Acute Ischaemic Stroke

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Acute Ischaemic Stroke
Table of Contents
 Preface
 Introduction
 Immediate Tasks
 Recognition of a suspected stroke and transfer
 Assessment
 Treatment
 Clinical Diagnosis
 Clinical assessment
 Mechanism and localisation of stroke
 Diagnostic Procedures
 Cerebral computed tomography (CCT) and its interpretation
 Magnetic resonance imaging
 Electrocardiogram
 Ultrasound studies
 Laboratory tests
 General Critical Care and Stroke Treatment
 Reperfusion therapy
 Which stroke patients should be admitted to the ICU?
 Managing the critically ill patient with stroke
 Secondary prophylaxis
 Rehabilitation
 Conclusion
 
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+Preface?page_ref_id=2400
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+Introduction?page_ref_id=2372
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+Immediate+Tasks?page_ref_id=2373
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+IMMEDIATE+TASKS%3A+Recognition+of+a+suspected+stroke+and+transfer?page_ref_id=2374
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+IMMEDIATE+TASKS%3A++Assessment?page_ref_id=2375
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+IMMEDIATE+TASKS%3A+Treatment?page_ref_id=2376
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+Clinical+Diagnosis?page_ref_id=2377
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+CLINICAL+DIAGNOSIS%3A+Clinical+assessment?page_ref_id=2378
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+CLINICAL+DIAGNOSIS%3A+Mechanism+and+localisation+of+stroke?page_ref_id=2379
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+Diagnostic+Procedures?page_ref_id=2380
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+DIAGNOSTIC+PROCEDURES%3A+Cerebral+computed+tomography+%28CCT%29+and+its+interpretation?page_ref_id=2381
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+DIAGNOSTIC+PROCEDURES%3A+Magnetic+resonance+imaging?page_ref_id=2382
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+DIAGNOSTIC+PROCEDURES%3A+Electrocardiogram?page_ref_id=2383
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+DIAGNOSTIC+PROCEDURES%3A+Ultrasound+studies?page_ref_id=2384
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+DIAGNOSTIC+PROCEDURES%3A+Laboratory+tests?page_ref_id=2385
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+General+Critical+Care+and+Stroke+Treatment?page_ref_id=2386
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+GENERAL+CRITICAL+CARE+AND+STROKE+TREATMENT%3A+Reperfusion+therapy?page_ref_id=2387
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+GENERAL+CRITICAL+CARE+AND+STROKE+TREATMENT%3A+Which+stroke+patients+should+be+admitted+to+the+ICU%3F?page_ref_id=2388
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+GENERAL+CRITICAL+CARE+AND+STROKE+TREATMENT%3A+Managing+the+critically+ill+patient+with+stroke?page_ref_id=2389
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+GENERAL+CRITICAL+CARE+AND+STROKE+TREATMENT%3A+Secondary+prophylaxis?page_ref_id=2390
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+GENERAL+CRITICAL+CARE+AND+STROKE+TREATMENT%3A+Rehabilitation?page_ref_id=2391
https://collaboration.esicm.org/Acute+Ischaemic+Stroke%3A+Conclusion?page_ref_id=2392
Acute Ischaemic Stroke
 
Current Status 2020
Completed 
This module is updated and maintained by the (NIC) section
Latest Update
Third Edition
Neuro-Intensive Care
Chair
Fabio Silvio Taccone MD, Assistant Professor, Department of Intensive Care,
Erasme Hospital, Professor of Emergency Medicine, the Université Libre de
Bruxelles (ULB), Brussels, Belgium
Deputy
Chiara Robba MD, PhD, Anaesthesia and Intensive Care, IRCCS for Oncology,
Genova, Italy
Section Editor
Valentina Della Torre MD, MSc, Department of Critical Care, Imperial College
NHS Foundation Trust, London, UK
ELearning Committee
Chair
Kobus Preller Dr., Consultant, John Farman ICU, Cambridge University Hospitals
NHS Foundation Trust, Cambridge, UK
Deputy
Mo Al-Haddad MD, Consultant in Anaesthesia and Critical Care, Queen Elizabeth
University Hospital; Honorary Clinical Associate Professor University of Glasgow,
Glasgow UK
Project Manager
Estelle Pasquier , European Society of Intensive Care Medicine
Third Edition 2018
Module Authors
Arnaldo Alves da Silva MD, MSc, PhD, Department of Critical Care Medicine,
Hospital Israelita Albert Einstein, São Paulo, Brazil Research Assistant Brazilian
Cochrane Centre
Matthew A. Kirkman MBBS, MRCS, MEd, The National Hospital for Neurology
and Neurosurgery, London, United Kingdom
Module Reviewers
Marcellina Isabelle Haeberlin MD, Neurocritical Care Unit Department of
Neurosurgery University of Zurich Switzerland
Emanuela Keller MD, Neurocritical Care Unit Department of Neurosruregry,
University of Zurich, Switzerland
J. Claude Hemphill III MD,MAS,FNCS, Neurocritical Care, San Francisco
General Hospital Department of Neurology, University of California, San Francisco
Section Editor
Lara Prisco MD (IT), MSc (IT), Neurointensive Care Unit, John Radcliffe Hospital
and Nuffield Department of Clinical Neurosciences Oxford University Hospitals
NHS Foundation Trust and University of Oxford, Oxford, United Kingdom
CoBaTrICE Mapping Contributors
Cristina Santonocito MD, Dept. of Anesthesia and Intensive Care, IRCSS-
ISMETT-UPMC, Palermo, Italy
Victoria Anne Bennett MD, St George’s Hospital, London, United Kingdom
Co-Ordinating Editor
Stephanie C. Cattlin MBBS, Bsc, FRCA, FFICM, Consultant in Intensive Care,
Imperial College Healthcare NHS Trust, London, UK
Executive Editor
Mo Al-Haddad MD, Consultant in Anaesthesia and Critical Care, Queen Elizabeth
University Hospital; Honorary Clinical Associate Professor University of Glasgow,
Glasgow UK
Second Edition 2010
Module Authors
Julian Bosel , Dept of Neurological Intensive Care University Hospital Heidelberg
Heidelberg, Germany
Thorsten Steiner , Dept of Neurological Intensive Care University Hospital
Heidelberg Heidelberg, Germany
First Edition 2003
Module Authors
Markus Bertram , Dept of Neurological Intensive Care University Hospital
Heidelberg Heidelberg, Germany
Didier Payen , Dept of Anaesthesia & Intensive Care Lariboisière University
Hospital Paris, France
Module Reviewers
Emanuela Keller MD, Neurocritical Care Unit Department of Neurosruregry,
University of Zurich, Switzerland
Tarek Sharshar , Department of Intensive Care Medicine, Raymond Poincaré
Hospital, Garches, France
Janice Zimmerman Dr., Dept of Internal Medicine Division of Critical Care The
Methodist Hospital Houston, Texas, USA
Update Info 
 
