CHAPTER 333 Initial Resuscitation, Prehospital Care, and Emergency Room Care in Traumatic Brain Injury
A critical objective of management of traumatic brain injury (TBI) is to prevent secondary injury. The two most common causes of secondary injury are intracranial mechanisms (e.g., hematoma and elevated intracranial pressure [ICP]) and systemic mechanisms (e.g., shock and hypoxemia). Efficient management by trauma and neurosurgery teams prevents secondary brain damage through adequate oxygenation and maintenance of adequate cerebral perfusion pressure. During the past decade, there has been remarkable improvement in prehospital evaluation and treatment, which significantly affects patient outcome. Universal implementation of advanced trauma life support protocols and Glasgow Coma Scale (GCS) has helped in standardizing trauma care. The latter has become the standard scoring system for assessing the level of consciousness and helps prognosticate head injury outcome.1
Prehospital Management
Rapid removal of the accident victim to a trauma care facility is critical to improve the chances of survival. Guidelines for prehospital management outlined by the Brain Trauma Foundation have been useful in this respect (Table 333-1). Paramedical personnel must work with the police and fire service to secure the scene and remove the patient safely without causing injury either to the casualty or other personnel at the scene.2 Wilmink and coworkers, following a review of 737 motor vehicle crashes, recommended a target of less than 30 minutes for the extrication of entrapped victims. 3 However, they emphasized that uncontrolled release is indicated only if there is an immediate threat to the victim’s life. Although expertise in safely extricating patients is crucial, there is considerable evidence that the experience of rescuers, medical training, and the timeliness of transport to an appropriate hospital also influence patient outcomes.
TABLE 333-1 Guidelines for Prehospital Management of Traumatic Brain Injury
The importance of prehospital services has been underlined by a prospective study comparing the overall mortality rate, in severe and moderate TBI patients, in two different environments: New Delhi, India, and Charlottesville, Virginia.4 The overall mortality rate was 11% in New Delhi versus 7.2% in Charlottesville. The mortality rates for victims with severe injuries (GCS motor score of 1 to 4) and those with mild injuries (GCS motor score of 6) were similar at both centers. Those patients with moderate injuries (GCS motor score of 5) had a mortality rate of 12.5% in New Delhi, compared with 4.8% in Charlottesville. This dramatic difference is attributed to the differences in prehospital emergency services. In New Delhi, 2.7% of victims received first aid administered by paramedical personnel or police before arriving at the hospital, whereas in Charlottesville, paramedics attended to 84.3% of victims and transported them by ambulance. The differences in transportation were also reflected in the percentage of patients admitted to the hospital within 1 hour of being injured: 6.9% in New Delhi, compared with 50.2% in Charlottesville. In regions where air transport is a feasible means of decreasing transport time to the trauma center, reductions in predicted mortality rates as high as 52% have been reported.5
Introduction of helicopter emergency medical services (HEMS) has revolutionized trauma care and has been shown to improve survival outcome. Proper identification of critically injured patients who need rapid transport is important for optimal use of this expensive mode of transport.6 The concept of physician-staffed HEMS was introduced to provide more definitive care to blunt trauma victims without prolonging the on-scene time.7–9 Initial studies showed up to a 35% decrease in mortality rate among patients treated by a nurse-physician team.8 Recent studies, however, have not shown any benefit in outcome compared with nonphysician-staffed HEMS.9
All patients with a GCS score equal to or less than 8 must be intubated and given controlled ventilation with continuous monitoring of oxygenation by pulse oximetry. Preventing hypoxemia and hypercapnia is a crucial step in prehospital management. Treatment is similar in head injury patients with significant deterioration of level of consciousness, seizures, respiratory distress, or severe facial and thoracoabdominal injuries. The priority for emergency medical service (EMS) is to immobilize the spine and achieve safe airway for use of rapid sequence intubation (RSI). A study at Harborview Medical Center showed a decrease in mortality among TBI patients after early prehospital intubation, although the rate of severe hypercapnia was 18%. Patients with severe hypercapnia had higher Injury Severity Scores and were more likely hypotensive, hypoxic, and acidotic.10,11 The San Diego Paramedics RSI Trial documented an increase in mortality after paramedic RSI, with hyperventilation and aspiration pneumonia identified as the major risk factors.12 Adequate training, regular experience, and close monitoring of a limited group of providers helps to maximize their exposure and experience with RSI.13
