Brain Injury – Post Acute Care Issues
Traumatic brain injury (TBI) is a brain injury due to externally inflicted trauma; may result in significant impairment of an individual’s physical, cognitive, and psychosocial functioning. TBI: leading mortality cause in North America for ages 1–45.
- Predominant age: Highest incidence in the very young (ages 0–4), in persons 15–24 years of age and those >75 years old
- Predominant sex: Male > Female (2:1)
- 1.2–1.7 million Americans sustain TBI per year.
- 50,000 deaths per year
- 80,000–90,000 sustain long-term disabilities
5.3 million Americans are living with TBI-related disabilities for which they require long-term assistance with activities of daily living.
- High risk: Male, age 15–34
- Moderate risk <5 years and >60 years
- Lower socioeconomic status (head injury)
Improved safety standards and programs designed to minimize injury from vehicular-related events (motor vehicle, motorcycle, bicycle, pedestrian), falls, violence, sports, and recreation provide best prevention against TBI (1)[C].
- Cortical contusions due to coup–contrecoup injuries. While axonal rupture from shear and tensile forces can occur at the time of severe head injury, milder degrees of axonal damage may play a role in mild TBI.
- Disruption of axonal neurofilament organization impairs axonal transport, leading to axonal swelling, Wallerian degeneration, and transection.
- Release of excitatory neurotransmitters acetylcholine, glutamate, and aspartate, and generation of free radicals may contribute to secondary injury.
- Leading causes of TBI: falls and motor vehicle accidents (MVA). Violence-related TBI has increased during the past decade and accounts for about 10% of all cases. Sports and recreation injuries are also an important cause of TBI, especially in teenagers and young adults.
- As the conflict in the Middle East continues, the number of soldiers returning to the US with diagnosed and undiagnosed blast-related TBI will continue to increase.
Commonly Associated Conditions
- Suicide attempts
- Substance abuse
- Attention deficit disorder
- Non-neurologic complications: Pulmonary, metabolic and endocrinologic, nutritional, GI, musculoskeletal, genitourinary, dermatologic, chronic pain
- Most neurologic complications are apparent within the 1st days following injury. Long-term sequelae include seizures, headache, hydrocephalus, visual defects, neuroendocrine abnormalities, and movement and sleep disorders.
- Cognitive consequences: Memory impairment, difficulties in attention and concentration, language deficits, visual perception problems, and poor problem-solving, reasoning, insight, judgment, and information processing
- Behavioral problems: Decreased ability to initiate responses, verbal and physical aggression, agitation, learning difficulties, shallow self-awareness, altered sexual functioning, impulsivity, social disinhibition
- Psychological consequences: Mood disorders, personality changes, altered emotional control, depression, anxiety
- Social consequences: Risk of suicide, divorce, unemployment, economic strain, alcohol/substance abuse.
Interactions of physical, cognitive, and behavioral sequelae interfere with new learning. Effects of early TBI may not become apparent until later in the child’s development.
- TBI’s severity is classified based on the Glasgow Coma Scale (GCS) as follows: Mild injury GCS 13–15; moderate injury GCS 9–12; severe injury GCS 8 or less.
- Glasgow Coma Scale (GCS). For all 3 categories, score best response:
|Withdraws from pain||4|
|Abnormal flexion to pain||3|
|Abnormal extension to pain||2|
Diagnostic Tests & Interpretation
- Evoked potentials (auditory, visual, somatosensory)
- Behavioral assessment, neuropsychological testing, vocational assessment
- Cognitive test for orientation and arousal; use Western Neuro Sensory Stimulation Profile or Galveston Orientation Amnesia Test
- Electroencephalograph (EEG)
Initial lab tests
As needed for suspected metabolic complications
- Bone scan: Heterotopic ossification
- CT: Hydrocephalus, atrophy, hematoma
- Video fluoroscopic swallowing study
- MRI to evaluate diffuse axonal injury
- EEG: To evaluate subclinical seizure activity. Limited predictive value in the setting of acute TBI.
- Evidence of microscopic axonal injury, axon retraction bulbs, and microglial clusters
- Hydrocephalus with periventricular edema
- Joint contractures result in collagen cross-linking: Decreased range of motion
- Heterotopic ossification: Disorganized osteoid calcification in soft tissue
- The diagnosis of pain following TBI can be difficult in light of limitations imposed by cognitive, language, and behavioral deficits.