Learning Objectives
After studying this module on Acute Ischaemic Stroke, you should be able to:
List the possible causes of stroke
Describe the difference between an ischaemic and a haemorrhagic stroke
Outline manage complications in a patient with stroke
Describe how to initiate appropriate treatment in a timely manner
 
eModule Information
Expiry date: 10/2020
COBATrICe competencies covered in this module:
Competencies
Adopts a structured and timely approach to the recognition, assessment and
stabilisation of the acutely ill patient with disordered physiology
Manages the care of the critically ill patient with specific acute medical conditions
Triages and prioritises patients appropriately, including timely admission to ICU
Recognises and manages the patient with neurological impairment
Faculty Disclosures: 
The authors of this module have not reported any disclosures.
Duration: 8 hours
Copyright©2017. European Society of Intensive Care Medicine. All rights reserved.
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1. Introduction
Acute ischaemic stroke (AIS) is a common cause of morbidity and mortality throughout
the world. Over 17 million strokes occur annually worldwide, with 6 million deaths as a
result. One in 6 people will have a stroke in their lifetime, and the vast majority of
survivors have persisting neurological deficits which impair the qualityof their life. 
 Important
Stroke is an emergency with a huge social and economic burden.
Over the years there have been significant research efforts in the search for effective
treatments for stroke. Although many putative neuroprotectants with promising pre-
clinical data have failed to translate into clinical benefit, we now have five aspects of
acute stroke therapy with class I evidence of improved outcomes. They are:
1. Stroke care in specialised units (Stroke units)
2. Platelet inhibitors such as acetylsalicylic acid within 48 hours 
3. Intravenous thrombolysis within 4.5 hours
4. Endovascular therapy within 6 hours
5. Decompressive craniectomy as soon as possible and ideally within 48 hours
(see reference below)
 
This chapter will help you better understand the complexity of treatment in AIS.
In text References
(Kirkman, Citerio and Smith. 2014; Go et al. 2013) 
 
 References
Kirkman MA, Citerio G, Smith M., The intensive care management of acute
ischemic stroke: an overview., 2014, PMID:24658914
Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Borden WB,
Bravata DM, Dai S, Ford ES, Fox CS, Franco S, Fullerton HJ, Gillespie C,
Hailpern SM, Heit JA, Howard VJ, Huffman MD, Kissela BM, Kittner SJ,
Lackland DT, Lichtman JH, Lisabeth LD, Magid D,, Heart disease and
stroke statistics--2013 update: a report from the American Heart
Association., 2013, PMID:23239837
1. 1. Immediate Tasks
https://www.ncbi.nlm.nih.gov/pubmed/24658914
https://www.ncbi.nlm.nih.gov/pubmed/23239837
The main goals of the acute management of AIS are:
Resuscitation and rapid recognition of the symptoms and signs of AIS
Timely commencement of treatment appropriate to the individual, including
thrombolysis or endovascular therapy
Early management of the key factors that can modulate outcomes, including
oxygenation, blood pressure, body temperature, and blood glucose levels
Prompt recognition of those patients who will need intensive care unit (ICU)
admission (see “Section 5.2 Which stroke patients should be admitted to the
ICU?”)
The first-line assessment and treatment are closely related and include the following
tasks:
Securing the airway and optimising oxygenation 
Haemodynamic stabilisation, intravenous access and fluid administration
Basic monitoring (including the rapid determination of blood glucose)
Obtaining a clinical history
Carrying out a physical examination
Treatment of symptoms such as agitation, vomiting, and pain
Recognition of contraindications to acute treatments, including thrombolysis and
endovascular therapy
Initiation of diagnostic procedures and interventions
 Note
The ABC of resuscitation clearly takes precedence and some procedures may
occur in parallel. For example, while taking the patient's history or undertaking
the physical examination, a nurse or other assistant may draw blood, initiate a
standard crystalloid infusion, and establish electrocardiogram (ECG) monitoring
and pulse oximetry.
1. 1. 1. Recognition of a suspected stroke and transfer
The most common early signs and symptoms of acute stroke start outside the hospital.
Prompt recognition of the signs and symptoms of stroke has become an important
public health issue, and the subject of several public awareness campaigns. The FAST
(Face, Arm, Speech, Time) tool is used by UK ambulance staff for this purpose, and in
the emergency room the ROSIER (Recognition of Stroke in the Emergency Room) test
can be utilised.
 Note
Stroke is a major public health issue.
Current consensus is that care should take place in specialised stroke units with
readily available access to thrombolysis, antiplatelet therapy, and neurointensive and
neurosurgical care facilities. A Cochrane systematic review involving 28 trials of 5,855
patients found stroke patients who receive organised inpatient care in stroke units are
more likely to be alive, independent, and living at home one year after the stroke.
Therefore, pre-hospital care networks have been developed that facilitate patient
transfer directly to hospitals with stroke units, so that delays in starting treatment are
minimised. A systematic review suggested that stroke units reduce mortality rates
through prevention of complications. In addition, the provision of acute rehabilitation is
also likely to influence outcome. Although care on an acute stroke unit is more costly
than care on a regular ward, it reduces post-acute inpatient care costs.
In text References
(Audebert et al. 2013; Weber, Ebinger and Audebert. 2015; Aoki et al. 2013; Stroke
Unit Trialists'. 2007; Govan, Langhorne and Weir CJ; Stroke Unit Trialists. 2007;
Epifanov et al. 2007; NHS 2018; UCLA Health 2016; Know 2011) 
 References
Audebert HJ, Saver JL, Starkman S, Lees KR, Endres M., Prehospital
stroke care: new prospects for treatment and clinical research., 2013,
PMID:23897876
Weber J, Ebinger M, Audebert HJ., Prehospital stroke care: telemedicine,
thrombolysis and neuroprotection., 2015, PMID:26109228
Aoki J, Kimura K, Koga M, Kario K, Nakagawara J, Furui E, Shiokawa Y,
Hasegawa Y, Okuda S, Yamagami H, Okada Y, Shibazaki K, Sakamoto Y,
Toyoda K., NIHSS-time score easily predicts outcomes in rt-PA patients: the
SAMURAI rt-PA registry., 2013, PMID:23433814
Stroke Unit Trialists' Collaboration., Organised inpatient (stroke unit) care
for stroke., 2007, PMID:17943737
Govan L, Langhorne P, Weir CJ; Stroke Unit Trialists Collaboration., Does
the prevention of complications explain the survival benefit of organized
inpatient (stroke unit) care?: further analysis of a systematic review., 2007,
PMID:17690313
Epifanov Y, Dodel R, Haacke C, Schaeg M, Schöffski O, Hennerici M, Back
T., Costs of acute stroke care on regular neurological wards: a comparison
with stroke unit setting., 2007, PMID:16930763
NHS, Stroke, 2018, https://www.nhs.uk/conditions/stroke/
UCLA Health System, Los Angeles Prehospital Stroke Screen (LAPSS),
2016, http://stroke.ucla.edu/workfiles/prehospital-screen.pdf
Know Stroke, NIH Stroke Scale, 2011, http://www.strokecenter.org/wp-
content/uploads/2011/07/NIH_Stroke_Scale_Booklet.pdf
https://www.ncbi.nlm.nih.gov/pubmed/23897876
https://www.ncbi.nlm.nih.gov/pubmed/26109228
https://www.ncbi.nlm.nih.gov/pubmed/23433814
https://www.ncbi.nlm.nih.gov/pubmed/17943737
https://www.ncbi.nlm.nih.gov/pubmed/17690313
https://www.ncbi.nlm.nih.gov/pubmed/16930763
https://www.nhs.uk/conditions/stroke/
http://stroke.ucla.edu/workfiles/prehospital-screen.pdf
http://www.strokecenter.org/wp-content/uploads/2011/07/NIH_Stroke_Scale_Booklet.pdf
1. 1. 2. Assessment
1. 1. 2. 1. Clinical history
Taking the clinical history is important to:
Decide whether it is a stroke
Determine whether the patient is within the time window for reperfusion therapy
Obtain clues to the mechanism of the stroke (course of symptoms, risk factors).
This may aid the following technical investigative procedures
Avoid potential complications of acute therapy
Concerning the therapeutic window, you should be aware that time is limited and that
history taking has to be focused.
It can be very difficult to accurately establish the time of stroke onset, for example if
the patient is unable to communicate what happened to them, or if they woke up with
new deficits having gone to sleep neurologically intact. In such instances, it is
important to take the last time that they were seen without the neurological deficit(s) as
the time of stroke onset and not the time they were found or woke up. This has
important implications, particularly regarding the eligibility for reperfusion therapy.
 Note
History taking and physical examination are crucial but should not delay specific
treatment
Consider the following items in history taking:
When did the first symptoms occur? Did the patient awake with symptoms/signs?
How have the symptoms evolved since onset? How rapidly have symptoms
developed?
Has the patient had a stroke before? Does she/he have any vascular risk factors?
What medication is the patient taking?
Does the patient suffer from diabetesor hypertension?
Are there any contraindications to thrombolytic treatment, endovascular therapy or
anticoagulation?
1. 1. 2. 2. Physical examination
The neurologic examination must be focussed and done with simultaneous
quantification of the NIHSS (National Institutes of Health Stroke Scale) in the
Emergency Room (ER). Neurological screening examination in this setting can follow
the NIHSS evaluation as follows:
Level of consciousness: orientation in time and place
Cranial nerves: pupils, visual fields, eye movements, facial weakness
Higher cortical dysfunction (aphasia, neglect)
Limb power: presence of drift/reaction to pain (in patients with reduced
consciousness)
Presence of limb ataxia
Sensory examination
Reflexes: including biceps, triceps, knee and ankle jerk, plantars (Babinski).
 Note
There are a range of videos freely available on the internet demonstrating how
to perform the NIHSS assessment as well as a physical examination in the
patient with suspected stroke. The learner is advised to use a search engine to
find these.
 Note
In patients with an impaired level of consciousness, neurological assessment
will be difficult. Nevertheless, examination of pupils, other brainstem reflexes,
and the reflex status along with observation of spontaneous activity and reaction
to painful stimuli (asymmetry?) may provide enough information for the
suspicion of stroke and the possible location of the injury.
A general physical exam is also important, and may suggest the underlying aetiology
of the stroke and any associated complications. It should include:
ABC assessment
Observation for early signs of dysphagia, preferably with a validated assessment
form
Cardiovascular examination for evaluation for concomitant heart disease, atrial
fibrillation, other arrhythmias, carotid bruits, and/or murmurs
Respiratory examination, including evaluation for the presence of pulmonary
oedema or (aspiration) pneumonia
 Note
 
