Ischaemic Stroke FM

Ischaemic stroke
Straight to the point of care
Last updated: Jan 24, 2023

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Risk factors 4
Aetiology 7
Pathophysiology 8
Classification 8
Case history 9
Diagnosis 11
Recommendations 11
History and exam 27
Investigations 31
Differentials 38
Management 41
Recommendations 41
Treatment algorithm overview 75
Treatment algorithm 77
Emerging 107
Primary prevention 107
Secondary prevention 108
Patient discussions 109
Follow up 110
Monitoring 110
Complications 113
Prognosis 114
Guidelines 115
Diagnostic guidelines 115
Treatment guidelines 116
References 119
Images 132
Disclaimer 135
Ischaemic stroke Overview
Summary
Ischaemic stroke is a leading cause of morbidity and mortality. If you suspect stroke, work rapidly through the
initial assessment and aim for quick access to CT scan. Early initiation of thrombolysis (i.e., within 4.5 hours
OVERVIEW
from onset of symptoms, if not contraindicated) is associated with improved functional outcomes.
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.
Admit everyone with suspected stroke directly to a hyperacute or acute stroke unit within 4 hours of
presentation.
Request an immediate (i.e., ideally in the next available time slot and definitely within 1 hour of arrival at
hospital) non-enhanced CT scan if indicated. Ischaemic stroke is a clinical diagnosis based on signs and
symptoms. A normal CT scan does not rule out a stroke but will rule out intracranial haemorrhage, which
must be excluded before starting thrombolysis.
Admit the patient directly to a hyperacute or acute stroke unit as soon as possible; UK guidelines recommend
doing this within 4 hours of presentation to hospital.
Intravenous alteplase should be given (if not contraindicated) if treatment is started as soon as possible
within 4.5 hours of onset of symptoms AND intracranial haemorrhage has been excluded by imaging.
Mechanical thrombectomy can be performed in selected patients within 6 to 24 hours of symptoms onset.
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 further subdivided into ischaemic stroke (caused by vascular occlusion or stenosis) and
haemorrhagic stroke (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid
haemorrhage). Central venous sinus thrombosis is a rare form of stroke that occurs due to thrombosis of the
dural venous sinuses. This topic focuses on the first 24 hours of acute care of patients with ischaemic stroke.
For information on other types of stroke, see Stroke due to spontaneous intracerebral haemorrhage ,
Subarachnoid haemorrhage , and Cavernous sinus thrombosis .
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jan 24, 2023.
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.
Ischaemic stroke 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.[5] [6] [7] People are most likely to have a stroke over the age of 55.[6] [8] Ischaemic
THEORY
stroke prevalence can be further sub-divided according to pathophysiological mechanism: extracranial

atherosclerosis (10%), intracranial atherosclerosis (10%), cardioembolic (25%), lacunar infarction ([small
vessel disease] 15%), indeterminate aetiology ([i.e., cryptogenic] 30%), or other defined causes (10%).
Ischaemic stroke is more common in older people, people with lower levels of education, and African-
American or Hispanic people.[9]
The overall incidence of stroke as well as stroke mortality has been decreasing over the last few decades
in high-income countries; this is thought to be driven by effective primary prevention and improvements in
stroke care.[10] However, there is some evidence of increasing incidence among young adults.[10] [11] The
bulk of the global stroke burden (86% of deaths and 89% of disability-adjusted life-years, or DALYs) is in
lower-income and lower-middle-income countries where stroke incidence has increased.[12] [13] [14] [15]
Between 1990 and 2016, the highest risks for stroke were seen in East Asia, Central Europe, and Eastern
Europe, and the lowest risk was in eastern sub-Saharan Africa.[14]
Risk factors
Strong
older age
Even after controlling for other age-related conditions such as hypertension, this remains a strong non-
modifiable risk factor.[9]
family history of stroke

Stroke-causing genetic disorders with mendelian inheritance are rare. However, twin studies show that
a significant portion of stroke risk is heritable, and epidemiological studies show that family history of
stroke is a risk factor.[17]
Numerous candidate genes have been proposed, but none have yet been consistently replicated as a
strong risk factor for stroke.[18]
history of ischaemic stroke or TIA

History of previous ischaemic stroke indicates that the patient may sustain more ischaemic strokes
in the future (particularly if risk factors, e.g., hypertension, are not corrected). Stroke rate has been
reported as 1.5%, 2.1%, 2.8%, 3.7%, and 5.1% on days 2, 7, 30, 90, and 365, respectively, after
transient ischaemic attack (TIA).[19] Studies show that the rate of post-TIA stroke might have
decreased slightly since 1999, likely related to advances in cardiovascular risk prevention.[20] [21]
hypertension
Strongly associated with increased incidence of ischaemic stroke.[22]
smoking
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jan 24, 2023.
diabetes mellitus
atrial fibrillation
THEORY
Strongly implicated in the risk of cardioembolic stroke but not other ischaemic stroke sub-types.[25]
comorbid cardiac conditions

Several other cardiac conditions have been reported as potential causes of cardioembolism, with
varying degrees of evidence. These conditions include myocardial infarction with regional wall
motion abnormalities or decreased left ventricular ejection fraction, valvular disease, patent foramen
ovale with or without atrial septal aneurysm, mitral valve prolapse, prosthetic heart valve, and
cardiomyopathy.[26]
carotid artery stenosis

Modestly associated with risk of first ever ipsilateral ischaemic stroke and strongly associated with
stroke recurrence after ipsilateral ischaemic stroke.[27] [28]
Degree of stenosis is related to the risk of recurrent stroke.[29]
sickle cell disease

Associated with vascular stenosis, brain ischaemia, and Moyamoya disease (vascular occlusion
affecting circle of Willis). In children, prophylactic transfusion based on transcranial Doppler ultrasound
criteria has been shown to lower subsequent stroke risk.[30]
dyslipidaemia
Large prospective studies have shown that increased serum total cholesterol is modestly associated
with an increased risk of ischaemic stroke.[31]
There are few studies on the association of low-density lipoprotein cholesterol with stroke, and the
results are conflicting.[26] A meta-analysis showed that increased high-density lipoprotein is protective
against ischaemic stroke.[32]
lower levels of education

Stroke symptoms are more likely among those with lower income and lower educational attainment.[9]
Weak
African-American or Hispanic ancestry
Have been associated with increased incidence of ischaemic stroke.[9] [33] [34] Compared with white
people, the risk of having a first stroke is nearly twice as high for black people, and black people are
twice as likely to die from stroke.[9] [35] Higher rates of hypertension, obesity, and diabetes mellitus
among black people might account for some of this disparity.[34] [36]
poor diet and nutrition

Epidemiological studies show a relationship between decreased stroke risk and increased
consumption of fruits and vegetables, decreased consumption of sodium, and increased consumption
of potassium.[37] [38] [39] [40]
5
The effects of decreased sodium and increased potassium intake may be mediated by a lower risk of
hypertension.
physical inactivity
THEORY
Decreased physical activity has been associated with increased risk of ischaemic stroke.[41]
obesity
Overweight and obese people have a modestly increased risk of ischaemic stroke.[42] [43]
alcohol abuse
Heavy alcohol use is associated with an increased risk of ischaemic stroke.[44]
Light to moderate alcohol consumption may be protective against ischaemic stroke.[44]
oestrogen-containing therapy
A small increased risk of ischaemic stroke may be present in users of oral contraceptive pills; however,
studies are conflicting.[45]
Clinical trials of oestrogen or oestrogen plus progestogen in post-menopausal women have shown an
increased incidence of ischaemic stroke.[46] [47]
obstructive sleep apnoea

Severe obstructive sleep apnoea doubles the risk for incident stroke, especially in young to middle-
aged people. Continuous positive airway pressure (CPAP) may reduce stroke risk, but trials have not
provided a high level of evidence to support the benefits of CPAP for primary stroke prevention.[48]
[49]
illicit drug use

Several drugs may influence stroke risk. Cocaine and other drugs may cause changes in blood
pressure or vasculitic-type changes in the intracranial circulation.
Unsafe intravenous injections may lead to infective endocarditis with subsequent cardioembolism, or
paradoxical embolism of injected foreign material.
migraine
Case-control studies show an elevated risk of stroke associated with migraine, particularly in younger
women and in those with migraine with aura.[50]
hyperhomocysteinaemia
Prospective and case-control studies show that higher serum homocysteine levels are associated with
a higher risk of ischaemic stroke. However, a randomised trial of homocysteine lowering to prevent
stroke showed no benefit of therapy.[51] Subsequent studies with stroke as a secondary endpoint have
shown varying results.[52] [53] Therefore, although homocysteine is clearly a marker of ischaemic
stroke risk, it remains unclear whether homocysteine itself causes stroke.
elevated lipoprotein(a)
Most studies of lipoprotein(a) and ischaemic stroke show increased risk with higher lipoprotein(a)
levels. Lipoprotein(a) levels can be lowered with niacin, but it is not known whether lipoprotein(a)
reduction reduces the risk of ischaemic stroke.
THEORY
hypercoagulable states
Elevated anti-cardiolipin or anti-beta2-glycoprotein-1 antibody levels have been associated with stroke.
Hereditary conditions associated with venous thromboembolism (e.g., antithrombin III deficiency,
protein C deficiency, protein S deficiency, factor V Leiden mutation, or prothrombin gene mutations)
have not been found to be risk factors for ischaemic stroke but are related to the risk of cerebral
venous sinus thrombosis.[26] [54]
The possibility that hypercoagulable states may be more strongly associated with certain stroke sub-
groups, including stroke in young people, is plausible but has not been evaluated in large studies.
elevated C-reactive protein

Associated with an increased risk of stroke after controlling for other risk factors.[55] Whether it directly
causes stroke or is merely a marker of risk is uncertain.
aortic arch plaques

Aortic arch plaques may be a risk factor for recurrent stroke and death. In cases of cryptogenic
strokes, further diagnostic tests are warranted to search for large aortic plaques.[56]
Aetiology
Ischaemic stroke is a syndrome, not a disease. It is caused by a transient or permanent critical reduction
in cerebral blood flow due to arterial occlusion or stenosis. Identification of the underlying mechanisms and
aetiologies is important so that appropriate therapy can be initiated to decrease the risk of recurrent stroke.
A classification scheme for ischaemic stroke developed for the Trial of Org 10172 in Acute Stroke Treatment
(TOAST) provides a framework for determining the stroke mechanism, with implications for identifying the
underlying aetiology:[3]
• Large artery atherosclerosis affects the extracranial carotid or vertebral arteries, or less commonly the
major intracranial arteries. It is a site for thrombus formation that then embolises to distal sites and/or
occludes the vessel.
• Small vessel (lacunar) stroke is caused by thrombotic occlusion of a small penetrating artery affected
by lipohyalinosis (lipid accumulation due to ageing and hypertension), resulting in a <1.5-cm infarct in
the perfusion territory of the affected small vessel.
• Cardioembolism results from thrombus formation in the heart, which then embolises to the intracranial
circulation, and is associated with cardiac disease such as atrial fibrillation. Accumulating evidence
suggests that aortic atherosclerotic plaque is another potential source of thrombus formation with
embolism.
• Strokes of other determined aetiology may be caused by various diseases of the intracranial or
extracranial vessels (e.g., dissection, vasculitis, venous thrombosis) or haematological system (e.g.,
sickle cell anaemia, antiphospholipid antibody syndrome, and other hypercoagulable states).
7
• Strokes of indeterminate aetiology, despite complete work-up, are not uncommon. In the Northern
Manhattan Stroke Study, 32% of strokes had no identifiable aetiology.[16]
THEORY
Pathophysiology
Regardless of the aetiology, ischaemic stroke occurs when blood supply in a cerebral vascular territory is
critically reduced due to occlusion or critical stenosis of a cerebral artery. A minority of ischaemic strokes are
caused by cerebral sinus or cortical vein thrombosis. These are frequently associated with a prothrombotic
(hypercoagulable or hyperaggregable) state, with resulting venous insufficiency and reduced blood flow.
Pathophysiologically, ischaemic stroke can be broadly classified as:
• Primary vascular pathologies (e.g., atherosclerosis, aortic arch atherosclerosis, arterial dissection,
migraine, or vasculitis) that directly reduce cerebral perfusion and/or result in artery-to-artery embolism
(i.e., stenosis or occlusion of a distal artery by an embolus originating in a proximal artery)
• Cardiac pathologies (e.g., atrial fibrillation, myocardial ischaemia/infarction, patent foramen ovale) that
lead to cerebral arterial occlusion due to embolism
• Haematological pathologies (e.g., prothrombotic hypercoagulable or hyperaggregable states) that

directly precipitate cerebrovascular thrombosis (particularly venous), or facilitate systemic venous or
intracardiac thrombus formation and cardioembolism.
Classification
Oxford Community Stroke Project classification system (also
known as the Bamford or Oxford classification)[2]
Classifies ischaemic stroke based on the initial presenting symptoms and clinical signs. This system does not
require imaging to classify the stroke, instead, it is a purely clinical diagnosis.
• Total anterior circulation stroke

• Partial anterior circulation stroke
• Posterior circulation stroke
• Lacunar syndrome
Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria[3]

Classifies ischaemic stroke according to pathophysiology:
Large artery atherosclerosis
• Infarction in the perfusion territory of an extracranial or intracranial artery with >50% stenosis, and no
other likely cause of stroke.
Cardioembolism
• Infarction in the presence of at least 1 cardiac condition strongly associated with stroke, such as atrial
fibrillation.
Small vessel occlusion
THEORY
• Infarction <1.5 cm in diameter in the perfusion territory of a small penetrating blood vessel.
Stroke of other determined aetiology
• Examples include cerebral infarction caused by vasculitis, arterial dissection, and hypercoagulable
states.
Stroke of indeterminate aetiology
• Infarction in the setting of 2 or more different potential aetiologies, no potential aetiology despite
complete diagnostic evaluation, or an incomplete evaluation.
Causative classification of stroke modified TOAST criteria[4]

This web-based validated classification algorithm sub-types ischaemic stroke according to pathophysiological
mechanism. Categories are:
• Large artery atherosclerosis

• Cardio-aortic embolism
• Small artery occlusion
• Other causes
• Indeterminate causes.
Indeterminate causes are divided into:
• Unknown - embolic stroke of undetermined source

• Unknown - multiple causes
• Unknown - incomplete evaluation.
Each sub-type except for the indeterminate group is sub-divided based on the weight of evidence as:
• Evident
• Probable
• Possible.
Case history
Case history #1
A 70-year-old right-handed man is discovered by a family member to have difficulty speaking and
comprehending spoken language, and an inability to raise his right arm. He was last known to be fully
9
functional 1 hour ago when the family member spoke to him by phone. There is a history of treated
hypertension and diabetes.
Other presentations
THEORY
The presenting symptoms of stroke vary by cerebral location. Most common symptoms are partial or
total loss of strength in upper and/or lower extremities, expressive and/or receptive language dysfunction,
sensory loss in upper and/or lower extremities, visual field loss, slurred speech, or difficulty with fine
motor co-ordination and gait. In most cases the symptoms appear rapidly, over seconds or minutes,
and may be preceded by one or more transient ischaemic attacks. There are no symptoms or signs
that reliably distinguish between ischaemic and haemorrhagic stroke. The acute onset of neurological
symptoms referable to the brain territory of a cerebral artery strongly suggests ischaemic stroke, but
mimicking conditions such as intracerebral haemorrhage, focal seizure, and complicated migraine need to
be considered and excluded.
Ischaemic stroke 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.
• Early initiation of intravenous thrombolysis (i.e., within 4.5 hours of onset of symptoms, if it is not
contraindicated) is associated with improved functional outcomes.[60] [61]
Suspect stroke in a patient with sudden (new, acute onset, or on awakening from sleep) focal
neurological symptoms:[62]
• 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.
Exclude hypoglycaemia (a stroke mimic) as the cause of these symptoms.[63]
Use a validated tool to aid diagnosis in people with suspected stroke:[63]
• In the emergency department: use the ROSIER scale (Recognition of Stroke in the
Emergency Room) to establish the diagnosis rapidly.[63]
• In the community: use FAST (Face Arm Speech Test) to screen people with sudden onset of
neurological symptoms for stroke.[63]
Admit everyone with suspected stroke directly to a hyperacute (or acute) stroke unit as soon as
possible; UK guidelines recommend doing this within 4 hours of presentation.[63] [64]
DIAGNOSIS
Determine the time of symptom onset because this is the main factor that will determine eligibility for
thrombolysis (i.e., within 4.5 hours of onset for intravenous thrombolysis).[63] [64]
• If the onset was unwitnessed, the definition of symptom onset is the time when the patient was
last seen well.[63]
Request an immediate non-contrast CT scan of the head to exclude intracerebral

haemorrhage (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:[63] [64]
• 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.
11
Remember:
• Ischaemic stroke is a clinical diagnosisbased on signs and symptoms.

• A normal CT scan does not rule out a stroke; particularly in the first few hours, the CT scan
can be normal, or show very subtle changes of ischaemia.
Key Recommendations
Obtain a brief history (including from witnesses or next of kin) followed by an abbreviated neurological
examination using the National Institutes of Health Stroke Scale.[65]
• 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.
• In people with an altered level of consciousness or coma, exclude haemorrhage and other mimics
such as seizures. See Differentials .
In people without indications for immediate CT head, request scan as soon as possible and
definitely within 24 hours of symptom onset.[63]
• Consider diffusion-weighted magnetic resonance imaging (MRI) of the head if the

diagnosis remains uncertain despite radiology.[64]
In patients with a suspected large vessel occlusion who are candidates for endovascular
thrombectomy, request CT angiography or MR angiography (CTA/MRA) after the initial non-enhanced
CT-head.[63]
• Candidates for thrombectomy alone include patients who cannot receive thrombolysis (e.g., with
contraindications including recent major surgery or current anticoagulation use, for example
patients on warfarin with INR >1.7).[64]
In candidates for thrombectomy in addition to thrombolysis, request CTA or MRA with contrast after (or
with) the initial CT head.[63]
DIAGNOSIS
Do not delay therapy with intravenous thrombolysis (if indicated)while:
• Waiting for results or waiting to perform tests, unless you suspect contraindications that must be
ruled out first (eg., hypoglycaemia, coagulopathy).[66] [67] Treatment should be started within 4.5
hours of onset of stroke symptoms AND after excluding intracranial haemorrhage.[63] [64]
• Waiting to perform CTA or MRA, or waiting for results.[66]
Order in all patients:
• Serum glucose to exclude hypoglycaemia and hyperglycaemia before giving thrombolysis.[63]

[65]
• Serum electrolytes to exclude electrolyte disturbance as a cause for sudden onset neurological
signs.
• Serum urea and creatinine to exclude renal failure because it may be a potential
contraindication to some stroke interventions.
• Cardiac enzymes to exclude concomitant myocardial infarction.
• Full blood count to exclude anaemia or thrombocytopenia prior to possible initiation of
thrombolysis, anticoagulants, or antithrombotics.
• Prothrombin time and partial thromboplastin time (with international normalised ratio)
to exclude coagulopathy.
• ECG to exclude cardiac arrhythmia or ischaemia, which are relatively common in ischaemic stroke.
Consider a serum toxicology screen if you suspect ingestion of toxic substances. Signs and
symptoms may mimic stroke.
Full Recommendations
Clinical presentation
Suspect stroke in a patient with sudden (new, acute onset, or on awakening from sleep) focal
neurological symptoms:[62]
• 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.
Be aware that one or more transient ischaemic at tacks (TIAs), which may be stereotypical, might
precede a stroke (as warning signs or symptoms).
• A TIA is a medical emergency heralding a significant risk of stroke. TIAs typically last a matter
of minutes. They should be treated and investigated promptly. The National Institute for Health
and Care Excellence (NICE) and the Royal College of Physicians, both in the UK, recommend
that people who have had a suspected TIA (without risk stratification) should have specialist
assessment and investigation within 24 hours of symptom onset.[63] [64] See Transient ischaemic
attack .
Initial assessment
The goal of the initial assessment is to recognise a stroke quickly - “time is brain.
DIAGNOSIS
• Efficient, rapid initial assessment and rapid access to CT scan (within 1 hour of
presentation) allow for early initiation of intravenous thrombolysis (i.e., within 4.5 hours of onset of
symptoms, if it is not contraindicated) which is associated with improved functional outcomes.[60]
[61]
In the emergency department

Use the ROSIER scale (Recognition of Stroke in the Emergency Room) in those with suspected
stroke or TIA to establish the diagnosis rapidly.[63] [68]
• 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
13
• Asymmetrical arm weakness
• Asymmetrical leg weakness
• Speech disturbance
• Visual field defect
• A score >0: stroke likely; a score ≤0: stroke unlikely (but not excluded).
In the community
Use a validated tool such as FAST (Face Arm Speech Test) to screen people with sudden onset of
neurological symptoms (such as visual disturbance or balance problems) for a diagnosis of stroke:[63]
[69]
• 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 despite a negative FAST.
Continue to manage them as you would someone with acute stroke.[64]
DIAGNOSIS
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. [63] [70]
Guidelines from the European Academy of Neurology and the 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.[71]
• The review included 8 studies and 7 scales.[71] Of the scales included, FAST (Face Arm
Speech Test) and ROSIER (Recognition of Stroke in the Emergency Room) had the highest
sensitivity (both 97%); specificity was 13% and 18% respectively (both in one study of 295
patients in the UK).[72]
The UK National Institute for Health and Care Excellence (NICE) stroke guideline from 2008 (not
changed in the 2019 update) recommends using a validated tool, such as FAST, outside hospital.[63]
• 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%).[69]
NICE also recommends using a validated tool, such as ROSIER, in the emergency department.[63]
• This recommendation is underpinned by evidence from a prospective cohort study which

included 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.[68]
Symptoms/signs according to the location of infarct
Anterior circulation stroke
DIAGNOSIS
Associated with ischaemia related to occlusion of the anterior circulation arteries - the carotid territory,
including the anterior and middle cerebral arteries and their branches.[73] Anterior circulation strokes are
the most common of all ischaemic strokes.[74]
Look for one or more of the following symptoms/signs:[73]
• Limb and/or facial weakness
• Complete or partial loss of muscle strength in face, arm, and/or leg; a typical presentation of
stroke.
• Weakness in face, arms, and legs (all three at same time) suggests deep hemispheric
involvement, although this may not differentiate stroke mechanism.
• Expressive and/or receptive dysphasia

• Sensory loss (numbness) in face and upper and/or lower extremities
• Patients often describe sensory loss and paraesthesias as “numbness”.

