The intent of this chapter is to provide a brief overview of common conditions and topics that may be encountered on a general inpatient rehabilitation unit; for an in-depth review of the topics, please see the corresponding chapters in this textbook.
Acute inpatient rehabilitation is a post–acute hospital level of care defined by the Center for Medicare and Medicaid Services (CMS). Acute inpatient rehabilitation can take place in a specific defined inpatient rehabilitation facility (IRF) within a hospital or as a stand-alone rehabilitation hospital. In the United States, to be recognized as an IRF, the center must provide at least 3 hours of therapy a day 5 days a week, nursing care 24 hours a day, and supervision at least 3 days a week by a physician with an expertise in rehabilitation.1
To be eligible for inpatient rehabilitation, patients must require complex nursing care, ongoing medical management, and sufficient rehabilitation needs. The required rehabilitation needs include active and ongoing interventions by physical therapy and occupational therapy with possible contributions from speech-language pathology and/or prosthetic or orthotic specialists. In complex cases such as a patient who requires dialysis, CMS allows therapies to be spread out over 7 days, provided that the patient completes 15 hours of intensive therapy per week. Furthermore, patients should make measurable gains during inpatient rehabilitation that result in improved functional capacity, adaptation to impairments, or independence in a reasonable amount of time. This is usually quantified by a functional independence measure (FIM) score2 (Fig. 55–1).
IRFs provide holistic and coordinated interdisciplinary care for their patients. The treatment team is led by the rehabilitation physician, and the team may include some or all of the following: physical therapists, occupational therapists, speech and language pathologists, nutritionists/dietitians, neuropsychologists, pharmacists, case managers, social workers, therapeutic recreation therapists, and other consulting services. The treatment team is expected to have regular conferences to communicate goals and coordinate care for each patient.1
Other levels of post–acute care include long-term acute care hospitals (LTACs or LTCHs) and skilled nursing facilities (SNFs). LTAC centers provide daily physician evaluations for patients with elevated medical needs, 24-hour nursing care, and variable amounts of rehabilitation. SNFs are typically short-term facilities within or affiliated with a nursing home and must provide nursing supervision for 8 hours a day and physician supervision at least every 30 days.
CMS requires IRFs to operate under the “60-40 rule.” This means that 60% of patients admitted to that IRF must fall within specific diagnostic categories to maintain IRF accreditation3 (Table 55–1).
Stroke is defined as the death of brain cells due to either ischemia or hemorrhage with subsequent neurologic changes. Ischemic stroke is the more common type of stroke, which occurs when blood flow is disrupted. This may occur due to thrombosis of an artery from an atherosclerosis plaque, or alternatively, an embolic disruption may occur when a blood clot becomes lodged in a smaller brain vessel. The source of embolic clots is typically the heart but could also be other vessels.4 Lacunar stroke is another, less common type of ischemic stroke. It affects deep brain structures and is almost always associated with hypertension.5 Alternatively, a hemorrhagic stroke typically occurs when there is a vessel rupture. The etiology of intracerebral hemorrhage is most commonly uncontrolled hypertension.5 The pattern of deficits will reflect the area of the brain that has been affected (Fig. 55–2).
Figure 55–2
Vascular distribution of the brain parenchyma. An understanding of the territories of the major intracranial vessels is important in the diagnosis of stroke and other vascular lesions. The anterior cerebral arteries (blue) supply the anterior parasagittal regions. The middle cerebral arteries (pink) supply most of the lateral cortex of the frontal and superior temporal lobes. The posterior cerebral arteries (green) supply the inferior temporal and occipital lobes. (Reproduced with permission from DeKoning E. Thermal Burns. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016.)
Brain dysfunction occurs after any insult to the brain that causes pathologic changes in physical, cognitive, language, and/or behavioral functioning. One common form of brain dysfunction is traumatic brain injury. The most common cause of traumatic brain injury occurs when the head endures enough force to cause the brain to move within the skull.6,7 Traumatic brain injuries result in both primary and secondary injuries. A primary injury to the brain, such as a cerebral contusion, occurs immediately. A secondary injury occurs due to a cascade of chemical and molecular events associated with brain swelling and edema.8 Traumatic brain injuries can be focal or diffuse. Diffuse axonal injury occurs due to centripetal forces acting on the brain and results in a stretching and injury of nerves and nerve connections. Due to location and differences in density within the brain, the primary location of diffuse centripetal injury occurs between the white and gray matter in the brain and around the corpus callosum.9 Hypoxic brain injuries are another type of brain dysfunction and are the result of lack of oxygen. Situations such as cardiopulmonary failure and near-drowning are common etiologies. Metabolic brain injuries can occur from other insults, such as prolonged severe hypoglycemia.10 Other brain injuries include but are not limited to tumors, infection, and other noxious processes that affect the brain.
