Stroke Due To Spontaneous Intracerebral Haemorrhage FM

Stroke due to spontaneous
intracerebral haemorrhage
Straight to the point of care
Last updated: Oct 12, 2022

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Risk factors 4
Aetiology 6
Pathophysiology 7
Classification 8
Case history 8
Diagnosis 10
Recommendations 10
History and exam 19
Investigations 22
Differentials 25
Criteria 26
Management 27
Recommendations 27
Treatment algorithm overview 44
Treatment algorithm 45
Emerging 57
Primary prevention 57
Secondary prevention 58
Patient discussions 58
Follow up 59
Monitoring 59
Complications 60
Prognosis 61
Guidelines 62
Diagnostic guidelines 62
Treatment guidelines 63
Evidence tables 64
References 66
Images 74
Disclaimer 75
Stroke due to spontaneous intracerebral haemorrhage Overview
Summary
Stroke due to spontaneous intracerebral haemorrhage is an emergency.
“Time is brain”. If you suspect stroke, work rapidly through the initial assessment and aim for quick access
OVERVIEW
to computed tomography (CT) scan. CT enables quick differentiation between ischaemic stroke and
spontaneous intracerebral haemorrhage (ICH), which must be done before reversing anticoagulation in
anticoagulation-induced ICH and before starting thrombolysis in ischaemic stroke. Both are critical and
urgent interventions.
Use a validated tool to aid recognition: use ROSIER (Recognition of Stroke in the Emergency Room) in the
emergency department; use FAST (Face Arm Speech Test) in the community.
Manage any airway, breathing, and circulatory insufficiencies requiring urgent treatment.
Request an immediate non-enhanced CT scan (i.e., ideally in the next available time slot and definitely
within 1 hour of arrival at hospital) if indicated. A CT-scan will confirm the diagnosis of ICH (i.e., presence of
hyperattenuation suggesting acute blood).
Prioritise rapid admission of the patient directly to a hyperacute or acute stroke unit (UK guidelines
recommend doing this within 4 hours of presentation to hospital); review by a neurosurgeon; reversal of
clotting abnormalities, if indicated; lowering of blood pressure, if indicated.
Definition
The World Health Organization defines stroke as “a clinical syndrome consisting of rapidly developing clinical
signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with
no apparent cause other than that of vascular origin".[1]
Stroke can be subdivided into ischaemic stroke (caused by vascular occlusion or stenosis) and haemorrhagic
stroke (caused by vascular rupture, resulting in intracerebral [intraparenchymal], subarachnoid, or
intraventricular haemorrhage). Central venous sinus thrombosis is a rare form of stroke that occurs due to
thrombosis of the dural venous sinuses.
Most intracerebral haemorrhages occur in the absence of vascular malformations, aneurysms, or

other structural causes, and are presumed to be due to diseases affecting small cerebral vessels
(arteriolosclerosis or cerebral amyloid angiopathy); this is often called primary intracerebral haemorrhage
(ICH) but this term discourages adequate investigation and accurate diagnosis so is not recommended. ICH
from an identifiable vascular malformation or as a complication of other medical or neurological diseases that
either impair coagulation or promote vascular rupture is termed secondary ICH.
This topic focuses on the first 24 hours of acute care of patients with a stroke due to spontaneous ICH. For
information on other types of stroke, see Ischaemic stroke , Subarachnoid haemorrhage , and Cavernous
sinus thrombosis .
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Oct 12, 2022.
BMJ Best Practice topics are regularly updated and the most recent version
3
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2023. All rights reserved.
Stroke due to spontaneous intracerebral haemorrhage Theory
Epidemiology
There are more than 100,000 strokes in the UK each year causing 38,000 deaths, making it a leading cause
of death and disability.[4] [5] [6] People are most likely to have a stroke over the age of 55.[7] [6] Stroke is the
THEORY
second largest cause of death globally (5.5 million deaths) after ischaemic heart disease.[8]
In 2017, the global prevalence of stroke was 104.2 million people; that of ischaemic stroke was 82.4 million
people and intracerebral haemorrhage (ICH) 17.9 million people.[9]
The incidence of ICH rises with age and is increased in certain groups. Overall, men have a higher incidence
compared with women. Moreover, Asian people have a higher rate of ICH compared with other ethnic
groups, including black people and people of Hispanic ethnicity.[10] [11]
Risk factors
Strong
hypertension
Uncontrolled hypertension is the most common risk factor for spontaneous intracerebral haemorrhage
(ICH).[22]
older age
Associated with increased incidence of ICH.[22]
male sex
Associated with increased incidence of ICH.[10]
Asian, black and/or Hispanic

Associated with increased incidence of ICH.[10] [23] Some, but not all, of this increased risk is
accounted for by higher prevalence of hypertension.[24] [25]
There is a two times higher rate of ICH in Asian people compared with other ethnic groups. Japanese
men had a higher incidence than Japanese women. This suggests a difference in cardiovascular risk
factors as well as influence from environmental factors.[11]
heavy alcohol use

Associated with an increased risk of ICH.[22]
illicit sympathomimetic drugs

Illegal drugs, particularly sympathomimetic drugs, such as cocaine and amphetamine, have been
associated with intracerebral haemorrhage.[22]
family history of intracerebral haemorrhage

Epidemiological studies show that a significant portion of sporadic ICH risk is heritable, and that family
history of ICH is a risk factor.[26]
haemophilia
Hereditary bleeding disorders, including haemophilia, may be complicated by ICH.
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Oct 12, 2022.
cerebral amyloid angiopathy
Most cases of cerebral amyloid angiopathy are non-familial. Cerebral amyloid angiopathy can rarely
be caused by autosomal dominant mutations involving the amyloid precursor protein, cystatin-C, or
transthyretin genes.[14]
THEORY
Additional non-modifiable risk factors for recurrent primary lobar haemorrhage have been identified
in those with presumed cerebral amyloid angiopathy: number of MRI microbleeds, presence of
white matter lesions on CT, and the presence of one or more apolipoprotein E epsilon 2 or epsilon 4
alleles.[12] [27] [28] [29]
autosomal dominant mutations in the COL4A1 gene

Rare autosomal dominant mutations in the COL4A1 gene cause intracerebral haemorrhage, retinal
haemorrhages, and porencephaly (cyst or cavity in the cerebral hemispheres).[30]
hereditary haemorrhagic telangiectasia

Caused by mutations in the ACVRL1, ENG, or SMAD4 gene. High prevalence of brain arteriovenous
malformations, which in turn increases the risk of ICH.[17]
autosomal dominant mutations in the KRIT1 gene, CCM2 gene, or PDCD10

gene
May lead to cavernous malformations.
anticoagulation
Clinical trials show that aspirin confers a very small increased risk, with warfarin conferring a more
substantial risk.[31] [32]
vascular malformations
These include arteriovenous malformations, dural arteriovenous fistulas, and cavernous
malformations.[33]
The risk of bleeding depends on the type of malformation, pattern of venous drainage, and history of
previous bleeds.
Moyamoya disease
Moyamoya syndrome and Moyamoya disease are associated with parenchymal and intraventricular
haemorrhage, predominantly in paediatric patients. The re-bleeding rate is approximately 7% per
year.[34] Patients with this vasculopathy also have an increased risk for cerebral aneurysms.
Weak
smoking
The association with ICH is unclear, with only a few studies documenting risk.[35]
non-steroidal anti-inflammatories (NSAIDs)

As a single group, NSAIDs did not have significant correlation with higher incidence of ICH, although
among users of specific agents (diclofenac and meloxicam) a significant increased risk was
observed.[36]
5
diabetes mellitus
Not a well-recognised risk factor despite some study findings.[35]
sympathomimetic medications
THEORY
A case-control study showed a relationship between the over-the-counter drug phenylpropanolamine,

now discontinued from the market, and ICH.[37] There is no consistent evidence that other
sympathomimetic drugs, including cold remedies, are associated.
Use of higher doses of the herbal medicine ephedra has been linked with haemorrhage risk in a case-
control study.[38]
cerebral vasculitis
Although a relatively infrequent cause of intracerebral or subarachnoid haemorrhage, cerebral
vasculitis should be considered in a setting of relevant systemic symptoms, an unexplained
progressive neurological disorder, or in a patient lacking risk factors for haemorrhagic stroke.
Diagnosis is achieved after a high level of suspicion with conventional angiography and
leptomeningeal biopsy.[39]
thrombocytopenia
Platelet counts less than 20,000/microlitre are associated with spontaneous ICH. Factors such
as uraemia and heavy alcohol use are well known to cause dysfunctional platelet aggregation
(thrombocytopathy) and act as the main mechanism for bleeding.
leukaemia
Leukaemia is associated with parenchymal haemorrhage and cerebral venous thrombosis
independently of thrombocytopenia.
Aetiology
Cerebrovascular changes induced by long-standing hypertension account for the large majority of primary
intracerebral haemorrhages (ICHs).
• Cerebral amyloid angiopathy (CAA) accounts for a significant number of primary ICHs, specifically in
the older population. While prevalence remains low in those aged younger than 55 years, it increases
with age.[12] CAA is caused by beta-amyloid deposition in the walls of medium-and small-sized
arteries restricted to the brain cortex (overlying leptomeninges) and cerebellum.[13] Rare hereditary
cases may be due to genetic mutations in cystatin-C, amyloid precursor protein, or transthyretin.[14]
The amyloid deposition in the blood vessels causes damage to the vascular architecture, fibrinoid
necrosis, and splitting of the vessel wall, which causes microbleeds from perivascular accumulation
of haemosiderin-laden macrophages. These cerebral microbleeds are only visible on magnetic
resonance imaging and result from the erythrocyte extravasation from small blood vessels. It is well
established that patients with apolipoprotein (Apo) E4 allele have an increased risk for CAA compared
with those who lack the allele. Heterozygotes of ApoE4 are at increased risk of an extreme form of
CAA, while homozygotes are at increased risk for an even more severe form of CAA. The presence
of ApoE2 has also been correlated with an increased risk for ICH in those with CAA. Typically, the
cerebral microbleeds in CAA are located in the cortical-subcortical regions of the brain parenchyma;
therefore, CAA is a major cause of lobar haemorrhage but is not a cause of haemorrhage in other
intracranial locations.[12]
• Hypertension can cause haemorrhage in any intracranial location. Chronic hypertension can also
result in cerebral microbleeds caused by damaged small vessels, yet these are typically within the
deeper brain structures. The presence and quantity of cerebral microbleeds are believed to be a
marker for the severity of underlying small vessel disease.[15]
THEORY
• It is important to recognise that most experts consider anticoagulation-associated haemorrhage to also
be a form of primary ICH.
Secondary ICH arises from an identifiable vascular malformation or as a complication of other medical or
neurological diseases that either impair coagulation or promote vascular rupture. Aetiologies include:
• Cerebral infarction or cerebral tumour with haemorrhage into the diseased tissue.
• Sympathomimetic drugs of misuse, such as cocaine and amphetamine. Cocaine and amphetamines
share pharmacological characteristics as well as physiological effects, yet amphetamine has a
longer half-life and, therefore, has more sustained systemic effects. It has been established that
amphetamine use is associated with a highly increased risk of haemorrhagic stroke among those aged
18 to 44 years. The higher risk is specific to this age group because of an overall higher prevalence
of illicit drug use among the younger population. Approximately 80% of amphetamine-related strokes
are haemorrhagic. There is no association between a particular route of administration (i.e., oral,
inhalation, or injection) and the incidence of haemorrhagic stroke. However, a literature review found
that ischaemic stroke associated with amphetamine use was more common with inhalation use.[16]
The sympathomimetic effect of amphetamine and amphetamine-like drugs (e.g., cocaine) cause
transient increases in both systolic and diastolic blood pressure that can lead to vascular damage due
to arteriosclerosis pathogenesis, arterial weakness, and intracranial haemorrhage.
• Brain arteriovenous malformations (AVMs) are a rare type of congenital vascular lesion that can
present with spontaneous ICH (58%), new-onset seizure (34%), or headache (8%). They are present
in 0.1% of the population and tend to be incidental findings after neuroimaging is done for other
neurological complaints. There is a higher prevalence of brain AVMs associated with haemorrhagic
hereditary telangiectasia (HHT). In fact, neuroimaging showing more than one brain AVM is highly
predictive of HHT. AVMs are direct arterial-to-venous connections without an intervening capillary bed.
The high-flow arteriovenous connection potentiates flow-related phenomena such as shear forces that
can result in arterialisation of the venous limb, vascular steal phenomenon, and even development
of aneurysms within the AVM. Overall, intracranial haemorrhage due to an AVM has a more benign
natural history than primary intracranial haemorrhage. The annual risk of intracranial haemorrhage
due to an unruptured AVM is 1.3%, while the annual risk of bleeding after a ruptured AVM is 4.8%.
Therefore, the most important risk for ICH from a brain AVM is an initial brain AVM rupture.[17]
Pathophysiology
Intracerebral haemorrhage (ICH) is caused by vascular rupture with bleeding into the brain parenchyma,
resulting in a primary mechanical injury to the brain tissue. The expanding haematoma may shear additional
neighbouring arteries, resulting in further bleeding and haematoma expansion, which can result in secondary
injury due to mass effect, increased intracranial pressure, reduced cerebral perfusion, secondary ischaemic
injury, and even cerebral herniation.[18] Significant haematoma growth (30% to 40% increase) over
several hours following presentation is common in those who present within 3 to 4 hours of the onset of
symptoms.[19] The period of bleeding may be extended even longer in anticoagulated patients. Arresting
haematoma growth is therefore a key objective for medical or surgical therapies. As a consequence of
haematoma growth, the haemorrhage may rupture into the subarachnoid space or the intraventricular space.
7
The role of matrix metalloproteinases in the genesis of neuroinflammation and haematoma growth is being
extensively investigated.[20] Mortality is increased when intraventricular haemorrhage is present, in part due
to the associated increased risk of communicating or non-communicating hydrocephalus.[21] Mortality from
ICH is high and may result from direct destruction of critical brain areas, compression of critical brain areas
THEORY
by adjacent haematoma, or cerebral circulatory arrest caused by globally increased intracranial pressure.
Classification
Aetiology of intracerebral haemorrhage[2]
Primary spontaneous
• Idiopathic (no identifiable vascular malformations or associated diseases)

