01Core principlesThe concepts and mechanisms needed to understand the subject.
Primary spontaneous ICH commonly arises from rupture of small arteries affected by hypertensive arteriopathy or cerebral amyloid angiopathy. Deep perforator territories include basal ganglia, thalamus, pons and cerebellum; amyloid angiopathy more often produces lobar haemorrhage in older adults. Secondary causes include arteriovenous malformation, aneurysm, dural fistula, cavernoma, cerebral venous thrombosis, tumour, vasculitis, sympathomimetic drugs and haemostatic disorders. Location suggests possibilities but never proves aetiology.
Injury develops through the initial mechanical disruption, haematoma expansion, surrounding oedema, inflammation, intraventricular blood and raised pressure. Expansion is most likely early, making onset time, antithrombotic status, blood pressure and repeat examination consequential. A small strategically located pontine bleed can be devastating, while a larger lobar collection may initially spare consciousness; volume alone cannot replace anatomy and trajectory.
Evidence contains important boundaries. The 2025 ESO/EANS guideline supports early smooth blood-pressure reduction most clearly in minor-to-moderate ICH below 30 mL, while cautioning about very high presenting pressure, large clots, planned evacuation and excessive falls. Its reversal recommendations are drug-specific and not equivalent to UK authorisation or commissioning. Surgery may be life-saving for obstructive hydrocephalus or selected cerebellar disease, but routine open evacuation for every supratentorial ICH is not justified.
Key points
- Spontaneous ICH is bleeding into brain parenchyma without trauma; keep it separate from traumatic contusion, aneurysmal SAH, haemorrhagic transformation of infarction and extra-axial bleeding.
- Non-contrast CT confirms blood and defines location, volume, intraventricular extension, hydrocephalus and mass effect. Repeat CT is driven by early expansion risk and any neurological decline.
- Deep basal-ganglia, thalamic, pontine or cerebellar bleeding often reflects small-vessel arteriopathy; lobar bleeding broadens the differential to cerebral amyloid angiopathy, macrovascular lesions, tumour, venous disease and drug-associated causes.
- NICE says to consider rapid lowering when acute ICH presents within 6 hours with systolic BP 150–220 mmHg: aim for 140 mmHg or lower, but do not drop more than 60 mmHg in the first treatment hour. Separately, ESO/EANS suggests below 140 mmHg within 6 hours only for adults with minor or moderate ICH under 30 mL, avoiding a fall over 70 mmHg or active reduction below 110 mmHg and using caution above 220 mmHg, with larger clots or planned evacuation.
- Stop antithrombotics and use an agent-specific specialist pathway: VKA ICH needs four-factor PCC plus IV vitamin K and adult dabigatran life-threatening bleeding uses idarucizumab 5 g. Do not use andexanet routinely class-wide: its adult licence covers life-threatening or uncontrolled apixaban/rivaroxaban bleeding, not edoxaban; NICE TA697 commissioning is restricted to gastrointestinal bleeding, and BSH April 2026 warns that thrombotic and stroke risk may outweigh benefit.
- Surgery is diagnosis-, location- and patient-specific. Hydrocephalus with reduced consciousness supports EVD; 2025 ESO/EANS suggests cerebellar evacuation above 15 mL for survival, while supratentorial strategies carry weaker, selected evidence.
02Mechanisms and patternsImportant relationships and how to distinguish them.
Sudden hemiparesis, hemisensory loss, aphasia, neglect, ataxia, vertigo, gaze deviation or dysarthria can resemble ischaemic stroke. Headache, vomiting, seizure and reduced consciousness increase suspicion of haemorrhage but imaging is required.
Record last known well, witnessed onset, pre-hospital change, GCS and NIHSS-compatible findings. New deterioration after the first scan may represent expansion, intraventricular extension, hydrocephalus, seizure, hypoxia or systemic instability.
Putaminal haemorrhage often causes contralateral weakness with gaze toward the lesion; thalamic disease may cause sensory loss and ocular signs; pontine bleeding can produce coma and small reactive pupils; cerebellar bleeding causes headache, vomiting, ataxia and brainstem compression. These patterns overlap.