• Unilateral sensory loss on neurological examination may involve some or all primary
modalities.
15
• Cortical sensory loss usually impairs fine sensory processing abilities such as two-point
discrimination, graphaesthesia, or stereognosis.
• Vision loss in one eye or visual field deficit
• Monocular vision loss may occur and is often transient.[75] This is a common early warning
signal for cervical carotid stenosis. It can present as amaurosis fugax or retinal stroke
(branch or central retinal artery occlusion); recognise and investigate with the same urgency.
See Carotid artery stenosis .
• Gaze paresis (often horizontal and unidirectional): in stroke, the eyes will look at the affected side
of the brain
• Consider seizure in people with wrong-way eye deviation (i.e., gaze deviation away from the
side of the brain lesion, towards the hemiparetic side).
• Visuospatial disturbances/neglect
• Homonymous quadrantanopia.
Practical tip
Coma is unusual; it is more common in people with brain stem ischaemia.
Posterior circulation stroke

Associated with ischaemia related to occlusion of the posterior circulation arteries - the vertebral arteries
in the neck, the intracranial vertebral, basilar, and posterior cerebral arteries, and their branches.[73]
Look for one or more of the following symptoms/signs:[73]
• Double vision
• Motor and/or sensory deficits
• Motor deficits: weakness, clumsiness, or paralysis of any combination of arms and legs, up
DIAGNOSIS
to quadriplegia, sometimes changing from one side to another in different attacks.

• Sensory deficits: numbness, including loss of sensation or paraesthesia in any combination
of extremities, sometimes including all four limbs or both sides of the face or mouth.
• Vertigo, with or without nausea and vomiting
• Typically reported as a spinning sensation; may also be described as feeling like being “on a
ship in choppy seas”.
• It is often associated with nystagmus.
• Ataxia or disequilibrium
• Dysarthria
• Dysphagia
• Specific cranial nerve deficits (eg., unilateral tongue weakness, diplopia)
• Horner's syndrome (hemilateral triad of miosis, ptosis, and facial anhidrosis)
• Homonymous hemianopia (ie., visual field loss on the left or right side of the vertical midline on the
same side of both eyes)
• ‘Crossed’ syndromes:
• Ipsilateral cranial nerves signs

• Contralateral long motor or sensory tract dysfunction
• Altered level of consciousness and coma.
Practical tip
Posterior circulation stroke remains more difficult to recognise and treat effectively than other types
of stroke. Taking a careful history will help to identify patients with posterior circulation stroke, who
may present with recurrent, stuttering, or progressive symptoms, which may include altered level of
awareness (not a typical stroke symptom but seen in bilateral thalamic ischaemia).[73]
Lacunar stroke syndromes

The following clinical features and physical examination findings are characteristic of the type of lacunar
syndrome:
Pure motor hemiparesis • Weakness on one side of the body (face,

arm, and leg) without cortical signs and
sensory symptoms
Pure sensory stroke • Unilateral numbness of the body (face,

arm, and leg) without cortical signs or
motor deficits
• All sensory modalities are impaired
Ataxic hemiparesis • Unilateral limb weakness and ataxia that

is out of proportion to the strength/motor
deficit
DIAGNOSIS
Sensorimotor stroke • Weakness and numbness of the face,
arm, and leg without cortical signs
Dysarthria-clumsy hand syndrome • Facial weakness

• Dysarthria
• Dysphagia
• Dysmetria/clumsiness of one upper
extremity
History
Take a careful history. Be sure to establish contact with witnesses or next of kin, not only for an
accurate history but also to seek consent for invasive tests or treatments, if these are needed.
• Determine the time of symptom onset because this is the main factor that will determine
eligibility for thrombolysis.
17
• If the onset was unwitnessed, the time of symptom onset is when the patient was last
seen well.[63]
• Ask about onset (sudden or gradual), duration, intensity, and fluctuation of symptoms.
• The symptoms and signs of ischaemic stroke appear suddenly and are maximum at
onset.
• Patients with posterior circulation stroke may present with recurrent, stuttering, or
progressive symptoms, which may include an altered level of consciousness.[73]
• Ask specifically about relevant past medical history that will influence management. This
includes (brief history):
• Recent stroke
• Seizure or epilepsy
• Myocardial infarction
• Atrial fibrillation
• Recent surgery
• Recent trauma
• Bleeding
• Haemorrhagic stroke
• Comorbidities (specifically hypertension and diabetes)
• Current or past illicit drug use
• Medicines (specifically anticoagulants, insulin, and antihypertensives).
Practical tip
The time of onset is not always easy to determine, particularly if the onset was not witnessed and
the patient is unable to communicate, if symptoms are mild and not immediately noticeable, or if
there is a stuttering or fluctuating course.
DIAGNOSIS
Bear in mind key risk factors for ischaemic stroke:
• Age ≥55 years
• A strong non-modifiable risk factor, even after controlling for other age-related conditions
such as hypertension.[9]
• History of transient ischaemic at tack (TIA)
• Patients with a history of TIA, particularly a recent TIA, are at a significant risk of subsequent
stroke. Most of these strokes occur within days of the TIA. Stroke rate has been reported
as 1.5%, 2.1%, 2.8%, 3.7%, and 5.1% on days 2, 7, 30, 90, and 365, respectively, after
TIA.[19] Studies show that the rate of post-TIA stroke might have decreased slightly since
1999, likely related to advances in cardiovascular risk prevention.[20] [21]
• History of ischaemic stroke
• Indicates that the patient may have more ischaemic strokes in the future (particularly if risk
factors such as hypertension are not corrected).[76]
• Family history of stroke at young age
• Stroke-causing genetic disorders with Mendelian inheritance are rare. Twin studies suggest a
small genetic contribution to stroke; epidemiological studies show that family history of stroke
is a risk factor.[17]
• Hypertension
• Strongly associated with an increased risk of ischaemic stroke.[77]
• Smoking
• Diabetes mellitus
• Causes at least one fifth of ischaemic strokes and is one of the strongest individual stroke
risk factors.[78]
• Comorbid cardiac conditions
• Including myocardial infarction, valvular disease, patent foramen ovale with or without atrial
septal aneurysm, prosthetic heart valve, and cardiomyopathy.[26]
• Carotid artery stenosis [27] [28]

• Sickle cell disease
• Associated with vascular stenosis, brain ischaemia, and Moyamoya disease (vascular
occlusion affecting the circle of Willis).
• Dyslipidaemia
• Increased total cholesterol is associated with an increased risk of ischaemic stroke. The risk
DIAGNOSIS
of ischaemic stroke is decreased with elevated high-density lipoprotein (HDL) cholesterol.[79]
Stroke mimics
Exclude stroke mimics such ashypoglycaemia, brain tumours, seizures, sepsis, or migraine to ensure
timely treatment. See Differentials .
Bear in mind the key clinical featuresthat may help distinguish between stroke and mimics (e.g.,
seizures, hypoglycaemia) at the initial bedside assessment:
19
Suggestive of mimic Suggestive of stroke
• Neurological symptoms and signs • Exact time of onset[80]

that are gradual in onset, progressive, • Sudden onset of neurological symptoms
and signs[80]
migratory • Symptoms are maximum at onset
• Positive neurological symptoms, (e.g.,
• Negative neurological symptoms (e.g.,
flashing lights or tingling, jerking, or visual loss, numbness, or weakness)[62]
shaking of limbs) • Definite focal symptoms[80]
• Known history of cognitive impairment[80] • Abnormal vascular findings (e.g., systolic
• Respiratory, abdominal or other abnormal blood pressure >150 mm Hg, atrial
signs[80] fibrillation, valvular heart disease, or
absent peripheral pulses)[80]
• Signs that can be lateralised to the left or
right side of the brain[80]
• Determination of a clinical stroke
subclassification[80]
Practical tip
Ischaemic stroke is a clinical diagnosis based on symptoms and signs. Therefore, distinguishing
true stroke from mimics is an essential skill that cannot be replaced by imaging alone.
Physical examination
Assess the patient’s level of consciousness using the Glasgow Coma Scale.
• In people with an altered level of consciousness or coma, exclude haemorrhage and other mimics
such as seizures. See Differentials .
• Consider seizure (Todd’s paresis) in people with reduced consciousness.
Practical tip
Haemorrhagic stroke is more often associated with seizures, decreased level of consciousness, and
DIAGNOSIS
signs of increased intracranial pressure than ischaemic stroke.
Perform an abbreviated neurological examinationusing the National Institutes of Health Stroke

Scale.[65]
• This tool measures the degree of neurological deficits. Higher scores indicate a more severe stroke.
Check for evidence of cardiac arrhythmias (e.g., atrial fibrillation) or valvular pathology.
• Auscultate the heart.

• Arrhythmias, murmurs, and pulmonary oedema are associated with cardiac comorbidities, which
predispose patients to stroke.
Refer to hyperacute or acute stroke unit

Transfer everyone 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.[63] [64]
• This is to begin thrombolysis as quickly as possible (if indicated), and to help prevent
complications.[63] [64]
Imaging
CT head
Request an immediate(i.e., ideally in the next available time slot and definitely within 1 hour of arrival at
hospital) non-enhanced CT scan of the headin people with suspected stroke in people with suspected
stroke if any of the following apply:[63] [64]
• 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
Use the CT scan to differentiate between ischaemic stroke and haemorrhagic stroke; which
must be done before starting thrombolysis in ischaemic stroke, and before reversing anticoagulation in
anticoagulation-induced intracerebral haemorrhage.[81]
• Only healthcare professionals with appropriate training should interpret acute stroke imaging for
thrombolysis or thrombectomy decisions.[81]
Remember that ischaemic stroke is a clinical diagnosis based on signs and symptoms; a
#normal CT scan does not rule out a stroke - particularly in the first few hours, the CT scan
can be normal or show very subtle ischaemic changes.
Practical tip
DIAGNOSIS
Ring through to a radiologist on call to advise an immediate CT scan; speak to the radiographer to
ensure the patient has the next available time slot.
Aim to take a collateral history from relatives regarding medications/past medical history while the
patient is in the CT scanner.
21
Non-contrast CT scan of brain showing sub-acute isolated

left basal ganglion infarction with left frontal horn mass effect
Courtesy of BMJ Case Reports 2009; doi:10.1136/bcr.10.2008.1139
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.[63]
Diffusion-weighted MRI
DIAGNOSIS
Consider diffusion-weighted MRI of the head if the diagnosis remains uncertain despite
radiology.[64]
Practical tip
If there is clinical doubt but the patient lies outside the thrombolysis or thrombectomy window (i.e.,
within 4.5 hours and 6-24 hours of onset of symptoms, respectively), it is reasonable to consider
a non-urgent MRI to confirm the diagnosis. An MRI scan in the presence of ongoing symptoms
is extremely likely to show the stroke. A normal MRI scan is very unlikely if the patient has had a
stroke.
DIAGNOSIS
(A) Non-contrast T1-weighted MRI. (B) Post-contrast T1-weighted MRI showing minimal increase
in leptomeningeal vessels over the right frontal region. (C) Diffusion-weighted image (DWI) showing
a hyperintense area in the right frontal region. (D) Apparent diffusion coefficient (ADC) map shows
hypointense lesion, indicating restricted diffusion that correlates with high intensity on DWI and
exponential diffusion. (E) ADC value is 0.22 x 10³ mm²/second, corresponding to a hyperacute infarct
From the personal collection of Eric E. Smith; used with permission
In candidates for endovascular thrombectomy

Patients presenting within 6 to 24 hours of symptom onset (i.e., from when they were last known to be
well) may be potential candidates for endovascular thrombectomy.[63]
• The selection of patients for mechanical thrombectomy (endovascular intervention) should be made
by clinicians experienced in the use of thrombolysis for stroke and in interpretation of
relevant imaging. The procedure should only be carried out by appropriately trained specialists
with regular experience in intracranial endovascular interventions, with appropriate facilities and
neuroscience support.[82]
23
CT angiography or MR angiography (CTA/MRA)
In patients with a suspected large vessel occlusion who are candidates for thrombectomy,
request a CTA or MRA following the initial non-enhanced CT.[63]
• Do not delay therapy with intravenous thrombolysis (if indicated) while waiting to
perform CTA or waiting for results. [66] In practice, hospitals that undertake CTA routinely in
acute stroke give thrombolysis without waiting for the CTA report; they review the initial plain CT at
the same time as performing the CTA.[66]
• Use CTA preferentially over MRA because CTA gives quicker results.[63]
In candidates for endovascular thrombectomy in addition to

thrombolysis
CTA/MRA with contrast

If the patient is a potential candidate for thrombectomy in addition to thrombolysis, request
CTA/MRA with contrast after (or with) the initial CT to confirm occlusion of the proximal anterior or
posterior circulation.[63]
CT perfusion imaging (or MR equivalent)

Add CT perfusion imaging (or MR equivalent) if thrombectomy might be indicated beyond
6 hours of symptom onset.[63] Studies have supported the use of perfusion scanning in patients to
extend the thrombectomy window above 6 hours.[83] [84] [85]
DIAGNOSIS
DIAGNOSIS
MRI arterial spin labelling image showing extensive hypoperfusion in the right
cerebral hemisphere. There is a clear mismatch between diffusion and perfusion
In the UK, the National Institute for Health and Care Excellence (NICE) recommends thrombectomy
(+/- thrombolysis) in patients who were last known to be well between 6 hours and 24 hours
previously (including wake-up strokes) with confirmed occlusion of the proximal anterior or
posterior circulation, if there is potential to salvage brain tissue as shown by CT perfusion or
diffusion-weighted MRI scanning.[63]
In suspected carotid stenosis: carotid ultrasound

Request an ultrasound of the carotids in anterior circulation strokes to determine if there is
symptomatic carotid stenosis.[63] See Carotid artery stenosis .
Practical tip
Request a chest x-ray in patients with cardiopulmonary signs or symptoms to detect other relevant
conditions such as cardiomegaly, aortic dissection, or pneumonia.
25
Echocardiogram
If you suspect cardioaortic embolism, consider contrast transthoracic echocardiography (TTE) to
evaluate the cardiac and aortic sources of embolus.[86] If no source is identified on TTE, use contrast
transoesophageal echocardiography (TOE) in selected patients instead.[86]
• Cardioaortic embolism to the brain accounts for approximately 15% to 30% of ischaemic strokes.[3]
[87]
Other investigations
Do not delay intravenous thrombolysis (if within the licensed time window and not contraindicated)
while waiting for results or waiting to perform tests, unless you suspect contraindications that must be
ruled out first (e.g., hypoglycaemia, coagulopathy).[66] [67]
Blood tests
While CT/MRI transport is being organised, insert an intravenous catheter with blood sampling.[64]
Order in all patients:
• Serum glucose
• Hypoglycaemia is a stroke mimic; hyperglycaemia has been associated with

intracerebral bleeding and worse clinical outcomes in patients treated with intravenous
thrombolysis. You need to exclude both before giving thrombolysis.[63] [65]
• Serum electrolytes
• To exclude electrolyte disturbance (e.g., hyponatraemia) as a cause for sudden onset

neurological signs.
• Serum urea and creatinine
• To exclude renal failure because it may be a potential contraindication to some stroke

DIAGNOSIS
interventions.
• Cardiac enzymes
• To exclude concomitant myocardial infarction.
• Full blood count
• To exclude anaemia or thrombocytopenia prior to possible initiation of thrombolysis,

anticoagulants, or antithrombotics.
• Prothrombin time and partial thromboplastin time (with international normalised ratio)
• To exclude coagulopathy.
• Don’t delay thrombolysis (e.g., by waiting for test results) if the patient has no history of
anticoagulant use, coagulopathy, or a condition that may lead to coagulopathy.[65]
Consider a serum toxicology screen if you suspect ingestion of toxic substances. Signs and symptoms
may mimic stroke.
ECG
Perform an ECG in all patientsto exclude cardiac arrhythmia (such as atrial fibrillation) or ischaemia,
which are both relatively common in ischaemic stroke.[78]
• Atrial fibrillation is an independent risk factor for ischaemic stroke and indicates a poor
prognosis.[25] See New-onset atrial fibrillation .
In people who would be eligible for secondary prevention treatment for atrial fibrillation:[64]
• Perform prolonged ECG monitoring(at least 12 hours)

• Consider longer ECG monitoring(24 hours or more) in those in whom no other cause of
stroke has been found, particularly if they have a pattern of cerebral ischaemia on brain imaging
suggestive of cardioembolism.
Practical tip
Atrial fibrillation is a major preventable cause of ischaemic stroke. Monitor all patients with
suspected stroke for atrial fibrillation and other arrhythmias.[64] See New-onset atrial fibrillation .
The presence of paroxysmal atrial fibrillation has previously been underestimated, and latest
guidance from the National Institute for Health and Care Excellence (NICE) in the UK is to consider
longer monitoring and implantable devices in more patients.[88]
History and exam

Key diagnostic factors
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 a typical presentation of
stroke.[62]
Weakness of all three suggests deep hemispheric involvement, although this may not differentiate
stroke mechanism.
DIAGNOSIS
Hemiparesis is a feature of any type of stroke which occludes the penetrating arteries that supply the
posterior limb of the internal capsule.
• If it is purely the penetrating arteries involved then the patient may have one of the lacunar
syndromes (e.g., pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, etc.).[89]
• If it is the middle cerebral artery (from which the penetrating arteries branch off) that is
occluded, there will be hemiparesis but with other neurological deficits.
As with most stroke signs and symptoms, bilateral involvement is uncommon and may reflect
alternative aetiologies. See Differentials .
dysphasia (common)
Impairment in any language function, either expressive or receptive, is a sign of dominant hemispheric
ischaemia.[62]
27
ataxia (common)
In the absence of muscle weakness, ataxia points to ischaemia involving the cerebellum or its
connections with the rest of the brain.
Posterior circulation strokes are more commonly associated with difficulty with fine motor coordination
and gait than anterior circulation strokes.
visual disturbance (common)

Loss of sight in one eye may occur and is often transient.
• This is a common early warning signal for cervical carotid stenosis. It can present as amaurosis
fugax or retinal stroke (branch or central retinal artery occlusion); recognise and investigate with
the same urgency. See Carotid artery stenosis .
Homonymous hemianopia involves vision loss on the same side of the visual field in both eyes.
Diplopia may occur in patients with posterior circulation ischaemia.[73]
risk factors (common)

Consider risk factors that make people more likely to have a stroke:
• Age ≥55 years[9]

• History of transient ischaemic attack (TIA)[19] [90]
• History of ischaemic stroke[76]
• Family history of stroke at a young age[17]
• Hypertension[77]
• Smoking[23]
• Diabetes mellitus[24]
• Atrial fibrillation[25] [78]
• Comorbid cardiac conditions[26]
DIAGNOSIS
• Carotid artery stenosis[27] [28]

• Sickle cell disease [30]
• Dyslipidaemia[79]
Other diagnostic factors

sensory loss (numbness) (common)
Patients often describe sensory loss and paraesthesias as 'numbness'.
• Unilateral sensory loss on neurological examination may involve some or all primary modalities.
• Cortical sensory loss usually impairs fine sensory processing abilities such as two-point
discrimination, graphaesthesia, and stereognosis.
dysarthria (common)
May accompany facial weakness, or brainstem or cerebellar dysfunction.
headache (common)
Headache is not uncommon in acute stroke but may indicate other pathologies such as:
• Intracerebral haemorrhage (may be insidious and gradually increasing).

