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The Management of Traumatic Brain Injury 

The Management of Traumatic Brain Injury
Chapter:
The Management of Traumatic Brain Injury
Author(s):

Jeremy G. Stone

, David M. Panczykowski

, and David O. Okonkwo

DOI:
10.1093/med/9780199375349.003.0009
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date: 07 December 2019

General Principles

Epidemiology

In the United States, traumatic brain injury (TBI) results in 2.5 million emergency department (ED) visits per year with 280,000 requiring hospitalization and is responsible for 53,000 deaths annually. The leading causes of TBI resulting in hospitalization include falls, motor-vehicle collisions, and assaults. Age-adjusted rates of TBI-related ED visits are increasing (457.5 in 2007 to 715.7 in 2010) whereas TBI-related hospitalizations have remained the same (91.7 per 100,000 people) and TBI-related deaths have decreased (18.2 to 17.1 per 100,000 people) over the same time period. Taken together, the prevalence of TBI confers an immense burden on the health care system with regard to direct medical expenditures, rehabilitation of long-term TBI-related disability, and indirect cost related to loss of productivity.

Definitions

The most widely utilized grading system for TBI severity is the Glasgow Coma Scale (GCS), which stratifies TBI into mild (e.g., concussion; GCS 13–15), moderate (GCS 9–12), and severe (GCS 3–8). The GCS assesses a patient’s level of consciousness based on scores for eye opening, verbal response, and motor response (detailed in assessment section later).

The primary injury, which occurs at the time of initial trauma, may be caused by blunt, blast, and/or penetrating mechanisms and is defined as death or dysfunction of central neurons secondary to the initial traumatic impact. Secondary injury includes progressive neuronal injury that develops subsequent to the initial trauma caused by inflammatory, ischemic, and/or cytotoxic insults that may be secondary to or modulated by both intracranial and systemic processes. In the critical care setting, nothing can be done to mitigate primary injury, which by definition has already occurred. However, prophylaxis, early recognition, and rapid treatment of subsequent insults may modulate secondary injury and improve outcome after TBI.

Key physiologic factors implicated in secondary brain injury include hypotension, hypoxia, intracranial hypertension, and inadequate cerebral perfusion pressure, all of which ultimately result in cerebral ischemia. Evidence-based protocols in severe TBI management are directed toward avoidance and treatment of cerebral ischemia and have reduced mortality rates in severe TBI from 50% to less than 25% over the past 30 years.

Pathophysiology of Cerebral Ischemia

When there is insufficient cerebral blood flow (CBF) to meet the metabolic demands of the brain, cerebral ischemia results. Unique among our organs, the brain lacks the capacity for significant oxygen storage, has minimal capacity to store glycogen, and is nearly completely dependent on blood flow to provide substrates of metabolism. As such, normal central nervous system physiology has autoregulatory mechanisms which couple the cerebral metabolic rate of oxygen to CBF to ensure that the high metabolic demands of the brain parenchyma are met. Cerebral autoregulation allows CBF to be kept constant over a wide range of blood pressures. Through dynamic vasoconstriction and dilation, cerebral arterioles can maintain a consistent level of blood and oxygen delivery when systolic blood pressure ranges between 50 and 150 mm Hg (Figure 9.1). Outside of this autoregulatory threshold, however, arteriolar vasoconstriction or dilation fail to maintain constant CBF and cerebral ischemia may ensue.

Figure 9.1 Cerebral blood flow is maintained at relatively constant rate over a wide range of cerebral perfusion pressures via dynamic arteriolar dilation and vasoconstriction.

Figure 9.1 Cerebral blood flow is maintained at relatively constant rate over a wide range of cerebral perfusion pressures via dynamic arteriolar dilation and vasoconstriction.

Source: White H, Venkatesh B. Cerebral perfusion pressure in neurotrauma: a review. Anesth Analg. 2008;107:979–988. Printed with permission of Wolters Kluwer Health, Inc.

