Classification of Head Injuries
• Closed versus penetrating
• Isolated versus multisystem injuries
• Mild (GCS 13–15)
• Moderate (GCS 9–12)
• Severe (GCS 3–8)
Pathologic Findings with Closed Head Injuries
• Skull fractures
• Epidural hematomas
• Subdural hematomas
• Parenchymal contusions
• Intraparenchymal hematomas
• Diffuse axonal injury
Management of Elevated Intracranial Pressure
• Prevention of venous engorgement
• CO2 control (mild hyperventilation)
• Sedation and pain control
• Cerebrospinal fluid drainage
• Hypertonic saline
• Decompressive craniectomy
• Pentobarbital coma
Traumatic brain injury (TBI) most commonly results from motor vehicle crashes (MVC) and typically affects males in the 2nd through 4th decades of life. These sudden random acts can have long-lasting effects on the patient and family, but these events also impact society as a whole when a young, viable, working-age individual becomes suddenly disabled and dependent on the care of others. TBI has no regard for age or gender, however, and can be seen in infants as a result of nonaccidental trauma as well as in geriatric patients following falls. The management of these patients can become extremely complicated and often requires the close interaction of numerous health care providers ranging from trauma, orthopaedic, and neurologic surgeons to nurses, social workers, and speech, occupational, and physical therapists. Unfortunately, current interventions are still limited to the avoidance or minimization of secondary injury and rehabilitative intervention. However, when these patients are managed with aggressive, comprehensive, multidisciplinary approaches, the outcomes at times can be rewarding.
TBI can be categorized based on numerous factors. Most commonly it is differentiated based on mechanism and injury type (closed versus penetrating), whether it has occurred with or without systemic injuries (isolated versus multisystem), and the severity (mild, moderate, severe). The Glasgow Coma Scale (GCS) (Table 1), which was initially developed as a prognostic indicator following closed head injury, has become the principal triage tool for evaluating these patients. Patients are scored based on their best response in each of the three categories (eye opening, verbal responses, and motor score) and then subdivided into mild (13–15), moderate (9–12), and severe (3–8). One caveat to this assessment tool is that it can be affected by numerous alterations, such as hypoxia, hypotension, hypothermia, intoxication, infection, and other metabolic derangements, which are commonly seen in the trauma population.
Glasgow Coma Scale
|Best Motor Score Best Verbal Response Best Eye Opening|
|6 Obeys commands||5 Normal speech||4 Spontaneous|
|5 Localizes to pain||4 Confused||3 To voice|
|4 Withdraws to pain||3 Inappropriate words||2 To pain|
|3 Flexor posturing||2 Incomprehensible sounds||1 No eye opening|
|2 Extensor posturing||1 No verbal response|
|1 No motor response||Intubated patients receive a 1 with the suffix T added to score|
Another common classification system following TBI is based on pathophysiologic findings. Concussion commonly occurs following mild or moderate TBI as the result of transient (typically seconds to minutes) neurologic dysfunction in the setting of a normal computed tomography (CT) scan. Brief loss of consciousness, commonly with amnesia regarding the event, is not uncommon and is often associated with nausea, vomiting, headache, dizziness, and transient visual obscuration. These symptoms may persist for several hours to weeks as part of the postconcussive syndrome and, in rare instances, especially following repetitive injury, these alterations may become long-lasting. As a result of these persistent problems, in addition to a better understanding of the neurocognitive effects following this type of injury, there has been an enormous emphasis placed on their prevention (see text following).
Skull fractures may occur in isolation or be associated with other types of brain injuries. They are commonly classified based on whether they are open (overlying laceration) or closed, linear or comminuted, and nondepressed or depressed. Skull fractures occur either as the result of a large force directed to a small area (i.e., depressed skull fracture following a blow to the head with a golf club) or when larger forces are dissipated throughout the skull resulting in fracture through the weakest area (linear fractures through frontal skull base petrous, or squamous temporal bone). Linear fractures are commonly associated with raccoon eyes (frontal skull base fractures), Battle’s sign (posterior skull base fracture), cerebrospinal fluid leak (otorrhea or rhinorrhea), or olfactory, facial or acoustic nerve injury (amnesia, facial palsy, sensorineuronal deafness).