• Anticoagulation.
Secondary
• An identifiable vascular malformation

• Medical or neurological diseases that impair coagulation or promote vascular rupture (e.g., cerebral
infarction or tumour, sympathomimetic drugs of misuse, haematological malignancies).
Location of intracerebral haemorrhage[3]

It is helpful to subdivide ICH by location because aetiologies and prognosis vary by site.
• Lobar: occurs in the cortex or subcortical white matter of the cerebral hemispheres.
• Deep hemispheric: occurs in the supratentorial deep grey matter structures, most commonly the
putamen and thalamic nuclei.
• Brain stem: occurs mostly in the pons.
• Cerebellar: occurs mostly in the dentate nucleus.
Case history
Case history #1
A 70-year-old man with a history of chronic hypertension and atrial fibrillation is witnessed by a family
member to have nausea, vomiting, and right-sided weakness as well as difficulty speaking and
comprehending language. The symptoms started with only mild slurred speech before progressing over
several minutes to severe aphasia and right arm paralysis. The patient is taking warfarin.
Other presentations
Headache occasionally accompanies intracerebral haemorrhage, but its absence does not rule out the
diagnosis.
THEORY
9
Stroke due to spontaneous intracerebral haemorrhage Diagnosis
Recommendations
Urgent
Time is brain” - if you suspect a stroke, work rapidly through the initial assessment and aim
for quick access to computed tomography (CT) scan.
• CT enables quick differentiation between ischaemic stroke and spontaneous intracerebral

haemorrhage (ICH) which must be done before reversing anticoagulation in anticoagulation-
induced ICH, and before starting thrombolysis in ischaemic stroke.[42] [43] Both are critical and
urgent interventions.
Suspect stroke in a patient with sudden onset of focal neurological symptoms:[44]
• Unilateral weakness or paralysis in the face, arm, or leg

• Unilateral sensory loss
• Dysarthria or expressive or receptive dysphasia
• Vision problems (e.g., hemianopia)
• Headache (sudden severe and unusual headache)
• Difficulty with coordination and gait
• Vertigo or loss of balance, especially with the above signs.
Suspect subarachnoid haemorrhage in anyone presenting with sudden severe (thunderclap)

headache, stiff neck, photophobia and blurred vision.[44] See our topic Subarachnoid haemorrhage.
Use a validated tool to aid diagnosis in people with suspected stroke:
• In the emergency department: use the ROSIER scale (Recognition of Stroke in the Emergency
Room) in people with suspected stroke.[42]
• In the community: use FAST (Face Arm Speech Test) to screen people with sudden onset of
neurological symptoms for stroke.[42]
DIAGNOSIS
Exclude hypoglycaemia (a stroke mimic) as the cause of sudden neurological symptoms.[42]
Request an immediate non-contrast CT scan of the head (i.e., ideally in the next available time slot
and definitely within 1 hour of arrival at hospital, whichever is sooner) if any of the following apply:[42] [43]
• Indications for thrombolysis or thrombectomy

• On anticoagulant treatment
• A known bleeding tendency
• A depressed level of consciousness (Glasgow Coma Scale score <13)
• Unexplained progressive or fluctuating symptoms
• Papilloedema, neck stiffness or fever
• Severe headache at onset of stroke symptoms
• Uncertain diagnosis.
Once you have managed any airway, breathing, and circulatory insufficiencies requiring urgent
intervention and following your initial assessment, prioritise rapid:
• Admission of the patient 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[42] [43]
• Review by a neurosurgeon[45]
• Reversal of clotting abnormalities, if indicated[43]
• Lowering of blood pressure, if indicated.[42] [43]
See Management section for details.
Key Recommendations
Obtain a brief history (from witnesses or next of kin) followed by an abbreviated neurological
examination using the National Institutes of Health Stroke Scale.[43]
• This tool measures the degree of neurological deficit. Higher scores indicate a more severe stroke.
Assess the patient’s level of consciousness using the Glasgow Coma Scale.
• Exclude mimics such as seizures in people with an altered level of consciousness/coma. See
Differentials section.
In people with suspected acute stroke without indications for immediate CT-head, request a scan as
soon as possible and definitely within 24 hours of symptom onset.[42]
Order in all patients:
• Serum glucose[42] [46]

• Serum electrolytes
• Serum urea and creatinine
• Liver function tests
• Full blood count
• Clotting screen
• ECG[45]
Consider a serum toxicology screen if you suspect use of toxic substances.[45]
DIAGNOSIS
Full Recommendations
Clinical presentation
Suspect stroke in a patient with sudden onset focal neurological symptoms:[44]
• Unilateral weakness or paralysis in the face, arm, or leg
• Complete or partial loss of muscle strength in face, arm, and/or leg is among the most
common presentations of stroke.
• As with most stroke signs and symptoms, bilateral involvement is uncommon and may reflect
alternative aetiology (but can be seen with bilateral brainstem or spinal infarcts).
• Sensory loss (numbness)
• Patients often describe sensory loss and paraesthesias as “numbness”, “tingling” or “pins
and needles”.
• Sensory inattention is a useful cortical sign, localising to the contralateral parietal region.
11
• Cortical sensory loss usually impairs fine sensory processing abilities such as two-point
discrimination, graphaesthesia, or stereognosis.
• Thalamic haemorrhages can present with sensory loss and pseudoathetosis.
• Dysarthria or expressive or receptive dysphasia
• Dysarthria may accompany facial weakness or cerebellar dysfunction.

• Impairment in any language function (fluency, naming, repetition, comprehension) is a sign of
dominant hemispheric stroke.
• Visual disturbance
• Homonymous hemianopia (i.e., visual field loss on the left or right side of the vertical midline
on the same side of both eyes) may result from haemorrhage in the visual pathways,
including the occipital lobe.
• Diplopia may result from brain stem haemorrhage.
• Spontaneous ICH can often cause photophobia.
• Headache
• Usually of insidious onset and gradually increasing intensity in ICH.

• More common in ICH than in ischaemic stroke, but the absence of headache does not rule
out ICH.
• Thunderclap headache (defined as sudden, severe headache that reaches maximum
intensity upon onset) is characteristic of subarachnoid haemorrhage. See our topic
Subarachnoid haemorrhage.
• Difficulty with coordination and altered gait
• In the absence of muscle weakness, impaired coordination points to haemorrhage involving

the cerebellum or its connections with the rest of the brain.
DIAGNOSIS
Other symptoms include:
• Vertigo
• Often reported as a spinning sensation; may also be described as feeling like being “on a
ship in choppy seas”.
• Typically seen in cerebellar or brainstem haemorrhage.
• Nausea/vomiting
• May either be due to posterior circulation haemorrhage or reflect increased intracranial

pressure.
• With cerebellar haemorrhage, nausea and vomiting may be the only presenting symptoms,
with an unremarkable neurological examination except for gait ataxia.
• Altered level of consciousness/coma
• Urgently diagnose (rule out haemorrhage) and manage (breathing and airway protection) any
patient with altered consciousness or in a coma.
• Reduced alertness may accompany very large hemispheric haemorrhages or posterior fossa
haemorrhages.
• Coma is more common in people with brain stem haemorrhage.
• Exclude conditions mimicking stroke (e.g., seizures).
• Confusion
• Common especially in older people with previous strokes or cognitive dysfunction.