Cerebral autoregulation is often impaired in TBI, thus several physiologic parameters involved in autoregulation are implicated in increased risk for cerebral ischemia (Figure 9.2). Cerebral perfusion pressure (CPP) is defined as mean arterial pressure (MAP) minus intracranial pressure (ICP) and is a surrogate marker for CBF. Low CPP is associated with higher mortality and morbidity in TBI, particularly when systemic hypotension occurs concomitantly. Likewise, hypoxia (arterial oxygen saturations <60%), systemic hypotension (systolic blood pressures <100–110 mm Hg), elevated ICP (ICP >20 mm Hg), low brain tissue oxygen saturation (PbtO2 <15–20 mm Hg), and hyperthermia (core temperature >38.5 °C, or brain tissue temperature >37.5 °C) are linked with higher morbidity and mortality in severe brain injury.

Figure 9.2 Cerebral perfusion pressure autoregulation in normal patients (A) versus patients with traumatic brain injury (B).

Figure 9.2 Cerebral perfusion pressure autoregulation in normal patients (A) versus patients with traumatic brain injury (B).

Source: Rangel-Castilla L, Gasco J, Nauta HJ, Okonkwo DO, Robertson CS. Cerebral pressure autoregulation in traumatic brain injury. Neurosurg Focus. 2008;25:1–8.

ICP is a key factor influencing CPP. Dictated by the fundamental principles of the Monro-Kellie doctrine, ICP is determined by the dynamic interplay between blood, cerebrospinal fluid (CSF), and brain parenchyma, the three components which occupy the fixed volume within the skull. If any one of these three components enlarges in volume or there is a new mass lesion introduced within the skull by trauma, there must be a compensatory corresponding decrease in volume of the other components in order to maintain the same pressure. The system has some capacity to compensate for new intracranial mass lesions by decreasing venous blood volume and/or CSF volume; however, once compensatory measures are overcome, there is an inevitable rise in ICP. Elevated ICP may ultimately lead to decreased CPP and cerebral ischemia or brain herniation, thereby contributing to secondary injury.

Clinical Assessment and Classification

General Principles

As in all traumatic injury, primary assessment and management should proceed based on Advanced Trauma Life-Support recommendations. Of patients with GCS ≤8, 60% have one or more other organ systems injured. As such, a focus on airway, breathing, and circulatory systems precedes neurologic assessment.

Neurologic Assessment and Classification

The GCS developed by Teasdale and Jennett in 1974 is the most widely used, reproducible, and rapid initial clinical assessment tool in TBI. Three components including eye opening, verbal response, and motor response are assessed and summed to quickly determine a patient’s overall level of consciousness (Table 9.1). Mechanical ventilation via endotracheal tube or tracheostomy precludes a patient’s ability to produce a verbal response, thus the verbal score of 1 is designated with a following “T” to highlight the mechanically ventilated status of the patient. Limitations of the GCS include scenarios with concomitant use of sedating alcohol, drugs, and/or administered medications; presence of facial trauma limiting eye opening or verbal responses; and/or assessment shortly after rapid sequence intubation in which neuromuscular blockade is in effect.

Table 9.1 The Glasgow Coma Scale

Best Response

Score

Eye Opening (E)

  • Spontaneous

4

  • To speech

3

  • To pain

2

  • Not open

1

Verbal Response (V)

  • Conversant and oriented

5

  • Confused

4

  • Nonsense

  • Sounds (moans)

3

2

  • Silent

1

  • Intubated

1T

Motor Response (M)

  • Follows commands

6

  • Localizes to pain

5

  • Withdraws from pain

4

  • Arm flexion to pain

3

  • Arm extension to pain

2

  • No response

1

GCS score = E + V + M (range 3 or 3T to 15)

Coupled with the GCS, pupillary and motor examinations are key components of an initial rapid neurologic assessment. A unilateral dilated, nonreactive pupil suggests ipsilateral uncal herniation with subsequent ipsilateral oculomotor nerve dysfunction. Alternatively, bilaterally dilated and unresponsive pupils may by observed in severe irreversible brainstem injury, hypotension, hypoxia, or bilateral oculomotor nerve dysfunction. Patients with an admission GCS of 3 and bilaterally dilated unresponsive pupils have near 100% mortality. The presence of focal weakness on motor examination may suggest a lateralized mass lesion. Most often, uncal herniation of the medial temporal lobe causes disruption of the corticospinal tracts on the side of the mass lesion and presents with contralateral weakness. However, in 10% of cases, a Kernohan notch phenomenon or “false localizing sign” may be observed in which a lateralized mass lesion will cause weakness on the same side as the lesion due to the contralateral corticospinal tracts being compressed against the contralateral edge of the tentorium cerebelli.