It is not possible to distinguish ischaemic from haemorrhagic stroke by clinical
examination alone; for that reason, appropriate imaging is required.
1. 1. 2. 3. Emergency diagnostic tests
The following tests are recommended as emergency diagnostic tests in patients with
AIS 
All patients:
Cranial imaging (see note below)
Blood glucose (hypoglycaemia is a stroke mimic)
Oxygen saturation (the most important vital sign to monitor in a patient with
stroke)
Serum electrolytes/renal function tests*
Complete blood count, including platelet count*
Markers of cardiac ischemia*
Prothrombin time/INR*
Activated partial thromboplastin time*
ECG*
 Note
Noncontrast computed tomography (CT) is the most widely used first-line
imaging tool in patients with suspected acute stroke, largely because it is easy
to acquire, widely available and is able to reliably differentiate between
ischaemia and haemorrhage. Other useful imaging tests include CT with
contrast, CT angiography (CTA), CT perfusion (CTP), magnetic resonance
imaging (MRI), magnetic resonance angiography (MRA) and magnetic
resonance perfusion imaging. Time is brain, and it is crucial that the specific
imaging strategy chosen does not significantly delay stroke workflow. For this
reason, CT-based imaging is generally preferred over MRI/MRA. The imaging
chosen will vary by centre, but it is common to perform a noncontrast CT to rule
out haemorrhage, followed by CTA to evaluate for target vessel occlusion and
facilitate planning of endovascular treatment. Multiphase CTA (mCTA) can be
useful to evaluate for collateral supply, which may influence decision-making
about endovascular therapy (it has been shown in multiple studies that patients
with good collaterals on CTA are likely to fare better with endovascular therapy
compared to intravenous thrombolysis). Contrast CT is recommended to
exclude, for example, intracranial tumour as a cause for the patient’s clinical
status - a contraindication to thrombolysis. CTP may identify the ischaemic core
of a stroke more sensitively than noncontrast CT, provides information about the
area of at-risk tissue (penumbra), and can facilitate the evaluation of collateral
supply. The acquisition and processing time for CTP is in the order of several
minutes in experienced centres and thus it should not delay the administration of
thrombolysis where indicated.
Selected patients:
Thrombin time and/or ecarin clotting time if it is suspected the patient is taking
direct thrombin inhibitors or direct factor Xa inhibitors
Liver function tests
Toxicology screen
Blood alcohol level
Pregnancy test
Arterial blood gas analysis (if hypoxia is suspected)
Chest radiography (if lung disease is suspected)
Lumbar puncture (if subarachnoid haemorrhage is suspected and CT scan is
negative for blood
Electroencephalogram (if seizures are suspected)
Duplex sonography of the intracranial vessels
Echocardiography
Of note, although it is desirable to know the results of the tests marked with an asterisk
(*) prior to commencing thrombolysis, the American Stroke Association guidelines
emphasise that thrombolysis should not be delayed while awaiting the results of these
tests unless:
1. There is clinical suspicion of thrombocytopaenia
2. The patient has received heparin or warfarin, or
3. The patient has received other anticoagulants (direct thrombin inhibitors or
direct factor Xa inhibitors)
 Note
Due to the time pressures, diagnostic procedures have to be initiated as
soon as possible. Clinical assessment may need to be interrupted in order to
carry out an essential cranial CT. Emergency laboratory tests and monitoring
can be performed in parallel (see above)
In text References
(Jauch et al. 2013; Menon et al. 2015) 
 References
Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk
BM, Khatri P, McMullan PW Jr, Qureshi AI, Rosenfield K, Scott PA,
Summers DR, Wang DZ, Wintermark M, Yonas H, American Heart
Association Stroke Council, Council on Cardiovascular Nursing, ,
Guidelines for the early management of patients with acute ischemic stroke:
a guideline for healthcare professionals from the American Heart
Association/American Stroke Association., 2013, PMID:23370205
Menon BK, Campbell BC, Levi C, Goyal M, Role of imaging in current acute
ischemic stroke workflow for endovascular therapy., 2015, PMID:25944319
1. 1. 3. Treatment
A consensus panel convened by the National Institutes of Neurological Disorders and
Stroke (NINDS) established time targets for the evaluation of stroke patients in the
Emergency Department. They are:
Door to physician ≤ 10 min
Door to stroke team ≤ 15 min
Door to CT initiation ≤ 25 min
Door to CT interpretation ≤ 45 min
Door to drug (≥80% compliance) ≤ 60 min
Door to stroke unit admission ≤ 3 hours
The management principles for AIS are highlighted in the following table.
Table 1:Immediate management of acute ischaemic stroke
https://www.ncbi.nlm.nih.gov/pubmed/23370205
https://www.ncbi.nlm.nih.gov/pubmed/25944319
Intervention Recommendations
Airway,
oxygenation and
ventilation
Continuous pulse oximetry 
If intubated: regular ABG to maintain PaO2
levels >80 mm Hg (10.6 KPa) 
In self-ventilating patients: SpO2 > 92%
during endovascular procedures and >94%
on ICU 
Blood pressure
Regular BP monitoring (at least every 3 min
during endovascular treatment) and
prevention of extremes of BP 
Invasive BP monitoring in those with unstable
BP and/or necessitating active hemodynamic
management and/or MV 
Acute BP lowering is currently only
recommended before commencing
thrombolysis (< 185/110 mm Hg for 24 h after
thrombolysis) or in the presence of extreme
hypertension (>220/120 mmHg) in those
without severe comorbidities (e.g. severe
cardiac failure, aortic dissection, hypertensive
encephalopathy) not undergoing thrombolysis
– IV labetalol, urapidil, clevedipine or
nicardipine can be used. 
First-line treatment of hypotension is fluid
resuscitation, followed by norepinephrine
and/or metaraminol
Blood glucose
monitoring
Regular (at least hourly) glucose monitoring 
Continuousinsulin infusion to prevent
hyperglycaemia
Target during endovascular therapy: 70-
140 mg/dL(4-8 mmol/l)
Target in the ICU: 140-180 mg/dL (8-10
mmol/l)
Temperature
management
Exclusion or treatment of underlying infection 
No clear evidence to direct specific
temperature targets, but recommendations
are: 
Target during endovascular therapy: 35-
37°C
Target in the ICU: prevent temperatures
>37.5°C
 
