Traumatic brain injury (TBI) is one of the leading causes of death and lifelong disability in the United States today. According to statistics from the Centers for Disease Control and Prevention (CDC), out of the estimated 1.5 million yearly survivors of TBI in the United States, approximately 90,000 are left with permanent disabilities. As a result, more than 5 million people are living with TBI-related disabilities. Men are affected 3 times as often as women, with the leading causes of TBI being motor vehicle accidents (MVAs), falls, and violence (CDC, 1999).
The overall mortality rate secondary to TBI has declined by 20% since 1980, and the decrease in mortality rates secondary to MVAs has been the primary cause of this decline. However, firearm-related TBIs have actually increased during the same period. Although firearms cause only 10% of all TBIs, they are the leading cause of TBI-related death in the United States. When the data are not controlled for socioeconomic factors and low income, nonwhite males seem to experience more TBI-related morbidity secondary to violent acts than other males (Harrison-Felix, 2001).
Age-related differences in the incidence and causes of TBI are reported. The incidence of TBI has bimodal peaks in the pediatric population, with the first peak occurring in children younger than 5 years. In this group, the increased incidence of TBI is due to child abuse and falls. Morbidity in the child abuse group is thought to be secondary to the brain anoxia and hypotension that occur as a result of delayed medical attention when TBI occurs. The second peak in the pediatric population occurs in mid-to-late adolescence and is caused by MVAs (Gedeit, 2001; Adelson, 1998). The prevalence of TBI increases in individuals older than 65 years, with the primary cause being falls. Risk factors for traumatic falls are female sex, poor vision, previous falls, dementia, and polypharmacy (Tinetti, 1995).
The pathophysiology of TBI can be separated into primary injury and secondary injury. Primary injury occurs at the time of impact. Secondary injury occurs after the impact secondary to the body's response to primary injury and can be influenced by medical interventions. Primary and secondary injuries can each be subdivided into focal and diffuse types. Focal injuries tend to be caused by contact forces, whereas diffuse injury is more likely to be caused by noncontact, acceleration-deceleration, or rotational forces (Greenwald, 2003).
Both cortical contusions and intracranial hematomas are common causes of primary focal TBI. Contusions usually occur after direct injuries over bony prominences of the skull, with the most commonly affected areas being the orbitofrontal and anterotemporal regions. Intracranial hematomas are divided into epidural hematomas, subdural hematomas, and subarachnoid hemorrhages. Epidural hematomas result from rupture of the middle meningeal artery where it crosses the squamous portion of the temporal bone and cause focal injury by increasing pressure over a cortical region of the brain. Subdural hematomas and subarachnoid hemorrhage occur as a result of disruption of the bridging vessels in their respective spaces; both cause focal injury due to increased intracranial pressure (ICP) (Greenwald, 2003).
Diffuse axonal injury (DAI) is caused by forces associated with acceleration-deceleration and rotational injuries. This type of injury most commonly occurs during the high-impact collisions of MVAs, but these injuries can also be due to contact sports and shaken-baby syndrome. DAI is an axonal shearing injury of the axons that is most often observed in the midline structures, including the parasagittal white matter of the cerebral cortex, the corpus callosum, and the pontine-mesencephalic junction adjacent to the superior cerebral peduncles (Meythaler, 2001).
Causes of secondary brain injury include the following: neurochemical and cellular changes, hypotension, hypoxia, increased ICP with decreased cerebral perfusion pressure (CPP) and a risk of herniation, electrolyte imbalances, and ischemia. Recent advances in minimizing secondary injury include minimizing the risk of early hypotension (systolic blood pressure <90 mm Hg) and hypoxia (arterial oxygen <60 mm Hg). In addition, early monitoring for and treatment of elevations in ICP along with the judicious use of pressors has minimized the risk of ischemic injury from low CPP (CPP = mean arterial pressure - ICP) (BTF, 2000). Hypothermia is a promising treatment in the acute stages to limit secondary brain injury.