In addition, temporal bone fractures may also be associated with epidural hematomas (EDHs). These extra-axial blood clots are most commonly caused by laceration of the middle meningeal artery and result in accumulation of high-pressure arterial bleeding in the potential space between the dura and skull. EDHs are more commonly seen in younger individuals, probably because of the decreased skull thickness and lack of adhesions between the skull and dura mater in this population. Commonly, these lesions appear on CT scan as lens- shaped, extra-axial hematomas most often in the temporal region and can be rapidly expansive secondary to the high-pressure arterial bleeding. The clinical course in these patients is classically described by a brief loss of consciousness from the initial concussion, followed by a “lucid interval” in which the patient may be awake and alert, which then gives way to another episode of decreased mental status that may be rapidly progressive and associated with signs of brain stem compression (flexor or extensor posturing, dilated nonreactive pupil). EDHs are usually treated surgically unless they are extremely small and constitute one of the few true neurosurgical emergencies where mere minutes may make an enormous difference in the patient’s outcome.
Unlike EDHs, subdural hematomas (SDHs) are often associated with other types of brain injury and thus typically involve an altered level of consciousness (LOC) from the onset. SDHs are typically caused by bleeding from bridging veins that get torn when the brain moves within its cerebrospinal fluid (CSF) buffer while the veins remain tethered at their dural insertions; however, other causes such as venous or arterial hemorrhage from a brain laceration also exist. CT scanning reveals that these lesions commonly appear more crescent- shaped but never cross the dural boundaries (falx or tentorium).
Unlike the high-pressure EDHs, SDHs typically expand at a slower rate but still cause devastating neurologic dysfunction from compression of the underlying brain. In addition, mortality rates tend to be higher with worse outcome for SDH as a result of the common underlying brain injury. Once again, these extra-axial clots frequently require surgical evacuation unless they are small and fail to have substantial compression on the underlying brain, where they are managed with serial imaging and close neurologic observation. In patients for whom a small SDH is not treated surgically, the physician must remain cognizant of the fact that a small proportion of these will increase in size between 1 and 4 weeks following the trauma and can be a cause of delayed deterioration or increased headache and new neurologic findings.
Intraparenchymal hematomas occur quite commonly following TBI and can be either hemorrhagic or nonhemorrhagic. These lesions range in size from 1 to 2 mm up to several centimeters, and can cause a full range of symptoms and neurologic findings based on their location, size, and degree of compression on surrounding structures. Just like extra-axial hematomas, these lesions may increase in size and commonly coalesce or mature and blossom during the first 12 to 24 hours following the trauma. In addition, larger hematomas incite an inflammatory reaction in the surrounding brain, resulting in increased edema around the lesion, which may result in increases in the intracranial pressure (ICP) (commonly seen on postinjury days [PIDs] 3–7). Management of these lesions depends on their size, location, and associated findings and ranges from serial observation and repeat imaging, surgical evacuation of the hematoma, or decompressive craniectomy with or without lobectomy.
The final category of pathologic abnormalities following TBI occurs as the result of shear injury to the axons themselves, called diffuse axonal injury (DAI). This is caused by either acceleration and deceleration or rotational forces to the axons resulting in micro- or macroscopic areas of injury and axonal transection. Most commonly this is encountered in the setting where a patient clinically has signs of a severe TBI, often with a GCS score less than 6; however, the CT scan is either unimpressive or shows only small areas of petechial hemorrhage. In addition, ICP recording typically shows normal or only slightly elevated values. Magnetic resonance imaging (MRI) is commonly used in this subset of patients and can be used as a predictive indicator for determining the severity of injury, especially if CT is negative. MRI commonly shows areas of increased intensity on fluid attenuation inversion recovery (FLAIR) and T2-weighted sequences in the brainstem, diencephalon, deep white matter tracts, or corpus callosum. Recovery following this type of injury is variable and depends more on the injury location (reticular activating system of brainstem versus supratentorial white matter tracts) than on the injury volume.