Abbreviations: ABG, arterial blood gas; BP, blood pressure; MV, mechanical
ventilation.
Cerebral perfusion and the penumbra 
Adequate cerebral perfusion is crucial in preserving the penumbra, where cerebral
autoregulation is impaired, and the cerebral blood flow (CBF) is passively dependent
on mean arterial pressure (MAP); post-stenotic flow requires stable circulatory
conditions.
The control of blood pressure is a major issue. If the pressure is too high, this may
exacerbate reperfusion injury to the penumbra and lead to increased oedema, cellular
hypoxia or haemorrhagic transformation. If the pressure is too low, CBF in the
penumbra can decrease to a level causing irreversible neuronal damage. Additionally,
this can cause vessels in intact brain regions to dilate, which can then lead to a
potential ‘steal-effect', further promoting ischaemia in the penumbra. Most
haemorrhagic strokes occur in hypertensive patients, whose CBF autoregulation is
impaired and whose blood pressure should therefore not be lowered too aggressively.
Blood pressure lowering should always be cautious, i.e. <15% in the first 24 hours in
those not receiving thrombolysis (more aggressive blood pressure lowering is
permitted prior to thrombolysis).
 Note
There are some conditions where these rules for blood pressure management
are not applicable e.g. known or suspected aortic dissection, hypertensive
encephalopathy, subarachnoid or intracerebral bleeding, severe heart failure,
acute myocardial infarction or unstable angina. In these situations, a
compromise is required.
 Notes
Local guidelines often preclude arterial puncture/cannulation before, during
and up to 24 hours after thrombolysis, and similar caution is required for
other invasive investigations outlined below.
In selected cases, transthoracic (TTE) or transesophageal (TEE)
echocardiography;
In selected cases, insertion of a central venous catheter to measure
central venous pressures or to administer vasoactive drugs;
When indicated (e.g. cardiac or septic shock), insertion of catheters
for cardiac output monitoring (pulmonary artery or femoral artery
thermodilution catheters).
In text References
(European Stroke Organisation (ESO) Executive Committee; ESO Writing. 2008;
Jauch et al. 2013; Kirkman, Citerio and Smith. 2014; Kirkman, Lambden and Smith.
2016) 
 References
Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk
BM, Khatri P, McMullan PW Jr, Qureshi AI, Rosenfield K, Scott PA,
Summers DR, Wang DZ, Wintermark M, Yonas H, American Heart
Association Stroke Council, Council on Cardiovascular Nursing, ,
Guidelines for the early management of patients with acute ischemic stroke:
a guideline for healthcare professionals from the American Heart
Association/American Stroke Association., 2013, PMID:23370205
Kirkman MA, Citerio G, Smith M., The intensive care management of acute
ischemic stroke: an overview., 2014, PMID:24658914
European Stroke Organisation (ESO) Executive Committee; ESO Writing
Committee., Guidelines for management of ischaemic stroke and transient
ischaemic attack 2008., 2008, PMID:18477843
Kirkman MA, Lambden S, Smith M., Challenges in the Anesthetic and
Intensive Care Management of Acute Ischemic Stroke., 2016,
PMID:26368664
https://www.ncbi.nlm.nih.gov/pubmed/23370205
https://www.ncbi.nlm.nih.gov/pubmed/24658914
https://www.ncbi.nlm.nih.gov/pubmed/18477843
https://www.ncbi.nlm.nih.gov/pubmed/26368664
2. Clinical Diagnosis
The history allows identification of the possible cause of stroke, especially if technical
diagnostic tests are not immediately available. It is also essential for the assessment
of the reperfusion time window.
 Note
This section of the module is largely beyond the scope of what the average
intensive care physician would need to know for the care of a stroke patient.
However, it is included as an advanced resource for your perusal.
2. 1. Clinical assessment
Clinical examination is important in localising the stroke, determining the extent of the
lesion, evaluating prognosis, and assessing overall stability of the patient.
Assessments influence:
The therapeutic options in the acute phase (e.g. no intravenous thrombolysis in
extending infarction within the 3-4.5 hour window)
Hospital management (e.g. decision about transfer to the ICU)
Ideally, all stroke patients should be treated on a stroke unit
Indications for admission to the ICU are shown in Section 5.2.