It is difficult to attribute improved outcomes in patients treated in the prehospital setting to a specific intervention; however, prevention of hypoxia and hypotension appears to be vital.14,15 The incidence of hypoxia or hypotension on arrival at the hospital has been shown to be decreased from 30% to 12% by simple improvements in prehospital airway management, including an increased use of intubation and mechanical ventilation.16,17 Patients with hypotension after severe TBI have twice the mortality rate of normotensive patients.18 Therefore, aggressive resuscitation with intravenous fluids is recommended in current guidelines for the management of patients with severe TBI.19 Treatment of increased ICP in patients with TBI is also likely to improve outcomes.20 A double-blind randomized controlled trial has shown the efficacy of hypertonic saline as resuscitation fluid in TBI patients in the prehospital setting without affecting the long-term neurological outcome.21
Adequate resources must include paramedics or physicians in the emergency response group who are capable of intubating patients in the prehospital setting. When a GCS score is determined in the prehospital setting, it can be useful as a comparison with the score in the emergency department. Winkler and coworkers demonstrated that patients whose GCS did not improve between the prehospital and initial hospital evaluation had worse outcomes.22
General Trauma Resuscitation and the Trauma Team
The American College of Surgeons (ACS) Committee on Trauma has outlined guidelines regarding responsibilities of the trauma response team.23 The composition and organization of the trauma response team vary with the resources available, the volume of trauma cases treated at each medical center, and local government guidelines. The goal of this group is to receive patients in the emergency room, treat the primary injuries, and prevent additional injury. A center with few trauma cases may assess and resuscitate patients in a general “code room,“ whereas larger centers use a designated trauma bay within the emergency department. Immediate access to a ventilator, operative instruments, unmatched O-negative packed red blood cells, and plain radiographs are necessary. Prompt availability of a computed tomography (CT) scanner, preferably within the emergency department, is essential.
Trauma centers, particularly level I centers, play an important role in the management of head injury patients. A multi-institutional, prospective study that involved the examination of costs and outcomes of care received by more than 5000 adult trauma patients 18 to 84 years of age treated at 69 hospitals located in 12 states concluded that the overall risk for death is significantly lower when care is provided in a trauma center rather than in a nontrauma center.24 Severely injured patients with an Injury Severity Score higher than 15 treated in ACS level I trauma centers have considerably better survival outcomes than those treated in ACS level II centers.25
The trauma population can have a higher incidence of blood-borne infections compared with the general emergency department population.26 Tardiff and colleagues studied patients who died from trauma in New York City.27 Overall, 7.2% were HIV positive, and 20.8% of patients 35 to 44 years old were HIV positive. Kelen and associates tested all patients visiting an inner-city emergency department in Baltimore and found that 24% were infected with at least one of the following: HIV, hepatitis B virus, or hepatitis C virus.28 Because of this increased risk, all participants in the trauma bay must strictly follow universal precautions. These include a fluid-impervious gown, mask, eye shield, head covering, and gloves.29
Primary Survey
The initial management of any trauma patient, including the head injured patient, is based on Advanced Trauma Life Support (ATLS) guidelines from the ACS. This initial management follows a sequential flow, known as the primary survey. This sequential flow aims to address the life-threatening issues by a systematic method to ensure these issues are addressed (Table 333-2). During the primary survey, the steps addressed are the “ABCDEs.” Although thought of as a sequential flow, these steps can be performed at the same time if enough personnel are available.
| Airway |
B (Breathing)
Breathing can be assessed at the time of evaluation of the airway. The chest wall is observed for symmetrical movement and is auscultated to confirm air movement. If a flail chest, pneumothorax, hemothorax, or any another abnormality is identified, it should be treated immediately. Adequate oxygenation is particularly important in the head injury patient, as is preventing hypercarbia. Determining the right blood CO2 level is controversial to some extent. Cerebral bold flow (CBF) increases in proportion to CO2 concentration. Thus, for each unit of elevation of CO2, the CBF increases by 2% to 4%.30 This could lead to an increase in ICP in a patient with a mass lesion or diffuse edema who is not adequately ventilating. Consequently, a low threshold for instituting mechanical ventilation is advised to minimize the chance of hypercarbia in a patient suspected of having a moderate or severe head injury. Muizelaar and colleagues, however, reported worse outcome for empirical hyperventilation in head injury patients during a randomized prospective study.31 Hence, a low-normal range of CO2 (an arterial CO2 of 30 to 35 mm Hg) should be targeted and maintained during the early evaluation of a trauma victim.