• Subarachnoid haemorrhage (severe and of sudden onset “thunderclap headache”).
• Intracranial hypertension (which may be caused by, for example, a cerebral venous sinus
thrombosis or space-occupying lesion).
• Migraine.
See Differentials .
ga ze paresis (common)
Often horizontal and unidirectional.
More common in anterior circulation strokes than in posterior circulation strokes.
Consider seizure with wrong-way eye deviation (i.e., gaze deviation away from the side of the brain
lesion, towards the hemiparetic side).
arrhythmias, murmurs, or pulmonary oedema (common)

Associated with cardiac comorbidities, which predispose patients to stroke.
• Atrial fibrillation is the cause of one fifth of ischaemic strokes and is one of the strongest
individual stroke risk factors.[25] [78] See New-onset atrial fibrillation .
vertigo (uncommon)
This is a common presentation of posterior circulation ischaemia.[73]
• Typically reported as a spinning sensation; may also be described as feeling like being “on a
ship in choppy seas”.
DIAGNOSIS
• It is often associated with nystagmus.
nausea and/or vomiting (uncommon)

May be due to posterior circulation ischaemia, or reflect increased intracranial pressure.[73]
neck or facial pain (uncommon)

May be associated with arterial dissection.
miosis, ptosis, and facial anhidrosis (hemilateral) (uncommon)

Horner's syndrome may be associated with posterior circulation strokes.[73]
Practical tip
In anterior circulation stroke accompanied by Horner’s syndrome, consider whether carotid

artery dissection could be the cause.
29
decreased level of consciousness or coma (uncommon)
A decreased level of consciousness may accompany large anterior circulation, thalamic,
bihemispheric, or brain stem strokes.
Consider seizure (Todd’s paresis) in people with reduced consciousness.
Coma is more common in people with brain stem ischaemia.
Practical tip
Haemorrhagic stroke is more often associated with seizures, decreased level of consciousness,
and signs of increased intracranial pressure than ischaemic stroke.
DIAGNOSIS
Investigations
1st test to order
Test Result
non-contrast CT head • hypoattenuation
Request an immediate non-enhanced CT of the head(i.e., (darkness) of the brain
ideally in the next available time slot and definitely within 1 hour) if parenchyma
any of the following apply:[63] [64] • loss of grey matter-
• Indications for thrombolysis or thrombectomy white matter
• On anticoagulant treatment differentiation, and
• A known bleeding tendency sulcal effacement
• A depressed level of consciousness (Glasgow Coma Scale • hyperattenuation
score <13) (brightness) in an
• Unexplained progressive or fluctuating symptoms artery indicates clot
• Papilloedema, neck stiffness, or fever within the vessel lumen
Practical tip
Ring through to a radiologist on call to advise an immediate CT

scan; speak to the radiographer to ensure the patient has the
next available time slot.
Aim to take a collateral history from relatives regarding
medications/past medical history while the patient is in the CT
scanner.
Use the CT scan to differentiate between ischaemic stroke

and haemorrhagic stroke; which must be done before starting
DIAGNOSIS
thrombolysis in ischaemic stroke and before reversing anticoagulation
in anticoagulation-induced intracerebral haemorrhage.[81]
• Only healthcare professionals with appropriate training

should interpret acute stroke imaging for thrombolysis or
thrombectomy decisions.[81]
Remember that ischaemic stroke is a clinical diagnosis

based on signs and symptoms; a normal CT scan does not
rule out a stroke - particularly in the first few hours following a
stroke, the CT scan can be normal or show very subtle ischaemic
changes.
31
Test Result
Non-contrast CT scan of brain showing sub-acute isolated

left basal ganglion infarction with left frontal horn mass effect
In people without indications for immediate brain imaging,

DIAGNOSIS
request scan as soon as possible and definitely within 24 hours of

symptom onset.[63]
serum glucose may be normal; may

Hypoglycaemia is a stroke mimic; hyperglycaemia has been show hypoglycaemia or
associated with intracerebral bleeding and worse clinical outcomes in hyperglycaemia
patients treated with intravenous thrombolysis.[63] [65] You need to
exclude both before giving thrombolysis.
serum electrolytes may be normal; may show
To exclude electrolyte disturbance (e.g., hyponatraemia) as a cause electrolyte disturbances
for sudden onset 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.
cardiac enzymes may be normal; may
To exclude concomitant myocardial infarction. show evidence of cardiac
ischaemia
Test Result
FBC may be normal; may show
To exclude anaemia or thrombocytopenia prior to possible initiation of anaemia or thrombocytopenia
thrombolysis, anticoagulants, or antithrombotics.
ECG may be normal; may show
To exclude cardiac arrhythmia (such as atrial fibrillation) or ischaemia, arrhythmia or signs of
which are relatively common in ischaemic stroke.[78] ischaemia
In people who would be eligible for secondary prevention treatment
for atrial fibrillation:[64]
• Perform prolonged ECG monitoring (at least 12 hours)

• Consider longer ECG monitoring (24 hours or more)
in those in whom no other cause of stroke has been found,
particularly if they have a pattern of cerebral ischaemia on
brain imaging suggestive of cardioembolism.
Practical tip
Atrial fibrillation is a major preventable cause of ischaemic

stroke.[25] Monitor all patients with suspected stroke for atrial
fibrillation and other arrhythmias.[64] See New-onset atrial
fibrillation .
The presence of paroxysmal atrial fibrillation has previously
been underestimated, and latest National Institute for Health
and Care Excellence guidance is to consider longer monitoring
and implantable devices in more patients.[88]
prothrombin time and PTT (with INR) may be normal; may show
To exclude coagulopathy. Don’t delay thrombolysis (e.g., by waiting coagulopathy
for test results) if the patient has no history of anticoagulant use,
coagulopathy, or a condition that may lead to coagulopathy.[65]
DIAGNOSIS
33
Other tests to consider
Test Result
serum toxicology screen may exclude alcohol and drug
Consider a serum toxicology screen if you suspect ingestion of toxic ingestion
substances. Signs and symptoms may mimic stroke.
diffusion-weighted MRI head • acute ischaemic infarct
Consider diffusion-weighted MRI if the diagnosis remains uncertain appears bright on
despite radiology.[64] diffusion-weighted
Practical tip imaging
• at later stages, T2
If there is clinical doubt but the patient lies outside the images may also show
thrombolysis or thrombectomy window (i.e., within 4.5 hours
increased signal in the
and 6-24 hours of onset of symptoms, respectively), it is
reasonable to consider a non-urgent MRI to confirm the ischaemic territory
diagnosis. An MRI scan in the presence of ongoing symptoms
is extremely likely to show the stroke. A normal MRI scan is
very unlikely if the patient has had a stroke.
DIAGNOSIS
Test Result
(A) Non-contrast T1-weighted MRI. (B) Post-contrast T1-weighted

MRI showing minimal increase in leptomeningeal vessels over
DIAGNOSIS
the right frontal region. (C) Diffusion-weighted image (DWI)
showing a hyperintense area in the right frontal region. (D)
Apparent diffusion coefficient (ADC) map shows hypointense
lesion, indicating restricted diffusion that correlates with high
intensity on DWI and exponential diffusion. (E) ADC value is
0.22 x 10³ mm²/second, corresponding to a hyperacute infarct
CT angiography or MR angiography ± contrast may be normal; may show

Request a CT angiography or MR angiography (CTA/MRA) without arterial occlusion or stenosis
contrast in patients with a suspected large vessel occlusion
who are candidates for thrombectomy following the initial non-
enhanced CT.[63]
Do not delay therapy with intravenous thrombolysis (if

indicated) waiting to perform CTA or waiting for results.
[66] In practice, hospitals that undertake CTA routinely in acute stroke
give thrombolysis without waiting for the CTA report; they review the
initial plain CT at the same time as performing the CTA.[66]
Use CTA preferentially over MRA because CTA gives quicker

results.[63]
35
Test Result
If the patient is a potential candidate for thrombectomy (i.e.,
onset of symptoms 6-24 hours) in addition to thrombolysis,
request a CTA/MRA with contrast after (or with) the initial
CTto confirm occlusion of the proximal anterior circulation.[63]
CT or MRI perfusion-weighted imaging shows areas with reduced

Add CT perfusion imaging (or MR equivalent) if blood flow that may be at risk
thrombectomy might be indicated beyond 6 hours of for subsequent infarction
symptom onset. [63] Studies have supported the use of perfusion
scanning in patients to extend the thrombectomy window above 6
hours.[83] [84] [85]
• In the UK, the National Institute for Health and Care Excellence
recommends thrombectomy for people who were
last known to be well between 6 hours and 24 hours
previously (including wake-up strokes) if there is
potential to salvage brain tissue as shown by perfusion
imaging.[63]
DIAGNOSIS
MRI arterial spin labelling image showing extensive

hypoperfusion in the right cerebral hemisphere. There
is a clear mismatch between diffusion and perfusion
Test Result
carotid ultrasound cervical artery occlusion or
Request an ultrasound of the carotids in anterior circulation strokes critical stenosis
to determine if there is symptomatic carotid stenosis.[63] [86] See
Carotid artery stenosis .
echocardiogram left atrial appendage
If you suspect cardioaortic embolism, consider contrast transthoracic thrombosis in patients with
echocardiography (TTE) to evaluate the cardiac and aortic sources atrial fibrillation, valvular
of embolus.[86] If no source is identified on TTE, use contrast
and prosthesis vegetations
transoesophageal echocardiography (TOE) in selected patients
instead.[86] and thrombosis, aortic arch
atheroma, patent foramen
• Cardioaortic embolism to the brain accounts for approximately ovale, atrial septal defect, and
15% to 30% of ischaemic strokes.[3] [87]
intracardiac tumours
DIAGNOSIS
37
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Intracerebral • No symptoms or signs • CT or MRI demonstrates
haemorrhage reliably distinguish haemorrhage
haemorrhagic stroke from (hyperattenuation).
ischaemic stroke.
• Haemorrhagic stroke is
more often associated
with reduced level of
consciousness and signs
of increased intracranial
pressure than ischaemic
stroke.
Transient ischaemic • Transient neurological • CT or MRI may be normal or

at tack (TIA) symptoms, with no evidence may reveal evidence of older
of acute infarct. A TIA has infarcts.
a sudden onset and may
last anything from a few
minutes to 24 hours. Most
patients with TIA usually
have complete resolution
of symptoms and signs
within 1 hour.[62] Suspect a
stroke if sudden-onset, focal
neurological deficit persists
for longer than 24 hours.
Hypertensive • The combination of • Cerebral oedema on CT or

encephalopathy headache, cognitive MRI.
abnormalities or decreased
level of consciousness,
DIAGNOSIS
and hypertension
significantly above patient's
baseline blood pressure
indicates hypertensive
encephalopathy. Other
possible signs/symptoms
include visual changes or
loss, or signs of increased
intracranial pressure.[91]
Hypoglycaemia • There may be a history of • Low serum glucose at time

diabetes with use of insulin of symptoms.
or insulin secretagogues.
• Decreased level of
consciousness.
Complicated migraine • Repetitive history of similar • MRI shows no evidence of

events; preceding aura, infarction.
headache in a marching
pattern differentiates
complicated migraine.[91]

symptoms
• Stroke often presents with
negative symptoms (e.g.,
visual loss, numbness, or
weakness).
• Positive symptoms (e.g.,
marching paraesthesias,
visual hallucinations,
and abnormal motor
manifestations) are more
likely with complicated
migraine.
Seizure and postictal • History of seizures; • Electroencephalogram

deficits witnessed seizure followed confirms evidence of seizure.
by postictal deficits: for • MRI shows no evidence of
example, drowsiness and infarction.
tongue-biting.[91]
• Wrong-way eye deviation
(i.e., gaze deviation
away from the side of the
brain lesion, towards the
hemiparetic side) should
prompt consideration of
seizure but can also occur
with strokes affecting the
pons or thalamus.
Conversion and somatic • Neurological signs and • MRI shows no evidence of

symptom disorders symptoms do not fit a infarction.
vascular territory.
• No cranial nerve deficits.
• Additionally, conversion
disorder displays multiple
DIAGNOSIS
signs that are neurologically
inconsistent.
Wernicke's • History of alcohol abuse. • Decreased blood thiamine

encephalopathy • Irritability, confusion, and level and successful
delirium common presenting therapeutic trial of thiamine.
features.
Brain tumour • Symptoms and signs more • CT head demonstrates

likely to have been on-going. lesion or lesions.
• May be history of cancer if
metastatic lesion causing
symptoms.
Sepsis • Clinical evidence or strong • No diagnostic test is

suspicion of infection in an available that can reliably
acutely unwell patient. confirm or exclude sepsis in
the timeframe within which
treatment should be started
for suspected sepsis.[92]
• Undertake intensive efforts,
including imaging, to identify
39

symptoms
the source of infection in all
patients with sepsis.[93] [94]
Ingestion of toxic • History of alcohol or drug • Toxicology screen positive

substances abuse. for alcohol or drugs.
DIAGNOSIS
Ischaemic stroke Management
Recommendations
Urgent
Time is brain” - ischaemic stroke is an emergency.
• Early initiation of intravenous thrombolysis (i.e., within 4.5 hours from onset of symptoms, if
it is not contraindicated) is associated with improved functional outcomes.[60] [61] [95]
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 for
those presenting with a Glasgow Coma Scale score ≤8. This should be done by an anaesthetist or
trained emergency department staff.[96]
• Give supplemental ox ygen only if ox ygen saturation drops below 93%. [97] Although the
National Institute for Health and Care Excellence (NICE) in the UK recommends starting oxygen
only if oxygen saturation drops below 95%, latest evidence suggests that in patients with stroke
there are no benefits to initiating oxygen therapy when SpO₂ is ≥93%, and it may cause harm.[63]
[97]
• Monitor controlled ox ygen therapy. An upper SpO 2 limit of 96% is reasonable when
administering supplemental oxygen to most patients with acute illness who are not at risk
of hypercapnia. Evidence suggests that liberal use of supplemental oxygen (target SpO 2
>96%) in acutely ill adults is associated with higher mortality than more conservative oxygen
therapy.[98] A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of
hypercapnic respiratory failure.[99]
• Do not routinely give ox ygen to people who are not hypoxic.[63]
Assess the patient’s level of consciousness using the Glasgow Coma Scale. In patients with
decreased level of consciousness or coma, urgently exclude haemorrhage and stroke mimics such as
seizures.
Admit everyone with suspected stroke directly to a hyperacute (or acute) stroke unit as soon as
possible; UK guidelines recommend doing this within 4 hours of presentation to hospital.[63] [64]
Intravenous alteplase should be given (if not contraindicated) if treatment is started as soon as
possible within 4.5 hours of onset of symptoms, AND if intracranial haemorrhage has been
excludedby imaging.[63] [95]
• Do not delay intravenous thrombolysis (if indicated) while waiting for results or waiting
to perform tests, unless you suspect contraindications that must be ruled out first (eg.,
MANAGEMENT
hypoglycaemia, coagulopathy), or while monitoring for further improvement.[66] [67] Reperfusion

(via thrombolysis, thrombectomy or both) is a time-critical intervention.
41
• Exclude hypoglycaemia and hyperglycaemia before giving thrombolysis;
hypoglycaemia is a stroke mimic and hyperglycaemia is associated with intracerebral bleeding
and worse clinical outcomes.[63] [65]
In the community: arrange immediate emergency admission to an hyperacute (or acute, depending on
availability) stroke unit for anyone with:
• Persisting neurological symptoms who is suspected of having acute stroke (or emergent transient
ischaemic attack [TIA]) [63] [64]
• Resolved neurological symptoms who has a bleeding disorder or is taking an anticoagulant
because haemorrhage must be excluded.[64]
In people with suspected TIA, follow the recommendations in our topic Transient ischaemic attack.
Key Recommendations
Monitor temperature and maintain normal body physiology.[64] [100]
• Give an antipyretic (e.g., paracetamol) in patients with high temperature.

• Do not use therapeutic hypothermia (i.e., active cooling) to reduce the risk of secondary brain
damage.[63]
Maintain blood glucose concentration between 4 and 11 mmol/L.[63]
• Give intravenous insulin and glucose to all adults with type 1 diabetes with threatened or actual
stroke. Follow your local protocol.[63]
Give antihypertensive treatment only if there is a hypertensive emergency with one or more
of the following serious concomitant conditions: [63]
• Hypertensive encephalopathy
• Hypertensive nephropathy
• Hypertensive cardiac failure/myocardial infarction
• Aortic dissection
• Pre-eclampsia/eclampsia.

• Consider longer ECG monitoring (24 hours or more) in those in whom no other cause of stroke has
been found, particularly if they have a pattern of cerebral ischaemia on brain imaging suggestive of
cardioembolism.
Monitor the patient for signs of elevated intracranial pressure (ICP). Repeat the CT head immediately if
MANAGEMENT
you suspect elevated ICP which may present as:
• A reducing level of consciousness

• Severe headache
• Nausea/vomiting
• A sudden increase in blood pressure.
Refer immediately to a neurosurgeon any patients with large middle cerebral artery territory
infarcts and those with large infarctions affecting the cerebellum.[64] [65] These types of stroke
have a very high mortality if urgent neurosurgical intervention is delayed.[65]
Consult immediately with a neurologist or neurosurgeon if the patient has uncontrolled or

recurrent seizures, or status epilepticus. The choice of anticonvulsant will depend on the patient
characteristics.[65] See Status epilepticus .
• Follow your hospital protocol. Levetiracetam and sodium valproate are commonly used.
Mechanical thrombectomy should be performed: [63]
• As soon as possible and within 6 hours of symptom onset (together with intravenous
thrombolysis, if not contraindicated and within the licensed time window) in patients who have
confirmed occlusion of the proximal anterior circulation demonstrated by CT angiography or
MR angiography (CTA/MRA).
• As soon as possible in patients who were last known to be well between 6 and 24 hours
previously (including wake-up strokes) who have confirmed occlusion of the proximal
anterior circulation demonstrated by CTA or MRA and if there is potential to salvage brain
tissue, as shown by perfusion imaging.
Thrombectomy should be considered together with thrombolysis(if not contraindicated and

within the licensed time window) as soon as possible for patients known to be well up to 24 hours
previously (including wake-up strokes):[63]
• Who have confirmed occlusion of the proximal posterior circulation (i.e., basilar or posterior
cerebral artery) demonstrated by CTA or MRA
AND
• If there is potential to salvage brain tissue, as shown by perfusion imaging.
Candidates for thrombectomy alone include patients who cannot receive thrombolysis (e.g., with
contraindications including recent major surgery, bleeding disorders such as haemophilia, current
anticoagulation use).[64]
Offer aspirin (or an alternative antiplatelet agent if the patient is allergic to or intolerant of aspirin)
as soon as possible and definitely within 24 hours#to all patients in whom intracerebral
haemorrhage has been excluded by imaging.[63]
Do not use anticoagulation treatment routinely to treat acute stroke.[63]
Do not start statin treatment immediately.There is consensus that it is safe to start statins after 48
hours.[63]
MANAGEMENT
• Offer high intensity statin therapy (unless contraindicated) to all patients.[64]

• Continue statin treatment in people who are already receiving statins.[63]
43
Full Recommendations
Treatment goals
“Time is brain” - ischaemic stroke is an emergency.
• Early initiation of intravenous thrombolysis (i.e, within 4.5 hours from onset of symptoms, if it is not
contraindicated) is associated with improved functional outcomes.[60] [61]
The goals of treatment are to:
• Restore blood flow
• This is the main goal of reperfusion either by giving intravenous alteplase (thrombolysis) or
by performing mechanical thrombectomy, or both.[63] [64]
• Support energy metabolism in ischaemic tissue