In addition to these abnormalities, patients with TBI are also at risk for damage to the spinal cord and vertebral and carotid arteries. Thus, patients with altered LOC should be assumed to have spinal instability and possible spinal cord injury (SCI); they should remain immobilized until the absence of these can be confirmed. The incidence of carotid and vertebral artery injury associated with severe TBI is unknown, but patients with facial or cervical fractures and those with soft tissue neck or chest injury (seat belt sign) have been found to be at higher risk. The appropriate screening for and treatment of these injuries have become a topic of intense debate in recent years but should be suspected in a patient with focal neurologic findings without identifiable cause on other imaging.
Intracranial Pressure and the Monroe-Kellie Doctrine
Regardless of the pathophysiologic type of injury, the end result commonly is the generation of increases in the ICP, which can then lead to secondary brain injury. ICP dynamics are easily understood if one considers the principles of the volume pressure relationships outlined by the Monroe-Kellie doctrine. The basis of this principle resides on the fact that the skull is a fixed and rigid volume; because of this any changes to the volume of its contents will directly affect the pressure within this rigid space. In simplest terms the intracranial cavity contains blood, water, and tissue. Blood may be intravascular (IV) or extravascular (EV) in the case of extra-axial blood clots; water includes not only CSF, which may build up in cases of hydrocephalus, but also edema following traumatic injuries; brain parenchyma typically compromises the tissue component, but in select instances tumors or cysts may also fall into this category.
As increases in any or all three of these categories occur, the pressure inside the cranial cavity increases proportionally. At first, compensatory changes occur, which accommodate for these increases, resulting in only mild pressure changes; however, eventually a critical volume is reached where the compensatory mechanisms are saturated, resulting in rapid and dramatic pressure changes. The following scenario illustrates these principles. A patient is involved in a motor vehicle crash and suffers a head injury with a small epidural hematoma. Initially he is awake and alert without any focal neurologic findings. The epidural hematoma creates an increase in the EV blood component of the Monroe-Kellie doctrine; however, compensatory changes in intracranial CSF volume result in decreases in the water component, thus preventing significant changes in ICP. However, the hematoma continues to enlarge, causing increases in ICP exhibited clinically by slow deterioration in the patient’s level of consciousness. The patient is now intubated and mildly hyperventilated, causing vasoconstriction, thereby decreasing the intravascular blood component and reducing ICP with an improvement in the patient’s neurologic condition. Unfortunately, as the operating room (OR) is being prepared, the patient suffers a rapid decrease in his level of consciousness, becoming unresponsive with flexor posturing and a nonreactive pupil. Although the hematoma has expanded at a constant rate over time, the rapid change in the patient’s condition is the result of him reaching the critical point where all compensatory mechanisms have been exhausted, thus causing profound, rapid changes in the patient’s ICP.
Treatment of Elevated Intracranial Pressure
Acute changes in ICP result in altered LOC, and at times other localizing neurologic findings such as blown (dilated, nonreactive) pupils and flexor or extensor posturing, and such findings may be the sign of impending herniation and death without immediate intervention. In a patient without a ventricular drain already in place, hyperventilation is the most rapid mechanism for acutely lowering elevated ICP. Currently, aggressive hyperventilation (Pco2 <30) is recommended only for short durations in cases of impending cerebral herniation while patients are being stabilized. As stated previously, hyperventilation causes vasoconstriction, which reduces intravascular blood within the cranial vault and almost instantaneously lowers ICP. However, several studies have now shown that the routine use of aggressive hyperventilation in the management of patients with severe closed head injury (CHI) results in decreased outcomes because of hypoxic injury and possible stroke caused by the sustained hyperventilation. Our current practice is to maintain Pco2 values between 35 and 38 with controlled ventilation in all patients with severe CHI; because of this, we leave all these patients intubated and mechanically ventilated until their ICPs normalize and all other therapies are withdrawn.