Spinal cord injury is damage to the cord with resulting disruption of motor function, sensation, and/or autonomic function below the level of injury. Spinal cord injuries can be further classified as complete, where the patient has no motor function or sensation below the level of injury, or incomplete, where there is preserved function below the level of injury. Spinal cord injuries are also classified as traumatic (resulting from a traumatic injury to the spinal cord) or nontraumatic (any other injury to the spinal cord).
The most common cause for a traumatic spinal cord injury is a motor vehicle accident. Falls are the second most common cause with a bimodal distribution for the young and elder populations.11 Traumatic spinal cord injuries may be further classified according to the International Standards for Neurological Classification of Spinal Cord Injury.12 Nontraumatic spinal cord injuries occur from processes including tumors, infections, and infarctions of the spinal cord. There are specific syndromes associated with certain spinal cord injuries (Fig. 55–3).
Central cord syndrome. This syndrome is characterized by weakness in the arms with relative sparing of the legs with loss of pain sensation, light touch, and proprioception below the level of injury.
Anterior cord syndrome. Often associated with vascular injury, this syndrome results in changes below the level of injury resulting in loss of motor function, pain sensation, and temperature sensation, while sense of touch and proprioception (sense of position in space) remain intact.
Posterior cord syndrome. This syndrome present as loss of proprioception and sense of vibration below the level of injury, while motor function and sensation of pain, temperature, and touch remain intact.
Brown-Séquard syndrome. This syndrome results from an injury that occurs to one side of the spinal cord, with the same side of the injury losing motor function, proprioception, vibration, and touch. On the opposite side, the patient loses pain and temperature sensation due to the location of decussation of the spinothalamic tract.
Conus medullaris syndrome. This syndrome is associated with T12–L2 vertebral level injuries and involves the sacral segments that include the bowel, bladder, sexual function, and sensation.
Cauda equine syndrome. This syndrome occurs when the injury is below where the spinal cord splits at approximately the L2 vertebral level. The damage involves the individual nerve roots, and the syndrome includes pain, paralysis of the lower limbs, and loss of sensation. While this can affect both legs, typically only one leg is involved.
A multiple major trauma is defined using the injury severity score (ISS), an established scoring system used to assess trauma severity in patients with multiple injuries, and correlates with morbidity and mortality. The ISS ranges from 1 to 75; multiple major trauma (or polytrauma) is defined by an ISS > 15, and a score of 75 is considered unsurvivable. This scale is largely used in trauma centers, and the calculation of scores is fairly limited.13,14
The most common causes of amputation in the United States are vascular disease, including diabetes mellitus and peripheral arterial disease, along with trauma and cancer.15 Pediatric patients can also have congenital limb deficiencies.16 At present, vascular causes of amputation are increasing, while traumatic and cancer-related amputations are decreasing. Typically, inpatient rehabilitation is more appropriate for individuals with lower limb amputations, but there have been cases where patients with upper limb amputations have benefited from inpatient rehabilitation.17
Proximal femur fractures are typically referred to as “hip fractures” and do typically qualify for inpatient rehabilitation per CMS guidelines. Osteoporosis is a major risk factor.18 Intertrochanteric femur fracture is the most common type of fracture.19 Fractures proximal to the lesser trochanter are more common in females and older people. Femoral neck fractures are less common but typically included in this grouping. Rehabilitation may start immediately postoperatively for intertrochanteric and femoral neck fractures depending on the surgical approach. Of note, fractures below the level of the trochanter are not considered “hip fractures” and may not qualify for inpatient rehabilitation.
There are many different diagnoses that may fall under the diagnosis of polyarthritis, but all of them have difficulty qualifying for inpatient rehabilitation according to CMS guidelines20 (Fig. 55–4).
