Evidence-Based Guidelines for the Management of Traumatic Brain Injury

Abstract

The management of traumatic brain injury has changed as a result of evidence-based treatment guideline first established in 1995. They have promoted standardization of care and as a result improved outcomes. In addition, the guidelines have helped identify gaps in our knowledge-base that can direct future research efforts.

Introduction

Traumatic brain injury (TBI) is a leading cause of death and disability for individuals in the United States. Of the estimated 1.4 million people who sustain a TBI annually, 1.1 million are evaluated and discharged from an emergency room, 235,000 are hospitalized and 50,000 will die. Males have the highest rates of TBI; while a motor vehicle accident is the most common mechanism of injury.¹

The Brain Trauma Foundation (BTF) was founded in 1986 by Dr. Jamshid Ghajar and the board of Sunny van Bulow Coma and Head Trauma Research Foundation, in order to support research on TBI. The BTF partners with the American Association of Neurological Surgeons (AANS), Congress of Neurological Surgeons (CNS) and AANS/CNS Joint section on Neurotrauma and Critical Care. The first evidenced-based guidelines for the management of TBI were published in 1995 and two subsequent editions in 2000 and 2007. The guidelines are widely accepted in the United States and have also been implemented in Europe, South America and China. They encompass all aspects and settings for the management of TBI including pre-hospital, in-hospital, surgical, pediatric and combat-related field management.² The guidelines can be accessed at www.braintrauma.org and an online interactive tool for TBI guidelines can be found at www.tbiclickandlearn.org.

Management

The principal goal for the management of traumatic brain injury is the prevention of secondary injury. The primary brain injury is often irreversible, however, maintaining adequate cerebral blood flow and oxygenation will assist in preventing further injury to the unaffected brain and as a result improve overall outcomes.

Treatment begins with adequate resuscitation. This includes maintaining a systolic blood pressure above 90 mmHg and blood oxygen saturation above 90%. Outcomes are significantly worse with only short periods of hypotension or hypoxia.³

In addition to adequate resuscitation, maintaining sufficient cerebral perfusion is critical. Measuring cerebral blood flow directly is not practical within the clinical setting; however, cerebral perfusion pressure (CPP) serves as an adequate substitute and can be calculated easily. CPP is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP, CPP=MAP-ICP) and is the pressure gradient across the cerebrovascular bed. The goal of management is to maintain the CPP between 50–70 mmHg which is accomplished through the adequate control of MAP and ICP. Control of MAP can be achieved with crystalloids and vasopressors. Vasopressors should be started if adequate fluid resuscitation fails to maintain a sufficient MAP.

Intracranial pressure is the pressure within the cranial vault relative to atmospheric pressure. Normal ICP ranges from 7 to 15 mmHg. The cranial vault has a fixed volume and is comprised of brain parenchyma (80% of volume), blood (10% of volume) and cerebrospinal fluid (CSF, 10% of volume). The Monro-Kellie doctrine describes the relationship between these three components and the ICP. When one pressure component increases, the other pressures will decrease to maintain a constant ICP. These compensatory mechanisms keep ICP within normal limits by shifting CSF from the ventricles into the spinal compartment, increasing CSF absorption, or removing blood from cerebral venous vessels. When the pressure from any of the three components exceeds the compensatory mechanism, ICP increases.

Patients with a Glasgow Coma Scale (GCS) score < 9 (See Table 1) are at highest risk for intracranial hypertension. An ICP monitor is useful for determining prognosis and for guiding therapy in severe TBI. When a patient has an abnormal CT scan (hematoma, contusions, swelling, herniation or compressed basal cisterns) and a GCS< 9 after resuscitation, placement of an ICP monitor should be considered assuming there is a reasonable prospect for survival. ICP monitoring should also be considered in patients with a GCS< 9 and a normal CT if two or more of the following exist: age > 40 years, unilateral or bilateral motor posturing or SBP < 90 mmHg. ICP monitors can be placed in the ventricle, brain parenchyma, subarachnoid space, subdural space or epidural space. However, a ventricular catheter connected to an external gauge transducer has been shown to be the most accurate and cost effective method of monitoring ICP (See Figure 1). A pressure of 20–25 mmHg can lead to herniation and is a reasonable threshold at which treatment should be initiated; although, ICP less than 20–25 mmHg can lead to herniation if there is a critically placed intracranial mass such as a hematoma.

Table 1.

Glasgow Coma Scale

GCS=Best Eye Opening+Best Verbal+Best Motor (range 3–15)

Points	Best Eye Opening	Best Verbal	Best Motor
6			obeys
5		oriented	localizes pain
4	spontaneous	confused	withdrawals to pain
3	to speech	inappropriate	flexion (decorticate)
2	to pain	incomprehensible	extensor (decerebrate)
1	none	none	none

Figure 1.

