Intracerebral haemorrhage

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

Spontaneous ICH is bleeding directly into brain parenchyma, sometimes extending into the ventricles or subarachnoid space. Deep basal ganglia, thalamic, pontine and cerebellar haemorrhages often reflect hypertensive arteriopathy; lobar haemorrhage raises cerebral amyloid angiopathy, vascular malformation, tumour, venous thrombosis or drug-related causes. Anticoagulation, stimulant drugs, coagulopathy and severe hypertension may contribute. Location, age, imaging and history guide later aetiological work-up, but acute priorities are physiological stability and limiting expansion.

Haematoma expansion occurs most often early and worsens outcome. Care therefore runs in parallel: urgent CT, controlled blood-pressure treatment in eligible patients, rapid anticoagulant reversal, neurosurgical triage and close neurological observation. Airway protection may be required for declining consciousness or bulbar dysfunction, while intubation drugs and ventilation should avoid hypotension. Blood-pressure treatment follows a monitored intravenous protocol; a generic instruction to make pressure normal can compromise cerebral perfusion.

Prognosis must not be decided from an admission score alone. Severity tools support communication and audit but can create a self-fulfilling prophecy if used to withdraw active care prematurely. Repeat assessment after stabilisation, include premorbid function and expressed wishes, and obtain specialist input. Survivors require cause investigation, blood-pressure control and a carefully timed decision on restarting antithrombotics, balancing the indication against lobar location, microbleeds, amyloid markers and recurrence risk.

Key points

Intracerebral haemorrhage commonly presents with sudden focal deficit, headache, vomiting, seizure or reduced consciousness and cannot be distinguished reliably from ischaemic stroke without urgent brain imaging.
Obtain non-contrast CT immediately, define haematoma site and volume, intraventricular extension, hydrocephalus and mass effect, and consider CTA for an underlying vascular lesion or expansion risk.
Record anticoagulant and antiplatelet exposure, exact last dose, blood pressure, glucose, platelets, INR, renal function and time of onset while stabilising airway, breathing and circulation.
Reverse warfarin-related haemorrhage urgently with four-factor prothrombin complex concentrate plus intravenous vitamin K, and use anticoagulant-specific emergency pathways for dabigatran or factor Xa inhibitors.
For eligible spontaneous intracerebral haemorrhage presenting within 6 hours with systolic pressure 150–220 mmHg and no NICE exclusion, consider controlled reduction to 140 mmHg or lower while ensuring the fall does not exceed 60 mmHg in the first hour; avoid hypotension and individualise when perfusion or raised-pressure concerns exist.
Routine platelet transfusion for spontaneous ICH in a patient taking antiplatelets is not beneficial and may be harmful unless a specific surgical or haematological indication is established.
Early neurosurgical discussion is essential for cerebellar haemorrhage with deterioration, brainstem compression or hydrocephalus, and for selected lobar or intraventricular cases; not every deep haemorrhage benefits from evacuation.
Prevent aspiration, VTE, fever, glucose extremes and pressure injury on a specialist stroke or neurocritical unit, and investigate deterioration with repeat imaging rather than assuming the initial bleed is static.

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

Hypertensive small-vessel disease

Chronic pressure-related arteriolar damage commonly causes deep haemorrhage in basal ganglia, thalamus, pons or cerebellum in chronically hypertensive adults.

Cerebral amyloid angiopathy

Amyloid deposition weakens cortical and leptomeningeal vessels, producing lobar haemorrhage and microbleeds, particularly in older adults.

Antithrombotic and coagulation disorders

Anticoagulants, severe thrombocytopenia and acquired or inherited coagulopathy increase bleeding risk and can amplify haematoma expansion.

Structural vascular or neoplastic lesion

Arteriovenous malformation, aneurysm, venous thrombosis and haemorrhagic tumour are important causes in younger people or atypical locations.

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

1
Arterial rupture
A weakened small artery or vascular lesion breaks, releasing blood directly into brain tissue under pressure.
2
Haematoma expansion
Continuing bleeding and local coagulation failure enlarge the clot, mechanically disrupting tissue and compressing adjacent pathways.
3
Perihaematomal injury
Thrombin, blood products, inflammation and blood–brain barrier disruption cause surrounding oedema and secondary neuronal dysfunction after the initial bleed.
4
Pressure and ventricular effects
Large or strategically placed haemorrhage raises intracranial pressure, enters ventricles or obstructs cerebrospinal-fluid flow, threatening herniation.

