You are in: eMedicine Specialties > Neurosurgery > Trauma Closed Head TraumaArticle Last Updated: Feb 7, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Leonardo Rangel-Castilla, MD, Staff Physician, Division of Neurosurgery, University of Texas Medical Branch at Galveston Leonardo Rangel-Castilla is a member of the following medical societies: American Association of Neurological Surgeons and Congress of Neurological Surgeons Coauthor(s): Jaime Gasco, MD, Staff Physician, Department of Neurosurgery, University of Texas Medical Branch at Galveston; Fadi Hanbali, MD, Assistant Professor, Division of Neurosurgery, Department of Surgery, Texas Tech University Health Sciences Center; Adjunct Professor, Departments of Neurosurgery and Orthopedic Surgery, Division of Neurosurgery, University of Texas Medical Branch, Galveston; Paul Salinas, MD, Staff Physician, Department of Neurosurgery, University of Texas Medical Branch at Galveston Editors: Paul L Penar, MD, Professor, Department of Surgery, Division of Neurosurgery, University of Vermont School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Ryszard M Pluta, MD, PhD, Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences at Warsaw, Poland; Senior Researcher, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH; Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy; Allen R Wyler, MD, Former Medical Director, Northstar Neuroscience, Inc Author and Editor Disclosure Synonyms and related keywords: traumatic brain injury, TBI, closed head injury, nonpenetrating head injury, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, SAH, intraventricular hemorrhage, intracranial hemorrhage, intracerebral hemorrhage, ICH, cerebral contusion, coup injury, contrecoup injury, diffuse axonal injury, DAI, generalized brain ischemia, Duret hemorrhage, brain stem injury, brain death, intracranial pressure, ICP, cerebral perfusion pressure, CPP, cerebrospinal fluid, CSF, decompressive craniotomy, motor vehicle collisions, motor vehicle accident, MVCs, contemporary neuromonitoring INTRODUCTIONSection 2 of 11
  BackgroundIn the United States, the incidence of closed head injury is estimated to be approximately 200 cases per 100,000 persons per year.1, 2, 3, 4, 5, 6 In a population of 291.6 million people, this rate equates to more than 570,000 patients annually.7 Approximately 15% of these patients succumb to the injury upon arrival to the emergency department. Traumatic injuries remain the leading cause of death in children and in adults aged 45 years or younger. Head injuries cause immediate death in 25% of acute traumatic injuries.8 Traumatic brain injury (TBI) results in more deaths than does trauma to other specific body regions.9 Penetrating intracranial injuries have worse outcomes than closed head injuries.10 Motor vehicle collisions (MVCs) are the most common cause of closed head injuries for teenagers and young adults.11 Alcohol or drug use contributes to as many of 38% of cases of severe head trauma in younger patients.12 A recent development has been the apparent increase in brain injuries among the elderly; this increase is thought to be related to the use of anticoagulant and antiplatelet drugs.13 Head injury significantly contributes to deaths from trauma.6 Annual mortality from closed head injuries is approximately 100,000 patients or 0%, 7%, and 36% of mild, moderate, and severe head injuries, respectively.6, 8 Patients with severe head injury have a 30-50% mortality rate, and those who survive are often left with severe neurological deficits that may include a persistent vegetative state.8 Permanent disability in survivors ranges from 10-100%, depending on the severity of the injuries. This produces more than 90,000 newly disabled patients annually, including 2500 who are in a persistent vegetative state.6, 8 The last 3 decades have been alternately exhilarating and frustrating for clinicians and researchers interested in TBI. Laboratory and bedside research has greatly improved our understanding of posttraumatic cerebral pathophysiology. These new insights have failed to make the transition to clinically used therapies. Many of the major clinical trials of the last decades have been negative studies that have shown us what does not work. Demonstrating the efficacy of new treatments has been extraordinarily difficult.15 PathophysiologyClosed head injuries are classified as either primary or secondary. A primary injury results from the initial anatomical and physiological insult, which is usually direct trauma to the head, regardless of cause. A secondary injury results from hypotension, hypoxia, acidosis, edema, or other subsequent factors that can secondarily damage brain tissue (see Secondary injuries). Free radicals are thought to contribute to these secondary insults, especially during ischemia. Primary InjuriesThe primary injury usually causes structural changes, such as epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intraventricular hemorrhage, or cerebral contusion. Cerebral concussion is defined as an altered mental state that may or may not include loss of consciousness that occurs as a result of head trauma. Concussion is also known as mild traumatic brain injury (MTBI). The Table 1. American
