticoagulation in TBI patients. One uncontrolled prospective study of 82 patients found a mortality reduction in those treated with a warfarin reversal protocol (10% mortality) compared to historical mortality rate in head injured patients on anticoagulation (48%). 174 The study was limited by lack of a control group and a majority of patients (84%) with only minor head injury (GCS >14). A subsequent study 175 by the same authors failed to demonstrate a benefit of a warfarin reversal protocol. In patients with spontaneous intracranial hemorrhage (ICH), several studies have shown that reversal of anticoagulation improves outcomes Various formulations have been used including fresh frozen plasma (FFP), clotting factor concentrates, and vitamin K. It is unclear whether the benefit of 13 Emergency Medicine Practice 2008

14 warfarin reversal in ICH patients translates into a meaningful benefit for patients with severe TBI. Controversies/Cutting Edge Several novel medications as well as management strategies are currently being investigated as potential treatments for severe traumatic brain injury. Most have had animal studies that demonstrated some benefit, while others have had more robust human studies that have thus far failed to show efficacy. Hypothermia In the most recent guidelines published by the Brain Trauma Foundation, the subject of therapeutic hypothermia for the treatment of severe TBI was raised. 179 A review of several small randomized controlled trials revealed no consistent clinical benefit for mortality or neurologic recovery None of the trials compared mild (> 33 C) with moderate (32 C-33 C) hypothermia, and trials using mild hypothermia were not more or less likely to show an outcome benefit compared with moderate hypothermia. In some of the trials, there was a trend towards improved neurologic recovery, particularly in patients kept hypothermic for more than 48 hours. On the other hand, the cold trauma patient may be more prone to bleeding and infections, such as pneumonia. 179 A well-designed randomized controlled trial is still needed to establish the efficacy or possible harm of therapeutic hypothermia. The means of inducing hypothermia also warrant future study including the use of cooling helmets, cold gastric lavage, and cooling blankets. Hyperbaric Oxygen Therapy (HBOT) In a 2003 literature review regarding hyperbaric oxygen therapy in TBI, 2 randomized controlled trials and several case controlled trials were identified. 185 The first randomized trial reviewed was published in 1976 with a total of 60 patients and found no clear benefit or harm from HBOT. 186 The second randomized trial published in 1994 with 168 patients demonstrated a decreased mortality in the HBOT group that was statistically significant. 187 There was no difference in neurological outcome between the 2 groups because the few additional survivors in the HBOT group were severely neurologically impaired. The case controlled trials showed some of the physiologic effects of HBOT but failed to demonstrate a consistent treatment benefit. Activated Factor VII (VIIa) To date, there is no randomized controlled trial examining the efficacy of factor VIIa for the treatment of the severe TBI patient with intracranial hemorrhage. Currently, the only FDA approved uses of factor VIIa are for treatment of bleeding episodes in hemophilia A or B patients with inhibitors to Factor VIII or Factor IX. There was a 2005 phase IIb trial examining the off-label use of VIIa in spontaneous intracranial hemorrhage. 188 The study of 399 patients was a well-designed randomized controlled trial demonstrating a significant reduction in hematoma growth as well as reduction in mortality and improved functional outcomes. The subsequent phase III trial did not show a mortality benefit in patients treated with VIIa. The most recent off-label trial involved polytrauma patients and assessed the safety of VIIa in 143 patients. A post-hoc analysis of the 30 patients with TBI found no difference in the treatment and placebo groups in terms of mortality, ventilator requirement, and length of ICU stay. 189 There are currently several ongoing trials assessing the safety and efficacy of VIIa in the treatment of trauma patients, including those with severe TBI, that will guide its future use. Ketamine Ketamine has long been thought to be detrimental to patients with TBI due to its potential to increase ICP. Key Points 1. Rapid identification of severe traumatic brain injury in the field should prompt rapid transport to a Level I trauma center if possible. 2. Assume concomitant cervical spine injury and use full spinal precautions throughout assessment and treatment. 