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

Deep hypertensive haemorrhage

Putaminal or thalamic bleeding may cause dense contralateral weakness or sensory loss, gaze disturbance and reduced consciousness, often with chronic hypertension or small-vessel disease.

Lobar haemorrhage

Cortical signs, visual field loss, aphasia, neglect or seizure with a superficial bleed suggests amyloid angiopathy, vascular lesion, tumour or another lobar cause.

Cerebellar haemorrhage

Abrupt vertigo, vomiting, occipital headache, gait or limb ataxia and declining consciousness may rapidly progress as the fourth ventricle and brainstem become compressed.

Pontine haemorrhage

Coma, pinpoint reactive pupils, abnormal eye movements, quadriparesis and respiratory dysfunction indicate a severe brainstem event requiring immediate critical-care assessment.

Intraventricular extension

Acute drowsiness, headache, vomiting and hydrocephalus accompany ventricular blood and can create a neurosurgical cerebrospinal-fluid diversion question.

Expansion pattern

Neurological worsening, rising pressure, repeated vomiting or falling consciousness in the first hours should be considered haematoma expansion or oedema until repeat imaging clarifies it.

Red flags requiring action

GCS decline, unequal pupils, extensor posturing or respiratory irregularity indicates impending herniation and needs immediate airway, neurocritical and neurosurgical action.
Cerebellar blood with hydrocephalus, brainstem compression or neurological deterioration is a time-critical surgical emergency.
Recent anticoagulant exposure with ICH requires reversal to begin as soon as clinically possible; do not wait for non-essential investigations or transfer.
Marked pressure elevation with cardiac, renal or neurological target-organ injury requires monitored treatment while preserving cerebral perfusion.
Young age, lobar location, subarachnoid extension or unusual calcification should prompt urgent vascular imaging for malformation, aneurysm or venous thrombosis.

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
Non-contrast CT brainFirst step
Why
Confirm haemorrhage and define location, size, ventricular extension, hydrocephalus, oedema and mass effect.
Interpretation and limitations
Compare with any later scan for expansion; location guides aetiology and surgical discussion, while a fluid level or disproportionate oedema may suggest coagulopathy or underlying lesion.
02
CT angiography
Why
Identify aneurysm, arteriovenous malformation or another vascular cause and assess contrast extravasation associated with expansion.
Interpretation and limitations
Use especially in younger patients, lobar or posterior fossa bleeds and atypical imaging; a negative CTA may still require delayed MRI or catheter angiography.
03
Full blood count and coagulation profile
Why
Find thrombocytopenia, anaemia, warfarin effect or another coagulopathy relevant to urgent treatment.
Interpretation and limitations
INR informs vitamin K antagonist reversal, but normal PT and APTT do not exclude clinically important DOAC activity; use drug-specific history and assays where available.
04
Renal function and anticoagulant timing
Why
Estimate persistence of direct oral anticoagulant effect and guide reversal, contrast and later dosing decisions.
Interpretation and limitations
Record the named drug, exact last dose and Cockcroft–Gault-relevant variables; renal impairment can prolong exposure, especially to dabigatran.
05
Repeat CT brain
Why
Detect expansion, hydrocephalus or new mass effect after deterioration or at the protocol surveillance interval.
Interpretation and limitations
Clinical decline requires immediate imaging; apparent stable focal signs do not eliminate planned follow-up in a high-risk early bleed.
06
MRI brain with blood-sensitive sequences
Why
Investigate underlying tumour, cavernoma, cerebral amyloid angiopathy or prior microhaemorrhage after the acute phase.
Interpretation and limitations
Strictly lobar microbleeds and cortical superficial siderosis support amyloid angiopathy, while timing must account for patient stability and acute blood artefact.
07
Toxicology or cause-directed tests
Why
Assess stimulant exposure, systemic disease, pregnancy-related hypertension or haematological causes when history indicates.
Interpretation and limitations
Target testing to the phenotype and avoid delaying reversal or neurosurgical care for broad panels that cannot change immediate management.