Sport-related concussions are frequent, with 300,000 cases reported each year.16 Football players and boxers are particularly exposed to repetitive concussions, leading to the condition now known as chronic traumatic encephalopathy syndrome. Repetitive concussions may result in chronic subclinical motor dysfunctions linked to intracortical inhibitory system abnormalities.17 Parkinsonian cognitive decline due to strionigral degeneration is now a well-known consequence of repetitive concussions; cumulative diffuse axonal injury effects in the midbrain are due to increased vulnerability to shear forces in that region. Increasing a player's neck strength may be an effective way to minimize the risk of future concussions, as studies with Hybrid III dummies seem to indicate.18 Cerebral contusion Cerebral contusions are commonly seen in the frontal and temporal lobes. They may accompany skull fracture, the so-called fracture contusion. The most worrisome trait of these contusions is their tendency to expand. This usually occurs from 24 hours to as long as 7-10 days after the initial injury. For this reason, cerebral contusions are often followed with a repeat head CT scan within 24 hours after injury. Coup injuries (contusions) are caused by direct transmission of impact energy through the skull into the underlying brain and occur directly below the site of injury. Contrecoup injuries are caused by rotational shear and other indirect forces that occur contralateral to the primary injury. Rotational force causes the basal frontal and temporal cortices to impact or sweep across rigid aspects of the skull, the sphenoid wing, and petrous ridges. Delayed enlargement of traumatic intraparenchymal contusions and hematomas is the most common cause of clinical deterioration and death. However, progression of contusion is highly variable, and although most remain unchanged for days, a few enlarge, some quite rapidly. In a retrospective study, well-known prognostic factors were found to predict contusion enlargement. The strongest prognostic factor is the presence of traumatic subarachnoid hemorrhage. The size of the intraparenchymal hemorrhage means that large lesions are probably in an active phase of progression at the time of the initial CT scan. The concurrent presence of a subdural hematoma was also predictive. Clinical features, such as the initial Glasgow Coma Score (GCS) and intracranial pressure (ICP), were not predictive of progression. The ideal time for a rescan is unclear, although most of the growth seems to occur within the first 24 hours of injury.19 Epidural hematoma The incidence of epidural hematomas is 1% of all head trauma admissions (see Image 1).20 Epidural hematomas most commonly (85%) result from bleeding in the middle meningeal artery. Epidural hematomas, however, may occur in locations other than in the distribution of the middle meningeal artery. Such hematomas may develop from bleeding from diploic vessels injured by overlying skull fractures.8 Epidural hematomas are often associated with a "lucid interval," a period of consciousness between states of unconsciousness. The lucent period is presumed to end when the hematoma expands to the point that the brainstem is compromised. Subdural hematoma The most common surgical intracranial lesion is a subdural hematoma. These occur in approximately 20-40% of patients with severe injuries (see Image 2).12, 21 A surface or bridging vessel (venous) can be torn because the brain parenchyma moves during violent head motion. The resulting bleeding causes a hematoma to form in the potential space between the dural and arachnoid. A lucid interval is less likely to develop in this type of injury than in epidural hematomas. Subdural hematomas can be the result of an arterial rupture as well; these hematomas have the peculiar location in the temporoparietal region and differ in form from those caused by the bridging vein rupture, which typically rupture in the frontoparietal parasagittal region. Hematoma thickness and the midline shift of the brain are often analyzed; when the midline shift exceeds the hematoma thickness (positive displacement factor), a poorer prognosis has been found.22 Intraventricular hemorrhage An intraventricular hemorrhage is another intracerebral lesion that often accompanies other intracranial hemorrhages (see Image 3). Intraventricular blood is an indicator of more severe head trauma. Intraventricular blood also predisposes the