Stroke due to spontaneous intracerebral haemorrhage

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

INITIAL

suspected intracerebral haemorrhage

1st line – stabilisation and urgent referral to hyperacute or acute stroke unit

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1st line –

stabilisation and urgent referral to hyperacute or acute stroke unit

Manage any airway, breathing, and circulatory insufficiencies requiring urgent treatment. In particular:

Consider endotracheal intubation for patients who are unable to protect their airway or those presenting with a depressed level of consciousness (Glasgow Coma Scale score ≤8 [ Glasgow Coma Scale Opens in new window ] ).[68] This should be done by an anaesthetist or trained emergency department staff.
Give supplemental oxygen only if oxygen saturation drops below 93%.[69] Although the National Institute for Health and Care Excellence (NICE) in the UK recommends starting oxygen only if oxygen saturation drops below 95%, latest evidence suggests that in patients with stroke there are no benefits to initiating oxygen therapy when SpO ₂ is ≥93%, and it may cause harm.[69]
- Monitor controlled oxygen therapy. An upper SpO ₂ limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.
  Evidence suggests that liberal use of supplemental oxygen (target SpO ₂ >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[73]
- A lower target SpO ₂ of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[70]
- Do not routinely give oxygen to people who are not hypoxic.[69]

Evidence: Target oxygen saturation in acutely ill adults

Too much supplemental oxygen increases mortality.

Evidence from a large systematic review and meta-analysis supports conservative/controlled oxygen therapy versus liberal oxygen therapy in acutely ill adults who are not at risk of hypercapnia.

Guidelines differ in their recommendations on target oxygen saturation in acutely unwell adults who are receiving supplemental oxygen. The 2017 British Thoracic Society (BTS) guideline recommends a target SpO ₂ range of 94% to 98% for patients not at risk of hypercapnia, whereas the 2022 Thoracic Society of Australia and New Zealand (TSANZ) guideline recommends 92% to 96%.[70][74]
The Global Initiative For Asthma (GINA) guidelines recommend a target SpO ₂ range of 93% to 96% in the context of an acute exacerbation of asthma.[75]
A systematic review including a meta-analysis of data from 25 randomised controlled trials (RCTs), published in 2018, found that in adults with acute illness, liberal oxygen therapy (broadly equivalent to a target saturation >96%) is associated with higher mortality than conservative oxygen therapy (broadly equivalent to a target saturation ≤96%).[73]
- In-hospital mortality was 11 per 1000 higher for the liberal oxygen therapy versus the conservative therapy group (95% CI 2 to 22 per 1,000 more).
- Mortality at 30 days was also higher in the group who had received liberal oxygen (RR 1.14, 95% CI 1.01 to 1.29).
- The trials included adults with sepsis, critical illness, stroke, trauma, myocardial infarction, and cardiac arrest, and patients who had emergency surgery. Studies that were limited to people with chronic respiratory illness or psychiatric illness, and patients on extracorporeal life support, receiving hyperbaric oxygen therapy, or having elective surgery, were all excluded from the review.
An upper SpO ₂ limit of 96% is therefore reasonable when administering supplemental oxygen to medical with acute illness who are not at risk of hypercapnia. However, a higher target may be appropriate for some specific conditions (e.g., pneumothorax, carbon monoxide poisoning, cluster headache, and sickle cell crisis).[69]
In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis and decided an interim update was not required.[70]
- The committee noted that the systematic review supported the use of controlled oxygen therapy to a target.
- While the systematic review showed an association between higher oxygen saturations and higher mortality, the BTS committee felt the review was not definitive on what the optimal target range should be. The suggested range of 94 to 96% in the review was based on the lower 95% confidence interval and the median baseline SpO ₂ from the liberal oxygen groups, along with the TSANZ guideline recommendation.
Subsequently, experience during the COVID-19 pandemic has also made clinicians more aware of the feasibility of permissive hypoxaemia.[76]
Management of oxygen therapy in patients in intensive care is specialised and informed by further evidence (not covered in this summary) that is more specific to this setting.[77][78][79]

Practical tip

An immediate (i.e., at most within 1 hour of arrival at hospital) non-contrast CT scan of the head confirms the diagnosis of intracerebral haemorrhage by the presence of hyperattenuation suggesting acute blood.[63] See the Diagnosis recommendations section for indications for CT scan in patients with suspected stroke.