Monitoring in TBI

CPP is used as a surrogate for the adequacy of CBF, therefore ICP and MAP should be monitored in severe TBI. Continuous systemic blood pressure monitoring via indwelling arterial line, ICP monitoring via invasive intracranial monitor, and continuous pulse oximetry are recommended in the critical care setting. ICP monitors may take the form of intraparenchymal monitors or external ventricular drains (EVD), which are placed within the ventricle. With regard to intraparenchymal monitors, devices on the market employ various technologies including fiberoptic transduction, microtip strain gauge transduction, or pneumatic transduction to measure ICP. Notably, EVDs have the dual ability to both directly transduce ICP and treat elevated ICP via diversion of CSF. However, when an EVD is open to drain, ICPs are unable to be transduced. Thus, per protocol at our institution, all severe TBI patients undergo tandem placement of EVDs and intraparenchymal ICP monitors, permitting ICP to be continuously transduced even while CSF is actively being diverted via EVD. This practice is not universal, and local protocols should be established by the managing teams.

While these physiologic parameters serve as surrogate markers for cerebral oxygenation, brain tissue oxygenation (PbtO2) may also be directly assessed via invasive fiberoptic catheter placement into the brain parenchyma. Low PbtO2 levels (<15–20 mm Hg) and longer duration of decreased PbtO2 (>30 minutes) are associated with higher mortality rates in severe TBI. Many protocols set a PbtO2 level of ≥20 mm Hg as the targeted goal for patient management.

Management of TBI

Care Setting

Patients with severe TBI should be cared for in a tertiary care center with a high volume of TBI patients. All severe TBI patients should be managed in the intensive care unit.

CPP: Goal >60 mm Hg

Current management guidelines for severe TBI advocate for a CPP threshold of 60 to 70 mm Hg. Driving CPP above 70 mm Hg with the use of vasopressors and/or intravascular volume expansion has been associated with significantly higher rates of acute respiratory distress syndrome. Thus, aggressive management of CPP greater than 70 mm Hg is not recommended. Overall, hypotension should be avoided, with a goal systolic blood pressure of 100 to 110 mm Hg and greater. When inadequate CPP is encountered clinically without elevated ICP, differential diagnosis should include systemic causes of hypotension including bleeding, tension pneumothorax, and spinal or cardiac shock. Intravascular resuscitation with isotonic fluids should be an initial step in therapy. In cases of refractory low CPPs, vasopressors may be required.

ICP: Goal <20 mm Hg

Intracranial hypertension has been associated with worse patient outcomes in severe TBI. In the neurocritical care setting, aggressive management of ICP is a management cornerstone. Intracranial hypertension treatment is based on a multimodal approach involving patient positioning, pharmacologic interventions, and potentially surgical intervention.

First-line treatments, when intracranial hypertension is encountered, include the following:

  • Patient positioning: head in neutral position with head of bed raised to at least 30 degrees

  • Cervical spine clearance and removal of rigid cervical collars should be expedited

  • Normocapnea (PaCO2 between 35 and 40 mm Hg)

  • Appropriate analgesia and pharmacologic sedation

  • Hyperosmolar therapy

Second-line treatments must be employed in up to 25% of severe TBI patients who will demonstrate intracranial hypertension refractory to first-line therapies:

  • Neuromuscular blockade

  • Hyperventilation (PaCO2 between 30 and 35 mm Hg)

  • Hypothermia (Temperature <36° C)

