Raised intracranial pressure from brain metastases

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

Brain metastases reach the central nervous system through the bloodstream, commonly from lung, breast, melanoma and renal cancers. Many lodge near the grey-white junction, but any compartment can be involved. Neurological harm depends more on location, oedema, haemorrhage and cerebrospinal-fluid obstruction than on diameter alone. A posterior-fossa metastasis can obstruct the fourth ventricle and threaten the brainstem quickly, while several small supratentorial lesions may present through seizure or subtle cognition.

The skull has fixed volume. Initially cerebrospinal fluid and venous blood are displaced to accommodate tumour and vasogenic oedema. Once this reserve is exhausted, further swelling creates a steep pressure rise, lowers cerebral perfusion and drives tissue across the tentorium or foramen magnum. Headache worsened by cough, strain or lying flat, morning vomiting and papilloedema are classic, but focal deficit, seizure, gait change or confusion may appear first. A fixed pupil, abnormal posturing or declining consciousness signifies late pressure and possible herniation.

In an unstable patient, non-contrast CT is the fastest examination for haemorrhage, hydrocephalus, major oedema and shift. Add contrast or proceed to MRI after stabilisation. Contrast-enhanced MRI with appropriate thin slices is the reference standard for number, size, posterior-fossa disease, leptomeningeal clues and local-treatment planning. Imaging still does not automatically establish histology: a solitary lesion without a known cancer, an atypical abscess-like appearance or a long interval from the primary may require resection or biopsy.

Dexamethasone reduces vasogenic oedema and often improves symptoms within hours, but it neither treats tumour nor reliably resolves obstructive hydrocephalus. Use the smallest regimen that controls neurological symptoms and taper as definitive treatment takes effect. Surgery is valuable for a large accessible symptomatic lesion, tissue uncertainty or hydrocephalus; stereotactic radiosurgery controls selected limited-volume disease; whole-brain radiotherapy has a selective role when distribution and prognosis justify its cognitive burden. Modern systemic agents with intracranial activity may contribute, but a patient with herniation physiology still needs immediate local and supportive rescue.

Key points

Brain metastases cause raised pressure through tumour volume, vasogenic oedema, haemorrhage and obstructive hydrocephalus; posterior-fossa lesions can deteriorate with little reserve.
Key features are progressive headache worse with cough or lying flat, vomiting, papilloedema, focal deficit, seizure, cognitive change and declining consciousness.
Immediate CT head is the first emergency study for herniation, haemorrhage or sudden deficit because it is fast; contrast-enhanced MRI is the reference standard for detecting and planning brain metastases when stable.
Give dexamethasone promptly for symptomatic tumour-related oedema or raised pressure, using the acute-oncology dose matched to severity and the shortest effective course with a documented taper.
Do not give prophylactic antiseizure medicine routinely to a patient with brain metastases who has never seized; treat a first seizure and review interactions with anticancer therapy.
A large accessible lesion causing mass effect, obstructive hydrocephalus or uncertain diagnosis may need urgent neurosurgical resection or CSF diversion.
Stereotactic radiosurgery is preferred local treatment for selected limited-volume disease; surgery, radiosurgery, whole-brain radiotherapy and systemic therapy are chosen from number, size, biology, prognosis and goals.
Monitor neurological examination, glucose, infection and steroid myopathy and re-image unexpected worsening to separate tumour progression, haemorrhage, treatment oedema and radionecrosis.

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

Haematogenous cerebral spread

Lung, breast, melanoma, renal and other cancers enter the arterial circulation and seed the grey-white junction and other well-perfused brain regions.

Large or strategically placed lesion

A growing metastasis, posterior-fossa mass or lesion near cerebrospinal-fluid pathways can create dangerous pressure despite a modest total tumour volume.

Intratumoral haemorrhage

Fragile tumour vessels can bleed spontaneously or with anticoagulation, abruptly enlarging mass effect and worsening neurological function.

Treatment-associated swelling

Radiotherapy, immunotherapy and tumour necrosis can temporarily increase inflammation and oedema, while radionecrosis can cause later symptomatic mass effect.