• Treat complications of stroke-related oedema, such as elevated intracranial pressure, and
prevent common acute complications such as those associated with acute reperfusion
therapy (e.g., orolingual angioedema secondary to alteplase). See Complications .
Urgent initial management

People with disabling ischaemic stroke are candidates for hyperacute treatment with thrombolysis,
mechanical thrombectomy, or both.
For those with non-disabling ischaemic stroke (i.e., minor stroke [NIHSS ≤3]) see Non-urgent initial
management, below.
Stabilisation
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 for
those presenting with a depressed level of consciousness (Glasgow Coma Scale score ≤8). This
should be done by an anaesthetist or trained emergency department staff.[96]
• Give supplemental ox ygen only if ox ygen saturation drops below 93%. [97] Although the
National Institute for Health and Care Excellence (NICE) in the UK recommends starting oxygen
only if oxygen saturation drops below 95%, latest evidence suggests that in patients with stroke
there are no benefits to initiating oxygen therapy when SpO₂ is ≥93%, and it may cause harm.[63]
[97]
administering supplemental oxygen to most patients with acute illness who are not at risk
of hypercapnia. Evidence suggests that liberal use of supplemental oxygen (target SpO 2
>96%) in acutely ill adults is associated with higher mortality than more conservative oxygen
MANAGEMENT
therapy.[98] A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of
MANAGEMENT
45
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 SpO₂ range of
94% to 98% for patients not at risk of hypercapnia, whereas the 2022 Thoracic Society of
Australia and New Zealand (TSANZ) guideline recommends 92% to 96%.[99] [101]
• The 2022 Global Initiative For Asthma (GINA) guidelines recommend a target SpO 2
range of 93% to 96% in the context of acute asthma exacerbations.[102]
• A systematic review including a meta-analysis of data from 25 randomised controlled trials

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%).[98] In-hospital mortality was
11 per 1000 higher for the liberal oxygen therapy group versus the conservative therapy group
(95% CI 2 to 22 per 1000 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 SpO₂ limit of 96% is therefore reasonable when administering supplemental oxygen
to 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).[97]
• In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis
and decided an interim update was not required.[103]
• 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 earlier 2015 TSANZ guideline recommendation.
MANAGEMENT
• Subsequently, experience during the COVID-19 pandemic has also made clinicians more aware
of the feasibility of permissive hypoxaemia.[104]
• Management of oxygen therapy in patients in intensive care is specialised and informed by
further evidence (not covered in this summary) that is more specific to this setting.[105] [106]
[107]
Refer to hyperacute or acute stroke unit

In hospital
Admit everyone 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.[63] [64]
• This is to begin thrombolysis as quickly as possible (if indicated) and to help prevent
complications.[63] [64]
MANAGEMENT
47
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 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.[64]
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.[108]
• It included 28 randomised controlled trials (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).[109]
• 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 outcomes (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 who is suspected of having acute stroke (or emergent transient
ischaemic attack)[63] [64]
• Resolved neurological symptoms who has a bleeding disorder or is taking an anticoagulant
because haemorrhage must be excluded.[64]
Thrombolysis
Follow your local protocols for recommendations on intravenous thrombolysis.
The National Institute for Health and Care Excellence (NICE) in the UK and the European Stroke
Organisation (ESO) recommend to give intravenous alteplase (recombinant tissue plasminogen
activator) to eligible patients if not contraindicated and:[63] [95] [110]
• Treatment is started as soon as possible within 4.5 hours of onset of stroke symptoms
AND
• Intracranial haemorrhage has been excluded using appropriate imaging techniques.
The ESO further recommends intravenous thrombolysis for:[95]
• Patients who were last seen well 4.5 to 9 hours earlier (known onset time), with CT or MRI core/
perfusion mismatch, and for whom mechanical thrombectomy is either not indicated or not planned
• Patients with acute ischaemic stroke on awakening from sleep, who were last seen well more than
4.5 hours earlier, who have MRI DWI-FLAIR mismatch (diffusion-weighted MRI and fluid-attenuated
MANAGEMENT
inversion recovery MRI mismatch), and for whom mechanical thrombectomy is either not indicated
or not planned.
49
Refer to the prescribing information for contraindications to thrombolysis with alteplase. Examples include
recent major surgery, bleeding disorders such as haemophilia, and current anticoagulation use.
Do not delay treatment with alteplase while waiting for results or waiting to perform tests, unless
you suspect contraindications that must be ruled out first (eg., hypoglycaemia, coagulopathy), or while
monitoring for further improvement.[66] [67]
Consider reducing blood pressure to 185/110 mmHg or lower in people who are candidates for
intravenous thrombolysis.[63] [111]
MANAGEMENT
Thrombolysis with alteplase
Alteplase improves functional outcomes after acute ischaemic stroke if given within 4.5 hours
of onset of symptoms. There is an increased risk of intracranial haemorrhage with alteplase but
this does not seem to affect death or dependency at 3 months.
A Cochrane systematic review (published 2014) assessed thrombolysis compared with placebo for
patients with acute ischaemic stroke. It included 27 trials (n=10,187); most of the evidence came from
the use of alteplase (12 trials; n=7012).[60]
• There was a significant reduction in death or dependency by the end of follow-up when
alteplase was given up to 6 hours from onset (8 randomised controlled trials [RCTs]; n=6729;
OR 0.84, 95% CI 0.77 to 0.93; significant heterogeneity)
• However, treatment within 3 hours was substantially more beneficial and there was no
heterogeneity (6 RCTs; n=1779; OR 0.65 95% CI 0.54 to 0.80).
In 2012 the UK National Institute for Health and Care Excellence (NICE) updated their guidance
on alteplase to extend the window for treatment from 3 hours to up to 4.5 hours after the onset of
symptoms.[110]
• The decision was based mainly on the third European Cooperative Acute Stroke Study (ECASS
III).[112]
• 821 people with acute ischaemic stroke were randomised to receive alteplase or placebo.
• Alteplase increased the proportion of people with a favourable outcome (modified Rankin
Scale [mRS] score 0-1; 52.4% with alteplase vs. 45.2% with placebo; RR 1.16, 95% CI
1.01 to 1.34).
• There was an increased risk of intracranial haemorrhage with alteplase (27.0% vs. 17.6%,
P=0.001) including symptomatic intracranial haemorrhage (2.4% with alteplase vs. 0.3%
with placebo; RR 4.82, 95% CI 1.06 to 21.87).
• There was no statistically significant difference in other serious adverse events or in all-
cause mortality at 3 months (7.7% with alteplase vs. 8.4% with placebo, P=0.68).
• In an additional analysis for NICE by the Evidence Review Group there was no significant
difference in death or dependency at 90 days (RR 0.87, 95% CI 0.73 to 1.05), although
there was a trend towards a better outcome with alteplase.[113]
• NICE excluded the third International Stroke Trial (IST-3) because it included people over 80
years old and treatment up to 6 hours, and therefore went beyond the UK market authorisation
of alteplase.
• A reanalysis of ECASS III published in 2020 raised concerns about the effectiveness of
alteplase when used 3 to 4.5 hours after the onset of stroke symptoms.[114] However, the
NICE guideline recommendation to use alteplase within its market authorisation (i.e., as early
as possible within 4.5 hours of onset of stroke symptoms, and if intracranial haemorrhage has
been excluded by appropriate imaging techniques) has remained unchanged and should be
MANAGEMENT
followed.[110] [115]
An individual patient-data meta-analysis (8 randomised trials, N=6136, published in 2018) included

analyses based on current and extended US and European labels for alteplase.[116]
51
• 40% of people in the trials were aged ≤80 years and treated within 4.5 hours (i.e., met the
current European label).
• Among these participants, alteplase increased the odds of achieving an excellent

outcome (mRS score 0-1; OR 1.42, 95% CI 1.21 to 1.68) and of gaining any improvement
in mRS score (OR 1.27, 95% CI 1.11 to 1.47).
• There was an increase in intracranial haemorrhage at 24 to 36 hours (OR 8.27, 95% CI
2.47 to 27.64) and fatal haemorrhage within 7 days (absolute excess risk 1.7%, 95% CI
0.9% to 2.5%). There was, however, no significant increase in 90-day all-cause mortality
(HR 0.98, 95% CI 0.76 to 1.25).
In the UK, alteplase should only be administered within a well-organised stroke service by staff trained
in delivering thrombolysis and in monitoring for complications.[63] [64] Trained staff in emergency
departments can also administer alteplase provided that the patient can be managed in an acute stroke
service.[63]
The Royal College of Physicians in the UK recommends to consider for alteplase treatment: [64]
• All patients regardless of age or stroke severity in whom treatment can be started within 3
hours of known onset of symptoms
• Patients aged <80 years in whom treatment can be started between 3 and 4.5 hours of known
onset.
• Patients aged >80 years in whom treatment can be started between 3 and 4.5 hours of known
onset on an individual basis.
• The benefits of treatment are smaller than if treated earlier, but the risks of a worse outcome,
including death, will on average not be increased.
Patients presenting between 6 and 24 hours after stroke onset may be considered for thrombectomy
alone.[63]
MANAGEMENT
Thrombolysis in people aged >80 years
People over 80 years old with acute ischaemic stroke may benefit from treatment with
alteplase; however, the decision needs to be made according to the risk-benefit profile of the
individual patient.
In 2015 the Medicines and Healthcare products Regulatory Agency (MHRA) in the UK reviewed the
evidence for alteplase, including the third International Stroke Trial (IST-3), the first trial to include a
large number of people aged >80 years (n=1617, 53% of total trial population).[117] [118]
• The MHRA made the case for people aged over 80 years being considered for treatment
on an individual basis, although they stopped short of specifically stating this in their overall
conclusions and recommendations.
The UK Royal College of Physicians (RCP) in their 2016 guideline recommended that anyone
presenting with acute ischaemic stroke within 3 hours of the onset of symptoms should be treated with
alteplase. For people >80 years presenting 3 to 4.5 hours from the onset of symptoms they stated that
treatment with alteplase should be considered on an individual basis.[64]
• This was mostly based on a Cochrane systematic review (published in 2014) that assessed the
effect of age under or over 80 years on death or dependency (defined as modified Rankin Scale
[mRS] 3-5).[60]
• Most of the evidence for people aged >80 years old came from IST-3.
• The subgroup analyses for death or dependency in people aged >80 years compared with
people aged ≤80 years showed similar results at both 6 hours (>80 years: OR 0.80, 95% CI
0.64 to 0.99; P=0.04 [3 trials,1696 participants]; ≤80 years: OR 0.85, 95% CI 0.76 to 0.95;
P=0.004 [10 trials, 5175 participants]) and 3 hours (>80 years: OR 0.56, 95% CI 0.40 to 0.78;
P=0.0007 [2 trials, 726 participants]; ≤80 years: OR 0.66, 95% CI 0.52 to 0.85; P=0.001 [6 trials,
1039 participants]).
The RCP guidance is also supported by a more recent individual patient-data meta-analysis of 8
randomised trials (published in 2018) which compared outcomes among a subgroup of patients aged
≤80 and >80 years, who otherwise met extended European Medicines Agency (EMA) marketing label
criteria at the time of the study for treatment with alteplase, but with no upper age limit (total 3491 of
the 6136 trial participants; 57%).[116]
• Overall, the OR for achieving an excellent functional outcome on the modified Rankin Scale of 0
to 1 was 1.43 (95% CI 1.23 to 1.65) and for gaining any improvement in mRS was 1.29 (95% CI
1.14 to 1.45).
• There was excellent functional outcome (OR 1.43, 95% CI 1.23 to 1.65), with no excess risk of
90-day mortality (16.1% with alteplase vs. 16.5% with control: HR 1.01, 95% CI 0.86 to 1.19).
Fatal haemorrhage within 7 days (absolute excess risk 2.1%, 95% CI 1.3% to 2.8%) was similar
MANAGEMENT
between subgroups.
• In a further subgroup analysis just considering those aged >80 years, the odds ratio for
achieving an excellent functional outcome was 1.69 (95% CI 1.17 to 2.44).
53
A 2020 pooled analysis of randomised trials of alteplase and registry data (almost 3000 patients)
examined outcomes in patients aged >80 years who met existing European regulatory criteria
including receipt of alteplase within 4.5 hours of stroke onset.[119]
• Among patients aged >80 years, alteplase versus placebo was associated with a higher
proportion of good stroke outcome (modified Rankin Scale score 0-1; 99/518 [19.1%] vs.
67/510 [13.1%]; P=0.0109) and similar 90-day mortality (153/518 [29.5%] vs. 154/510 [30.2%];
P=0.8382).
• The odds of a good stroke outcome following alteplase allocation in the full randomised
controlled trial (RCT) population were independent of age (P=0.7383).
• Registry data showed that outcomes among patients aged >80 years who received alteplase
for acute ischaemic stroke in routine clinical practice correspond well with those in RCTs. The
incidence of spontaneous intracranial haemorrhage (1.4% vs. 3.7%) and overall mortality
(29.0% vs. 29.5%) following thrombolysis of patients aged >80 years who otherwise met
European regulatory criteria was not increased in routine practice versus clinical trials.
Mechanical thrombectomy
The decision to offer mechanical thrombectomy (endovascular intervention) should be made by
clinicians experienced in the use of thrombolysis for stroke and in interpretation of relevant
imaging. The procedure should only be carried out by appropriately trained specialists with regular
experience in intracranial endovascular interventions, with appropriate facilities and neuroscience
support.[82]
Candidates for thrombectomy alone include those who cannot receive thrombolysis (e.g., with
contraindications including recent major surgery, bleeding disorders such as haemophilia, current
anticoagulation use).[64]
The team should take into account the patient’s clinical status and the extent of established
infarction on initial brain imaging to inform decisions about thrombectomy. Select people who have (in
addition to the specific additional factors from NICE stated below):[63]
• A pre-stroke functional status <3 on the modified Rankin Scale, and

• A score >5 on the National Institutes of Health Stroke Scale (NIHSS)
In addition, the National Institute for Health and Care Excellence (NICE) in the UK specifically
recommends for people with acute ischaemic stroke:[63]
• Offering mechanical thrombectomy:
• As soon as possible and within 6 hours of symptom onset (together with intravenous
thrombolysis, if not contraindicated and within the licensed time window) to patients with
confirmed occlusion of the proximal anterior circulation (demonstrated by CT
angiography or MR angiography [CTA/MRA]).
MANAGEMENT
• As soon as possible to patients who were last known to be well between 6 and 24
hours previously (including wake-up strokes):
• Who have confirmed occlusion of the proximal anterior circulation demonstrated by
CTA or MRA
AND
• Considering thrombectomy together with intravenous thrombolysis (where not

contraindicated and within the licensed time window) as soon as possible for patients known
to be well up to 24 hours previously (including wake-up strokes):
• Who have confirmed occlusion of the proximal posterior circulation(i.e., basilar or

posterior cerebral artery) demonstrated by CTA or MRA,
AND
The role of thrombectomy alone without intravenous thrombolysis (e.g., where there are contraindications
for thrombolysis) has not yet been ascertained.
• One systematic review found that, even in patients with mild strokes due to large vessel occlusion
(LVO) who were not eligible for thrombolysis with intravenous alteplase, mechanical thrombectomy
resulted in better 90-day functional outcomes, and suggested that this treatment can play an
important role for patients not eligible for intravenous alteplase.[120]
• Analysis from three randomised controlled trials (RCTs; 1092 patients) detected no differences
in functional outcomes of intravenous thrombolysis-eligible patients with an acute LVO receiving
direct endovascular treatment compared with endovascular treatment preceded by intravenous
thrombolysis.[121] However, the authors note that because uncertainty for most end points remains
large and the available data are not able to exclude the possibility of overall benefit or harm, further
RCTs are needed.
MANAGEMENT
55
Evidence: Mechanical thrombectomy in anterior circulation stroke
Mechanical thrombectomy, with or without thrombolysis, compared with thrombolysis or

standard care, improves functional outcome (measured by the modified Rankin Scale [mRS])
and potentially quality of life in adults with anterior circulation stroke confirmed by non-
invasive angiography.
For most studies, the direction of effect favoured thrombectomy in terms of mortality at 90
days or 1 year, although only one study found a significant difference.
Due to the development of new neurointerventional techniques, numerous multicentre randomised

controlled trials (RCTs) in this area have been published since 2015. The UK National Institute for
Health and Care Excellence (NICE) performed an updated evidence search for their 2019 guideline on
acute ischaemic stroke in adults.[63]
They compared endovascular therapy (mechanical thrombectomy) with or without intravenous

alteplase versus alteplase or standard care (for example, aspirin) in patients with proven large
vessel occlusion on CT or MRI. They found 10 RCTs, all in adults with anterior circulation stroke.
Results were reported by time from symptom onset to treatment, a planned subgroup analysis, due to
heterogeneity.[63]
• For patients treated within 6 hours of symptom onset, they found 6 RCTs (MR CLEAN,
THRACE, EXTEND IA, SWIFT PRIME, THERAPY, and PISTE) in a total of 1334 adults.[63]
• Thrombectomy improved functional independence (increased the number of patients

with mRS 0 to 2 at 90 days; RR 1.47, 95% CI 1.28 to 1.68; moderate-quality evidence
assessed using GRADE).
• There was no difference in serious adverse events, quality of life, or mortality at 90 days
(GRADE moderate) or in intracerebral haemorrhage at 90 days (GRADE low). However,
quality of life was only reported in one study (THRACE).
• For treatment within 8 hours, they found one RCT (REVASCAT) involving 206 people.[63]
• Thrombectomy increased the number of patients with mRS 0 to 2 at 90 days (RR 1.55,
95% CI 1.06 to 2.27; low quality evidence assessed using GRADE) and quality of life
scores (median EQ-5D [scores range from -0.33 to +1.00, with higher scores indicating a
better quality of life]: 0.33 higher in intervention group; GRADE moderate).
• There was no difference in intracerebral haemorrhage or mortality at 90 days (GRADE
low).
• For treatment within 12 hours, they found one RCT (ESCAPE) involving 316 people.[63]
95% CI 1.36 to 2.42; GRADE moderate) and increased quality of life (median EQ-5D
MANAGEMENT
visual analogue scale [score ranges from 0 to 100]: 15 higher in intervention group;
GRADE moderate).
• Thrombectomy reduced the risk of malignant middle cerebral syndrome (RR 0.26, 95%
CI 0.12 to 0.55; GRADE high) and mortality at 90 days (RR 0.54, 95% CI 0.31 to 0.95;
GRADE moderate).
• There was no significant difference in intracerebral haemorrhage (GRADE low).
• For treatment after 6 hours but within 24 hours, they found 2 RCTs (DAWN and DEFUSE 3)
involving a total of 388 patients. In these trials few patients in either group received thrombolysis
because most were outside of the licenced time window.[63]
95% CI 2.17 to 4.59; GRADE moderate).
• There was no significant difference in intracerebral haemorrhage (GRADE low) or
mortality (GRADE very low).
• Procedural complications were reported as a harm of thrombectomy in one study (OR
7.27, 95% CI 1.61 to 32.73; GRADE high), but were considered to be outweighed by the
benefits of functional outcome improvement.
• NICE considered the evidence to be applicable to people over the age of 16 and put no upper
age limit on their recommendation. Overall, 3 studies had inclusion criteria of up to 80 years of
age, one up to 85 years and one of up to 90 years, the remaining 5 studies included everyone
eligible who was aged over 18 years.
• NICE noted that following the presentation of results of MR CLEAN, which showed a benefit
of thrombectomy, most other trials stopped recruitment early (EXTEND IA, SWIFT PRIME,
THERAPY, PISTE, REVASCAT, ESCAPE, DEFUSE 3). Some trials conducted an interim
analysis; others acknowledged they were underpowered. It is possible that the treatment effect
was overestimated in the trials that terminated early, although NICE felt there was no need to
downgrade the evidence because of this.
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57
Evidence: Mechanical thrombectomy in posterior circulation stroke
Mechanical thrombectomy, with or without thrombolysis, may be beneficial in selected patients