Why perform such a thorough clinical assessment when a cranial
CT is available?
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 Cranial CT in the early phase of ischaemic stroke, and therefore
within the therapeutic window can often be negative. Imaging studies
have to always be interpreted within the overall clinical context to guide
treatment decisions.
Clinical symptoms and signs vary with the brain territory involved (Figure 1).
Figure 1: Localisation of stroke deficits can be
facilitated by a good working knowledge of
neuroanatomy. This figure lists some of the
commoner features by anatomical location of the
stroke. A more detailed list of potential clinical
signs or symptoms by vascular territory is
provided in section Large artery thrombosis or
embolism below.
 Note
 
 When you are confronted with a patient presenting with one, or a
combination of these symptoms, consider: Is it really a stroke?
These symptoms can also be caused by other pathologies, such as inflammatory
processes, tumours, some metabolic disorders and intoxications. These possibilities
will, in part, need other acute diagnostic and therapeutic investigations. A thorough
history to enquire about previous symptoms is therefore important.
 Note
Stroke is a medical emergency demanding rapid, appropriate treatment, and
has to be confirmed or ruled out immediately.
2. 1. 1. Differential diagnosis
Stroke is a sudden or rapidly developing neurological deficit. The differential diagnostic
considerations below can be of help. 
It is important to differentiate between stroke and stroke mimics, which comprise up to
one-third of stroke-like presentations, to ensure appropriate and safe management.
This relies on thorough history-taking, clinical examination and the use of appropriate
imaging.
The principal condition to identify in the differential diagnosis of AIS is intracerebral
haemorrhage (ICH).
Clinical findings favouring the diagnosis of ICH include: 
Onset during a hypertensive crisis
Progression of symptoms within minutes
Early, excessive vomiting
Early/immediate loss of consciousness
Acute onset of headache
https://collaboration.esicm.org/dl869?display
In text References
(Chong TT and Fedi. 2013; Waldmann. 2008) 
The diagnosis cannot, however, be confirmed by history and clinical examination
alone. Neuroimaging (CT/MRI) is urgently required.
Other differential diagnoses of ischaemic stroke are shown in the below table.
Table 2: Stroke mimics
Condition Comments
Hypoglycaemia
Can produce hemiplegia and aphasia as well as
the more common symptoms of confusion and
reduced level of consciousness
Intracranial space occupying
lesions
Tumours, cerebral abscess, and intracranial
bleeding such as a subdural hematoma may
produce a stroke-like presentation. More acute
presentations in the setting of tumours may be
due to intratumoural haemorrhage, seizures or
the development of obstructive hydrocephalus
Seizures and the postictal state
Todd’s paresis usually follows partial motor
seizures, but can result from generalised
seizures too. Can also be a complication of a
stroke
Migraine
Can mimic a stroke in the presence of a
hemiplegic migraine,or can itself precipitate a
stroke
Encephalopathies and
metabolic disorders
Hyperglycaemia can result in focal neurological
deficits and seizures. Hypertensive
encephalopathy may present with headaches
and cortical blindness. Hyponatremia and hepatic
encephalopathy may also cause stroke-like
presentations
Sepsis
Relies on a thorough systemic examination for
diagnosis and identification of a focus of
infection. Sepsis can be a risk factor for stroke
itself, for example mycotic emboli, and when co-
existing, differentiating the two is difficult
Drug toxicity
Examples include lithium, carbamazepine and
phenytoin
Functional disorders
Often presents with acute weakness or sensory
disturbance that is triggered, for example by a
panic attack. An inconsistent clinical examination
is key to diagnosis
 
In text References
(Fernandes et al. 2013) 
 