- Dysautonomia: Tachypnea, hypertension, painful posturing/contractions, diaphoresis
- Neuropathic pain: Burning, shocklike, or pins and needles; allodynia/hyperpathia. 3 most common: Complex regional pain syndrome, central pain syndrome, and peripheral neuropathy.
- Spasticity or spastic dystonia
- Headache: Posttraumatic headache, hydrocephalus, increased intracranial pressure
- Myofascial pain syndrome
- Neurogenic heterotopic ossification: Bone formation in soft tissue
- Deep vein thrombosis
- Constipation and urinary retention
- Trauma: Fractures, musculoskeletal injuries
- Shoulder: Subluxation, acromioclavicular separation, rotator cuff tendonitis/tear
- Chronic infection, depression, hypothyroidism, hydrocephalus, intracerebral hemorrhage, seizures, fractures, tracheal stricture, pain, alcohol, drugs, polypharmacy, and/or central nervous system depressant
- Psychostimulants may affect speed of cognitive processing, mood, and behavior:
- Methylphenidate 20–40 mg/d in 2 divided doses; dextroamphetamine [B]
- Also likely to improve memory, attention, concentration, and mental processing in children/adults (2)[A]
- Treat epilepsy or depression 1st.
- Minimize the use of antipsychotics and benzodiazepines, as they worsen cognition.
- β-Blockers have best evidence for efficacy in agitation/aggression (3)[A].
- Antidepressants (SSRIs) and AEDs in the context of an affective disorder or epilepsy, respectively, may help agitation/aggression (4)[B].
- If necessary, use antipsychotics of the atypical class (clozapine, olanzapine, quetiapine, risperidone, and ziprasidone) (5)[B].
- Abulia (lack of initiative): Amantadine (Symmetrel), bromocriptine, methylphenidate, levodopa (5)[C]
- Epilepsy: American Academy of Physical Medicine and Rehabilitation does not recommend AEDs for preventing late (>7 days post TBI) posttraumatic seizures (6)[B]. If epilepsy occurs, avoid phenobarbital; too sedating (6).
- Spasticity caution: Be aware of potential negative consequences of all agents:
- Use dantrolene sodium 25–200 mg/d divided t.i.d.; baclofen; intrathecal baclofen; diazepam, clonidine, tizanidine, and gabapentin; botulinum toxin injections for focal spasticity (7)[B].
- Neurogenic bladder: Oxybutynin 2.5 mg t.i.d. -10 mg q.i.d. if bladder pressures low and/or postvoid residuals low (1)[B]
- Bowel routine: Stool softener such as docusate sodium (daily) combined with laxative (night before suppository), high-fiber diet, and suppository (every other day) (1)[C]
- Heterotopic ossification: Indomethacin 25–50 mg t.i.d. If severe, progressive, or history of GI ulceration, then etidronate (Didronel) 20 mg/kg for 6 months or alendronate 20 mg/d (1)[C].
- Neurobehavioral problems: Weak evidence supports psychostimulants as effective in treatment of inattention, apathy, and slowness; high-dose β-blockers in treatment of agitation and aggression; and anticonvulsants and antidepressants in treatment of agitation and aggression with an affective disorder (4)[B].
- Precautions: Medications may have significant adverse effects in persons with TBI and can impede rehabilitation progress.
- Diminished level of arousal: Identify best modality for communication, assess functional skills (proper seating, hand function) with behaviorist/neuropsychologist.
- Social work (family education and long-term planning) and nursing
- Reduce sedatives
- Neurogenic bladder—treat urinary tract infection:
- If postvoid residual <50 mL, then try regular voiding routine q2h
- If still incontinent, add oxybutynin
- If still incontinent, try condom catheter during the day; incontinence pads at night.
- If high postvoid residuals or high pressure bladder or dyssynergic bladder on urodynamics: Intermittent catheter q4–6h
- Neurogenic bowel: Regular bowel routine
- Contractures and spasticity; stretching:
- If no progress after 4 weeks, consider serial casting or custom-made orthotic
- Contractures >45°: Consider tendon release.
- Heterotopic ossification: Stretch soft tissue to decrease maturation of osteoid, consider orthotics/splinting, bone scan at baseline
- Skin: Turn patient q2h; avoid sitting such as in bed at 45°, observe for erythema around tube sites, and rule out latex allergy.