with posterior circulation stroke; however, evidence is very limited and current practice
is largely influenced by evidence from people with anterior circulation stroke and clinical
experience of these interventions in people with posterior circulation stroke.
In the 2019 guideline on acute ischaemic stroke in adults, the UK National Institute for Health and
Care Excellence (NICE) looked for direct evidence on the effectiveness of mechanical thrombectomy
in people with posterior circulation stroke. NICE did not find any published evidence (RCTs
or observational studies) that met their criteria. The guideline committee therefore made their
recommendation based on clinical knowledge of outcomes of basilar artery occlusion and current best
practice.[63] [115]
• The committee noted that prognosis is usually poor, with around 80% mortality, and that
without intervention only 2% to 5% of people make a full neurological recovery. However, good
outcomes can be achieved with intervention even up to 24 hours post-stroke onset.
• The committee agreed that current best practice is to consider intravenous thrombolysis and
mechanical thrombectomy following brain imaging to look for established tissue damage,
particularly in the brainstem, to ascertain which patients may benefit from treatment. This
reduces the number of people surviving with severe neurological disability. Intervention should
be as soon as possible after presentation.
• They also felt the evidence from anterior circulation stroke was supportive for intervention in
posterior stroke. Therefore, the committee recommended that thrombectomy, and thrombolysis
within its licensed indications, should be considered for people with posterior circulation
proximal occlusions - a weaker recommendation than the one they made for people with anterior
circulation stroke.
The NICE guideline group was aware of two relevant study protocols. One, the Basilar Artery
International Cooperation Study (BASICS) study is a randomised, multicentre, open label, controlled
trial that is estimated to complete around January 2020.[122] The other, the BEST study, a multicentre,
randomised, open-label trial in China, was published in December 2019.[123]
• This study found no difference between thrombectomy and standard care for post-circulation
stroke for functional outcomes (modified Rankin Scale [mRS] 0 to 3 at 90 days; 28/66 with
thrombectomy vs. 21/65 with standard care; adjusted OR 1.74, 95% CI 0.81 to 3.74) or 90-day
mortality (22/66 with thrombectomy vs. 25/65 with standard care; P=0.54).
• However, the study may have been underpowered and it was stopped early due to the large
number of crossovers between groups and poor recruitment. Further pre-specified analysis
showed a benefit of thrombectomy on mRS at 90 days in both per-protocol (28/63 patients with
thrombectomy vs. 13/51 with standard care; adjusted OR 2.90, 95% CI 1.20 to 7.03]) and as-
treated (36/77 with thrombectomy vs. 13/54 with standard care; adjusted OR 3.02, 95% CI 1.31
to 7.00) analyses.
MANAGEMENT
Monitoring and supportive care
Monitor the patient’s clinical status closely and provide supportive care as appropriate. [64]
In particular, monitor:
• Level of consciousness
• Blood glucose
• Blood pressure
• Oxygen saturations
• Hydration
• Temperature
• Cardiac rhythm and rate.
Monitor the patient for complications such as signs of raised intracranial pressure and seizures.
Level of consciousness
Assess and monitor the patient’s level of consciousness using the Glasgow Coma Scale.
• In patients with decreased level of consciousness or coma, urgently exclude haemorrhage

and stroke mimics such as seizures. See Differentials .
Practical tip
Haemorrhagic stroke is more often associated with seizures, decreased level of consciousness, and
signs of increased intracranial pressure than ischaemic stroke.
Blood glucose
Monitor blood glucose regularly. Maintain a blood glucose concentration between 4 and 11 mmol/L
in people with acute stroke.[63]
MANAGEMENT
59
Evidence: Glycaemic control in acute stroke
Despite evidence of an increased risk of poor functional outcome and death in patients with
ischaemic stroke who develop post-stroke hyperglycaemia, limited available data do not show
a significant benefit with tight glycaemic control compared with usual care. In addition, there is
an increased risk of hypoglycaemia with tight glycaemic control. [63] [64] [124] [125] [126]
• A Cochrane systematic review found no significant difference in terms of dependency or

death when intensive insulin therapy was compared with usual care to maintain blood glucose
levels in adults with acute stroke, but rates of hypoglycaemia were higher with intensive insulin
therapy.[127]
• The review (search date September 2013) included 11 randomised controlled trials
(RCTs), involving a total of 1583 participants (with and without diabetes) with blood
glucose levels >6.1 mmol/L after a stroke.
• The intensive insulin treatment intervention aimed to maintain blood glucose within the
normal range of 4 to 7.5 mmol/L and was started in the first 24 hours of ischaemic stroke.
Control interventions included placebo, no treatment, or loose control with insulin.
• The mean blood glucose level during treatment was significantly lower in the intensive
insulin intervention group than in the control group (6.7 mmol/L vs. 7.3 mmol/L; mean
difference -0.63, 95% CI -0.80 to -0.46 mmol/L).
• There was no significant difference between the treatment and control groups for the
primary outcome of dependency or death (OR 0.99, 95% CI 0.79 to 1.23), or final
neurological deficit (standardised mean difference -0.09, 95% CI: -0.19 to +0.01).
• However, there was a significant increase in the incidence of symptomatic hypoglycaemia
in the intensive treatment group compared with the control group (OR 14.6, 95% CI 6.6 to
32.2).
• Results from an RCT including 1151 adults who received either intensive treatment for
hyperglycaemia (target blood glucose concentration of 4.4 to 7.2 mmol/L) or standard treatment
(target glucose concentration of 4.4 to 9.9 mmol/L) for up to 72 hours did not show a significant
difference in favourable functional outcome at 90 days. Treatment was stopped early for
hypoglycaemia or other adverse events in 11.2% of patients in the intensive treatment group
and in 3.2% in the standard treatment group.[126]
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 to 11 mmol/L (this was not changed in the 2022
update of this guideline).[63]
• This recommendation is underpinned by:

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• 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 stroke.[128]
• Consensus of the NICE guideline panel on the 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 recommends
a broader target range of 5 to 15 mmol/L, with close monitoring to avoid hypoglycaemia.[64]
• This guideline cites the same trial as the NICE guideline to support this
recommendation.[128]
• The recommendation in the European Stroke Organisation guidelines from 2018 is underpinned
by evidence from a systematic review including almost all the same studies as those included in
the 2014 Cochrane review (above).[125]
• This guideline makes 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 (low-quality evidence as assessed using GRADE).[125]
Give optimal insulin therapy with intravenous insulin and glucose to all adults with type 1 diabetes with
threatened or actual stroke. Follow your local protocol.[63]
Blood pressure
Monitor blood pressure regularly and give antihypertensive treatment only if there is
a hypertensive emergency with one or more of the following serious concomitant
conditions:[63]
The National Institute for Health and Care Excellence (NICE) in the UK recommends to consider reducing
blood pressure to 185/110 mmHg or lower in people who are candidates for intravenous thrombolysis.[63]
[111] In patients with acute ischaemic stroke not treated with intravenous thrombolysis or mechanical
thrombectomy and blood pressure >220/120 mmHg, the European Stroke Organisation states that careful
blood pressure reduction (<15% systolic blood pressure reduction in 24 hours) is reasonable and likely
to be safe.[111] In patients on antihypertensive medication, resume oral treatment once the patient is
medically stable and as soon as they can swallow medication safely.[64]
MANAGEMENT
61
Evidence: Lowering blood pressure
The 2019 UK National Institute for Health and Care Excellence (NICE) guideline on stroke
recommends that blood pressure should not be lowered routinely after an ischaemic stroke
unless there are serious coexisting medical issues. [63]
• The NICE guideline committee reported a lack of evidence from their analysis of two Cochrane
reviews and four additional randomised controlled trials for benefit in manipulating blood
pressure using beta-blockers or calcium-channel blockers in the first 72 hours of acute
ischaemic stroke compared with control/placebo.[129] [130] However, they agreed there may
be individual clinical circumstances where active management of severe hypertension would be
indicated.
A Cochrane systematic review (search date 2014) addressed the question of whether to
continue or discontinue existing antihypertensive regimens in patients with acute stroke.
[131]
• The review included 26 trials involving a total of 17,011 adults with acute ischaemic stroke or
intracerebral haemorrhage. Interventions for lowering blood pressure included alpha-blockers,
ACE inhibitors, angiotensin-II receptor antagonists, calcium-channel blockers, nitric oxide
donors, or thiazide-like diuretics.
• Among the patients with ischaemic stroke who were not already on antihypertensive treatment,
blood pressure lowering did not significantly change the following outcomes: “death or
dependency” (OR 1, 95% CI 0.92 to 1.08; 8 trials; n=11,015), “death” (OR 0.95, 95% CI 0.78 to
1.16; 10 trials; n=11,238), “dependency” (mean difference in Barthel Index 0.84, 95% CI -3.21
to +4.89; 2 trials; n=3,681), “early neurological deterioration” (OR 0.58, 95% CI 0.09 to 3.82; 2
trials; n=3349), “length of stay” (mean difference -0.03; 95% CI -0.33 to +0.28; 2 trials; n=7393)
or “quality of life” (mean difference in EuroQol 0.13, 95% CI -0.14 to +0.4; 2 trials; n=4038).
• Among the patients with ischaemic stroke who were already taking antihypertensives who
continued or stopped this treatment, there was no significant difference in the following
outcomes: “death or dependency” at day 90 (OR 1.06, 95% CI 0.87 to 1.28; 1 trial; n=1,832),
“death” (OR 1.24, 95% CI 0.96 to 1.61; 1 trial; n=1,832), “early neurological deterioration” (OR
1.27, 95% CI 0.89 to 1.82; 1 trial; n=2097), or “length of stay” (mean difference 1.2, 95% CI
-0.87 to +3.27; 1 trial; n=2097). However, “dependency” was lower among those who stopped
treatment (mean difference on the Barthel Index -3.8, 95% CI -7.23 to -0.37; 1 trial; n=2097) and
“quality of life” was better among those who stopped treatment (mean difference on the EuroQol
-0.03, 95% CI -0.06 to 0.00; 1 trial; n=2097).
Ox ygen saturations
Monitor oxygen saturations and give supplemental ox ygen only if ox ygen saturation drops
below 93%.[97] See Stabilisation under Urgent initial management above for more information.
MANAGEMENT
administering supplemental oxygen to most patients with acute illness who are not at risk of
hypercapnia. Evidence suggests that liberal use of supplemental oxygen (target SpO 2 >96%) in
acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[98] A
lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory
failure.[99]
Hydration
Assess the patient’s hydration within 4 hours of their arrival at hospital.[63] Review regularly; manage as
needed to maintain normal hydration.[63] [64]
Temperature
Monitor temperature.[64] [100] Patients with stroke can lose their thermoregulation acutely and may need
interventions even in the absence of infection.
• Give an antipyretic (e.g., paracetamol) in patients with high temperature. Do not give antipyretics
to patients with a normal temperature to prevent hyperthermia.[100]
The National Institute for Health and Care Excellence (NICE) in the UK does not recommend the use of
therapeutic hypothermia (a cooling device used to lower the body’s temperature by 2ºC to 4°C for several
hours immediately after a stroke) to reduce the risk of secondary brain damage.[132]
Cardiac rhythm and rate


• Consider longer ECG monitoring (24 hours or more) in those in whom no other cause of
stroke has been found, particularly if they have a pattern of cerebral ischaemia on brain imaging
Atrial fibrillation is an independent risk factor for ischaemic stroke and indicates a poor prognosis.[25] See
New-onset atrial fibrillation .
Intracranial pressure
Monitor the patient for signs of elevated intracranial pressure (ICP). For information on other
complications, see Complications .
Repeat the CT head immediately if you suspect elevated ICP, which may present as:

• Severe headache
• Nausea/vomiting
Refer immediately to a neurosurgeon any patients with large middle cerebral artery territory
MANAGEMENT
infarcts and those with large infarctions affecting the cerebellum. These types of stroke have a
very high mortality if urgent neurosurgical intervention is delayed.[65]
63
• Patients with large middle cerebral artery territory infarcts (at risk of malignant middle
cerebral artery syndrome) may need decompressive hemicraniectomy (neurosurgical removal
of part of the skull to reduce intracerebral pressure).[65]
• Patients with large infarctions affecting the cerebellum may need ventriculostomy
(placement of an external ventricular drain) or posterior fossa craniectomy.[65]
Practical tip
Patients with large infarctions affecting the cerebellum or middle cerebral artery are at risk of
developing oedema and elevated intracranial pressure. If left unchecked, the oedema compromises
blood flow and causes brain herniation, which is frequently fatal.
In line with recommendations from the National Institute for Health and Care Excellence (NICE) in the
UK, decompressive hemicraniectomy should be considered (performed within 48 hours of
symptom onset) in any patient who meets all of the following criteria:[63]
• Clinical deficits that suggest infarction in the territory of the middle cerebral artery, with a
score >15 on the National Institutes of Health Stroke Scale (NIHSS)
• Decreased level of consciousness, with a score of 1 or more on item 1a of the NIHSS
• Signs on CT of an infarct of at least 50% of the middle cerebral artery territory:
• With or without additional infarction in the territory of the anterior or posterior cerebral artery
on the same side
or
• 3
With infarct volume greater than 145 cm , as shown on diffusion-weighted MRI scan.
MANAGEMENT
Evidence: Decompressive hemicraniectomy
Decompressive hemicraniectomy reduces mortality, with some evidence of improved

functional outcomes (although overall functional outcomes are poor in this population) and a
variable impact on quality of life (which is generally low with or without surgery). There is no
evidence that there should be an age cut-off for surgery, with the patient’s pre-stroke functional
status being a more useful indicator of the potential outcomes of surgery.
There has been much debate about the net benefits of hemicraniectomy, especially in patients aged
over 60 years due to the possibility of an increased risk of surviving with a serious disability, compared
with people under 60 years.
The 2008 UK National Institute for Health and Care Excellence (NICE) guideline recommended
hemicraniectomy only in people aged under 60 years. This was updated in 2019 to recommend
that patients or their family members or carers should be given specific information on the risks
and benefits in terms of functional outcomes and risk of mortality, so that personal values and
preferences, especially regarding disability, are considered in shared decision-making.[133] This
updated recommendation followed new evidence focusing on patient age, in particular the 2014
DESTINY II trial.[133]
• The review by NICE found 5 randomised controlled trials (RCTs) of patients with an average age
<60 years (HeMMi, HeADDFIRST, HAMLET, DESTINY and DECIMAL).[133]
• In these studies, decompressive hemicraniectomy reduced mortality at 30 days (1 study;

n=32; risk difference 416 fewer per 1000 [95% CI 64 fewer to 501 fewer]; moderate-
quality evidence assessed using GRADE), 6 months (3 studies; n=86; risk difference 262
fewer per 1000 [95% CI 76 fewer to 371 fewer]; GRADE moderate) and 1 year (3 studies;
n=134; risk difference 392 fewer per 1000 [95% CI 261 fewer to 469 fewer]; GRADE
high).
• There was a clinically important difference in functional outcomes (score 0 to 3 on
modified Rankin Scale) at 6 months (risk difference 110 more per 1000 [95% CI 68 fewer
to 441 more]; GRADE very low) or 1 year (risk difference 130 more per 1000 [95% CI 25
fewer to 392 more]; GRADE low).
• There was no clinically important difference for quality of life at 1 year as measured by
the SF-36 mental summary score (1 study; n=35; GRADE very low) or as measured
using visual analog scales (1 study; n=32; GRADE low), but a clinically important harm
of surgery for the SF-36 physical summary scale (1 study; n=35; GRADE low). Overall,
quality of life scores were low in both groups.
• NICE found 3 RCTs in patients with an average age over 60 years (including DESTINY II).[133]
• In these studies, decompressive hemicraniectomy reduced mortality at 6 months (1

study; n=29; risk difference 487 fewer per 1000 [95% CI 122 fewer to 579 fewer]; GRADE
moderate) and 1 year (3 studies; n=162; risk difference 364 fewer per 1000 [95% CI 227
MANAGEMENT
fewer to 462 fewer]; GRADE moderate).

• There was no difference in functional outcomes between groups at 6 months (2 studies;
n=141; risk difference 23 more per 1000 [95% CI 7 fewer to 159 more]; GRADE very low)
65
but a significant benefit for surgery at 12 months (3 studies; n=165; risk difference 100
more per 1000 [95% CI 10 more to 180 more]; GRADE very low).
• Quality of life was higher at 1 year after surgery (1 study; n=100; GRADE low). Overall
quality of life scores were low in both groups.
In all of the trials in people aged over 60 years, surgery had to be within 48 hours of symptom
onset. Two of the trials in those aged under 60 years included people who had surgery longer
than 48 hours after symptom onset (HeMMi 72 hours and HAMLET 96 hours). The NICE
guideline group felt the beneficial results were largely driven by studies which only allowed
surgery up to a maximum of 48 hours after onset, hence the time limit for surgery in their
recommendation.
The NICE guideline committee notes that there was a clear mortality benefit of surgery at any
age and that the patient’s pre-morbid state is more important than their age when making a
decision about the risks of surgery. However, survivors have a high likelihood of moderate or
severe disability with or without surgery.
Discuss the risks and benefits of the procedurewith the patient or their family members or
carers. Take into account the patient’s functional status before the stroke, and their wishes and
preferences.[63] A shared decision-making process should include a careful discussion with the patient or
their representatives about the risk of survival with substantial disability.[134]
Seizures
Consult immediately with a neurologist or neurosurgeon if the patient has uncontrolled or
recurrent seizures, or status epilepticus. The choice of anticonvulsant will depend on individual
patient characteristics.[65] See Status epilepticus .
• Follow your hospital protocol. In practice, levetiracetam and sodium valproate are commonly
used.
Non-urgent initial management

In people with non-disabling ischaemic stroke (i.e., minor stroke) who are not candidates for hyperacute
treatment with thrombolysis and/or mechanical thrombectomy, secondary prevention of stroke
assessment and management may be prioritised. See Prevention .
• A minor ischaemic stroke is defined as a score <3 on the National Institutes of Health Stroke Scale
(NIHSS), and no persistent disabling neurological deficit.[135]
Subsequent acute treatment
Antiplatelet therapy
MANAGEMENT
Offer an antiplatelet agent as soon as possible but certainly within 24 hours (unless
contraindicated) to any patient presenting with acute stroke who has had intracerebral haemorrhage
excluded by imaging:[63]
• Aspirin orally (for those with no dysphagia), or
• Aspirin rectally or by enteral tube (for those with dysphagia).
Offer an alternative antiplatelet agent to anyone who is allergic to or genuinely intolerant of

aspirin.[63] In practice, clopidogrel is often used.
Antiplatelet treatment may be contraindicated or delayed in patients with active bleeding (e.g., from the
gastrointestinal tract).
Evidence: Aspirin
The UK National Institute for Health and Care Excellence (NICE) guideline recommendation
to give aspirin within 24 hours to patients with acute ischaemic stroke with a diagnosis of
primary intracerebral haemorrhage excluded by brain imaging is underpinned by evidence from
a Cochrane systematic review. [63] [136]
A 2003 Cochrane Review was used as evidence to support the NICE guideline recommendation:[137]
• The review found that aspirin compared with placebo was associated with:
• A significant reduction in death or dependency at 1 month or more after follow-up (OR

