Neurology

Raised Intracranial Pressure

Raised intracranial pressure is a dangerous final pathway in which increased volume within the fixed skull reduces cerebral perfusion and may cause herniation; the cause, visual risk and speed of neurological deterioration determine the emergency pathway.

In a nutshell

Raised intracranial pressure is a syndrome caused by added volume, impaired CSF drainage or venous congestion within the fixed skull. It can reduce cerebral perfusion and cause herniation. Treat the deteriorating patient immediately with ABCDE, oxygenation, perfusion, head elevation, urgent imaging and specialist escalation; use hyperosmolar therapy or temporary hyperventilation only under neurocritical-care direction while treating the cause. Papilloedema is important but may be absent in acute disease, and lumbar puncture is unsafe when mass effect or obstructed CSF pathways could cause herniation.

Classic presentation

A person develops progressive headache, vomiting and visual disturbance with papilloedema or a sixth-nerve palsy, then worsening consciousness, seizure, focal signs or pupillary change. The immediate priorities are neurological trend, pupils, airway, imaging and identifying the cause.

Key points

Monro–Kellie explains why intracranial pressure can rise steeply after compensatory CSF and venous reserves are exhausted.
Raised pressure is a syndrome: consider haemorrhage, tumour, abscess, hydrocephalus, venous thrombosis, infection, severe infarction, trauma and IIH.
A falling conscious level, new pupillary asymmetry, abnormal posturing or irregular breathing is possible herniation and requires immediate critical-care and neurosurgical action.
CT is the rapid first test for acute deterioration; CT does not itself exclude raised pressure, and MRI or venous imaging may be needed.
Attempt fundoscopy and assess vision, but absence of papilloedema does not exclude acute raised pressure.
Do not perform lumbar puncture until imaging and senior review exclude mass effect or obstructed CSF pathways; raised pressure alone is not an absolute contraindication in IIH.
Hyperosmolar therapy is a temporising specialist treatment, not routine prophylaxis; monitor renal, sodium, osmolality, fluid and haemodynamic effects.
Hyperventilation is a short bridge for impending herniation, not routine prophylaxis, because it can reduce cerebral blood flow.
Dexamethasone is selective for vasogenic tumour or abscess oedema and is not routine treatment for cytotoxic stroke or traumatic oedema.
Sight-threatening visual decline in IIH is an emergency requiring neuro-ophthalmology and possible CSF diversion.

First-line investigation

Immediate neurological and physiological assessment, fundoscopy or visual assessment, urgent CT and cause-directed vascular or MRI imaging, with LP only after anatomical safety review.

Management

Resuscitate and prevent secondary injury

Use ABCDE, protect the airway, avoid hypoxia, hypotension and hypercapnia, treat fever, pain, agitation and seizures, elevate the head when appropriate and escalate immediately for deterioration or herniation signs.^2,1

Image urgently and identify the cause

Arrange urgent CT, add venous or MRI imaging when indicated, attempt fundoscopy and discuss with neurosurgery, critical care, neurology, infection, stroke or oncology according to the cause.^2,3,7

Use specialist temporising ICP treatment

Use hyperosmolar therapy under neurocritical-care protocol for acute intracranial hypertension or impending herniation, and temporary controlled hyperventilation only as a monitored bridge; do not use either routinely.^1,8,5

Treat the cause

Use evacuation, decompression, tumour or abscess treatment, CSF diversion, antimicrobial therapy, CVST anticoagulation or IIH treatment as the cause requires; use dexamethasone only for appropriate vasogenic oedema.^2,6,4,7,5

Protect vision and monitor recurrence

For IIH or other chronic pressure syndromes, monitor visual fields and acuity with specialist teams, reassess the cause and give safety-net advice for headache, vomiting, visual change, seizure or neurological deterioration.^3,5

Exam traps

Cushing response and a fixed dilated pupil are late danger signs, not reassuring diagnostic criteria to wait for.
Normal fundoscopy or CT does not safely exclude acute raised pressure.
Do not perform LP in the presence of mass effect or obstructed CSF pathways; image and seek senior review first.
Raised pressure in IIH is different from a mass lesion: after safe imaging, LP opening pressure is part of diagnosis.
Dexamethasone reduces vasogenic tumour or abscess oedema, not cytotoxic oedema from ischaemic stroke or trauma.
Routine hyperventilation can worsen cerebral ischaemia; use only as a monitored bridge for imminent herniation.

Illustrations

Brain herniation syndromesAn illustration of subfalcine, uncal and tonsillar herniation, labelled with the clinical consequences of third-nerve, vascular and brainstem compression. Include a warning that these are late emergency signs.RupertMillard, Wikimedia Commons · CC-BY-SA-3.0

Papilloedema on fundoscopyA fundoscopic image of a swollen optic disc with blurred margins, with a note that papilloedema indicates sustained optic-nerve sheath pressure but may be absent in acute raised intracranial pressure.DocSee04, Wikimedia Commons · CC-BY-4.0

Key sources

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.