  • Barbiturate-induced burst suppression

  • Decompressive craniectomy

First-Line ICP Treatments

Rational for prioritizing these first-line treatments includes that the treatments are relatively low risk with a low adverse event profile, they can be rapidly administered, and they are the least invasive. Elevating the head of bed and maintaining a neutral head position serves to reduce ICP via maximization of venous blood outflow from the head, thereby decreasing intracerebral blood volume while concomitantly modulating CBF and CPP. Regarding cervical spine clearance, expeditious removal of external cervical collars allows decreased kinking of neck veins which, similar to bed positioning, can facilitate venous outflow from the head. Based on mounting evidence highlighting the sensitivity and specificity of helical computed tomography (CT) scanning of the cervical spine for determination of unstable cervical spine injuries, our institutional policy is to clear cervical spine precautions following negative helical CT scans in patients with no neurological deficit that can be ascribed to a cervical spinal cord injury.

Additionally, analgesia and pharmacologic sedation are first-line therapies with the goal of minimizing pain and agitation, which physiologically are shown to induce elevations in blood pressure, ICP, body temperature, and resistance to controlled mechanical ventilation, all of which can contribute to secondary brain injury. Sedation in TBI patients can render accurate neurologic assessment problematic, however, a variety of pharmacologic agents are good candidates for use in the TBI population. Propofol and dexmedetomidine are have relatively short half-lives and thus are able to be turned off for accurate neurologic assessments and are shown to reduce ICP and have neuroprotective properties, respectively. Boluses of short-acting opioids, such as fentanyl, are also highly effective for pain and agitation control without significantly impacting the ability to complete a neurologic exam.

Last among first-line therapies, hyperosmolar therapy, including use of hypertonic saline or mannitol, may be employed for effective medical control of ICP. Hypertonic saline in the form of 3% continuous infusions and/or 30 cc boluses of 23.4% saline may be introduced via central venous catheter to reduce ICP via both an osmotic and rheologic effect. Mannitol is administered via bolus dosing of 0.25 g/kg to 1 g/kg body weight; it reduces ICP and also exhibits dual rheologic and osmotic effects. Rheologic properties include the ability to expand plasma volume, reduce hematocrit, and increase red blood cell deformability, all of which ultimately decrease blood viscosity, increase CBF, and subsequently decrease ICP via arteriolar vasoconstriction. Osmotically, mannitol creates a gradient between intravascular and interstitial space in brain parenchyma, thereby encouraging water diffusion from the parenchyma into the cerebral vasculature.

Increasing evidence suggests hypertonic saline is overall more effective in a greater percentage of patients for ICP reduction than mannitol. Rebound intracranial hypertension is a troubling adverse phenomenon which can be observed with mannitol use and is thought to be secondary to uptake of mannitol into the brain, causing a paradoxical reverse osmotic gradient. The blood brain barrier, however, is thought to be less permeable to hypertonic saline solutions, and thus rebound ICP spikes are less commonly seen with hypertonic saline use. Importantly, mannitol can precipitate acute tubular necrosis, leading to acute renal failure, particularly in cases with elevated serum osmolarity greater than 320 mOsm. Mannitol encourages profound diuresis, which can precipitate electrolyte abnormalities and intravascular volume depletion as well. Hypertonic saline use is also not without risk. Vigilant attention to serum sodium levels is critical when administering hypertonic saline, as a rapid rise in serum sodium can precipitate central pontine myelinolysis, especially in patients with underlying chronic hyponatremia. Other risks of hypertonic saline use include pulmonary edema, seizures, coagulopathy, phlebitis, and other electrolyte abnormalities. Goal sodium levels in this setting are generally 140 to 160 mEq/L.

Second-Line ICP Treatments

When first-line therapies are exhausted and intracranial hypertension remains refractory, second-line therapies may be necessary, including neuromuscular blockade, hypothermia, barbiturate-induced coma, hyperventilation, and surgical decompression. Neuromuscular blockade via continuous infusion of agents with mechanism of action at the neuromuscular junction reduces ICP via decreasing intrathoracic pressure, facilitating venous blood outflow from the head and completely removing the patient’s ability to resist against controlled mechanical ventilation. Agents with a short half-life (e.g., cisatracurium) are preferred to reduce interference with neurologic examination as much as possible, and dosing can be titrated to a patient’s twitch response to a train of four peripheral nerve stimulator. Complications of neuromuscular blockade include higher rates of infection (e.g., pneumonia, sepsis) and longer intensive care unit stays.

