Post-Acute Management of Traumatic Brain Injury

Scope and geriatric context. The post-acute phase begins once the patient is medically and neurosurgically stable, and covers rehabilitation, prevention of secondary complications, and management of long-term sequelae. In older adults, TBI is usually caused by falls, is frequently complicated by antiplatelet or anticoagulant use, and carries higher mortality and worse functional outcome for any given injury severity.

Structured multidisciplinary rehabilitation. Refer early to a team comprising a rehabilitation physician, physiotherapist, occupational therapist, speech and language therapist, neuropsychologist, dietitian and social worker. Set goal-directed, individualised targets and measure progress with GOS-E, FIM or Barthel Index and formal cognitive testing. Early, intensive, specialist inpatient rehabilitation produces better functional outcomes than generic ward care.

Cognitive rehabilitation. Measure the duration of post-traumatic amnesia (a key prognostic marker) with the GOAT or Westmead scale. Deficits in attention, memory, processing speed and executive function are managed with compensatory strategies, memory aids and diaries, environmental structuring and errorless learning. Formal screening is essential in older adults, in whom these deficits are easily mislabelled as dementia.

Neurobehavioural and psychiatric sequelae. Agitation and aggression, apathy, disinhibition, emotional lability, depression (up to 50%), anxiety, post-traumatic stress, disturbed sleep–wake cycle and fatigue. Manage behaviour non-pharmacologically first — routine, environmental modification, identifying triggers. Use SSRIs for depression; avoid typical antipsychotics and benzodiazepines, which impair motor and cognitive recovery. Methylphenidate or amantadine may improve arousal and attention in selected patients.

Medical complications to anticipate. Post-traumatic seizures — prophylaxis only for the first 7 days; longer-term antiseizure medication (preferably levetiracetam) only if seizures actually occur. Post-traumatic hydrocephalus — suspect when recovery plateaus or reverses; image and consider shunting. Also spasticity and contractures, heterotopic ossification, dysphagia and aspiration, malnutrition, bladder and bowel dysfunction, pressure ulcers, venous thromboembolism, chronic pain and post-traumatic headache, post-traumatic hypopituitarism (growth hormone, thyroid, cortisol and gonadal deficiency — commonly missed), and chronic subdural haematoma appearing weeks later.

Long-term, social and geriatric issues. Assess mental capacity and undertake advance care planning; give explicit driving cessation and return-to-activity advice; train and support caregivers and arrange respite. Prevent the next injury — falls prevention: home hazard assessment, vision and hearing, footwear, gait aids, medication review, bone health — and decide with the cardiology team on reintroducing antithrombotics. Counsel that TBI raises the long-term risk of dementia, epilepsy and Parkinson’s disease, and arrange disability certification and welfare access under NPHCE and the Rights of Persons with Disabilities Act 2016.

Contemporary guidance and evidence syntheses (2023–2025) add three practice points. (i) Blood biomarkers GFAP and UCH-L1 (available as an FDA-cleared point-of-care assay) assist triage and prognostication after TBI and reduce unnecessary CT scanning — useful in frail patients in whom repeated imaging is undesirable. (ii) Systematic screening for post-traumatic hypopituitarism at 3–6 and 12 months is recommended, since untreated hypopituitarism mimics and worsens post-concussive fatigue, apathy and cognitive slowing. (iii) Age alone must not be used to withhold or limit rehabilitation — outcome data consistently show that older TBI survivors achieve meaningful functional gains when given adequate rehabilitation intensity.