Admit anyone with suspected stroke directly to a hyperacute or acute (depending on availability) stroke unit as soon as possible; UK guidelines recommend doing this within 4 hours of presentation to hospital.[55]

On admission, ensure the patient has their swallowing function assessed by appropriately trained staff before being given any oral food, fluid, or medication.[30][55]
Start nutrition support for people who are at risk of malnutrition. Routine nutritional supplementation is not recommended for people who are adequately nourished on admission.[55]

ACUTE

confirmed intracerebral haemorrhage

1st line – supportive care plus monitoring

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1st line –

supportive care plus monitoring

Monitor the patient’s clinical status closely for complications, particularly signs of elevated intracranial pressure and seizures. Provide supportive care as appropriate.[30]

Do not start statin treatment in patients with spontaneous ICH unless required for other indications.[30]

Refer immediately for repeat brain imaging if the patient deteriorates.[30][55]

Level of consciousness

Assess the patient’s level of consciousness using the Glasgow Coma Scale. [ Glasgow Coma Scale Opens in new window ] Monitoring of consciousness should continue once the patient is on the hyperacute or acute stroke unit.[30]

Blood glucose

Monitor blood glucose regularly. Maintain a blood glucose concentration between 4 and 11 mmol/L in people with acute stroke.[55]

Give optimal insulin therapy with intravenous insulin and glucose to all adults with type 1 diabetes with threatened or actual stroke. Follow local protocols.[55]

Blood pressure

Monitor blood pressure intensively and follow recommendations in the rapid blood pressure control treatment option, below.

Oxygen saturation

Give supplemental oxygen only if oxygen saturation drops below 93%.[69] Although the National Institute for Health and Care Excellence (NICE) in the UK recommends starting oxygen only if oxygen saturation drops below 95%, latest evidence suggests that in patients with stroke there are no benefits to initiating oxygen therapy when SpO ₂ is ≥93%, and it may cause harm.[69] Monitor controlled oxygen therapy. An upper SpO ₂ limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.

Evidence suggests that liberal use of supplemental oxygen (target SpO ₂ >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[73]

A lower target SpO ₂ of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[70]

Do not routinely give oxygen to people who are not hypoxic.[69]

Hydration

Assess the patient’s hydration using multiple methods within 4 hours of their arrival at hospital. Review regularly; manage as needed to maintain normal hydration.[30][55]

Cardiac rate and monitoring

Use your clinical judgement to determine the most appropriate method of monitoring cardiac rhythm and rate based on the individual patient and follow your hospital protocol.

Intracranial pressure

Consider monitoring the patient for signs of elevated intracranial pressure (ICP) and treatment if any of the following is present:[23]

Glasgow Coma Scale score ≤8 that is presumed related to haematoma mass effect [ Glasgow Coma Scale Opens in new window ]
Clinical evidence of transtentorial herniation
Significant intraventricular haemorrhage or hydrocephalus.

Refer any patient who develops hydrocephalus to a neurosurgeon.[30][55]

Seizures

Consult immediately with a neurologist if the patient has uncontrolled or recurrent seizures, or status epilepticus. New-onset seizures in the context of spontaneous ICH are relatively common (affecting between 2.8% and 28% of patients); most of these seizures occur within the first 24 hours of the haemorrhage.[23] See Status epilepticus.

Choose an anticonvulsant based on individual patient characteristics.[23] Follow your hospital protocol. In clinical practice, levetiracetam and sodium valproate are commonly used.

Temperature

Monitor temperature.[30] Give an antipyretic (e.g., paracetamol) in patients with high temperature.[85]

Primary options

paracetamol: oral: 500-1000 mg orally every 4-6 hours when required, maximum 4000 mg/day; intravenous (<51 kg body weight): 15 mg/kg intravenously every 4-6 hours when required, maximum 60 mg/kg/day; intravenous (≥51 kg body weight): 1000 mg intravenously every 4-6 hours when required, maximum 4000 mg/day (3000 mg/day if risk factors for hepatotoxicity)

Plus – immediate referral for neurosurgery assessment

Consider – rapid blood pressure control

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Consider –

rapid blood pressure control

Additional treatment recommended for SOME patients in selected patient group

Consider rapid lowering of blood pressure (BP) for patients with ICH who have a systolic BP of 150 to 220 mmHg AND:[55]

Present within 6 hours of symptom onset
Do not have: an underlying structural cause (e.g., tumour, arteriovenous malformation, or aneurysm); a Glasgow Coma Scale score <6; a massive haematoma with poor expected prognosis [ Glasgow Coma Scale Opens in new window ]
Are not going to have early neurosurgery to evacuate the haematoma.