- Respiratory: Night humidification for tracheotomy
- Endocrine: Monitor fluid balance
- Dental: Assessment and radiographs
- Rehabilitative practices: Rehabilitative programs should be interdisciplinary, comprehensive, and include cognitive and behavioral assessment and intervention (1)[C]
Issues for Referral
- Refer to multidisciplinary rehabilitation programs.
- Suicide attempts and ideation (SI) are more prevalent in people with TBI, even after controlling for psychiatric disorders (8)[C]. Assess hopelessness and SI proactively.
Complementary and Alternative Medicine
- Cognitive exercises (including computer-assisted strategies), compensatory devices (memory books, paging systems), psychotherapy, behavior modification, vocational rehabilitation, school rehabilitation, nutritional support, music and art therapy, therapeutic recreation
- Hyperbaric oxygen therapy (HBOT) cannot be routinely recommended for patients with TBI because of few trials, methodologic shortcomings, and poor reporting (9)[A].
Patients make slow, steady gains; review medical status monthly.
- Ensure adequate hydration; 2–2.5 L of water/d.
- Bolus feeds preferred if fed by gastrostomy.
- Upright and quiet for 1/2 hour following feeds, as aspiration can occur even with a g-tube
- Early feeding is associated with trend toward better survival and disability outcomes (10)[A].
- For information and family support groups:
- Brain Injury Information Network www.tbinet.org/
- Brain Injury Association of America www.biausa.org/
- Families need support, advocacy, education, information (verbally and written), opportunity to have input regarding priorities and treatment plans, and to discuss limits of treatment for patient (advance directive).
- Most rapid return of function is during 1st 2 years, but some improve slowly for 5–10 years
- Highly variable (80% of individuals with severe injuries become independent in dressing and self-care at 1 year)
- Negative prognostic factors:
- Age >40 years old
- Abnormal pupillary responses or extraocular eye movements
- Prolonged coma
- Abnormal evoked potentials
- Accurate prediction of return to work is not feasible, with rates in the 12–70% range.
Major affective disorder (depression, psychosis) in up to 50% of patients, family and caregiver burnout, substance abuse, social isolation, dental caries, osteoporosis, aspiration pneumonia, pressure ulcers, dysphagia, esophagitis, bladder incontinence, contractures/spasticity
1. Consensus conference. Rehabilitation of persons with traumatic brain injury. NIH Consensus Development Panel on Rehabilitation of Persons With Traumatic Brain Injury. JAMA. 1999;282:974–83.
2. Siddall OM. Use of methylphenidate in traumatic brain injury. Ann Pharmacother. 2005;39:1309–13.
3. Fleminger S, et al. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev. 2003/2006;(1):CD003299.
4. Deb S, Crownshaw T. The role of pharmacotherapy in the management of behaviour disorders in traumatic brain injury patients. Brain Inj. 2004;18:1–31.
5. Elovic EP, et al. The use of atypical antipsychotics in traumatic brain injury. J Head Trauma Rehab. 2003;18(2):177–95.
6. Bushnik T, et al. Medical and social issues related to posttraumatic seizures in persons with traumatic brain injury. J Head Trauma Rehab. 2004;19(4):296–304.
7. Zafonte R, et al. Acute care management of post-TBI spasticity. J Head Trauma Rehab. 2004;19(2):89–100.
8. Simpson G, Tate R, et al. Suicidality in people surviving a traumatic brain injury: prevalence, risk factors and implications for clinical management. Brain Inj. 2007;21:1335–51.
9. Bennett M, Heard R. Hyperbaric oxygen therapy for multiple sclerosis. Cochrane Database Syst Rev. 2004:CD003057.
10. Perel P, Yanagawa T, Bunn F, et al. Nutritional support for head-injured patients. Cochrane Database Syst Rev. 2006:CD001530.
- 339.20 Post-traumatic headache, unspecified
- 854.00 Intracranial injury of other and unspecified nature, without mention of open intracranial wound, with state of consciousness unspecified
- 907.0 Late effect of intracranial injury without mention of skull fracture
- 127295002 Traumatic brain injury (disorder)
- 429656004 Late effect of traumatic injury to brain (disorder)
- 54012000 Posttraumatic headache (finding)
- TBI can cause both neurologic and non-neurologic manifestations.
- Best approach to treatment includes multi- and interdisciplinary team member participation.
- TBI can lead to devastating sequelae; prevention is key.