Head Injury Management

Classification by Severity

Primary Survey (ATLS Approach)

1. Airway + C-spine control - Assume cervical spine injury until ruled out. Use in-line manual stabilisation + hard collar. Chin-lift and head-tilt are contraindicated. Rapid sequence intubation (RSI) for all comatose patients (aspiration risk). Blind nasal intubation is relatively contraindicated if skull base fracture is suspected.
2. Breathing - Target PaO2 >11 kPa. Exclude tension pneumothorax (absent breath sounds, hyperresonance, haemodynamic shock, tracheal deviation) - treat with needle decompression then chest tube.
3. Circulation - Target MAP 80-90 mmHg. Haemorrhagic shock is the most common cause of hypotension. Give crystalloid initially; proactive blood product replacement (equal ratios of RBCs : plasma : platelets) for massive haemorrhage. Activate institutional massive transfusion protocol as needed. Exclude hypoglycaemia.
4. Neurological assessment - GCS, pupils (size, equality, reactivity), focal deficits. Document at scene, during transfer, on admission, and serially. A falling GCS signals developing secondary injury - act immediately.

Secondary Survey - Head Examination

• Scalp: inspect and palpate for lacerations (can bleed profusely), subgaleal haematoma, overlying fractures
• Skull base fracture signs: Battle's sign (mastoid bruising), "raccoon/panda eyes" (bilateral periorbital bruising), haemotympanum, CSF rhinorrhoea/otorrhoea
• Cranial nerves: facial or vestibulocochlear nerve injury with skull base fractures; gaze paresis, dysconjugate gaze indicate brainstem involvement
• Signs of raised ICP: Cushing's reflex (hypertension + bradycardia + irregular breathing), vomiting, decorticate/decerebrate posturing
• Signs of uncal herniation: ipsilateral fixed dilated pupil + contralateral motor weakness
• Cerebellar tonsillar herniation: mid-size unreactive or pinpoint pupils + flaccid paralysis

Imaging

• CT head is the first-line investigation for moderate/severe TBI and in mild TBI when risk factors are present (anticoagulants, age >65, focal neuro signs, GCS not fully recovered, vomiting, seizure)
• CT shows: extradural haematoma (lentiform/biconvex hyperdense lesion), subdural haematoma (crescentic), contusions (heterogeneous with blood), diffuse axonal injury (haemorrhagic foci in corpus callosum/dorsolateral brainstem)
• MRI is more sensitive for diffuse axonal injury - used when patient fails to improve neurologically
• CT angiography if arterial dissection suspected (carotid or vertebral)
• All extremities with deformity or restricted range of motion should be radiographed (tertiary survey)
• Cervical spine MRI for ligamentous injury should be obtained within 48 hours (specificity decreases after this)

Types of Intracranial Injury

Extradural Haematoma (EDH)

• Classic: temporal bone fracture + middle meningeal artery tear
• "Talk and die" pattern: transient LOC → lucid interval → rapid deterioration (occurs in ~1/3)
• CT: lentiform (biconvex) hyperdense lesion with midline shift
• Management: urgent craniotomy and evacuation in deteriorating/comatose patients or large bleeds; close observation + serial imaging for smaller stable bleeds
• Prognosis: excellent if evacuated promptly without associated primary brain injury

Acute Subdural Haematoma (ASDH)

• Tearing of bridging veins; common in older/anticoagulated patients
• CT: crescentic hyperdense collection
• Management: craniotomy for acute SDH with mass effect; burr-hole or twist-drill for subacute/chronic SDH

Intracerebral Haemorrhage (ICH)

• Occurs in ~40% of TBI from tearing of small/medium vessels
• Contusional lesions may worsen within 24 hours; reassess with repeat CT
• Most managed conservatively unless mass effect is severe

Traumatic Subarachnoid Haemorrhage

• Most common form of subarachnoid haemorrhage (SAH) overall
• Managed conservatively; not typically associated with vasospasm (unlike aneurysmal SAH)
• Consider CT angiography to exclude a ruptured aneurysm as the precipitating event

Diffuse Axonal Injury (DAI)

