Traumatic brain injury

Overview

Head injury is the main killer and disabler of children, teenagers and young adults. Road traffic accidents cause up to half of cases; falls and assaults make up most of the rest.

Brain damage happens in two stages:

• Primary injury: the damage done at the moment of impact (contusion, laceration, axonal shearing). It cannot be undone.
• Secondary injury: further damage over hours and days from hypoxia, hypotension, raised ICP, seizures, fever, hypoglycaemia and expanding haematomas. It is preventable, and this is where treatment works.

Glasgow Coma Scale

• Range 3 to 15. Record the parts (e.g. E3 V3 M5), not just the total.
• Use the best response. If one side flexes and the other localises, the motor score is M5.
• Intubated patients get "T" for verbal. If an item cannot be tested, mark it NT.
• The motor score is the best single predictor of outcome.
• Painful stimuli: trapezius squeeze, supraorbital pressure or nail-bed pressure.

Severity

Initial assessment (ATLS approach)

1. Airway with cervical spine protection: assume a neck injury until cleared (cervical fractures occur in up to 10% of moderate and severe head injuries).
2. Breathing: oxygen; avoid hypoxia.
3. Circulation: treat hypotension. Bleeding inside the head does not cause haemorrhagic shock in an adult; if the patient is shocked, look for chest, abdominal, pelvic or long bone bleeding. Scalp wounds can bleed heavily and need control.
4. Disability: GCS, pupils (size in mm and reaction), gross limb deficit, blood glucose. Do this before giving sedatives or paralysing drugs for intubation.
5. Exposure and secondary survey: scalp, face, ears, nose, spine (log-roll), full neurological exam.

History from paramedics: mechanism and energy, loss of consciousness and its length, amnesia (retrograde and anterograde), seizures, vomiting, anticoagulant or antiplatelet use, whether the patient was moving all limbs before intubation.

Non-accidental injury in children: delayed presentation, injuries of different ages, retinal haemorrhages, chronic subdural collections on both sides, several skull fractures.

Imaging: who needs a CT?

Based on Bailey & Love (UK NICE guidance) and ATLS.

• Non-contrast CT is the investigation of choice. Patients having a head CT after significant injury should have the cervical spine scanned too.
• Repeat CT whenever the clinical state changes, and within 24 hours for contusions, anticoagulated or elderly patients.
• A midline shift of 5 mm or more usually means the clot or contusion needs evacuation.

Discharge after minor/mild injury needs: GCS 15 with no deficit, normal CT if one was indicated, not intoxicated, a responsible adult at home, and written head injury advice (return if headache worsens, repeated vomiting, drowsiness, visual change or limb weakness).

Skull fractures

Focal intracranial lesions

Other lesions

• Traumatic subarachnoid haemorrhage: overall, SAH is most often due to trauma, not aneurysm. Managed conservatively; vasospasm is uncommon. Ask whether an aneurysm bleed caused the fall.
• Contusions: bruised brain at the frontal lobe undersurface and the temporal tips (rough skull base). Coup (under the impact) and contre-coup (opposite side). Can enlarge and coalesce over 24–48 hours, so repeat CT.
• Diffuse axonal injury (DAI): shearing of axons in high-speed acceleration-deceleration. Patient deeply comatose but the CT may look nearly normal; small haemorrhages at the grey-white junction, corpus callosum and dorsolateral brainstem. MRI shows it better; definitive diagnosis is pathological.
• Arterial dissection: carotid or vertebral, often with skull base fractures; causes delayed stroke.

Medical management of moderate and severe TBI

Aim: prevent secondary injury. Early transfer to a neurosurgical centre improves survival.

• Intubate and ventilate severe injuries (GCS ≤ 8) and agitated moderate injuries needing transfer.
• Fluids: normal saline or Ringer's lactate; no hypotonic or glucose-only fluids (they worsen brain swelling).
• Reverse anticoagulation promptly (vitamin K and prothrombin complex concentrate for warfarin; platelets for antiplatelets; protamine for heparin; idarucizumab for dabigatran).
• ICP control: head up, loosen collar, sedation, analgesia, paralysis, mannitol (1 g/kg bolus for signs of herniation in a normovolaemic patient) or hypertonic saline, CSF drainage by EVD. Barbiturate coma, hypothermia and decompressive craniectomy lower ICP but have limited proof of better long-term outcome.
• Seizures: early (within 7 days) or late. Phenytoin prophylaxis reduces early seizures but does not prevent late post-traumatic epilepsy. Adult loading dose about 1 g IV given no faster than 50 mg/minute. Treat active fits with a benzodiazepine.
• Late epilepsy risk is highest with early seizures, intracranial haematoma and depressed skull fracture.
• Nutrition: start enteral feeding within 72 hours.
• Pituitary and sodium problems: SIADH and cerebral salt wasting (hyponatraemia), or diabetes insipidus (hypernatraemia).

Concussion and late effects

• Concussion: a brief, non-focal disturbance of brain function after a closed head injury with a normal CT; confusion and amnesia are key; loss of consciousness is not required.
• Second impact syndrome: a second blow while still symptomatic may cause severe brain swelling; symptomatic players should not return to sport.
• Post-concussion syndrome: prolonged headache, dizziness, poor concentration, insomnia, mood change.
• Glasgow Outcome Scale: 5 good recovery, 4 moderate disability, 3 severe disability, 2 persistent vegetative state, 1 dead.

Brainstem death

• Definition: irreversible loss of cerebral and brainstem function; legally equal to death and allows heart-beating organ donation.
• Preconditions: a known cause of irreversible coma, and reversible causes excluded (drugs, hypothermia, metabolic or endocrine upset).
• Tests (done twice, by two senior doctors in UK practice): absent pupillary, corneal, vestibulo-ocular (caloric), oculocephalic and gag reflexes, no motor response to pain in the cranial nerve territory, and apnoea despite a raised PaCO2 (above 6.7 kPa).

Quick revision

• GCS 15 max, 3 min; severe 3–8; intubate at 8 or less.
• Secondary injury = hypoxia, hypotension, raised ICP: prevent them.
• EDH: middle meningeal artery, temporal fracture, lucid interval, biconvex, urgent craniotomy, good prognosis.
• ASDH: bridging/cortical vessels, crescent, severe primary injury, worse prognosis.
• CSDH: elderly on anticoagulants, hypodense crescent, burr holes.
• Basal fracture: Battle's, raccoon eyes, CSF leak, haemotympanum; no blind NG tube.
• Depressed fracture → elevation; risk of epilepsy and infection.
• DAI: coma with near-normal CT; corpus callosum and brainstem.
• Phenytoin cuts early seizures only; steroids are harmful.

Written by The House Job from standard surgical references (Bailey & Love; ATLS Student Course Manual).

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