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

1
Blood-brain barrier leaks
Tumour mediators disrupt capillary tight junctions, allowing protein-rich fluid into white matter and producing vasogenic oedema responsive to corticosteroid.
2
Fixed cranial volume is exhausted
Tumour, oedema and blood consume compensatory cerebrospinal-fluid and venous reserve until small volume increases cause steep pressure rises.
3
Perfusion pressure falls
As intracranial pressure approaches mean arterial pressure, cerebral perfusion declines, causing ischaemia, reduced consciousness and a self-reinforcing oedema cycle.
4
Tissue shifts across compartments
Pressure gradients displace temporal, central or cerebellar tissue across rigid dural openings, compressing brainstem and cranial nerves.

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

Raised-pressure headache

Progressive diffuse headache that is worse on waking, lying flat, coughing or straining and accompanied by vomiting suggests pressure rather than uncomplicated tension pain.

Focal cortical syndromeRed flag

Weakness, aphasia, neglect, visual-field loss or focal seizure localises a lesion or haemorrhage and requires urgent imaging.

Posterior-fossa syndromeRed flag

Gait or limb ataxia, vertigo, dysarthria, cranial-nerve dysfunction and vomiting may precede abrupt hydrocephalus or brainstem compromise.

Papilloedema and sixth-nerve palsy

Optic-disc swelling, transient visual obscurations or impaired abduction supports raised pressure, but absence does not exclude rapid or focal mass effect.

Herniation physiologyRed flag

Declining consciousness, unequal or fixed pupils, abnormal posturing, irregular breathing, hypertension and bradycardia demands immediate neurocritical action.

Steroid-responsive oedema

Rapid improvement in headache or deficit after dexamethasone supports an oedema component but cannot distinguish metastasis from another steroid-responsive lesion.

Red flags requiring action

Reduced consciousness, pupillary asymmetry, abnormal posturing or a Cushing physiological pattern requires immediate herniation management.
A first seizure, status epilepticus or failure to recover promptly after a seizure in a cancer patient needs emergency assessment and imaging.
New focal weakness, aphasia, visual field loss, ataxia or rapidly worsening confusion may represent metastasis, haemorrhage or acute stroke.
Headache worse on waking, coughing, straining or lying flat with vomiting or papilloedema suggests raised intracranial pressure.
Anticoagulation and haemorrhage-prone melanoma, renal, thyroid or choriocarcinoma metastases increase concern for intratumoral bleeding.

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
First emergency non-contrast CT headFirst step
Why
Detect haemorrhage, major mass effect, hydrocephalus and shift rapidly in an unstable or suddenly deteriorating patient.
Interpretation and limitations
A normal CT does not exclude small metastases, posterior-fossa disease or leptomeningeal spread; proceed to contrast MRI when clinically safe.
02
Reference-standard contrast-enhanced brain MRI
Why
Define lesion number, size, location, oedema, posterior-fossa involvement and suitability for surgery or stereotactic treatment.
Interpretation and limitations
Use a dedicated metastasis protocol with thin post-contrast imaging; compare treatment dates because radiation change and immunotherapy inflammation can mimic progression.
03
Serial neurological and consciousness assessment
Why
Detect herniation progression and establish response to steroid, seizure treatment and decompression.
Interpretation and limitations
Document GCS, pupils, cranial nerves, power, language, fields, coordination and gait when safe; a worsening trend overrides a scheduled scan slot.
04
Glucose, electrolytes, calcium and organ profile
Why
Identify reversible seizure or encephalopathy contributors and establish corticosteroid and treatment safety.
Interpretation and limitations
Correct hypoglycaemia and severe sodium or calcium disturbance urgently without assuming they fully explain focal signs or mass effect.
05
Systemic staging and molecular review
Why
Define extracranial control, prognosis and therapies with intracranial activity.
Interpretation and limitations
Review current histology and actionable biomarkers; do not postpone emergency local treatment for a complete elective restaging sequence.
06
Tissue diagnosis when uncertainty changes care
Why
Differentiate metastasis from primary tumour, abscess, lymphoma or treatment effect.
Interpretation and limitations
Resection can provide tissue and decompression simultaneously for an accessible dominant lesion; biopsy route is planned by the neuro-oncology MDT.