Induction of hypothermia to a temperature below 36° C may lower brain metabolism and reduce ICP and can be trialed in refractory intracranial hypertension. This treatment should not be used prophylactically, as multiple studies have shown there is no benefit on long-term outcomes. Hyperventilation has also been shown to reduce ICP by producing vascular constriction and lowering CBF. This intervention should only be used transiently as it may lead to cerebral ischemia and infarction, thus resulting in additional secondary injury.

Therapy with barbiturate-induced coma requires continuous EEG monitoring. The most common agent used is pentobarbital, and treatment should be initiated with a test bolus dose of 10 mg/kg. If there is a reduction in the ICP in response to the test dose, then an infusion of pentobarbital should be started at 1 mg/kg. The infusion dose is titrated up until electrographic burst suppression of cerebral activity is achieved on EEG. Additional boluses of 5 mg/kg should be given every 30 to 60 minutes up to a total bolus dose of 20 mg/kg to achieve loading and facilitate transition to a burst suppression pattern. The mechanism by which pharmacologic burst suppression promotes ICP reduction is incompletely understood but thought to be secondary to decreased cerebral metabolism, cerebral vasoconstriction, and prevention of neurotoxic excitatory cascades. There is no benefit to prophylactic treatment with burst suppression in severe TBI; however, patients with intracranial hypertension refractory to all other interventions have decreased mortality if ICPs respond to barbiturate therapy. Complications of barbiturate-induced burst suppression include systemic hypotension and increased infection rates. Pharmacologic burst suppression unfortunately obviates the ability to complete neurologic exams for long periods of time, often 24 to 48 hours after barbiturate infusions are stopped.

Surgical Intervention

In cases where medical therapy fails and in other specific circumstances involving focal mass lesions with mass effect and midline shift, surgical intervention may be indicated. In patients with severe TBI, 25% will have lesions in which surgical intervention is generally indicated. Additionally, patients who show decreases in GCS score by ≥2 from the field to the ED are more likely to require neurosurgery. Neurosurgical intervention for management of ICP involves decompression via removal of a portion of the cranial vault. Taking into account the Monro-Kellie doctrine, surgical decompression serves to treat elevated ICP by removing the volumetric constraint of the nonexpansile rigid skull (Figure 9.3). Most commonly, lateralized mass lesions such as subdural hematoma, epidural hematoma, or contusion are treated with ipsilateral decompressive hemicraniectomy. Much less commonly, bifrontal lesions such as bifrontal contusions or generalized multifocal brain edema are treated with bifrontal craniectomy. Rarely, a posterior fossa traumatic mass lesion will require a posterior approach for suboccipital craniectomy. Surgical intervention can be lifesaving and highly effective for ICP management in medically refractory intracranial hypertension.

Figure 9.3 The rigid skull with fixed intracranial volume (represented by the rectangle) contains brain, cerebrospinal fluid (CSF), and blood. Intracranial pressure (ICP) is influenced by the dynamic interplay among the individual components (1). The addition of another component within the intracranial space, such as posttraumatic cerebral edema or mass lesion, will result in concomitant decrease in volume of another component in s compensated state where ICP does not rise (2). However, an uncompensated state with elevations in ICP will eventually ensue when compensatory measures are exhausted (3).

Figure 9.3 The rigid skull with fixed intracranial volume (represented by the rectangle) contains brain, cerebrospinal fluid (CSF), and blood. Intracranial pressure (ICP) is influenced by the dynamic interplay among the individual components (1). The addition of another component within the intracranial space, such as posttraumatic cerebral edema or mass lesion, will result in concomitant decrease in volume of another component in s compensated state where ICP does not rise (2). However, an uncompensated state with elevations in ICP will eventually ensue when compensatory measures are exhausted (3).

