Head injury (GCS, types of haematoma, management)

Overview

Traumatic brain injury (TBI) is a leading cause of death and disability in young adults. Road traffic accidents (especially motorbikes) and falls are the main causes in Pakistan, and alcohol is a common factor in many countries.

Brain damage happens in two stages:

• Primary injury: at the moment of impact (contusion, axonal shearing, laceration). It cannot be undone.
• Secondary injury: develops over the next minutes to days from hypoxia, hypotension, raised intracranial pressure (ICP), expanding haematoma, seizures, fever and low sodium. This is what treatment aims to prevent.

Glasgow Coma Scale (GCS)

• Total 3 to 15. Record the parts as well as the total (for example E2 V2 M4).
• If a part cannot be tested (eyes swollen shut, intubated), it is marked non-testable rather than scored.
• The motor score is the best single predictor of outcome. If the two sides differ, use the better side for scoring.

Grading the severity

The length of post-traumatic amnesia (PTA) is also used: PTA beyond 24 hours marks a severe injury, and PTA over a week makes lasting cognitive problems very likely.

Types of injury

Skull fractures

• Linear vault fracture: shows that the blow was strong. It does not itself damage the brain, but in a conscious patient it makes an intracranial haematoma far more likely.
• Depressed fracture: fragment pushed inwards; high risk of post-traumatic epilepsy; usually needs surgical elevation, especially if open.
• Basal (base of skull) fracture: often missed on plain films; needs CT with bone windows. Signs:
  • Raccoon (panda) eyes: bruising around both eyes (anterior fossa).
  • Battle's sign: bruising behind the ear over the mastoid (middle fossa).
  • CSF rhinorrhoea or otorrhoea; haemotympanum.
  • VIIth and VIIIth nerve damage (facial weakness, deafness); loss of smell with cribriform plate fractures.
• Complications: meningitis through a CSF leak, carotid injury, and cranial nerve palsies.

Diffuse brain injuries

• Concussion: brief, non-focal loss of function (often brief loss of consciousness) with a normal CT.
• Diffuse axonal injury (DAI): shearing of axons from rapid acceleration–deceleration and rotation; many small bleeds at the grey–white junction; the patient is deeply comatose, often out of proportion to a near-normal first CT. Poor outcome.
• Hypoxic–ischaemic injury from shock or apnoea; diffuse swelling with loss of grey–white differentiation.

Focal injuries

• Contusions: bruises, mostly in the frontal and temporal lobes, sometimes on the side opposite the blow (contrecoup). They can grow into an intracerebral haematoma, so a repeat CT is often done.
• Extradural, subdural and subarachnoid bleeding, compared below.

Extradural versus subdural haematoma

Traumatic subarachnoid haemorrhage is the commonest form of SAH overall and is managed conservatively.

Raised intracranial pressure and herniation

• Monro–Kellie doctrine: the skull is a rigid box of brain, blood and CSF. A new mass is first compensated by pushing out CSF and venous blood. When this reserve is used up, ICP rises steeply with small further increases in volume.
• Normal resting ICP is about 10 mmHg; sustained pressure above about 22 mmHg carries a poor outcome.
• Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − ICP. Aim to keep CPP at 60 mmHg or more.

Uncal (transtentorial) herniation

The medial temporal lobe (uncus) is pushed through the tentorial opening:

• Compresses the oculomotor (III) nerve: the parasympathetic pupil fibres on its surface fail first, so the pupil on the side of the clot dilates ("blown pupil") and stops reacting.
• Compresses the cerebral peduncle: contralateral hemiparesis.
• Compresses the reticular formation: falling GCS.

Tonsillar herniation (coning)

Cerebellar tonsils pushed through the foramen magnum compress the medulla, producing the Cushing triad: rising blood pressure (widened pulse pressure), falling pulse (bradycardia) and irregular breathing, followed by respiratory arrest. It is a late, pre-terminal sign.