Three scales are commonly used to measure severity of TBI. First is the Glasgow Coma Scale (GCS), which is used immediately after brain injury. The GCS is a 3- to 15-point scale that reflects the level of arousal, as determined by using the patient's motor, verbal, and eye responses. The severity of injury can then be stratified into mild, moderate, and severe. Mild brain injury corresponds to a GCS score of 13-15, moderate corresponds to a score of 9-12, and severe injury corresponds to a score of 3-8.
In the second commonly used scale, the severity of brain injury is determined by the duration of loss of consciousness. Loss of consciousness of 30 minutes or less is defined as mild TBI. Loss of consciousness between 30 minutes and 6 hours is moderate TBI, and loss of consciousness of greater than 6 hours is considered severe TBI (Greenwald, 2003).
The last tool commonly used to measure the severity of TBI is the length of posttraumatic amnesia (PTA). The length of PTA is positively correlated with the severity of TBI. The presence of PTA is judged by using the Galveston Orientation Amnesia Test (GOAT) (Zafonte, 1997).
The brain is intimately connected with almost every organ system in the body, including the integumentary, gastrointestinal (GI), genitourinary (GU), and musculoskeletal systems. Medical complications after TBI arise from the concomitant injuries, alterations in neurologic function, and the effects of prolonged immobility. With so many possible complications of TBI, this section focuses on those complications that occur most frequently and on those that cause the most morbidity.
Posttraumatic seizures are one of the more serious complications of TBI. The standard classification includes generalized, partial, and absence seizures. Absence seizures are uncommon in TBI.
About 5% of all patients with TBI experience at least one late seizure, and as many as 50% of those patients with penetrating injuries experience late seizure activity (Yablon, 1993). If a patient has one posttraumatic seizure, the likelihood of him or her having another is 50% (Yablon, 1993).
In regard to seizure prevention, Temkin et al showed in a 1990 report that the prophylactic use of phenytoin is effective in the first week but not beyond that. In patients with TBI who have had a seizure, causes such as a tumor, hypoglycemia, hypoxia, an electrolyte imbalance, infection, and even drug abuse must be considered. The evaluation usually includes an analysis of serum chemistries, a complete blood cell count, and proper diagnostic imaging (ie, CT scanning, MRI, EEG).
Hydrocephalus is characterized as either communicating or noncommunicating on the basis of the location of the causative obstruction. Noncommunicating hydrocephalus occurs secondary to an obstruction within the ventricular system before the exit of cerebrospinal fluid (CSF) from the forth ventricle. Communicating hydrocephalus, which is more common in TBI, occurs when the obstruction is in the subarachnoid space (Hammond, 1999). In TBI, subarachnoid obstruction is commonly caused by inflammation and impaired CSF absorption by arachnoid granulations.
Clinically, hydrocephalus can occur with nausea, vomiting, headache, papilledema, obtundation, dementia, ataxia, and urinary incontinence. The diagnosis is made based on clinical suspicion and diagnostic imaging studies, including MRI, CT scanning, and radioisotope cisternography. The treatment of hydrocephalus consists of primarily lumbar puncture or shunt placement.
Deep venous thrombosis
In the population with TBI, deep venous thrombosis (DVT) is both common, with an incidence as high as 54%, and critical, in that the first clinical sign is often sudden death due to pulmonary embolus (Hammond, 1999). Because of the rapid decline in pulmonary function when a pulmonary embolus has completely occluded the pulmonary capillary system, sudden death is usually the first clinical sign. Other clinical signs (eg, shortness of breath, chest pain, pulmonary crackles) are also common, but these are usually present with smaller emboli.
In patients with TBI, risk factors for DVT include immobility, a lower-extremity fracture, and indwelling catheters.
The most common modes of detection of DVT are Doppler ultrasonography, B-mode ultrasonography, and contrast-enhanced venography. Venography remains the criterion standard for the diagnosis of symptomatic DVT, but noninvasive Doppler ultrasonography is most commonly used.