3. Identify and treat other traumatic injuries simultaneously. 4. Avoid hypotension and hypoxemia. 5. Endotracheal intubation by EMS should only be performed when adequate airway or oxygenation is not otherwise possible. 6. Avoid prophylactic or inadvertent hyperventilation. 7. Resuscitation of shock should follow ATLS protocols, using saline and blood products when necessary. 8. Non-contrast CT scanning offers the most rapid delineation of brain injury. 9. Intracranial pressure monitoring should be obtained early, and appropriate cerebral perfusion pressures should be maintained. 10. Sedation with opiates, benzodiazepines, and low dose propofol should be used when intracranial hypertension is present; care must be taken to treat resulting systemic hypotension. Emergency Medicine Practice EBMedicine.net December 2008

15 Clinical Pathway: Evaluation Of Severe Traumatic Brain Injury Patient arrives, GCS 8. Class I: Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective. Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. Class IIa: Weight of evidence or opinion is in favor of the procedure or treatment. Class IIb: Usefulness/efficacy is less well established by evidence or opinion. Class III: Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful. Adapted from: Sacco RL, Adams R, Albers G et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack. Stroke. 2006;37; This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Already intubated? Yes Confirm tube placement: breath sounds, chest x-ray, and ETCO 2. Avoid hyperventilation. (Class II) Avoid hypoxemia. (Class III) Hypotension present? NO Identify and stabilize other immediate life-threatening injuries. NO Yes Premedicate: Lidocaine 1.5 mg/kg (Class III) Vecuronium 0.01mg/kg (Class III) BVM assist for 3 minutes Etomidate 0.3 mg/kg Succinylcholine 1.5 mg/kg (Class III) Orotracheally intubate, maintaining in-line stabilization. Resuscitate with normal saline and blood - ATLS protocol. (Class III) Avoid using albumin. (Class III) Copyright 2008 EB Practice, LLC No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. Signs of herniation present? NO Yes Initiate hyperosmolar therapy with mannitol 0.25 mg mg/kg (Class II) Order noncontrast CT scan of brain. Order early neurosurgical consultation. Lesion with mass effect? Lesion without clear mass effect? Normal CT scan? Begin immediate neurosurgical decompression. Place ventriculostomy. (Class III) Treat intracranial hypertension with sedatives, paralytics, and CSF drainage. (Class III) Admit to ICU. Place ventriculostomy if 2 or more of the following are present: age > 40, unilateral or bilateral motor posturing, or systolic BP < 90. (Class III) Investigate other causes for low GCS. Admit to ICU. December 2008 EBMedicine.net 15 Emergency Medicine Practice 2008

16 Recent studies are challenging this belief and may allow clinicians to use this agent for sedation In each small randomized controlled study, ketamine sedation was compared with various other sedative medications using a variety of parameters including ICP, CPP, and need for additional ICP lowering therapy. The results consistently showed no significant difference in these parameters. The most recent randomized controlled study of 25 patients compared an opiate/benzodiazepine combination to ketamine/ benzodiazepine for sedation and found no difference in ICP or CPP between the 2 groups. 193 The total number of patients enrolled in all of these trials combined was less than 100. A larger randomized trial is needed to confirm that ketamine is a safe sedative agent to use in the severe TBI population. Progesterone Progesterone has recently received attention as a potential neuroprotective agent in the treatment of patients with severe TBI. The ProTECT trial 194 published in 2007 was conducted on the basis of animal research showing that infusion of progesterone shortly after TBI reduces cerebral edema, prevents neuronal loss, and improves functional outcomes. The human trial was a phase II well-designed RCT of 100 patients designed to test the safety of progesterone in TBI patients compared with placebo. The study found no significant increase in adverse events and a marginally statistically significant decrease in mortality of 13% in the treatment group compared with 30.4% in the placebo group (relative risk [RR] 0.43; 95% CI, 0.18 to 0.99). A future phase III study to examine the efficacy of progesterone is currently in the planning stage. Other Agents Through the last 20 years, a variety of other agents have been studied with inconclusive results regarding their efficacy. These include magnesium sulfate, 195 granulocyte colony-stimulating factor, 196 dexanabinol, 197 and rivastigmine. 