C (Circulation)
Acute blood loss after scalp and open skull injury can lead to hypovolemic hypotension. Although laceration of a major intracranial artery resulting in heavy blood loss is easily recognized, the rather brisk bleeding that can arise from scalp lacerations of the galeal blood vessels is often overlooked. Hence, close examination of the head for lacerations should be an essential part of the general secondary survey. Scalp clips, staples, or large running temporary sutures can be used to rapidly stop significant bleeding and permit further examination before definitively repairing the laceration. Hypotension with bradycardia suggests neurogenic shock associated with spinal cord injury and should be treated with pressors rather than aggressive volume expansion after other possible sources of occult hemorrhage have been excluded. In such cases, central venous pressure measurement through a central line is essential. The occurrence of hypertension, bradycardia, and respiratory irregularity suggests a Cushing response32 as a late event from raised ICP and herniation, as described by Cushing in 1901. Although respiratory changes are seldom seen clinically because patients will be mechanically ventilated at this point, deviations from the typical tachycardia response seen in trauma patients should alert the trauma team to potential intracranial hypertension.
Secondary Survey and Neurological Assessment
A detailed secondary survey is important because more than half of patients with severe head injury have other major injuries.33 A review of injuries co-occurring with head trauma showed pelvis or long bone fracture in 32%, major chest injury in 23%, facial fracture in 22%, abdominal visceral injury in 7%, and spinal cord injury in 2% of patients.33 The incidence of cervical spine injury in patients with head injury is between 1.2% and 7.8%.34–37
History
General trauma information provides valuable data in addition to neurological history in diagnosing an acute brain injury. People who witnessed the injury, medical personnel at the scene, family members, and police officers can all give helpful information. Details of the mechanism of trauma, the speed, the damage the vehicle has sustained, injuries to other people, the patient’s location in relation to the vehicle (driver or passenger, inside or thrown from the vehicle), and the presence of safety features (e.g., airbags, seat belts) are some of the facts that could provide information about forces the victim was subjected to during the crash. A patient’s progress after acute trauma provides insight to neurological functioning. However, the accuracy of this information should be evaluated by bearing in mind the validity of the source. Witnesses may be able to describe seizure activity, an awake but confused state, flaccid unconsciousness, focal weakness, or posturing. Although some emergency medical teams have good understanding of neurological signs, other movements are often mistaken as posturing. A detailed description of witnessed events allows one to resolve the validity of the claim. A patient who deteriorates into coma who was reported as lucid initially suggests an 80.5% chance of having a focal intracranial mass lesion on CT.38 A first emergency room GCS evaluation that has not improved from the initial prehospital evaluation correlates with a worse outcome.22
Examination
Along with the GCS, pupillary examination should be part of the initial neurological assessment, but it may be much less reliable in a medicated patient (e.g., large doses of narcotics or atropines). Pupillary findings and the age of the patient are two of the factors that have great prognostic significance independent of the GCS.39,40 Neurological worsening can be identified easily during resuscitation by reexamining the pupil. A unilateral dilated pupil that does not react to light (or does so very slowly) in a trauma patient should be considered to be caused by ipsilateral uncal transtentorial herniation until proved otherwise. Direct trauma to the eye can also cause unilateral pupil dilation. An unreactive pupil, with light response in the contralateral eye (an afferent pupillary defect or Marcus Gunn pupil), may indicate an optic nerve injury. Bilateral dilated pupils are not easy to interpret and may result from hypoxia, hypotension, mydriatic drugs, or bilateral third nerve dysfunction. Total loss of third nerve function results in an inferiorly and laterally deviated eye, but given that in most unconscious head injury patients, the third nerve deficit will be partial, reversible, and possibly at the level of the brainstem, this is seldom seen.41 Bilateral pupillary constriction is commonly a drug response (especially if narcotics were given) but can also represent a pontine lesion. Unilateral pupil constriction is often accompanied by mild ptosis when Horner’s syndrome is present, suggesting carotid dissection.
