Raised intracranial pressure and cerebral oedema

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The Monro-Kellie principle describes a skull containing brain, blood and cerebrospinal fluid. Early increases in one component are buffered by displacement of venous blood and fluid, so intracranial pressure may remain stable until reserve is exhausted. Beyond that point small volume changes produce steep pressure rises. Cerebral perfusion pressure is the difference between mean arterial pressure and intracranial pressure; both hypotension and intracranial hypertension therefore threaten perfusion. A single normal pressure or CT does not replace continued assessment when the neurological state deteriorates.

Herniation patterns reflect the direction of tissue displacement. Uncal shift can compress the ipsilateral third nerve and cerebral peduncle; central descent produces progressive diencephalic and brainstem dysfunction; tonsillar descent threatens medullary respiration; subfalcine shift can compromise anterior cerebral circulation. Pupillary asymmetry is clinically important but can have ocular or drug causes, so examine size and reactivity before and after interventions while treating the whole trajectory.

Treatment distinguishes generic physiological rescue from cause-specific care. Airway control must avoid hypoxia and large blood-pressure drops. Analgesia and sedation reduce metabolic demand but can obscure examination and require ventilation planning. Hyperosmolar therapy buys time; it does not remove a tumour, drain obstructed ventricles or reverse haemorrhage. Intracranial monitoring is used in selected severe brain injury and other neurocritical illness through current local thresholds, with management based on sustained pressure, examination, imaging and cerebral physiology.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Expanding intracranial lesion

Tumour, abscess, traumatic or spontaneous haemorrhage and large infarction add tissue or blood volume within the rigid skull.

Hydrocephalus

Obstruction or impaired absorption enlarges cerebrospinal-fluid spaces and transmits pressure to surrounding brain during acute progression.

Venous and pressure disorders

Cerebral venous thrombosis and idiopathic intracranial hypertension raise venous or cerebrospinal-fluid pressure without a primary mass.

Diffuse cellular injury

Hypoxia, liver failure, infection and severe metabolic disturbance cause cytotoxic or vasogenic oedema across broad brain regions.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Compensatory reserve exhaustion
Cerebrospinal fluid and venous blood initially shift to accommodate added volume until fixed cranial capacity is exhausted.
2
Exponential pressure rise
Further tissue, blood or fluid expansion then causes a steep increase in intracranial pressure and widespread tissue compression.
3
Reduced cerebral perfusion
Rising intracranial pressure opposes arterial pressure, reducing blood flow and creating secondary ischaemia and cytotoxic oedema.
4
Tissue shift and herniation
Pressure gradients displace brain beneath dural partitions or through the foramen magnum, compressing cranial nerves, brainstem and vital centres.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Progressive pressure headache

Headache worsens over days or weeks, may be prominent on waking or with cough and bending, and accompanies vomiting or transient visual dimming.

Papilloedema syndrome

Blurred disc margins, vessel obscuration and haemorrhages with preserved central acuity early indicate transmitted raised cerebrospinal-fluid pressure after ocular mimics are excluded.

Sixth-nerve palsy

Horizontal diplopia from impaired abduction can be a false-localising sign of intracranial hypertension and does not identify the lesion side.

Acute brain swelling

Declining consciousness, worsening focal findings and repeated vomiting after trauma, haemorrhage, large infarction or hypoxia suggests rapidly shrinking intracranial reserve.

Impending herniationRed flag

A newly dilated pupil, extensor posturing, irregular respiration or hypertension with bradycardia requires immediate critical-care and neurosurgical action.

