Archives of Physical Medicine and Rehabilitation
Volume 89, Issue 3, Supplement 1 , Pages S9-S14, March 2008

Congenital and Acquired Brain Injury. 2. Medical Rehabilitation in Acute and Subacute Settings

  • Steven R. Flanagan, MD

      Affiliations

    • Mount Sinai Hospital, New York, NY
    • Corresponding Author InformationCorrespondence to Steven R. Flanagan, MD, Mt Sinai Hospital, Box 1240B, 1 Gustave L. Levy Pl., New York, NY 10029-6504
    • ,
  • Christina Kwasnica, MD

      Affiliations

    • Barrow Neurologic Institute, Phoenix, AZ
    • ,
  • Allen W. Brown, MD

      Affiliations

    • Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN
    • ,
  • Elie P. Elovic, MD

      Affiliations

    • Kessler Medical Rehabilitation Research and Education Center, West Orange, NJ
    • ,
  • Sunil Kothari, MD

      Affiliations

    • The Institute for Rehabilitation and Research, Houston, TX.

Article Outline

Abstract 

Flanagan SR, Kwasnica C, Brown AW, Elovic EP, Kothari S. Congenital and acquired brain injury. 2. Medical rehabilitation in acute and subacute settings.

This self-directed learning module reviews common clinical problems and issues pertaining to early management of persons with traumatic brain injury (TBI). It is part of the study guide on brain injury medicine in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. Acute TBI is frequently complicated by agitation, dystonia, and numerous orthopedic and neurologic comorbidities, often causing a decrement in function, which requires careful assessment and treatment. Individuals with acute brain injury typically receive rehabilitation in a setting determined by numerous factors, including medical stability and tolerance to rehabilitation interventions.

Overall Article Objectives

To describe (a) common traumatic brain injury−related comorbidities and treatment strategies, (b) potential causes of declining patient performance, and (c) appropriate settings for rehabilitation interventions.

Key Words: Brain injuries, Comorbidity, Muscle spasticity, Psychomotor agitation, Rehabilitation

 

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2.1 Clinical Activity: Using both pharmacologic and nonpharmacologic means, manage a 30-year-old patient with traumatic brain injury in the critical care unit who is demonstrating agitated, unsafe, and/or aggressive behaviors 

POSTTRAUMATIC AGITATION has been defined as a delirium present during the period of posttraumatic amnesia, manifested by behavioral excesses such as aggression, akathisia, disinhibition, emotional lability, destructiveness, or combativeness.1 However, experts2 report that when assessment and treatment are indicated, it is more important to target individual undesirable behaviors rather than to focus on defining agitation.

Assessing Agitation Level 

In addition to directly targeting a particular behavior, one needs an objective, validated, agitation scale, both to determine agitation level and to evaluate treatment effects. Validated scales provide extensive information that quantifies maladaptive behavior. Two such scales that are commonly used in the rehabilitation environment are the Agitated Behavior Scale (ABS) and the Overt Aggression Scale (OAS)3 (appendix 1). The ABS consists of 14 items that are scored 1 to 4 based on the frequency of a particular behavior. The OAS quantifies the severity of the aggressive behavior in 4 categories: verbal and physical, aggression against self, aggression against other people, and aggression against objects. The time required to administer these metrics is often lacking in the intensive care unit (ICU), with other less time-consuming metrics such as the Ramsey Scale, the Sedation Agitation Scale, or the Motor Activity Scale being preferable in these settings (appendix 2).2, 4

Potential Sources of Agitation 

Agitation in the ICU may result from disinhibited behavior secondary to the traumatic brain injury (TBI) or from numerous other issues that must be considered during evaluation. See appendix 3 for a list of issues to be considered in assessing agitation in a person with TBI.