Source: Exo J, Smith C, Bell MJ. Emergency treatment options for pediatric traumatic brain injury. Pediatric Health. 2009;3:533–541.

Brain Tissue Oxygen: PbtO2 >20 mm Hg

Current guidelines state that the use of advanced monitoring of brain oxygenation in conjunction with ICP and CPP monitoring should provide additional information regarding the metabolic demands of the brain. Evidence to support the routine use of PbtO2 monitoring remains controversial. Based on clinical evidence of worse outcomes in patients with low PbtO2, if monitoring is undertaken, the usual goal is to maintain levels >20 mm Hg. This can be achieved in a number of ways, such as adjusting ventilator settings, increasing CPP, red blood cell transfusions, or temperature control. There are potential risks with any of these interventions, thus careful consideration must be used based on the individual clinical scenario.

Hypoxia: Goal Arterial Oxygen Saturation >90%

A multimodal approach is necessary to prevent secondary brain injury related to cerebral ischemia. Establishing an early protected airway via endotracheal intubation improves outcomes in severe TBI. Arterial oxygen saturations should be treated to maintain above 90%. Given oxygen delivery to the brain is highly dependent on oxygen content of blood, anemia may also enhance secondary brain injury. There is no current consensus on appropriate transfusion thresholds in severe TBI; however, low hemoglobin is associated with increased morbidity and mortality. Transfusion of packed red blood cells may improve outcomes for the severely injured via multiple mechanisms including improving cerebral oxygenation and increasing blood pressure which thereby modulates CPP. However, transfusion is also associated with increased thromboembolic events, transfusion reactions, and increased rates of acute respiratory distress syndrome.

Hyperpyrexia: Goal Normothermia, Core Body Temperature <38.5°C

An elevated core body temperature >38.5°C is shown to increase cerebral metabolism and increases mortality in severe head injury. Cornerstones in effective fever management include antipyretics, cooling blankets, and intravascular cooling catheters. Our institutional protocol for severe TBI patients involves immediate placement of a femoral or subclavian intravascular cooling catheter which remains in place for at least 36 hours for close temperature control in the acute postinjury period. Infectious workups should be pursued aggressively in appropriate cases.

Glycemic Control: Goal Serum Glucose <180 mg/dL

Hyperglycemia is common after TBI secondary to activation of the sympathetic nervous system and adrenergic catecholamine release. Both early and persistent hyperglycemia is associated with poor functional outcomes in severe TBI. Frequent glucose checks and tight glycemic control via sliding scale insulin administration are paramount.

Fluid Balance and Electrolytes

Electrolyte abnormalities are common in the TBI population, with up to 60% demonstrating an electrolyte abnormality in the acute posttrauma period. Abnormal serum sodium concentrations are the most common alteration, and posttraumatic hyponatremia is associated with worse outcomes and increased hospital days. Underlying pathophysiology involved with posttraumatic hyponatremia most often involves cerebral salt wasting or syndrome of inappropriate antidiuretic hormone (SIADH). These two entities are distinguished based on volume status with SIADH resulting in eu- or hypervolemia, whereas cerebral salt wasting results in hypovolemia. Distinguishing between the two is important, as management differs. In SIADH, fluid restriction is indicated, while sodium supplementation is the mainstay of therapy for cerebral salt wasting.

Hypernatremia is not uncommon after TBI and is most often secondary to central diabetes insipidus related to pituitary stalk dysfunction. Incidence of posttraumatic central diabetes insipidus is directly related to severity of brain injury. Management may involve a combination of free-water boluses or administration of hypotonic fluids, and rarely necessitates use of desmopressin (DDAVP). Following initial fluid resuscitation, the intravenous maintenance fluid of choice in TBI is normal saline (0.9% NaCl). Fluids with dextrose should be avoided given concern for inducing or worsening hyperglycemia.