patient to posttraumatic hydrocephalus and intracranial hypertension, which may warrant placement of an intraventricular catheter (if emergent drainage needed) or ventriculoperitoneal shunt for chronic hydrocephalus. Diffuse axonal injury Despite the absence of any intracranial mass lesion or history of hypoxia, some patients remain unconscious after a TBI. Brain MRI studies have demonstrated a clear correlation between white matter lesions and impairment of consciousness after injury. The deeper the white matter lesion, the more profound and persistent the impairment of consciousness.23 The usual cause for persistent impairment of consciousness is the condition referred to as diffuse axonal injury (DAI; see Image 4). Approximately 30-40% of individuals who die from TBI reveal postmortem evidence of DAI and ischemia.24 This type of injury commonly results from traumatic rotation of the head, with mechanical forces that act on the long axons, leading to axonal structural failure. DAI is caused by an acceleration injury and not by contact injury alone. The brain is relatively incompressible and does not tolerate tensile or shear strains well. Slow application of strain is better tolerated than rapid strain. The brain is most susceptible to lateral rotation and tolerates sagittal movements best.25 Secondary injuriesSecondary insults can take many forms and can be summarized as follows:
The major focus in the management of acute closed head injury is the prevention of secondary injuries and the preservation of neurological functions that are not damaged by the primary injury. Cerebral ischemia Cerebral ischemia is inadequate oxygen perfusion to the brain as a result of hypoxia or hypoperfusion. The undamaged brain tolerates low PaO2 levels better than the severely injured brain. Traumatized brain tissues are very sensitive to even moderate hypoxia (90 mm Hg). Gordon and Ponten proposed 2 explanations for this phenomenon: (1) Respiratory alkalosis may shift the oxygen-hemoglobin curve to the left, thereby increasing the affinity of the hemoglobin to the oxygen and decreasing the ease of oxygen release, and (2) uneven cerebral blood flow (CBF) may result from focal vasospasm with loss of focal autoregulation in the area of injured brain tissue.25 Approximately one third of patients with severe head injuries have been demonstrated to experience ischemic levels of CBF.26 CBF is normally kept constant over a range (about 50-150 mm Hg) of cerebral perfusion pressure (CPP; see Image 6). This is made possible by adjustments in vascular tone known as autoregulation (solid line). In patients with brain trauma, this autoregulation may malfunction, and CBF may become dependent on the CPP (dashed lines). Autoregulation is absent, diminished, or delayed in 50% of patients with severe head injuries.26 The lowest CBF values occur within the first 6-12 hours after injury.27, 28, 29, 30 The overall outcome of patients who experience ischemia is much worse than that of initially nonischemic patients.26, 31, 32 The initial ischemia is thought to cause permanent irreversible damage even if CBF is eventually optimized. The use of Brain edema Brain edema is another form of secondary injury that may lead to elevated ICP and frequently results in increased mortality. Brain edema is categorized into 2 major types: vasogenic and cellular (or cytotoxic) edema. Vasogenic edema occurs when a breach in the blood-brain barrier allows water and solutes to diffuse into the brain. Most of this fluid accumulates in the white matter and can be observed on head CT scans as hypodense white matter (on T1-weighted images) or as a bright signal area on the T2-weighted MRI. The mechanism of cellular (cytotoxic) edema is less clear. Theories include the increased uptake of extracellular potassium by the injured brain cells or the transport of HCO3- and H+ for Cl- and Na+ by the injured brain tissue as the mechanism of insult.25 FrequencyUnited StatesThe incidence of closed head injury is estimated to be approximately 200 cases per 100,000 persons per year.1, 2, 3, 4, 5, 6 Mortality/MorbidityTraumatic injuries remain the leading cause of death in children and in adults aged 45 years or younger (see Background). RaceThe incidence in specific ethnic groups varies. SexThe incidence varies in males and females. AgeThe incidence varies by age, but children and young people experience closed head trauma more often than older populations. CLINICALSection 3 of 11