Young age, no hypertension, lobar or unusual location, prodromal headache, malignancy, infection, pregnancy, stimulant exposure or a vascular bruit lowers the threshold for CTA, venography, MRI or catheter angiography.
Identify vitamin K antagonist, direct thrombin inhibitor, factor Xa inhibitor, heparin and antiplatelet therapy separately. Record dose, last ingestion, renal function, indication and relevant assays; do not wait for a complete panel before specialist reversal action.
Age, GCS, volume, infratentorial origin and intraventricular extension inform the ICH score, but calibration varies and historical cohorts predate current stroke-unit care. Reassess after stabilisation before using prognosis in shared decisions.
03Interpreting evidenceInformation, measurements and their limitations.
Consider the information, its meaning and its limitations before deciding what follows.
- 01
Immediate non-contrast CT head - Why
- Differentiate ICH from ischaemic stroke and define the anatomical threat.
- Interpretation and limitations
- Describe location, estimated volume, intraventricular extension, hydrocephalus, midline shift, basal cisterns and signs of herniation. Look for subarachnoid blood, mass or venous pattern that redirects the diagnosis.
- 02
Repeat non-contrast CT - Why
- Detect haematoma expansion or new hydrocephalus during the high-risk early course and after deterioration.
- Interpretation and limitations
- Compare volume, ventricular blood, shift and cisterns with the baseline scan. Neurological decline should prompt urgent repeat imaging even if the initial clot appeared small.
- 03
CT angiography with cause-directed MRI, venography or catheter angiography - Why
- Find a macrovascular, venous, neoplastic or other secondary cause in an appropriate phenotype.
- Interpretation and limitations
- The DIAGRAM approach combines age, location, small-vessel-disease signs and CTA result to estimate macrovascular probability, but external validation was only moderate before CTA. A negative test does not end investigation when suspicion remains high.
- 04
Full blood count, glucose, electrolytes, renal and liver function, PT/INR, APTT and agent-relevant assays - Why
- Identify physiological mimics, organ dysfunction and haemostatic factors that alter treatment.
- Interpretation and limitations
- INR guides vitamin K antagonist reversal, but PT or APTT cannot reliably quantify every direct anticoagulant. Interpret a drug level or anti-Xa assay only with its calibrated agent, sampling time and local laboratory capability.
- 05
Serial neurological and physiological monitoring - Why
- Recognise expansion, seizure, pressure crisis and complications of blood-pressure or haemostatic treatment.
- Interpretation and limitations
- Trend GCS components, focal signs, pupils, blood pressure and variability, oxygenation, temperature and glucose. A smooth target trajectory matters; hypotension, a large rapid fall or worsening examination triggers immediate review.
04Applied reasoningWorked examples connecting principles to decisions.
01Worked case: first-hour ICH careAcute focal deficit with CT-confirmed ICHAn adult presents within hours with spontaneous parenchymal haemorrhage and no trauma.+
- 1Activate stroke and neurocritical teams, stabilise airway and oxygenation, obtain immediate CT, record exact onset, GCS, focal deficit, baseline function, blood pressure and all antithrombotic exposure.
- 2Classify location, volume, ventricular extension, hydrocephalus and mass effect; send core bloods, stop antithrombotics and seek haematology input. Use four-factor PCC plus IV vitamin K for VKA-associated ICH and idarucizumab 5 g for adult dabigatran-associated life-threatening bleeding. For factor-Xa exposure, make an agent-specific specialist decision: andexanet is licensed in adults for life-threatening or uncontrolled apixaban/rivaroxaban bleeding, not edoxaban; NICE TA697 commissioning is restricted to gastrointestinal bleeding, and the April 2026 BSH position warns that thrombosis and ischaemic-stroke risk may outweigh benefit, so it is not routine class-wide ICH reversal.
