20.1 Traumatic Brain Injury Management & Paroxysmal Sympathetic Hyperactivity

Primary and Secondary Injury

Primary injury happens at impact: contusion, axonal shearing (diffuse axonal injury), epidural and subdural hematoma, traumatic subarachnoid hemorrhage, and skull fracture. Nothing in the ICU reverses it.

Secondary injury develops over hours to days and is what critical care prevents:

• Hypotension and hypoxemia: a single episode of systolic pressure below 90 mmHg roughly doubles mortality, and hypoxemia compounds it. These are the two prehospital variables most strongly linked to death.
• Intracranial hypertension and reduced cerebral perfusion pressure.
• Fever, seizures, hyperglycemia and hypoglycemia, hyponatremia, and anemia.
• Excitotoxicity, mitochondrial failure, and inflammation.

Early Management

CRASH-3 randomized more than 12,000 patients with traumatic brain injury to tranexamic acid or placebo. Treatment within 3 hours reduced head injury-related death in mild-to-moderate injury (GCS 9 to 15) without an excess of vascular occlusive events; benefit was not seen in patients with a GCS of 3 or bilateral unreactive pupils. Note the contrast with CRASH-2, where tranexamic acid reduced death from bleeding in general trauma within 3 hours.

Surgical indications include an epidural hematoma larger than 30 mL regardless of GCS, an acute subdural hematoma with a thickness above 10 mm or midline shift above 5 mm, a contusion with mass effect and deterioration, posterior fossa lesions with compression, and depressed open skull fractures. Decompressive craniectomy decisions follow the DECRA and RESCUEicp evidence discussed in the intracranial hypertension section.

Monitoring: place an intracranial pressure monitor for severe injury (GCS 3 to 8) with an abnormal CT, or a normal CT with two of age over 40, motor posturing, or systolic pressure below 90 mmHg. An external ventricular drain also allows CSF drainage. Multimodality options include brain tissue oxygen tension (the BOOST-3 trial compared management strategies), jugular venous oximetry, and continuous EEG.

Specific Problems After Head Injury

• Cerebral contusion blossoming: lesions expand over 24 to 72 hours, so repeat imaging and deterioration thresholds matter.
• Traumatic subarachnoid hemorrhage: vasospasm occurs but is less common than after aneurysmal bleeding.
• Post-traumatic hydrocephalus: consider it with failure to improve or late deterioration.
• Pituitary dysfunction: diabetes insipidus and anterior pituitary failure occur acutely and chronically; screen for cortisol deficiency in refractory hypotension.
• Neurogenic pulmonary edema and cardiac stunning from the catecholamine surge.
• Coagulopathy: tissue factor release can cause disseminated intravascular coagulation; follow fibrinogen and platelets.
• Hyponatremia: distinguish SIADH (euvolemic, concentrated urine, treated with fluid restriction) from cerebral salt wasting (hypovolemic, high urine sodium with volume depletion, treated with salt and volume). Treating one as the other worsens the patient.

Blunt Cerebrovascular Injury

• Mechanism: carotid or vertebral artery dissection from hyperextension and rotation, direct blow, or fracture through the foramen transversarium or carotid canal.
• Screen with CT angiography (expanded Denver criteria): cervical spine fracture (especially C1 to C3, subluxation, or transverse foramen involvement), basilar skull fracture involving the carotid canal, Le Fort II or III fracture, a seat-belt sign or neck hematoma, severe traumatic brain injury (GCS below 6), near-hanging with anoxia, or an unexplained focal neurologic deficit.
• Grading (Biffl) runs from intimal irregularity (grade I) to occlusion (grade IV) and transection (grade V).
• Treatment: antithrombotic therapy (aspirin or systemic heparin) reduces stroke in grades I to III; endovascular treatment is used for pseudoaneurysms and selected high-grade lesions. Weigh bleeding risk from other injuries, and repeat imaging in 7 to 10 days for low-grade lesions.

Paroxysmal Sympathetic Hyperactivity (PSH)

• Setting: usually 1 to 2 weeks after severe traumatic brain injury (also after hypoxic injury, stroke, and hemorrhage), in patients with diffuse axonal injury.
• Presentation: paroxysms lasting minutes to hours, often several times a day, with hypertension, tachycardia, tachypnea, hyperthermia, profuse sweating, and dystonic posturing or rigidity. Episodes are triggered by pain, suctioning, turning, bladder distension, or constipation.
• Diagnosis uses the PSH Assessment Measure, which combines a clinical feature scale with a diagnostic likelihood score. It is a diagnosis of exclusion: rule out sepsis, pulmonary embolism, seizures, withdrawal syndromes, pain, serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia, thyroid storm, and raised intracranial pressure.
• Consequences: high energy expenditure with weight loss, muscle contractures and heterotopic ossification, secondary brain injury from hyperthermia, and prolonged ICU stay.
• Treatment:
  • Reduce triggers: analgesia, bowel and bladder care, cluster care, and a quiet environment.
  • Propranolol: a nonselective beta-blocker with central penetration, which also reduces energy expenditure.
  • Gabapentin: targets the paroxysmal allodynic component and is often the most effective long-term agent.
  • Clonidine or dexmedetomidine: central alpha-2 agonists for sympathetic outflow.
  • Opioids, particularly morphine, abort acute episodes.
  • Bromocriptine for hyperthermia and dystonia, baclofen or intrathecal baclofen and benzodiazepines for severe posturing.
  • Avoid chasing each episode with antibiotics and cultures once the pattern is established, and avoid antipyretics alone, which do not control the syndrome.