198 None of these agents has clearly been shown to cause harm, but they also have not demonstrated efficacy in a welldesigned trial. Cost-Effective Strategies In the treatment of severe traumatic brain injury, there are few meaningful strategies to reduce the cost of care for the acutely injured patient. Most of the care provided to this patient population involves critical care, intensive monitoring, surgical treatment, as well as prolonged rehabilitation. The only study 203 to date showing a significant cost benefit to a treatment modality is the implementation of a severe TBI protocol. The authors used matched historical controls with severe TBI prior to the implementation of a protocol based on the Brain Trauma Foundation s evidence-based guidelines in These controls were compared with 2 groups of patients: those in whom some of the guideline recommendations were followed and those in whom most of the guidelines were followed. Outcome measures included mortality, days in the ICU, days in the hospital, cost of care, and Glasgow Coma Outcome scores. The authors reported positive impact on outcomes post guideline implementation, thus supporting that the use of a protocol for care improves outcomes. Of note, critical analysis of this report introduces some caution in accepting the findings at face value: it is unclear if other changes took place in the hospital such as facilitated discharge planning which would explain the decreased length of stay. It is also unclear if it was following the guidelines per se that improved care or the increased attention to care that is commensurate with a protocol, but in either case it appears that patients benefited. Additional reduction of costs can also be accomplished through prevention programs. These programs can include car safety systems, motorcycle/bicycle helmet laws, and education about helmets for other sports including skiing, snowboarding, skateboarding, rollerblading, and others. Laws, education, and enforcement aimed at unsafe and intoxicated drivers may also help reduce the frequency and severity of TBI. Disposition Patients with severe TBI all need to be admitted to the hospital, preferably to a trauma ICU or to a neurosciences ICU. Early consultation with neurosurgery and trauma surgery will help guide admission to the appropriate service. When TBI is one of many injuries, the patient is best cared for initially by a trauma surgery service. Patients presenting to an ED without trauma support should be transferred to a tertiary hospital with neurosurgery and trauma surgery capabilities as soon as the patient is stable for transport and after consultation with both of these services. Transport to a Level I trauma center has been associated with decreased mortality for multisystem trauma and a recent study in the Journal of the American College of Surgeons found that this mortality benefit was most notable in the TBI subgroup. 202 Summary Severe traumatic brain injury is a complex and challenging clinical entity. The EP must not only identify the injury early in the course of evaluation but also must quickly initiate treatment. This review summarizes current recommendations for diagnosis, treatment, and disposition of severe TBI based on the most recent available data. Rapid treatment and referral to trauma and neurosurgical specialty care have dramatically reduced mortality and neuro- Emergency Medicine Practice EBMedicine.net December 2008

17 Risk Management Pitfalls For Severe Traumatic Brain Injury 1. I thought we could wait to see the blood glucose on the chemistry sent to the lab. Both hypoglycemia and hyperglycemia can cause altered mental status and can either mimic or may have been the mechanism leading to TBI. All patients with altered mental status should have rapid bedside assessment of blood glucose as early as possible. Hypoglycemia and hyperglycemia should be treated because correction may improve level of consciousness. Severe hypoglycemia or hyperglycemia may worsen outcomes in patients with TBI. 2. EMS said he was just drunk. Patients with alcohol or drug intoxication may have altered mental status that can mimic TBI. Blood alcohol levels and urine toxicology screens may help prove that intoxication is present. However, these tests take time to perform and no patient should be presumed to be just drunk. Unless trauma can be reasonably excluded by reliable history and supported by physical examination, evaluation for TBI should proceed. 