Head Injury: Extradural Haematoma

Brief posttraumatic loss of consciousness.

Followed by recovery and a ‘lucid interval’ (between initial trauma and subsequent neurological deterioration).

Leading to neurological decline with decreasing GCS.

Finally, if untreated, death due to ‘herniation’ (usually uncal).

Other presenting complaints: Headache, vomiting and seizures.
Deterioration usually over ‘few’ hours.

Remember: Only up to one-third of cases with EDHs have the characteristic lucid interval before deterioration; therefore, even in the absence of the ‘textbook presentation’, EDHs must be suspected and ruled out in patients presenting with decreased GCS, headache, vomiting, seizure or focal neurological deficits following head trauma.

Examination

Scalp laceration or bony step-off in the area of injury, otorrhoea, rhinorrhoea and haemotympanum.
Decreased or fluctuating GCS with or without focal neurological deficits.
Ipsilateral pupillary dilatation (due to increased ICP and compression of oculomotor nerve) (see Chapter 30).
Contralateral hemiparesis (due to compression of ipsilateral cerebral peduncle).
Ipsilateral hemiplegia or hemiparesis: Can occur as a ‘false localising sign’ due to compression of contralateral cerebral peduncle against the tentorial edge (the so-called ‘Kernohan’ notch phenomenon).
In later stages due to progression and herniation:

Coma and decerebrate rigidity.

Cushing response (hypertension, bradycardia and respiratory irregularity) and death.

Investigation

Plain skull X-ray: May show skull fracture.
Unenhanced head CT scan (Figure 34.1): Compare with acute subdural haematoma (Table 34.1) (also see Chapter 33)—

Done urgently as a procedure of choice for diagnosis.