In order to qualify for inpatient rehabilitation, the patient must have significant functional impairment of ambulation and other activities of daily living (ADLs). The patient must also have either tried extensive alternatives to inpatient rehabilitation and failed or have a recent disease flare that cannot be addressed in another level of care (Table 55–2).
Polyarticular rheumatoid arthritis | An autoimmune inflammatory disorder affecting multiple organ systems including diarthrodial joints. The disease causes synovial lining inflammation leading to pannus formation and joint destruction. |
Psoriatic arthritis | Seronegative arthropathies that include multiple-joint arthritis and can have exacerbations. |
Hemochromatosis | Excessive iron stores lead to organ dysfunction and progressive arthritis, including the hips. |
Alkaptonuria | Deficiency in homogentisic acid oxidase leading to arthritis of the large joints. |
Wilson’s disease | Copper deposition in organs, knee joints, and spine. |
Osteoarthritis (OA) is a chronic degenerative joint disease leading to deterioration of the articular cartilage. Patients with severe OA involving two or more weight-bearing joints (including the hips, knees, shoulders, and elbows) who have joint deformity, a decreased range of motion, atrophy of muscles surrounding the joints, and a significant decrease in their mobility and ability to perform their ADLs meet the criteria for inpatient rehabilitation admission. These individuals meet the CMS requirements only after they have failed other, less intensive rehabilitation interventions, and they must demonstrate that improvement cannot be achieved with other interventions or at another level of care.
Multiple sclerosis (MS) is an autoimmune demyelinating disease that can affect the brain and spinal cord, leading to a multitude of different symptoms. Common impairments include loss of sensation, weakness or paralysis, and cognitive disorders. There are many different subclassifications of MS, including relapsing-remitting, secondary progressive, primary progressive, and progressive-relapsing.21 Symptoms may improve or disappear between attacks, but as the disease progresses, there may be permanent neurologic deficits. Imaging of brain and spinal cord usually show periventricular white matter plaques. Spasticity is common.
Parkinson’s disease is a neurodegenerative disorder involving death of the cells that comprise the substantia nigra in the midbrain. This results in a decrease in dopamine release and movement-related deficits with tremors and rigidity.22 Cognitive deficits usually occur later in the disease. Autonomic instability is possible.
Polyneuropathies include a heterogeneous group of diseases with numerous causes and presentations. The common characteristic inherent to all these diseases is underlying peripheral nerve pathology. A few examples include
Inherited neuropathies, which tend to have symptoms such as sensory loss, ataxia, and an increased incidence of muscle cramping.
Hereditary motor and sensory neuropathies (HMSNs) or Charcot-Marie-Tooth disease, which is common, and deficits involving strength and sensation are frequently reported.23,24
Hereditary sensory and autonomic neuropathies (HSANs), which include such symptoms as loss of pain and temperature sensation, thermal dysregulation, bladder dysfunction, and cognitive defects.23
Hereditary motor neuropathies (HMNs), which include abnormalities in anterior horn cells that result in atrophy of distal spinal muscles and weakness of the upper and lower extremities.23,25
Acquired neuropathies are peripheral nerve injuries typically associated with medical conditions, inflammatory processes, or medications. Common causes including diabetes mellitus, thyroid disorders, amyloidosis, sarcoidosis, Sjögren’s syndrome, porphyria, uremia, exposure to lead, exposure to mercury, lack of folate, chemotherapy agents, alcohol abuse, vitamin B12 deficiency, lack of pyridoxine (vitamin B6), acute inflammatory demyelinating polyradiculopathy (AIDP)/Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculopathy (CIDP), exposure to arsenic, monoclonal gammopathy, diphtheria, HIV/AIDS, leprosy, Lyme disease, and many more.23 Critical illness can result in severe inflammation that damages peripheral nerves.26 This is known as critical illness neuropathy and is addressed later. Acquired neuropathies tend to have similar symptoms, including burning, pain, and paresthesias and sometimes ascending paralysis.
There are a number of neuromuscular junction diseases. The more common are as follow:
Myasthenia gravis is an autoimmune response to postsynaptic acetylcholine receptors.27 Symptoms include ocular and proximal weakness that improves with rest.
