Synopsis
Recognise intracranial hypertension before herniation, identify the mechanism and cause, stabilise cerebral perfusion, and use imaging, hyperosmolar rescue and definitive neurosurgical treatment safely.
- Intracranial pressure rises when the fixed cranial volume can no longer compensate for expansion of brain tissue, blood or cerebrospinal fluid, eventually reducing cerebral perfusion and shifting tissue.
- Causes include traumatic or spontaneous haemorrhage, tumour, infarction, infection, hydrocephalus, venous thrombosis, hepatic failure, hypoxic injury and idiopathic intracranial hypertension, each requiring different definitive treatment.
- Progressive headache, vomiting, transient visual obscurations, diplopia from sixth-nerve palsy and papilloedema support a slower rise, but papilloedema can be absent in acute catastrophic pressure.
- Reduced consciousness is the most important bedside trajectory; unilateral pupillary dilation, abnormal posturing and Cushing hypertension with bradycardia are late findings.
- Vasogenic oedema reflects blood-brain-barrier leakage around tumours and inflammation, cytotoxic oedema reflects cellular energy failure in ischaemia, and interstitial oedema accompanies hydrocephalus.
- Priorities are oxygenation, normocapnia, avoidance of hypotension, neutral neck alignment, head elevation and treatment of fever, agitation, seizures and hypoglycaemia.
- Brief controlled hyperventilation is a rescue bridge for imminent herniation, not routine prolonged therapy, because cerebral vasoconstriction can worsen ischaemia.
- Hypertonic saline or mannitol can rapidly reduce brain water; selection and repeat dosing depend on haemodynamics, sodium, osmolality, kidney function and the neurocritical-care protocol.
- Corticosteroids help vasogenic oedema from selected tumours but are harmful in traumatic brain injury and are not routine therapy for ischaemic or hypoxic cytotoxic oedema.
- Definitive management may require haematoma evacuation, external ventricular drainage, tumour treatment, abscess drainage, venous thrombosis therapy or decompressive surgery.
Key red flags
A newly dilated pupil, extensor posturing, irregular respiration or hypertension with bradycardia requires immediate critical-care and neurosurgical action.
Investigation priorities
Detect haemorrhage, mass, hydrocephalus, infarct signs and major tissue shift quickly.
Management branches
Consciousness, pupils or posture deteriorates with suspected intracranial hypertension.
- Activate critical-care and neurosurgical teams, secure airway and oxygenation as necessary, maintain blood pressure and place the head up with neck midline and venous drainage unobstructed.
- Treat seizure, fever, agitation, hypoglycaemia and severe hypercapnia, using brief hyperventilation only as a monitored bridge when herniation is imminent.
- Give local-protocol hypertonic saline or mannitol when indicated and move to emergency CT and definitive neurosurgical intervention without waiting to assess headache response.
A stable patient has headache, visual obscurations or optic-disc swelling without acute herniation signs.
- Confirm true papilloedema, measure blood pressure and arrange urgent brain imaging with venography where cerebral venous thrombosis is possible.
- After mass and obstruction are excluded, perform protocol-led lumbar puncture with accurate lateral-position opening pressure and appropriate cerebrospinal-fluid studies.
- Refer promptly to the relevant neurology, ophthalmology, neurosurgery or oncology pathway and monitor visual fields rather than treating headache alone.
Key medicines
Hypertonic sodium chlorideConcentration, bolus volume and repeat limits follow the local neurocritical-care protocol, central or peripheral access policy and measured sodium rather than a generic ward prescription.Monitor sodium, chloride, osmolality, renal function, volume status and infusion site; overcorrection and repeated unmeasured dosing can cause serious metabolic and neurological harm.
MannitolUse a weight-based intravenous bolus from the current BNF and local intracranial-pressure protocol, with response and osmolar monitoring before any repeat dose.Hypotension, diuresis, kidney injury and accumulation can reduce cerebral perfusion; avoid automatic use in hypovolaemia and monitor fluid balance closely.