Severe Traumatic Brain Injury
By Douglas Lowery, MD
Severe traumatic brain injuries (tbi) refer to those brain injuries leaving patients with an initial Glasgow Coma Scale score of 8 or less. The evolution of a time-critical component of cerebral resuscitationa term referring to the aggressive management of cerebral perfusion pressurehas resulted in a growing emphasis on the early management of patients with traumatic brain injuries. Early management of severe brain injuries now refers to the prehospital and ED treatment, rather than the surgical and initial intensive care unit treatment. It is increasingly clear that precious moments of cerebral resuscitation lost during the prehospital and ED phases of therapy render significant damage to the outcomes of severely head-injured patients. Never has it been more important that emergency physicians have a solid understanding of the bases and methods for performing cerebral resuscitation.
Pathophysiology of TBI
Commonly, the TBI disease process is divided into two main mechanisms: primary brain injuries and secondary brain injuries. Primary brain injuries are immediate and are the direct result of the biomechanical dispersion of kinetic forces throughout the brain tissues, resulting in bleeding, contusion, laceration, and axonal injury. Head injury prevention programs and immediate surgical interventions focus on the primary brain injuries.
Secondary brain injuries may develop over hours to weeks, and these injuries include the cascade of injury processes resulting from the brain’s cellular, inflammatory, and neurochemical responses to the primary injuries.1 This cascade often results in brain swelling. Since the cranium is essentially a closed container, relatively small changes in volume from brain swelling or mass effect will result in large intracranial pressure differences. Cerebral perfusion pressure (CPP)a measure of blood flow to the brainis defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). As ICP rises, CPP falls, resulting in a cerebral nutrient imbalance (often an imbalance of oxygen supply and demand) that, within minutes, can lead to neuronal injury and death. Cerebral resuscitation zeroes in on prevention and correction of decreased cerebral perfusion pressure within minutes, if possible. Most of our ED interventions are aimed at discouraging these secondary brain injuries.
Diagnosis
The diagnosis of severe TBI is straightforward and should be afforded high priority since the central nervous system is so sensitive to injury and ischemia. The physical examination may reveal clues of brain injury and resulting intracranial hypertension. The Glasgow Coma Scale is the parlance of brain injury severity and should be conjoined with careful head and neurologic examinations when determining the nature of brain injury, triaging diagnostic and treatment interventions, and communicating with neurosurgeons. Declining neurologic function not due to extracranial causes, anisocoria, and posturing may all be signs of rising intracranial pressure or herniation.
Computed tomographic (CT) scanning of the brain has become a mainstay for the ED physician in diagnosing brain injuries and intracranial mass effects. Furthermore, CT has become virtually an imperative for assisting neurosurgeons in determining operative procedures and approaches. Coordinating rapid CT imaging (usually outside the ED) while diagnosing and treating extracranial injuries and performing time-critical cerebral resuscitation is a challenging but requisite role for the emergency physician treating the severely brain-injured patient.
Following cerebral perfusion pressure by monitoring serial arterial blood pressure and intracranial pressure in severely brain-injured patients is often reserved for the operating room or intensive care unit. However, early monitoring of these two parameters (possibly in the ED) in addition to pulse oximetry and end-tidal CO2 monitoring will aid the emergency physician in optimizing cerebral perfusion pressure during the vitally important early resuscitation phase of severely brain-injured patients. If available, these modalities should be employed at the earliest possible opportunity.
Cerebral Resuscitation
The ED management of severely brain-injured patients focuses on two simultaneous tasks: the recognition of primary brain injuries and other injuries needing acute (usually surgical) intervention, and the maintenance of cerebral perfusion pressure despite the cascade of secondary mechanisms of brain injury mentioned above. A recent collaboration among members of the Joint Section on Neurotrauma and Critical Care of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons resulted in the publication of Guidelines for the Management of Severe Head Injury, an evidence-based analysis of the published literature to date.2 This important reference critically examines the gamut of treatments, both proven and unproven, for severe traumatic brain injuries and recommends specific management guidelines for practitioners dealing with severely head-injured patients.