Coma Scales
Among the numerous injury scales for evaluation of a patient’s neurological status, the GCS has become the standard owing to its ease of application and usefulness in communicating a patient’s status among the various specialties involved.42 It requires only about 30 seconds in assessing three categories of the GCS. Before assessing the GCS, one should confirm that the patient is not hypotensive or pharmacologically paralyzed, either of which hinders correct scoring. While approaching the patient, look for spontaneous eye opening, then address the patient with a greeting and a simple command and note his or her verbal, eye opening, and motor response. If the patient is unresponsive, a painful stimulus is given with a sternal rub or supraorbital pressure. The GCS score that has the most prognostic importance is referred to as the postresuscitation GCS, obtained after the patient’s airway and hemodynamic status have been stabilized.
The sum of motor and eye opening scores followed by a T indicates an intubated patient who cannot be given verbal scores. For example, an intubated patient with spontaneous eye opening4 and localizing to painful stimuli5 would be given a GCS score of 9T. When assigning a score, the best response should be noted; thus, a patient with decorticate posturing on the right and decerebrate posturing on the left would be given a motor score of 3. This type of focality is not formally a part of the GCS, but it should be noted, because early signs of herniation due to a mass lesion are generally unilateral. Deterioration of GCS during resuscitation calls for attention to secondary injuries that require management; hence, it is essential to reevaluate the GCS as resuscitation proceeds. At a minimum, the motor score must be documented; this portion of the assessment is the most reproducible and carries the most prognostic information.39
Presence of clinical herniation syndromes has great significance in trauma patients. Herniation of the uncus and parahippocampal gyrus between the tentorial notch and the midbrain is the most common type and leads to uncal tentorial herniation syndrome. This may be due to an ipsilateral mass lesion such as an epidural hematoma or to temporal lobe edema or hemorrhage. Direct compression of the ipsilateral third cranial nerve and the ipsilateral cerebral peduncle results in ipsilateral pupillary enlargement and contralateral hemiparesis. In addition, compression of the posterior cerebral artery that occurs in some cases leads to occipital lobe infarction unless rapidly corrected. Kernohan’s notch effect occurs if the uncal herniation results in ipsilateral pupillary dilatation and ipsilateral hemiparesis due to pressure on the contralateral cerebral peduncle that is pushed against the contralateral tentorial edge.43 Thus, the side of the pupillary changes provides important clues in localizing the side of the uncal herniation. Untreated herniation with third nerve compression affects eye motility with lateral and inferior eye deviation and hemiparesis progressing to decerebrate posturing. This corresponds to functional disconnection of cerebral cortex from brainstem and was first demonstrated by Sherrington in animal models by transecting the brainstem at the intercollicular level, reproducing decerebrate posturing.44
Tonsillar herniation occurs when cerebellar tonsils are forced downward through the foramen magnum, giving rise to medullary compression. This results from continued supratentorial downward compression or a primary posterior fossa mass. The medullary compression causes rapid loss of respiratory drive and irreversible brainstem damage unless swiftly decompressed. Both uncal and tonsillar herniation can result in brainstem hemorrhage that is located in the midline (Duret’s hemorrhage), which can be differentiated from the punctate hemorrhage seen in diffuse axonal injury,45 which is usually located dorsally in the corpora quadrigemina.
Radiographic Evaluation
Computed Tomography
The CT-based protocol for cervical spine clearance has become the standard practice in many emergency departments. However, there is lack of consensus regarding an efficient and effective method of cervical spine evaluation after blunt trauma. Gale and coworkers showed that plain cervical spine films fail to fully assess the cervical spine after blunt trauma, and they advocate the routine use of screening CT scans.47 Physical examination should precede imaging, especially in patients without clinical evidence of neurological injury, intoxication, or distracting injury. Patients who do not meet these criteria should undergo helical CT scanning of the entire cervical spine. Magnetic resonance imaging (MRI) should be considered in all patients with neurological deficits.