HistoryThe specific patient history varies. PhysicalThe Glasgow Coma Scale (GCS), first introduced by Teasdale and Jennett in 1974, has been the standard for objectively assessing individuals with traumatic head injuries (see Table 2).34 It comprises motor, verbal, and eye scores. The overall score generally refers to the best response/examination obtained within the first 6-8 hours after injury and following resuscitation and is considered to be a predictor of the patient's overall outcome.35, 36, 37, 12, 38 The GCS has 2 main advantages in that it provides a reproducible, objective evaluation of neurological status, and it is a relatively simple way to monitor a patient's neurological condition over time. The GCS has shortcomings because its reliability depends on the absence of confounding factors (eg, sedation, paralytics, hypothermia, hypotension, hypoxia). Additionally, it cannot compensate for lack of eye opening in patients with periorbital trauma or loss of verbal response in intubated patients, and it omits brainstem reflex assessment.39, 40 Most clinicians assign a verbal score of 1 and apply the modifier "T" to intubated individuals. This may not be an accurate assessment of the patient's true verbal score.41 The motor component of the GCS score is most predictive of the severity of the brain injury and correlates most strongly with overall outcome.41
Patients should also be evaluated for basic brainstem reflexes. This assessment includes the evaluation of pupillary reflex, corneal reflex, gag/cough reflex, oculocephalic reflex, vestibuloocular reflex, and spontaneous breathing. Pupillary asymmetry or anisocoria of more than 1 mm (up to 1 mm may be physiological) must be attributed to an intracranial lesion until proven otherwise.41 Careful attention must be given to the evaluation of spontaneous breathing in the ventilated patient. A common pitfall is to mistakenly assess a patient as taking spontaneous breaths when the sensitivity on the ventilator is set to a level that triggers a mechanical breath at the slightest effort by the patient. Proper evaluation entails setting the ventilator sensitivity to zero, then reevaluating the patient after a few seconds, which does not allow time for hypoxia or hypercapnia to develop. The presence of any of the above reflexes confirms that the patient has at least basic brainstem reflexes. A complete absence of brainstem reflexes is an ominous sign. Causes
DIFFERENTIALSSection 4 of 11
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Advantages | Disadvantages |
| Noninvasive and rapid | Traumatic vascular lesions may be missed. |
| Very sensitive for acute hemorrhage | DAI is likely to be missed. |
| Defines nature of ICH (ie, SDH† , SAH‡) | Motion artifact may limit study. |
| Defines anatomical location of lesion | Posterior fossa lesions are poorly depicted. |
| Identifies fractures of the cranium | Depressed skull fractures at the vertex (or along the plane of an axial scan) are poorly depicted. |
| Sensitive to detecting intracranial air | The scanner has a weight limit, and a patient may be too heavy. |
| Sensitive in identifying foreign objects | A patient may decompensate while in the scanner. |
Order serum sodium, urine specific gravity, urine osmolarity, and serum osmolarity tests for individuals with urine output of 250 mL/h or more for 3 or more consecutive hours (pediatric patients, >3 mL/kg/h) and for patients who are thought to have diabetes insipidus. Large doses of mannitol can mask diabetes insipidus by producing a high urine output.
Intracranial hypertension is a common neurologic complication in patients who are critically ill. Intracranial hypertension is the common pathway in the presentation of traumatic head injury. The underlying pathophysiology of increased intracranial pressure (ICP) is the subject of intense basic and clinical research, which has led to advances in the understanding of the physiology related to ICP. Few specific treatment options for intracranial hypertension have been subjected to randomized trials, however, and most management recommendations are based on clinical experience.
Normal values of intracranial pressure
In healthy individuals with closed cranial fontanelles, central nervous systems contents, including brain, spinal cord, blood, and cerebrospinal fluid (CSF), are encased in a noncompliant skull and vertebral canal, constituting a nearly incompressible system. In the average adult, the skull encloses a total volume of 1450 mL: 1300 mL of brain, 65 mL of CSF, and 110 mL of blood. The Monroe-Kellie hypothesis states that the sum of the intracranial volumes of blood, brain, CSF, and other components is constant, and that an increase in any one of these must be offset by an equal decrease in another.
The reference range of ICP varies with age. Values for pediatric subjects are not as well established. Normal values are less than 10-15 mm Hg for adults and older children, 3-7 mm Hg for young children, and 1.5-6 mm Hg for term infants. ICP can be subatmospheric in newborns. ICP values greater than 20-25 mm Hg require treatment in most circumstances. Sustained ICP values of greater than 40 mm Hg indicate severe, life-threatening intracranial hypertension.
