Head Injury

Injury to the brain or skull from external mechanical force, ranging from mild concussion to severe TBI with structural brain damage.

Primary injury (at the moment of impact; irreversible) is distinguished from secondary injury (subsequent hypoxia, hypotension, raised ICP, seizures; potentially preventable and treatable, and the focus of emergency management).

Classified by GCS at presentation (best post-resuscitation score):

• Mild: GCS 13-15

• Moderate: GCS 9-12

• Severe: GCS ≤8 ; requires airway protection/intubation

Pathology types: extradural hematoma (arterial, typically middle meningeal artery, biconvex on CT), subdural hematoma (venous, bridging veins, crescentic on CT), traumatic subarachnoid hemorrhage, intracerebral hemorrhage/contusion, diffuse axonal injury (shearing forces, often normal initial CT despite a severe clinical picture), skull fracture (linear, depressed, basal).

• GCS assessment (Eye 1-4, Verbal 1-5, Motor 1-6) ; serial monitoring is more important than a single value

• Extradural hematoma classic pattern: initial loss of consciousness → "lucid interval" → rapid deterioration as the hematoma expands; do not be falsely reassured by a lucid interval

• Signs of raised ICP: headache, vomiting, deteriorating GCS, Cushing's triad (hypertension, bradycardia, irregular breathing ; a late, pre-terminal sign), unilateral then bilateral pupil dilation (uncal herniation)

• Basal skull fracture signs: Battle's sign (mastoid bruising, delayed), raccoon eyes (periorbital bruising), CSF rhinorrhea/otorrhea, hemotympanum

• Focal neurological deficit: localizes the lesion

• Seizures: early (within 24h, common, doesn't necessarily predict epilepsy) vs. late (>7 days, higher epilepsy risk)

Red flags requiring urgent CT: GCS <15 at 2 hours post-injury, suspected open/depressed skull fracture, signs of basal skull fracture, post-traumatic seizure, focal neurological deficit, more than one episode of vomiting, age ≥65, dangerous mechanism, retrograde amnesia >30 min, anticoagulant use, GCS <13 at initial assessment.

• CT head (non-contrast) : investigation of choice: identifies hemorrhage, mass effect, midline shift, skull fracture; do not delay for mild-moderate injury meeting the criteria above

• C-spine imaging: high association with head injury (assess per NEXUS/Canadian C-spine rules), CT C-spine if high-risk mechanism/symptoms

• GCS and pupillary response: serial reassessment is the primary monitoring tool, not a single CT

• Bloods: FBC, coagulation profile (critical if on anticoagulants/antiplatelets : reverse urgently if intracranial bleed present), glucose (exclude hypoglycemia as cause of reduced GCS), alcohol level if relevant : do not attribute reduced GCS to intoxication without excluding structural injury

• MRI: superior for diffuse axonal injury, not first-line acutely

Differentials for altered consciousness post-trauma: hypoglycemia, alcohol/drug intoxication, post-ictal state, hypoxia, hypotension/shock, pre-existing intracranial pathology.

Primary survey first : hypoxia and hypotension are the two most important preventable secondary insults; treat these before focusing on the head injury itself.

• Airway protection: intubate if GCS ≤8, maintain C-spine precautions

• Maintain cerebral perfusion: target SBP ≥110-120mmHg (a single hypotensive episode significantly worsens outcome), normocapnia, normothermia, normoglycemia

Signs of raised ICP/herniation (unilateral dilated pupil, deteriorating GCS, Cushing's triad):

• Head elevation 30 degrees, midline neck position (avoid venous obstruction)

• Hyperosmolar therapy: mannitol 0.5-1g/kg IV bolus, or hypertonic saline (3%) 150-250mL bolus : temporizing while arranging definitive management

• Brief hyperventilation (target PaCO2 ~30-35mmHg) as a temporizing bridge to surgery only, not sustained therapy

• Urgent neurosurgical referral for evacuation (extradural/subdural with mass effect, depressed skull fracture)

Other measures:

• Seizure management: benzodiazepine for active seizure; consider prophylactic levetiracetam in severe TBI (reduces early post-traumatic seizures, no proven effect on late epilepsy)

• Reverse anticoagulation urgently if intracranial hemorrhage (vitamin K + prothrombin complex concentrate for warfarin, specific reversal agents for DOACs where available)

• Mild TBI/concussion: observation period, safety-netting advice (return if worsening headache, vomiting, drowsiness, confusion), avoid return to contact sport until symptom-free with graduated return-to-play

• ICU admission for severe TBI (GCS ≤8) : ICP monitoring, ventilation, neuroprotective management (target ICP <20-22mmHg, cerebral perfusion pressure 60-70mmHg)

Disposition: discharge with head injury advice if low-risk, normal CT, and responsible adult supervision available; admit for observation if risk factors present even with a normal CT; neurosurgical transfer for any surgical lesion or GCS ≤8.