 References
Waldmann CS. , Oxford Desk Reference: Critical Care, 2008,
ISBN:9780199229581
Chong TT-J, Fedi M. , Acute management of stroke – II: haemorrhagic
stroke., 2013, https://www.anaesthesiajournal.co.uk/article/S1472-
0299(13)00197-5/fulltext
Fernandes PM, Whiteley WN, Hart SR, Al-Shahi Salman R., Strokes:
mimics and chameleons., 2013, PMID:23315456
2. 2. Mechanism and localisation of stroke
Before reading the next section you may wish to refresh your memory of the normal
anatomy of the brain and the deficits likely to follow occlusion of individual cerebral
vessels. The classification of stroke subtypes helps physicians differentiate between
small vessel disease and other aetiologies.
 Note
The mechanism of stroke can often be determined by history taking and clinical
examination.
In text References 
(Caplan. 2009; Adams HP and Biller 2015) 
The following mechanisms and types of stroke do not always lead to conditions that
require to be treated by the intensivist; however, secondary deterioration in the acute
case is always possible.
2. 2. 1. Microangiopathic or lacunar stroke
The mode of onset and clinical course of lacunar infarcts often differ from those
originating elsewhere:
https://www.anaesthesiajournal.co.uk/article/S1472-0299(13)00197-5/fulltext
https://www.ncbi.nlm.nih.gov/pubmed/23315456
Preceding transient ischaemic attacks (TIAs) (15-20%) occur shortly (several
days) before onset of infarction, tend to occur in clusters and are more
stereotypical compared with large vessel TIAs
Insidious onset and a gradually progressive, 'stuttering' course
Lacunar lesions are small and may become symptomatic in regions with a high
density of axons and with multiple extensions, e.g. the cerebral peduncles and the
brainstem. They may present as:
Pure motor stroke
Pure sensory stroke
Sensory-motor stroke
Ataxic hemiparesis
Dysarthria-clumsy-hand syndrome
2. 2. 2. Systemic embolism
A history of cardiac disease may be mentioned by the patient, relatives or referring
doctor. This may involve: mechanical or cardiac valve dysfunction, atrial fibrillation, left
atrial and/or ventricular thrombus, dilated cardiomyopathy, recent myocardial infarction
(<4 weeks), left ventricular aneurysm, sick sinus syndrome, infective myocarditis, or
atrial myxoma.
Characteristic features in the history include:
Sudden onset, with maximal severity at onset
Onset usually during activity, in awake state; presentation on awakening is
unusual
Recurrent TIAs in different anatomical areas
The typical clinical presentation of various arterial territories is shown in section 3.2.3
“Large artery thrombosis or embolism” below.
2. 2. 3. Large artery thrombosis or embolism
Large vessel disease may cause stroke by post-stenotic perfusion deficit, sudden
atherothrombotic occlusion, or arterio-arterial embolism. The clinical picture may not
differ significantly from that in systemic embolism. However, the clinical history may
reveal:
Typical atherogenic risk factors
Frequent TIAs, e.g. amaurosis fugax (internal carotid artery stenosis), in the same
arterial territory
Onset often during sleep or atherothrombotic stroke during activity, a gradual
progression or stepwise course over minutes to hours is characteristic
(attributable to gradual accumulation of thrombus or to lowering of blood pressure,
e.g. following antihypertensive therapy).
Acute occlusion of the basilar artery comprises around 1% of all strokes but is a
medical emergency. It can result in thalamic or brainstem infarction, and typically
presents with a sudden and severe neurological impairment dependent on the position
of the occlusion within the basilar artery. Proximal occlusions can result in
quadriparesis with preserved consciousness, whereas distal occlusions can be
associated with visual and oculomotor deficits, behavioural disturbance, somnolence
and/or hallucinations. Sudden death or loss of consciousness is also possible. Rapid
treatment is essential to minimise the risk of death, and therefore patients with acute
basilar occlusion require urgent transfer to a comprehensive neurosciences centre
with interventional neuroradiology facilities for endovascular intervention.
The typical clinical presentations of different arterial territories that may be affected by
systemic embolism, large artery thrombosis or embolism are as follows:
Infarcts of the middle cerebral artery (MCA) territory
Contralateral motor weakness and/or sensory deficit (face and arm more than leg)
Aphasia: language disturbances (dominant hemisphere damage) – Broca,
Wernicke, or global
Apraxia
Dysarthria
Conjugated ipsilateral eye deviation in large infarcts
Homonymous visual field defects, alone or in combination with above
Impaired spatial perception or neglect (non-dominant hemisphere damage)
Infarcts of the anterior cerebral artery territory
Contralateral hemiparesis and/or sensory deficit (more pronounced in the lower
limbs)
Urinary incontinence
Apraxia
Anosmia
Bilateral: apathy, motor inertia and muteness
Posterior (vertebral, basilar and posterior cerebral artery) circulation infarcts (usually
embolic)
Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
Bilateral motor and/or sensory deficit
Disorder of conjugate eye movement (vertical=midbrain, horizontal=pons)
Cerebellar dysfunction without ipsilateral long-tract deficit
Altered consciousness
Dysarthrophonia, dysphagia
Horner syndrome (also in carotid artery dissection)
https://collaboration.esicm.org/s
Contralateral homonymous hemianopsia
Bilateral lesions: cortical blindness (Anton's syndrome)
Behavioural disturbance
2. 2. 4. Dissection of cervical arteries
Apart from cardiac embolism, consider dissection of cervical arteries. The (typically
younger) patient's history may reveal risk factors such as:
Recent trauma
Previous infection
Signs of connective tissue abnormalities (hyperextensible joints, Marfan
syndrome, Ehlers-Danlos syndrome, known mitral valve prolapse).
The characteristic clinical presentation is a focal neurological syndrome in combination
with unilateral headache or neck pain, pulsatile tinnitus, and an ipsilateral Horner
syndrome in the case of internal carotid artery dissection.
 Note
Stroke also occurs in young persons, including children.
There are many other mechanisms of stroke and stroke-like episodes. You can find
further information in the following references.
In text References 
(Caplan 2008; Caplan. 2009; Paciaroni et al. 2012) 
 References
Caplan LR. , Caplan’s Stroke: A Clinical Approach. 4th ed. , 2009, ISBN:
9781416047216
Adams HP Jr, Biller J, Classification of subtypes of ischemic stroke: history
of the trial of org 10172 in acute stroke treatment classification., 2015,
PMID:25813192
Caplan LR, Uncommon Causes of Stroke. 2nd ed., 2008,
ISBN:9780521874373
Paciaroni M, Agnelli G, Caso V, Bogousslavsky J., Manifestations of
Stroke., 2012, ISBN:9783805599108
https://www.ncbi.nlm.nih.gov/pubmed/25813192
3. Diagnostic Procedures
Technical diagnostic tests are performed for the following purposes:
The main 'switch point' in the direction of your acute treatment and secondary
prophylaxisis the early differentiation of ischaemic stroke from intracerebral
haemorrhage or subarachnoid haemorrhage (SAH). This is crucial for the early
management of stroke.
Based on the physical and neurological evaluation and skilled use and
interpretation of emergency diagnostic tests, different causes of ischaemic stroke
can be identified. These may indicate the need for specific therapeutic procedures
and influence the choice of a secondary prophylaxis.
After appropriate clinical suspicion of stroke and patient stabilization, the ultimate
diagnosis relies on neuroimaging that must be performed promptly, especially for those
within the therapeutic window for thrombolysis. A 30-minute delay in commencing
thrombolysis treatment has been shown to reduce favourable three-month outcomes
by 10%. Use of the NIHSS can permit objective quantification of the impairment
caused by a stroke, and its use is especially important if considering revascularization
therapy.
Useful cranial imaging modalities include noncontrast CT, CT with contrast, CTA, CTP,
MRI, MRA and magnetic resonance perfusion imaging. In the acute setting, a
noncontrast CT scan of the brain is the imaging modality of choice in many units as it
is readily available and allows rapid image acquisition. In addition to differentiating
between haemorrhage and infarct, the CT scan can provide prognostic information and
exclude some stroke mimics. A contrast CT can be performed at the same time and is
highly recommended to exclude other pathologies, for example intracranial tumour, as
a cause for the patient’s clinical status - a contraindication to thrombolysis. Magnetic
resonance imaging (MRI) has higher sensitivity and specificity in detecting ischemia
than CT, and is increasingly being used in the acute phase after AIS. However, it is
more time-consuming, less accessible, and not as well tolerated by patients than CT. It
also presents logistical difficulties in comatose, ventilated patients.
Additional imaging is often performed to aid diagnosis and management, although it
should not delay thrombolysis in eligible patients. CT angiography (CTA) can identify
the site of arterial occlusion, collateral circulation, and underlying pathophysiology
such as vessel dissection, and can be conducted at the same time as the structural CT
image. MR angiography can also provide this information. CT and MRI perfusion
imaging can help delineate the necrotic core and ischemic penumbra, as well as
evaluation of collateral supply.
In text References
(Parsons et al. 2005; Jauch et al. 2013; Singer et al. 2004; Lees et al. 2010) 
 