3. I didn t realize that he had a cervical fracture. Severe TBI implies significant forces applied to the head and by definition also to the cervical spine. All patients with moderate to severe TBI should be assumed to have concomitant spine injury until such injuries are radiographically ruled out. Health care providers should maintain spinal immobilization, including rigid cervical collar, throughout the initial evaluation and treatment. 4. I called the neurosurgeon in, so I let her handle it. The initial resuscitation of the trauma patient still remains the domain of the EP, and other injuries must first be excluded or treated prior to transfer of care to a neurosurgeon. ED and hospital overcrowding has moved much of the early ICU care of the trauma patient to the ED setting. Though the bulk of the decision-making responsibility may be assumed by the trauma or neurosurgical service, the EP should still feel obligated to render ongoing assessment and emergency treatment should the patient s status change. 5. I gave him mannitol, but now he s getting worse. The diuretic mannitol serves as a temporizing measure in patients with imminent herniation but it has a limited duration of action and does not provide definitive treatment of intracranial hypertension. Any patient requiring mannitol should receive rapid neuroimaging (CT scan) December 2008 EBMedicine.net and prompt re-evaluation by a neurosurgeon for possible surgical decompression. 6. He didn t have any external signs of trauma, so I didn t get a CT. Severe TBI may exist without external evidence of cranial trauma. Care should be taken to take a thorough history for possible traumatic mechanisms of injury. In cases where a patient has altered mental status and no clear history can be obtained, TBI should be considered and a CT scan should be obtained. 7. The neurologic examination was fine an hour ago, but now he s unresponsive. Patients with TBI may rapidly deteriorate either from extension of the initial/primary injury or from the development of secondary injuries. All patients with TBI should have frequent neurologic re-assessment. 8. We just intubated the patient but his blood gas shows a PaCO 2 of 25 mm Hg. Routine hyperventilation is not recommended for patients with TBI as vasoconstriction may decrease cerebral perfusion pressure and worsen secondary injuries. However, when patients are being oxygenated and ventilated via bag-valvemask by hand, the provided respiratory rate is often much too high which can lead to inadvertent hyperventilation and hypocarbia. Care should be taken to monitor the rate of respiration/ventilation either by ventilator or when hand-bagging a patient and to follow blood gasses for measurement of PaO 2 and PaCO The CBC just came back and the hematocrit is 20, and he has persistent hypotension. Many patients with TBI have multi-system trauma. Do not forget to fully evaluate the trauma patient for other injuries and particularly for sources of hemorrhage. Severe anemia or hemorrhagic shock can affect outcomes for patients with TBI. 10. I didn t know the patient was on warfarin. Anticoagulants such as warfarin may cause patients with even minor mechanisms of injury to suffer severe TBI due to their coagulopathic state. A full history including medication history should be performed on every patient. Especially in patients where this information is not available, measurement of INR can help the EP identify patients who may be at risk for increased bleeding. 17 Emergency Medicine Practice 2008

18 logical morbidity in the last several decades. There are several novel therapies in development, but the most important treatment at present and in the foreseeable future is early resuscitation and prevention of secondary brain injury, a task well suited to the trained EP. Case Conclusions The blown pupil raised concern for uncal herniation and consequently you began to hyperventilate the patient and administered mannitol 0.5 gm / kg. Once the pupil normalized, the hyperventilation was discontinued and mechanical ventilation was initiated with a goal arterial PaCO 2 of 35 mm Hg. A continuous IV infusion of propofol was started for sedation and prevention of ICP elevation. The on-call neurosurgeon was contacted while the patient was quickly transported to radiology for a non-contrast CT scan of the head, which revealed a large left epidural hematoma. The patient was taken to the operating room for surgical evacuation and decompressive craniotomy. He was subsequently transferred to the intensive care unit for recovery and close monitoring for vasospasm, edema, and secondary injury. After a brief