• High-energy mechanism; renders patient comatose immediately; associated with poor outcomes
• Strictly a pathological diagnosis (petechial haemorrhages in white matter tracts)
• CT: haemorrhagic foci in corpus callosum/dorsolateral brainstem (MRI more sensitive)

Cerebral Contusions

• Occur at inferior frontal lobes and temporal poles (coup and contre-coup mechanism)
• Rarely require surgery; may warrant delayed evacuation if mass effect develops

Surgical Management

• Early discussion with neurosurgery is mandatory - UK data show higher mortality for severe TBI managed in non-neurosurgical centres
• Indications for urgent surgical evacuation: EDH in deteriorating patient; acute SDH with mass effect; parenchymal haematoma with significant mass effect; open/depressed skull fracture
• Decompressive craniectomy: prophylactic craniectomy in the absence of haematoma is NOT recommended (supported by randomised trial data) - Bailey & Love, p.387; Plum & Posner, p.582

ICP Management - Stepwise Approach

Step 1 - Basic measures

• Head of bed elevated 30°
• Loosen cervical collar to improve venous drainage
• Actively control seizures and fever
• Ensure eunatraemia (target Na+ >140 mmol/L)

Step 2 - Sedation/analgesia/ventilation

• Intubate and ventilate for GCS ≤8 or deteriorating moderate TBI
• Target PaCO2 4.5-5.0 kPa (eucapnia) - hyperventilation is only a temporising measure for acute herniation, not sustained treatment
• Target PaO2 >11 kPa
• Escalating doses of sedatives and analgesics, then muscle relaxants if needed

Step 3 - Osmotherapy

• Mannitol or hypertonic saline (equally effective in TBI with documented elevated ICP)
• Target Na+ >140 mmol/L

Step 4 - ICP monitoring + CSF drainage

• Bolt ICP monitor or external ventricular drain (EVD) - EVD also allows CSF drainage to reduce ICP
• All comatose TBI patients require ICP monitoring (10-20% will develop ICP elevation)

Step 5 - Refractory ICP

• High CPP strategy where autoregulation is preserved (induces vasoconstriction)
• Barbiturate coma, therapeutic hypothermia - limited evidence for long-term benefit
• Decompressive craniectomy as last resort

Adjunctive Medical Management

Anticoagulation Reversal

• Check medications: reverse anticoagulants urgently; consider platelet transfusion for antiplatelet agents, especially pre-operatively

Seizure Prophylaxis

• Early seizures (within 7 days) occur in 2% (mild TBI) to 60% (severe TBI with ICH, depressed fracture, dural tear)
• Phenytoin is the traditional prophylactic agent for high-risk patients

Corticosteroids

• Routine administration is NOT recommended in severe head injury - associated with increased mortality (CRASH trial data)

Pituitary Function

• All aspects of pituitary function may be compromised after TBI
• Screen pituitary hormone levels; liaise with endocrinology

Nutrition

• Commence enteral nutrition within 72 hours of injury (preferred over parenteral)
• Prokinetics (metoclopramide, erythromycin) if gastric motility impaired

Minor / Mild TBI Management

• Most patients do not require CT - use validated decision rules (NICE head injury guidelines, Canadian CT Head Rule, NEXUS II)
• Observe for 4-6 hours; discharge with head injury advice if GCS returns to 15 and no risk factors
• Concussion features: headache, amnesia, confusion, vomiting, somnolence - resolve over days to weeks
• Post-concussive syndrome: persistent headache, memory/cognitive impairment, fatigue beyond 3 months

Special Situations

Head Injury in Children

• Children have proportionally large heads - predisposed to head and neck injury
• Paediatric GCS adapted for pre-verbal children
• Non-accidental injury (NAI) must always be considered: ensure mechanism matches developmental stage, examine for injuries outside normal distribution

Arterial Dissection

• Carotid dissection (extracranial/at skull base) and vertebral artery dissection
• Presents with headache, neck pain, and focal ischaemia
• Associated with skull base fractures; may cause subarachnoid bleeding (vertebral)
• Investigate with CT/MR angiography

Outcomes - Glasgow Outcome Scale (GOS)