Agitation Management in the ICU 

Behavioral management strategies are often not used in the ICU because of limited staff time, patients’ diminished learning capacity, and the fact that medical needs often take precedence over behavioral problems. However, some simple environmental strategies can be implemented, such as minimizing stimulation, limiting visitation, and facilitating patient orientation. Orienting patients consists of staff introducing themselves and explaining the rationale for interventions in simple terms, providing a clock and calendar, and writing the names of the treating clinicians where they can be readily seen. Establishing regular sleep-wake cycles with lights out at night and providing pharmacologic assistance are also helpful.

Pharmacologic Intervention 

Medications that are commonly administered for sedation in the ICU are often not those normally used by clinicians during TBI rehabilitative care. The agents most typically used in the ICU for patients with TBI are described later.

Propofol infusion, an anesthetic agent believed to manifest its effect through the GABA-A system, is used for sedation in patients who are intubated in the ICU. It has a relatively favorable side-effect profile, with a rapid return to consciousness after the infusion is discontinued.2 Although haloperidol is frequently cited as the drug of choice in the management of sedation of the patient with delirium (with benzodiazepines reported as useful in other cases),5 both animal6 and human evidence7, 8 suggests that their use may be detrimental after TBI. The atypical antipsychotics have less dopamine-blockading effect than haloperidol, activate 5-HT2 serotonergic pathways, and may be considered an option in managing TBI-related agitation. These antipsychotic agents are available in both enteral and injectable formulations; however, clinicians should exercise caution when using them because of their potentially life-threatening cardiac side effects, most notably QT prolongation.

Pharmacologic management of TBI-related agitation is often accomplished by manipulating the serotonin and catecholamine pathways. Dopamine in particular has been shown to be elevated in animal models of aggression, with the administration of a dopamine agonist shown to increase agitation and akathisia in both animal models and humans.9 Manipulation of the serotonin system with selective serotonin reuptake inhibitors or trazodone as a means to ameliorate agitation is also a rational choice, although sufficient time is required to assess its clinical effectiveness in each person. Human studies showed lower levels of serotonin metabolites in subjects with poor impulse control and aggression, justifying their use. Although no studies have been performed to evaluate their efficacy in the ICU, certain anticonvulsants (eg, lamotrigine, valproate, carbamazepine) are favored by many clinicians for agitation management. Unfortunately, little clinical evidence from clinical trials exists to support their decision in using these agents. The Cochrane Database Review reported that the best evidence for medication management in the treatment of TBI-related agitation exists for inderal.10

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2.2 Educational Activity: To discuss the evaluation of an 18-year-old patient whose performance during the last 2 days of inpatient therapies has declined 

During rehabilitation, the expected clinical course after brain injury is that of steady improvement. Any decline should be considered abnormal and warrants clinical evaluation. In appendix 4, we present the most common causes of clinical decline and suggestions for what the assessment might include. A thorough history and physical examination are, of course, the cornerstone of the evaluation.

Patients at a low neurologic level (ie, the minimally conscious patient) present a special challenge. Not only may changes in their clinical status be subtle and hard to detect, but the history and physical examination are more difficult to perform. One should also keep in mind that even minor changes in physiologic status, such as significant constipation, can affect the clinical level of these patients.

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2.3 Clinical Activity: To manage an 18-year-old patient with a TBI who presents with generalized spasticity affecting all 4 extremities and who also exhibits posturing and dysautonomia 

Two conditions that are commonly encountered after severe TBI include dysautonomia and severe generalized spasticity. Dysautonomia, also known as sympathetic storming or hypothalamic-midbrain dysregulation syndrome, is characterized by severe, paroxysmal increases in heart rate, temperature, and blood pressure with decerebrate or decorticate posturing. The syndrome is associated with severe diffuse axonal injury, preadmission hypoxia, younger age, and brainstem injury. It is associated with longer ICU and rehabilitation stays as well as worse outcomes at discharge.11 The first step in any clinical situation is to identify and address noxious stimuli such as infection, decubitus ulceration, heterotopic ossification, or undiagnosed fractures. Elevated temperatures always require an extensive workup for infectious etiologies, even in the presence of coexisting dysautonomia.