Plain Radiographs
Plain skull radiographs played an important role in investigation of head trauma before the widespread availability of CT scan. In recent years, the use of plain radiography in the initial evaluation of head injury patients has become controversial. A management strategy that shifted the focus of neuroimaging of head trauma from skull radiography to CT scanning was developed and tested by Master and colleagues.48 Nevertheless, skull radiography is useful for imaging of calvarial fractures, penetrating injuries, and radiopaque foreign bodies. A fracture seen on plain films significantly increases the risk for an important intracranial hematoma.48 In patients with severe abdominal or thoracic injuries who require immediate surgical intervention before obtaining CT scan, plain radiographs of the skull can be taken in the operating room. If these have positive findings or there is physical or neurological evidence of a head injury, a ventriculostomy can be done in the operating room.49 Anteroposterior and lateral radiographs have traditionally been required to clear the thoracolumbar spine after blunt trauma.
Magnetic Resonance Imaging
MRI provides excellent visualization of hematomas and diffuse axonal injury, although bony details are more difficult to assess. MRI technology has limited application in the acute phase of head trauma, the major limitation being the time required to carry out the scan. Magnetic resonance angiography is helpful in evaluating arterial injuries, including dissection and occlusion. Other magnetic resonance techniques, such as diffusion imaging and spectroscopy, have proved to be important research tools in understanding the pathophysiology of brain injury and may be of benefit in determining long-term prognosis. These are covered in more detail in Chapter 330.
Cerebral Angiography
Although cerebral angiography is the gold standard for assessing the cerebral vasculature, CT angiography has largely replaced it in the initial evaluation of TBI. Intracranial vascular occlusion or dissection occurs in up to 10% of cases in some series of blunt trauma and should always be considered in patients with focal neurological deficits not explained by the injuries on CT scans. The deficit occurs acutely, and there may be a lucid interval between the trauma and neurological deterioration.50 Traumatic intracranial aneurysms usually become symptomatic days to weeks after the trauma; hence, angiography is not routinely indicated during the initial assessment of these patients except in patients with brisk epistaxis or a mechanism of injury that implies a vascular injury.51 Conventional angiography allows the use of a range of endovascular techniques in managing these vascular injuries (see Chapter 336).
Acute Trauma Management
Hypoxia (PaO2 < 60 mm Hg) after head injury correlates poorly with patient outcome. Therefore, patients should be rapidly intubated, and adequate oxygenation should be maintained with frequent arterial blood gas measurement and pulse oximetry monitoring. In acutely deteriorating patients with signs of herniation, hyperventilation can be attempted while preparing to transport the patient for scanning or to the operating room. During acute resuscitation, systolic blood pressure should be maintained above 100 mm Hg. Low systolic blood pressure results in additional cerebral ischemia and further rise in ICP.52,53 Increased risk for mortality has been shown in patients with at least one episode of hypotension between the time of injury and completion of resuscitation. Hypotension without tachycardia should alert the trauma team to a possible spinal cord injury resulting in neurogenic shock.
Control of ICP remains a cornerstone of acute trauma care management. An ICP greater than 20 mm Hg correlates with neurological deterioration and increased mortality. Mannitol is an osmotic diuretic that rapidly lowers ICP and increases CBF by volume expansion and decreased blood viscosity, which permits cerebral vasoconstriction, resulting in lower ICP.54,55 Serum osmolality should be checked and maintained below 320 mOsm to prevent acute tubular necrosis.56 If a patient has overt signs of herniation or there is acute deterioration in the GCS score, a bolus of 0.5 to 1.0 g/kg mannitol may be administered if hemodynamically stable. Because of the diuretic effects, a Foley catheter must be in place, and volume replacement should be given to maintain euvolemia.
In addition to ICP control, the prevention of seizures in the acute setting is also important. The effectiveness of phenytoin in preventing posttraumatic seizures was evaluated with a randomized trial involving 404 patients.57 Those receiving phenytoin had a 3.6% rate of seizures during the first week, compared with 14.2% in the placebo group. After the initial week, there was no reduction in seizure frequency in the treatment group. Based on these results, phenytoin is given for the first week after injury. Rapid infusion of intravenous phenytoin can cause cardiac arrhythmia and hypotension, especially in patients with known cardiovascular disease.58,59 Fosphenytoin has fewer cardiovascular side effects.60 Given the danger of hypotension in these patients, the phenytoin loading dose is generally not administered until the patient has been fully resuscitated and is hemodynamically stable.