Adequate sedation and pain control are also important elements of ICP control. Patients who are restless and agitated will have higher ICPs than similar patients who are resting quietly in bed. Another important point is the prevention of venous congestion. This occasionally is evident in cervical collars, which are fastened too tightly or with the use of trach ties that are wrapped too tightly around the neck to hold the endotracheal tube in place.
Several medications are available for the treatment of elevated ICP, with the most common one being mannitol. Although this agent acts as an osmotic diuretic and helps pull excess interstitial fluid into the vascular space and thus lower ICP, there are several other hypothetical mechanisms that probably also increase its efficacy such as increasing RBC flexibility, decreasing RBC and platelet clumping in small arterioles and capillaries, and increasing intravascular volume, thus improving cardiac function. Other diuretics such as furosemide (Lasix)1 or urea (Ureaphil) may also be used but have less dramatic effects on ICP. Hypertonic saline (NaCl 3% to 5%)1 has also been used more recently by some physicians and has been shown to have many of the same effects as mannitol.
CSF diversion is one of the simplest, quickest-acting methods for decreasing ICP, especially if a ventricular drain is already in place. The emergent surgical evacuation of mass lesions such as large epidural, subdural, or intraparenchymal hematomas is also extremely effective for controlling ICP, and in many instances it is also life- saving. However, in some instances, underlying brain injury or stroke from prolonged brain compression may be exhibited as massive intraoperative brain swelling and in these instances may necessitate that the bone flap be left off (craniectomy).
Management of Severe Closed Head Injury
The current recommendations of the Brain Trauma Foundation Guidelines for the management of closed head injuries call for the placement of ICP monitors in all patients who fall into the severe category (GCS score <9). At our institution we routinely place combination intraventricular monitors and drains in all patients with a postresuscitation GCS score of less than 7. Monitors are inserted into patients with a GCS score of 7 to 9 on an individual basis depending on whether there are distracting reasons, such as intoxication, to cause the altered LOC. If patients are intubated and not following commands but are purposeful in their movements, we will sometimes elect not to place a ventriculostomy and follow the patient’s clinical course over several hours. Other factors include CT findings and the need to go to the operating room during the acute period for the treatment of other life-threatening injuries, age, or for heavy sedation secondary to other injuries or pulmonary problems. At times patients in this GCS range will be given 6 to 12 hours and treated medically to see whether or not they improve prior to placement of an ICP monitor.
Once an ICP monitor and drain have been placed, elevations in ICP are treated in a systematic order. Target values include attempts to keep ICP less than 15 to 20 and cerebral perfusion pressure (CPP) greater than 60. Low CPP (CPP = mean arterial blood pressure [MAP] − ICP) is caused by either elevated ICP or low MAP. For patients with low MAP or uncontrolled ICP, vasopressors may be used to increase blood pressure (BP) and central venous pressure. At the University of Louisville, dopamine (Intropin) is used as a first-line agent, followed by phenylephrine (Neo-Synephrine) and norepinephrine (Levophed) in refractory cases. ICP elevations are initially treated with adequate sedation and pain control, such as midazolam (Versed),1 propofol (Diprivan), and/or morphine (Lioresal),1 to prevent agitation and elevated airway pressures, which can further increase ICP and intermittent CSF diversion. In cases where this fails to control ICP, mannitol is then added to the treatment protocol along with more continuous CSF diversion and finally chemical paralysis. Mannitol is administered as a bolus infusion in doses ranging from 0.25 to 1.0 mg/kg body weight every 4 to 8 hours with the endpoints being either ICP control or measured serum osmolarity greater than 315 mOsmL.