• Differentiate aphasia from confusion; aphasia is a specific sign of dominant hemisphere
injury.
• Gaze paresis
• Often horizontal and unidirectional.
About 11% of all patients presenting to hospital in the UK with acute stroke have spontaneous ICH as the
cause.[43]
Suspect subarachnoid haemorrhage in anyone presenting with sudden severe (thunderclap)

headache, stiff neck, photophobia, and blurred vision.[44] See our topic Subarachnoid haemorrhage.
Initial assessment
The goal of the initial assessment is to recognise a stroke quickly - “time is brain.
In the emergency department

Use the ROSIER scale (Recognition of Stroke in the Emergency Room) in patients with suspected
DIAGNOSIS
stroke or transient ischaemic attack (TIA) to establish the diagnosis rapidly.[42]
• Score -1 point for each feature (clinical history):
• Loss of consciousness or syncope

• Seizure activity
• Score +1 point for each feature (neurological history):
• Asymmetrical face weakness

• Asymmetrical arm weakness
• Asymmetrical leg weakness
• Speech disturbance
• Visual field defect
• A score >0: stroke likely; a score ≤0: stroke unlikely (but not excluded).
13
In the community
Use a validated tool such as FAST (Face Arm Speech Test) to screen people with sudden onset of
neurological symptoms for a diagnosis of stroke:[42]
• Score 1 point for each feature:
• Face weakness
• Arm (or leg) weakness
• Speech disturbance
• Suspect stroke if score > 0; refer for emergency medical care in hospital (by 999 ambulance in the
UK).
Practical tip
Be aware that the patient may have ongoing focal neurological deficits (such as visual disturbance
or balance problems) despite a negative FAST. Continue to manage them as you would someone
with acute stroke.[43]
Evidence: FAST and ROSIER scales to identify stroke
Despite limited evidence, guidelines recommend using screening tools to expedite access to
specialist care for patients with stroke, since the benefits are likely to outweigh any harms and
the tools require minimal resources. [42] [47]
Guidelines from the European Academy of Neurology and European Stroke Organisation in 2017
identified a 2014 systematic review assessing the diagnostic accuracy of various scales for emergency
medical services technicians and paramedics to identify patients who have had a stroke prior to
hospital assessment.[47] [48]
• The review included 8 studies and 7 scales.[48] Of the scales included, FAST and ROSIER had
the highest sensitivity (both 97%); specificity was 13% and 18%, respectively (both in one study
of 295 patients in the UK).[49]
The UK National Institute for Health and Care Excellence (NICE) stroke guideline from 2008 (not
DIAGNOSIS
changed in the 2022 update) recommends using a validated tool, such as FAST, outside hospital.[42]
• This recommendation is underpinned by evidence from a prospective cohort study of 487

patients. In this study, ambulance paramedics’ stroke diagnosis using FAST gave a positive
predictive value (PPV; i.e., the proportion with a positive test who in reality actually have the
condition or characteristic) of 78% (95% CI 72% to 84%).[50]
NICE also recommends using a validated tool, such as ROSIER, in the emergency department.[42]
• This recommendation is underpinned by evidence from a prospective cohort study which

involved 343 patients in the development phase and 173 in the validation phase. In this study,
ROSIER showed a PPV of 90% (95% CI 85% to 95%) when used by emergency department
clinicians.[51]
History
Take a careful history. Establish contact with witnesses or the patient’s next of kin, not only for
an accurate history but also to seek consent from next of kin for invasive tests or treatments, if these are
needed.
• Determine the time of stroke onset because this is the main factor that will determine some
stroke interventions.
• If the onset was unwitnessed, the time of symptom onset is when the patient was last
seen well.[42]
• Ask about onset (sudden or gradual), duration, intensity, and fluctuation of symptoms.
• The symptoms and signs of ICH often start suddenly and progress over several minutes.[45]
• Symptoms of ischaemic stroke may, in contrast, be maximal at onset, particularly in embolic
infarction. See our topic Ischaemic stroke.
• Symptoms that spontaneously improve or resolve suggest ischaemia rather than
haemorrhage.
• Ask specifically about relevant past medical history that will influence management. This
includes:[45]
• Vascular risk factors: history of stroke or ICH, hypertension, diabetes mellitus, or smoking
• Medications: anticoagulants, antiplatelet agents, antihypertensives, stimulants (including diet
pills), and sympathomimetic drugs
• Recent trauma or surgery: carotid endarterectomy or carotid stenting
• ICH may be related to hyperperfusion after such procedures.
• Dementia: associated with amyloid angiopathy

• Alcohol or illicit drug use: cocaine and other sympathomimetic drugs (e.g., amphetamine,
methamphetamine)
• Seizures
• Liver disease, cancer, and haematological disorders: may be associated with coagulopathy.
Practical tip
DIAGNOSIS
The time of onset is not always easy to determine, particularly if the onset was not witnessed and
the patient is unable to communicate, symptoms are mild and not immediately noticeable, or if there
is a stuttering or fluctuating course.
Ask about common risk factors for spontaneous ICH:
• Hypertension
• Uncontrolled hypertension is the most common risk factor.[22]
• Older age[22]
• History of heavy alcohol, amphetamine/methamphetamine, or cocaine use[22]
• Family history of ICH
• Anticoagulant use.[22]
Stroke mimics
Exclude stroke mimics such as hypoglycaemia, seizures, brain tumours, sepsis, or migraine to
ensure timely treatment. See Differentials section.
15
Bear in mind the key clinical features that may help distinguish between stroke and mimics (e.g.,
seizures, hypoglycaemia) at the initial bedside assessment:
Suggestive of mimic Suggestive of stroke
• Neurological symptoms and signs • Exact time of onset[52]

that are gradual in onset, progressive, • Sudden onset of neurological symptoms
and signs[45]
migratory • Symptoms are maximal at onset or
• Positive neurological symptoms (e.g.,
progress suddenly over several minutes
flashing lights, tingling, jerking, or shaking • Negative neurological symptoms (e.g.,
of limbs) visual loss, numbness, or weakness)[44]
• Known history of cognitive • Definite focal symptoms[52]
impairment[52] • Abnormal vascular findings (e.g., systolic
• Respiratory, abdominal, or other blood pressure >150 mmHg, atrial
abnormal signs[52] fibrillation, valvular heart disease, or
absent peripheral pulses)[52]
• Signs that can be lateralised to the left or
right side of the brain[52]
• Clinical stroke subclassification can be
determined[52]
Physical examination
Perform a general physical examination focusing on the head, heart, lungs, abdomen, and
extremities.[45]
• ICH is more often associated with reduced level of consciousness than ischaemic stroke.[45]
Perform an abbreviated neurological examination using the National Institutes of Health Stroke
Scale (NIHSS).[45]
• This tool measures the degree of neurological deficits. Higher scores indicate a more severe stroke.
DIAGNOSIS
• People with ICH more often have depressed consciousness on initial presentation than patients
with ischaemic stroke, reducing the utility of the NIHSS.
The most common findings on neurological examination are:
• Altered level of consciousness

• Partial or total loss of strength in upper and/or lower extremities (usually unilateral)
• Fluent or non-fluent language dysfunction
• Sensory loss in upper and/or lower extremities (associated with sensory neglect if non-dominant
hemisphere stroke)
• Gaze deviation (towards the damaged sphere)
• Gaze paresis (often horizontal and unidirectional)
• Visual field loss
• Dysarthria
• Difficulty with fine motor coordination and gait.
Practical tip
Brainstem and cerebellar haemorrhages are more frequently associated with altered levels of
consciousness, coma, and vomiting than ischaemic strokes.
Refer to hyperacute or acute stroke unit

Transfer 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.[42] [43]
• Patients with spontaneous ICH can deteriorate quickly and require urgent specialist assessment
and monitoring.[42] [43]
Imaging
CT-head
Request an immediate non-contrast CT scan of the head (i.e., ideally in the next available time slot
and definitely within 1 hour of arrival at hospital, whichever is sooner) if any of the following apply:[42] [43]

• A depressed level of consciousness (Glasgow Coma Scale score <13 )
• Papilloedema, neck stiffness, or fever
Practical tip
Aim to take a collateral history from relatives regarding medications/past medical history while the
DIAGNOSIS
patient is in the CT scanner.
Confirm ICH by the presence of hyperattenuation (brightness) suggesting acute blood, often with
surrounding hypoattenuation (darkness) due to oedema.[53]
17
Intracranial haemorrhage on CT scan

Massachusetts General Hospital personal case files; used with permission
Use the CT scan to differentiate between ischaemic stroke and ICH; this must be done before
reversing anticoagulation in anticoagulation-induced ICH and before starting thrombolysis in ischaemic
stroke.[42] [43] See our topic Ischaemic stroke.
• Only healthcare professionals with appropriate training should interpret acute stroke imaging for
thrombolysis or thrombectomy decisions.[43]
DIAGNOSIS
In people with suspected acute stroke without indications for immediate brain imaging,
request a scan as soon as possible and definitely within 24 hours of symptom onset.[42]
General investigations
Blood tests
While CT transport is being organised, insert an intravenous catheter with blood sampling.[43] Order in
all patients:
• Serum glucose
• Hypoglycaemia is a stroke mimic; hyperglycaemia has been associated with intracerebral

bleeding.[42] [46]
• Serum electrolytes
• To exclude electrolyte disturbance (e.g., hyponatraemia) as a cause for neurological signs.
• Serum urea and creatinine
• To exclude renal failure because it may be a potential contraindication to some stroke
interventions.
• Liver function tests
• To exclude liver dysfunction as a cause of haemorrhage.
• Full blood count
• To exclude thrombocytopenia as a cause of haemorrhage.
• Clot ting screen
• To exclude coagulopathy as a cause of haemorrhage. Check international normalised ratio

(INR) or factor Xa levels, if available.
Consider a serum toxicology screen if you suspect use of toxic substances.
• Cocaine and other sympathomimetic drugs of misuse are associated with ICH, especially in
younger people.[45]
ECG
Perform an ECG in all patients to assess for active coronary ischaemia or prior cardiac injury; ECG
abnormalities can indicate concomitant myocardial injury.[45]
History and exam

Key diagnostic factors
DIAGNOSIS
unilateral weakness or paralysis in the face, arm, or leg (common)
Complete or partial loss of muscle strength in face, arm, and/or leg is among the most common
presentations of stroke.
As with most stroke signs and symptoms, bilateral involvement is uncommon and may reflect
alternative aetiology (but can be seen with bilateral brainstem or spinal infarcts).
sensory loss (numbness) (common)

Patients often describe sensory loss and paraesthesias as “numbness”, “tingling” or “pins and
needles”.
Sensory inattention is a useful cortical sign, localising to the contralateral parietal region.
Cortical sensory loss usually impairs fine sensory processing abilities such as two-point discrimination,
graphaesthesia, or stereognosis.
Thalamic haemorrhages can present with sensory loss and pseudoathetosis.
19
dysphasia (common)
Expressive or receptive dysphasia may occur.
Impairment in any language function (fluency, naming, repetition, comprehension) is a sign of

dominant hemispheric stroke.
Differentiate fluent, non-repetitive (Wernicke's) aphasia from confusion; aphasia is a specific sign of
dominant hemisphere injury.
dysarthria (common)
May accompany facial weakness or cerebellar dysfunction.
visual disturbance (common)

Homonymous hemianopia (i.e., visual field loss on the left or right side of the vertical midline on the
same side of both eyes) may result from haemorrhage in the visual pathways, including the occipital
lobe.
Diplopia may result from brain stem haemorrhage.
photophobia (common)
Spontaneous intracerebral haemorrhage (ICH) can often cause photophobia.
headache (common)
Usually of insidious onset and gradually increasing intensity in ICH.
More common in ICH than in ischaemic stroke, but the absence of headache does not rule out ICH.
Thunderclap headache (defined as sudden, severe headache that reaches maximum intensity upon
onset) is characteristic of subarachnoid haemorrhage. See our topic Subarachnoid haemorrhage.
ataxia (common)
DIAGNOSIS
In the absence of muscle weakness, impaired coordination points to haemorrhage involving the
cerebellum or its connections with the rest of the brain.
risk factors (common)

Common risk factors for spontaneous ICH include:
• Hypertension
• Uncontrolled hypertension is the most common risk factor.[22]
• Older age[22]
• History of heavy alcohol, amphetamine/methamphetamine, or cocaine use[22]
• Family history of ICH
• Anticoagulant use.[22]
Other diagnostic factors

vertigo (uncommon)
Often reported as a spinning sensation; may also be described as feeling like being “on a ship in
choppy seas”.
Typically seen in cerebellar or brainstem haemorrhage.
nausea/vomiting (uncommon)
May either be due to posterior circulation haemorrhage or reflect increased intracranial pressure.
With cerebellar haemorrhage, nausea and vomiting may be the only presenting symptoms, with an
unremarkable neurological examination except for gait ataxia.
decreased level of consciousness/coma (uncommon)

