Traumatic Brain Injury Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH
Case 27
An 18-year-old man had an unintentional fall from a second story balcony. He had a Glasgow coma scale (GCS) of 5 (El, Vl, M3), normal blood pressure, and normal pulse rate in the emergency department. The patient was immediately intubated, and a brain CT scan revealed linear skull fractures, bilateral frontal lobe contusions, intraparenchymal hematoma, and diffuse cerebral swelling. The neurosurgeon determined that these injuries do not warrant surgical treatment at this time. A ventriculostomy drain was placed in the ICU for monitoring and revealed intracranial pressure (ICP) of 26 mm Hg.
⯈What is the primary goal in the management of this patient?
⯈What are appropriate management steps?
ANSWER TO CASE 27:
Traumatic Brain Injury
Summary: An 1 8-year-old man has fallen from 20 ft and has a traumatic brain injury. His CT scan shows intraparenchymal hemorrhage and diffuse swelling. Placement of the ventriculostomy shows that he has intracranial hypertension.
- Primary goal in the management: The primary goal in the treatment of this patient is to decrease the amount of secondary brain injury.
- Appropriate management steps: This patient has a traumatic brain injury (TBI) and an elevated ICP. The next steps need to include measures to reduce the ICP and maintain the cerebral perfusion pressure (CPP). These measures include the use of mannitol, vasopressors, brief hyperventilation, elevation of the head of bed (if possible), and maintaining the head in midline position. If these measures do not work, surgical intervention may be necessary.
ANALYSIS
Objectives
- To learn the prognostic factors for traumatic brain injuries.
- To learn the optimal supportive strategies (ventilation, fluid/electrolyte, and hemodynamic strategies) for patients with severe brain injuries and intracranial hypertension.
- To learn the factors that contribute to secondary brain injury.
Considerations
This patient suffered a significant fall and presented with a GCS that is indicative of severe intracranial injury. His CT scan has shown that he has skull fractures and severe injury to the brain. The ability to minimize swelling and maintain adequate perfusion to the brain is of the utmost importance, as secondary injury to the brain significantly worsens the outcome. Special attention needs to be paid to ensure that there are no episodes of hypotension or hypoxia. A ventriculostomy is helpful in the diagnosis and treatment of traumatic brain injury. This device can be used not only for ICP measurements, but it can be used to remove cerebrospinal fluid (CSF) for temporary relief of intractable intracranial hypertension.
Approach To:
Traumatic Brain Injury
DEFINITIONS
TRAUMATIC BRAIN INJURY: Injury to the brain as a result of an external force leading to disruption of brain tissue and blood vessels. The injury can consist of skull fractures, intracranial bleeding (subdural, epidural, intraparenchymal), and diffuse axonal injury.
MONRO-KELLIE DOCTRINE: Doctrine that describes cerebral compliance. Within the skull, there is brain tissue, cerebrospinal fluid, and intracranial blood. As the volume of one of these increases, the skull does not allow for expansion, so there is a mandatory increase in ICP. Only with the reduction of one of these (skull restrictions, tissue, fluid, or blood) can there be a reduction in ICP.
CEREBRAL PERFUSION PRESSURE (CPP) = MAP - ICP. Under normal circumstances, the cerebral blood flow remains constant over a wide range of cerebral perfusion pressure. This is often referred to as the zone of autoregulation. Normally, CPP below 50 mm Hg causes ischemic damage, while CPP above 150 can cause hyperperfusion injury. Acute disease processes can alter the range of the zone of autoregulation, leading to increased risk of cerebral damage.
CLINICAL APPROACH
Prognostic Factors for Traumatic Brain Injuries
Traumatic brain injury remains one of the major causes of morbidity and mortality. In the United States, brain injury was only recently surpassed by gunshot wounds as the number 1 cause of death in trauma patients. There is a significant amount of post-injury care needed in this population, since many patients require rehabilitation or suffer from posttraumatic stress disorder (PTSD). The goal in treating patients with TBI is to minimize the risk for developing secondary brain injury. Identifying those factors which tend toward a worse prognosis is not as clear, however. The prognosis for TBI is dependent on a multitude of factors including the type and severity of the injury, the time before initiation of treatment, and physiologic occurrences after the injury. There have been models based on large numbers of retrospective analysis that have identified some prognostic factors for TBI.