examination of the second patient, you noticed equal sized pupils with normal reactions to light. You found a right-sided hemiparesis and a positive Babinski s reflex on the right toe. You identified the GCS as 7 and recommended orotracheal intubation. Using full spinal precautions and inline stabilization, you preoxygenated with 100% supplemental oxygen. An IV bolus of lidocaine and a defasciculating dose of vecuronium was given followed by successful rapid sequence intubation with etomidate and succinylcholine. A noncontrast head CT revealed a hyperdense subdural hemorrhage with midline shift. After drainage of the venous hemorrhage, the patient was extubated and discharged back to the nursing home after 14 days without neurologic sequelae. References Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. 1. Teasdale G, Jennett B. Assessment of Coma and Impaired Consciousness; a practical scale. Lancet. 1974;2: (Descriptive) 2. Teasdale G, Jennett B. Assessment and Prognosis of Coma after Head Injury. Acta Neurochir. 1976;34: (Retrospective; 92 subjects) 3. Jennett B, Teasdale G, Galbrath S, et al. Severe Head Injuries in Three Countries. J Neurol Neurosurg Psych. 1977;40: (Prospective;700 patients) 4. Shackford SR, Wald SL, Ross SE, et al. The clinical utility of computed tomographic scanning and neurologic examination in the management of patients with minor head injuries. J Trauma. 1992; 33: (Retrospective; 2766 patients) 5. Stein SC, Ross SE. Mild head injury: a plea for routine early CT scanning. J Trauma. 1992;33: (Retrospective; 1448 patients) 6. ACS ATLS: Advanced Trauma Life Support for doctors, 7th Ed., Chicago: American College of Surgeons; 2004 (Textbook) 7. Kraus J, McArthur D. Epidemiology of Brain Injury. In: Cooper P., Golfinos J, ed. Head Injury. 4th ed. McGraw-Hill Publishers. New York. 2000: (Textbook) 8. Zinc B. Traumatic brain injury outcome: Concept in emergency care. Ann Emerg Med. 2001; 37(3): (Review) 9. Guidelines.gov (Guidelines) 10. The Brain Trauma Foundation. The American Association of Neurological Surgeons.The Joint Section on Neurotrauma and Critical Care. J Neurotrauma. 2007; 24: S (Guidelines) 11. Badjatia N, Carney N, Crocco T, et al, Guidelines for Pre-Hospital Management of Traumatic Brain Injury, 2nd Ed, Pre-Hosp Em Care. 2007: 12(1), Supplement, pg S1-S52. (Guidelines) 12. Nrayan TK, et al. Clinical trials in head injury. Journal of Neurotrauma. 2002; 19:503 (Review) 13. Langlois J, Rutland-Brown W, Thomas K, Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths, Centers for Disease Control and Prevention, national Center for Injury Prevention and Control (Government Report) 14. Bullock MR, Chestnut R, Ghajar J, et al. Surgical management of acute subdural hematoma. Neurosurgery. 2006; 58(Supplement 3): S16-S24. (Review) 15. Lenzlinger PM, Saatman KE, Raghupathi R, et al. Overview of basic mechanisms underlying neuropathological consequences of head trauma. In: Head Trauma Basic, Pre-clinical, and Clinical Directions. New York. 2001: (Review) 16. Kirsh, R: Head Injury. In: Tintinalli JE, et al. Emergency Medicine: A Comprehensive Study Guide, 6th ed. New York: McGraw-Hill. (Textbook) 17. Munch E, Horn P, Schurer L, et al. Management of Severe Traumatic Brain Injury by Decompressive Craniectomy. Neurosurgery. 2000;47(2): (Retrospective; 49 patients) 18. Servadei F, Murray G, Teasdale G, et al. Traumatic Subarachnoid Hemorrhage: Demographic and Clinical Study of 750 Patients from the European Brain Injury Consortium Survey of Head Injuries. Neurosurgery. 2002;50(2): (Prospective; 750 patients) 19. Oertel M, Kelly DF, McArthur D, et al. Progressive Hemorrhage after Head Trauma: Predictors and Consequences of the Evolving Injury. Journal of Neurosurgery. 2002;96(1): (Retrospective; 142 patients) 20. Arundine M, Aarts M, Lau A, et al. Vulnerability of Central Neurons to Secondary Insults after In Vitro Mechanical Stretch. Journal of Neuroscience. 2004;24(37): (Basic science research) 21. Wolf JA, Stys PK, Lusardi T, et al. Tramautic Axonal Injury Induces Calcium Influx Modulated by Tetrodotoxin-Sensitive Sodium Channels. Journal of Neuroscience. 2001; (6): (Basic science research) 22. Iwata A, Stys PK, Wolf JA, et al. Traumatic Axonal Injury Induces Proteolytic Cleavage of the Voltage- Gated Sodium Channels Modulated by Tetrodotoxin and Protease Inhibitors. Journal of Neuroscience. 2004; 24(19): (Basic science research) 23. Heegaard W, Biros M. Traumatic Brain Injury. Emerg Med Clinic North Am. 2007; 25(3): (Review) 24. Chesnut R. The management of severe traumatic brain injury. Emerg Med Clinic North Am. 1997; 15(3): (Review) 25. Zweinenberg M, Muizellar J. Vascular aspects of severe head injury. In: Head Trauma Basic, Pre-clinical, and Clinical Directions. New York. 2001: (Review) 26. D Onofrio G, Degutis L. Preventive care in the emergency department: screening and brief intervention for alcohol problems in the emergency department: a systematic review. Acad Emerg Emergency Medicine Practice EBMedicine.net December 2008