Urgently diagnose (rule out haemorrhage) and manage (breathing and airway protection) any patient
with altered consciousness or in a coma.
Reduced alertness may accompany large hemispheric haemorrhages or posterior fossa

haemorrhages.
Coma is more common in people with brain stem haemorrhage.
Exclude conditions mimicking stroke (e.g., seizures).
confusion (uncommon)
Common especially in older people with previous strokes or cognitive dysfunction.
ga ze paresis (uncommon)
Often horizontal and unidirectional.
DIAGNOSIS
21
Investigations
1st test to order
Test Result
non-contrast CT head hyperattenuation (brightness),
Request an immediate non-contrast CT scan of the head (i.e., suggesting acute blood,
ideally in the next available time slot and definitely within 1 hour often with surrounding
of arrival at hospital, whichever is sooner) if any of the following
hypoattenuation (darkness)
apply:[42] [43]
due to oedema
• A depressed level of consciousness (Glasgow Coma Scale
score <13 )
• Papilloedema, neck stiffness, or fever
Practical tip
Aim to take a collateral history from relatives regarding

medications/past medical history while the patient is in the
scanner.
DIAGNOSIS
Intracranial haemorrhage on CT scan

Massachusetts General Hospital
personal case files; used with permission
Use an urgent non-enhanced CT head to differentiate between

ischaemic stroke and ICH, which must be done before reversing
anticoagulation in anticoagulation-induced ICH and before starting
thrombolysis in ischaemic stroke.[44] [45] See our topic Ischaemic
stroke.
Test Result
In people without indications for immediate brain imaging,
request a scan as soon as possible and definitely within 24 hours of
symptom onset.[42]
serum glucose may be normal; may

Hypoglycaemia is a stroke mimic; hyperglycaemia has been show hypoglycaemia or
associated with intracerebral bleeding.[42] [46] hyperglycaemia
serum electrolytes may be normal; may show

To exclude electrolyte disturbance (e.g., hyponatraemia) as a cause electrolyte disturbances
for neurological signs.
serum urea and creatinine may be normal; may show
To exclude renal failure because it may be a potential contraindication renal failure
to some stroke interventions.
liver function tests may be normal; may show
To exclude liver dysfunction as a cause of haemorrhage. liver dysfunction
• Significant liver dysfunction can seriously compromise the

coagulation system and induce bleeding, and also promote
the development of cerebral oedema (mainly due to impaired
ammonia metabolism) and intracranial hypertension, especially
in cases of acute liver failure.
FBC may be normal; may show

To exclude thrombocytopenia as a cause of haemorrhage. anaemia or thrombocytopenia
Thrombocytopenia suggests a secondary cause of haemorrhage.
DIAGNOSIS
clot ting screen usually normal
To exclude coagulopathy as a cause of haemorrhage.
Check INR or factor Xa levels, if available.
If elevated, results suggest a secondary cause of haemorrhage.

ECG may be normal; may show
To assess for active coronary ischaemia or prior cardiac injury; ECG arrhythmia or signs of
abnormalities can indicate concomitant myocardial injury.[45] ischaemia
23
Other tests to consider
Test Result
serum toxicology screen may exclude alcohol and drug
Consider a toxicology screen if you suspect use of toxic substances. ingestion
Signs and symptoms may mimic stroke.
• Cocaine and other sympathomimetic drugs are associated with

ICH, especially in younger people.[45]
DIAGNOSIS
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Ischaemic stroke • No symptoms or signs • Acute haemorrhage
reliably distinguish ischaemic appears bright due to
stroke from spontaneous hyperattenuation of the x-
intracerebral haemorrhage. ray beams in CT scan. In
contrast, ischaemic infarct
appears as hypoattenuation
(darkness), although may not
appear for many hours after
stroke onset.
Hypertensive • Hypertension significantly • Cerebral oedema on CT

encephalopathy above patient's baseline or MRI. Certain patients
blood pressure associated present characteristic
with headache, decreased changes in the posterior
consciousness or cognitive aspect of the brain.
abnormalities, visual
changes or loss, and signs
of increased intracranial
pressure. Less frequently
these patients present with
focal abnormalities in the
neurological examination.
Hypoglycaemia • Sweating, tremor, hunger, • Low serum glucose on blood

confusion, and ultimately chemistry.
a decreased level of
consciousness.
• May have known history
of diabetes mellitus and
insulin use or medical
DIAGNOSIS
conditions associated with
hypoglycaemia.
Complicated migraine • Repetitive history of similar • MRI shows no evidence of

events preceding aura; infarction.
headache in a marching
pattern.
Seizure disorder • A history of seizures and/or • EEG results may identify

a witnessed seizure followed seizure activity.
by postictal deficits. • MRI shows no evidence of
infarction.
Conversion and somatic • Neurological signs and • CT and MRI show no

symptom disorders symptoms do not fit a evidence of infarction or
vascular territory. No cranial haemorrhage in conversion
nerve deficits. disorder.
• Additionally, conversion
disorder displays multiple
signs that are neurologically
inconsistent.
25
Criteria
Cerebral amyloid angiopathy (CAA) accounts for a significant number of primary intracerebral haemorrhages
(ICHs), specifically in the older population. A definitive diagnosis of cerebral amyloid angiopathy (CAA) can
only be made on the basis of brain tissue biopsy showing deposits of amyloid in the cerebral vessel walls. In
routine clinical practice the modified Boston criteria, which combine neuroimaging and clinical findings, are
used in order to establish a probable diagnosis.
Boston criteria[54]
Used to estimate the likelihood of underlying CAA as a cause of lobar ICH.
• Definite CAA: autopsy verification.

• Probable CAA with supporting pathology: single or multiple lobar haemorrhages with CAA identified on
a biopsy or resection specimen.
• Probable CAA: multiple lobar haemorrhages that may include lobar microbleeds on magnetic
resonance imaging (MRI) gradient-echo sequence; patient 55 years old or older.
• Possible CAA: single lobar haemorrhage; patient 55 years old or older.
NOTE: Other potential causes of single or multiple haemorrhages are excluded, such as thrombocytopenia
or familial cavernous malformations. Haemorrhages and microbleeds should be present in the lobar regions
only.
DIAGNOSIS
Stroke due to spontaneous intracerebral haemorrhage Management
Recommendations
Urgent
“Time is brain” - spontaneous intracerebral haemorrhage (ICH) is an emergency.
• Aggressive early management of ICH is crucial. Early deterioration is common in the first few hours
after symptom onset.[45]
Manage any airway, breathing, and circulatory insufficiencies requiring urgent intervention. In particular:
• Consider endotracheal intubation.[55]

• Aim for a target ox ygen saturation of 94-96% in acutely ill patients who are not at
risk of hypercapnia. [56] A lower target of 88% to 92% is appropriate if the patient is at risk of
hypercapnic respiratory failure.[57]
Admit anyone with suspected stroke directly to a hyperacute or acute (depending on availability)
hospital.[42] [43]
Arrange an immediate review by a neurosurgeon to assess whether or not the patient will benefit
from neurosurgery.[45] [58]
Offer rapid lowering of blood pressure (BP) to patients with acute ICH who have a systolic BP of 150
to 220 mmHg AND:[42]
• 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
• Are not going to have early neurosurgery to evacuate the haematoma.
Follow your local protocol for urgent BP lowering in these patients.[43]
Consider rapid BP lowering for patients with acute ICH who have a systolic BP of >220 mmHg
OR present beyond 6 hours of symptom onset AND:[42]

aneurysm); a Glasgow Coma Scale score <6; a massive haematoma with poor expected prognosis
Aim for a systolic BP target of 130 to 140 mmHg within 1 hour of starting treatment and maintain this
BP for at least 7 days.[42]
MANAGEMENT
Reverse anticoagulation treatment urgently. Return clotting levels to normal as soon as possible in
people who were on:
27
• 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.[42]
[43]
• Dabigatran: reverse with idarucizumab.[43]
• Factor Xa inhibitor treatment: give prothrombin complex concentrate (4-factor).[43]
Key Recommendations
• Continue to monitor consciousness once the patient is on the hyperacute or acute stroke unit.[43]
Monitor blood glucose regularly. Maintain a blood glucose concentration between 4 and 11 mmol/L in
people with acute stroke.[42] Give optimal insulin therapy with intravenous insulin and glucose to all adults
with type 1 diabetes with threatened or actual stroke. Follow local protocols.[42]
Consider monitoring the patient for signs of elevated intracranial pressure if any of the following is
present:[45]
• Glasgow Coma Scale score ≤8 that is presumed related to haematoma mass effect
• Clinical evidence of transtentorial herniation
• Significant intraventricular haemorrhage or hydrocephalus.
Refer any patient who develops hydrocephalus to a neurosurgeon. The neurosurgeon will
consider surgical intervention (e.g., insertion of an external ventricular drain).[42] [43]
Consult immediately with a neurologist if the patient has uncontrolled or recurrent seizures, or
status epilepticus. Follow your local protocol. See our topic Status epilepticus.
Do not start statin treatment in patients with primary ICH unless required for other indications.
Full Recommendations
Treatment goals
Ensure urgent specialist input and treatment to reduce bleeding as patients with ICH can deteriorate
rapidly.[43]
Anticoagulation reversal, intensive blood pressure lowering, neurosurgery and access to critical
care might all be beneficial in acute ICH but high-quality evidence for these interventions is currently
lacking.[58]
Urgent initial management
Stabilisation
MANAGEMENT
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 ).[55] This
should be done by an anaesthetist or trained emergency department staff.
• Aim for a target ox ygen saturation of 94-96% in acutely ill patients 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.[56]
• A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic
respiratory failure.[57]
• The National Institute for Health and Care Excellence in the UK recommends starting oxygen
if oxygen saturation drops below 95%.[42]
MANAGEMENT
29
Evidence: Target ox ygen saturation in acutely ill adults
Too much supplemental oxygen increases mortality .
Evidence from a large systematic review and meta-analysis supports conservative/

controlled ox ygen therapy versus liberal ox ygen therapy in non-hypercapnic acutely ill
adults.
• 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 2015 Thoracic Society of Australia and New Zealand (TSANZ) guideline
recommends 92% to 96%.[57] [59]
• 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%).[56]
• 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 patients 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).[60]
• In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis
and decided an interim update was not required.[57]
• 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.
MANAGEMENT
• Management of oxygen therapy in patients in intensive care is specialised and informed by

further evidence that is more specific to this setting.[61] [62] [63]
Refer to hyperacute or acute stroke unit
In hospital
Admit anyone with suspected stroke directly to a hyperacute or acute (depending on availability)
hospital.[42] [43]
• These patients require urgent specialist assessment and monitoring as they can deteriorate
quickly.[42] [43]
• If the patient deteriorates refer immediately for repeat brain imaging.[42] [43]
MANAGEMENT
31
Evidence: Hyperacute stroke units
People who have had a stroke are more likely to be alive, independent, and living at home at
1 year post-stroke if they received care in an acute inpatient stroke unit, compared with less-
organised alternative care. Care in a dedicated stroke ward seems to be the most effective
approach.
The 2016 UK Royal College of Physicians (RCP) national clinical guideline on stroke cites a 2013
Cochrane review by the Stroke Unit Trialists’ Collaboration to support its recommendation to admit
patients with suspected acute stroke to a hyperacute stroke unit.[43]
This Cochrane review (search date January 2013) assessed the effect of organised inpatient stroke
unit care compared with alternative less-organised forms of care for people with acute stroke.[64]
• It included 28 RCTs, involving a total of 5855 patients admitted to hospital with stroke (using a
clinical definition of stroke: focal neurological deficit due to cerebrovascular disease, excluding
subarachnoid haemorrhage and subdural haematoma).
• Results for organised stroke unit care versus alternative care (general wards or mixed
rehabilitation units) showed that patients in stroke units had a reduced “risk of death”, “death
or institutionalised care”, and “death or dependency” at final follow-up (median 1 year), 5 years
follow-up, and 10 years follow-up.
The Cochrane review has since been updated (search date April 2019).[65]
• The update included 29 RCTs (n=5902).

