Management of Delirium in Post-Traumatic Brain Injury
Begin by identifying and correcting reversible causes of delirium—including drug-induced delirium, inadequate pain control, metabolic disturbances, hypoxia, and sepsis—before initiating pharmacological treatment, as up to 50% of delirium cases are reversible. 1
Initial Assessment and Screening
- Use validated delirium screening tools specifically the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) or Intensive Care Delirium Screening Checklist (ICDSC) to systematically evaluate for delirium 1
- Delirium occurs in approximately 46-90% of TBI patients, making it nearly universal in this population 2, 3
- Assess Glasgow Coma Scale (particularly the verbal component score), as lower GCS scores at emergency department presentation predict higher delirium risk 2
- Perform frequent neurological examinations to distinguish delirium from secondary neurological deterioration requiring repeat imaging 1
Identify and Correct Reversible Causes
Before any pharmacological intervention, systematically address the following reversible factors: 1
- Medications: Discontinue or reduce benzodiazepines, anticholinergics, corticosteroids, and other psychoactive drugs that may precipitate delirium 1
- Pain control: Optimize analgesia, as poorly controlled pain is a major contributor to delirium 1
- Metabolic disturbances: Correct electrolyte imbalances, dehydration, hypo/hyperglycemia 1
- Hypoxia and hypotension: Maintain adequate oxygenation and cerebral perfusion pressure (CPP ≥60 mmHg when ICP monitoring available) 4
- Sepsis and infection: Identify and treat any infectious sources 1
Pharmacological Management
When non-pharmacological measures fail and delirium persists, use intravenous haloperidol or droperidol as first-line agents for both hyperactive (RASS +1 to +4) and hypoactive (RASS 0 to -3) delirium. 1
Haloperidol Dosing
- Initial dose: 0.5-2 mg IV slow bolus 1
- Haloperidol is the drug of choice for pharmacological treatment of post-traumatic delirium 1
- Important caveats: Monitor for extrapyramidal side effects and QT prolongation 1
- Some evidence suggests typical neuroleptics like loxapine may be more effective than atypical agents (olanzapine) in TBI-induced delirium 5
Alternative Considerations
- Dexmedetomidine and remifentanil are associated with decreased delirium risk in general ICU patients, though specific evidence in TBI populations is limited 6
- Avoid benzodiazepines as they are implicated in drug-induced delirium 1
Non-Pharmacological Interventions
Implement multi-component care bundles targeting modifiable risk factors: 7
- Analgesia-prioritized sedation: Use sedation algorithms that prioritize pain control over deep sedation 7
- Spontaneous awakening and breathing trials: Conduct regular trials when clinically appropriate 7
- Early mobilization: Initiate as soon as safely possible given TBI precautions 7, 3
- Sleep cycle optimization: Minimize nighttime disruptions and promote normal circadian rhythms 3
- Family engagement: Encourage family presence and familiar stimuli 7
Monitoring and Follow-up
- Delirium symptoms in TBI patients typically include prominent cognitive deficits (orientation, attention, long-term memory, visuospatial ability) in the first 4 days 2
- Motor agitation and lability of affect are common non-cognitive symptoms that often resolve rapidly 2
- Most delirium symptoms improve within the first week, but persistent delirium beyond this period warrants reassessment for ongoing secondary brain injury 2
- Critical pitfall: Do not attribute all behavioral changes solely to the TBI itself—delirium is a distinct organ dysfunction syndrome requiring active management 6
Special Considerations in TBI Populations
- TBI patients have unique pathophysiology including primary injury to arousal/attention structures, progressive inflammatory destruction, and neurotransmitter dysregulation 7
- Post-traumatic delirium is independently associated with prolonged hospitalization, increased mortality, and worse long-term cognitive outcomes 7
- Up to two-thirds of TBI survivors develop agitation and delirium, which contributes to long-term cognitive impairment 6
- Despite high prevalence, post-traumatic delirium often goes unrecognized and undertreated 6