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

Acute ischaemic stroke

Focal onset is clinically indistinguishable; urgent non-contrast CT identifies blood and prevents unsafe reperfusion or antithrombotic treatment.

Subarachnoid haemorrhage

Thunderclap headache with blood concentrated in basal cisterns or sulci favours subarachnoid bleeding, though intraparenchymal extension can coexist.

Haemorrhagic venous infarction

Headache, seizure and a lesion crossing arterial territories with venous occlusion support cerebral venous thrombosis despite intraparenchymal blood.

Haemorrhagic tumour

Disproportionate oedema, an underlying enhancing mass or atypical evolution raises tumour and may require delayed contrast imaging after blood resolves.

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

01FIRSTFirst hour after diagnosisFirst stepUrgent CT confirms spontaneous intracerebral haemorrhage.

1Stabilise airway, breathing and circulation, elevate the head appropriately, correct hypoxia and glucose emergencies and establish frequent neurological observations.
2EscalationNotify stroke or neurocritical care and neurosurgery according to location and severity, and document onset, premorbid function and escalation wishes without delaying active treatment.
3Review antithrombotic exposure and begin indicated reversal immediately while obtaining full blood count, coagulation, renal function and group-and-save samples.
4Start protocol-led blood-pressure management when eligible and obtain CTA or repeat imaging according to the clinical and anatomical risk.

02REVERSEAnticoagulant-associated ICHThe patient has current warfarin, dabigatran, apixaban, rivaroxaban, edoxaban or heparin exposure.

1Identify the exact agent, last administration, dose, renal function and relevant laboratory result, but do not let incomplete history postpone haematology and pharmacy contact.
2For warfarin use four-factor PCC plus intravenous vitamin K; for dabigatran use the licensed specific antidote when indicated; follow the current commissioned protocol for factor Xa inhibitors.
3Stop all anticoagulant and antiplatelet agents, control blood pressure and repeat coagulation or drug-related testing after reversal as the protocol requires.
4Document the thrombotic indication and defer any restart decision until haemorrhage stability, cause and longer-term risks are reviewed multidisciplinary.

03SWELLMass effect or hydrocephalusExamination or imaging shows falling consciousness, ventricular obstruction, cerebellar compression or major midline shift.

1Call neurosurgery and critical care immediately, secure the airway when needed and prevent hypoxia, hypotension, fever and severe glucose disturbance.
2Repeat CT if the clinical state has changed and communicate clot site, volume, intraventricular blood, hydrocephalus and current GCS.
3Consider external ventricular drainage, posterior fossa decompression or selected clot evacuation through the specialist team; avoid lumbar puncture.
4Use temporary intracranial-pressure measures only as a bridge under specialist direction and reassess goals after treatment options are defined.

04LATERSurvivor prevention planThe haemorrhage is stable and acute surgical or reversal decisions are complete.

1Determine likely cause from location, vascular imaging, MRI markers, blood pressure history and drug exposure and arrange any delayed angiography or tumour assessment.
2Establish sustained blood-pressure treatment, adherence support and home monitoring while addressing smoking, alcohol, stimulants and sleep apnoea where relevant.
3Review every antithrombotic indication with stroke, cardiology or haematology input and decide whether, when and what to restart based on individual risks.
4Provide multidisciplinary rehabilitation, cognition and mood assessment and clear safety advice for recurrent neurological symptoms.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Rapidly replaces vitamin K-dependent coagulation factors and corrects the warfarin effect while vitamin K takes effect.

Four-factor prothrombin complex concentrate

For warfarin-associated intracranial bleeding, give an urgent intravenous dose based on presenting INR, body weight and the specific product or local major-haemorrhage protocol.

Use with intravenous vitamin K, monitor INR response and recognise thromboembolic risk; specialist advice must not create delay in life-threatening bleeding.

Provides sustained restoration of vitamin K-dependent clotting-factor synthesis after the short-lived infused factor correction.

Phytomenadione

Give intravenous vitamin K, commonly 5–10 mg under the major-haemorrhage protocol, at the same time as PCC for warfarin-associated intracerebral haemorrhage.