Lambert-Eaton myasthenic syndrome is autoimmune and typically a paraneoplastic syndrome. The target is the presynaptic membrane, and the result is decreased release of acetylcholine.27 Symptoms include proximal weakness (especially of the lower legs) that improves with exercise. Autonomic instability symptoms may be present.
Botulism is the Clostridium botulinum toxin that blocks presynaptic release of acetylcholine.28 Symptoms include bulbar symptoms (ptosis, dysphasia), gastrointestinal (GI) symptoms, and respiratory and cardiac dysfunction.
Myopathies are a collection of medical diagnoses that all have underlying muscle pathology and result in weakness. Recently, many physiatrists have used the term disuse muscle atrophy, but the exact diagnostic criteria remain controversial.29 Other myopathies are listed by category as follows:
Metabolic: Pompe’s disease (acid maltase deficiency), McArdle’s disease (myophosphorylase deficiency), phosphofructokinase deficiency, hyper-/hypokalemic periodic paralysis
Inflammatory: Polymyositis/dermatomyositis, sarcoidosis, infectious
Endocrine: Thyroid, parathyroid, adrenal, pituitary
Toxic: Alcohol, diuretic, vincristine, steroid, statin
Motor neuron diseases are a group of diagnoses with similar underlying pathology. Individuals with these diseases may benefit from a rehabilitation facility stay, but goals should revolve around adapting to the disease and providing caregiver education. Therapeutic exercise, instead of strength training, and improving endurance are typical goals given the risk of worsening weakness in these patients with overfatiguing muscles.30
Type I (Werdnig-Hoffman disease) affects lower motor neurons and has both the earliest onset (3–6 months) and worse prognosis (usually fatal early in life) of all types of SMA. Characteristic symptoms include floppy baby syndrome (hypotonia), weak cry, tongue fasciculations, and respiratory failure requiring ventilation support.31
Type II (chronic Werdnig-Hoffman disease) is similar to type I but it is slower to progress. This disease is usually fatal during midlife.31
Type III (Kugelberg-Welander disease) progresses slowly with symmetric ascending weakness and normal life expectancy.31
Poliomyelitis/post-polio syndrome is a lower motor neuron disease caused by the picornavirus with degeneration of the anterior horn cells. Acute infection is typically marked by severe weakness with some recovery in function. These patients remain stable for years or decades until the weakness slowly returns.32
Amyotrophic lateral sclerosis (ALS) is an upper and lower motor neuron disease due to unexplained degeneration of the anterior horn cells. This is most commonly seen in men in their fifties who first develop asymmetric ascending atrophy and weakness along with increased tone. The prognosis is very poor, and half of patients die within 3 years of diagnosis.33
Critical illness neuromuscular diseases are typically diagnosed in the intensive care unit (ICU) setting or in patients who have spent prolonged times with inflammatory processes. Common risk factors include infection, trauma, or other insult causing a systemic inflammatory response syndrome (SIRS).
Septic encephalopathy is a complication of SIRS postulated to be related to changes in the blood-brain barrier. Symptoms include altered mental status and/or cognitive deficits, but the disease may manifest initially with issues of coordination or planning of movement.34
In critical illness polyneuropathy (CIP), nerve conduction studies (NCS)/electromyelographic (EMG) assessment may demonstrate axonal and demyelinating motor and sensory peripheral polyneuropathy. Nerve biopsy could be considered but is not typical. Weakness and sensory loss are typical manifestations.35
Critical illness myopathy (CIM) is likely related to prolonged immobility, SIRS, neuromuscular blocking agents, or steroids, resulting in an acute inflammatory myopathy leading to muscle cell breakdown. It is typically diagnosed on physical examination, but NCS/EMG and/or muscle biopsy could be considered.35
There are innumerable possible deficits that can be present at birth. Despite many of them being relatively uncommon, the possible diagnoses that may be seen in an inpatient rehabilitation setting are briefly reviewed as follows:
Congenital limb deficiencies typically occur during the first trimester of pregnancy, with risk factors including thalidomide and misoprostol.36 Goals for inpatient rehabilitation include improving ADLs, mobility, and transfers and addressing any prosthetic needs.
Congenital scoliosis results from abnormal spinal formation during development.37 Goals for inpatient rehabilitation include improving ADLs, mobility, and transfers and addressing any orthotic or surgery needs.