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

Acute stroke or haemorrhage

Sudden focal deficit or reduced consciousness may be vascular, and cancer increases both thrombosis and bleeding; emergency stroke imaging remains necessary.

Primary brain tumour or abscess

A solitary enhancing lesion may be glioma, abscess, lymphoma or metastasis; clinical context, diffusion, perfusion and sometimes tissue establish diagnosis.

Leptomeningeal metastatic disease

Multifocal cranial neuropathy, radicular symptom or communicating hydrocephalus suggests meningeal spread rather than pressure from one parenchymal mass.

Metabolic or treatment encephalopathy

Sepsis, sodium or calcium disorder, hepatic failure, opioids and immune-related encephalitis can alter cognition without structural mass effect and may coexist.

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

01DeterioratingProtect brain and identify herniationFirst stepConsciousness, pupils, posture, breathing or focal neurology is worsening rapidly.

1Use ABCDE with cervical-neutral head elevation, oxygen for hypoxaemia, glucose and blood gas, seizure control and avoidance of hypotension and hypercapnia.
2Give dexamethasone promptly for suspected tumour-associated oedema, obtain immediate CT and contact neurosurgery, critical care and acute oncology together.
3DefinitiveTreat obstructive hydrocephalus or a surgically accessible dominant mass urgently; use temporary hyperosmolar rescue only under neurocritical guidance while definitive decompression is mobilised.

02Stable symptomaticDefine all intracranial diseaseA cancer patient has new headache, focal symptom, seizure or cognitive change without herniation physiology.

1Obtain contrast-enhanced MRI with a metastasis protocol and review anticoagulants, steroid exposure, previous brain treatment and current systemic cancer control.
2Use dexamethasone for clinically important oedema, provide analgesia and antiemetic, and treat actual seizure with an interaction-conscious antiseizure medicine.
3Present imaging, performance, histology and prognosis at the neuro-oncology MDT to select resection, stereotactic radiotherapy, whole-brain treatment or systemic therapy.

03Local treatmentMatch surgery and radiation to volumeImaging confirms brain metastases and urgent physiology is controlled.

1Offer resection for selected large accessible symptomatic lesions, tissue uncertainty or obstructive mass effect when functional and systemic prognosis support benefit.
2Use stereotactic radiosurgery or fractionated stereotactic radiotherapy for selected limited-volume lesions and postoperative cavities according to size and critical anatomy.
3Consider whole-brain radiotherapy selectively for diffuse disease when expected symptom or control benefit outweighs neurocognitive burden; integrate systemic treatment with intracranial activity.

04Follow-upSeparate progression from treatment effectNeurological symptoms or MRI abnormality evolves after surgery, radiosurgery, whole-brain or systemic treatment.

1Reassess steroid dose, seizure, metabolic and infection causes and obtain MRI with advanced sequences when conventional enhancement cannot distinguish viable tumour from treatment change.
2Discuss short-interval imaging, amino-acid or metabolic imaging where available, surgery or biopsy when the distinction will change care and the patient is stable.
3Taper corticosteroid to the lowest effective dose, rehabilitate focal and cognitive disability and establish a rapid pathway for recurrent neurological deterioration.

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

Reduces tumour-associated vasogenic oedema and temporarily improves headache, vomiting and focal neurological function.

Dexamethasone for symptomatic cerebral oedema

Use 4 to 8 mg daily orally or intravenously in divided doses for mild to moderate symptoms and up to 16 mg daily for severe raised-pressure or focal symptoms under the acute neuro-oncology protocol, then taper as rapidly as clinically tolerated.

Give promptly in a deteriorating known-cancer presentation, but obtain diagnostic tissue before prolonged steroid when lymphoma is possible and physiology allows. Monitor glucose, infection, delirium, sleep, gastric risk and proximal weakness.