Prophylaxis for DVT should be started as early as possible, although no method allows the complete prevention of thrombus formation (Cifu, 1996). However, a number of prophylactic measures have been implemented to reduce the risk of thrombus formation. These include the use of elastic compression stockings, intermittent pneumatic compression, vena cava filters, warfarin, unfractionated heparin, and low-molecular-weight heparin. Even more of the controversy surrounding DVT prophylaxis in TBI is due to the possible increase in risk for intracerebral hemorrhage associated with some of the above prophylactic measures.
The treatment for DVT in the TBI population includes intravenous (IV) or subcutaneous heparin for 10 days, with the overlapping administration of warfarin. Prothrombin time (PT)/international normalized ratio (INR) should be monitored until a therapeutic response is achieved, at which time heparin therapy can be discontinued. The risk attributable to treatment is the same of that for prophylaxis, and each patient should be individually evaluated for a risk of falling and for a risk of intracerebral hemorrhage.
Because clinical signs and symptoms are often absent in the diagnosis of DVT, a high index of suspicion and timely medical intervention is of utmost importance in the patient with TBI.
Heterotopic ossification (HO) is described as ectopic bone formation in the soft tissue surrounding the joints. In TBI, the incidence of neurogenic heterotopic ossification (NHO) ranges from 11-76%, with a 10-20% incidence of clinically significant NHO (Melamed, 2002). NHO generally causes joint pain and decreased range of motion (ROM), and it often has associated low-grade fever, periarticular swelling, periarticular warmth, and periarticular erythema. The morbidity that results from HO ranges from incidental radiologic findings to complete ankylosis.
HO most commonly occurs in the hips, followed by the knees, elbows, shoulders, hands, and spine (in decreasing order of incidence). Risk factors associated with the development of HO following TBI are posttraumatic coma lasting longer than 2 weeks, limb spasticity, and decreased mobility (Hammond, 1999). The greatest risk for HO is during the first 3-4 months after injury (Hammond, 1999).
The pathophysiology of HO remains unclear; however, inappropriate differentiation of mesenchymal cells into osteoblasts is postulated to be the basic defect. Autonomic dysregulation (through increased vascularity and venous hemostasis), humoral factors, and local inflammatory mediators contribute to the development of HO.
Because of these nonspecific signs, laboratory and radiologic data are critical in the diagnosis of HO. Although both serum alkaline phosphatase levels and erythrocyte sedimentation rates are nonspecific, they are both elevated early in the disease process of HO, and thus they can be used as indicators for further workup. Radiologic evidence is the criterion standard for diagnosing HO, and the 3 main tools are plain radiography, sonography, and triple-phase bone scanning. Plain radiography is useful early on to rule out underlying fracture. Sonographic findings lag by 1-2 weeks, and plain radiographic findings lag by 2-3 weeks because of lack of early calcification of HO. Triple-phase bone scanning depicts HO the earliest.
ROM plays a key role in the prophylaxis and treatment of HO in TBI. Some controversy exists over the use of forceful ROM as a cause of HO, but human studies have not demonstrated this mechanism.
Routine prophylaxis with etidronate for patients with severe brain injury has been proposed, but it is not currently standard practice (Spielman, 1983). The prophylactic role of nonsteroidal anti-inflammatory drugs (NSAIDs) and low-dose radiation (which is commonly used in other groups at risk for HO) remains unclear. NSAIDs and etidronate can help with pain management, and the risk and benefits of these drugs in established HO should be assessed.
Although a patient may have ROM, HO may result in functional impairment, which may require surgical excision. In the past, to minimize risk of recurrence, surgical excision was delayed 12-18 months to allow the heterotopic bone to mature. Recent investigators have questioned this practice (Melamed, 2002).
In one inpatient rehabilitation unit, spasticity was found in an estimated 25% of patients with TBI (Elovic, 2001).
Two terms that are often confused as being synonymous with spasticity are tone and rigidity. Tone is defined as “resistance to stretch or movement across a joint when the patient is relaxed” (Burnett, 2003). Spasticity is a function of tone and is defined as “velocity dependent increase in tone” (Burnett, in press). Rigidity is also a function of tone, but it is defined as the “non-velocity dependent increase in tone” (Burnett, 2003).