Pharmacologic management is largely empirical and based on limited retrospective case reviews. Benzodiazepines and intravenous opiates are often initiated in the ICU setting. In the rehabilitation setting, medications such as propranolol, bromocriptine, and oral antispasticity agents are frequently used.12 Bromocriptine is a dopamine agonist that acts both at the level of the hypothalamus and striatum; case studies of its successful use in adults with TBI have been reported.13 Recent research has focused on the use of intrathecal baclofen infusion to control symptoms of dysautonomia. One study14 examining continuous infusion via either a spinal catheter or an implantable pump revealed a correlation between baclofen doses and the number of paroxysmal episodes, defined as periods of hypertonia, hyperthermia, tachycardia, and swelling, during the acute period. The pathophysiologic hypothesis that supports the role of intrathecal baclofen in the treatment of dysautonomia remains unclear.14

Spasticity is commonly encountered acutely after TBI. It is defined as a velocity-dependent increase in muscle tone. Risk factors for developing spasticity include immobilization, motor impairment, associated hypoxic injury, concomitant spinal cord injury, and younger age. The evaluation must include an assessment of both active and passive range of motion (ROM), degree of tone, and identification of noxious factors similar to those seen in dysautonomia that may also increase spasticity. Clinical measurement should include objective measures such as the Modified Ashworth Scale (MAS) to grade the degree of tone or the Tardieu scale to grade the degree of spasticity.

Physical modalities can be instituted without fear of systemic effects. These include passive stretching, serial casting, splinting, and electric stimulation, all of which may maintain ROM or decrease tone mildly.15 The use of oral antispasticity agents, such as baclofen or dantrolene, during the acute phase after TBI has not been well studied. Concerns have been raised that these medications may cause lethargy and fatigue, decreasing a patient’s ability to participate in therapies. Oral agents, such as baclofen, which works at the spinal receptor level, have been shown to reduce spasticity in other diagnostic populations and may result in decreased lower-extremity spasticity after TBI. However, drug-related somnolence limits their use, as seen in study populations.16 Dantrolene sodium works peripherally at the muscle sarcomere, possibly providing some advantages. However, when studied in TBI, no oral antispasticity agents have ever evidenced functional improvement in subjects.

Regional treatment of spasticity can be useful in certain patients. Goals for treatment of the upper extremity with botulinum neurotoxin include the following: (1) preventing skin irritation and breakdown, (2) decreasing pain, and (3) decreasing amount of assistance needed for passive and active function.17 Neurolytic therapy with either phenol or botulinum toxin can be used in concert with serial casting, splinting, and other generalized interventions. An open-label trial of subjects with TBI found improvements in both wrist ROM and MAS scores.18 The findings were similar to those in stroke subjects, who also showed improvement in self-reported measures of disability. Studies have also shown no significant side effects with botulinum toxin; however, phenol may cause painful dysesthesia after injection.

Intrathecal baclofen administration can effectively control spasticity and dystonia after TBI. Continuous infusion of baclofen has resulted in a decrease in MAS scores in both the upper and lower limbs, which was maintained at 1 year.19 Risks associated with the placement of baclofen pumps include cerebrospinal fluid leak or seroma, infection, catheter migration, and seizures related to both overdose and withdrawal.20 The use of intrathecal baclofen can be done in conjunction with any of the other local or systemic treatments. The ideal timing of placement is yet to be determined, although many recommend early intervention. Orthopedic procedures such as tendon transfers and lengthening may decrease patient burden of care.21

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2.4 Clinical Activity: To provide consultation to a trauma surgeon who has treated a 25-year-old patient with a severe TBI for 6 weeks in the ICU 

A coordinated evidenced-based protocol for managing TBI, including early involvement of rehabilitation services, has been shown to increase care-delivery efficiency and improve outcome.22, 23 Early rehabilitation evaluation and management can serve several purposes. It can prevent complications related to immobility, initiate neurorehabilitation treatments, evaluate functional cognitive impairment, and manage behavioral and medical treatment for altered cognitive states.