Administer by the recommended rate with resuscitation readiness for rare reactions; vitamin K alone acts too slowly for emergency reversal.

Specifically binds dabigatran and rapidly reverses its anticoagulant effect during intracranial haemorrhage or emergency intervention.

Idarucizumab

For life-threatening dabigatran-associated bleeding, give 5 g intravenously as two consecutive 2.5 g doses according to the licensed product and local reversal pathway.

Confirm likely recent dabigatran exposure, monitor for rebound where renal impairment or high levels persist, and remember the patient's underlying thrombotic risk.

Reduces ongoing haematoma expansion risk in eligible patients with acute pressure elevation while maintaining cerebral and systemic perfusion.

Intravenous antihypertensive

Use titratable labetalol, nicardipine or the locally approved agent to achieve the acute ICH target gradually with continuous or very frequent pressure monitoring.

Agent choice and target require stroke expertise; avoid systolic hypotension, abrupt falls, bradycardia, bronchospasm and treatment that delays neurosurgical transfer.

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

Expansion and herniation

Early haematoma growth and oedema can abruptly reduce consciousness, compress brainstem structures and cause death during early deterioration.

Intraventricular haemorrhage and hydrocephalus

Blood entering ventricles obstructs cerebrospinal-fluid circulation, increasing pressure and sometimes requiring external drainage for acute pressure control.

Seizures and recurrent bleeding

Cortical blood provokes seizures, while untreated hypertension, amyloid disease or a vascular lesion leaves continuing haemorrhage risk.

Persistent disability and immobility harm

Motor, sensory, language and cognitive injury causes dependence, aspiration, venous thrombosis, pressure damage and prolonged rehabilitation needs.

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

Perform high-frequency GCS, pupil and focal neurological observations in a stroke or neurocritical environment, escalating any decline immediately.
Monitor blood pressure continuously or at short intervals during intravenous therapy and record achieved level and variability, not only the prescription.
Repeat INR after PCC for warfarin, and perform anticoagulant-specific or coagulation reassessment as directed after other reversal treatments.
Review follow-up CT for expansion, intraventricular extension and hydrocephalus, obtaining unscheduled imaging whenever symptoms worsen.
Monitor oxygenation, temperature, glucose, sodium, fluid balance, swallowing, VTE risk and pressure areas throughout immobility.
After discharge, track home and clinic pressure, renal function and adherence and revisit antithrombotic decisions when new imaging or rhythm information emerges.

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

Location suggests cause

Deep haemorrhage favours hypertensive arteriopathy, whereas recurrent lobar bleeding in an older adult raises cerebral amyloid angiopathy, but neither association is absolute.

Normal INR misses DOAC

Routine coagulation tests can appear normal despite clinically relevant factor Xa inhibitor or dabigatran exposure, so the medicine history is indispensable.

Pressure treatment needs a floor

Controlled lowering can limit expansion, but overshooting into hypotension threatens perihaematomal and systemic perfusion and worsens kidney or myocardial injury.

Scores do not set ceilings

An admission prognostic score can describe group risk but should not independently trigger early treatment limitation for an individual patient.

Posterior fossa space is scarce

A cerebellar clot can cause lethal hydrocephalus or brainstem compression at a volume tolerated more easily in a cerebral hemisphere.

Restart is a new decision

The original antithrombotic indication, bleed mechanism and subsequent risk control must be reassessed rather than automatically resuming the same agent on a fixed day.

11Common pitfallsFrequent interpretation and management errors.

01
Do not diagnose ischaemic stroke from the clinical syndrome and give aspirin before urgent imaging has excluded haemorrhage.
02
Do not wait for a routine ward round to reverse active warfarin or dabigatran effect in intracerebral bleeding.
03
Do not use a normal INR to declare that a recent direct oral anticoagulant has no clinically important effect.
04
Do not transfuse platelets routinely solely because the patient took aspirin or clopidogrel before spontaneous ICH.
05
Do not lower pressure abruptly to a normal outpatient value or ignore the lower safety boundary in the acute protocol.
06
Do not postpone neurosurgical referral for deteriorating cerebellar haemorrhage until profound coma develops.
07
Do not use a severity score alone to justify immediate withdrawal of active treatment before stabilisation and specialist assessment.