Spasticity is more often encountered in lesions of the upper motor neurons, whereas rigidity is more common in basal ganglia disorders. The morbidity that is associated with spasticity is variable because, in some people, spasticity may assist in leg extension for walking or finger flexion for grasping. Prolonged low tone after TBI is generally predictive of poor motor recovery.
Guidelines for the treatment of spasticity are generally based on the following: (1) any resulting limitation in function, (2) pain, (3) prevention of contracture, and (4) assistance with positioning (Elovic, 2001). The first-line treatment for spasticity is correct positioning of the involved body segment and ROM exercises. Second-line treatment includes splinting, casting, and other modalities.
Depending on a patient's response to first-line treatment, pharmacotherapy may be initiated. Therapy varies according to whether the spasticity is generalized or local. Generalized spasticity is usually treated systemically. Dantrolene sodium is considered a preferred medication in TBI because of its lack of cognitive and sedative adverse effects.
Other medications used for spasticity include baclofen, tizanidine, clonidine, and benzodiazepines, but their use may be limited by the sedative and cognitive effects. Local treatments for spasticity include chemical neurolysis with phenol or alcohol injections and botulinum toxin A and B injections. They differ mainly in their onset and mechanism of action (Burnett, 2003).
GI and GU complications
GI and GU complications remain among the more common in patients with a TBI. Some of the most frequent GI complications are stress ulcers, dysphagia, bowel incontinence, and elevated liver function test (LFT) results. Elevated LFT results are commonly secondary to either trauma or anticonvulsant therapy, and they can sometimes be premorbid findings. Underlying constipation and/or impaired communication and mobility are often the cause of bowel incontinence. The use of stool softeners and stimulants along with a rectal suppository to ensure full GI evacuation often resolves bowel incontinence.
GU complications include urethral strictures, urinary tract infections, and urinary incontinence. An appropriate workup of GU symptoms, including ruling out infection, is indicated. When impaired communication and mobility are the cause of urinary incontinence, a trial of a timed voiding program is indicated. For an effective timed voiding program, patients are taken to the bathroom and given the opportunity to void every 2 hours during the day and every 4 hours overnight. Although less preferable, diapers and condom catheters may be needed.
Posttraumatic agitation is observed in at least one third of patients with a TBI who are in the early stages of recovery. In a 1996 report, Sandel and Mysiw define agitation as a subtype of delirium unique to survivors of TBI in which the patient is in the state of PTA and in which excesses of behavior include some combination of aggression, akathisia, disinhibition, and/or emotional lability.
Prior to considering any intervention for an agitated patient, the physician should obtain a thorough history and perform a thorough physical examination to ensure the patient's medical stability. Pain is a common but often overlooked cause of agitation after TBI. Combined with a diminished ability to communicate and/or cope with pain, agitation not surprisingly results. The use of central-acting medications that may potentiate agitation should be minimized.
Environmental modifications may be necessary to minimize unnecessary stimuli and assist with the patient's orientation. Disordered sleep-wake cycles are common in patients with TBI, and they should be treated with environmental and pharmacologic interventions as needed. Physical restraints often exacerbate agitation and should not be used routinely; however, the use of less restrictive restraints, such as net covered beds (eg, Vail beds), has become acceptable and popular in the treatment of the agitated patient with a brain injury.
Pharmacologic treatment for agitation spans a broad range of medication classes, including anticonvulsants, antidepressants, antihypertensives, antipsychotics, benzodiazepines, buspirone, stimulants, and amantadine (Mysiw, 1997). The treatment of agitation requires a review of the action and adverse effect profiles for each of these medications. The choice of treatment is based on the type and frequency of target behaviors. Optimally, the medication should minimize the patient's agitation without impairing his or her arousal and cognition. When possible, choose a medication that also treats a coexisting condition. Careful monitoring of target behaviors and adverse effects by family and the treating team is critical for successful treatment.