 References
Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk
BM, Khatri P, McMullan PW Jr, Qureshi AI, Rosenfield K, Scott PA,
Summers DR, Wang DZ, Wintermark M, Yonas H, American Heart
Association Stroke Council, Council on Cardiovascular Nursing, ,
Guidelines for the early management of patients with acute ischemic stroke:
a guideline for healthcare professionals from the American Heart
Association/American Stroke Association., 2013, PMID:23370205
Parsons MW, Pepper EM, Chan V, Siddique S, Rajaratnam S, Bateman GA,
Levi CR., Perfusion computed tomography: prediction of final infarct extent
and stroke outcome., 2005, PMID:16240339
Singer OC, Sitzer M, du Mesnil de Rochemont R, Neumann-Haefelin T.,
Practical limitations of acute stroke MRI due to patient-related problems.,
2004, PMID:15159492
Lees KR, Bluhmki E, von Kummer R, Brott TG, Toni D, Grotta JC, Albers
GW, Kaste M, Marler JR, Hamilton SA, Tilley BC, Davis SM, Donnan GA,
Hacke W; ECASS, ATLANTIS, NINDS and EPITHET rt-PA Study Group,
Allen K, Mau J, Meier D, del Zoppo G, De Silva DA, Bu, Time to treatment
with intravenous alteplase and outcome in stroke: an updated pooled
analysis of ECASS, ATLANTIS, NINDS, and EPITHET trials., 2010,
PMID:20472172
3. 1. Cerebral computed tomography (CCT) and its interpretation
According to their density, the various structures of the head absorb radiation to a
different degree. The higher the density i.e. their absorption of radiation, the more
opaque is their appearance on the scan: bone, intraparenchymal calcification > blood
> thrombosed vessel > grey matter (e.g. thalamus, basal ganglia, cortex), white matter
> oedematous brain tissue.
The addition of CT angiography (CTA) and CT perfusion will not only help to make the
diagnosis of stroke, but these techniques will provide the physician with information on
location of vessel occlusion, presence and quality of collateral blood flow, cerebral
blood flow, cerebral abscesses and cerebral blood volume. These will allow the use of
the so-called ASPECTS score, which has some prognostic value regarding reperfusion
and clinical outcome.
 Notes
https://www.ncbi.nlm.nih.gov/pubmed/23370205
https://www.ncbi.nlm.nih.gov/pubmed/16240339
https://www.ncbi.nlm.nih.gov/pubmed/15159492
https://www.ncbi.nlm.nih.gov/pubmed/20472172
The Alberta Stroke Program Early CT Score (ASPECTS) is a 10-point score
used in patients with MCA stroke to predict outcomes. From an initial score
of 10, 1 point is deducted for every one of the following regions involved:
Caudate
Putamen
Internal capsule
Insular cortex
M1: anterior MCA cortex
M2: MCA cortex lateral to insular ribbon
M3: Posterior MCA cortex
M4: Anterior MCA territory immediately superior to M1
M5: Lateral MCA territory immediately superior to M2
M6: Posterior MCA territory immediately superior to M3
It has been shown that patients with an ASPECTS score of ≤7 have a worse functional
outcome score at 3 months, and an increased risk of thrombolysis-related
parenchymal haemorrhage.
In text References
(Dzialowski et al. 2006; Parsons et al. 2005) 
 Note
Before examining any CT scan always check the patient's details, the date
and time, and the anatomical orientation (i.e. right is left and left is right). In the
following section, we will review some cranial CT scans of patients with stroke.
The following video shows an axial CT head scan of a male patient who presented
with left sided hemiparesis. It demonstrates a right-sided ischaemic stroke in the
territory of the right MCA.
CT Right MCA Stroke 
Interpretation 
The patients in images 1 and 2 (Figure 2) both presented with severe right-sided
hemiparesis and aphasia. The onset of symptoms in both cases was two hours before
the scan was taken.
Figure 2: Axial CT scans of two different patients
with stroke due to different aetiologies.
The patient in image 1 is a 72-year-old male who has a hyperdense left MCA (arrow).
This is a sign of thromboembolic material within the lumen of the MCA and supports
the diagnosis of an acute ischaemic stroke.
By contrast the patient in image 2 (Figure 2) is a 45-year old hypertensive smoker who
has had an intracerebral haemorrhage (star) with extension into the ventricular system
(arrows). Given the presence of intraventricular haemorrhage, the patient is at risk of
hydrocephalus.
Despite both patients presenting in a similar manner, the underlying aetiology of their
symptoms is completely different, emphasising the importance of early cranial imaging.
CT imaging is able to reliably differentiate between ischaemic and haemorrhagic
stroke – as in the two cases here – which avoids the risk of administering thrombolysis
to a patient with intracranial haemorrhage.
CT imaging can also give an indication of the age of the stroke. Look at images 3 and
4, below. Both patients woke up with a left-sided hemiparesis.
Figure 3: The two patients in images 3 and 4
awoke with left-sided hemiparesis, but their scans
reveal a difference in the age of their stroke.
Image 3 (Figure 3) may appear normal on initial review, but on closer inspection, it is
possible to see early cranial CT signs of infarction. These include loss of grey-white
matter differentiation and hypoattenuation of deep nuclei, and cortical hypodensity with
associated parenchymal swelling and gyral effacement. In image 3 (Figure 3), there is
hypoattenuation of the right lentiform nucleus(small arrows) relative to the left
lentiform nucleus, as well as some loss of the right insular ribbon (large arrow).
https://collaboration.esicm.org/dl862?display
https://collaboration.esicm.org/dl863?display
Image 4 (Figure 3) shows a more established infarction of the right lentiform nucleus
(arrows).
The density will further decrease during subsequent days, indicating a progressive
liquefaction of the infarcted tissue. After several weeks, resorption of a haemorrhage
will also lead to a hypodense lesion, often considerably smaller than the primary
hyperdense lesion.
If the cranial CT has just been performed and the patient is still within the therapeutic
window, do not waste time with ultrasound evaluation; consider CT angiography for
quick and safe assessment of the patency or occlusion of large intracranial vessels
(Figure 4). Ensure that this procedure does not delay treatment.
Figure 4: Coronal CTA scan with 3D
reconstruction of a patient who presented with a
dense right hemiparesis and aphasia. The CTA
shows complete occlusion of the left MCA (red
arrow).
 