Patients who continue to have sustained increases in their ICP despite these interventions are considered to have refractory ICP and at our facility are considered for one of two potential salvage treatments. Pentobarbital (Nembutal)1 coma has been used successfully on occasion in young patients without mass lesions to decrease the metabolic demands of the brain during these periods of sustained ICP. Patients need to be chosen wisely for this therapy because it carries enormous risks in addition to the possibility of preserving the patient in a long-term, nonfunctional, persistent vegetative state. Initiation of pentobarbital coma causes severe hypotension, and patients almost always require the use of pressors in addition to volume expansion. At our facility we also place all of these patients on a Rotorest bed in an attempt to minimize the pulmonary complications that frequently occur with the use of this technique.
The second salvage therapy is decompressive craniectomy. This procedure involves the removal of a significant area of skull, typically almost an entire hemisphere or both frontal regions with opening of the dura. This permits the injured, swollen brain to herniate through the opening and is the only intervention that increases the volume of the intracranial compartment, thereby reducing pressure. In addition, this technique allows for the evacuation of large hemorrhagic contusions, or in cases of extreme ICP elevations it can be coupled with either frontal or temporal lobectomy. Once again, patients must be selected carefully for this intervention. Decompressive craniectomy is used much more frequently than pentobarbital coma at our institution. We use this strategy for patients with elevated ICP—more than 30 to 40 for more than 30 minutes—or a significant change in neurologic condition that is nonresponsive to all other interventions. In order for either of these two salvage approaches to be effective, they must be used at the first signs of refractory ICP prior to the occurrence of complications such as ischemic infarcts, brainstem compression, or hemorrhage.
Patients treated with decompressive craniectomies are at risk for significant alterations in CSF dynamics, which may result in delayed deterioration. Signs of hydrocephalus, either in the form of ventriculomegaly or extra-axial or interhemispheric CSF fluid collections, will be evident in 50% to 80% of these patients. When necessary these patients will be treated with external ventricular or subdural drains followed by early cranioplasty (replacement of the bone plate). In many instances these changes will resolve following cranioplasty and therefore avoid the need for ventriculoperitoneal shunting, with its associated risks and complications.
All patients with abnormal head CT scans (regardless of GCS score) are treated with close neurologic observation, most commonly in an intensive care unit (ICU) setting, and serial CT scans (4–6 hours later and on PID 1), and they are placed on 7 days of phenytoin (Dilantin). Temkin and colleagues showed that patients with post-traumatic intracranial hemorrhage were at increased risk of suffering seizures in the acute period; treatment with antiepileptics beyond 7 days did not decrease the risk of these patients developing epilepsy or delayed seizures, but there were increased risks associated with side effects from medication administration. Patients who experience a seizure following CHI (with the exception of acute post-traumatic seizures) should be maintained on antiepileptics for at least 3 to 6 months and possible indefinitely depending on their clinical condition and EEG results. Patients with acute post-traumatic seizures (within the first several minutes following the event) are not felt to be at increased risk for developing further seizures and receive the routine 7-day treatment. At the University of Louisville we have found that changing phenytoin dosing to a weight-based schedule (15 mg/kg load, 2 mg/kg every 8 hours unless elderly [≥70 years old], then 2 mg/kg every 12 hours) increases the chance of achieving a therapeutic dose earlier in the treatment course and lowers the costs of monitoring these agents.
Finally, the treatment of these patients requires a tight-knit group of specialists and ancillary service providers with open communication channels. We have found that the use of a time-independent phased outcome clinical pathway helps maximize the level of patient care and maintain cost-effectiveness. By using such an approach all routine interactions are initiated at the time of admission and each care provider has a clear role and responsibility; one of the most important aspects of this system is the involvement of a clinical coordinator whose responsibility includes ensuring that all aspects of patient care and family education are completed at the appropriate intervals. We believe another key component is our philosophy toward early feeding (prior to PID 3) and early tracheotomy and percutaneous endoscopic gastrostomy (PEG) feeding tube placement in a majority of these individuals (PID 4). We have shown that such an aggressive approach to these issues helps reduce infectious complications and minimizes length of ICU stay.
