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Practice Guideline
. 2025 Dec;10(4):1007-1086.
doi: 10.1177/23969873251340815. Epub 2025 May 22.

European Stroke Organisation (ESO) and European Association of Neurosurgical Societies (EANS) guideline on stroke due to spontaneous intracerebral haemorrhage

Thorsten Steiner  1   2 , Jan C Purrucker  2 , Diana Aguiar de Sousa  3   4   5 , Trine Apostolaki-Hansson  6 , Jürgen Beck  7 , Hanne Christensen  8 , Charlotte Cordonnier  9 , Matthew B Downer  10   11 , Helle Eilertsen  12   13 , Rachael Gartly  14 , Stefan T Gerner  15 , Leonard Ho  16   17 , Silje Holt Jahr  12   18 , Catharina Jm Klijn  19 , Nicolas Martinez-Majander  20 , Kateriine Orav  21 , Jesper Petersson  22 , Andreas Raabe  23 , Else Charlotte Sandset  24 , Floris H Schreuder  19 , David Seiffge  25 , Rustam Al-Shahi Salman  26
Affiliations
Practice Guideline

European Stroke Organisation (ESO) and European Association of Neurosurgical Societies (EANS) guideline on stroke due to spontaneous intracerebral haemorrhage

Thorsten Steiner et al. Eur Stroke J. 2025 Dec.

Abstract

Spontaneous (non-traumatic) intracerebral haemorrhage (ICH) affects ~3.4 million people worldwide each year, causing ~2.8 million deaths. Many randomised controlled trials and high-quality observational studies have added to the evidence base for the management of people with ICH since the last European Stroke Organisation (ESO) guidelines for the management of spontaneous ICH were published in 2014, so we updated the ESO guideline. This guideline update was guided by the European Stroke Organisation (ESO) standard operating procedures for guidelines and the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework, in collaboration with the European Association of Neurosurgical Societies (EANS). We identified 37 Population, Intervention, Comparator, Outcome (PICO) questions and prioritised clinical outcomes. We conducted systematic literature searches, tailored to each PICO, seeking randomised controlled trials (RCT) - or observational studies when RCTs were not appropriate, or not available - that investigated interventions to improve clinical outcomes. A group of co-authors allocated to each PICO screened titles, abstracts, and full texts and extracted data from included studies. A methodologist conducted study-level meta-analyses and created summaries of findings tables. The same group of co-authors graded the quality of evidence, and drafted recommendations that were reviewed, revised and approved by the entire group. When there was insufficient evidence to make a recommendation, each group of co-authors drafted an expert consensus statement, which was reviewed, revised and voted on by the entire group. The systematic literature search revealed 115,647 articles. We included 208 studies. We found strong evidence for treatment of people with ICH on organised stroke units, and secondary prevention of stroke with blood pressure lowering. We found weak evidence for scores for predicting macrovascular causes underlying ICH; acute blood pressure lowering; open surgery via craniotomy for supratentorial ICH; minimally invasive surgery for supratentorial ICH; decompressive surgery for deep supratentorial ICH; evacuation of cerebellar ICH > 15 mL; external ventricular drainage with intraventricular thrombolysis for intraventricular extension; minimally invasive surgical evacuation of intraventricular blood; intermittent pneumatic compression to prevent proximal deep vein thrombosis; antiplatelet therapy for a licensed indication for secondary prevention; and applying a care bundle. We found strong evidence against anti-inflammatory drug use outside of clinical trials. We found weak evidence against routine use of rFVIIa, platelet transfusions for antiplatelet-associated ICH, general policies that limit treatment within 24 h of ICH onset, temperature and glucose management as single measures (outside of care bundles), prophylactic anti-seizures medicines, and prophylactic use of temperature-lowering measures, prokinetic anti-emetics, and/or antibiotics. New evidence about the management of ICH has emerged since 2014, enabling this update of the ESO guideline to provide new recommendations and consensus statements. Although we made strong recommendations for and against a few interventions, we were only able to make weak recommendations for and against many others, or produce consensus statements where the evidence was insufficient to guide clinical decisions. Although progress has been made, many interventions still require definitive, high-quality evidence, underpinning the need for embedding clinical trials in routine clinical practice for ICH.