Conclusion
The primary goals of trauma resuscitation are preventing hypoxia and hypotension, maintaining low normocarbia, rapidly assessing and decompressing mass lesions, and controlling ICP. When possible, emergency medical technicians should begin these actions in the prehospital setting. In the emergency department, the traumatologist and neurosurgeon must develop an organized approach to evaluating and treating these patients. Among trauma surgeons, there is a movement to expand the role trauma surgeons play in the care of injured patients to include all operative emergencies, including those procedures normally performed by specialists.61–63 This expanded role would include procedures traditionally performed by neurosurgeons, including decompression of subdural or epidural hematomas. The American Association for the Surgery of Trauma (AAST) has developed a proposed training program for these new specialists in what is termed Acute Care Surgery. It is thought that the expanded role of acute care surgeons may increase access to and the speed with which care is provided to patients, particularly in rural areas, where there may be fewer neurosurgeons.
This new concept has been variably received by the neurosurgical community.64 Although some have found that life-saving decompression performed by trained general surgeons can be effective,65 a limited number of studies by non-neurosurgeons performing neurosurgical procedures suggest that outcome is improved if these procedures are performed by a neurosurgeon and further indicate that there is normally enough time to transfer these patients to a facility with specialists.66,67 In some very isolated communities, particularly where it is difficult to obtain neurosurgical trauma coverage, there may be an increasing role played by acute care surgeons, as demonstrated in Australia, Montana, Wyoming, and Norway.68 In all settings, the coordinated treatment by all personnel, including prehospital staff, trauma surgeons, emergency department physicians, and neurosurgeons, is required to ensure that the patient has the best possible outcome.
American College of Surgeons Committee on Trauma. Resources for Optimal Care of the Injured Patient: 1999. Chicago: American College of Surgeons; 1999.
Baxt WG, Moody P. The impact of a physician as part of the aeromedical prehospital team in patients with blunt trauma. JAMA. 1987;257:3246-3250.
Britt LD. Acute care surgery: the curriculum should address the needs. J Surg Edu. 2007;64:300-301.
Bullock RM, Chesnut RM, Clifton GL, et al. Management and prognosis of severe traumatic brain injury. J Neurotrauma. 2000;17:449-553.
Committee on Acute Care Surgery, American Association for the Surgery of Trauma. The acute care surgery curriculum. J Trauma Injury Infect Crit Care. 2007;62:553-556.
Cooper DJ, Myles PS, McDermott FT, et al. Prehospital hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: a randomized controlled trial. JAMA. 2004;291:1350-1357.
Cunningham P, Rutledge R, Baker CC, Clancy TV. A comparison of the association of helicopter and ground ambulance transport with the outcome of injury in trauma patients transported from the scene. J Trauma. 1997;43:940-946.
Davis DP, Dunford JV, Ochs M, et al. The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma. 2004;56:808-814.
Demetriades D, Martin M, Salim A, et al. Relationship between American College of Surgeons trauma center designation and mortality in patients with severe trauma (injury severity score > 15). J Am Coll Surg. 2006;202:212-215.
Fortune JB, Bock D, Kupinski AM, et al. Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning. J Trauma. 1992;32:618-627.
Gale SC, Gracias VH, Reilly PM, Schwab CW. The inefficiency of plain radiography to evaluate the cervical spine after blunt trauma. J Trauma. 2005;5:1121-1125.
Kaufmann GE, Clark K. Emergency frontal twist drill ventriculostomy: technical note. J Neurosurg. 1970;33:226-227.
King JTJr, Carlier PM, Marion DW. Early Glasgow Outcome Scale scores predict long-term functional outcome in patients with severe traumatic brain injury. J Neurotrauma. 2005;22:947-954.
Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991;75:731-739.
Ringburg AN, Spanjersberg WR, Frankema SP, et al. Helicopter emergency medical services (HEMS): impact on on-scene times. J Trauma. 2007;63:258-262.
Valadka AB, Ellenbogen RG, Wirth FPJr, Laws ERJr. Acute care surgery: challenges and opportunities from the neurosurgical perspective. Surgery. 2007;141:321-323.