0.95, 95% CI 0.91 to 0.99; P=0.008)
• A significant reduction in symptomatic pulmonary embolism (OR 0.71, 95% CI 0.53 to
0.97; P=0.03)
• A significant reduction in recurrent ischaemic stroke or stroke of unknown pathology
during treatment period (OR 1.22, 95%CI 0.69 to 0.87; P=0.00002)
• A small significant increase in risk of symptomatic intracranial haemorrhage (OR 1.22,
95% CI 1.00 to 1.50; P=0.05) and major extracranial haemorrhage (OR 1.69, 95% CI 1.35
to 2.11; P <0.0001).
• The NICE guideline panel noted that the two largest randomised controlled trials made up 98%
of the data in this Cochrane systematic review and these two trials recommended that aspirin
should be given as soon as possible after exclusion of haemorrhage and within 48 hours, and
then continued for 2 to 4 weeks following onset.[138] [139]
• Even though this Cochrane Review has since been updated (including an updated literature
search) and changed in scope to include only trials of oral antiplatelet agents, the same two
trials still contribute to 98% of the data.[136]
• The authors of the 2014 Cochrane review state that the hazard of bleeding associated with
aspirin, although significant, is more than offset by the benefit of aspirin in its associated
reduction in recurrent ischaemic stroke.[136]
Offer a proton-pump inhibitor, in addition to aspirin, to any patient who reports previous dyspepsia
associated with aspirin.[63]
MANAGEMENT
In practice, administration of aspirin (or alternative) is usually delayed 24 hours after

alteplase, once a further CT scan has excluded significant bleeding.
67
Continue aspirin daily until 2 weeks after the onset of stroke symptoms, then start definitive long-
term antithrombotic treatment. Start people on long-term treatment earlier if they are being discharged
before 2 weeks.[63]
Practical tip
Many ischaemic strokes are caused by conventional atherosclerosis, either in major vessels (such
as the aortic arch or carotid arteries) or more distal vessels in the brain itself. Strokes caused by
atherosclerosis, plaque rupture, platelet aggregation, and vessel occlusion by platelet-rich thrombus
or embolism of the thrombus should be treated with antiplatelet agents.[63] [64]
Anticoagulation
Do not use anticoagulant treatment routinely to treat acute stroke.[63]
MANAGEMENT
Evidence: Anticoagulation
There is evidence from one systematic review that early anticoagulation shows no net benefit
in acute ischaemic stroke.
A Cochrane systematic review (search date June 2014) assessed the effectiveness and safety of
early (within the first 14 days of onset; >90% within 48 hours) anticoagulation (with unfractionated
heparin, low molecular weight heparin, heparinoids, direct oral anticoagulants, and thrombin inhibitors)
in people with acute presumed or confirmed ischaemic stroke. The review included 24 randomised
controlled trials involving a total of 23,748 participants.[140]
• At the end of follow-up, anticoagulants did not reduce the risk of death (OR 1.05, 95% CI 0.98 to
1.12; 11 trials; 22,776 participants), or death or dependency (OR 0.99, 95% CI 0.93 to 1.04; 8
trials; 22,125 participants).
• Anticoagulants significantly reduced the odds of deep vein thrombosis (OR 0.21, 95% CI 0.15 to
0.29; 10 trials; 916 participants), although most deep vein thromboses detected were subclinical
and asymptomatic.
• Anticoagulants also significantly reduced the odds of fatal or non-fatal symptomatic pulmonary
embolism (OR 0.60, 95% CI 0.44 to 0.81; 14 trials; 2,544 participants) and recurrent ischaemic
stroke (OR 0.76, 95% CI 0.65 to 0.88; 11 trials; 21,605 participants).
• However, anticoagulation significantly increased symptomatic (fatal or non-fatal) intracranial
haemorrhages (OR 2.55, 95% CI 1.95 to 3.33; 16 trials, 22,943 participants) and major
extracranial haemorrhage (defined as bleeding serious enough to cause death or require
hospitalisation or transfusion; OR 2.99, 95% CI 2.24 to 3.99; 18 trials; 22,255 participants).
• The authors of the review concluded that the data do not support the routine use of early
anticoagulants in acute ischaemic stroke.
The 2008 UK guideline on stroke from the National Institute for Health and Care
Excellence (NICE) made recommendations on the use of anticoagulation in patients with
stroke based on evidence from an earlier version of this Cochrane review (search date
2003). [63] [141]
• These recommendations are unchanged in the most recent version (2019 update) of this NICE
guideline.[63]
• The conclusions of the 2015 update of this Cochrane review have not changed despite the
addition of two trials compared with the 2004 publication.[140] [141]
Indications for anticoagulation in people with stroke include:[63]
• A cardiac source of embolism

• Cerebral venous thrombosis
• Some cases of arterial dissection.
MANAGEMENT
See Complex presentations, below, for more information on anticoagulation treatment in complex
presentations.
69
Practical tip
The patient receiving thrombolysis on presentation should not necessarily affect when you
start anticoagulation. If there has been significant haemorrhagic transformation of the infarction
some clinicians would delay starting anticoagulation beyond 2 weeks, but there are no clear
guidelines covering this area of practice. If there is a full recovery with thrombolysis (or mechanical
thrombectomy), anticoagulation could and should be considered significantly earlier.[63] [64]
In terms of venous thromboembolism (VTE) prophylaxis in patients with ischaemic stroke, there may be
some people for whom the risk of VTE outweighs the risk of haemorrhagic transformation. People at
particularly high risk of VTE include anyone with: [63]
• Complete paralysis of the leg

• A previous history of venous thromboembolism
• Dehydration
• Comorbidities (such as malignant disease)
• Current or recent smoker.
Regularly review the patient if they are given prophylactic anticoagulation.[63]
Practical tip
Haemorrhagic conversion is most common in larger infarcts and in those receiving anticoagulation
or alteplase. See Complications .
Complex presentations
Seek senior advice for the management of more complex presentations, such as:
• Acute venous stroke
• Full-dose anticoagulation treatment (initially full-dose heparin and then warfarin [INR 2 to 3])
is indicated in patients diagnosed with cerebral venous sinus thrombosis (including those
with secondary cerebral haemorrhage) unless there are comorbidities that preclude its
use.[63] [142]
• Stroke associated with arterial dissection
• Either anticoagulants or antiplatelet agents are indicated in patients who have a stroke
secondary to acute arterial dissection.[63]
• Stroke associated with antiphospholipid syndrome
• Manage in the same way as acute ischaemic stroke without antiphospholipid syndrome.
There is insufficient evidence to support any recommendations on safety and efficacy of
MANAGEMENT
anticoagulants versus antiplatelet agents in this sub-population.[63]
• Atrial fibrillation or atrial flut ter
• For people with paroxysmal, persistent, or permanent atrial fibrillation (valvular or non-
valvular) or atrial flutter, AND:
• Disabling ischaemic stroke: defer anticoagulation until at least at least 2 weeks from
onset of symptoms.[63] [64] Give daily aspirin for the first 2 weeks.[63]
• Non-disabling ischaemic stroke: defer anticoagulation for an interval at the discretion
of the prescriber, but no later than 2 weeks from the onset of symptoms.[64]
• Atrial fibrillation causes at least one fifth of ischaemic strokes and is one of the strongest
individual stroke risk factors.[78]
• See New-onset atrial fibrillation and Atrial flutter .
• Patients with prosthetic valves and at risk of haemorrhage
• Stop anticoagulation treatment for 1 week and substitute aspirin.[63]
• Symptomatic proximal deep vein thrombosis or pulmonary embolism
• Treat with anticoagulation in preference to aspirin unless there are other contraindications to
anticoagulation.[63]
Statins
Do not start statin treatment immediately. There is consensus that it is safe to start statins after
48 hours.[63]
Offer high-intensity statin therapy (unless contraindicated) to all patients.[64]
• Give moderate- or low-intensity statin therapy at the maximum tolerated dose if a high-intensity
statin is unsuitable or not tolerated.[64]
Continue statin treatment in people who are already receiving statins.[63]
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:[63] [64]
• 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.[63]
Start nutrition support for people who are at risk of malnutrition. Routine nutritional supplementation is
MANAGEMENT
not recommended for people who are adequately nourished on admission.[63]
71
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.[63]
Evidence: Optimal positioning
Evidence shows no difference in outcomes when the patient with acute ischaemic stroke is
positioned lying flat or with their head elevated. Therefore the optimum position should be
individually tailored to suit the patient. [143]
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 new systematic review for their
stroke guideline comparing positioning patients with acute ischaemic 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.[143]
• In the pilot HeadPoST study (94 people), 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 maintained in this position for at least
48 hours.[144]
• In the full HeadPoST study (11,093 people), 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.[145]
• 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 to 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 that the average stroke severity was lower and not representative of the range of stroke
severities managed within UK stroke centres.
MANAGEMENT
• They 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.[143]
Help the patient to sit out of bed, stand, or walkas soon as their clinical condition permits as part of
an active management programme in a specialist stroke unit.[63]
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.
[146]
• In 2019, the UK National Institute for Health and Care Excellence (NICE) found two studies
examining early (within 48 hours) mobilisation involving a total of 75 people.[146] [147] [148]
• 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.
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.[63]
• High-intensity mobilisation refers to the very early mobilisation intervention from the AVERT
trial.[149] 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
73
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 .[146]
• In 2019, the UK National Institute for Health and Care Excellence (NICE) performed a review for
their stroke guideline and found six studies examining very early (within 24 hours) mobilisation
involving a total of 2475 people.[146]
• The majority of data was from the AVERT III 2016 trial.[149] [150] [151] [152] [153] 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 Scale 0 to 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 mRS 0 to 2 at 90 days (5 studies; n=2377; high-quality
evidence assessed using GRADE) or 12 months (2 studies; n=2152; moderate quality
evidence assessed using GRADE)
• There was also no significant difference between groups for recurrent stroke (1 study;
n=71; low quality evidence assessed using GRADE), neurological deterioration (1 study;
n=138; GRADE very low quality), adverse events (2 studies; n=209; GRADE moderate
quality), length of hospital stay (1 study; n=124; GRADE low quality) or mortality at 90
days (6 studies; n=2475; GRADE moderate quality).
• 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 quality) and at 90 days (n=80; GRADE moderate quality), but the guideline
committee did not consider this clinically meaningful.[146]
• 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.[146]
• 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. They advise
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
Prevention of deep venous thrombosis and pulmonary embolism
in immobile patients
Give intermittent pneumatic compression within 3 days of admission for the prevention of deep vein
thrombosis and pulmonary embolism. Give continuous treatment for 30 days or until the patient is mobile
or discharged, whichever is sooner.[64]
Do not routinely give low molecular weight heparin or graduated compression stockings.[64] However
in practice, prophylactic low molecular weight heparin may be considered if intermittent pneumatic
compression is contraindicated or not possible.
Discharge
Offer information on stroke to patients and their family/carers.[64] See Patient leaflets .
Arrange follow-up in primary care on discharge.
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 ischaemic stroke
1st stabilisation and referral to hyperacute or

acute stroke unit
MANAGEMENT
75
Acute ( summary )
confirmed ischaemic stroke
presentation within 4.5 1st supportive care plus monitoring

hours AND thrombolysis
not contraindicated
plus alteplase
consider mechanical thrombectomy
plus antiplatelet agent
consider venous thromboembolism prophylaxis

plus early mobilisation
plus high-intensity statin
presentation after 4.5 1st supportive care plus monitoring

hours OR thrombolysis
contraindicated


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 ischaemic stroke
1st stabilisation and 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 for those presenting with
a depressed level of consciousness
(Glasgow Coma Scale score ≤8). This
should be done by an anaesthetist or
trained emergency department staff.[96]
• Give supplemental ox ygen only if
ox ygen saturation drops below 93%.
[97]
• Monitor controlled ox ygen

therapy. An upper SpO 2 limit
of 96% is reasonable when
administering supplemental
oxygen to most patients with acute
illness who are not at risk of
hypercapnia. Evidence suggests
that liberal use of supplemental
oxygen (target SpO 2 >96%) in
acutely ill adults is associated
with higher mortality than more
conservative oxygen therapy.[98] A
lower target SpO 2 of 88% to 92% is
appropriate if the patient is at risk of
• Do not routinely give ox ygen to
peoplewho are not hypoxic.[63]
Evidence: Target ox ygen saturation in

acutely ill adults
Too much supplemental oxygen increases

mortality.
MANAGEMENT
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.
77
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 2022 Thoracic
Society of Australia and New
Zealand (TSANZ) guideline
recommends 92% to 96%.[99]
[101]
• The 2022 Global Initiative For
Asthma (GINA) guidelines
recommend a target SpO
2 range of 93% to 96% in
the context of acute asthma
exacerbations.[102]
• A systematic review including a meta-

analysis of data from 25 randomised
controlled trials 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%).[98] In-hospital mortality was 11
per 1000 higher for the liberal oxygen
therapy group versus the conservative
therapy group (95% CI 2 to 22 per
1000 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 SpO₂ limit of 96% is therefore
MANAGEMENT
reasonable when administering

supplemental oxygen to 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
Initial
monoxide poisoning, cluster headache,
and sickle cell crisis).[97]
• In 2019 the BTS reviewed its guidance
in response to this systematic review
and meta-analysis and decided an
interim update was not required.[103]
• 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 earlier 2015 TSANZ
guideline recommendation.
• Subsequently, experience during the

COVID-19 pandemic has also made
clinicians more aware of the feasibility
of permissive hypoxaemia.[104]
• Management of oxygen therapy in
patients in intensive care is specialised
and informed by further evidence (not
covered in this summary) that is more
specific to this setting.[105] [106] [107]
» Admit everyone 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.[63]
[64]
• On admission, ensure the patient has

their swallowing function assessed
by appropriately trained staff before
being given any oral food, fluid, or
medication.[63] [64]
MANAGEMENT
• 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.[63]
79
Acute
confirmed ischaemic stroke
presentation within 4.5 1st supportive care plus monitoring

hours AND thrombolysis
Primary options
not contraindicated
» 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
Assess and monitor the patient’s level of
consciousness using the Glasgow Coma Scale.
• In patients with decreased level of

consciousness or coma, urgently exclude
haemorrhage and stroke mimics such as
seizures. See Differentials .
Practical tip
Haemorrhagic stroke is more often

associated with seizures, decreased level
of consciousness, and signs of increased
intracranial pressure than ischaemic
stroke.
Blood glucose
Monitor blood glucose regularly. Maintain a
blood glucose concentration between 4 and 11
mmol/L.[63]
Give insulin and glucose to all adults with type 1

diabetes with threatened or actual stroke. Follow
your local protocol.[63]
Blood pressure
Monitor blood pressure regularly and give
antihypertensive treatment only if there is a
hypertensive emergency with one or more of the
following serious concomitant conditions:[63]
MANAGEMENT
• Hypertensive cardiac failure/myocardial
infarction
Acute
The National Institute for Health and Care

Excellence (NICE) in the UK recommends to
consider reducing blood pressure to 185/110
mmHg or lower in people who are candidates for
intravenous thrombolysis.[63]
Ox ygen saturations
Monitor oxygen saturations and give
supplemental oxygen only if oxygen saturation
drops below 93%.[97]
• Monitor controlled ox ygen therapy.

An upper SpO 2 limit of 96% is
supplemental oxygen to most patients
with acute illness who are not at risk
of hypercapnia. Evidence suggests
that liberal use of supplemental oxygen
(target SpO 2 >96%) in acutely ill adults is
associated with higher mortality than more
conservative oxygen therapy.[98] A lower
target SpO 2 of 88% to 92% is appropriate
if the patient is at risk of hypercapnic
respiratory failure.[99]
• Do not routinely give oxygen to people
who are not hypoxic.[63]

acutely ill adults

mortality.



MANAGEMENT

81
Acute
[101]
exacerbations.[102]

MANAGEMENT

to a target.
Acute

Hydration
Assess the patient’s hydration within 4 hours
of their arrival at hospital.[63] Review regularly;
manage as needed to maintain normal
hydration.[63] [64]

In people who would be eligible for secondary
prevention treatment for atrial fibrillation:[64]
• Perform prolonged ECG monitoring (at

least 12 hours)
• Consider longer ECG monitoring (24
hours or more) in those in whom no
other cause of stroke has been found,
particularly if they have a pattern of
cerebral ischaemia on brain imaging
MANAGEMENT
Atrial fibrillation is an independent risk factor

for ischaemic stroke and indicates a poor
83
Acute
Monitor the patient for signs of elevated
intracranial pressure (ICP). For information on
other complications, see Complications .
Repeat the CT head immediately if you suspect

elevated ICP, which may present as:

• Severe headache
• Nausea/vomiting
Refer immediately to a neurosurgeon any

patients with large middle cerebral artery
territory infarcts and those with large infarctions
affecting the cerebellum. These types of stroke
have a very high mortality if urgent neurosurgical
intervention is delayed.[65]
• Patients with large middle cerebral artery

territory infarcts (at risk of malignant
middle cerebral artery syndrome) may
need decompressive hemicraniectomy
(neurosurgical removal of part of the skull
to reduce intracerebral pressure).[65]
• Patients with large infarctions affecting
the cerebellum may need ventriculostomy
(placement of an external ventricular
drain) or posterior fossa craniectomy.[65]
Practical tip
Patients with large infarctions affecting the

cerebellum or middle cerebral artery are
at risk of developing oedema and elevated
intracranial pressure. If left unchecked,
the oedema compromises blood flow
and causes brain herniation, which is
frequently fatal.
In line with recommendations from the National

Institute for Health and Care Excellence (NICE)
in the UK,decompressive hemicraniectomy
should be considered (performed within 48
hours of symptom onset) in any patient who
meets all of the following criteria:[63]
MANAGEMENT
• Clinical deficits that suggest infarction

in the territory of the middle cerebral
artery, with a score >15 on the National
Institutes of Health Stroke Scale (NIHSS)
Acute
• Decreased level of consciousness, with
a score of 1 or more on item 1a of the
NIHSS
• Signs on CT of an infarct of at least 50%
of the middle cerebral artery territory:
• With or without additional infarction

in the territory of the anterior or
posterior cerebral artery on the
same side
or
• With infarct volume greater than
3
145 cm , as shown on diffusion-
weighted MRI scan.
Evidence: Decompressive
hemicraniectomy
Decompressive hemicraniectomy reduces

mortality, with some evidence of improved
functional outcomes (although overall
functional outcomes are poor in this
population) and a variable impact on
quality of life (which is generally low with
or without surgery). There is no evidence
that there should be an age cut-off for
surgery, with the patient’s pre-stroke
functional status being a more useful
indicator of the potential outcomes of
surgery.
There has been much debate about the

net benefits of hemicraniectomy, especially
in patients aged over 60 years due to the
possibility of an increased risk of surviving
with a serious disability, compared with
people under 60 years.
The 2008 NICE guideline recommended

hemicraniectomy only in people aged under
60 years. This was updated in 2019 to
recommend that patients or their family
members or carers should be given specific
information on the risks and benefits in terms
MANAGEMENT
of functional outcomes and risk of mortality,

so that personal values and preferences,
especially regarding disability, are considered
in shared decision-making.[133] This updated
recommendation followed new evidence
85
Acute
focusing on patient age, in particular the 2014
• The review by NICE found 5

randomised controlled trials (RCTs) of
patients with an average age <60 years
(HeMMi, HeADDFIRST, HAMLET,
DESTINY and DECIMAL).[133]
• In these studies, decompressive

hemicraniectomy reduced
mortality at 30 days (1 study;
n=32; risk difference 416 fewer
per 1000 [95% CI 64 fewer to
501 fewer]; moderate-quality
evidence assessed using
GRADE), 6 months (3 studies;
371 fewer]; GRADE moderate)
and 1 year (3 studies; n=134;
risk difference 392 fewer per
1000 [95% CI 261 fewer to 469
fewer]; GRADE high).
• There was a clinically important
difference in functional
outcomes (score 0 to 3 on
modified Rankin Scale) at 6
months (risk difference 110
more per 1000 [95% CI 68 fewer
to 441 more]; GRADE very low)
or 1 year (risk difference 130
to 392 more]; GRADE low).
• There was no clinically important
difference for quality of life at 1
year as measured by the SF-36
mental summary score (1 study;
n=35; GRADE very low) or as
measured using visual analog
scales (1 study; n=32; GRADE
low), but a clinically important
harm of surgery for the SF-36
MANAGEMENT
physical summary scale (1

study; n=35; GRADE low).
Acute
Overall, quality of life scores
were low in both groups.
• NICE found 3 RCTs in patients with an

average age over 60 years (including
DESTINY II).[133]

mortality at 6 months (1 study;
1000 [95% CI 227 fewer to 462
fewer]; GRADE moderate).
• There was no difference in
functional outcomes between
groups at 6 months (2 studies;
n=141; risk difference 23 more
per 1000 [95% CI 7 fewer to 159
more]; GRADE very low) but a
significant benefit for surgery at
12 months (3 studies; n=165;
risk difference 100 more per
1000 [95% CI 10 more to 180
more]; GRADE very low).
• Quality of life was higher at
1 year after surgery (1 study;
n=100; GRADE low). Overall
quality of life scores were low in
both groups.
In all of the trials in people aged over

60 years, surgery had to be within 48
hours of symptom onset. Two of the
trials in those aged under 60 years
included people who had surgery
longer than 48 hours after symptom
onset (HeMMi 72 hours and HAMLET
96 hours). The NICE guideline group
MANAGEMENT
felt the beneficial results were largely

driven by studies which only allowed
surgery up to a maximum of 48 hours
87
Acute
after onset, hence the time limit for
surgery in their recommendation.
The NICE guideline committee notes

that there was a clear mortality
benefit of surgery at any age and
that the patient’s pre-morbid state is
more important than their age when
making a decision about the risks of
surgery. However, survivors have a
high likelihood of moderate or severe
disability with or without surgery.
Discuss the risks and benefits of the

procedurewith the patient or their family
members or carers. Take into account the
patient’s functional status before the stroke,
and their wishes and preferences.[63] A shared
decision-making process should include a
careful discussion with the patient or their
representatives about the risk of survival with
substantial disability.[134]
Seizures
Consult immediately with a neurologist or
neurosurgeon if the patient has uncontrolled
or recurrent seizures, or status epilepticus.
The choice of anticonvulsant will depend on
individual patient characteristics.[65] See Status
epilepticus .
• Follow your hospital protocol. In practice,

levetiracetam and sodium valproate are
commonly used.
Temperature
Monitor temperature and maintain normal body
physiology.[64] [100]
Give an antipyretic (e.g., paracetamol) in

patients with high temperature.
• Do not use therapeutic hypothermia

(i.e., active cooling) to reduce the risk of
MANAGEMENT
secondary brain damage.[63]
plus alteplase
Acute
Treatment recommended for ALL patients in
selected patient group
Primary options
» alteplase: 0.9 mg/kg intravenously