Hydrocephalus pattern

Headache, gait or cognition change, vomiting and reduced alertness with ventricular enlargement suggests impaired cerebrospinal-fluid flow needing urgent drainage assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Emergency non-contrast CT brainFirst step
Why
Detect haemorrhage, mass, hydrocephalus, infarct signs and major tissue shift quickly.
Interpretation and limitations
Effaced sulci or cisterns, ventricular compression, midline shift and herniation support dangerous pressure; posterior-fossa and early disease may require MRI.
02
MRI brain with contrast and venous sequences
Why
Characterise tumour, infection, venous thrombosis, posterior-fossa disease and subtle oedema when stable enough.
Interpretation and limitations
Select diffusion, contrast and venography by suspected mechanism; transport risk may outweigh extra detail in an actively herniating patient.
03
Fundoscopy or optic-disc imaging
Why
Identify papilloedema in a subacute pressure syndrome.
Interpretation and limitations
True papilloedema prompts urgent brain imaging before lumbar puncture; pseudopapilloedema and malignant hypertension remain alternatives requiring ophthalmic correlation.
04
Intracranial pressure monitoring
Why
Guide therapy in selected severe traumatic and neurocritical illness.
Interpretation and limitations
Interpret sustained values and waveforms with mean arterial pressure, examination and imaging; exact insertion and treatment thresholds follow the specialist protocol.
05
Serum sodium, osmolality and renal function
Why
Choose and monitor hyperosmolar therapy safely.
Interpretation and limitations
Hypernatraemia, osmolar load, kidney injury and fluid state constrain repeat dosing; point-of-care results must be reconciled with laboratory values.
06
Arterial blood gas
Why
Assess oxygenation, carbon dioxide and acid-base contributors to cerebral blood volume.
Interpretation and limitations
Avoid hypoxia and marked hypercapnia; hypocapnia should be a short rescue target only in impending herniation under expert monitoring.
07
Lumbar puncture after imaging
Why
Measure opening pressure and analyse fluid only in selected stable syndromes without mass effect.
Interpretation and limitations
It is contraindicated when focal mass, obstructive hydrocephalus or herniation risk is present; normal imaging does not remove every clinical contraindication.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Migraine

Recurrent headache with sensory sensitivity and normal optic discs may be migraine, but vomiting, papilloedema, focal signs or reduced consciousness require urgent imaging.

Meningitis or encephalitis

Fever, meningism, seizures and cerebrospinal-fluid inflammation support infection, which can itself produce oedema alongside intracranial hypertension.

Low-pressure headache

Pain worse upright with brain sag and venous engorgement indicates cerebrospinal-fluid volume loss rather than intracranial hypertension.

Toxic or hypertensive encephalopathy

Systemic exposure, severe pressure or organ failure may cause diffuse cerebral dysfunction and oedema without a focal obstructing lesion.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Immediate rescueProtect cerebral oxygen deliveryFirst stepConsciousness, pupils or posture deteriorates with suspected intracranial hypertension.

1Activate 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.
2Treat seizure, fever, agitation, hypoglycaemia and severe hypercapnia, using brief hyperventilation only as a monitored bridge when herniation is imminent.
3DefinitiveGive local-protocol hypertonic saline or mannitol when indicated and move to emergency CT and definitive neurosurgical intervention without waiting to assess headache response.

02Cause identificationMatch definitive treatment to anatomyDefinitiveInitial stabilisation permits imaging and focused investigation.

1Review trauma, anticoagulation, cancer, infection, thrombosis, liver failure and toxic or metabolic context alongside non-contrast CT findings.
2Add contrast MRI, vascular imaging or microbiology only where the patient is stable and the result directs evacuation, drainage, anticoagulation, antimicrobial or oncological care.
3Avoid diagnostic lumbar puncture until imaging and senior assessment confirm no mass effect or obstructive process and the result is genuinely needed.

03Neurocritical controlTreat sustained pressure and prevent secondary injuryIntracranial hypertension persists despite first physiological measures.

1Optimise sedation, ventilation, temperature, sodium, seizures and perfusion using monitored targets, reassessing for a surgically correctable lesion after any worsening.
2Use repeat hyperosmolar therapy only with sodium, osmolality, kidney and haemodynamic review, avoiding automatic alternating regimens without evidence of effect.
3EscalationEscalate selected cases to cerebrospinal-fluid drainage, decompressive surgery or other tiered treatment through the neurocritical-care protocol and family discussion.