Types of Intracranial Pressure (ICP) Monitors

Treatment of Elevated Intracranial Pressure

Treatment of elevated ICP can be achieved by decreasing parenchymal, CSF or blood volume. The use of a ventricular catheter provides access to monitor ICP and also will allow for drainage of CSF to lower elevated ICP. The inclusion of a ventricular catheter to drain CSF, if needed, is a reasonable adjunct to the placement of an ICP monitor and can be highly effective in controlling an elevated ICP.

Hyperventilation effectively lowers ICP as a result of vasoconstriction and diminished cerebral blood flow; however, this contradicts the primary goal of maintaining adequate cerebral blood flow. Hypocapnia can worsen cerebral ischemia⁴ and in the injured brain prolong hyper ventilation is associated with worse outcomes and is not recommended. However, hyper ventilation can be used as a temporizing measure while other treatment modalities, such as surgical decompression, are being initiated.

Hyperosmolar therapy is effective in controlling elevated ICP primarily through the reduction of brain parenchymal volume. Mannitol is the primary agent utilized for this treatment, although, other agents including hypertonic saline are often utilized. Because mannitol induced dieresis can cause hypotension, blood pressure should be closely monitored. In order to monitor the effectiveness of treatment, the use of an ICP monitor should be considered when administering mannitol.

Surgical Treatment of Elevated Intracranial Pressure

Surgical treatments are also important in the management of elevated ICP. Removal of a mass (i.e. hematoma, contusion, etc) lowers the overall volume within the intracranial vault and as a result lowers ICP. In addition, it prevents further injury to the brain due to the direct pressure of the mass. These space occupying lesions include hematomas within the epidural space, subdural space or brain parenchyma (See Figure 2A & 2B). However, they can also include focal edematous or contused brain parenchyma that has mass effect. The indications for surgical intervention are based on the clinical findings, the size of the mass and the amount of associated mass effect on the brain. Small lesions that are asymptomatic and not associated with significant mass effect can be followed with serial neurological examinations and CT scans. Removal of mass lesions usually involves a large craniotomy that includes the frontal, temporal and parietal regions. This affords exposure that allows for the flexibility to alter surgical objectives as the procedure unfolds. Removal of hematomas, debridement of necrotic brain parenchyma and controlling hemorrhage are important surgical goals.⁵

Figure 2A. Gunshot Wound with Contusion and Diffuse Cerebral Edema.

(Thin arrow: Ventriculostomy tube, Arrowhead: Bone fragments, Open arrow: Contusion)

Figure 2B. After Craniectomy.

(Arrows: Craniectomy site)

In addition to removal of space occupying lesions to diminish intracranial volume, removal of a portion of the cranium (i.e. craniectomy) can also be useful. The portion of bone is sterilely stored or placed in a subcutaneous pouch within the patient’s abdominal wall. Thus a craniectomy allows for an increase in the overall volume of the cranial vault and lowering ICP. The bone flap can be replaced once the factors resulting in the elevation of ICP have resolved. A craniectomy is often combined with procedures to remove spaces occupying lesions such as a hematoma, however, it can be performed in isolation if there is no focal mass and other treatment modalities to control the ICP have failed. While further study is required to determine if a craniectomy improves outcomes, it has gained acceptance as an effective option to control ICP.

The use of steroids to reduce brain edema associated with brain neoplasms became prevalent in the 1960s. Because cerebral edema associated with TBI has different pathologic mechanisms than that which is associated with other processes such as tumors, the use of steroids in TBI is ineffective in controlling ICP and is associated with worse outcomes. Consequently, the guidelines recommend that steroids should not be used in the treatment of TBI.

Posttraumatic seizure (PTS) is classified as either early (< 7 days after TBI) or late (> 7 days after TBI). The use of prophylactic anticonvulsants to prevent late PTS has not shown to be effective and is not recommended. Evidence suggests that early PTS can be diminished if anticonvulsants are administered during the first seven days following a TBI; however, there is no associated improvement in outcomes with the use of anticonvulsants.

Conclusion

The establishment and implementation of the evidence-based guidelines for the treatment of TBI has been an important effort over the last 15–20 years. The widespread acceptance of the guidelines has standardized care across institutions and most importantly improved outcomes. In addition, the guidelines have helped direct research efforts to strengthen the evidence for the treatment modalities used in TBI.

Biography

John W. Gianino, MD, MBA, FACS, MSMA member since 2003, is Assistant Professor of Surgery at the University of Missouri – Kansas City School of Medicine and Chief of Neurosurgery at Truman Medical Centers in Kansas City. Lukuman O. Afuwape, MD, is a second resident in the Department of Surgery at the University of Missouri – Kansas City School of Medicine.

Contact: john.gianino@tmcmed.org