As a priority, the prehospital and ED resuscitation of severely head-injured patients must focus on the prevention and early treatment of hypoxia and hypotension.3 Hypoxia often follows severe head injuries and quickly leads to neuronal injury and death. For this reason, airway control using rapid sequence intubation and mechanical ventilation with supplemental oxygen should be initiated early in the management of these patients. The aim of airway control and supplemental oxygenation is to maintain peripheral oxygen saturation at 100% and minimize oxygen imbalance in the brain. If the patient has aspirated or has significant pulmonary injuries or incapacities, a high FIO2 may be required for this purpose and should not be avoided.
In addition to peripheral oxygen saturation, the emergency physician must attend to the ventilatory statusspecifically the prevention of hypercarbiain the severely brain-injured patient. Recent guidelines have debunked the long-standing practice of routine, mechanical hyperventilation of severely brain-injured patients. Cerebral ischemia resulting from the compensatory autoregulation of hypocarbia superimposed upon regions of the brain that might already be hypoperfused from the primary injuries may lead to worse outcomes in severely brain- injured patients.2 It is now recommended that the goal of immediate mechanical ventilation would be to maintain the pCO2 between 35 and 45 mmHg unless the patient demonstrates clinical signs of intracranial hypertension. More specifically, hyperventilation to a pCO2 of 25-30 mmHg is now only encouraged once the clinician finds good evidence of intracranial hypertension, such as clinical signs of herniation, worsening neurologic function, or radiographic signs of mass effect.
Similarly, maintaining the cerebral perfusion pressure greater than 70 mmHg is the prime incentive for preventing and aggressively treating hypotension, which is, at a minimum, defined as a systolic blood pressure less than 90 mmHg. Treating hypoxia, as well as maintaining intravascular volume, are important adjutants to the prevention of hypotension. Colloids, crystalloids (either hypertonic or isotonic), and blood products, when appropriate, all appear to be useful for restoring and maintaining intravascular volume in severely head-injured patients. Volume repletion is best accomplished using central venous pressure monitoring if possible. Pressors may be used to maintain blood pressure in severely head-injured patients but are a poor substitute for intravascular volume replacement. Cautious employment of pharmacologic agents that may lower blood pressure, such as barbiturates, is an important part of preventing hypotension. Acutely, mannitol may increase intravascular volume and improve cerebral perfusion as well; however, the use of mannitol in the absence of intracranial hypertension is not recommended.2
In addition to the primary goals of treating hypoxia and hypotension in the severely brain-injured patient, the emergency physician should pay careful attention to providing adequate analgesia and sedation to these patients. Even severely brain-injured patients can develop intracranial hypertension as a result of airway manipulation, pain, and instrumentation. Using narcotics for analgesia and benzodiazepines for sedation will assist in the management of intracranial hypertension. Obviously, one must use caution when administering these agents in hypovolemic patients because of the attendant risk of hypotension and subsequent cerebral hypoperfusion.
Mannitol, an osmotic diuretic that works by dehydrating the brain tissues, has long been an important adjutant to cerebral resuscitation. It should be administered by intravenous bolus to patients with clinical or radiographic signs of intracranial hypertension. While it is generally agreed upon that corticosteroids and barbiturates have no role in the early treatment of the severely brain-injured patient, the role of hypothermia early on is less clear and is currently under investigation.
Treatment Horizons
In severely head-injured patients, the immediate treatment of hypoxia and hypotension is the cornerstone of the initial cerebral resuscitation. Still, researchers in the neurosciences have never been more aggressive in their exploration of new treatment modalities aimed at discouraging the secondary brain injury cascades in TBI. Calcium antagonists, antioxidants, excitatory amino acid receptor antagonists, and steroid hormones are all under active investigation.4 Regardless of advances with these modalities, the early and rudimentary cerebral resuscitation of severely brain-injured patients as described above is certain to remain paramount in its priority. (Dr. Lowery is Assistant Professor of Emergency Medicine, Emory University School of Medicine, and Medical Director, Emergency Department, Emory University Hospital, Atlanta, GA.)
References
1. Siesjo BK. Basic mechanisms of traumatic brain damage. Ann Emerg Med 1993;22:959-969.
2. Bullock R, et al. Guidelines for the management of severe head injury. New York: Brain Trauma Foundation; 1996.
3. Chestnut, RM. The management of severe traumatic brain injury. Emerg Med Clin N Am 1997;15:581-604.
4. White BC, Krause GS. Brain injury and repair mechanisms: The potential for pharmacologic therapy in closed-head trama. Ann Emerg Med 1993;22:970-979.
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