When medical and surgical status permits and ongoing rehabilitation is indicated, timely movement along the continuum of trauma care should be anticipated. Decisions regarding postacute hospital rehabilitation can be influenced by the following things: the patient’s neurologic status and level of alertness; his/her level of physical endurance; functional limitations, including restrictions on weight bearing after fracture; financial and insurance issues, including policy coverage specific to rehabilitation and rehabilitation setting; availability of community resources, including subacute and skilled care; and the ability of family members or significant others to provide the anticipated level of care after discharge.

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Levels of Rehabilitation Care 

Inpatient Rehabilitation 

A prospective payment system (PPS) for care provided by an inpatient rehabilitation facility (IRF) to Medicare beneficiaries was implemented by the Center for Medicare & Medicaid Services (CMS)24 in 2002. To calculate a predetermined rate of payment for a given case-mix group, this system considers a patient’s age, level of impairment and function, and comorbid conditions. This process is similar to the system used in determining payment for Medicare beneficiaries in an acute care hospital based on their diagnosis-related group. The PPS for care provided in an inpatient rehabilitation facility is fast being adopted by private insurers as well, although some reimbursement levels have increased and the composition of patients admitted for inpatient rehabilitation has not significantly changed since implementation.25, 26

The CMS also developed eligibility guidelines24 for the admission of Medicare beneficiaries to an IRF. These guidelines direct the following: the majority of patients must have 1 of the 13 diagnoses selected as appropriate for this level of care, there must be a medical need for at least 2 therapeutic disciplines (eg, physical and occupational therapy), and the patient must be able (or has the potential) to tolerate 3 hours of therapy soon after admission26 (see the “3-hour rule” below). Furthermore, the patient must be medically stable, the admission should be authorized by the patient’s insurance carrier or other funding source, and a community discharge plan should be in place or anticipated. Brain injury is among the 13 diagnoses selected by the CMS as appropriate for inpatient rehabilitation.

The “3-Hour Rule” 

The CMS requirement that patients admitted for inpatient rehabilitation receive 3 hours of therapy daily, the “3-hour rule,” is a general guideline held by CMS. This standard is not defined in Medicare statutes or regulations and does not have the force of law. A patient is expected to be able to receive, tolerate, and benefit from 3 hours of daily therapy services within several days of admission and to do so for 5 out of 7 days. These services can be provided by clinicians other than occupational and physical therapists, such as speech and language therapy, and prosthetic or orthotic services. When medical or other conditions limit tolerance for or provision of 3 hours of therapy in a day for limited periods, compliance can be maintained by documenting the existence and extent of the complicating conditions. Guidelines for compliance to the “3-hour rule” vary by fiscal intermediary and among states. Private insurance company policies vary by agency, although many companies have adopted the CMS guidelines.

Alternatives to Inpatient Rehabilitation 

For patients who are severely impaired after TBI, an alternative to inpatient rehabilitation may be indicated. Where available, long-term acute care (LTAC) facilities provide an acute hospital level of care for patients requiring daily physician management for medically complex conditions such as prolonged mechanical ventilation, intravenous therapy, or complicated dialysis. Multidiscipline rehabilitation services are available in these settings, although the degree of coordination and comprehensiveness varies. A 25-day average length of stay is mandated for LTAC facilities. Most skilled nursing facilities (SNFs) also provide rehabilitation services to patients unable to tolerate intense rehabilitation treatment. Subacute rehabilitation in an SNF can serve as a transition to inpatient rehabilitation or home. For patients with severe impairment and adequate resources, community-based rehabilitation and nursing services can be provided in the home. Outpatient brain rehabilitation clinical services are crucial for maintaining coordination of these services and providing continuity of longitudinal care.