Treatment of Mild and Moderate Traumatic Brain Injury
In many circumstances patients with moderate TBI are treated almost as though they had severe TBI, with the exception of invasive ICP monitoring. Many patients will be intubated at the time of admission and require sedation and adequate pain management. This can be difficult because it is of utmost importance to maintain the ability to perform serial neurologic examinations. Therefore, we commonly use a combination of propofol (Diprivan) infusions and intermittent morphine (Lioresal)1 injections in these patients, thereby allowing hourly assessment of neurologic function. We have found that a subset of patients (older than age 45 years, multisystem trauma, presence of early pneumonia) with moderate TBI requires more aggressive treatment with early tracheostomy and PEG tube placement and, at times, ICP monitors.
The subset of patients with moderate TBI who are not intubated at the time of admission are also watched closely in the ICU. Once again, close monitoring of neurologic function and vigorous pulmonary toilet is of key importance because some patients may be lethargic and are at risk of pulmonary decompensation. We have found ipratropium (Atrovent)1 and albuterol (Proventil)1 nebulizers and early mobilization minimize pulmonary problems. Patients with progressive lethargy, worsening neurologic function, hypoxia, hypercapnia, or the inability to protect their airways are intubated and placed on mechanical ventilation. Once again, patients unable to tolerate a diet by PID 3 have a nasogastric feeding tube placed to allow for early enteral nutritional support; however, PEG tubes are not placed until later in the hospital course in the predischarge phase because many patients in this category will improve throughout their hospitalization and be able to tolerate an oral diet by the time of discharge.
Patients with mild TBI are treated over a much wider continuum, ranging from discharge from the emergency room (ER) with appropriate adult supervision to observation in the ICU to immediate surgical treatment of mass lesions. The two most important factors in determining treatment algorithms for these patients are presence or absence of abnormal CT findings and neurologic function, with associated symptoms such as nausea, vomiting, dizziness, or visual problems. Headache is a common complaint in all of these patients and must be taken in context with other complaints and imaging results. Patients with severe headaches, dizziness, and vomiting (postconcussive syndrome) may commonly require a brief hospital stay to allow for delayed imaging and at least partial resolution of some of the complaints.
Early and Delayed Neurologic Changes
Any patient suffering a significant neurologic injury requires close neurologic monitoring. Although most patients remain unchanged or show gradual improvement in the early phases, a small percentage will show signs of neurologic deterioration. At first these signs may be subtle (agitation, mild increase in lethargy, protracted vomiting); but eventually they may become more profound and can be precursors to impending neurologic demise and death. When these changes are the result of either expanding mass lesions or increases in ICP, treatment instituted in the early phases is more likely to be successful compared to instances when interventions are performed under conditions associated with cerebral herniation syndromes. Thus any patient showing persistent signs of neurologic decline should be promptly evaluated by a physician and many may also require repeat CT scanning.
However, not all neurologic changes are the result of changes in ICP or expansion of mass lesions, and such irregularities may be caused by a long list of other metabolic or neurologic conditions. Some of the more common causes are seizures, strokes (especially from carotid or vertebral dissections), electrolyte imbalances, hypoxia, hypercarbia, fever, excess sedation, or drug and/or alcohol withdrawal.
Concussions and Sports-Related Injuries: Return to Play Guidelines
Over the past 2 decades, knowledge regarding the detrimental effects of repetitive mild head injuries has led to intense public debate concerning whether athletes should be allowed to return to play following such injuries. Concussions are not uncommon among participants in competitive sports including football, hockey, baseball, and soccer. Concerns regarding the full negative impact of repetitive, almost innocuous injury have led many youth soccer leagues to ban or modify rules regarding heading of the ball. In addition, other concerns exist following more severe concussions, including development of other life-threatening neurologic injuries such as subdural or epidural hematomas, development of the double-impact syndrome (rapid, uncontrolled increases in ICP following sequential minor traumas), and the long-term neuropsychological impact of these injuries. As a result of these concerns, the guidelines concerning when and if an athlete should be allowed to return to play have undergone modification since development of the earlier criteria. Because of these frequent changes, readers are encouraged to check with their local medical agencies or recent publications and Internet sources if faced with these issues. In short, if a player loses consciousness or has persistent symptoms (>15–20 minutes), he or she should not be allowed to return to play on that day or even not for 1 to 2 weeks following the complete resolution of all symptoms. It should also be stressed that an individual may have a concussion without loss of consciousness and that concussion is defined as any transient change in mental status. To this end many organizations including the National Football League have developed a sideline neuropsychological screening test that can often help illustrate these deficits even when the athlete appears normal.