Cerebral dynamics overview
Cerebral perfusion pressure (CPP) depends on the mean systemic arterial pressure (MAP) and ICP, which is determined by the following relationship:
CPP = MAP – ICP where MAP = (1/3 systolic BP) + (2/3 diastolic BP)
As a result, CPP can be reduced from an increase in ICP, a decrease in blood pressure, or a combination of both factors. Through the normal regulatory process called pressure autoregulation, the brain is able to maintain a normal cerebral blood flow (CBF) with a CPP that ranges from 50-150 mm Hg. At CPP values less than 50 mm Hg, the brain may not be able to compensate adequately, and CBF falls passively with CPP.
After injury, the ability of the brain to autoregulate may be absent or impaired. When CPP is within the normal autoregulatory range (50-150 mm Hg), this ability of the brain to pressure autoregulate also affects the response of ICP to a change in CPP. When pressure autoregulation is intact, decreasing CPP results in vasodilation, which allows the CBF to remain unchanged. This vasodilation can result in an increase in ICP. Likewise, an increase in CPP results in the vasoconstriction of cerebral vessels and may reduce ICP. When pressure autoregulation is impaired or absent, ICP decreases and increases with changes in CPP.48
Perhaps the least invasive method of lowering ICP is to elevate the head of the patient to 30°. Some researchers have demonstrated improved ICP control with elevation (head of bed) to 45°, but recent evidence from using multimodality monitoring has suggested a 30° head elevation for maximum benefits.25 Note that head elevation may reduce cerebral perfusion, even as it lowers ICP.
Hyperventilation became a popular means of reducing ICP in the 1970s. However, recent studies raise concern that aggressive hyperventilation exacerbates cerebral ischemia. One study shows that patients who were hyperventilated to a PCO2 level of 25 mm Hg had worse outcomes than patients who were kept at a nearly normal PCO2 level.46 In addition, in most patients, hyperventilation is not necessary to control ICP.49, 50, 29, 51 Currently, hyperventilation (PCO2 of 30-35 mm Hg) is recommended to reduce ICP for only a short period, as a temporizing measure while other methods of ICP control are initiated. Hyperventilation reduces ICP only temporarily, progressively losing effectiveness after 16 hours of continuous use.52
Mannitol probably has several mechanisms of action. One obvious mechanism is through osmotic diuresis via drawing edema from the cerebral parenchyma. This usually takes 15-30 minutes, and the effect usually lasts 1.5-6 hours. Another mechanism is by immediate plasma expansion and decreased blood viscosity, thereby improving blood flow and eventually resulting in intracranial vasoconstriction in an attempt to maintain constant blood flow. This vasoconstriction ultimately leads to decreased intracranial volume (Monroe-Kelly hypothesis) and decreased ICP.53, 54 Mannitol is also considered a free radical scavenger.55 Administration of this drug in severe traumatic brain injury patients studied both with jugular bulb oxygen saturation56 as well as with multimodal brain monitoring57 suggests a potential change in the internal milieu that would improve cerebral oxygenation.
Serial serum osmolarity levels must be checked to maintain an osmolarity of no greater than 315-320 mOsm/kg H2O to avoid acute renal failure. Some studies have raised concern that the early use of mannitol can lead to hypotension, with an associated worse outcome.58 For this reason, patients treated with mannitol must be kept euvolemic with isotonic fluid resuscitation as required.
Although some evidence suggests that barbiturates may be effective in lowering refractory ICP, such administration often causes depressed myocardial function and CPP.41 These drugs often have an associated morbidity and do not significantly change outcome.59, 10
A barbiturate-induced coma with EEG burst suppression is often a "last ditch effort" to reduce the ICP and should be reserved only for patients with refractory ICP who are unresponsive to other measures. One may even consider decompressive craniectomy prior to the use of barbiturates. Barbiturate serum levels are a poor estimate of therapeutic effect and should not be followed for treatment purposes. For this reason, all patients should have EEG monitoring to monitor for induced burst suppression. A loading dose of pentobarbital can be administered as a 10 mg/kg bolus (over 30 min), followed by 5 mg/kg/h for 3 doses, titrated to a low level of bursts per minute (2-5). Barbiturates are contraindicated in hypotensive patients.
One must give special attention to preventing hypotension.24, 31 Data from the Traumatic Coma Data Bank (TCDB) reveal that hypotension in patients with severe TBI increases the mortality rate from 27% to 50%.25 Traditional management has included fluid restriction in order to minimize cerebral edema, but this practice may be dangerous in patients who already have intravascular volume depletion.