Cerebral palsy is a nonprogressive lesion of the immature brain that may cause any combination of movement and posture disorders (e.g., spastic or dyskinetic movement disorders), cognition impairments, and/or sensation problems. Dystonia and spasticity are common in this population and may require intensive therapy, medication, and modalities.38
Spina bifida is a term for a group of neural tube defects during embryonic development of the vertebral column and is the most common spinal cord disorder in children.39
These patients are rarely admitted to inpatient rehabilitation facilities, but some of them could have focused goals for inpatient rehabilitation. Some of the possible diagnoses are as follows:
Myopathies:
Dystrophic myopathies: Duchenne’s, Becker’s, congenital muscular dystrophies, facioscapulohumeral dystrophy, Emery-Dreifuss muscular dystrophy, and limb-girdle syndromes40
Congenital myopathies: Mitochondrial, central core, minicore disease, nemaline, myotubular, congenital type I fiber predominance and fiber disproportions, miscellaneous subcellular organelles, minimal-change, and other nonspecific congenital myopathies40
Myotonic myopathies: Myotonic muscular dystrophy (MMD), myotonia congenita, Schwartz-Jampel syndrome, and congenital myotonic dystrophy40
Congenital myasthenia syndromes. This is a group of inherited disorders caused by mutations in genes encoding proteins essential for the integrity of neuromuscular transmission.41
Peripheral nerve disorders:
Hereditary motor sensory neuropathy (HMSN)
Type I (Charcot-Marie-Tooth [CMT] disease) through type IV. This is the most frequent form of inherited neuropathy with great variety of phenotypes, inheritance patterns, and causative genes.42
Spinal muscular atrophy (SMA). This is a congenital disorder caused by degeneration of the anterior horn cells of the spinal cord and brainstem motor nuclei. It is characterized by weakness, muscle wasting, and both upper and lower motor neuron signs (SMA type I presents the earliest and is most severe).
Friedreich’s ataxia. This is a spinocerebellar degeneration syndrome due to lack of mitochondrial protein frataxin. This disease typically presents before age 20, and patients develop gait ataxia that progresses in ascending fashion.43,44
Juvenile rheumatoid arthritis and other arthridities. These are considered acceptable diagnoses for inpatient rehabilitation when appropriate goals are set.
A burn is an acute injury to the skin, most commonly from heat, but it could also occur from cold exposure, chemicals, electricity, and radiation. The exposed collagen causes an inflammatory response, increased capillary permeability, and reduced osmotic pressure that decrease intravascular volume acutely, leading to hypovolemia and shock.45 Burns are severely painful, prone to infection, and require adequate nutrition for healing.46 The goal of burn rehabilitation includes controlling scarring, and physiatrists apply early mobilization and splinting to maintain range of motion and prevent limitations due to scarring. Other complications include idiopathic peripheral polyneuropathies and heterotopic ossification, with the elbow being the most common joint affected (Fig. 55–5).
Figure 55–5
Percentage area of burns by body area. (Reproduced with permission from Ladde JG. Central Nervous System Procedures and Devices. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016.)
Systemic vasculitides can result in joint inflammation. The joint inflammation has subsequent weakness and pain, resulting in significant functional impairment of ambulation and other ADLs. Some examples include.
Polymyalgia rheumatic. This is associated with temporal arteritis (giant cell arteritis). Patients have symptoms affecting proximal muscles of the pelvis, shoulders, and neck with morning stiffness and muscle tenderness and associated myalgias/arthralgias.47
Polyarteritis nodosa. This is systemic necrotizing vasculitis involving small and medium-sized arteries and associated arthritis.48
Churg-Strauss syndrome. This is now called eosinophilic granulomatosis with polyangitis and involves eosinophil and granuloma formation with associated neuropathies.49
Patients with major joint replacements need to meet one or more of the criteria listed in Table 55–3 to qualify for inpatient rehabilitation in the United States per CMS guidelines.