(maximum 90 mg/dose); give 10% of the total
dose by intravenous bolus initially, then give
the remainder of the dose by intravenous
infusion over 60 minutes
» The National Institute for Health and Care

Excellence (NICE) in the UK and the European
Stroke Organisation (ESO) recommend to give
intravenous alteplase (recombinant tissue
plasminogen activator) to eligible patients if
not contraindicated and:[63] [95] [110]
• Treatment is started as soon as

possible within 4.5 hours of onset of
stroke symptoms
AND
• Intracranial haemorrhage has been
excluded using appropriate imaging
techniques
» The ESO further recommends intravenous

thrombolysis for:[95]
• Patients who were last seen well 4.5 to 9

hours earlier (known onset time), with CT
or MRI core/perfusion mismatch, and for
whom mechanical thrombectomy is either
not indicated or not planned
• Patients with acute ischaemic stroke on
awakening from sleep, who were last seen
well more than 4.5 hours earlier, who have
MRI DWI-FLAIR mismatch (diffusion-
weighted MRI and fluid-attenuated
inversion recovery MRI mismatch), and for
whom mechanical thrombectomy is either
not indicated or not planned.
» Refer to the prescribing information

for contraindications to thrombolysis
with alteplase. Examples include recent major
surgery, bleeding disorders such as haemophilia,
MANAGEMENT
and current anticoagulation use.
» Do not delay treatment with alteplase

while waiting for results or waiting to perform
tests, unless you suspect contraindications that
must be ruled out first (eg., hypoglycaemia,
89
Acute
coagulopathy), or while monitoring for further
improvement.[66] [67]
» Exclude hypoglycaemia and

hyperglycaemia before giving
thrombolysis hypoglycaemia is a stroke
mimic and hyperglycaemia is associated
with intracerebral bleeding and worse clinical
outcomes.[63] [65]
» In the UK, alteplase should only be

administered within a well-organised stroke
service by staff trained in delivering thrombolysis
and in monitoring for complications.[63] [64]
Trained staff in emergency departments can also
administer alteplase provided that the patient
can be managed in an acute stroke service.[63]
» The Royal College of Physicians in the UK

recommends to consider for alteplase
treatment: [64]
• All patientsregardless of age or stroke

severity in whom treatment can be started
within 3 hours of known onset of
symptoms
• Patients aged <80 years in whom
treatment can be started between 3 and
4.5 hours of known onset.
• Patients aged >80 years in whom
treatment can be started between 3 and
4.5 hours of known onset on an individual
basis.
» Consider reducing blood pressure to 185/110

mmHg or lower in people who are candidates for
intravenous thrombolysis.[63] [111]
Treatment recommended for SOME patients in
» The decision to offer mechanical
thrombectomy (endovascular intervention)
should be made by clinicians experienced
in the use of thrombolysis for stroke and in
interpretation of relevant imaging.[63]

Excellence (NICE) in the UK specifically
recommends:
MANAGEMENT
• In patients with confirmed occlusion of

the proximal anterior circulation (by
CT angiography or MR angiography [CTA/
MRA]):[63]
Acute
• Offering mechanical
thrombectomy as soon as
possible and within 6 hours of
symptom onset together with
intravenous thrombolysis
• Considering thrombectomy as
soon as possible in patients
last known to be well between 6
to 24 hours previously (including
wake-up strokes) if there is
potential to salvage brain
tissue, as shown by perfusion
imaging.

the proximal posterior circulation (by
CTA or MRA):[63]
• Considering thrombectomy
together with intravenous
thrombolysis as soon as
possible for patients known
to be well up to 24 hours
previously (including wake-up
strokes) as shown by perfusion
imaging.
» The team will take into account the

patient’s clinical status and the extent of
established infarction on initial brain imaging
to inform decisions about thrombectomy. Select
people who have (in addition to the specific
factors stated above):[63]
• A pre-stroke functional status <3 on the

modified Rankin scale (mRS), and
• A score >5 on the National Institutes of
Health Stroke Scale (NIHSS).
» The role of thrombectomy alone without

intravenous thrombolysis (e.g., where there are
contraindications for thrombolysis) has not yet
been ascertained.
• One systematic review found that, even

in patients with mild strokes due to large
vessel occlusion (LVO) who were not
eligible for thrombolysis with intravenous
alteplase, mechanical thrombectomy
MANAGEMENT
resulted in better 90-day functional

outcomes, and suggested that this
treatment can play an important role
for patients not eligible for intravenous
alteplase.[120]
91
Acute
• Analysis from three randomised controlled
trials (RCTs; 1092 patients) detected
no differences in functional outcomes
of intravenous thrombolysis-eligible
patients with an acute LVO receiving direct
endovascular treatment compared with
endovascular treatment preceded by
intravenous thrombolysis.[121] However,
the authors note that because uncertainty
for most end points remains large and
the available data are not able to exclude
the possibility of overall benefit or harm,
further RCTs are needed.

Primary options
» aspirin: 300 mg orally/rectally once daily
Secondary options
» clopidogrel: 75 mg orally once daily
» Offer an antiplatelet agent as soon

as possible but certainly within 24
hours (unless contraindicated) to any patient
presenting with acute stroke who has had
intracerebral haemorrhage excluded by
imaging:[63]
• Aspirin orally (for those with no

dysphagia), or
• Aspirin rectally or by enteral tube (for
those with dysphagia).
» Offer an alternative antiplatelet agent to

anyone who is allergic to or genuinely intolerant
of aspirin.[63] In practice, clopidogrel is often
used.
» Antiplatelet treatment may be contraindicated

or delayed in patients with active bleeding (e.g.,
from the gastrointestinal tract).
» Offer a proton-pump inhibitor, in addition to

aspirin, to any patient who reports previous
dyspepsia associated with aspirin.[63]
MANAGEMENT
» In practice, administration of aspirin (or

alternative) is usually delayed 24 hours after
alteplase, once a further CT scan has excluded
significant bleeding.
Acute
» Continue aspirin daily until 2 weeks
after the onset of stroke symptoms, then start
definitive long-term antithrombotic treatment.
Start people on long-term treatment earlier if
they are being discharged before 2 weeks.[63]
» Give intermittent pneumatic compression
within 3 days of admission for the
prevention of deep vein thrombosis and
pulmonary embolism. Do not routinely give
low molecular weight heparin or graduated
compression stockings.[64] However in practice,
prophylactic low molecular weight heparin
may be considered if intermittent pneumatic
» 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.[63]
» 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.[63]
• High-intensity mobilisation refers to

the very early mobilisation intervention
from the AVERT trial.[149] 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.

Primary options
» atorvastatin: 20-80 mg orally once daily
» Do not start statin treatment immediately.

There is consensus that it is safe to start statins
MANAGEMENT
after 48 hours.[63]
» Offer high-intensity statin therapy (unless

contraindicated) to all patients.[64]
93
Acute
• Give moderate- or low-intensity statin
therapy at the maximum tolerated dose if
a high-intensity statin is unsuitable or not
tolerated.[64]
» Continue statin treatment in people who are

already receiving statins.[63]
presentation after 4.5 1st supportive care plus monitoring
hours OR thrombolysis
Primary options
contraindicated
» 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
Assess and monitor the patient’s level of
consciousness using the Glasgow Coma Scale.
• In patients with decreased level of

consciousness or coma, urgently exclude
haemorrhage and stroke mimics such as
seizures. See Differentials .
Practical tip
Haemorrhagic stroke is more often

associated with seizures, decreased level
of consciousness, and signs of increased
intracranial pressure than ischaemic
stroke.
Blood glucose
Monitor blood glucose regularly. Maintain a
blood glucose concentration between 4 and 11
mmol/L.[63]
Give insulin and glucose to all adults with type 1

diabetes with threatened or actual stroke. Follow
your local protocol.[63]
Blood pressure
Monitor blood pressure regularly and give
MANAGEMENT
antihypertensive treatment only if there is a

hypertensive emergency with one or more of the
following serious concomitant conditions:[63]
Acute
• Hypertensive cardiac failure/myocardial
infarction
The National Institute for Health and Care

Excellence (NICE) in the UK recommends to
consider reducing blood pressure to 185/110
mmHg or lower in people who are candidates
for intravenous thrombolysis.[63] [111] In
patients with acute ischaemic stroke not treated
with intravenous thrombolysis or mechanical
thrombectomy and blood pressure >220/120
mmHg, the European Stroke Organisation states
that careful blood pressure reduction (<15%
systolic blood pressure reduction in 24 hours) is
reasonable and likely to be safe.[111] In patients
on antihypertensive medication, resume oral
treatment once the patient is medically stable
and as soon as they can swallow medication
safely.[64]
Ox ygen saturations
Monitor oxygen saturations and give
supplemental oxygen only if oxygen saturation
drops below 93%.[97]
• Monitor controlled ox ygen therapy.

An upper SpO 2 limit of 96% is
supplemental oxygen to most patients
with acute illness who are not at risk
of hypercapnia. Evidence suggests
that liberal use of supplemental oxygen
(target SpO 2 >96%) in acutely ill adults is
associated with higher mortality than more
conservative oxygen therapy.[98] A lower
target SpO 2 of 88% to 92% is appropriate
if the patient is at risk of hypercapnic
respiratory failure.[99]
• Do not routinely give oxygen to people
who are not hypoxic.[63]

acutely ill adults
MANAGEMENT

mortality.

95
Acute


[101]
exacerbations.[102]

MANAGEMENT

Acute

to a target.

Hydration
Assess the patient’s hydration within 4 hours
of their arrival at hospital.[63] Review regularly;
manage as needed to maintain normal
MANAGEMENT
hydration.[63] [64]

In people who would be eligible for secondary
prevention treatment for atrial fibrillation:[64]
97
Acute
• Perform prolonged ECG monitoring (at
least 12 hours)
• Consider longer ECG monitoring (24
hours or more) in those in whom no
other cause of stroke has been found,
particularly if they have a pattern of
cerebral ischaemia on brain imaging
Atrial fibrillation is an independent risk factor

for ischaemic stroke and indicates a poor
Monitor the patient for signs of elevated
intracranial pressure (ICP). For information on
other complications, see Complications .
Repeat the CT head immediately if you suspect

elevated ICP, which may present as:

• Severe headache
• Nausea/vomiting
Refer immediately to a neurosurgeon any

patients withlarge middle cerebral artery territory
infarcts and those with large infarctions affecting
the cerebellum. These types of stroke have
a very high mortality if urgent neurosurgical
intervention is delayed.[65]
• Patients with large middle cerebral artery

territory infarcts (at risk of malignant
middle cerebral artery syndrome) may
need decompressive hemicraniectomy
(neurosurgical removal of part of the skull
to reduce intracerebral pressure).[65]
• Patients with large infarctions affecting
the cerebellum may need ventriculostomy
(placement of an external ventricular
drain) or posterior fossa craniectomy.[65]
MANAGEMENT
Acute
Practical tip
Patients with large infarctions affecting the

cerebellum or middle cerebral artery are
at risk of developing oedema and elevated
intracranial pressure. If left unchecked,
the oedema compromises blood flow
and causes brain herniation, which is
frequently fatal.
In line with recommendations from the National

Institute for Health and Care Excellence (NICE)
in the UK, decompressive hemicraniectomy
should be considered (performed within 48
hours of symptom onset) in any patient who
meets all of the following criteria:[63]
• Clinical deficits that suggest infarction

in the territory of the middle cerebral
artery, with a score >15 on the National
Institutes of Health Stroke Scale (NIHSS)
• Decreased level of consciousness, with
a score of 1 or more on item 1a of the
NIHSS
• Signs on CT of an infarct of at least 50%
of the middle cerebral artery territory:
• With or without additional infarction

in the territory of the anterior or
posterior cerebral artery on the
same side
or
• With infarct volume greater than
3
145 cm , as shown on diffusion-
weighted MRI scan.
Evidence: Decompressive
hemicraniectomy
Decompressive hemicraniectomy reduces

mortality, with some evidence of improved
functional outcomes (although overall
functional outcomes are poor in this
population) and a variable impact on
quality of life (which is generally low with
MANAGEMENT
or without surgery). There is no evidence

that there should be an age cut-off for
surgery, with the patient’s pre-stroke
functional status being a more useful
indicator of the potential outcomes of
surgery.
99
Acute
There has been much debate about the
net benefits of hemicraniectomy, especially
in patients aged over 60 years due to the
possibility of an increased risk of surviving
with a serious disability, compared with
people under 60 years.
The 2008 NICE guideline recommended

hemicraniectomy only in people aged under
60 years. This was updated in 2019 to
recommend that patients or their family
members or carers should be given specific
information on the risks and benefits in terms
of functional outcomes and risk of mortality,
so that personal values and preferences,
especially regarding disability, are considered
in shared decision-making.[133] This updated
recommendation followed new evidence
focusing on patient age, in particular the 2014
• The review by NICE found 5

randomised controlled trials (RCTs) of
patients with an average age <60 years
(HeMMi, HeADDFIRST, HAMLET,
DESTINY and DECIMAL).[133]

mortality at 30 days (1 study;
501 fewer]; moderate-quality
evidence assessed using
GRADE), 6 months (3 studies;
1000 [95% CI 261 fewer to 469
fewer]; GRADE high).
• There was a clinically important
difference in functional
outcomes (score 0 to 3 on
MANAGEMENT
modified Rankin Scale) at 6

months (risk difference 110
to 441 more]; GRADE very low)
or 1 year (risk difference 130
Acute
to 392 more]; GRADE low).
• There was no clinically important
difference for quality of life at 1
year as measured by the SF-36
mental summary score (1 study;
n=35; GRADE very low) or as
measured using visual analog
scales (1 study; n=32; GRADE
low), but a clinically important
harm of surgery for the SF-36
physical summary scale (1
study; n=35; GRADE low).
Overall, quality of life scores
were low in both groups.
• NICE found 3 RCTs in patients with an

average age over 60 years (including
DESTINY II).[133]

mortality at 6 months (1 study;
1000 [95% CI 227 fewer to 462
fewer]; GRADE moderate).
• There was no difference in
functional outcomes between
groups at 6 months (2 studies;
n=141; risk difference 23 more
per 1000 [95% CI 7 fewer to 159
more]; GRADE very low) but a
significant benefit for surgery at
12 months (3 studies; n=165;
risk difference 100 more per
1000 [95% CI 10 more to 180
more]; GRADE very low).
• Quality of life was higher at
MANAGEMENT
1 year after surgery (1 study;

n=100; GRADE low). Overall
101
Acute
quality of life scores were low in
both groups.
In all of the trials in people aged over

60 years, surgery had to be within 48
hours of symptom onset. Two of the
trials in those aged under 60 years
included people who had surgery
longer than 48 hours after symptom
onset (HeMMi 72 hours and HAMLET
96 hours). The NICE guideline group
felt the beneficial results were largely
driven by studies which only allowed
surgery up to a maximum of 48 hours
after onset, hence the time limit for
surgery in their recommendation.
The NICE guideline committee notes

that there was a clear mortality
benefit of surgery at any age and
that the patient’s pre-morbid state is
more important than their age when
making a decision about the risks of
surgery. However, survivors have a
high likelihood of moderate or severe
disability with or without surgery.
Discuss the risks and benefits of the

procedurewith the patient or their family
members or carers. Take into account the
patient’s functional status before the stroke,
and their wishes and preferences.[63] A shared
decision-making process should include a
careful discussion with the patient or their
representatives about the risk of survival with
substantial disability.[134]
Seizures
Consult immediately with a neurologist or
neurosurgeon if the patient has uncontrolled
or recurrent seizures, or status epilepticus.
The choice of anticonvulsant will depend on
individual patient characteristics.[65] See Status
MANAGEMENT
epilepticus .
Acute
• Follow your hospital protocol.
Levetiracetam and sodium valproate are
commonly used.
Temperature
Monitor temperature and maintain normal body
physiology.[64] [100]
Give an antipyretic (e.g., paracetamol) in

patients with high temperature.
• Do not use therapeutic hypothermia

(i.e., active cooling) to reduce the risk of
secondary brain damage.[63]

» Candidates for thrombectomy alone include
patients who cannot receive thrombolysis (e.g.,
with contraindications including recent major
surgery, bleeding disorders such as haemophilia,
current anticoagulation use).[64]
» The decision to offer mechanical

thrombectomy (endovascular intervention)
should be made by clinicians experienced
in the use of thrombolysis for stroke and in
interpretation of relevant imaging.[63]

Excellence (NICE) in the UK specifically
recommends:

the proximal anterior circulation (by
CT angiography or MR angiography [CTA/
MRA]):[63]
• Offering mechanical
thrombectomy as soon as
possible and within 6 hours of
symptom onset
• Considering thrombectomy as
soon as possible in patients
last known to be well between 6
MANAGEMENT
to 24 hours previously (including

wake-up strokes) if there is
potential to salvage brain
tissue, as shown by perfusion
imaging.
103
Acute
the proximal posterior circulation (by
CTA or MRA):[63]
• Considering thrombectomy
together with intravenous
thrombolysis as soon as
possible for patients known
to be well up to 24 hours
previously (including wake-up
strokes) as shown by perfusion
imaging.
» The team will take into account the

patient’s clinical status and the extent of
established infarction on initial brain imaging
to inform decisions about thrombectomy. Select
people who have (in addition to the specific
factors stated above):[63]
• A pre-stroke functional status <3 on the

modified Rankin scale (mRS), and
• A score >5 on the National Institutes of
Health Stroke Scale (NIHSS).
» The role of thrombectomy alone without

intravenous thrombolysis (e.g., where there are
contraindications for thrombolysis) has not yet
been ascertained.
• One systematic review found that, even

in patients with mild strokes due to large
vessel occlusion (LVO) who were not
eligible for thrombolysis with intravenous
alteplase, mechanical thrombectomy
resulted in better 90-day functional
outcomes, and suggested that this
treatment can play an important role
for patients not eligible for intravenous
alteplase.[120]
• Analysis from three randomised controlled
trials (RCTs; 1092 patients) detected
no differences in functional outcomes
of intravenous thrombolysis-eligible
patients with an acute LVO receiving direct
endovascular treatment compared with
endovascular treatment preceded by
intravenous thrombolysis.[121] However,
the authors note that because uncertainty
MANAGEMENT
for most end points remains large and

the available data are not able to exclude
the possibility of overall benefit or harm,
further RCTs are needed.
Acute
Primary options
» aspirin: 300 mg orally/rectally once daily
Secondary options
» clopidogrel: 75 mg orally once daily
» Offer an antiplatelet agent as soon

as possible but certainly within 24
hours(unless contraindicated) to any patient
presenting with acute stroke who has had
intracerebral haemorrhage excluded by
imaging:[63]
• Aspirin orally (for those with no

dysphagia), or
• Aspirin rectally or by enteral tube (for
those with dysphagia).
» Offer an alternative antiplatelet agent to

anyone who is allergic to or genuinely intolerant
of aspirin.[63] In practice, clopidogrel is often
used.
» Antiplatelet treatment may be contraindicated

or delayed in patients with active bleeding (e.g.,
from the gastrointestinal tract).
» Offer a proton-pump inhibitor, in addition to

aspirin, to any patient who reports previous
dyspepsia associated with aspirin.[63]
» Continue aspirin daily until 2 weeks

after the onset of stroke symptoms, then start
definitive long-term antithrombotic treatment.
Start people on long-term treatment earlier if
they are being discharged before 2 weeks.[63]
» Give intermittent pneumatic compression
within 3 days of admission for the
prevention of deep vein thrombosis and
pulmonary embolism. Do not routinely give
MANAGEMENT
low molecular weight heparin or graduated

compression stockings.[64] However in practice,
prophylactic low molecular weight heparin
may be considered if intermittent pneumatic
105
Acute
» 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.[63]
» 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.[63]
• High-intensity mobilisation refers to

the very early mobilisation intervention
from the AVERT trial.[149] 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.