Warner KJ, Cuschieri J, Copass MK, et al. The impact of prehospital ventilation on outcome after severe traumatic brain injury. J Trauma. 2007;62:1330-1336.
Wester T, Fevang LT, Wester K. Decompressive surgery in acute head injuries: where should it be performed? J Trauma Injury Infect Crit Care. 1999;46:914-919.
Winkler JV, Rosen P, Alfry EJ. Prehospital use of the Glasgow Coma Scale in severe head injury. J Emerg Med. 1984;2:1-6.
1 King JTJr, Carlier PM, Marion DW. Early Glasgow Outcome Scale scores predict long-term functional outcome in patients with severe traumatic brain injury. J Neurotrauma. 2005;22:947-954.
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6 Cunningham P, Rutledge R, Baker CC, Clancy TV. A comparison of the association of helicopter and ground ambulance transport with the outcome of injury in trauma patients transported from the scene. J Trauma. 1997;43:940-946.
7 Singbartl G. Significance of preclinical emergency treatment for the prognosis of patients with severe craniocerebral trauma. Anaesth Intensivther Notfallmed. 1985;20:251-260.
8 Baxt WG, Moody P. The impact of a physician as part of the aeromedical prehospital team in patients with blunt trauma. JAMA. 1987;257:3246-3250.
9 Ringburg AN, Spanjersberg WR, Frankema SP, et al. Helicopter emergency medical services (HEMS): impact on on-scene times. J Trauma. 2007;63:258-262.
10 Warner KJ, Cuschieri J, Copass MK, et al. The impact of prehospital ventilation on outcome after severe traumatic brain injury. J Trauma. 2007;62:1330-1336.
11 Davis DP, Dunford JV, Ochs M, et al. The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma. 2004;56:808-814.
12 Davis DP, Stern J, Sise MJ, Hoyt DB. A follow-up analysis of factors associated with head-injury mortality after paramedic rapid sequence intubation. J Trauma. 2005;59:486-490.
13 Davis DP, Vadeboncoeur TF, Ochs M, et al. The association between field Glasgow Coma Scale score and outcome in patients undergoing paramedic rapid sequence intubation. J Emerg Med. 2005;29:391-397.
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20 Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993;34:216-222.
21 Cooper DJ, Myles PS, McDermott FT, et al. Prehospital hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: a randomized controlled trial. JAMA. 2004;291:1350-1357.
22 Winkler JV, Rosen P, Alfry EJ. Prehospital use of the Glasgow Coma Scale in severe head injury. J Emerg Med. 1984;2:1-6.
23 American College of Surgeons Committee on Trauma. Resources for Optimal Care of the Injured Patient: 1999. Chicago: American College of Surgeons; 1999.
24 Mackenzie EJ, Rivara FP, Jurkovich GJ, et al. The National Study on Costs and Outcomes of Trauma. J Trauma. 2007;63(6 suppl):S54-S67.
25 Demetriades D, Martin M, Salim A, et al. Relationship between American College of Surgeons trauma center designation and mortality in patients with severe trauma (injury severity score > 15). J Am Coll Surg. 2006;202:212-215.
26 Nagachinta T, Gold CR, Cheng F, et al. Unrecognized HIV-1 infection in inner-city hospital emergency department patients. Infect Control Hosp Epidemiol. 1996;17:174-177.
27 Tardiff K, Marzuk PM, Leon AC, et al. Human immunodeficiency virus among trauma patients in New York City. Ann Emerg Med. 1998;32:151-154.
28 Kelen GD, Green GB, Purcell RH, et al. Hepatitis B and hepatitis C in emergency department patients. N Engl J Med. 1992;326:1399-1404.
29 Marcus R, Culver DH, Bell DM, et al. Risk of human immunodeficiency virus infection among emergency department workers. Am J Med. 1993;94:363-370.
30 Fortune JB, Bock D, Kupinski AM, et al. Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning. J Trauma. 1992;32:618-627.
31 Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991;75:731-739.
32 Cushing H. Concerning a definite regulatory mechanism of the vasomotor center which controls blood pressure during cerebral compression. Johns Hopkins Hosp Bull. 1901;12:290-292.
33 Miller JD, Sweet RC, Narayan R, et al. Early insults to the injured brain. JAMA. 1978;240:439-442.
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