Keywords: Guideline; intracerebral haemorrhage; stroke; systematic review.

Plain language summary

BackgroundEvery year, around 3.4 million people have a type of stroke caused by bleeding in the brain that is not due to injury or another medical condition. The main causes of this kind of stroke include getting older, health issues like high blood pressure, and being exposed to air pollution. However, doctors and researchers are learning more and more about how to treat and prevent this condition, helping patients recover better and reducing the chances of it happening again. This guideline is an update of the last European Stroke Organisation guideline for people with bleeding in the brain, published in 2014.How We Created This GuideTo make sure this guide is based on the best available evidence, we followed a structured process recommended by the European Stroke Organisation (ESO) and the European Association of Neurosurgical Societies (EANS). We focused on finding the highest quality evidence about what care works best for patients with bleeding in the brain, and made recommendations guided by a framework called GRADE.We started with 37 important questions about care for people with stroke due to bleeding in the brain. To answer these, we looked at thousands of research papers and focused on the best available studies, especially ones where a treatment was compared reliably with an alternative. If there was not enough strong evidence to form a recommendation for clinical practice, we used expert opinions to create a consensus about a statement to guide clinical practice.What We FoundAfter looking at 115,647 studies, our findings for people with bleeding in the brain were:• What works best: We found strong evidence that patients get better when treated in specialized stroke units, and when their blood pressure is reduced to prevent more strokes.• What might help: There is weaker evidence supporting certain treatments, such as using scores to predict the cause of bleeding, early lowering of blood pressure, early use of some drugs to promote blood clotting, surgery to remove the bleeding (including approaches that use only a small hole in the skull), surgery to decompress the skull, drainage of blood in the fluid around the brain with a clot-busting drug, prevention of clots in veins by compression devices, and restarting blood-thinning medications for those who need them. There is also weaker evidence for patients getting better when a care bundle is used. These types of care require further study.• What should be avoided: We found strong evidence that anti-inflammatory drugs should not be used unless it’s part of a research study.• What might not help: We found weaker evidence against routine policies to limit treatment, controlling body temperature, controlling blood sugar, and routine treatment to prevent seizures, as well as evidence against giving a platelet transfusion (a type of blood product).• Uncertain areas: We did not find enough reliable evidence about tests to look for causes of bleeding, scores to predict outcome, early use of several drugs to promote blood clotting, surgery with drainage of fluid with a clot-busting drug, drainage of blood in the fluid around the brain, brain pressure monitoring, blood thinning drugs to prevent clots in veins, routine use of medicine to prevent seizures, blood thinning drugs and devices to prevent strokes and heart attacks for people with an irregular heartbeat, and statins to prevent strokes and heart attacks. In these cases, we provide expert opinions to help guide medical decisions and encourage more reliable research to be done.Why This MattersThis guideline summarises the best available evidence and expert opinions, to inform the care of people with stroke due to bleeding in the brain. This guideline may help doctors and other healthcare professionals to improve care for people with bleeding in the brain. Although a lot of progress has been made since the last edition of this guideline, more large, reliable, definitive clinical trials are needed to identify ways of improving outcome after bleeding in the brain.

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Conflict of interest statement

Declaration of conflicting interestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Intellectual and financial disclosures of the module working group members are presented in Supplemental Table.