Cerebral edema may occur regardless of the amount of intravenous fluid administered, and hypervolemia, per se, does not cause brain edema if the serum sodium level and osmolarity are within normal limits.25 However, managing patients who have closed head injuries with liberal amounts of hypotonic intravascular fluid may cause intracerebral hemorrhages to blossom. Smaller amounts of hypertonic solutions may be equally effective without the risk of fluid overload.60, 61 The ultimate goal of the management of patients with closed head injuries is to maintain a state of euvolemia. In a euvolemic patient who is hemodynamically stable, two-thirds maintenance of isotonic solution is recommended. Avoid hypotonic fluids because they may decrease serum osmolarity and increase brain swelling.
In addition, patients with closed head injuries are prone to acute coagulopathies. These coagulopathies are often the result of release of thromboplastin and tissue-activating protein from injured brain tissue. The release of these proteins leads to abnormal intravascular clotting, which consumes clotting factors, platelets, and fibrinogen and ultimately results in elevated PT and aPTT. In patients with acute intracranial hemorrhages, these coagulopathies must be addressed and corrected promptly.
Fresh frozen plasma (FFP) transfusions until the coagulopathy is corrected is the preferred method. This is especially true for individuals who are taking anticoagulants (eg, warfarin) and who are at high risk of continued bleeding. Winter and colleagues have shown that prophylactic FFP administration in individuals with closed head injuries is of no benefit.62 Vitamin K plays an important role in correcting the coagulopathy; however, it usually takes 24-48 hours to be activated. During this interval, the patient's intracranial hemorrhage is likely to worsen. Recombinant activated factor VII (rFVIIa) is a relatively new pharmaceutical agent developed for use in patients with hemophilia in whom inhibitors to clotting factors VIII or IX have developed.
The use of rFVIIa in neurosurgery has lagged behind its use in other fields, although the body of literature on such uses is growing. Various uses are pertinent to the neurosurgeon, including the treatment of patients with coagulation disorders, those patients who have experienced trauma, and those patients with perioperative hemorrhage, intracerebral hemorrhage, or subarachnoid hemorrhage. rFVIIa is a safe and effective agent with the potential to revolutionize the treatment of neurosurgical patients with hemorrhage. Cost is a major impediment to the widespread use of rFVIIa, and some evidence suggests that its use in the neurosurgical population may be subject to higher risk than in other populations studied thus far. Although further study is needed to better delineate the safety and efficacy of the drug, rFVIIa is clearly an agent with tremendous promise.63
Pyrexia commonly occurs in patients with head injuries, possibly because of posttraumatic inflammation, direct damage to the hypothalamus, or secondary infection. The most common cause is fever secondary to an underlying infection. Less common is an unexplained fever or "neurogenic" fever estimated to occur in approximately 8% of patients who have head injuries with pyrexia.64 Regardless of the cause of the elevated temperature, pyrexia alone increases metabolic expenditure, glutamate release, and neutrophil activity, while causing blood-brain barrier breakdown.
Pyrexia is also thought to exacerbate oxygen radical production and cytoskeletal proteolysis.65, 66 These changes may further compromise the injured brain and worsen neuronal damage. For this reason, the source of the fever must be identified and corrected.
Although the source of the infection is sought, maintain body temperature in a normothermic range with acetaminophen. However, despite sound physiological justification for treating fever in brain-injured patients, no evidence indicates that doing so improves outcome.
Hyperglycemia has also been shown to have a detrimental effect on induced brain ischemia. Clinical trials support the correlation between hyperglycemia and poor overall outcome in patients with head injuries and recommend that euglycemia be maintained at all times.67
Some patients with severe head injuries may develop hypertension, either from an exacerbation of a chronic process or as a result of the head injury. Keep systolic blood pressure less than 180 mm Hg, particularly in patients who have an intracranial hemorrhage. This value requires adjustment for patients with a history of uncontrolled hypertension. If possible, avoid nitroprusside because it is a cerebral vasodilator and may actually increase ICP. A nicardipine grip is preferred in patients whose blood pressure is difficult to control. Corticosteroids have occasionally been used but have no proven benefit for patients with severe head injuries.10
Effective treatment of intracranial hypertension involves the meticulous avoidance of factors that precipitate or aggravate increased ICP. When ICP becomes elevated, ruling out new mass lesions that should be surgically evacuated is important. Medical management of increased ICP should include sedation and paralysis, drainage of CSF, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension that results from TBI.48
As a general rule, indications for surgery include any intracranial mass lesion that causes significant or progressive neurological compromise, particularly a decreased level of consciousness. The overall outcome of individuals with an intracranial lesion that causes significant mass effect is improved with rapid decompression; therefore, operating on these patients as soon as possible is advisable.