Nutrition

Severe TBI and other frequently associated polytraumas can cause a hypermetabolic state. Enteral feeding (unless there is some absolute contraindication) should commence as soon as possible with full caloric replacement by postinjury day 5. Patients with malnutrition during the first two weeks after injury have significantly increased mortality when compared to patients who have caloric needs met by postinjury day 7. Additionally, early initiation of enteral feeding is associated with decreased infection rates.

In choosing between orogastric and nasogastric enteral feeding tubes, one must note the presence or absence of anterior skull base fractures. Placement of nasogastric tubes in the setting of severe skull base fractures can adversely result in intracranial penetration of the feeding tube. Other considerations in TBI patients include the increased prevalence of delayed gastric emptying and altered lower esophageal function which predispose to aspiration. The need for long-term feeding may indicate placement of percutaneous endoscopic jejunal or gastrostomy tube.

Prophylaxis

Seizure Prophylaxis

Seizures can profoundly enhance secondary brain injury via increased ICP and cerebral metabolic rate; decreased CBF, blood pressure, and oxygen delivery; and promotion of neurotoxic excitatory neurotransmitter release. Seizures are more likely to be observed in patients with depressed skull fractures, cortical contusions, penetrating injury mechanisms, and subdural/epidural hematomas and in those with initial GCS <10. Early posttraumatic seizures, which occur within seven days of injury, are observed in between 4% and 25% of TBI patients. Late posttraumatic seizures, which occur after the seven-day window, are seen in 9% to 42% of patients. Seizure prophylaxis with antiepileptic (AED) agents does not impact incidence of late posttraumatic seizures; however, it is shown to reduce early posttraumatic seizures. Thus, seven days of seizure prophylaxis with an AED remains a standard recommendation. Phenytoin is the most widely studied drug in the TBI population, thus it is frequently used; however, newer AEDs, such as levetiracetam, have reduced side effect profiles, particularly in the elderly, and may be another option. Dosing regimens that achieve therapeutic levels are recommended. Ongoing research seeks to elucidate if there is clinical superiority in seizure prevention and outcomes between the various AEDs that are available.

Gastrointestinal Prophylaxis

Sympathetic nervous system activation with resulting catecholamine surges can promote gastric ulcer formation after severe TBI. Routine use of histamine type 2 antagonists or proton pump inhibitors for ulcer prevention is common practice among mechanically ventilated patients with severe TBI. Additionally, early enteral feeding and appropriate fluid resuscitation aid in prevention of this complication.

Venous Thromboembolism Prophylaxis

Without the use of mechanical and pharmacologic prophylaxis, the incidence of deep venous thrombosis (DVT) in the severe TBI population may be as high as 20%. DVTs may lead to potentially life-threatening pulmonary embolism (PE), which is seen in 0.38% of TBI patients during the acute recovery phase. Given the immediate danger of PEs and the risk of progression of intracranial bleeding in TBI patients who must be fully anticoagulated to treat a DVT/PE, prevention of venous thromboembolism is critical. All in-hospital patients are fitted with pneumatic compression devices for mechanical DVT/PE prophylaxis. Pharmacologic prophylaxis does increase the risk a trauma-related intracranial bleed will progress; thus, our institutional policy is to commence pharmacologic prophylaxis with enoxaparin 30 mg every 12 hours on posttrauma day 1, as long as CT scanning demonstrates stability of trauma-related intracranial lesions.

Management to Avoid: Steroids

Steroid administration should be avoided in severe TBI as it is shown to increase mortality and is associated with other complications including hyperglycemia, gastric ulcer formation, and gastrointestinal bleeding.

Conclusions

The prevalence and consequences of TBI confer an immense burden on patients, families, and our health care system. Evidence-based managements strategies seek to intervene on pathophysiology which ultimately leads to cerebral ischemia and secondary brain injury. Modern care for TBI with multidisciplinary treatment teams employing multimodal physical, pharmacologic, and surgical therapies resulted in a drop in mortality from 50% to 25% in patients with severe head injury. While much progress has been made, there remains vast room for improvement in outcomes for TBI victims. Ongoing research is assessing novel neuroprotective drugs and the role of advanced neuromonitoring management of these patients, but much work remains to be done.

Further Reading

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