Elevated Intracranial Pressure and Brain Herniation

The cranium is a rigid compartment holding brain (about 80%), blood (about 10%) and CSF (about 10%). Any added volume must be offset by displacement of CSF into the spinal subarachnoid space or of venous blood out of the skull. Once these buffers are exhausted, compliance collapses and small volume increments produce steep ICP rises.

• Normal adult supine ICP is 5 to 15 mmHg. Sustained ICP above 20 to 22 mmHg for more than 5 minutes is pathological.
• Cerebral perfusion pressure equals MAP minus ICP. The usual target is 60 to 70 mmHg.
• Autoregulation failure makes cerebral blood flow pressure-passive, so both hypotension and hypertension become harmful.

Causes by mechanism

• Mass lesions: haematoma, tumour, abscess, empyema.
• Cerebral oedema: vasogenic (tumour, abscess), cytotoxic (infarct, hypoxia), interstitial (hydrocephalus), osmotic (hyponatraemia, hepatic failure).
• CSF obstruction: obstructive hydrocephalus, intraventricular haemorrhage.
• Venous outflow obstruction: cerebral venous thrombosis.
• Hyperaemia: hypercapnia, seizures, hyperthermia.
• Idiopathic intracranial hypertension.

Herniation syndromes are classified by the displaced tissue and the structure crossed:

• Subfalcine: cingulate gyrus under the falx.
• Uncal (lateral transtentorial): medial temporal lobe through the tentorial notch.
• Central transtentorial: downward diencephalic displacement.
• Tonsillar: cerebellar tonsils through the foramen magnum.
• Upward cerebellar: posterior fossa mass pushing the vermis up through the notch.
• Transcalvarial: through a craniectomy defect.

Raised ICP in the awake patient produces

• Headache worse supine, on waking and with Valsalva, with vomiting.
• Papilloedema, transient visual obscurations, and diplopia from false localising abducens palsy.
• Progressive drowsiness.

The Cushing response is a late sign of brainstem compromise

• Systolic hypertension with widened pulse pressure.
• Bradycardia.
• Irregular respiration.

Herniation patterns

• Uncal: ipsilateral dilated, poorly reactive pupil from CN III compression, then contralateral hemiparesis. Kernohan notch phenomenon (ipsilateral hemiparesis from compression of the opposite cerebral peduncle) is a false localising sign. PCA compression causes contralateral homonymous hemianopia.
• Central: progresses rostrocaudally.
• Diencephalic stage: small reactive pupils, Cheyne-Stokes breathing, decorticate posturing.
• Midbrain stage: midposition fixed pupils, central neurogenic hyperventilation, decerebrate posturing.
• Pontine stage: ataxic breathing, loss of oculovestibular responses.
• Medullary stage: apnoea and cardiovascular collapse.
• Subfalcine: contralateral leg weakness from ACA compression, often clinically silent.
• Tonsillar: neck stiffness, head tilt, sudden apnoea, hypotension.
• Duret haemorrhages in the midbrain and pons are a late sign of rostrocaudal deterioration.

In idiopathic intracranial hypertension, the patient is alert with papilloedema and a normal scan. In mass lesions, focal signs and falling GCS predominate.

Clinical assessment comes first and must not be delayed by imaging in a herniating patient. Record GCS, pupil size and reactivity, and brainstem reflexes serially.

Non-contrast CT head findings suggesting raised ICP

• Sulcal effacement and loss of grey-white differentiation.
• Effaced basal cisterns.
• Midline shift above 5 mm.
• Ventricular dilatation with transependymal flow.
• Tonsillar descent below the foramen magnum.

MRI and MR venography are used when venous thrombosis, posterior fossa pathology or idiopathic intracranial hypertension is suspected.

Invasive monitoring

• External ventricular drain is the reference standard, because it allows CSF drainage and is used when hydrocephalus is present.
• Intraparenchymal microtransducers are an alternative.
• Monitoring is indicated in severe head injury with an abnormal CT, and in comatose patients with space-occupying lesions.
• Look for Lundberg A (plateau) waves of 50 to 100 mmHg lasting 5 to 20 minutes, and a rising P2 above P1 indicating poor compliance.

Non-invasive adjuncts

• Optic nerve sheath diameter above about 5 mm by ultrasound suggests ICP above 20 mmHg.
• Transcranial Doppler with raised pulsatility index.

Lumbar puncture is contraindicated with mass effect or obstructive hydrocephalus. In idiopathic intracranial hypertension, opening pressure above 25 cm H2O confirms the diagnosis.

Baseline laboratory tests: sodium, osmolality, glucose, coagulation, ammonia in suspected hepatic encephalopathy, and blood gas.

Baseline measures for all patients

• Head of bed at 30 degrees, head midline, no tight cervical collars or tube ties compressing jugular veins.
• Intubate for GCS 8 or below or airway compromise. Maintain SpO2 above 94% and PaCO2 35 to 45 mmHg.
• Maintain euvolaemia with isotonic saline. Avoid hypotonic fluids and dextrose-containing solutions.
• Keep SBP above 110 mmHg and CPP 60 to 70 mmHg.
• Normothermia, glucose 140 to 180 mg/dL, sodium 140 to 150 mmol/L.
• Treat seizures promptly.

Tier 1: first-line ICP lowering

• Sedation and analgesia: propofol 1 to 4 mg/kg/h (watch propofol infusion syndrome above 4 mg/kg/h) with fentanyl 25 to 200 mcg/h.
• Mannitol 20%: 0.25 to 1 g/kg IV over 15 to 20 minutes, repeated every 4 to 6 hours. Hold if serum osmolality exceeds 320 mOsm/kg. Avoid hypovolaemia.
• Hypertonic saline 3%: 2 to 5 mL/kg (about 150 to 250 mL) over 10 to 20 minutes, targeting sodium 145 to 155 mmol/L. Check sodium every 4 to 6 hours and withhold above 160 mmol/L.
• CSF drainage via EVD, opened at an ICP threshold of 15 to 20 mmHg.

Impending herniation (emergency)

• Secure the airway and give brief hyperventilation to PaCO2 30 to 35 mmHg as a bridge only. Prolonged use causes ischaemia.
• Mannitol 1 g/kg, or 23.4% saline 30 mL via central line over 10 to 20 minutes.
• Urgent CT and neurosurgical review for evacuation, EVD or decompression.

Tier 2 and 3: refractory ICP

• Neuromuscular blockade: cisatracurium 0.15 mg/kg bolus then 1 to 3 mcg/kg/min.
• Barbiturate coma: pentobarbital 10 mg/kg over 30 minutes, then 5 mg/kg/h for 3 hours, then 1 to 4 mg/kg/h titrated to EEG burst suppression. Expect hypotension and ileus, and have vasopressors ready.
• Decompressive craniectomy, with a large frontotemporoparietal flap of at least 12 cm, reduces mortality in refractory ICP but increases survival with severe disability.
• Moderate hypothermia (32 to 34 C) is not routine.

Cause-directed therapy

• Vasogenic oedema from tumour or abscess: dexamethasone 10 mg IV then 4 mg every 6 hours. Do not use steroids in traumatic brain injury, where they increase mortality.
• Obstructive hydrocephalus: EVD or shunt.
• Idiopathic intracranial hypertension: acetazolamide 500 mg twice daily increased to 4 g/day as tolerated, weight loss, and optic nerve sheath fenestration or shunting for threatened vision.
• Evacuate surgical haematomas and treat infection or venous thrombosis as indicated.