Follow your local protocol for urgent BP lowering in these patients.[30] The National Clinical Guideline for Stroke for the UK and Ireland recommend to aim to achieve a systolic BP of 130-139 mmHg within one hour, to be sustained for at least 7 days.[30]

The European Stroke Organisation recommends to lower blood pressure to 140 mmHg (and to keep it above 110 mmHg) to reduce haematoma expansions in patients with hyperacute (<6 hours) ICH. Their expert consensus concludes decrease of systolic blood pressure should not exceed 90 mmHg from baseline values.[72]

The National Clinical Guideline for Stroke for the UK and Ireland notes there is limited randomised controlled trial evidence regarding intensive blood pressure lowering in patients after ICH with baseline systolic blood pressure greater than 220 mmHg or beyond 6 hours from onset and therefore do not make specific recommendations relating to this group of patients.[30] However, the National Institute for Health and Care Excellence (NICE) in the UK recommends considering rapid BP lowering on a case-by-case basis for patients, taking into account the risk of harm, with acute ICH who have a systolic BP of >220 mmHg OR present beyond 6 hours of symptom onset AND:[55]

Do not have: an underlying structural cause (e.g., tumour, arteriovenous malformation, or aneurysm); a Glasgow Coma Scale score <6; a massive haematoma with poor expected prognosis
Are not going to have early neurosurgery to evacuate the haematoma.

Aim to reach a systolic BP target of 140 mmHg or lower while ensuring that the magnitude drop does not exceed 60 mmHg within 1 hour of starting treatment.[55]

Evidence: Rapid BP lowering

Rapid BP lowering in patients with acute intracerebral haemorrhage and high systolic blood pressure is associated with a reduced risk of haematoma expansion at 24 hours and a possible improved quality of life at 90 days. There are no clear increased harms in most patients, although aggressive protocols should be avoided due to the risk of renal failure.

In 2022, based on new evidence from a pooled individual patient data (IPD) analysis of the multicentre ATACH-2 and INTERACT2 trials, the UK National Institute of Health and Care Excellence (NICE) updated their guidance on the efficacy and safety of lowering BP in people with acute haemorrhagic stroke.[81]

NICE included seven randomised controlled trials (RCTs) (n=5119) in the previous 2019 review with most of the evidence from ATACH-2 (n=1000) and INTERACT2 (n=2829). At the 2022 update they also included three post hoc analyses of the ATACH-2 study and separately considered the combined IPD analysis.[81]
- All trials compared intensive BP therapy with standard BP therapy, although target BP varied between studies and length of treatment ranged from 24 hours to 7 days.
Haematoma expansion was reduced with intensive therapy (6 trials; n=3417; RR 0.82 [95% CI 0.73 to 0.93]; GRADE moderate).
Quality of life at 90 days was better with intensive treatment in the INTERACT2 trial; however, there was no difference in quality of life in the pooled result (2 trials, n=3030, GRADE moderate).
Intensive BP lowering did not affect functional outcomes (modified Rankin Scale 0-2) at 90 days (3 trials; n=3832; RR 1.06 [95% CI 0.99 to 1.13]; absolute risk in control group 44 more per 100, absolute risk in intervention group 47 more per 100 [95% CI 43 fewer to 50 more]; moderate-quality evidence as assessed by GRADE).
There was no clinical difference at 90 days for mortality (7 trials; n=5099; GRADE high), recurrent stroke (3 trials; n=3832; GRADE moderate), or myocardial infarction (1 trial; n=629; GRADE low).
There was no difference at 24 hours in neurological deterioration (5 trials; n=5065, GRADE low) or symptomatic cerebral ischaemia (1 trial; n=201; GRADE low).
There was a possible clinical harm for renal failure at 90 days (4 trials; n=1647; RR 2.07 [95% CI 1.08 to 3.99]; GRADE moderate).
- In three of the studies there was no significant difference in renal failure (although all three had low event rates and wide confidence intervals).
- The ATACH-2 trial, however, used a more aggressive protocol for lowering BP and this was found to increase the risk of renal failure (21/500 with intensive treatment vs. 9/500 with standard treatment; RR 2.33 [95% CI 1.08 to 5.04]).
The IPD analysis showed that the BP target thresholds in the 2019 NICE recommendation may be harmful, as may a very large reduction (>60 mmHg) in blood pressure within the first hour.[81][82] Therefore, in 2022, the guideline committee decided to remove the aim of reaching the target within 1 hour. The committee also noted that:
- Only a third of participants in the INTERACT2 trial achieved the target of 140 mmHg within 1 hour.
- A reduction of more than 60 mmHg within 1 hour was associated with significantly worse outcomes such as renal failure, early neurological deterioration, and death, compared with standard treatment.
- There is sufficient evidence to show that intensive lowering of systolic blood pressure can be safe when using less aggressive protocols, although there is an absence of evidence in clinically frail adults.
TThe 2019 NICE guideline stated that treatment should start within 6 hours and continue for 7 days. However, this timeframe was removed from the 2022 guideline due to weak evidence and concerns about the potential impact on patient flow, bed management, and resource use.
There was limited evidence in people presenting beyond 6 hours of symptom onset and in people with a systolic BP over 220 mmHg at presentation, therefore NICE made a weaker recommendation for these groups.

