What are the management options for Traumatic Brain Injury (TBI)?

Management of Traumatic Brain Injury

Severe TBI patients must be immediately transferred to a specialized neurosurgical center by a medicalized prehospital team, as this approach significantly reduces mortality and improves neurological outcomes compared to management at non-specialized facilities. 1

Initial Assessment and Severity Evaluation

Assess TBI severity using the Glasgow Coma Scale (GCS), specifically focusing on the motor response component, along with pupillary size and reactivity. 1

• Age, initial GCS score, and pupillary examination are the key predictors of neurological outcome at 6 months 1
• Severe TBI is defined as GCS < 9, moderate TBI as GCS 9-14, and mild TBI as GCS 13-15 2
• Repeated neurological examinations should be performed frequently (every 15-30 minutes initially in moderate TBI) to detect secondary deterioration 3
• Any decrease of at least 2 points in GCS or new neurological deficit mandates immediate repeat CT imaging 3, 4

Transcranial Doppler (TCD) should be incorporated into the initial trauma assessment (FAST protocol) to evaluate cerebral perfusion. 1

• Concerning TCD findings include: diastolic blood flow velocity (Vd) < 20 cm/s with pulsatility index (PI) > 1.4 in severe TBI 1
• In moderate/mild TBI, Vd < 25 cm/s or PI > 1.25 predicts secondary neurological deterioration 1
• These thresholds should trigger immediate therapeutic measures to improve brain perfusion 1

Biomarkers should NOT be used in routine clinical practice for initial severity assessment. 1

Prehospital and Emergency Management

Transfer severe TBI patients immediately to specialized centers with neurosurgical facilities and neuro-intensive care capabilities. 1

• Mortality rates are significantly lower in neurosurgical centers even for patients not requiring surgical intervention 1
• This benefit stems from accumulated expertise and immediate neurosurgical availability 1

Prevent secondary brain injury by avoiding hypotension and hypoxia. 1, 5

• Maintain systolic blood pressure > 110 mmHg to ensure adequate cerebral perfusion 3, 4
• Ensure adequate oxygenation with PaO2 between 60-100 mmHg 3
• Control ventilation through tracheal intubation and mechanical ventilation with end-tidal CO2 monitoring 4
• Target EtCO2 between 30-35 mmHg prior to obtaining arterial blood gas samples 1

Imaging Strategy

Perform brain and cervical CT scan without delay in all severe TBI patients. 1

• Use inframillimetric sections reconstructed with thickness > 1 mm, visualized with double fenestration (CNS and bone windows) 1, 4
• CT scan is the first-line diagnostic tool for primary brain lesions due to availability and speed 1
• Initial CT guides neurosurgical procedures and monitoring techniques 1

Consider early CT-angiography of supra-aortic and intracranial arteries in patients with specific risk factors. 1, 4

• Risk factors include: cervical spine fracture, focal neurological deficit unexplained by brain imaging, and basal skull fractures 4

Neurosurgical Interventions

Immediate surgical intervention is indicated for: 4

• Symptomatic extradural hematoma (regardless of location)
• Acute subdural hematoma with thickness > 5 mm and midline shift > 5 mm
• Acute hydrocephalus requiring drainage
• Open displaced skull fracture requiring closure
• Closed displaced skull fracture with brain compression

Consider decompressive craniectomy for refractory intracranial hypertension. 3, 6

Intracranial Pressure Management

ICP monitoring is indicated in severe TBI patients (GCS < 9) with abnormal CT findings. 3, 4

First-Tier Interventions:

• Elevate head of bed 20-30 degrees 3, 4
• Maintain adequate cerebral perfusion pressure ≥ 60 mmHg 3
• Provide appropriate sedation and analgesia 1
• Restrict free water and avoid excess glucose 4
• Minimize hypoxemia and hypercarbia 4
• Treat hyperthermia aggressively 4

Second-Tier Interventions for Elevated ICP:

Use osmotic diuretics (mannitol) for ICP reduction. 4, 7

• Mannitol dosing: 0.25-0.5 g/kg IV (adults), administered as 15-25% solution over 30-60 minutes 7
• Pediatric dosing: 1-2 g/kg body weight or 30-60 g/m² body surface area over 30-60 minutes 7
• Small or debilitated patients: 500 mg/kg 7

Consider external ventricular drainage for persistent intracranial hypertension despite sedation and correction of secondary brain insults. 4

For acute ICP crises, temporary hyperventilation (PaCO2 30-35 mmHg) may be used cautiously. 3

• After stabilization in patients with chest trauma, maintain PaCO2 between 35-40 mmHg to prevent excessive cerebral vasoconstriction 4

In refractory cases, consider barbiturate coma or decompressive craniectomy. 2

Monitoring for Complications

Monitor for signs of increased ICP: 4

• Pupillary abnormalities
• Hypertension with bradycardia (Cushing's triad)
• Deteriorating neurological examination

Advanced neuromonitoring modalities show promise: 2, 5

• Brain tissue oxygen (PbtO2) monitoring provides strategies to optimize cerebral blood flow 2
• Multimodality monitoring has become more widely available for detecting pathophysiological derangements 8

Critical Pitfalls to Avoid

Do NOT use corticosteroids for ICP control in TBI patients. 3, 4

• Corticosteroids have failed to demonstrate beneficial effects on mortality or neurological outcomes 4

Avoid concomitant administration of nephrotoxic drugs or other diuretics with mannitol. 7

• Risk factors for renal complications include pre-existing renal disease and conditions predisposing to renal failure 7

Do NOT perform daily interruption of sedation in TBI patients with signs of high ICP. 3

Avoid hypo-osmolar fluids that may worsen cerebral edema. 3

Do NOT delay imaging or neurosurgical consultation in patients with history of lucid interval. 3, 4

• Deterioration after lucid interval most commonly occurs within 24 hours (71% of cases) 4
• Mass lesions are found in 81% of patients who deteriorate after lucid interval 4

Mannitol may increase cerebral blood flow and risk of postoperative bleeding in neurosurgical patients. 7

• It may worsen intracranial hypertension in children who develop generalized cerebral hyperemia during the first 24-48 hours post-injury 7

Additional Management Considerations

Optimize acute care by addressing: 2, 5

• Recognition and treatment of paroxysmal sympathetic hyperactivity (PSH) 2, 5
• Early seizure prophylaxis 2
• Venous thromboembolism (VTE) prophylaxis 2
• Nutrition optimization 2

Discontinue mannitol if renal, cardiac, or pulmonary status worsens, or CNS toxicity develops. 7

Apply palliative care principles early, as severe TBI remains a devastating injury with challenging long-term outcomes. 2