• There were improved outcomes at the end of scheduled follow-up (median 1 year) with stroke
unit care compared with alternative care:
• Poor outcome (OR 0.77, 95% CI 0.69 to 0.87; moderate-quality evidence as assessed by
GRADE).
• “Death” (OR 0.76, 95% CI 0.66 to 0.88; GRADE moderate).
• “Death or institutional care” (OR 0.76, 95% CI 0.67 to 0.85; GRADE moderate).
• “Death or dependency” (OR 0.75, 95% CI 0.66 to 0.85; GRADE moderate).
• Subjective health status may be better with stroke unit care, however it was only reported
in 3 studies (GRADE very low). No studies reported patient satisfaction.
• Organised stroke unit care did not seem to result in a longer hospital stay, however results
were very heterogeneous (standardised mean difference 0.16 lower [0.33 lower to 0.01
2
higher], I =85%, GRADE low).
• The results were independent of age, sex, severity of stroke, or stroke type.
• Three RCTs (n=1139) with extended follow-up found stroke unit care continued to be associated
with more favourable results at both 5 and 10 years post stroke, although there was increased
heterogeneity and loss of statistical significance over time.
• A network meta-analysis was used to compare different forms of organised inpatient care.
MANAGEMENT
Overall, care in a dedicated stroke ward was found to be the most effective approach.
• Poor outcome (stroke ward: OR 0.74, 95% CI 0.62 to 0.89, GRADE moderate; mobile
stroke team: OR 0.88, 95% CI 0.58 to 1.34, GRADE low; mixed rehabilitation ward: OR
0.70, 95% CI 0.52 to 0.95, GRADE low).
• “Death” (stroke ward: OR 0.62, 95% CI 0.47 to 0.82, GRADE moderate; mobile stroke
team: OR 1.23, 95% CI 0.67 to 2.27, GRADE low; mixed rehabilitation ward: OR 1.20,
95% CI 0.73 to 1.99, GRADE low).
• “Death or institutional care” (stroke ward: OR 0.72, 95% CI 0.62 to 0.83, GRADE
moderate; mobile stroke team: OR 1.46, 95% CI 1.03 to 2.05, GRADE low; mixed
rehabilitation ward: OR 0.75, 95% CI 0.58 to 0.96, GRADE low).
• “Death or dependency” (stroke ward: OR 0.71, 95% CI 0.58 to 0.86, GRADE moderate;
mobile stroke team: OR 0.87, 95% CI 0.57 to 1.32, GRADE low; mixed rehabilitation
ward: OR 0.69, 95% CI 0.51 to 0.9, GRADE low).
In the community
Arrange immediate emergency admission to an hyperacute (or acute, depending on availability) stroke
unit for anyone with:
• Persisting neurological symptoms suspected of having acute stroke[42] [43]

• Resolved neurological symptoms who has a bleeding disorder or is taking an anticoagulant as
haemorrhage must be excluded. This is standard practice.
Immediate neurosurgery assessment

Arrange an immediate review by a neurosurgeon to assess whether the patient will benefit from
neurosurgery.[45] [58]
• This review may happen at the emergency department or in the hyperacute or acute stroke unit
(depending on the availability of the neurosurgeon). The neurosurgeon often does this remotely
rather than attending in person. If in the stroke unit, it is the stroke team who liaises with the
surgical team.
• The role of surgery for most patients with spontaneous ICH remains controversial.[45]
Neurosurgery to evacuate the haematoma or treat hydrocephalus might improve outcomes, but
there is a lack of clear evidence and who to operate on remains uncertain.[58]
According to the UK National Institute for Health and Care Excellence (NICE), people with any of the
following clinical features rarely require surgical intervention and should receive medical treatment
MANAGEMENT
initially:[42]
• Small deep haemorrhages

• Lobar haemorrhage without either hydrocephalus or rapid neurological deterioration
• A large haemorrhage and significant comorbidities before the stroke
33
• Glasgow Coma Scale score <8 unless this is because of hydrocephalus
• Posterior fossa haemorrhage.
Rapid blood pressure lowering

Consider rapid lowering of blood pressure (BP) for patients with ICH who have a systolic BP of 150 to 220
mmHg AND:[42]

aneurysm); a Glasgow Coma Scale score <6 ; a massive haematoma with poor expected
prognosis
Follow your local protocol for urgent BP lowering in these patients.[43]
Taking into account the risk of harm, consider rapid BP lowering on a case-by-case basis for patients with
acute ICH who have a systolic BP of >220 mmHg OR present beyond 6 hours of symptom onset
AND:[42]

aneurysm); a Glasgow Coma Scale score <6; a massive haematoma with poor expected
prognosis
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.[42]
MANAGEMENT
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.[66]
• 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.[66]
• 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 possible a 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
MANAGEMENT
may be harmful, as may a very large reduction (>60 mmHg) in blood pressure within the
first hour.[66] [67] Therefore, in 2022, the guideline committee decided to remove the aim of
reaching the target within 1 hour. The committee also noted that:
35
• 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.
• The 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.
Urgent reversal of anticoagulation

Urgently reverse abnormalities of clotting, particularly in patients taking anticoagulants.[43]
• About 10% to 20% of acute ICHs occur in patients taking oral anticoagulants, and this aetiology is
associated with a high risk of early haematoma expansion.[58]
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)[42] [43]
• Dabigatran: reverse with idarucizumab[43]
• Factor Xa inhibitor: treat with prothrombin complex concentrate (4-factor).[43]
Monitoring and supportive care

Monitor the patient’s clinical status closely and provide supportive care as appropriate.[43] In
particular, monitor:
• Level of consciousness
• Blood glucose
• Blood pressure
• Oxygen saturation
• Hydration
• Temperature
MANAGEMENT
• Cardiac rhythm and rate.
Monitor the patient for complications, particularly signs of elevated intracranial pressure and seizures.
Refer immediately for repeat brain imaging if the patient deteriorates.[42] [43]
Level of consciousness
Assess the patient’s level of consciousness using the Glasgow Coma Scale. Monitoring of
consciousness should continue once the patient is on the hyperacute or acute stroke unit.[43]
Blood glucose
Monitor blood glucose regularly. Maintain a blood glucose concentration between 4 and 11 mmol/
Lin people with acute stroke.[42]
Give optimal insulin therapy with intravenous insulin and glucose to all adults with type 1 diabetes with
threatened or actual stroke. Follow local protocols.[42]
MANAGEMENT
37
Evidence: Glyacemic control in acute stroke
Limited available data do not show a significant benefit with tight glycaemic control compared
with usual care in patients with haemorrhagic stroke who develop post-stroke hyperglycaemia,
and there is an increased risk of hypoglycaemia. [68] [42] [43]
There is very little evidence from RCTs on glycaemic control in people with haemorrhagic stroke.
Guideline groups have therefore considered pragmatic studies (where every patient presenting
with acute stroke is included in the study) or large prospective studies when making their
recommendations.
Guidelines vary in their recommendations for target range for blood glucose in this
situation.
• The UK National Institute for Health and Care Excellence (NICE) guideline on stroke from 2008
recommends keeping blood glucose between 4 and 11 mmol/L (this was not changed in the
2022 update of this guideline).[42]
• This recommendation is underpinned by:
• Evidence from the United Kingdom Glucose Insulin in Stroke Trial (GIST-UK),
which found no support for tight blood glucose control in patients with mildly
or moderately elevated blood glucose levels following acute stroke (15% of
participants had haemorrhagic stroke)[69]
• Consensus of the guideline panel on recommended glucose range.
• The guideline panel agreed by consensus that patients with pre-existing diabetes should
continue to be treated according to current guidelines.
• The 2016 National Clinical Guideline published by the Royal College of Physicians in the
UK recommends a broader target range of 5 to 15 mmol/L, with close monitoring to avoid
hypoglycaemia.[43]
• This guideline also cites the GIST-UK trial to support this recommendation.[69]
• The European Stroke Organisation (ESO) guidelines from 2018 make a weak recommendation
against the routine use of intravenous insulin to achieve tight glycaemic control as a means to
improve functional outcome, survival, or infarct size (very low-quality evidence as assessed
using GRADE).[68]
• This recommendation is underpinned mostly by evidence from one small study (n=25)
comparing tight glycaemic control (4.4 to 6.0 mmol/L) with usual care (<8.3 mmol/L) that
found no significant difference in functional outcome (RR 0.72, 95% CI 0.14 to 3.61) or
survival (RR 0.81, 95% CI 0.40 to 1.65).[70]
MANAGEMENT
• Hypoglycaemic events (all asymptomatic) were more common with tight control (RR 3.25,
95% CI 0.39 to 27.15).
• The guideline group also considered prospective observational studies and post hoc
analysis of clinical trials on blood pressure management (ATACH, INTERACT2, and
SAMURAI-ICH) which report an association between hyperglycaemia and poor functional
outcome and an increased risk of death (although there were insufficient data to show
any impact on survival).[71] [72] [73] [74]
• There was conflicting evidence regarding haematoma growth. The ATACH post-hoc
analysis found a decline in serum glucose concentration was associated with a reduced
risk of haematoma expansion.[72] However, the INTERACT2 study did not find any
difference in haematoma growth.[74]
Blood pressure
Monitor blood pressure intensively and follow recommendations in the Rapid blood pressure lowing
section, above.
Ox ygen saturation
Aim for a target oxygen saturation of 94% to 96% in acutely ill patients 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.[56]
• A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory
failure.[57]
• The National Institute for Health and Care Excellence in the UK recommends starting oxygen if
oxygen saturation drops below 95%.[42]
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.[42] [43]
Temperature
Monitor temperature.[43] Patients with stroke can lose their thermoregulation acutely and may need
interventions in the absence of infection.
• Give an antipyretic (e.g., paracetamol) in patients with high temperature.[75]
Cardiac rhythm and rate

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
MANAGEMENT
the following is present:[45]
39
• Common causes of elevated ICP are hydrocephalus from intraventricular haemorrhage or mass
effect from the haematoma.[45]
• Haematoma evacuation and decompressive hemicraniectomy are options for treating elevated
ICP.[45]
Seizures
Consult immediately with a neurologist if the patient has uncontrolled or recurrent seizures, or
status epilepticus. See our topic Status epilepticus.
Choose an anticonvulsant based on individual patient characteristics.[45] Follow your hospital

protocol. In clinical practice, levetiracetam and sodium valproate are commonly used.
Statins
Do not start statin treatment in patients with spontaneous ICH unless required for other indications.[43]
Swallowing assessment and nutrition

On admission, ensure the patient has their swallowing function assessed by appropriately
trained staff before being given any oral food, fluid, or medication:[42] [43]
• If the admission screen indicates problems with swallowing, ensure specialist assessment
within 24 hours of admission (preferably) and not more than 72 hours afterwards.
• To avoid aspiration pneumonia, give food, fluids, and medication to people with dysphagia in a form
that can be swallowed without aspiration, after specialist assessment of swallowing.[42]
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.[42]
Optimal positioning and early mobilisation