Patients suffering any type of TBI can have long-lasting cognitive, psychological, and emotional dysfunction in addition to their functional and neurologic deficits. Although most people assume that the resolution of decreased alertness and consciousness symbolizes resolution of the overall neurologic injury, this is not the case in most patients. In our series of patients with moderate TBI, we found that almost 50% of patients at median follow-up of 27 months complained of persistent emotional or cognitive problems that interfered with their lifestyle despite the fact that they all were discharged from the hospital with a GCS score of 14 to 15. Long-term speech and cognitive therapies as well as individual, group, and family counseling will be helpful for many of these patients.
In the late hospital and early rehabilitative stages, numerous pharmacologic agents may be helpful to overcome some of the neurologic side effects following TBI. Patients with autonomic storms (intermittent episodes of diaphoresis, tachycardia, fever, agitation) may respond to adrenergic antagonists such as clonidine (Catapres)1 or propanolol (Inderal),1 in addition to volume resuscitation, morphine (Lioresal),1 baclofen,1 and bromocriptine (Parlodel).1 Patients with hypoarousal are treated with amantadine1 (Symmetrel), 100 mg at 8 am and 12 pm, and bromocriptine,1 5 to 15 mg every day.
Trazodone (Desyrel), 50 to 100 mg at bedtime, may be helpful in restoring sleep-wake cycles, whereas risperidone (Risperdal),1 olanzapine (Zyprexa),1 and quetiapine (Seroquel)1 may be helpful to control agitation and combativeness during the subacute recovery phases.
The previously mentioned treatment strategies include what is considered common practice at the University of Louisville; however, newer, more aggressive treatments and monitoring capabilities are always being developed. Some of the newer monitoring systems under development include cerebral oximetry measurements (frequently through invasive indwelling catheters) and cerebral microdialysis systems, in which continuous assessments are performed to determine the concentrations of critical markers such as lactate in the brain or CSF. Both of these methods provide physiologic feedback for the metabolic environment of the brain, are sensitive enough to predict changes in regional oxygenation, and have been found to be correlated with outcomes in small nonrandomized studies.
1. Brain Trauma Foundation. Management and Prognosis of Severe Traumatic Brain Injury. New York: Brain Trauma Foundation; 2000.
2. McIlvoy L., Spain D.A., Raque G., et al. Successful incorporation of the Severe Head Injury Guidelines into a phased-outcome clinical pathway. J Neurosci Nurs. 2001;33(2):72–78.
3. Miller P.R., Fabian T.C., Bee T.K., et al. Blunt cerebrovascular injuries: Diagnosis and treatment. J Trauma. 2001;51(2):279– 286.
4. Temkin N.R., Dikmen S.S., Wilensky A.J., et al. A randomized, double-blind study of phenytoin for the prevention of post- traumatic seizures. N Engl J Med. 1990;323:497–502.
5. Vitaz T.W., McIlvoy L., Raque G.H., et al. Development and implementation of a clinical pathway for severe traumatic brain injury. J Trauma. 2001;51(2):369–375.
6. Vitaz T.W., McIlvoy L., Raque G.H., et al. Development and implementation of a clinical pathway for spinal cord injuries. J Spinal Disord. 2001;14(3):271–276.
7. Vitaz T.W., Jenks J., Raque G.H., Shields C.B. Outcome following moderate traumatic brain injury. Surg Neurol. 2003;60(4):285– 291.
1 Not FDA approved for this indication.