International Classification of Function, Disability and Health 

Characterizing the TBI’s effect on functionality and social integration for patients who acquire long-term impairment from their TBI is a primary role of rehabilitation clinicians as they recommend a rehabilitation setting. The World Health Organization has developed a classification system that extends the International Classification of Diseases (ICD-9, ICD-10) to include a system of coding modifiers, the International Classification of Function, Disability and Health (ICF).27 This classification scheme characterizes the severity of impairment associated with a disease state as well as the subsequent effects this impairment has on personal activities, relationships with others, and interactions with the community. The ICF introduces concepts of limitation to activities (formerly termed disability) and restrictions to participation (formerly referred to as handicap) as primary consequences of impairment related to injury or disease. In this way, the ICF seeks to integrate the medical and social models of disease. This approach is particularly pertinent for diseases that are associated with long-term impairment, such as TBI. When fully implemented, the ICF program will have a standardized coding system that features comprehensive clinical classification along the continuum of recovery after TBI. This system will also support clinical stratification and will inform rehabilitation decision making regarding appropriate levels of care.

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2.5 Clinical Activity: To assess a 75-year-old pedestrian who sustained a TBI and multiple trauma in an automobile collision 4 weeks ago. He required an emergency craniotomy for evacuation of a subdural hematoma and now has a swollen left leg on admission to inpatient rehabilitation 

The presence of a swollen limb after TBI suggests several possible conditions, including heterotopic ossification (HO), venous thromboembolism (VTE), infection, complex regional pain syndrome, and undiagnosed trauma. Although it appears to be histologically normal, HO is bone that occurs in abnormal locations. After TBI it occurs predominantly at the elbows, hips, and shoulders, and less commonly at the knee. Reported prevalence rates of clinically significant HO vary widely but likely range from 10% to 20%.28 It occurs more frequently following severe TBI and is often associated with spasticity.28 The precise pathogenesis remains uncertain, but it appears to result from the inappropriate differentiation of mesenchymal cells into osteoblastic stem cells in response to yet-unidentified inducing agents.29 Early clinical signs include pain, swelling, and erythema, followed by restricted ROM, which may cause impaired mobility and function as well as joint ankylosis. As HO progresses, it may entrap peripheral nerves, resulting in neuropathies. HO typically cannot be seen on plain radiography until several weeks after clinical manifestations become evident. Therefore, radionuclide bone scanning is the preferred diagnostic test for early detection. Treatment options include diphosphonates for a period of 6 months and/or nonsteroidal anti-inflammatory agents in conjunction with ROM exercises to preserve joint mobility. Traditionally, surgical resection was postponed until at least 18 months after the inducing trauma because of the risk of recurrence. However, several case series30, 31 suggest that earlier resection results in improved function without significant risk of recurrence. Diphosphonates are an effective means of prophylaxis if initiated shortly after the trauma,32 although mineralization of the bone matrix resumes after drug discontinuation, making this practice controversial. Noninflammatory drugs and irradiation may offer some benefit after surgically resected TBI-induced HO.33

VTE occurs commonly after acquired brain injury, often occurring early as an asymptomatic condition. Overall prevalence ranges from 6.7% to 13% in acute inpatient rehabilitation settings.34, 35 There are no standards of care regarding VTE prevention after TBI, although methods used include low-dose heparin compounds and intermittent pneumatic compression (IPC), which are probably equally efficacious when used appropriately.36 However, IPC has a high failure rate in patients who have undergone brain tumor resections,37 with evidence suggesting that meaningful posttraumatic prophylaxis is achieved only with nearly continuous use of the IPC until the risk of VTE subsides.38 IPC has limited utility in persons with lower-limb fractures, casts, or dressing, and improper use has been documented39 as adversely impacting its effectiveness. Regarding the use of low-dose heparin, some concern exists about the risk of expanding intracranial hemorrhages after trauma, although evidence suggests that its early use after TBI is safe,40 acknowledging that large-scale multicenter studies have not yet been reported. A meta-analysis41 revealed that low doses of either low-molecular-weight or unfractionated heparin compounds significantly decreased the incidence of deep vein thrombosis (DVT) in neurosurgery patients, the majority of whom had brain tumors, with only a small risk of major hemorrhage. Class 3 evidence suggests that prophylactic inferior vena cava catheter filters effectively prevent pulmonary embolism in high-risk patients for whom anticoagulation is contraindicated,38 but their use is controversial because they may increase the risk of DVT and its associated morbidity.37 Many inpatient rehabilitation centers screen patients with brain injury for DVT by using venous duplex ultrasonography, although its cost-effectiveness in acquired brain injuries remains controversial.42 Although D-dimer assay is frequently abnormal in the presence of DVT, it is not a clinically useful screening tool because of its poor specificity in patients with TBI.43