Assess individual clinical needs and personal preferences to determine the patient’s optimal
head position. Take into account factors such as comfort, physical and cognitive abilities, and postural
control.[42]
MANAGEMENT
Evidence: Optimal positioning
Evidence shows no difference in outcomes when the patient with acute stroke is positioned
lying flat or with their head elevated. Therefore the optimum position should be individually
tailored to suit the patient. [76]
There is wide variation in clinical practice, with lying flat thought to help maintain blood flow to 'at-risk'
brain regions, but possibly increasing the risk of complications such as pneumonia. In 2019, the UK
National Institute for Health and Care Excellence (NICE) performed a systematic review for their 2019
stroke guideline update, comparing positioning patients with acute stroke lying flat versus sitting up.
The review included two studies, reported in six papers, both of PROBE (prospective, randomised,
open-label, controlled trial with blinded outcome evaluation) design.[76]
• In the pilot HeadPoST study (94 people) all participants had acute ischaemic stroke. The
intervention group lay flat for 24 hours, then from 24 to 48 hours had their heads raised slowly
to a maximum of 15°; after 48 hours, heads were elevated further to the standard 30° or more.
The control group sat up with heads elevated to 30° or more as soon as possible after the
diagnosis, and were maintained in this position for at least 48 hours.[77]
• In the full HeadPoST study (11,093 people), 8.4% of participants had acute haemorrhagic
stroke. The intervention group lay flat as soon as possible after presentation and for at least
24 hours. The control group sat up with heads elevated to at least 30° immediately upon
presentation to the emergency department and for at least 24 hours.[78]
• The NICE guideline review reported that:
• Despite the pilot trial finding that there was a possible benefit with lying down in terms
of function at 90 days, the larger full study did not find any difference between groups
(modified Rankin Scale 0-2 (2 studies; n=9840; RR 1.07; 95% CI 0.9 to 1.26; GRADE
very low quality).
• There was no clinically important difference in recurrent stroke (2 studies; n=11,185;
moderate-quality evidence assessed using GRADE), pneumonia at 90 days (1 study;
n=11,093; GRADE low quality), EQ-5D for pain/discomfort at 90 days (1 study; n=8830;
GRADE low quality), length of stay (1 study; n=94; GRADE low quality) or mortality at 90
days (2 studies; n=10,945; GRADE moderate quality).
• The guideline committee noted that large numbers of patients were excluded from enrolment
due to clinician discretion (particularly in relation to their ability to tolerate the lying flat position)
and the average stroke severity was lower and not representative of the range of stroke
severities managed within UK stroke centres.
• The committee therefore concluded that individual factors such as comfort, medical condition,
pressure care, pain, physical and cognitive abilities, orientation, alignment, postural control, and
compliance should be considered when positioning patients with acute stroke.[76]
• Despite the majority of patients in the included studies having acute ischaemic stroke, NICE
made a broad recommendation for all people with acute stroke.
MANAGEMENT
NICE’s recommendations on positioning were unchanged in the 2022 update of their stroke guideline.
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.[42]
41
Evidence: Early mobilisation (within 48 hours)
Guidelines suggest that early mobilisation (within 48 hours) may be appropriate in patients
who require minimal assistance to mobilise (e.g., those who have had a mild stroke, or are
experiencing language and/or upper limb dysfunction alone), although evidence is limited. [79]
When the UK National Institute for Health and Care Excellence (NICE) updated their guideline on
stroke in 2019, they found two studies examining early (within 48 hours) mobilisation involving a total
of 75 people.[80] [81] [79]
• The review by NICE incorporating these two studies reported that there was no significant
difference for the outcomes of mortality, functional outcome (modified Rankin Scale),
neurological deterioration, adverse events, or length of hospital stay (all very low-quality
evidence assessed using GRADE).
• The guideline panel made a consensus recommendation that mobilisation should be considered
as and when the patient’s clinical condition permits.
• Both studies were only in people with acute ischaemic stroke; however NICE made a broad
recommendation for all people with acute stroke.
NICE’s recommendations on early mobilisation were unchanged in the 2022 update of their stroke
guideline.
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.[42]
• High-intensity mobilisation refers to the very early mobilisation intervention from the AVERT
trial.[82] 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.
MANAGEMENT
Evidence: Very early mobilisation (within 24 hours)
Very early mobilisation does not seem to improve outcomes, and high intensity strategies may
cause clinical harm in early functional outcomes, possibly due to reduced cerebral perfusion.
Therefore very early mobilisation should not be actively pursued. However patients who can
mobilise with little or no help in the first 24 hours after stroke should not be discouraged from
doing so. [79] [Evidence B]
• The UK National Institute for Health and Care Excellence (NICE) review for their 2019 guideline
found six studies examining very early (within 24 hours) mobilisation involving a total of 2475
people.[79]
• Five of the studies included people with ischaemic and haemorrhagic stroke, the
remaining one only included people with ischaemic stroke.
• The majority of data was from the AVERT III 2016 trial.[83] [84] [85] [86] [82] This study used
a high-intensity mobilisation strategy beginning within 24 hours of stroke symptom onset and
including at least three additional out-of-bed (sitting, standing, or walking) sessions compared
with usual care.
• For functional outcomes there was a suggestion of clinical harm as a result of very
early mobilisation with fewer patients reaching a modified Rankin Score 0-2 at 7 days (2
studies; n=191; 118 fewer per 1000 [from 223 fewer to 20 more], low-quality evidence
assessed using GRADE); however there was no significant difference between very early
mobilisation and usual care for modified Rankin Score 0-2 at 90 days (5 studies; n=2377;
GRADE high) or 12 months (2 studies; n=2152; GRADE moderate).
• There was also no significant difference between groups for recurrent stroke (1 study;
n=71; GRADE low), neurological deterioration (1 study; n=138; GRADE very low),
adverse events (2 studies; n=209; GRADE moderate), length of hospital stay (1 study;
n=124; GRADE low) or mortality at 90 days (6 studies; n=2475; GRADE moderate).
• One small study found a statistically significant benefit of very early mobilisation for
functional outcomes measured by the Barthel index at discharge (n=90; GRADE
moderate) and at 90 days (n=80; GRADE moderate), but the guideline committee did not
consider this clinically meaningful.[79]
• NICE comments that evidence on very early mobilisation is difficult to interpret due to the
differences in intensity, timing and type of mobilisation used in the trials, and lack of stratification
by initial ability to mobilise independently.
• The NICE guideline committee consensus is not to restrict appropriate very early (within 24
hours) mobilisation in people who are independently mobile after having a stroke. NICE advises
not to start intense mobilisation (more frequent mobilisations of a longer duration than ‘usual
care’) within the first 24 hours among people who need help to sit out of bed, stand, or walk,
because this could reduce cerebral perfusion in these patients.
MANAGEMENT
NICE’s recommendations on very early mobilisation were unchanged in the 2022 update of their
stroke guideline.
43
Prevention of deep venous thrombosis and pulmonary embolism
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.[43]
Do not routinely give low molecular weight heparin (LMWH) or use graduated compression stockings.[43]
However, in practice, consider prophylactic LMWH if intermittent pneumatic compression is
contraindicated or not possible.
Procedural videos
Treatment algorithm overview

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 ( summary )
suspected intracerebral
haemorrhage
1st stabilisation and urgent referral to

hyperacute or acute stroke unit
Acute ( summary )
confirmed intracerebral haemorrhage
1st supportive care plus monitoring
plus immediate referral for neurosurgery

assessment
consider rapid blood pressure control
consider urgent reversal of anticoagulation
consider venous thromboembolism prophylaxis

plus early mobilisation
MANAGEMENT
Treatment algorithm
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 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 ).[55]
This should be done by an anaesthetist or
trained emergency department staff.
• Aim for a target ox ygen saturation of
94% to 96% in acutely ill patients 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.[56]
• A lower target SpO 2 of 88% to
92% is appropriate if the patient is
at risk of hypercapnic respiratory
failure.[57]
• The National Institute for Health
and Care Excellence in the UK
recommends starting oxygen if
oxygen saturation drops below
95%.[42]
Evidence: Target ox ygen saturation in

acutely ill adults
Too much supplemental oxygen increases

mortality .
Evidence from a large systematic review

MANAGEMENT
and meta-analysis supports conservative/

controlled oxygen therapy versus liberal
oxygen therapy in non-hypercapnic acutely ill
adults.
45
Initial
• 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 2015 Thoracic Society of Australia
and New Zealand (TSANZ) guideline
recommends 92% to 96%.[57] [59]
• 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%).[56]
• 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.
MANAGEMENT
• 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
Initial
for some specific conditions (e.g.,
pneumothorax, carbon monoxide
poisoning, cluster headache, and
sickle cell crisis).[60]
• In 2019 the BTS reviewed its guidance
in response to this systematic review
and meta-analysis and decided an
interim update was not required.[57]
• 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.
• Management of oxygen therapy in

patients in intensive care is specialised
and informed by further evidence that
is more specific to this setting.[61] [62]
[63]
Practical tip
An immediate (i.e., ideally in the next

available time slot and definitely within
1 hour of arrival at hospital, whichever
is sooner) non-contrast CT scan of
the head confirms the diagnosis of
intracerebral haemorrhage by the
presence of hyperattenuation suggesting
acute blood.[53] See the Diagnosis
recommendations section for indications
MANAGEMENT
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
47
Initial
guidelines recommend doing this within 4 hours
of presentation to hospital.[42] [43]
• On admission, ensure the patient has

their swallowing function assessed
by appropriately trained staff before
being given any oral food, fluid, or
medication:[42] [43]
• 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.[42]
MANAGEMENT
Acute
confirmed intracerebral haemorrhage
1st supportive care plus monitoring

Primary options
» paracetamol: 500-1000 mg orally every 4-6

hours when required, maximum 4000 mg/
day; 15 mg/kg (maximum 1000 mg/dose)
intravenously every 4-6 hours when required,
maximum 4000 mg/day
» Monitor the patient’s clinical status closely

for complications, particularly signs of elevated
intracranial pressure and seizures. Provide
supportive care as appropriate.[43]
» Do not start statin treatment in patients with

spontaneous ICH unless required for other
indications.[43]
» Refer immediately for repeat brain imaging if

the patient deteriorates.[42] [43]
Assess the patient’s level of consciousness
using the Glasgow Coma Scale. Monitoring of
consciousness should continue once the patient
is on the hyperacute or acute stroke unit.[43]
Blood glucose
Monitor blood glucose regularly. Maintain a
blood glucose concentration between 4 and 11
mmol/L in people with acute stroke.[42]
Give optimal insulin therapy with intravenous

insulin and glucose to all adults with type 1
diabetes with threatened or actual stroke. Follow
local protocols.[42]
Blood pressure
Monitor blood pressure intensively and follow
recommendations in the rapid blood pressure
control treatment option, below.
Ox ygen saturation
MANAGEMENT
Aim for a target oxygen saturation of 94-96%

in acutely ill patients who are not at risk of
hypercapnia.
49
Acute
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.[56]
A lower target SpO 2 of 88% to 92% is

appropriate if the patient is at risk of hypercapnic
respiratory failure.[57]
The National Institute for Health and Care

Excellence in the UK recommends starting
oxygen if oxygen saturation drops below
95%.[42]
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.[42] [43]
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.
Consider monitoring the patient for signs
of elevated intracranial pressure (ICP) and
treatment if any of the following is present:[45]
• Glasgow Coma Scale score ≤8 that is

presumed related to haematoma mass
effect
• Clinical evidence of transtentorial
herniation
• Significant intraventricular haemorrhage or
hydrocephalus.
Refer any patient who develops