Long-term physical impairments are generally less prominent with TBI than cognitive and behavioral impairments. Long-term physical impairments are the factors that most commonly limit the patients' reintegration into the community, including their return to employment.
Two years after a TBI, reported cognitive, behavioral, or emotional problems include memory problems (74%), fatigue (72%), word-finding difficulties (67%), irritability (67%), impaired speed of thinking (64%), and impaired concentration (62%) (Ponsford, 1995).
Cognitive rehabilitation plays an important role in assessment and treatment of TBI-related cognitive impairment. In 2000, Cicerone et al critically reviewed the scientific literature concerning the effectiveness of cognitive rehabilitation for persons with TBI and stroke, and these authors developed practice standards, guidelines, and options.
Interest in the use of pharmacologic agents to enhance cognitive performance after brain injury is growing, but few controlled clinical trials have been performed. Currently, no treatment is universally accepted for the amelioration of neurobehavioral deficits after TBI.
Methylphenidate is commonly used to treat patients with hypoarousal, initiation, and attention problems associated with TBI. Some evidence suggests that methylphenidate may hasten recovery after TBI; the positive effects of methylphenidate are improved speed in processing and sustained attention (Whyte, 1997). Through the potentiation of dopamine, amantadine has been reported to improve arousal, attention, and executive functions (Zafonte, 2001). In a small open-label study, donepezil (an acetylcholinesterase inhibitor) was reported to improve memory and behavior during 12 weeks of treatment (Masanic, 2001).
Depressed mood in the year after TBI has been reported in 40-50% of individuals, and this may compound the behavioral and cognitive impairments (Glenn, 2001). In 1998, Hibbard et al found that 61% of adults met the criteria for major depression at some time after their TBI. Risk factors for depression are an increased severity of TBI, premorbid behavioral impairments, and female sex. These risk factors are present in all age groups.
Treatment options for depression after TBI include counseling, support groups, and antidepressant medication. Early after a TBI, a grief reaction is common, and this is better treated with supportive therapies than with other approaches. If medications are used, the profile of the chosen medication, including its adverse effects and interactions must be carefully considered to avoid worsening any sedation or cognitive impairment.
In medicine today, tools that can be used to effectively measure outcome are increasingly needed. These tools must be universal and not population specific, and they must also measure medically relevant criteria. With such tools, outcome measures can improve medical management as well as patient education.
Three commonly used outcome measures include the Glasgow Outcome Scale (GOS), the Functional Independence Measure (FIM), and the Disability Rating Scale (DRS). The GOS is one of the earlier outcome measures used. The original scale has 5 categories, including dead, vegetative state, severe disability, moderate disability (defined as being able to live independently but unable to return to work or school), and good recovery (defined as being able to return to work or school). These categories are often too broad and therefore insensitive to detect changes in the spectrum of recovery.
The DRS was developed as a single scale to track a patient's progress from coma to community. It includes 8 items that include components of impairment (GCS), disability (activities of daily living [ADLs]), and handicap (work). The FIM is the most widely used functional scale in rehabilitation. It is an 18-item scale that is used to assess the level of independence for mobility, self-care, and cognition. It is often faulted as having limited sensitivity in both patients with low-level brain injuries and in outpatients. The Center for Outcome Measurement in Brain Injury (COMBI) Web site is an excellent resource for scales used in brain injury (Wright, 2000).
In predicting overall outcome following TBI, the clinician must have an understanding of the relationship between the variables that predict outcome and the various levels of outcome that exist. These predictors are both physiological and psychosocial and include age, pupillary response, motor response, presence of intracerebral lesions, depression, availability of social support, access to the community, and quality of life (Watanabe, 2003).
More severe injuries, as measured by using the GCS, and length of PTA (see Measures of Severity) are generally associated with a poorer outcome. Patients who have had an acute compromise in hemodynamic stability, oxygenation, or maintenance of adequate CPP are expected to have a poorer outcome (BTF, 2000).
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