Before operating, one must always consider the patient's condition and refrain from relying solely on radiographic evidence. For example, some patients with severe cerebral atrophy (eg, elderly patients) may accommodate a large intracranial hemorrhage, whereas most young individuals may experience neurological deficits with relatively smaller intracranial hemorrhages. Note that some intracranial hemorrhages may be actively bleeding during the initial head CT scan; what may appear as relatively small on the initial scan may actually become quite significant in a short period of time. In this case, the patient's physical examination findings are more valuable in evaluating his or her intracranial status than the initial head CT scan findings.
Some authors have suggested a decompressive craniotomy (ie, removal of a bone flap with or without dural opening) to provide more space for the brain to expand, for the treatment of uncontrollable ICPs before irreversible ischemic brain damage has occurred. The role of decompressive craniotomy in the absence of compressive pathology (such as subdural hematoma) in patients with closed head injuries has not been well documented. Most authors, however, agree that children benefit more from decompressive craniotomies than adults, and some authors are advocates of very early decompressive craniotomies for uncontrollable ICP in children.68 It seems clear that older individuals, particularly those older than 50 years, do less well with elective decompressive craniotomies.69, 70
Obtain consultations as necessary for other accompanying injuries (eg, plastic surgeons for facial lacerations), realizing that the patient's closed head injury takes precedence over all other non—life-threatening injuries once the patient is stabilized.
Before, physicians thought that patients with closed head trauma should be on NPO status. Now, the new modality is to provide nutrition as soon as possible. The consequences of hypermetabolism, hypercatabolism, and an altered immune function are part of the response to traumatic head injury. Once a person with acute traumatic brain injury develops this hyperdynamic state, the resultant excessive protein breakdown ensues. This can lead to malnutrition. Lack of nutrient supplementation in these patients is associated with increased morbidity and mortality. Enteral nutrition is the preferred mode of feeding but is often not tolerated in the patient with head injury. Parenteral nutritional support can be given to these patients without worsening cerebral edema.71
The patient should be prescribed bed rest.
Neurosurgeons have commonly given prophylactic anticonvulsants for individuals with intracranial hemorrhages. The appropriate duration of treatment is not well established. Individuals who have experienced seizure activity can reasonably be treated with anticonvulsants for 6-12 months, after which reevaluation is necessary. Temkin and colleagues suggest that treatment for longer than 8 days after injury does not reduce the frequency of long-term seizure disorders. Anticonvulsants may be used to treat early (<7 d) posttraumatic seizures. According to Greenberg, prophylactic anticonvulsants do not reduce the frequency of late (>7 d) posttraumatic seizures.72
The recommended anticonvulsant medication in adults is phenytoin or fos-phenytoin (18 mg/kg of loading dose), ensuring therapeutic levels of 10-20 mg/dL. Note that a "therapeutic level" does not necessarily have a direct bearing on adequate control of seizures. A relatively common adverse effect of chronic phenytoin use is gingival hyperplasia and hirsutism, which precludes chronic use in children. Phenobarbital is an acceptable alternative in children who require long-term anticonvulsive therapy (10-20 mg/kg loading dose, then 3-5 mg/kg/d divided bid/tid) to achieve a therapeutic level of 10-40 mg/dL.