MANAGEMENT
hydrocephalus to a neurosurgeon. [42] [43]
Seizures
Consult immediately with a neurologist if the
patient has uncontrolled or recurrent seizures,
Acute
or status epilepticus. See our topic Status
epilepticus.
• Choose an anticonvulsant based on

individual patient characteristics.[45]
Follow your hospital protocol. In clinical
practice, levetiracetam and sodium
valproate are commonly used.
Temperature
Monitor temperature.[43] Give an antipyretic
(e.g., paracetamol) in patients with high
temperature.[75]
plus immediate referral for neurosurgery
assessment
Treatment recommended for ALL patients in
selected patient group
» Arrange an immediate review by a
neurosurgeon to assess whether or not the
patient will benefit from neurosurgery.[45] [58]
» According to the UK National Institute for

Health and Care Excellence (NICE), people
with any of the following clinical features rarely
require surgical intervention and should receive
medical treatment initially:[42]
• Small deep haemorrhages

• Lobar haemorrhage without either
hydrocephalus or rapid neurological
deterioration
• A large haemorrhage and significant
comorbidities before the stroke
• Glasgow Coma Scale score <8 unless this
is because of hydrocephalus
• Posterior fossa haemorrhage.
consider rapid blood pressure control

Treatment recommended for SOME patients in
» Consider rapid lowering of blood pressure (BP)
for patients with ICH who have a systolic BP of
150 to 220 mmHg AND:[42]
MANAGEMENT

• 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
51
Acute
• Are not going to have early neurosurgery
to evacuate the haematoma.
» Follow your local protocol for urgent BP

lowering in these patients.[43]
» Taking into account the risk of harm, consider

rapid BP lowering on a case-by-case basis for
patients with acute ICH who have a systolic BP
of >220 mmHg OR present beyond 6 hours of
symptom onset AND:[42]
• 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.[42]
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.[66]
• NICE included seven randomised

controlled trials (RCTs) (n=5119) in
the previous 2019 review with most of
MANAGEMENT
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
Acute
study and separately considered the
combined IPD analysis.[66]
• 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
MANAGEMENT
for renal failure at 90 days (4 trials;

n=1647; RR 2.07 [95% CI 1.08 to
3.99]; GRADE moderate).
53
Acute
• 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.[66] [67] 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
MANAGEMENT
frail adults.
• TThe 2019 NICE guideline stated that

treatment should start within 6 hours
Acute
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

Primary options
Warfarin/vitamin K antagonist reversal
» prothrombin complex concentrate: consult
specialist for guidance on dose
-and-
» phytomenadione: consult specialist for
guidance on dose
OR
Dabigatran reversal
» idarucizumab: consult specialist for
guidance on dose
OR
Factor Xa inhibitor reversal

» prothrombin complex concentrate: consult
specialist for guidance on dose
» Urgently reverse abnormalities of clotting,

particularly in patients taking anticoagulants.[43]
» Return clotting levels to normal as soon as

possible in people who were on:
• Warfarin (and have elevated international

normalised ratio [INR]) or another
MANAGEMENT
vitamin K antagonist: give a combination

of prothrombin complex concentrate
(4-factor) and intravenous vitamin K
(phytomenadione)[42] [43]
• Dabigatran: reverse with idarucizumab[43]
55
Acute
• Factor Xa inhibitor: treat with prothrombin
complex concentrate (4-factor).[43]
consider venous thromboembolism prophylaxis

plus early mobilisation
» 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.[43]
• Do not routinely give low molecular

weight heparin (LMWH) or use graduated
compression stockings.[43] However, in
practice, consider prophylactic LMWH
if intermittent pneumatic compression is
contraindicated or not possible.
» 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.[42] 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.[42]
• High-intensity mobilisation refers to

the very early mobilisation intervention
from the AVERT trial.[82] 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.
MANAGEMENT
Emerging
Surgical techniques
Post hoc subgroup analyses of the STICH (Surgical Trial in Intracerebral Haemorrhage) trial suggested a
benefit for resection of haematomas <1 cm from the brain surface and possible harm from resection for
patients in coma (Glasgow Coma Scale ≤8).[179] Some data support the possibility of a good outcome
with early resection (<12 hours), despite a possible higher rate of recurrent bleeding.[45] Extensive
research is being done to assess the benefit of haematoma drainage through minimally invasive surgery.
An extensive meta-analysis showed that patients with supratentorial intracerebral haemorrhage (ICH) may
benefit from minimally invasive draining techniques, especially when suffering superficial 25 mL to 40 mL
haematomas.[180] The phase 2, randomised, controlled, open-label MISTIE trial showed that minimally
invasive surgery plus alteplase appears to be safe in patients with ICH; however, increased asymptomatic
bleeding was a major finding.[181] The STICH II trial confirmed that early surgery of superficial haemorrhage
may offer a small survival advantage, especially in the non-comatose group of patients that present with or
progress to a decreased level of consciousness (Glasgow Coma Score 9 -12).[182] The ICES study also
showed that early intraoperative stereotactic computed tomography (CT)-guided endoscopic surgery is a
safe and effective method to remove acute ICHs.[183] The use of recombinant tissue plasminogen activator
(r-TPA) has been shown to accelerate resolution of intraventricular haemorrhage.[184]
Andexanet alfa
A recombinant modified human factor Xa decoy protein that binds factor Xa inhibitors, resulting in decreased
anti-Xa activity and thrombin generation. It has been approved for use in adults treated with the direct factor
Xa inhibitors apixaban and rivaroxaban when reversal of anticoagulation is needed due to life-threatening
or uncontrolled bleeding. There is an ongoing trial, which aims to determine the efficacy and safety of
andexanet alfa compared to usual care in patients presenting with acute intracranial haemorrhage within 6
hours of symptom onset and within 15 hours of taking an oral factor Xa inhibitor.[185]
Haemostatic therapy
Treatment with recombinant activated factor VII prevented haematoma growth but failed to improve clinical
outcomes in a phase III trial.[19] Future trials may investigate whether recombinant activated factor VII is
more effective in selected patient subgroups. Additional basic research has been performed on cilostazol (a
phosphodiesterase-3 inhibitor) to prevent intravenous tissue plasminogen activator-associated haemorrhagic
transformation and warfarin-induced haemorrhage. Cilostazol has been shown to have protective properties
on endothelial cells, vascular smooth muscle cells, and the blood-brain barrier, yet clinical trials are needed
to investigate if such properties would be of benefit in haemorrhagic stroke or prevention of haematoma
expansion.[186]
Novel rehabilitation techniques

Newer techniques such as non-invasive brain stimulation with transcranial direct current stimulation (tDCS)
as well as repetitive transcranial magnetic stimulation (rTMS) are currently being studied. Such methods are
believed to increase functional recovery, when compared with traditional physiotherapy, via neuromodulatory
pathways.[187]
Primary prevention
Use the QRISK assessment tool to assess cardiovascular disease (CVD) risk for the primary prevention of
CVD (including intracerebral haemorrhage [ICH]) in people aged ≤84 years.[40] Hypertension and heavy
alcohol use are the strongest risk factors for ICH.
MANAGEMENT
Advise those at high risk of developing cardiovascular disease on lifestyle measures that reduce the risk of a
stroke, including recommendations to:[40]
• Exercise regularly
57
• Maintain a cardioprotective diet
• Manage weight
• Reduce alcohol consumption
• Stop smoking.
Manage underlying conditions that predispose a patient to stroke such as:[41]
• Hypertension
• Hypercholesterolaemia
• Type 1 and type 2 diabetes
• Atrial fibrillation
• Transient ischaemic attacks.
Secondary prevention
Start secondary prevention measures for all patients as soon as possible after the diagnosis is
confirmed.[43] Secondary prevention is started in hospital and should be followed up in primary care,
particularly blood pressure monitoring and treatment.[43] [190]
• Advise patients on lifestyle measures including recommendations to:[43]
• Exercise regularly
• Maintain a healthy diet
• Manage weight
• Reduce alcohol consumption
• Stop smoking
• Reduce caffeine intake in people with hypertension.[191]
• Review medications used in secondary prevention. In particular, monitor blood pressure lowering
treatment frequently and adjust treatment as tolerated to achieve and maintain a smooth target systolic
blood pressure below 130 mmHg.[43]
• Optimise management of other comorbidities and risk factors such as diabetes mellitus; cerebral
amyloid angiopathy; heavy alcohol, amphetamine drugs, or cocaine use; antiplatelet, anticoagulant,
and statin use.
Patient discussions
Advise patients to stop smoking, reduce their alcohol consumption, and exercise regularly.
MANAGEMENT
Stroke due to spontaneous intracerebral haemorrhage Follow up
Monitoring
Monitoring
FOLLOW UP
Monitor the patient’s clinical status closely for complications, particularly signs of elevated intracranial
pressure and seizures. Provide supportive care as appropriate.[43]
Refer immediately for repeat brain imaging if the patient deteriorates.[42] [43]
Assess the patient’s level of consciousness using the Glasgow Coma Scale. Monitoring of consciousness
should continue once the patient is on the hyperacute or acute stroke unit.[43]
Blood glucose
Monitor blood glucose regularly. Maintain a blood glucose concentration between 4 and 11 mmol/L in
people with acute stroke.[42]
Give optimal insulin therapy with intravenous insulin and glucose to all adults with type 1 diabetes with
threatened or actual stroke. Follow local protocols.[42]
Blood pressure
Monitor blood pressure intensively and follow recommendations in the Rapid blood pressure lowering
section of Management recommendations.
Ox ygen saturation
Aim for a target oxygen saturation of 94% to 96% in acutely ill patients 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.[56]
• A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory
failure.[189]
• The National Institute for Health and Care Excellence in the UK recommends starting oxygen if
oxygen saturation drops below 95%.[42]
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.[42] [43]
Temperature
Monitor temperature.[43] Give an antipyretic (e.g., paracetamol) in patients with high temperature.[75]
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.
Consider monitoring the patient for signs of elevated intracranial pressure (ICP) and treatment if any of
the following is present:[45]
59
FOLLOW UP
Refer any patient who develops hydrocephalus to a neurosurgeon.[42] [43]
Seizures
Consult immediately with a neurologist if the patient has uncontrolled or recurrent seizures, or status
epilepticus. See our topic Status epilepticus.
• Choose an anticonvulsant based on individual patient characteristics.[45] Follow your

hospital protocol. In clinical practice, levetiracetam and sodium valproate are commonly used.
Complications
Complications Timeframe Likelihood

infection short term medium
Preventable infections include aspiration pneumonia, urinary tract infection, and cellulitis from infected
pressure ulcers.
deep venous thrombosis/pulmonary embolism short term medium
Consider either anticoagulation or use of a vena caval filter in patients who develop symptomatic
deep venous thrombosis or pulmonary embolism to prevent the development of further pulmonary
emboli.[42] Use your clinical judgement to individually assess the risk-benefit balance of using (or
avoiding) anticoagulant treatment in a patient with intracerebral haemorrhage and pulmonary embolism.
There is no evidence to guide the management of these patients.[43]
seizures long term medium
Seizures may complicate up to 8% of intracerebral haemorrhages and may develop into epilepsy.[188]
The risk is higher with cortical bleeds.
delirium variable high
A period of delirium is common following intracerebral haemorrhage.
aspiration pneumonia variable medium
Stroke-related dysphagia results in aspiration and subsequent pneumonia.[46]
A dysphagia screen is recommended in stroke patients before oral intake.
When aspiration pneumonia occurs, treatment is with antibiotics with consideration of enteral feeding.
Prognosis
FOLLOW UP
Mortality is significantly higher than for ischaemic stroke, in the range of 35% to 40%.[10] Only 20% to 30%
of all patients are well enough to live independently by 3 to 6 months. Haemorrhage volume is the strongest
predictor of outcome. Advanced age, impaired consciousness at presentation, and rupture of the haematoma
into the ventricular system are also associated with worse outcomes.[21]
61
Stroke due to spontaneous intracerebral haemorrhage Guidelines
Diagnostic guidelines
United Kingdom
Stroke and transient ischaemic at tack in over 16s: diagnosis and initial
management
Published by: National Institute for Health and Care Excellence Last published: 2022
National clinical guideline for stroke