Primary options
» atorvastatin: 20-80 mg orally once daily
» Do not start statin treatment immediately.

There is consensus that it is safe to start statins
after 48 hours.[63]
» Offer high-intensity statin therapy (unless

contraindicated) to all patients.[64] Give
moderate- or low-intensity statin therapy at the
maximum tolerated dose if a high intensity statin
is unsuitable or not tolerated.[64]
» Continue statin treatment in people who are

already receiving statins.[63]
MANAGEMENT
Emerging
Aspirin and clopidogrel
The European Stroke Organisation (ESO) recommends that aspirin and clopidogrel should be combined in
adults with a moderate- to high-risk transient ischaemic attack (TIA; ABCD2 score ≥4) or minor ischaemic
stroke (National Institutes of Health Stroke Scale [NIHSS] ≤3) within 24 hours of either the TIA or ischaemic
stroke event. The ESO recommends that dual therapy should be continued for 21 days followed by single
antiplatelet therapy.[253]
This advice is supported by a 2018 systematic review of three randomised, placebo-controlled trials
(n=10,447). Compared with aspirin alone, dual antiplatelet therapy (clopidogrel and aspirin) started within 24
hours of high-risk TIA or minor ischaemic stroke reduced subsequent stroke by about 20 in 1000 patients,
with a possible increase in moderate to severe bleeding of 2 per 1000 population. Discontinuation of dual
antiplatelet therapy within 21 days, and possibly as early as 10 days, of initiation was likely to maximise
benefit and minimise harm.[254]
Although dual antiplatelet therapy is approved in some countries for this indication, monotherapy with
aspirin or clopidogrel is recommended by the National Institute for Health and Care Excellence (NICE) in the
UK.[115]
Aspirin and ticagrelor

In March 2021, the ESO guidelines made a weak recommendation based on moderate-quality evidence
for 30-days of dual antiplatelet therapy with aspirin and ticagrelor in people with non-cardioembolic
mild to moderate ischaemic stroke or high-risk TIA in the past 24 hours.[253] The ESO stated that this
regimen should be considered as an alternative to aspirin plus clopidogrel, particularly in people known
to be intolerant of clopidogrel or in people who have moderate stroke (NIHSS 4 or 5) and no other
contraindication.[253] The ESO guidance is supported by the THALES randomised controlled trial of 11,016
patients with high-risk TIA or minor ischaemic stroke (none of whom received thrombolysis or thrombectomy
or required anticoagulation). THALES demonstrated that compared with aspirin alone, dual treatment with
ticagrelor and aspirin reduced the risk of disabling stroke or death within 30 days (4.0% vs. 4.7%).[255]
Severe bleeding was more frequent with ticagrelor plus aspirin than with aspirin alone (0.5% vs. 0.1%),
including intracranial haemorrhage (0.4% vs. 0.1%). The use of dual antiplatelet therapy with aspirin and
ticagrelor is also supported by the European Society of Cardiology.[256]
However, an application to the European Medicines Agency (EMA) to change the marketing authorisation
of ticagrelor to include the prevention of stroke in adults who have had a mild to moderate ischaemic stroke
or high-risk TIA was withdrawn in December 2021. Based on trial data and the company’s response to their
questions, the EMA expressed concern that the benefits of short-term treatment with ticagrelor plus aspirin in
preventing stroke in these patients did not clearly outweigh the risks of fatal and non-fatal bleeding. It is not
currently approved in the UK for preventing stroke after previous ischaemic stroke or high-risk TIA. However,
ticagrelor has been approved for this indication by the US Food and Drug Administration.
Primary prevention
The UK National Institute for Health and Care Excellence (NICE) recommends in its 2016 guideline to use
the QRISK2 assessment tool to assess cardiovascular disease (CVD) risk for the primary prevention of CVD
in people aged ≤84 years.[57]
• An evidence review by NICE in 2018 concluded that the updated QRISK3 version of the tool performs
MANAGEMENT
better than QRISK2 in identifying those at greatest risk of heart disease and stroke.[58]
Advise those at high risk of developing cardiovascular disease on lifestyle measures that reduce the risk of a
stroke, including recommendations to:[57]
107
• Exercise regularly
• Maintain a cardioprotective diet
• Manage weight
• Reduce alcohol consumption
• Stop smoking.
Manage underlying conditions that predispose a patient to stroke such as:[59]
• Hypertension
• Hypercholesterolaemia
• Type 1 and type 2 diabetes
• Transient ischaemic attacks.
Secondary prevention
Start secondary prevention measures for all patients as soon as possible after the diagnosis is
confirmed.[64] Secondary prevention is started in hospital and should be followed up in primary care.[64]
[265]
• Advise patients on lifestyle measures including recommendations to:[64]
• Exercise regularly[266]
• Maintain a healthy diet
• Manage weight
• Reduce alcohol consumption
• Stop smoking
• Reduce caffeine intake in people with hypertension.[63]
• Review medications used in secondary prevention. Some patients may have been started on these
drugs at diagnosis. See Subsequent acute management under Management recommendations .
• Antiplatelet therapy
• For long-term secondary prevention, the Royal College of Physicians in the UK

recommends clopidogrel in people without paroxysmal or permanent atrial fibrillation;
aspirin can be given to people who are allergic or cannot tolerate clopidogrel.[64] If a
patient has been started on aspirin during the acute stage, it should be switched to
clopidogrel after 2 weeks.
• High-intensity statin therapy
• Should be started if not contraindicated.[64]
• Antihypertensives
MANAGEMENT
• Give a thiazide-like diuretic, calcium-channel blocker, or ACE inhibitor to treat

hypertension.[64]
• Monitor blood pressure lowering treatment frequently and adjust treatment as tolerated to
achieve a target systolic blood pressure below 130 mmHg (or 140–150 mmHg in people
with severe bilateral carotid artery stenosis).[64]
• Anticoagulants
• Should be started in people with stroke and paroxysmal, persistent, or permanent atrial
fibrillation or atrial flutter once intracranial bleeding and other contraindications (such as
uncontrolled hypertension) are excluded.[64]
• Optimise management of other comorbidities and risk factors such as diabetes mellitus,
obstructive sleep apnoea, heart failure, contraception, menopause, and influenza.
Patient discussions
Offer information and advice on stroke to patients and their family/carers.[64] See Patient leaflets.
• Patient education and follow-up information should be provided initially in the hospital and offered
again and reinforced in primary care.[64]
MANAGEMENT
109
Ischaemic stroke Follow up
Monitoring
Monitoring
FOLLOW UP
Monitor the patient’s clinical status closely and provide supportive care as appropriate.[64] In particular,
monitor:
• Level of consciousness
• Blood glucose
• Blood pressure
• Oxygen saturations
• Hydration
• Temperature
• Cardiac rhythm and rate.
Monitor the patient for complications such as signs of raised intracranial pressure and seizures.
Assess and monitor the patient’s level of consciousness using the Glasgow Coma Scale.
• In patients with decreased level of consciousness/coma, urgently exclude haemorrhage and

stroke mimics such as seizures.
• Haemorrhagic stroke is more often associated with seizures, decreased level of consciousness,
and signs of increased intracranial pressure than ischaemic stroke.
Blood glucose
Monitor blood glucose regularly. Maintain a blood glucose concentration between 4 and 11 mmol/
L.[63]
• Give intravenous insulin and glucose to all adults with type 1 diabetes with threatened or actual
stroke. Follow your local protocol.[63]
Blood pressure
Monitor blood pressure regularly and give antihypertensive treatment only if there is
a hypertensive emergency with one or more of the following serious concomitant
conditions:[63]
The National Institute for Health and Care Excellence (NICE) in the UK recommends to consider reducing
blood pressure to 185/110 mmHg or lower in people who are candidates for intravenous thrombolysis.[63]
[111] In patients with acute ischaemic stroke not treated with intravenous thrombolysis or mechanical
thrombectomy and blood pressure >220/120 mmHg, the European Stroke Organisation states that careful
blood pressure reduction (<15% systolic blood pressure reduction in 24 hours) is reasonable and likely
to be safe.[111] In patients on antihypertensive medication, resume oral treatment once the patient is
medically stable and as soon as they can swallow medication safely.[64]
Ox ygen saturations
FOLLOW UP
Monitor oxygen saturations and give supplemental ox ygen only if ox ygen saturation drops
below 93%.[97]
• Monitor controlled ox ygen therapy. An upper SpO 2 limit of 96%is reasonable when
administering supplemental oxygen to most patients with acute illness who are not at risk of
hypercapnia. Evidence suggests that liberal use of supplemental oxygen (target SpO 2 >96%) in
acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[98] A
lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory
failure.[99]
Hydration
Assess the patient’s hydration within 4 hours of their arrival at hospital.[63] Review regularly; manage as
needed to maintain normal hydration.[63] [64]
Temperature
Monitor temperature and maintain normal body physiology.[64] [100]
• Give an antipyretic (e.g., paracetamol) in patients with high temperature.

• Do not use therapeutic hypothermia (i.e., active cooling) to reduce the risk of secondary brain
damage.[63]

• Perform prolonged ECG monitoring(at least 12 hours)

• Consider more prolonged ECG monitoring (24 hours or longer) in those in whom no other
cause of stroke has been found, particularly if they have a pattern of cerebral ischaemia on brain
imaging suggestive of cardioembolism.
Atrial fibrillation is an independent risk factor for ischaemic stroke and indicates a poor prognosis.[25] See
New-onset atrial fibrillation .
Monitor the patient for signs of elevated intracranial pressure (ICP). For information on other
complications, see Complications .
Repeat the CT head immediately if you suspect elevated ICP, which may present as:
• A reduced level of consciousness

• Headache
• Nausea/vomiting
Refer immediately to a neurosurgeonany patients with large middle cerebral artery territory
infarcts and those with large infarctions affecting the cerebellum. These types of stroke have a
very high mortality if urgent neurosurgical intervention is delayed.[65]
111
• Patients with large middle cerebral artery territory infarcts (at risk of malignant middle
cerebral artery syndrome) may need decompressive hemicraniectomy (neurosurgical removal
of part of the skull to reduce intracerebral pressure).[65]
• Patients with large infarctions affecting the cerebellum may need ventriculostomy
FOLLOW UP
(placement of an external ventricular drain) or posterior fossa craniectomy.[65]
Patients with large infarctions affecting the cerebellum or middle cerebral artery are at risk of developing
oedema and elevated intracranial pressure. If left unchecked, the oedema compromises blood flow and
causes brain herniation, which is frequently fatal.
Seizures
Consult immediately with a neurologist or neurosurgeon if the patient has uncontrolled or recurrent
seizures, or status epilepticus. The choice of anticonvulsant will depend on individual patient
characteristics.[65] See Status epilepticus .
Complications
Complications Timeframe Likelihood
FOLLOW UP
deep venous thrombosis short term medium
Motor weakness with lack of mobility causes venous stasis in the lower limbs, resulting in deep venous
thrombosis. Prophylactic anticoagulation will reduce the risk of pulmonary embolism.[261] [262]
Intermittent pneumatic compression of the legs is recommended to reduce the risk of DVT in non-
ambulatory stroke patients.[65] [262]
haemorrhagic transformation of ischaemic stroke short term low
Haemorrhagic conversion can occur in any ischaemic stroke, but is more common in larger infarcts
and those for which anticoagulation or alteplase (recombinant tissue plasminogen activator) has been
given.[65] Petechial bleeding may be relatively common and is frequently asymptomatic.[65]
alteplase-related orolingual oedema short term low
Orolingual oedema can rarely complicate the use of alteplase. In most cases, patients improve after
alteplase treatment has been stopped and antihistamines and corticosteroids have been given. Sometimes
orolingual oedema involves the upper airways extensively, leading to severe respiratory distress. Referral
to an anaesthetist is required in these cases.
depression variable high
Depression is common after stroke, and may warrant treatment with psychotherapy or antidepressant
medicines.[260]
fatigue variable high
At least half of all stroke survivors experience fatigue.[263]
Post-stroke fatigue affects quality of life and exerts a negative impact on a patient’s daily activities, such as
decreased participation in physical activities and rehabilitation.[263] There is insufficient evidence on the
efficacy of any intervention to treat or prevent fatigue after stroke.[264]
aspiration pneumonia variable low
Stroke-related dysphagia results in aspiration and subsequent pneumonia. On admission, ensure the
patient has their swallowing function assessed by appropriately trained staff before being given any oral
food, fluid, or medication.[63] [64]
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.[63]
When aspiration pneumonia occurs, the pneumonia should be treated with antibiotics and consideration
given to whether enteral feeding is indicated.[65]
113
Prognosis
FOLLOW UP
In 2019, there were 6.5 million deaths from stroke worldwide. Stroke is a leading cause of serious long-term
disability in the US and worldwide.[12] [257] Prognosis of functional outcome can be reliably performed by
well-validated prognostic scores like the ASTRAL score or the iScore.[258] Intravenous thrombolysis and
dedicated stroke units are the only interventions shown to improve stroke outcome.
Common medical complications of stroke include aspiration pneumonia, depression, and deep vein
thrombosis.
A meta-analysis study on the efficacy of physiotherapy following stroke found that a variety of interventions
improved functional outcomes, even when they were applied late after stroke.[259]
Patients receiving alteplase

Patients treated with alteplase (if given within 4.5 hours of onset of symptoms) have a better functional
outcome than patients not treated with alteplase. There is, however, an increased risk of intracerebral
haemorrhage with alteplase; this does not seem to affect death or dependency at 3 months.[60] [113] [116]
Ischaemic stroke 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: Intercollegiate Stroke Working Party; Royal College of Last published: 2016
Physicians (UK)
Europe
EACVI recommendations on cardiovascular imaging for the detection of
GUIDELINES
embolic sources: endorsed by the Canadian Society of Echocardiography
Published by: European Association of Cardiovascular Imaging Last published: 2021
Organization consensus statement and practical guidance for pre-hospital

management of stroke
Published by: European Academy of Neurology; European Stroke Last published: 2017
Association
North America
2019 update to the 2018 guidelines for the early management of acute
ischemic stroke: a guideline for healthcare professionals
Published by: American Heart Association; American Stroke Last published: 2019
Association
Summary of evidence-based guideline update: prevention of stroke in

nonvalvular atrial fibrillation
Published by: American Academy of Neurology Last published: 2014
(reaffirmed in 2022)
115
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: Intercollegiate Stroke Working Party; Royal College of Last published: 2016
Physicians (UK)
Europe
Guidelines on intravenous thrombolysis for acute ischaemic stroke

GUIDELINES
Published by: European Stroke Organisation Last published: 2021
Guidelines on blood pressure management in acute ischaemic stroke and

intracerebral haemorrhage
Guidelines on the management of space-occupying brain infarction

Guidelines on mechanical thrombectomy in acute ischaemic stroke

Published by: European Stroke Organisation; endorsed by Stroke Last published: 2019
Alliance for Europe
Guidelines on glycaemia management in acute stroke

Guidelines for prophylaxis for venous thromboembolism in immobile

patients with acute ischaemic stroke
Guidelines for the management of temperature in patients with acute

ischemic stroke
North America
Acute stroke management

Published by: Heart and Stroke Foundation, Canada Last published: 2022
Guidelines for the prevention of stroke in patients with stroke and transient
ischemic at tack
Association
Clinical practice guidelines for management of extracranial cerebrovascular

disease
Published by: Society for Vascular Surgery Last published: 2021
Guidelines for the early management of acute ischemic stroke

GUIDELINES
Association
Guidelines for adult stroke rehabilitation and recovery

Association
Stroke and transient ischemic at tack - acute and long-term management

Published by: British Columbia Government (Canada) Last published: 2015
Summary of evidence-based guideline update: prevention of stroke in

nonvalvular atrial fibrillation
Published by: American Academy of Neurology Last published: 2014
(reaffirmed in 2022)
Guidelines for the primary prevention of stroke

Published by: American Heart Association Last published: 2014
Antithrombotic and thrombolytic therapy for ischemic stroke: antithrombotic

therapy and prevention of thrombosis, 9th ed
Published by: American College of Chest Physicians Last published: 2012
Diagnosis and management of cerebral venous thrombosis

Published by: American Heart Association Last published: 2011
Africa
The South African guideline for the management of ischemic stroke and
transient ischemic at tack: recommendations for a resource-constrained
health care set ting
Published by: South African Stroke Society Last published: 2011
117
Oceania
Clinical guidelines for stroke management

Published by: National Stroke Foundation (Australia) Last published: 2022
GUIDELINES
Ischaemic stroke References
Key articles
• National Institute for Health and Care Excellence. Stroke and transient ischaemic attack in over 16s:
REFERENCES
diagnosis and initial management. Apr 2022 [internet publication]. Full text
• Royal College of Physicians. National clinical guideline for stroke. October 2016 [internet publication].
Full text
• National Institute for Health and Care Excellence. Mechanical clot retrieval for treating acute ischaemic
stroke. February 2016 [internet publication]. Full text
• National Institute for Health and Care Excellence. Alteplase for treating acute ischaemic stroke.
September 2012 [internet publication]. Full text
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131
Ischaemic stroke Images
Images
IMAGES
Figure 1: Non-contrast CT scan of brain showing sub-acute isolated left basal ganglion infarction with left
frontal horn mass effect
Ischaemic stroke Images
IMAGES
Figure 2: (A) Non-contrast T1-weighted MRI. (B) Post-contrast T1-weighted MRI showing minimal increase
in leptomeningeal vessels over the right frontal region. (C) Diffusion-weighted image (DWI) showing a
hyperintense area in the right frontal region. (D) Apparent diffusion coefficient (ADC) map shows hypointense
lesion, indicating restricted diffusion that correlates with high intensity on DWI and exponential diffusion. (E)
ADC value is 0.22 x 10³ mm²/second, corresponding to a hyperacute infarct
133
IMAGES Ischaemic stroke Images
Figure 3: MRI arterial spin labelling image showing extensive hypoperfusion in the right cerebral hemisphere.
There is a clear mismatch between diffusion and perfusion
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Consultant in Stroke Medicine
Addenbrooke’s Hospital, Associate Lecturer, School of Clinical Medicine, University of Cambridge,
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Acknowledgements,
BMJ Best Practice would like to gratefully acknowledge the previous expert contributor for this topic, whose
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Ischaemic stroke

Straight to the point of care

Last updated: Jan 24, 2023

stroke prevalence can be further sub-divided according to pathophysiological mechanism: extracranial

family history of stroke

history of ischaemic stroke or TIA

comorbid cardiac conditions

carotid artery stenosis

Degree of stenosis is related to the risk of recurrent stroke.[29]

sickle cell disease

lower levels of education

poor diet and nutrition

Light to moderate alcohol consumption may be protective against ischaemic stroke.[44]

obstructive sleep apnoea

illicit drug use

elevated C-reactive protein

aortic arch plaques

Pathophysiologically, ischaemic stroke can be broadly classified as:

• Haematological pathologies (e.g., prothrombotic hypercoagulable or hyperaggregable states) that

• Total anterior circulation stroke

Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria[3]

Large artery atherosclerosis

Small vessel occlusion

Stroke of other determined aetiology

Stroke of indeterminate aetiology

Causative classification of stroke modified TOAST criteria[4]

• Large artery atherosclerosis

Indeterminate causes are divided into:

• Unknown - embolic stroke of undetermined source

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

Exclude hypoglycaemia (a stroke mimic) as the cause of these symptoms.[63]

Use a validated tool to aid diagnosis in people with suspected stroke:[63]

Request an immediate non-contrast CT scan of the head to exclude intracerebral

• Indications for thrombolysis or thrombectomy

• Ischaemic stroke is a clinical diagnosisbased on signs and symptoms.

• Consider diffusion-weighted magnetic resonance imaging (MRI) of the head if the

Do not delay therapy with intravenous thrombolysis (if indicated)while:

Order in all patients:

• Serum glucose to exclude hypoglycaemia and hyperglycaemia before giving thrombolysis.[63]

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

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

Symptoms/signs according to the location of infarct

Anterior circulation stroke

Look for one or more of the following symptoms/signs:[73]

• Limb and/or facial weakness

• Expressive and/or receptive dysphasia

• Patients often describe sensory loss and paraesthesias as “numbness”.

• Vision loss in one eye or visual field deficit

Coma is unusual; it is more common in people with brain stem ischaemia.

Posterior circulation stroke

Look for one or more of the following symptoms/signs:[73]

to quadriplegia, sometimes changing from one side to another in different attacks.

• Vertigo, with or without nausea and vomiting

• Ipsilateral cranial nerves signs

• Altered level of consciousness and coma.