The most commonly identified factors in almost all models that identify risk factors for poor outcomes are age, initial motor score in the GCS, and pupillary reactivity at admission. Additional prognostic information is provided by the initial CT scan. The inclusion of other clinical information such as secondary insults (hypotension and hypoxia), and laboratory parameters (glucose and hemoglobin) appears to strengthen the prognostic indication.
The GCS (Table 27-1) was introduced to help improve uniformity, reproducibility, and communication of patients' neurological conditions between different care providers. The routine use of the GCS allows stratification of patients for initial therapy. The GCS measures the patient's consciousness in 3 separate components.
They are scored for their eye-opening response, their verbal response, and their motor response with a minimum score of 3 and maximum of 15. The patient is awarded the best score possible for each category. For example, a patient who is a new paraplegic, but can follow commands with their arms is given a score of 6 on the motor scale (not a 1 because he does not move his legs). A low score for the motor component of the GCS has been identified as the most important predictor of poor outcome.
The pupillary examination is an essential component of the initial examination for all trauma patients. Detection of a pupil asymmetry, dilation or loss of light reflex in an unconscious patient is concerning for ipsilateral intracranial pressure increase. The mass effect of intracranial injuries increases the intracranial pressure and this is reflected by compression of the cranial nerves and pupillary changes. Patients who have concerns for intracranial injury and have unequal or nonreactive pupils should have rapid lowering of their ICP.
The type of injury seen on the CT scan appears to indicate the likelihood of poor outcome. Direct lacerations of epidural arteries produce epidural hematomas, while it is the disruption of bridging subdural veins that causes subdural hematomas. Intracerebral contusions are most likely the result of tissue disruption from the direct force of the injury. Contra-coup injuries are common and can be on the more severely injured side. A subarachnoid hemorrhage has been stated to double the mortality. Conversely, an epidural hematoma was associated with a better outcome, possibly due to the ability to emergently evacuate the hematoma. The brain damage caused by an epidural hematoma is secondary to compression, instead of intrinsic brain injury. Relief of this pressure likely results in full recovery.
Diffuse axonal injury (DAI) may not be seen on initial CT scan, but often results in poor long-term outcome. Small punctate lesions seen on initial CT scan may hint toward DAI, but MRI is the definitive imaging for diagnosis. The MRI for diagnosis of DAI does not need to be done in the early treatment stages. CT findings can also correlate with increased intracranial pressures. The loss or compression of the basilar cisterns is an indication of elevated ICP and predictor of poor outcome. With improved transport times and rapid access to CT scans, there is new risk for underestimating early intracranial injuries seen on the initial CT scan. Therefore, any patient with TBI who has intracranial pathology should have an early follow-up CT image.
Supportive strategies for severe brain injuries and intracranial hypertension: Aggressive restoration of intravascular volume, maintenance of adequate cerebral perfusion pressure, and avoidance of hypoxia are the primary endpoints in the supportive therapy for patients with intracranial hypertension. There are several different therapies and maneuvers that can be utilized to achieve these goals. Cerebrospinal fluid drainage, controlled hyperventilation, mannitol, and barbiturates are among the most commonly used therapies to alleviate intracranial hypertension. Maneuvers directed at improving cerebral perfusion require that patients have appropriate continuous monitoring with intracranial pressure monitors, central venous catheters, and arterial lines. Patients with increased intracranial pressures should be positioned to optimize venous drainage from the brain, and this can be accomplished with elevation of the head of the bed and positioning the head in a neutral, midline position.
The monitoring of ICP is essential for all patients with severe head injury. The concern for herniation from elevated ICP is the impetus for placement of ICP monitoring. The range for when to treat elevated ICP is not as clear, but is usually recommended at ICP >20 to 25 mm Hg. Increased intracranial pressure may have a direct injurious effect on the brain tissue, but the greatest harm associated with increased ICP is the increase in resistance to cerebral blood flow, which produces additional secondary brain injury.