Figures

Graphical abstract
Graphical abstract
Figure 1.
Figure 1.
Percent of total DALYs lost to intracerebral haemorrhage by country in 2021.
Figure 2.
Figure 2.
Effect on good functional outcome (mRS 0–2) at 3–6 months after intensive blood pressure lowering with any vasodepressor drug (note: some trials allowed use of non-vasodepressor blood-pressure lowering-drugs) compared with control in adults with acute intracerebral haemorrhage.
Figure 3.
Figure 3.
Effect on good functional outcome (mRS 0–2) at 3–6 months of intensive blood pressure (BP) lowering with any vasodepressor drug (note: some trials allowed use of non-vasodepressor blood-pressure lowering-drugs) compared with control following symptom onset in subgroups of adults with acute intracerebral haemorrhage stratified by time to treatment. This included trials enrolling patients within 6 h, those enrolling within 24 h (excluding trials enrolling patients within 6 h), and studies involving treatment within 72 h (excluding trials enrolling within 24 h).
Figure 4.
Figure 4.
Effect on death within 3–6 months of intensive blood pressure (BP) lowering with any vasodepressor drug (note: some trials allowed use of non-vasodepressor blood-pressure lowering-drugs) compared with control in adults with acute intracerebral haemorrhage.
Figure 5.
Figure 5.
Effect on death within 3–6 months following symptom onset in subgroups of adults with spontaneous ICH stratified by time to treatment of intensive blood pressure (BP) lowering with any vasodepressor drug (note: some trials allowed use of non-vasodepressor blood-pressure lowering-drugs) compared with control. This included trials enrolling patients within 6 h, those enrolling within 24 h (excluding trials enrolling patients within 6 h), and studies involving treatment within 72 h (excluding trials enrolling within 24 h).
Figure 6.
Figure 6.
Effect on haematoma expansion of intensive blood pressure (BP) lowering with any vasodepressor drug (note: some trials allowed use of non-vasodepressor blood-pressure lowering-drugs) compared with control in adults with acute intracerebral haemorrhage.
Figure 7.
Figure 7.
The effect on haematoma expansion in subgroups stratified by time to treatment of intensive blood pressure (BP) lowering with any vasodepressor drug (note: some trials allowed use of non-vasodepressor blood-pressure lowering-drugs) compared with control in adults with spontaneous ICH. This included studies enrolling patients within 6 h and those enrolling within 24 h (excluding trials enrolling within 6 h).
Figure 8.
Figure 8.
Effect on death or dependence (mRS 4–6) at day 90 of rFVIIa or placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 9.
Figure 9.
Effect on death from any cause by day 90 of rFVIIa versus placebo/open control for adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 10.
Figure 10.
Effect on haematoma expansion by 24 h of rFVIIa or placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 11.
Figure 11.
Effect on thromboembolic adverse events of rFVIIa or placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 12.
Figure 12.
Effect on Death or dependence (mRS 4–6) at day 90 of tranexamic acid versus placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 13.
Figure 13.
Effect on death from any cause by day 90 of tranexamic acid versus placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 14.
Figure 14.
Effect on Death from any cause by day 7 of tranexamic acid versus placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 15.
Figure 15.
Effect on haematoma expansion by 24 h of tranexamic acid versus placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 16.
Figure 16.
Effect on thromboembolic adverse events of tranexamic acid versus placebo/open control in adults with spontaneous ICH not associated with antithrombotic drug use.
Figure 17.
Figure 17.
Effect on death or dependence (mRS 4–6) at day 90 of platelet transfusion versus open control in adults with spontaneous ICH associated with antiplatelet drug use.
Figure 18.
Figure 18.
Effect on death by day 90 of platelet transfusion versus open control in adults with spontaneous ICH associated with antiplatelet drug use.
Figure 19.
Figure 19.
Effect on haematoma expansion of spontaneous ICH associated with antiplatelet drug use treated with platelet transfusion versus open control.
Figure 20.
Figure 20.
Effect on thromboembolic adverse events of platelet transfusion versus open control in adults with spontaneous ICH associated with antiplatelet drug use.
Figure 21.
Figure 21.
Effect on death at day 90 of desmopressin versus placebo for adults with spontaneous ICH associated with antiplatelet drug use.
Figure 22.
Figure 22.