Other causes of a unilateral swollen leg after TBI include a ruptured Baker’s cyst, complex regional pain syndrome (CRPS), undiagnosed trauma, and infection. CRPS type 1, formerly known as reflex sympathetic dystrophy, can occur after TBI, resulting in limb pain associated with edema, skin texture and temperature changes, and localized bone demineralization. A swollen limb may also be caused by an unidentified orthopedic injury because 11% of fractures and 34% of peripheral nerve lesions associated with TBI are first recognized in the rehabilitation setting.44 Whenever feasible, long-bone fractures are best managed initially by definitive internal fixation, which reduces the chances of joint contracture by permitting early mobilization of injured limbs. Other factors contributing to peripheral neuropathies include pressure from hemorrhage or HO, prolonged coma, spasticity, and poorly fitted plaster casts or orthotics.

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Appendix 1. Scales to Assess Agitation During Rehabilitation 


1.Agitated Behavior Scale

2.Overt Aggression Scale

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Appendix 2. Scales to Assess Agitation in the ICU 


1.Ramsey Scale

2.Sedation Agitation Scale

3.Motor Activity Scale

Appendix 3. Agitation Sources to Consider After TBI
EtiologyDescription
DirectBrain lesion in locales that control mood, judgment, or behavior
Indirect or not TBI related
Premorbid personality

Premorbid psychiatric issues

Substance/drug withdrawal

Hypoxemia

Pain

Overstimulation from staff and medical care

Environment (light, temperature, noise, other patients)

Disturbance/sleep-wake cycle

Medical issues (cardiac, pulmonary, infection, lines, tubes)

Medication effect

Physical restraints

Appendix 4. Potential Causes of Clinical Decline After TBI
Possible EtiologyEvaluation Might IncludeComments
Occult or early infectionReview of vital signs, laboratory and other testsMost commonly a urinary tract infection
Electrolyte abnormalityLaboratory testsMost commonly sodium disturbance
Medication changesReview of current medications and recent changesOf note, any change, either adding or removing a medication, might cause a decline
Occult hypoxemiaOxygen saturation, arterial blood gas, hemoglobinFor instance, from an early pneumonia or a pulmonary embolus
HypoglycemiaBlood glucoseFor instance, from decreased insulin requirements with recovery
Relative hypotensionReview of vital signs, orthostatic vital signsFor instance, from a decreased need for antihypertensive medications with recovery
Intracranial complicationNeuroimagingMost commonly the development of hydrocephalus but other lesions possible
Endocrine abnormality45Laboratory testsMost commonly thyroid or adrenal deficiency but other hormones should also be investigated
Psychiatric disordersCareful historyFor example, from depression affecting initiation
Excessive fatigueCareful history, selected laboratory tests, sleep studyFor instance, from poor sleep or anemia
Electroencephalographic abnormalities46EncephalogramFor instance, nonconvulsive seizures
Constipation/obstipationCareful history, abdominal radiographNot uncommonly can have a significant impact on mental status

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  • ⁎ Key reference.

 No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated.

 Reprints are not available from the author.

PII: S0003-9993(07)01858-8

doi:10.1016/j.apmr.2007.12.010

Archives of Physical Medicine and Rehabilitation
Volume 89, Issue 3, Supplement 1 , Pages S9-S14, March 2008

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