Published by: Royal College of Physicians Last published: 2016
Europe
EFNS guidelines on the use of imaging in cerebrovascular disease

GUIDELINES
Published by: European Academy of Neurology (European Federation Last published: 2011
of Neurological Societies)
North America
ACR appropriateness criteria: cerebrovascular disease

Published by: American College of Radiology Last published: 2021
Guidelines for the management of spontaneous intracerebral hemorrhage

Published by: American Heart Association; American Stroke Last published: 2015
Association
Canadian stroke best practice recommendations: acute stroke management

Published by: Heart and Stroke Foundation of Canada Last published: 2018
Oceania
Clinical guidelines for stroke management

Published by: National Stroke Foundation (Australia) Last published: 2019
Stroke due to spontaneous intracerebral haemorrhage Guidelines
Treatment guidelines
United Kingdom
Stroke and transient ischaemic at tack in over 16s: diagnosis and initial
management
Published by: National Institute for Health and Care Excellence Last published: 2022
National clinical guideline for stroke

Published by: Royal College of Physicians Last published: 2016
Europe
Management of spontaneous intracerebral hemorrhage
GUIDELINES
Published by: European Stroke Organisation Last published: 2014
North America
An evidence based guideline: prophylaxis of venous thrombosis in

neurocritical care patients
Published by: Neurocritical Care Society Last published: 2016
Guidelines for the management of spontaneous intracerebral hemorrhage

Published by: American Heart Association; American Stroke Last published: 2015
Association
Canadian stroke best practice recommendations: acute stroke management

Published by: Heart and Stroke Foundation of Canada Last published: 2018
Parenteral anticoagulants: antithrombotic therapy and prevention of

thrombosis, 9th ed. American College of Chest Physicians evidence-based
clinical practice guidelines
Published by: American College of Chest Physicians Last published: 2012
Oceania
Clinical guidelines for stroke management

Published by: National Stroke Foundation (Australia) Last published: 2019
63
Stroke due to spontaneous intracerebral haemorrhage Evidence tables
Evidence tables
How does very early mobilisation compare with standard care after stroke?
EVIDENCE TABLES
This table is a summary of the analysis reported in a Cochrane Clinical Answer that focuses on the
above important clinical question.
View the full source Cochrane Clinical Answer
Evidence B * Confidence in the evidence is moderate or low to moderate where GRADE has been
performed and there may be no difference in effectiveness between the intervention
and comparison for key outcomes.
Population: Adults with acute stroke (mean age 60 to 77 years) #

Intervention: Very early mobilisation (median time to mobilisation after stroke 18.5 hours: range 13.1 to 43
hours)
Comparison: Standard care (median time to mobilisation after stroke 33.3 hours: range 22.5 to 71.5 hours)
† ‡
Outcome Effectiveness (BMJ rating) Confidence in evidence (GRADE)
Mortality (median 3‐month No statistically significant Moderate

follow‐up) difference
Death or dependency (median No statistically significant Moderate

3‐month follow‐up) difference
Death or institutional care No statistically significant GRADE assessment not performed for
difference this outcome
Activities of daily living (ADL) Favours intervention Low

score (median 3‐month follow‐
up)
Able to walk No statistically significant GRADE assessment not performed for

difference this outcome
Duration of acute hospital stay Favours intervention Low
Complications (median 3‐ No statistically significant Low

month follow‐up) difference
Note
The Cochrane review which this Cochrane Clinical Answer (CCA) is based on states that a cautious
approach to active mobilisation within 24 hours of a stroke is supported due to the evidence suggesting that
it may carry some increased risk. It notes that although they included nine studies (N=2958), most of the
Stroke due to spontaneous intracerebral haemorrhage Evidence tables
evidence was based on the largest study (AVERT III, N=2104). The Cochrane review also performed an
exploratory network meta-analysis that suggested mobilisation at 24 hours may produce the best outcome
(low-quality evidence as assessed by GRADE).
EVIDENCE TABLES
# For the included studies the median percentage of people with an intracerebral haemorrhage was 12%.
See CCA for more details.
* Evidence levels
The Evidence level is an internal rating applied by BMJ Best Practice. See the EBM Toolkit for details.
Confidence in evidence
A - High or moderate to high

B - Moderate or low to moderate
C - Very low or low
† Effectiveness (BMJ rating)

Based on statistical significance, which demonstrates that the results are unlikely to be due to chance, but
which does not necessarily translate to a clinical significance.
‡ Grade certainty ratings
High The authors are very confident that the true

effect is similar to the estimated effect.
Moderate The authors are moderately confident that
the true effect is likely to be close to the
estimated effect.
Low The authors have limited confidence in the
effect estimate and the true effect may be
substantially different.
Very Low The authors have very little confidence in
the effect estimate and the true effect is
likely to be substantially different.
BMJ Best Practice EBM Toolkit: What is GRADE?
65
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Stroke due to spontaneous intracerebral haemorrhage Images
Images
IMAGES
Figure 1: Intracranial haemorrhage on CT scan

Massachusetts General Hospital personal case files; used with permission
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Contributors:
// Peer Reviewers:
David Werring, FRCP, PhD, FESO

Professor of Clinical Neurology
Head of Research Department, Brain Repair and Rehabilitation, UCL Institute of Neurology, Honorary
Consultant Neurologist, National Hospital for Neurology and Neurosurgery, University College Hospitals
NHS Foundation Trust, North Thames Clinical Research Specialty Lead for Stroke, NIHR Clinical Research
Network, London, UK
DISCLOSURES: DW has received honoraria (speaking) from Bayer 2016, 2017, 2018 (talks or debates
on intracerebral haemorrhage, atrial fibrillation, dementia) and honoraria (chairing) from Portola and Bayer
2019. DW has received consultancy fees from Bayer (2017; embolic stroke of undetermined source),
JFB consulting (2018; PCSK9 inhibitors in stroke), Alnylam (2019; cerebral amyloid angiopathy), Portola
(2019, 2020; andexanet alpha). JW was UCL Principle Investigator for NIHR clinical trials NAVIGATE-
ESUS (Bayer, 2016-19), B2341002 (Pfizer 2014-2016), Action-2 (Biogen, 2016-19); Chief Investigator for
OPTIMAS; steering committee and co-investigator for RESTART, TICH-2.
// Expert Advisers:
Mat thew Jones, MD, FRCP

Consultant Neurologist
Greater Manchester Neurosciences Centre, Salford Royal Foundation Trust, Honorary Senior Lecturer,
University of Manchester, Manchester, UK
DISCLOSURES: MJ is the chair of the Association of British Neurologists Education Committee (unpaid
position). MJ is a faculty member of an MRCP revision course.
Acknowledgements,
BMJ Best Practice would like to gratefully acknowledge the previous expert contributors, whose work has
been retained in parts of the content:
Fernando D. Goldenberg, MD, Clinical Associate of Neurology, Medical Director, Neuroscience ICU,
Director, Neurocritical Care Education, Co-Director, Stroke Center, University of Chicago, Chicago, IL, Raisa
C. Martinez, MD, Neurocritical Care Fellow, Department of Neurology, University of Chicago, Chicago, IL
DISCLOSURES: FDG and RCM declare that they have no competing interests.
// Editors:
Helena Delgado-Cohen,
Section Editor, BMJ Best Practice
DISCLOSURES: HDC declares that she has no competing interests.
Tanna z Aliabadi-Oglesby,
Lead Section Editor, BMJ Best Practice
DISCLOSURES: TAO declares that she has no competing interests.
Julie Costello,
Comorbidities Editor, BMJ Best Practice
Contributors:
DISCLOSURES: JC declares that she has no competing interests.
Adam Mitchell,
Drug Editor, BMJ Best Practice
DISCLOSURES: AM declares that he has no competing interests.

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Stroke due to spontaneous

Straight to the point of care

Last updated: Oct 12, 2022

Most intracerebral haemorrhages occur in the absence of vascular malformations, aneurysms, or

Asian, black and/or Hispanic

heavy alcohol use

illicit sympathomimetic drugs

family history of intracerebral haemorrhage

autosomal dominant mutations in the COL4A1 gene

hereditary haemorrhagic telangiectasia

autosomal dominant mutations in the KRIT1 gene, CCM2 gene, or PDCD10

non-steroidal anti-inflammatories (NSAIDs)

A case-control study showed a relationship between the over-the-counter drug phenylpropanolamine,

• Idiopathic (no identifiable vascular malformations or associated diseases)

• An identifiable vascular malformation

Location of intracerebral haemorrhage[3]

• CT enables quick differentiation between ischaemic stroke and spontaneous intracerebral

Suspect stroke in a patient with sudden onset of focal neurological symptoms:[44]

• Unilateral weakness or paralysis in the face, arm, or leg

Suspect subarachnoid haemorrhage in anyone presenting with sudden severe (thunderclap)

Use a validated tool to aid diagnosis in people with suspected stroke:

Exclude hypoglycaemia (a stroke mimic) as the cause of sudden neurological symptoms.[42]

• Indications for thrombolysis or thrombectomy

See Management section for details.

Order in all patients:

• Serum glucose[42] [46]

Consider a serum toxicology screen if you suspect use of toxic substances.[45]

• Unilateral weakness or paralysis in the face, arm, or leg

• Sensory loss (numbness)

• Dysarthria or expressive or receptive dysphasia

• Dysarthria may accompany facial weakness or cerebellar dysfunction.

• Usually of insidious onset and gradually increasing intensity in ICH.

• Difficulty with coordination and altered gait

• In the absence of muscle weakness, impaired coordination points to haemorrhage involving

Other symptoms include:

• May either be due to posterior circulation haemorrhage or reflect increased intracranial

• Common especially in older people with previous strokes or cognitive dysfunction.

• Often horizontal and unidirectional.

Suspect subarachnoid haemorrhage in anyone presenting with sudden severe (thunderclap)

In the emergency department

• Score -1 point for each feature (clinical history):

• Loss of consciousness or syncope

• Score +1 point for each feature (neurological history):

• Asymmetrical face weakness

• Score 1 point for each feature:

Evidence: FAST and ROSIER scales to identify stroke

• This recommendation is underpinned by evidence from a prospective cohort study of 487

• This recommendation is underpinned by evidence from a prospective cohort study which

• ICH may be related to hyperperfusion after such procedures.

• Dementia: associated with amyloid angiopathy

Ask about common risk factors for spontaneous ICH:

• Uncontrolled hypertension is the most common risk factor.[22]

Suggestive of mimic Suggestive of stroke

• Neurological symptoms and signs • Exact time of onset[52]

The most common findings on neurological examination are:

• Altered level of consciousness

Refer to hyperacute or acute stroke unit

• Indications for thrombolysis or thrombectomy

Intracranial haemorrhage on CT scan

• Hypoglycaemia is a stroke mimic; hyperglycaemia has been associated with intracerebral

• To exclude electrolyte disturbance (e.g., hyponatraemia) as a cause for neurological signs.

• Serum urea and creatinine

• Liver function tests