Management

Primary survey (ABCDE)

• Airway with cervical spine protection: assume a neck injury in every significant head injury. Intubate if GCS is 8 or less, the airway is at risk, or ventilation is inadequate.
• Breathing: avoid hypoxia; aim for normal oxygen and normal PaCO2 (about 35–45 mmHg).
• Circulation: avoid hypotension; in severe brain injury, low blood pressure on arrival more than doubles mortality. Look for bleeding elsewhere, because an isolated head injury rarely causes shock in adults. ATLS advises keeping systolic BP at 100 mmHg or more at age 50–69 and 110 mmHg or more at age 15–49 or over 70.
• Disability: GCS, pupils (size and reaction), lateralising signs; check blood glucose.
• Use normal saline or Ringer's lactate; avoid hypotonic and glucose-containing fluids, and prevent low sodium.

CT scanning in mild head injury (GCS 13–15)

A patient with loss of consciousness, amnesia or disorientation needs a CT if any of the following is present:

All moderate and severe injuries get a CT. On CT, look for blood, contusions, midline shift (5 mm or more often needs surgery) and effacement of the basal cisterns.

Lowering a raised ICP

• Head up about 30 degrees, neck straight, avoid tight tube ties (helps venous drainage).
• Mannitol 20%: give a rapid 1 g/kg bolus for acute deterioration (new dilated pupil, hemiparesis, falling GCS) in a patient with normal blood volume, then go straight to CT or theatre. It is an osmotic diuretic, so do not give it to a hypotensive patient.
• Hypertonic saline (3% or stronger): equally effective, and preferred when the patient is hypotensive because it does not cause diuresis.
• Brief hyperventilation (PaCO2 about 25–30 mmHg) lowers ICP by cerebral vasoconstriction. Use it only briefly for impending herniation; prolonged or prophylactic use causes cerebral ischaemia.
• Barbiturates for ICP that does not respond to other measures, only if the patient is haemodynamically stable.
• Surgery: evacuate the haematoma; decompressive craniectomy in selected cases.
• ICP monitoring in severe TBI.

Other measures

• Reverse anticoagulants quickly (vitamin K, prothrombin complex concentrate or FFP for warfarin; protamine for heparin; idarucizumab for dabigatran; platelets for antiplatelet drugs).
• Seizures: treat them. Phenytoin or fosphenytoin is used in the acute phase. Early anticonvulsants reduce early seizures but do not prevent late post-traumatic epilepsy.
• Corticosteroids are not used for head injury.
• Treat fever, keep glucose and sodium normal, and give DVT prophylaxis once bleeding is controlled.

Mild head injury: discharge

If the patient is fully alert with a normal examination (and CT where needed), they can go home with a responsible adult for the next 24 hours and a head injury advice sheet: return at once for worsening headache, repeated vomiting, drowsiness, confusion, weakness or seizures. About 3% of mild injuries deteriorate unexpectedly.

Complications and late effects

• Post-traumatic epilepsy: risk is highest with early seizures (first week), an intracranial haematoma, and a depressed skull fracture.
• Post-concussion syndrome: headache, dizziness, poor concentration, fatigue, irritability and depression, even after minor injury.
• Chronic subdural haematoma and hydrocephalus (communicating) later on.
• CSF leak and meningitis after basal fracture.
• Diabetes insipidus and hypopituitarism after fractures through the sella or stalk injury.
• Cognitive and behavioural change: frontal lobe contusions cause disinhibition and poor judgement.
• Chronic traumatic encephalopathy ("punch-drunk" syndrome) after repeated blows, as in boxers.
• Benign paroxysmal positional vertigo.

Quick revision

• GCS = E4 + V5 + M6; minimum 3; 8 or less = coma, intubate.
• Mild 13–15, moderate 9–12, severe 3–8.
• Extradural: temporal fracture, middle meningeal artery, lucid interval, biconvex, urgent craniotomy, good outcome.
• Subdural: bridging veins, crescent; chronic form in elderly or anticoagulated weeks after trivial injury, burr holes.
• Basal fracture: raccoon eyes, Battle sign, CSF leak, haemotympanum, VII/VIII palsy.
• Uncal herniation: ipsilateral blown pupil, contralateral hemiparesis. Cushing triad: high BP, low pulse, irregular breathing.
• CPP = MAP − ICP; keep CPP 60 or more; normal ICP about 10 mmHg.
• Mannitol 1 g/kg (not if hypotensive); hypertonic saline if hypotensive; hyperventilation only briefly; no steroids.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; ATLS Student Course Manual; Bailey and Love's Short Practice of Surgery).

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