Effect on death or dependence at day 90 of desmopressin versus placebo for adults with spontaneous ICH associated with antiplatelet drug use.
Figure 23.
Figure 23.
Effect on haematoma expansion at 24 h of desmopressin versus placebo for adults with spontaneous ICH associated with antiplatelet drug use.
Figure 24.
Figure 24.
Effect on thromboembolic events of desmopressin versus placebo for adults with spontaneous ICH associated with antiplatelet drug use.
Figure 25.
Figure 25.
Effect on death of any cause by day 90 of PCC versus FFP for ICH associated with vitamin K-antagonist use.
Figure 26.
Figure 26.
Effect on death or dependence (mRS 4–6) at 90 days of PCC versus FFP for ICH associated with vitamin K-antagonist use.
Figure 27.
Figure 27.
Effect on haematoma expansion by 24 of PCC versus FFP for ICH associated with vitamin K-antagonist use.
Figure 28.
Figure 28.
Effect on death by day 30 of andexanet alfa compared with standard care in adults with ICH associated with use of FXaI (intention-to-treat extended population).
Figure 29.
Figure 29.
Effect on death or dependence (mRS 4–6) at day 30 of andexanet alfa compared with standard care in adults with ICH associated with use of FXaI (intention-to-treat extended population).
Figure 30.
Figure 30.
Effect on haematoma expansion ⩽ 35% by 12 h of andexanet alfa compared with standard care in adults with ICH associated with use of FXaI (data from the Efficacy Analysis Extended Population of the ANNEXA-I trial).
Figure 31.
Figure 31.
Effect on thromboembolic adverse events of andexanet alfa compared with standard care in adults with ICH associated with use of FXaI (intention-to-treat extended population).
Figure 32.
Figure 32.
Effect on death at 3–12 months of surgery aimed at haematoma removal compared with no surgery in adult people with acute spontaneous supratentorial ICH.
Figure 33.
Figure 33.
The effect on 3–12 months good functional outcome of surgery aimed at haematoma removal compared with no surgery in adult people with acute spontaneous supratentorial ICH.
Figure 34.
Figure 34.
The effect on death at 3–12 months of surgery aimed at haematoma removal by means of craniotomy and open standard surgical technique compared with no surgery in adults with acute spontaneous supratentorial ICH.
Figure 35.
Figure 35.
The effect on good functional outcome (mRS 0–3) of surgery aimed at haematoma removal by means of craniotomy and open standard surgical technique compared with no surgery on 3–12 months in adults with acute spontaneous supratentorial ICH.
Figure 36.
Figure 36.
The effect on functional outcome of minimally invasive surgical removal compared with no surgery in adults with acute spontaneous supratentorial.
Figure 37.
Figure 37.
The effect on death of minimally invasive surgical removal compared with no surgery in adults with acute spontaneous supratentorial ICH.
Figure 38.
Figure 38.
The effect on death at 6–12 months of surgery with catheter placement plus thrombolysis compared with no surgery in adults with acute spontaneous supratentorial ICH.
Figure 39.
Figure 39.
The effect on good functional outcome at 6–12 months of surgery with catheter placement plus thrombolysis compared with no surgery in adult people with acute spontaneous supratentorial ICH.
Figure 40.
Figure 40.
The effect on death at 6 months of decompressive craniectomy without haematoma removal compared with no surgery in adult people with acute spontaneous deep, severe ICH.
Figure 41.
Figure 41.
The effect on good functional outcome (mRS 0–4) at 6 months of decompressive craniectomy without haematoma removal compared with no surgery in adult people with acute spontaneous deep, severe ICH.
Figure 42.
Figure 42.
The effect on death of external ventricular drainage with intraventricular thrombolysis versus external ventricular drainage without intraventricular thrombolysis in adult people with acute spontaneous ICH and intraventricular extension.
Figure 43.
Figure 43.
The effect on good functional outcome of external ventricular drainage with intraventricular thrombolysis versus external ventricular drainage without intraventricular thrombolysis in adult people with acute spontaneous ICH and intraventricular extension.
Figure 44.
Figure 44.
The effect on shunt dependence of external ventricular drainage with intraventricular thrombolysis versus external ventricular drainage without intraventricular thrombolysis in adult people with acute spontaneous ICH and intraventricular extension.
Figure 45.
Figure 45.
The effect on death at 1–6 months of surgical removal of the intraventricular blood compared with no surgical removal of intraventricular blood in adult people with acute spontaneous ICH and intraventricular extension of the haemorrhage.