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Davis D, Serrano J, Vilke G, et al, The Predictive Value of Field Versus Arrival Glasgow Coma Scale Score and TRISS Calculations in Moderate-to-Severe Traumatic Brain Injury, J Trauma May: 60(5) (Retrospective review; 12,882 patients) 44. Holly L, Kelly D, Counelils G, et al, Cervical Spine trauma associated with moderate and severe head injury: incidence, risk factors, and injury characteristics, J Neurosurg Apr; 96(3 Suppl) (Prospective case series; 447 patients) 45. The Brain Trauma Foundation. The American Association of Neurological Surgeons.The Joint Section on Neurotrauma and Critical Care. J Neurotrauma 2007; 24: S (Guidelines) 46. McConnell K, Newgard C, Mullins R, et al, Mortality Benefit of Transfer to Level I versus Level II Trauma Center for Head Injured Patients, Health Services Research April: 40(2): (Retrospective cohort; 551 patients) 47. 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Davis D, Peay J, Serrano J, et al: The Impact of Aeromedical Response to Patients with Moderate to Severe Traumatic Brain Injury. A Em Med. 2005: 46 (2), (Retrospective; 10,314 patients) 53. Chesnut RM, Marshall LF, Lauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993; 34: (Prospective; 717 patients) 54. Fearnside MR, Cook RJ, McDougall P, et al: The Westmead Head Injury Proect outcomes in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables. Br J Neurosurg. 1993; 7: (Prospective; 315 patients) 55. Wade C, Grady J, Kramer G, et al, Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension, J Trauma May;42(5 Suppl):S61-65 (Cohort analysis; 223 patients) 56. 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Davis D, Idris A, Sise M, et al: Early ventilation and outcome in patients with moderate to severe traumatic brain injury. Crit Care Med. 2006; 34(4): (Retrospective; 3,804 patients) 62. Davis D, Dunford J, Poste J, et al, The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. Trauma Jul; 57(1):1-8, discussion 8-10 (Retrospective case control; 57 patients) 63. Davis D, Dunford J, Ochs M, et al, The use of quantitative end-tidal capnometry to avoid inadvertent hyperventilation in patients with head injury after paramedic rapid sequence intubation, J Trauma Apr: 56(4): (Prospective; 426 patients) 64. Davis D, Ochs M, Hoyt D, et al, Paramedic-administered neuromuscular blockade improves prehospital intubation success in severely head-injured patients, J Trauma. 2003;55(4): (Prospective; 249 patients) 65. Bulger E, Copass M, Sabath D, et al, The use of neuromuscular blocking agents to facilitate prehospital intubation does not impair outcome after traumatic brain injury, J Trauma Apr: 58(4): ; discussion (Retrospective; 2012 patients) 66. Ochs M, Davis D, Hoyt D, et al, Paramedic-performed rapid sequence intubation of patients with severe head injuries, Ann Emerg Med. 2002: (40(2): (Prospective; 114 patients) 67. ATLS: Advanced Trauma Life Support for doctors, 7th Ed., Chicago: American College of Surgeons; 2004 (Textbook). 68. Chesnut R, Marshall L, Klauber M, et al, The role of secondary brain injury in determining outcome from severe head injury, J Trauma Feb;34(2): (Prospective; 717 patients) 69. Fearnside M, Cook R, McDougall P, McNeil R, The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables, Br J Neuro- December 2008 EBMedicine.net 19 Emergency Medicine Practice 2008

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Acad Emerg Med. 2001; 8: (Randomized, Prospective; 30 patients) 112. Schramm, WM, Strasser, K: Effects of rocuronium and vecuronium on intracranial pressure, mean arterial pressure and heart rate in neurosurgical patients. Br J Anaesth. 1996; 77(5): (Prospective; 20 patients) 113. Schneider R, Caro D. Sedative and Induction Agents. In: Walls R, Luten R, Murphy M, Schneider R eds. Manual of Emergency Airway Management.: Lippincott Williams & Wilkins; 2004: (Textbook chapter) 114. Jagoda A, Bruns J. Increased Intracranial Pressure. In: Walls R, Luten R, Murphy M, Schneider R eds. Manual of Emergency Airway Management: Lippincott Williams & Wilkins; 2004: Emergency Medicine Practice EBMedicine.net December 2008

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