04Subacute papilloedemaProtect vision while establishing causeA stable patient has headache, visual obscurations or optic-disc swelling without acute herniation signs.

1Confirm true papilloedema, measure blood pressure and arrange urgent brain imaging with venography where cerebral venous thrombosis is possible.
2After mass and obstruction are excluded, perform protocol-led lumbar puncture with accurate lateral-position opening pressure and appropriate cerebrospinal-fluid studies.
3Refer promptly to the relevant neurology, ophthalmology, neurosurgery or oncology pathway and monitor visual fields rather than treating headache alone.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Creates an osmotic gradient that can rapidly reduce cerebral water and support perfusion during intracranial hypertension.

Hypertonic sodium chloride

Concentration, 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.

Provides short-term osmotic reduction of brain water while definitive treatment is organised.

Mannitol

Use 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.

Reduces blood-brain-barrier leakage and neurological symptoms around selected intracranial tumours.

Dexamethasone for tumour oedema

A neurosurgical or oncology team chooses the lowest effective loading and maintenance regimen for symptomatic tumour-related vasogenic oedema, then tapers deliberately.

Not indicated for traumatic brain injury or routine stroke oedema; monitor infection, glucose, mood, muscle, gastrointestinal and thrombotic complications.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Brain herniation and death

Continuing pressure shift causes fixed pupils, abnormal posturing, respiratory failure and irreversible brainstem injury without intervention.

Secondary cerebral ischaemia

Reduced perfusion and vessel compression extend neuronal injury beyond the original lesion and may leave additional permanent disability.

Optic-nerve damage

Sustained papilloedema causes optic atrophy and permanent visual-field or acuity loss when raised pressure persists untreated.

Rescue-treatment harm

Hyperosmolar therapy, hyperventilation and drainage can cause electrolyte, kidney, perfusion, bleeding and infection complications without definitive cause control.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record Glasgow Coma Scale components, pupil size and reactivity, focal deficits and posturing frequently, escalating small trends rather than waiting for a large total-score drop.
Monitor blood pressure, oxygenation, carbon dioxide, temperature, glucose and seizures because each can create secondary brain injury independent of pressure.
During hyperosmolar therapy trend sodium, chloride, osmolality, creatinine, urine output and haemodynamics at protocol-defined intervals.
Repeat imaging urgently after unexpected decline and at specialist-selected intervals after surgery, drainage or treatment of the causal lesion.
When papilloedema is present, document acuity, colour, pupils, fields and optic-disc appearance because headache relief does not guarantee visual protection.
Review thrombosis, infection, nutrition, skin, rehabilitation and family communication during prolonged neurocritical illness.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Papilloedema can lag

Acute lethal pressure may develop before optic-disc swelling, so a normal fundus cannot reassure against rapidly evolving herniation.

Pupils are a trajectory

Baseline anisocoria exists, but a new enlarging poorly reactive pupil during neurological decline is a time-critical change.

Perfusion needs pressure

Aggressively lowering blood pressure in an intracranial-pressure crisis can worsen cerebral perfusion even when systemic hypertension looks alarming.

Osmotherapy buys time

A temporary neurological improvement after saline or mannitol does not remove the haematoma, hydrocephalus or mass that created the crisis.

Steroids depend on mechanism

They reduce tumour-related vasogenic leakage but do not reverse cytotoxic cellular swelling and worsen outcome in traumatic brain injury.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for papilloedema before recognising acute intracranial hypertension.
02
Using pulse oximetry while ignoring carbon dioxide and blood pressure.
03
Performing lumbar puncture before excluding a focal mass or obstruction.
04
Using prolonged hyperventilation as routine pressure control.
05
Repeating hyperosmolar boluses without sodium, renal and volume review.
06
Giving corticosteroid for traumatic or ischaemic cerebral oedema.
07
Treating a monitor number while missing an evacuable lesion.