Treats focal or bilateral seizures with relatively few hepatic enzyme interactions with systemic anticancer therapy.

Levetiracetam after seizure

A common adult starting regimen after a brain-tumour seizure is levetiracetam 500 mg orally or intravenously twice daily, increased according to recurrence, renal function and specialist neurology advice.

Do not prescribe prophylactically to every seizure-naive patient. Adjust for renal impairment and monitor somnolence, agitation, depression and suicidality; status epilepticus follows the emergency seizure protocol.

Controls headache, nausea and vomiting while corticosteroid and definitive decompression take effect.

Antiemetic and analgesic support

Select the BNF antiemetic and analgesic route according to vomiting, consciousness, QT interval, bowel function, renal function and the need for rapid titration.

Sedation can obscure neurological decline and dopamine antagonists can cause dystonia or akathisia; repeated symptomatic dosing must not delay imaging or hydrocephalus treatment.

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

Brain herniation

Tissue displacement compresses midbrain or medulla, producing fixed pupils, coma, abnormal breathing, cardiovascular instability and death without immediate rescue.

Seizure and status epilepticus

Cortical irritation from tumour, oedema or haemorrhage can cause focal or bilateral convulsion, aspiration, hypoxia and prolonged neuronal injury.

Hydrocephalus

Posterior-fossa or ventricular disease can obstruct cerebrospinal-fluid circulation, rapidly worsening headache, vomiting, gait and consciousness and requiring drainage.

Steroid and treatment toxicity

Prolonged dexamethasone causes infection, hyperglycaemia, delirium and proximal weakness, while radiation can cause necrosis, cognitive decline and oedema.

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

During acute deterioration, repeat GCS, pupils, power and cardiorespiratory observations frequently and escalate any new asymmetry or consciousness decline.
Track headache, vomiting, focal function and steroid response while checking capillary glucose, infection, sleep, mood and proximal strength.
After a seizure, monitor recovery, recurrence, aspiration, driving advice and antiseizure toxicity and review renal function and anticancer interactions.
Use protocolled MRI after local treatment and investigate earlier when symptoms worsen; apparent enhancement may represent progression, haemorrhage, oedema or radionecrosis.
Review systemic disease, performance and patient goals at each intracranial treatment decision because benefit from local control depends on the whole cancer trajectory.
Provide rehabilitation, falls and safety assessment and a 24-hour route for new seizure, weakness, vomiting or altered consciousness.

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

CT rescues and MRI maps

CT is fastest for haemorrhage and herniation, while contrast MRI finds smaller lesions and defines the true local-treatment burden.

Posterior fossa has little reserve

A relatively small cerebellar lesion can obstruct cerebrospinal fluid or compress brainstem before dramatic supratentorial signs appear.

Steroid treats oedema not cancer

Rapid symptomatic response is valuable but cannot replace decompression, radiotherapy or tumour-active systemic treatment.

No seizure means no routine drug

Antiseizure medicines add cognitive and psychiatric toxicity and are not routinely used before a first seizure solely because a metastasis exists.

Enhancement is not always progression

Radiation necrosis and immune inflammation can mimic tumour growth, requiring temporal, clinical and advanced-imaging correlation.

11Common pitfallsFrequent interpretation and management errors.

01
Sending a patient with falling consciousness directly to routine MRI without immediate resuscitation and CT capability.
02
Waiting for papilloedema before considering raised intracranial pressure.
03
Using dexamethasone as definitive tumour treatment or continuing it indefinitely without a taper plan.
04
Giving prophylactic antiseizure medicine to every seizure-naive patient with brain metastases.
05
Assuming sudden focal deficit is tumour progression and missing stroke or intratumoral haemorrhage.
06
Choosing whole-brain radiotherapy automatically without considering surgery, stereotactic treatment, systemic options and prognosis.
07
Calling every enlarging post-radiotherapy lesion recurrent cancer without assessing treatment effect.