Maintaining adequate blood flow to the brain is important treatment therapy, but it is not as easy as it would seem. Under normal circumstances, cerebral pressure autoregulation maintains CBF stable over a wide range of CPP (approximately 50-150 mm Hg). However, this zone of autoregulation is disrupted in patients with traumatic brain injuries, resulting in an increased reliance on raised MAP for brain perfusion. Previously, a CPP of >70 mm Hg was the goal for treating patients with TBI. However, data from the National Institutes of Health (NIH) -funded North American Brain Injury Study on Hypothermia suggested that transient decreases in CPP <60 mm Hg were not associated with worse outcome than CPP >60 mm Hg. The recent data seem to question the utility of maintaining the MAP artificially high to improve CPP, and this practice in fact may increase the duration of intracranial hypertension. It appears that attention to CPP is important; however, the best strategy for management is not clear. However, it is accepted that routinely elevating CPP to values above 60 mm Hg is not associated with improved outcome.
Brain cell metabolism is more important than total blood flow; thus, methods have been devised to try and monitor cerebral cellular metabolism. Two methods involve measuring 1) the oxygen saturation in the internal jugular vein (JVSo2), and 2) the tissue oxygen tension i n the brain (Ptio2). These methods have obvious limitations. The JVSo2 is a measurement of entire brain oxygen utilization which may not help when there is a focal lesion. Conversely, the brain tissue oxygenation measures only a focal area of tissue and may not be representative of other areas of injury. Currently no device can be singled out as an ideal monitor.
Avoidance of hypotensive episodes is important and is accomplished by use of plasma expansion (crystalloids, colloids, blood products) and vasopressors. It is important to recognize that while patients with TBI may have hypotension as a result of their TBI, this is an uncommon occurrence, so any hypotension in a patient with a TBI should be considered to be hypovolemic in nature. The achievement of euvolemia is necessary prior to the addition of vasopressors, as the constriction of cerebral blood vessels in a hypovolemic patient can contribute to worsening ischemia. Crystalloid administration is best accomplished by use of normal saline. This is different from patients who need volume resuscitation as the result of hemorrhage. The normal saline can aid in expanding the intravascular volume and may aid in decreasing brain tissue swelling. For similar reason, fluids containing dextrose and water should not be given to patients with TBI, as the free water may infuse into the brain tissue and thereby increase brain swelling. Vasopressor use usually involves an α-agonist that has focused activity on vasculature. Treatment of hypertension is rarely indicated in the patient with head injury. There is no evidence that hypertension promotes continued intracranial hemorrhage.
Patients with severe brain injury (GCS <8) require early intubation for protection of their airway. This also allows for the provision of increased oxygen administration to reduce hypoxia. Additionally, the minute ventilation can be controlled, and the patient can be hyperventilated to decrease the Paco2 and thus cause vasoconstriction. This will decrease both the cerebral blood flow and cerebral blood volume. The decrease in blood volume can aid in the acute decrease in elevated ICP. Potential benefits of controlled hyperventilation are probably most prominent in the first 24 to 48 hours after injury, so hyperventilation to decrease ICP should be used with extreme caution and only for short periods of time. Thereafter, if intracranial hypertension persists, controlled hyperventilation to Paco2 values of 30 to 35 mm Hg may be considered, but again for only short time periods. For the majority of individuals, controlled ventilation to maintain Paco2 between 35 and 40 mm Hg is optimal.
Cerebral edema in patients with TBI can result from direct cellular injuries from the traumatic event or later from vasogenic edema during the recovery phase. Currently, the strategies for removing cerebral edema are limited to osmotic agents, usually mannitol or hypertonic saline. Mannitol increases the osmotic gradient and by Starling forces, draws fluid from the interstitial compartment of the brain into the plasma, thereby decreasing the brain volume and ICP. Mannitol can have adverse consequences as it is a potent diuretic and can significantly decrease the intravascular volume and, consequently, decrease the CBF. As such, it should only be given to patients who have documented euvolemia and ongoing continuous monitoring to avoid treatment-related hypotension. Hypertonic saline has been implemented more recently in the treatment of patients with TBI. The same mechanism of action to reduce ICP is hypothesized for hypertonic saline, but there is currently no data to support its efficacy.