Consider – urgent reversal of anticoagulation

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Consider –

urgent reversal of anticoagulation

Additional treatment recommended for SOME patients in selected patient group

Urgently reverse abnormalities of clotting, particularly in patients taking anticoagulants.[30][72]

Return clotting levels to normal as soon as possible in people who were on:

Warfarin (and have elevated international normalised ratio [INR]) or another vitamin K antagonist: give a combination of prothrombin complex concentrate (4-factor) and intravenous vitamin K (phytomenadione).[30][55]
Dabigatran: reverse with idarucizumab. If idarucizumab is unavailable, prothrombin complex concentrate (4-factor) may be considered.[30][72]
Factor Xa inhibitor: treat with prothrombin complex concentrate (4-factor).[30][72] Recombinant coagulation factor Xa (andexanet alfa) may be considered in the context of a randomised controlled trial.[30] See Emerging treatments for more information on andexanet alfa.

Primary options

Warfarin/vitamin K antagonist reversal

prothrombin complex concentrate: consult specialist for guidance on dose

and

phytomenadione: consult specialist for guidance on dose

Dabigatran reversal

idarucizumab: consult specialist for guidance on dose

Factor Xa inhibitor reversal

prothrombin complex concentrate: consult specialist for guidance on dose

Consider – venous thromboembolism prophylaxis plus early mobilisation

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Consider –

venous thromboembolism prophylaxis plus early mobilisation

Additional treatment recommended for SOME patients in selected patient group

Give intermittent pneumatic compression within 3 days of admission for the prevention of deep venous thrombosis and pulmonary embolism in immobile patients. Give continuous treatment for 30 days or until the patient is mobile or discharged, whichever is sooner.[30]

Do not routinely give low molecular weight heparin (LMWH) or use graduated compression stockings.[30] However, in practice, consider prophylactic LMWH if intermittent pneumatic compression is contraindicated or not possible.

Arrange assessment of patients with mobilisation difficulties by an appropriately trained healthcare professional as soon as possible. Ensure this assessment is conducted within the first 24 hours of onset to determine the most appropriate and safe methods of transfer and mobilisation.[30] Help the patient to sit out of bed, stand, or walk as soon as their clinical condition permits as part of an active management programme in a specialist stroke unit.[55] Mobilisation typically begins between 24 and 48 hours of stroke onset.[30] If the patient needs help to sit out of bed, stand, or walk, do not provide high-intensity mobilisation in the first 24 hours after symptom onset.[30][55]

High-intensity mobilisation refers to the very early mobilisation intervention from the AVERT trial.[30][97] It includes mobilisation that: begins within the first 24 hours of stroke onset; includes at least three additional out-of-bed sessions compared with usual care; focuses on sitting, standing, and walking (that is, out of bed) activity.

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Stroke due to spontaneous intracerebral haemorrhage

suspected intracerebral haemorrhage

stabilisation and urgent referral to hyperacute or acute stroke unit

Evidence: Target oxygen saturation in acutely ill adults

Practical tip

confirmed intracerebral haemorrhage

supportive care plus monitoring

Level of consciousness

Blood glucose

Blood pressure

Oxygen saturation

Hydration

Cardiac rate and monitoring

Intracranial pressure

Seizures

Temperature

Primary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

immediate referral for neurosurgery assessment

rapid blood pressure control

Evidence: Rapid BP lowering

urgent reversal of anticoagulation

Primary options

Warfarin/vitamin K antagonist reversal

Dabigatran reversal

Factor Xa inhibitor reversal

These drug options and doses relate to a patient with no comorbidities.

Primary options

Warfarin/vitamin K antagonist reversal

Dabigatran reversal

Factor Xa inhibitor reversal

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

Warfarin/vitamin K antagonist reversal

Dabigatran reversal

Factor Xa inhibitor reversal

venous thromboembolism prophylaxis plus early mobilisation

Stroke due to spontaneous intracerebral haemorrhage

Treatment algorithm

suspected intracerebral haemorrhage

stabilisation and urgent referral to hyperacute or acute stroke unit

Evidence: Target oxygen saturation in acutely ill adults

Practical tip

confirmed intracerebral haemorrhage

supportive care plus monitoring

Level of consciousness

Blood glucose

Blood pressure

Oxygen saturation

Hydration

Cardiac rate and monitoring

Intracranial pressure

Seizures

Temperature

Primary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

immediate referral for neurosurgery assessment

rapid blood pressure control

Evidence: Rapid BP lowering

urgent reversal of anticoagulation

Primary options

Warfarin/vitamin K antagonist reversal

Dabigatran reversal

Factor Xa inhibitor reversal

These drug options and doses relate to a patient with no comorbidities.

Primary options

Warfarin/vitamin K antagonist reversal

Dabigatran reversal

Factor Xa inhibitor reversal

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

Warfarin/vitamin K antagonist reversal

Dabigatran reversal

Factor Xa inhibitor reversal

venous thromboembolism prophylaxis plus early mobilisation