- 3Apply the exact NICE blood-pressure rule only when its conditions fit: consider rapid lowering for acute ICH presenting within 6 hours with systolic BP 150–220 mmHg, aiming for 140 mmHg or lower without a fall greater than 60 mmHg in the first treatment hour. Separately, ESO/EANS suggests below 140 mmHg within 6 hours for adults with minor or moderate ICH under 30 mL, avoiding a fall over 70 mmHg or active reduction below 110 mmHg and using caution above 220 mmHg, in larger clots or when evacuation is planned.
- 4Discuss immediately with neurosurgery for posterior-fossa bleeding, hydrocephalus with impaired consciousness, herniation, progressive decline or a potentially treatable selected supratentorial lesion.
- 5Repeat examination and CT according to early risk and any change, then investigate the cause through vascular or MRI pathways when phenotype warrants it.
02Neurosurgical emergencyIVH, hydrocephalus or cerebellar compressionICH extends into ventricles with obstructive hydrocephalus and reduced consciousness, or a cerebellar clot causes brainstem compression or deterioration.+
- 1Escalate immediately to neurosurgery and neurocritical care while protecting airway, perfusion and ventilation; repeat CT if the clinical state has changed.
- 2Use EVD for intraventricular blood with hydrocephalus contributing to impaired consciousness; in cerebellar ICH, assess clot volume, compression and the need for evacuation rather than relying on drainage alone.
- 3Continue cause-specific haemostasis and monitoring because CSF diversion does not stop the original bleeding source.
03Aetiology pathwayPossible secondary ICHAge, location, history or CT features are atypical for small-vessel arteriopathy.+
- 1Perform CTA promptly when appropriate and select venography, MRI or catheter angiography with neuroradiology based on suspected malformation, venous thrombosis, tumour or other cause.
- 2If initial vascular imaging is negative but pre-test probability remains high, agree delayed or alternative imaging rather than labelling the event primary by exclusion.
- 3Carry the established cause into secondary prevention, genetic or family assessment and follow-up rather than defaulting every survivor to a hypertension-only plan.
05Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.
- Use frequent GCS, pupil and focal-neurology checks with continuous cardiorespiratory monitoring during the acute phase.
- Chart blood pressure continuously or at short intervals, including treatment start, rate of fall, variability and any renal or neurological adverse effect.
- Repeat CT for clinical decline and according to the stroke service’s expansion-risk protocol; compare ventricular extension and hydrocephalus as well as parenchymal volume.
- After any reversal strategy, monitor haemostasis, thrombosis, renal function and the need and timing for restarting thromboprophylaxis or long-term antithrombotics.
- Screen swallowing before oral intake, prevent aspiration and immobility complications, manage fever and glucose, and begin multidisciplinary rehabilitation when stable.
06Special situationsVariants, exceptions and circumstances that change the usual approach.
Location guides, not proves
A deep clot supports hypertensive arteriopathy and a lobar clot supports amyloid or secondary disease, but vascular and drug-related causes can occur in either.
Expansion is a process
A CT is one time point. Worsening deficit or consciousness after imaging demands a search for growth, IVH, hydrocephalus and seizure.
Pressure targets have edges
Trial populations mainly had minor-to-moderate volumes. Severe, very large, very hypertensive or operative patients need individual perfusion-aware decisions.
EVD has one job
Ventricular drainage can relieve obstructive hydrocephalus; it neither evacuates a parenchymal clot nor guarantees recovery.
A score cannot set a ceiling
Prognostic scores communicate severity and support audit, but early self-fulfilling treatment limitation can distort their apparent accuracy.
07Common pitfallsFrequent interpretation and management errors.
- 01
Calling an ICH hypertensive from location alone without considering macrovascular, venous, tumour and drug-associated causes.
- 02
Using one blood-pressure number without stating onset time, initial SBP, haematoma volume, perfusion and surgical context.
- 03
Assuming a normal PT or APTT excludes clinically important direct anticoagulant activity.
- 04
Treating EVD as complete management of intraventricular extension or cerebellar mass effect.
- 05
Applying traumatic acute SDH or aneurysmal SAH operative and medical rules to spontaneous ICH.
- 06
Using the ICH score alone to withdraw active care or deny neurosurgical review.