Painful and noxious stimuli in patients with TBI can contribute to increase in ICP. Adequate pain control and sedation is critical when caring for these patients. However, the use of such agents can limit the neurologic examination; therefore, short-acting agents are preferred. Barbiturate comas have also been utilized to aid in the decrease of cerebral metabolism, but this intervention should be limited to situations where sedation alone is insufficient to maintain patient comfort. Neuromuscular blockade may be added if further ICP control is needed, but again, it interferes with the ability for neurological examination.
Factors Contributing to Secondary Brain Injury
Secondary brain injury refers to the injurious events that occur after the initial injury. Other than public safety intervention measures (ie, requirement of helmet wearing, etc), there is little that can be done to prevent the primary injury. It is the severity of the secondary insult that often determines the overall outcome of patients with TBI and as such, it has become the major goal in the treatment of patients with TBI. The 2 factors that are most injurious are hypotension and hypoxia. Another significant factor that can contribute to secondary brain injury is secondary hemorrhage, often referred to as "blossoming" of the initial hemorrhage.
The pathophysiology behind secondary injury involves biochemical processes and injury to the "supporting cells" in the brain including microglia, astrocytes, oligodendrocytes, and endothelial cells; these are critical to the survival of neurons. Numerous clinical trials of patients with brain trauma have investigated of use of various pharmacologic agents to mitigate secondary injury. However, to date, there has been limited success demonstrated in these investigations.
Since there are no real pharmacologic interventions that can prevent or reverse secondary injury, the primary management is to minimize hypotension and hypoxia. A single episode of systolic blood pressure of <90 mm Hg that occurs during the period from injury through resuscitation doubles the mortality and significantly increases the morbidity of any given brain injury. This reinforces the priority of avoiding hypovolemia and early consideration for vasopressor initiation when hypotension is refractory to fluid management.
Hypoxia is also known as a significant contributor to poor outcome in patients with TBI. The incidence of hypoxic episodes has decreased with the practice of early intubation and mechanical ventilator support. The avoidance of decreased oxygencarrying capacity (anemia) is often cited in the literature as a need to maintain a hematocrit of above 30%. Currently, this level of hematocrit is not substantiated by the literature, and the adverse effects of blood transfusions are well known. However, it is generally accepted that patients with TBI should avoid significant anemia and the need for transfusion is left to the judgment of individual physicians.
Secondary brain hemorrhage is certainly one of the most devastating forms of secondary injury. The additional blood volume increases the mass effect and ICP, limiting the ability to maintain adequate CBF. Additionally, the increased bleeding initiates oxidative stress, inflammation, and edema, which all can result in cell death. Reducing secondary hemorrhage after CNS trauma may have profound effects on overall outcome. Monitoring the patient's coagulation status, especially those who have undergone significant blood transfusions is critical, as coagulophathies will contribute to further bleeding and increased mass effects.
Another important source of secondary injury is continued fever. It is not clear as to how or why continued fever increases secondary brain injury, but it is thought that the increased metabolic requirement of the cells is the cause. Patients with severe brain injuries and fevers should be treated aggressively with medications and mechanical cooling devices to reduce their core temperatures.
CLINICAL CASE CORRELATION
- See Case 7 (Ethics in Critical Care), Case 28 (Blunt Trauma), and Case 30 (Altered Mental Status).
COMPREHENSION QUESTIONS
27.1 An 1 8-year-old man is riding his motorcycle when he crashed into a light pole. On presentation to the trauma bay, his eyes open to pain, he his mumbling, and he has flexor posturing. What is his GCS?
A. 6
B. 7
c. 8
D. 9
E. 10
27.2 A 35 -year-old woman i s the passenger in a car that i s involved in rollover. When she arrives at the trauma bay, her GCS is 5 (E1 V1 M3 ), and she is intubated. She is hypotensive with a systolic blood pressure of 80 mm Hg that is not responsive to fluid resuscitation. Her FAST shows free fluid in the abdomen. The initial management should be:
A. Immediately place a ventriculostomy in the trauma bay.
B. Take the patient to the CT scanner to image their brain and cervical spine.
C. Take the patient immediately to the operating room.
D. Admit to the ICU, start fluid boluses and blood transfusions.
E. Take patient to the angiography suite for aortic angiography and embolization.
27.3 A 21-year-old man had a bicycle crash with subsequent intracerebral hemorrhage and ventriculostomy placement. Later that day, his ICP rises to 35 mm Hg and he is given 100 g of mannitol. Over the next hour, his blood pressure decreases from 120/80 to 90/60 mm Hg. The most likely cause of his hypotension is:
A. Increased intracerebral pressure
B. New intracranial bleeding
C. Spinal shock
D. Decreased intravascular volume
E. Myocardial depression
27.4 A 19-year-old man is hit in the head with a baseball bat and is brought to the hospital by his friends 5 minutes after being assaulted. His GCS is 10 and his blood pressure is 150/90 mm Hg. He has a CT scan of his brain that shows a small area with intraparenchymal hemorrhage (~3 cm in diameter) . He is taken to the ICU for monitoring. His treatment should include which of the following:
A. Mannitol administration, repetition of CT scan in 24 to 48 hours, and monitoring in the ward
B. Ventriculostomy placement and admission to the ICU for monitoring
C. Intubation, fluid administration, vasopressors, and repetition of CT in 6 hours
D. Admission to the ICU for monitoring and repetition of CT in 6 hours
E. Emergent craniectomy and evacuation of the intracerebral hematoma
ANSWERS TO QUESTIONS
27.1 B. His GCS is 7 . Using this value, he receives 2 points for opening his eyes to pain, 2 points for incoherent speech, and 3 points for flexor posturing.
27.2 C. This patient was involved in a significant trauma and presents to the trauma bay with a decreased GCS. She is intubated for airway protection. She is receiving fluid for her hypotension, but it does not respond to fluid administration and her FAST examination shows that there is free fluid in the abdomen. The 2 most injurious events in a patient with a TBI is hypotension and hypoxia. It appears that the patient has continued bleeding in her abdomen as seen by free fluid there and a blood pressure that does not respond to fluids. Controlling the bleeding in the operating room is the best method to decrease the likelihood of hypotensive episodes.
27.3 D. Mannitol works to decrease cerebral edema by increasing the osmotic gradient from brain tissue to the plasma, thereby drawing the fluid out of the brain tissue. However, mannitol also acts as a significant diuretic and can deplete the total intravascular volume. This can lead to hypotension and increase the risk of secondary brain injury. It should only be used in patients who are known to be euvolemic.
27.4 D. This patient has a moderate head injury as indicated by his GCS. He has a small intraparenchymal bleed, but because of his rapid presentation to the emergency department, this bleed may "blossom" later. His injury is not severe enough at the moment to warrant intubation, ventriculostomy placement, vasopressors, or surgical decompression. However, because of the risk of increased bleeding, he does need to be monitored in the ICU with frequent neurologic examinations and a repeat head CT in about 6 hours.
CLINICAL PEARLS
⯈ Early supportive therapy in patients with TBI includes restoration of intravascular volume, maintenance of adequate cerebral perfusion pressure, and avoidance of hypoxia.
⯈ Hypotension in a patient with TBI should be considered to be hypovolemic first, and efforts should be concentrated on identifying and correcting the source of hypovolemia.
⯈ Reducing the ICP can be accomplished with elevation of the head of bed, neutral head position, osmotic diuresis, and brief hyperventilation.
⯈ Reduction of secondary brain injury is the primary goal in treating patients with TBI.
References
Chang CWJ. Neurologic injury: prevention and initial care. In: Gabrielli A, Layon AJ, Yu M, eds. Civetta, Taylor, & Kirby's Critical Care. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009:1245-1260.
Clifton GL, Drever P, Valadka A, Zygun D, Okonkwo D. Multicenter trial of early hypothermia in severe brain injury.] Neurotrauma. 2009 Mar;26(3 ):393-397.
Nortje J, Menon DK. Traumatic brain injury: physiology, mechanisms, and outcome. Curr Opin Neural. 2004 Dec;17(6):711-718.
Winter CD, Adamides AA, Lewis PM, Rosenfeld JV. A review of the current management of severe traumatic brain injury. Surgeon. 2005;3:329-337.
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