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While 60% of patients must meet the criteria in the table, 40% can have other diagnoses not related to those criteria and still be appropriate for inpatient rehabilitation. Examples include but are not limited to medical debility, deconditioning, diffuse muscle weakness, heart/lung/liver/kidney transplant, left ventricular assistive device (LVAD), autonomic dysfunction, cardiac impairment, pulmonary disease, cancers, and other orthopedic injuries without required comorbidities.50
Patients who qualify under CMS criteria for inpatient rehabilitation should be able to engage in rehabilitation therapies. The patient must have his or her needs addressed by at least two therapy disciplines (physical therapy, occupational therapy, and speech and language pathology) where one of the disciplines must be physical therapy. The patient should be able to tolerate 3 hours of rehabilitation over the course of the day or be ready to tolerate 3 hours within 48 hours of admission. The patient must have the ability to significantly improve his or her level of independence. In addition, the patient should have a reasonable discharge plan with an appropriate level of assistance on discharge.50 Further surgeries or invasive procedures should be completed as able before admission to inpatient rehabilitation.
Autonomic dysreflexia (AD) is a complication of spinal cord injury and is defined as a sudden increase of systolic blood pressure about 20 mm Hg above the patient’s baseline.51 AD is typically associated with complete spinal cord injuries above the T6 level.51 In addition to hypertension, AD is associated with bradycardia, headache, nasal congestion, and sweating or flushing above the level of the lesion. Symptoms noted during AD are typically triggered by noxious stimuli below the lesion. Common triggers are kinked indwelling catheters, constipation, ingrown toenails, pressure ulcers, menstruation, and other noxious stimulus.51
Initial management includes raising the head of the bed and taking off all compressive garments (including compression stockings, abdominal binders, jewelry, tight pants, etc.). If an indwelling catheter is present, irrigate the catheter to make sure that there is not an obstruction. Consider a bladder scan, and catheterize the patient if indicated. If the patient is constipated and needs a suppository, it is important to numb the rectal area with lidocaine jelly, wait 15 to 20 minutes, and then insert the suppository. Optimization of pain management is essential because pain below the level of the lesion can also trigger AD.51
Acute management includes an assessment of the patient’s blood pressure every 5 minutes. If the blood pressure continues to be above the patient’s baseline, a fast-acting blood pressure medication such as nitroprusside paste or patch is recommended.51 Long-acting hypertensive medications are a last resort. If AD persists over 1 to 2 hours, consideration should be given to transferring the patient to the emergency room/critical care unit for continuous blood pressure monitoring. AD can lead to seizures, stroke, and death if pressures continue to be uncontrolled. Special attention needs to be paid to pregnant patients; if their blood pressure continues to be elevated after removing noxious stimuli, consider preeclampsia and associated labor. Transferring these patients to an OB-GYN unit for close monitoring may be prudent.52
Many blood pressure issues arise during inpatient rehabilitation; therefore, blood pressure should be closely monitored as activity intensity increases. Typically, blood pressure issues are more common during the first few days of rehabilitation and then stabilize over time. A few more common issues are addressed next.
Orthostastic hypotension is a drop in systolic blood pressure below 20 mm Hg from baseline with reflex tachycardia. It is usually associated with dizziness and presyncopal symptoms. Orthostatic blood pressure is often observed in individuals who have lost control of the autonomic nervous system due to prolonged bedrest or neurologic injury.
First-line management involves increasing venous return to the heart by laying patient flat, using compression stockings and an abdominal binder, and potentially placing the patient in a Tredelenberg position. Antihypertensive medications often need to be adjusted during early inpatient rehabilitation, and the diet should be modified as medically indicated53 (Table 55–4).
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High blood pressure can also limit inpatient rehabilitation. High systolic blood pressures above 140 mm Hg or diastolic pressures above 95 mm Hg are concerning.53 It is essential to monitor for signs and symptoms of hypertensive emergency, such as headaches, blurry vision, chest pain, dizziness, and even agitation. In patients with recent stroke (<1 month), hypotension needs to be avoided to decrease hypoperfusion.53 There are many choices for medications to lower blood pressure, and difficult cases may benefit from consultation with internal medicine or neurology.
Aspiration is the penetration of particles or oral secretions from the oral and nasal cavity into the larynx, trachea, and lower respiratory tracts. It can be manifested as cough, wet voice, dysphonia, dyspnea, or wheezing.54 Aspiration typically affects patients who have had a change in the ability to swallow.