Figure 46.
Figure 46.
The effect on functional outcome at 2–6 months of surgical removal of the intraventricular blood compared with no surgical removal of intraventricular blood in adult people with acute spontaneous ICH and intraventricular extension of the haemorrhage.
Figure 47.
Figure 47.
The effect on shunt dependence at 1–6 months of surgical removal of the intraventricular blood compared with no surgical removal of intraventricular blood in adult people with acute spontaneous ICH and intraventricular extension of the haemorrhage.
Figure 48.
Figure 48.
The effect on death at 3 and 12 months of surgical haematoma evacuation compared with no surgery in adult people with acute cerebellar ICH.
Figure 49.
Figure 49.
The effect on functional outcome at 3 months of surgical haematoma evacuation compared with no surgery in adult people with acute cerebellar ICH.
Figure 50.
Figure 50.
Prevention of deep venous thrombosis by physical interventions versus routine care (follow-up: 30 days).
Figure 51.
Figure 51.
Prevention of pulmonary embolism by physical interventions versus routine care (follow-up: 30 days).
Figure 52.
Figure 52.
Prevention of death by physical interventions versus routine care (follow-up: 30 days).
Figure 53.
Figure 53.
Prevention of death by short-term anticoagulation versus routine care for (follow-up: range 10 days–90 days).
Figure 54.
Figure 54.
Prevention of symptomatic or asymptomatic venous thrombosis by short-term anticoagulation versus routine care for (follow-up: range 10 days–21 days).
Figure 55.
Figure 55.
Prevention of symptomatic or asymptomatic pulmonary embolism by short-term anticoagulation versus routine care (follow-up: range 10 days–90 days).
Figure 56.
Figure 56.
Risk of recurrent intracerebral haemorrhage by short-term anticoagulation versus routine care (follow-up range: up to 10 days).
Figure 57.
Figure 57.
Effect on death of corticosteroids versus control in adults with acute ICH (follow-up: range at discharge to 6 months).
Figure 58.
Figure 58.
Effects on death of deferoxamine versus control in acute ICH.
Figure 59.
Figure 59.
Effects on good functional outcome of deferoxamine treatment versus routine care in acute ICH (follow-up 21 days–6 months).
Figure 60.
Figure 60.
Effects on the occurrence of clinical seizures of anti-seizure treatment versus control in acute ICH (follow-up: range 3–12 months).
Figure 61.
Figure 61.
Effect on death of primary prophylactic anti-seizure treatment versus control in acute ICH (follow-up: range 3–12 months).
Figure 62.
Figure 62.
Effects on good functional outcome (mRS 0–2) of an implementation of a care-bundle versus standard management (follow-up: range 3–6 months).
Figure 63.
Figure 63.
Effects on deaths of an implementation of a care-bundle versus standard management (follow-up: range 30 days–6 months).
Figure 64.
Figure 64.
Effect on recurrence of any stroke after ICH of applying versus not applying an intensive antihypertensive treatment in adults with an acute ICH beyond the acute period. (Post-hoc/sub-group analysis)
Figure 65.
Figure 65.
Effect on ICH recurrence of intensive blood pressure control versus standard blood pressure control in adults with acute ICH beyond the acute period.,
Figure 66.
Figure 66.
Effects on death of restarting oral anticoagulant therapy compared with avoiding oral anticoagulation in adults with ICH and NVAF.
Figure 67.
Figure 67.
Effect of major adverse cardiovascular events of restarting oral anticoagulant therapy compared with avoiding oral anticoagulation in adults with ICH and NVAF.
Figure 68.
Figure 68.
Effects on recurrent ICH of restarting oral anticoagulant therapy compared with avoiding oral anticoagulation in adults with ICH and AF.
Figure 69.
Figure 69.
Effects on recurrent ICH of restarting antiplatelet therapy compared with avoiding antiplatelet therapy in adults with ICH.
Figure 70.
Figure 70.
Effects of Major occlusive vascular events of restarting antiplatelet therapy compared with avoiding antiplatelet therapy in people with ICH.
Figure 71.
Figure 71.
Effects on death of restarting antiplatelet therapy compared with avoiding antiplatelet therapy in people with ICH.
Figure 72.
Figure 72.
Effect on death of statins versus no statins in observational studies in people with ICH.
Figure 73.
Figure 73.
Effect on major vascular events of statins versus no statins of observational studies and a sub-study of the SPARCL trial in people with ICH.
Figure 74.
Figure 74.
Effects on recurrence of ICH of statins versus no statins in observational studies and a sub-study of the SPARCL trial in people with ICH.
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