Uncal Herniation

Uncal herniation is displacement of the medial temporal lobe (uncus and hippocampal gyrus) over the free edge of the tentorium, compressing the oculomotor nerve, the midbrain and the posterior cerebral artery. It is the commonest form of transtentorial herniation and results from a lateral mass lesion.

Epidemiology. It complicates acute subdural and extradural haematoma, temporal intracerebral haemorrhage, malignant hemispheric infarction and tumour. Mortality is high once the pupil is fixed and dilated.

Causes. Traumatic extradural or subdural haematoma, hypertensive or traumatic temporal haemorrhage, middle cerebral artery infarct, abscess, tumour and diffuse swelling.

Pathophysiology. The uncus is pushed medially and downward, compressing the ipsilateral third nerve (parasympathetic fibres on its surface), the cerebral peduncle (contralateral hemiparesis) and the posterior cerebral artery (occipital infarction). The midbrain may be pushed against the opposite tentorial edge (Kernohan notch, giving ipsilateral hemiparesis, a false localising sign).

Presentation is headache, falling consciousness, ipsilateral pupillary dilation (sluggish, then fixed), ptosis and a down-and-out eye, contralateral hemiparesis, extensor posturing, hypertension and bradycardia, and loss of consciousness. Visual field loss from occipital infarction is seen in survivors.

Red flags.

• Unilateral dilated pupil with falling consciousness.
• New hemiparesis or posturing.
• Cushing response, or rapid fall in the Glasgow Coma Scale.

Treatment starts on clinical grounds. CT head (temporal haematoma, midline shift, effacement of the ipsilateral perimesencephalic cistern, uncus displacement), with CT angiography if vascular lesion is suspected. Check glucose, coagulation, sodium, gas and group and crossmatch. Do not perform lumbar puncture.

Differential diagnosis. Direct orbital or third nerve trauma, posterior communicating artery aneurysm, diabetic third nerve palsy, Horner syndrome, drug induced mydriasis (atropine, nebulised ipratropium into the eye) and Adie pupil.

Immediate.

• Airway: intubate with ketamine 1 to 2 mg/kg or etomidate 0.3 mg/kg and rocuronium 1.2 mg/kg, avoiding hypotension and hypoxia.
• Head up 30 degrees, neck neutral, systolic pressure at least 110 mmHg, normoxia and normocapnia.
• Hyperosmolar therapy: 3% sodium chloride 250 mL IV over 15 to 20 minutes (or 23.4% sodium chloride 30 mL IV over 10 to 20 minutes through a central line), or mannitol 20% 0.5 to 1 g/kg IV over 15 to 20 minutes (osmolality under 320 mOsm/kg). Repeat for a recurrent dilated pupil.
• Brief hyperventilation to PaCO2 of 4.0 to 4.5 kPa (30 to 35 mmHg) as a bridge to surgery.

Reverse coagulopathy. Warfarin: prothrombin complex concentrate 25 to 50 units/kg and vitamin K 10 mg IV. Dabigatran: idarucizumab 5 g IV. Factor Xa inhibitors: prothrombin complex concentrate 50 units/kg (maximum 5000 units) or the specific reversal agent. Platelets for thrombocytopenia (over 100 x 10^9/L before neurosurgery).

Tranexamic acid. 1 g IV over 10 minutes within 3 hours of head injury, then 1 g over 8 hours.

Seizure prophylaxis. Levetiracetam 60 mg/kg IV (maximum 4500 mg), then 500 to 1000 mg every 12 hours (adjusted to eGFR) for a limited period in traumatic haematoma.

Surgery. Immediate craniotomy for evacuation of extradural or subdural haematoma, decompressive craniectomy for refractory pressure, and burr hole decompression if transfer is delayed and the cause is a large extradural haematoma.

Monitoring. Pupils and Glasgow Coma Scale every 15 minutes, intracranial pressure, cerebral perfusion pressure (60 to 70 mmHg), sodium and repeat CT.

Referral and escalation. Neurosurgery and neurocritical care at once. Transfer without delay if neurosurgery is not available.

Special groups. In children, 3% sodium chloride is 2 to 5 mL/kg and mannitol 0.5 to 1 g/kg. In older adults and anticoagulated patients, reverse anticoagulation and expect lower tolerance of fluid shifts.