The new antiepileptic drug levetiracetam is used in the setting of acute brain injury for seizures treatment or prophylaxis; it is a desirable alternative to phenytoin. It is associated with fewer complications when it is used as monotherapy. Checking for therapeutic levels is not needed. The dose is 500 mg bid IV or
These agents are indicated for short-term (1 wk) or long-term (6- to 12-mo) posttraumatic seizure control for patients who have experienced posttraumatic seizure activity. Phenobarbital may be considered in children for long-term anticonvulsive therapy.
| Drug Name | Phenytoin (Dilantin) |
|---|---|
| Description | Used for acute seizure prophylaxis in individuals with closed head injuries. |
| Adult Dose | Loading dose: 15-20 mg/kg PO/IV once Initial dose: 100 mg (125 mg suspension) IV/PO tid Maintenance dose: 300-400 mg/d PO/IV divided tid, or qd/bid if using extended release; increase to 600 mg/d (625 mg/d susp) may be necessary; do not exceed 1500 mg/d Infusion rate must not exceed 50 mg/min in order to avoid hypotension and arrhythmias; alternatively, 1 g loading dose, then 100 mg tid, checking level qd to achieve therapeutic level of 10-20 mg/dL |
| Pediatric Dose | <6 years: 15-20 mg/kg PO/IV loading dose once or in divided doses; follow by initial 5 mg/kg/d maintenance dose (range, 4-8 mg/kg) PO/IV divided bid/tid >6 years: May require minimum adult dose (300 mg/d); not to exceed 300 mg/d; alternatively, loading dose of 10-20 mg/kg IV, then 5 mg/kg administered qd or divided tid |
| Contraindications | Documented hypersensitivity; sinoatrial block, second- and third-degree AV block, sinus bradycardia, Adams-Stokes syndrome |
| Interactions | Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity; effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, or sucralfate; may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid. |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Perform blood cell counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugar levels); discontinue use if hepatic dysfunction occurs |
| Drug Name | Phenobarbital (Barbita, Luminal, Solfoton) |
|---|---|
| Description | Used for acute seizure prophylaxis in children with closed head injuries. |
| Adult Dose | 30-120 mg/d PO qd or 2-3 divided doses; not to exceed 400 mg/d; frequency determined by response |
| Pediatric Dose | 1-3 mg/kg IV/IM |
| Contraindications | Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis |
| Interactions | May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur) |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema |
Most patients require physical and occupational therapy, depending on the severity of the head injury.
Most patients with moderate-to-severe head injuries likely benefit from outpatient physical and occupational therapy. Once patients' acute issues have been addressed, many patients require cognitive rehabilitation (outpatient or inpatient).
Initially, an anticonvulsant regimen should be started for patients with moderate or severe head injuries. Cease administration if no seizure activity occurs within the first 7 days after injury. For patients who have seizure activity in this time period, or who have undergone surgical procedures, one may opt to continue anticonvulsants for 6-12 months.
Once the patient's acute issues have been addressed, seek long-term placement (eg, long-term acute care, skilled nursing facility, inpatient cognitive rehabilitation center) if the patient continues to require significant medical attention or assistance (eg, because of ventilation, need for significant nursing care).
See Secondary injuries.
Educate the family about the type of injury the patient has sustained and what natural progression or recovery should be expected. The patient and the patient's family can be instructed regarding home exercises, wound care, and administration of long-term antibiotics.
| Media file 1: CT scan of left frontal acute epidural hematoma (black arrow) with midline shift (white arrow). Note the left posterior falx subdural hematoma and left frontoparietal cortical contusion. | |
 | View Full Size Image | Media type: CT |
| Media file 2: CT scan of left frontoparietal acute subdural hematoma (black arrow). Note the moderate amount of midline shift. | |
 | View Full Size Image | Media type: CT |
| Media file 3: CT scan of bilateral acute intraventricular hemorrhages (black arrow). Note the comminuted skull fractures that involve bilateral frontal, temporal, and parietal bones (white arrow). Note the ischemic changes in both frontal lobes, subarachnoid hemorrhages in the intrahemispheric fissure and left frontal lobe, and multiple intraparenchymal hemorrhages in both frontal poles. | |
 | View Full Size Image | Media type: CT |
| Media file 4: MRI of the brain that shows diffuse axonal injury (DAI) and hyperintense signal in the corpus callosum (splenium), septum pellucidum, and right external capsule. | |
 | View Full Size Image | Media type: CT |
| Media file 5: MRI of the brain (sagittal view) that shows a Duret hemorrhage in the splenium of the corpus callosum. | |
 | View Full Size Image | Media type: CT |
| Media file 6: Cerebral blood flow/cerebral perfusion pressure chart. | |
 | View Full Size Image | Media type: Graph |