Traumatic Brain Injury and Spinal Cord Injury
Traumatic Brain Injury and Spinal Cord Injury
TBI care rests on preventing secondary injury: avoid hypotension (systolic below 90–100 mmHg) and hypoxia (SpO2 below 90%), maintain cerebral perfusion pressure (CPP = MAP − ICP), and treat elevated ICP in a stepwise fashion. Targets: ICP below 22 mmHg, CPP 60–70 mmHg. First-tier measures include head-of-bed elevation, sedation, analgesia, normocapnia, osmotherapy with mannitol or hypertonic saline, and CSF drainage. Hyperventilation to PaCO2 30–35 mmHg is a temporary bridge for impending herniation only, because it causes vasoconstriction and ischemia. Steroids are contraindicated in TBI.
Seizure prophylaxis is typically seven days after severe TBI; it does not prevent late epilepsy. Anticoagulation reversal is urgent. Know the CT patterns: epidural hematoma (lens-shaped, arterial), subdural (crescent, venous), contusion, and diffuse axonal injury. Decompressive craniectomy is considered for refractory ICP.
Spinal cord injury: use the ASIA examination, secure the airway with manual in-line stabilization, and maintain MAP 85–90 mmHg for about seven days in acute cervical injury. Neurogenic shock causes hypotension with bradycardia; spinal shock refers to transient areflexia. Methylprednisolone is not routinely recommended. Watch for respiratory failure, ileus, pressure injury, and autonomic dysreflexia.
Trap: attributing hypotension solely to head injury when concomitant hemorrhage exists, or missing a cervical injury because the patient is intoxicated.
Worked example: MAP 70 mmHg with ICP 25 mmHg gives CPP 45 mmHg-below target; lower ICP and support MAP.