Patients with aspiration usually present with shortness of breath and anxiety. It is important to determine oxygen saturation and to obtain an arterial blood gas determination, as well as to provide supplemental oxygen as needed. If the patient is stable and there are no signs of asphyxiation, one should monitor for signs of infection, such as fever, tachycardia, elevated white cell count, and decreased arousal. These signs, however, may not be evident until days later. Patients at risk for aspiration need to be closely monitored by a speech/language pathologist. If necessary, obtain a chest x-ray or chest CT scan and repeat a swallow study. If infection is suspected, consultation with internal medicine, pulmonology, or infectious disease may be warranted.
Previous research studies of gurgled wet voices showed no association between the voice quality and penetration or aspiration of oral/nasal materials during swallowing.54 However, voice quality may represent patients at risk for aspiration. Aspiration precautions should be put in place during meals and tube feedings by maintaining the head of the bed at between 45 and 90 degrees. Also, maintaining the head of the bed above 30 degrees while patients sleep helps avoid aspiration of regurgitated materials in case of gastroesophageal acid reflux.
Adrenergic Dysfunction (Also Known As Dysautonomia, Sympathetic Hyperactivity, Paroxysmal Autonomic Instability with/without Dystonia, and Storming)
Autonomic dysfunction is dysregulation of the body’s autonomic nervous system and is a common finding in severe traumatic brain injury. It occurs most commonly during ICU hospitalization and early stages of recovery. Such dysfunction typically improves over time, but there is a small percentage of patients who have persistent symptoms.55
The proposed mechanism involves an imbalance of neurotransmitters between the thalamus and hypothalamus and their connections to the cortex. This results in a catecholamine surge into the circulation secondary to physical or environmental stimuli.55 Adrenergic dysfunction is usually manifested by hypertension, with systolic blood pressure usually above 140 mm Hg, tachycardia (heart rate [HR] > 120 beats/min), hyperthermia (>38.5°C), diaphoresis, restlessness, worsening of spasticity, dystonia, and posturing.55
Similar to autonomic dysreflexia, the first step is to remove noxious stimuli. Initially, evaluation of the bladder for retention, removal of noxious stimuli, and exclusion of infection, constipation, and/or menstruation are warranted. Clinicians should monitor blood pressure and temperature every 15 to 20 minutes for the initial hour. Sometimes medication, such as acetaminophen, can be helpful in managing fever and pain. If the patient presents with severe pain, short-acting opioids may help decrease pain and inhibit sympathetic hyperactivity. If there is concern for temperatures greater than 102°F, consider a cooling blanket or chilled normal saline intravenously to help reduce the temperature.56
Beta blockers (such as propranolol) may be considered for patients with a sustained elevated blood pressure who have failed the preceding measures for more than 30 to 60 minutes.55 The patient needs to be monitored closely for hypotension after administration. In cases of severe adrenergic dysfunction, regularly scheduled propranolol, morphine, and/or gabapentin may help.55 In refractory cases, a number of case reports have documented an improvement with intrathecal baclofen.55
Any change from the patient’s baseline mental status needs to be monitored closely. There are innumerable possible causes, but physiatrists should have a high suspicion for new or recurrent stroke, hydrocephalus, seizures, infection, hypoglycemia, hypoxia, delirium, and electrolyte imbalance.56 Patients with a brain injury or stroke can have decreased communication abilities, and changes in mental status may be a useful sign that further workup is needed.
Assessment of acute change in mental status may benefit from recording whether changes are sudden or gradual. This can assist in determining etiology, such as possible hypoglycemia or related hypotension. Similarly, delirium, especially worsening delirium at night, can be predicated on environmental cues. It is also typically important to rule out infection, neuroendocrine dysfunction, and other causes of encephalopathy, such as high ammonia, when appropriate56 (Fig. 55–6). A head CT scan without contrast material may be warranted to assess for hydrocephalus or a new intracranial event.56 Lastly, avoiding medications that can cause oversedation such as benzodiazepines or antipsychotics is encouraged because they can worsen confusion.56
Figure 55–6
Delirium pathophysiology represents a complex series of interrelated events. Multiple pathways to delirium may be present in a single patient. (Reprinted with permission from Flacker JM, Lipsitz LA, et al. Neural mechanisms of delirium: current hypotheses and evolving concepts. J Gerontol A Biol Sci Med Sci. 1999;54(6):B239–46.)
Patients with hypoarousal strictly related to the location of their brain injury may benefit from neurostimulants such as modafinil, amantadine, or methylphenidate.57 These medications are not free from side effects and should be administrated with caution.