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.

Risk Factors

  • High risk: Male, age 15–34
  • Moderate risk <5 years and >60 years
  • Lower socioeconomic status (head injury)

General Prevention

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

  • Psychosis
  • Suicide attempts
  • Substance abuse
  • Attention deficit disorder

Glasgow Coma Scale, Traumatic brain injury, Neurological Disorders, traumatic brain injury, excitatory neurotransmitters, neurotransmitters acetylcholine, moderate risk, head injury,



  • 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.

Pediatric Considerations

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.

Physical Exam

  • 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:
Verbal response Score
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible speech 2
No response 1
Eye opening
Spontaneous 4
To speech 3
To pain 2
No response 1
Motor response
Obeys commands 6
Localizes pain 5
Withdraws from pain 4
Abnormal flexion to pain 3
Abnormal extension to pain 2
No response 1

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


Initial approach

  • 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.

Pathological Findings

  • 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

Differential Diagnosis

  • 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



Support's development and hosting
  • 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]
  • Agitation:
    • 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.

Additional Treatment

General Measures

  • 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].

Ongoing Care

Follow-Up Recommendations

Patient Monitoring

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].

Patient Education

  • For information and family support groups:
    • Brain Injury Information Network
    • Brain Injury Association of America
  • 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)

Clinical Pearls

  • 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.


About the author

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