13.5 Head Injury & Traumatic Brain Injury: Preventing Secondary Brain Injury

13.5 Head Injury & Traumatic Brain Injury: Preventing Secondary Brain Injury

Traumatic brain injury (TBI) is the leading cause of trauma death and lifelong disability in Canada, and it is the injury where prehospital care changes outcome most reliably. The reason is simple and worth stating at the outset: you cannot undo the primary injury, but almost everything that determines the final outcome is secondary injury you can prevent.

Primary Versus Secondary Brain Injury

The Physiology You Must Be Able to Reason With

Three relationships drive every management decision in TBI.

1. The Monro-Kellie doctrine. The adult cranium is a rigid box containing brain, blood, and cerebrospinal fluid in a fixed total volume. Adding a haematoma or oedema forces compensatory displacement of CSF and venous blood. Compensation is remarkably effective — and then it is suddenly exhausted, at which point intracranial pressure (ICP) rises steeply for a small further volume increase. This is why a patient can appear stable and deteriorate precipitously.

2. Cerebral perfusion pressure.

CPP = MAP - ICP

Cerebral perfusion pressure is what actually delivers oxygen to brain tissue. Because ICP is rising and you cannot lower it much in the field, mean arterial pressure is the variable you protect. A single episode of hypotension roughly doubles mortality in severe TBI; hypotension combined with hypoxia is worse again.

3. Carbon dioxide controls cerebral vessel calibre. Cerebral arterioles dilate with hypercapnia and constrict with hypocapnia.

• Hypercapnia (under-ventilation) → vasodilation → increased cerebral blood volume → increased ICP.
• Aggressive hyperventilation → vasoconstriction → cerebral ischaemia in tissue that is already injured.

Hyperventilation is therefore not a treatment for raised ICP; it is a brief, last-resort temporizing manoeuvre for active herniation only, and it causes harm when used prophylactically.

Recognition: The Anatomy of the Bleeds

Clinical Signs of Rising ICP and Herniation

Cushing's triad is a late sign of brainstem compression:

1. Hypertension with a widening pulse pressure
2. Bradycardia
3. Irregular respirations (Cheyne-Stokes, cluster, or ataxic breathing)

[!CAUTION] Cushing's triad is not an early warning — it means herniation is under way. The early signs are far subtler: a falling GCS, particularly a drop of 2 or more points; new agitation or combativeness; repeated vomiting; a worsening headache; and a unilateral dilated, sluggish or non-reactive pupil from uncal compression of the oculomotor nerve.

Other findings that should change your index of suspicion:

• Basal skull fracture: periorbital ecchymosis ("raccoon eyes"), retroauricular ecchymosis (Battle's sign), cerebrospinal fluid rhinorrhoea or otorrhoea, haemotympanum. Do not pack the ears or nose; do not insert a nasopharyngeal airway or nasogastric tube.
• Posturing: decorticate (flexion, GCS motor 3) is less ominous than decerebrate (extension, GCS motor 2); progression from flexion to extension signals deterioration.
• Seizure after head injury, which both raises ICP and worsens hypoxia.

Prehospital Management: The Secondary-Injury Bundle

Management is a short, evidence-driven checklist. Every item exists to protect CPP and oxygen delivery.

1. Oxygenation. Avoid any hypoxia. Target normal saturations — commonly 94% to 98% — and treat SpO2 below 90% as an emergency. Both hypoxia and sustained hyperoxia are harmful.
2. Ventilation to normocapnia. Use waveform capnography and target a normal EtCO2, commonly 35 to 40 mmHg. Ventilate at a normal rate; the reflex to "bag fast" is the most common iatrogenic injury in TBI.
3. Blood pressure. Treat hypotension aggressively within your scope — control haemorrhage, position appropriately, and give fluid where authorized. A single hypotensive episode is a major independent predictor of death.
4. Spinal motion restriction where indicated by the Canadian C-Spine Rule (Section 13.2) — but never at the cost of airway control.
5. Head-up positioning to approximately 30 degrees where the spine is cleared or the stretcher can be tilted as a unit, with the head midline, to promote venous drainage. Avoid tight cervical collars and anything that occludes jugular outflow.
6. Glucose. Check it in every altered patient. Hypoglycaemia mimics TBI and independently injures the brain; treat it.
7. Temperature. Prevent hyperthermia, which sharply increases cerebral metabolic demand. Prevent shivering.
8. Seizure management per local directive, with attention to the airway and ventilation during and after.
9. Analgesia and sedation where authorized — pain and agitation raise ICP — balanced against the need to monitor level of consciousness.
10. Transport decision. A patient with a significant TBI belongs at a centre with computed tomography and neurosurgical capability. Recognizing that early, and saying so, changes outcomes more than anything else in this list.

The Anticoagulated and the Older Patient

The combination the blueprint weights heavily — geriatric patients are 37 to 47 examination items — and the combination that kills quietly:

• Ground-level falls in older adults produce the majority of serious TBI in Canada.
• Anticoagulants and antiplatelets (warfarin, apixaban, rivaroxaban, dabigatran, clopidogrel, ASA) convert a minor bump into a large intracranial bleed, often with a delayed presentation.
• Cerebral atrophy means a substantial subdural haematoma can accumulate before any clinical change, and the "baseline" you are told about may already be abnormal.
• Treat the medication list as a mechanism modifier. A GCS of 15 in an anticoagulated 84-year-old who struck their head is not reassuring, and that patient needs assessment and imaging regardless of how well they look.

Paediatric Considerations

• Children have proportionally larger heads, thinner cranial bones, and weaker neck musculature, so head injury is common and the cervical spine is at risk.
• Infants can lose clinically significant blood volume into the cranial vault through open fontanelles and expandable sutures — a bulging fontanelle is an important sign, and hypovolaemic shock from an intracranial bleed is possible in infants though not in older children and adults.
• Vomiting after head injury is more common and less specific in children, but persistent vomiting still warrants assessment.
• Consider non-accidental injury when the history does not match the injury, when the history changes, or when presentation is delayed, and follow the mandatory reporting duty in your province.