 References
Parsons MW, Pepper EM, Chan V, Siddique S, Rajaratnam S, Bateman GA,
Levi CR., Perfusion computed tomography: prediction of final infarct extent
and stroke outcome., 2005, PMID:16240339
Dzialowski I, Hill MD, Coutts SB, Demchuk AM, Kent DM, Wunderlich O,
von Kummer R., Extent of early ischemic changes on computed
tomography (CT) before thrombolysis: prognostic value of the Alberta
Stroke Program Early CT Score in ECASS II., 2006, PMID:16497977
3. 2. Magnetic resonance imaging
Magnetic resonance imaging (MRI) has become increasingly established as an
investigative tool for the diagnosis of acute stroke in many hospitals. The equipment is
https://collaboration.esicm.org/dl864?display
https://www.ncbi.nlm.nih.gov/pubmed/16240339
https://www.ncbi.nlm.nih.gov/pubmed/16497977
not, however, available in all hospitals admitting and treating patients with stroke.
MRI is more sensitive than CT scan in detecting hyperacute stroke. Diffusion-weighted
imaging (DWI) can show alterations minutes from the ictus time (Figure 5). Perfusion-
weighted imaging (PWI) is helpful in quantifying ischemic penumbra tissue. The
PWI/DWI mismatch show both the size of the perfusion lesion and diffusion lesion.
MRI angiography (MRA) can visualise large vessel occlusion or stenosis. MRI with fat
suppression technique, may confirm a suspected dissection and demonstrate the
mural haematoma. Stroke MRI, including MRA/DWI/PWI, can be helpful in patients
who wake up with strokes or those who present later in the time window for assessing
the potential benefits of thrombolysis. Sometimes, intravenous thrombolysis can be
initiated, and stroke MRI is then performed without time loss with the purpose of
gaining more information and further guiding reperfusion therapy (bridging concept). In
the case of haemorrhagic stroke, MRI might immediately provide information on the
underlying cause such as arteriovenous malformations.
Figure 5: Diffusion-weighted MRI demonstrating
increased DWI signal, in keeping with acute
ischaemic stroke, located in the region of the left
basal ganglia and insula.
In text References
(Köhrmann and Schellinger 2007; Nour and Liebeskind. 2011; Kim et al. 2014) 
 References
Köhrmann M, Schellinger PD, Stroke-MRI: extending the time-window:
recent trials and clinical practice., 2007, PMID:18705990
Nour M, Liebeskind DS., Brain imaging in stroke: insight beyond diagnosis.,
2011, PMID:21556679
Kim BJ, Kang HG, Kim HJ, Ahn SH, Kim NY, Warach S, Kang DW.,
Magnetic resonance imaging in acute ischemic stroke treatment., 2014,
PMID:25328872
https://collaboration.esicm.org/dl865?display
https://www.ncbi.nlm.nih.gov/pubmed/18705990
https://www.ncbi.nlm.nih.gov/pubmed/21556679
https://www.ncbi.nlm.nih.gov/pubmed/25328872
3. 3. Electrocardiogram
An electrocardiogram (ECG) is indispensable because of the high incidence of heart
disease in stroke patients. Arrhythmias, in particular atrial fibrillation, or recent
myocardial infarction may be responsible for emboli.
3. 4. Ultrasound studies
Continuous wave (cw)-Doppler of extracranial arteries and pulsed wave (pw)- Doppler
of intracranial arteries facilitates identification of an occluded or stenotic vessel,
evaluation of the quality of collaterals, and confirmation of reperfusion. Duplex
sonography allows visualisation of the extracranial vessels with good quality
visualisation of intracranial vessels in patients with sufficient temporal bone windows.
Currently, vascular pathology including stenoses/dissections/thrombi/atherosclerosis
can be detected over a wide range of cerebral vessels. Doppler evaluation is non-
invasive and repeatable and is, therefore, excellent for dynamic assessments over
time. It is, however, quite investigator-dependent. It is very important to keep in mind
that ultrasound must not delay radiographic cerebral imaging.

What is the impact of the result of an ultrasound study during the
acute phase?
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 If you find an occlusion or high-grade stenosis 
• You will control arterial pressure even more carefully, attempt to
maintain blood pressure in the higher range and observe the
relationship between clinical symptoms and the pressure levels 
• For secondary prophylaxis, you might prefer platelet inhibitors to
anticoagulants. Consider carotid revascularisation e.g. by referral to the
vascular surgeons with a view to a carotid endarterectomy (CEA) 
• You might omit further unnecessary diagnostic tests such as
transoesophageal echocardiography (TEE).
Other ultrasound studies include transthoracic and transoesophageal
echocardiography to screen for cardioembolic conditions. They are not usually
performed acutely but may be useful within the first 24 hours after the onset of stroke.
3. 5. Laboratory tests
The following tests are important in the management of stroke patients. They have
been sub-divided into urgent (U) and subsequent (S) tests.
Table 1: Tests in stroke patients management
Category Type of test Importance
U Electrolytes
For hypo- or
hypernatraemia. Important
for cerebral oedema,
seizures and arrhythmias
U Glucose
Hypoglycaemia may mimic
stroke and has to be treated
immediately.
Hyperglycaemia may
increase infarction size and
impair late functional
outcome
U Haemoglobin/Haematocrit/RBC/WBC
Anaemia may aggravate
brain ischaemia.
Haemoconcentration may
impair oxygen supply to the
penumbra
U Blood urea and creatinine
Elevated serum urea and
creatinine indicate renal
insufficiency – nephrotoxic
agents and contrast agents
should be avoided where
possible
U CK, CKMB, Troponin I
Important to detect
associated myocardial
infarction
U Transaminases
To eliminate chronic or
acute liver disease
(particularly in those at high-
risk)
U Coagulation– Fibrinogen, APTT, INR
To check potential
contraindication for
anticoagulation and
thrombolysis
U Arterial blood gas analysis
To control pO2, pCO2 and
PH
S
Specific coagulation tests – Protein
C, S, At III
As part of aetiologies for
stroke
S Sedimentation rate, CRP
To assess inflammatory
context
S Cholesterol, Triglycerides As a stroke risk factor
 
 Note
Tests may be different in your institution.
In younger patients where there is no clear cause of stroke, the following special
laboratory tests are used:
Protein C, S, aPC-resistance
Cardiolipin-AB
Homocysteine
Vasculitis-screening
CSF (in case of suspected SAH, meningitis or vasculitis)
 Urine toxicology screening.

 Why is an initial laboratory assessment so important in the acute
setting? Which variables may influence your diagnostic and
therapeutic options? 
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 Coagulation tests: These results have to be known e.g. INR,
thrombocytopenia, and sometimes adjusted before starting a
thrombolytic therapy or invasive procedures. 
Blood glucose: Exclusion of hypoglycaemia is crucial since hypoglycaemia can mimic
an acute ischaemic infarction.Diagnosis and treatment of hypoglycaemia may thus
prevent misdiagnosis with possibly dangerous diagnostic and therapeutic
consequences. Furthermore, hypoglycaemia worsens functional outcome and
increases infarct size in stroke patients. At the same time, significant hyperglycaemia
is associated with a worse stroke outcome, and thus should be treated. 
Blood urea and creatinine may influence your choice of diagnostic imaging
procedure such as avoidance of IV contrast agents. 
Acute phase/infection parameters: these might explain fever, which is detrimental in
stroke and may suggest the need to identify a source of infection and start antibiotic
treatment.
4. General Critical Care and Stroke Treatment
The past two decades have seen a significant change in the management approach to
patients with acute ischaemic stroke. There is now class I evidence to support five
interventions for patients with acute stroke:
1. Care on a stroke unit
2. Intravenous tissue plasminogen activator (rt-PA) within 4.5 hours of stroke
onset (even if endovascular treatments are being considered)
3. Aspirin within 48 hours of stroke onset
4. Decompressive craniectomy for supratentorial malignant hemispheric cerebral
infarction within 48 hours of symptom onset, and
5. Endovascular therapy with stent retriever in selected patients with anterior
circulation stroke within 6 hours of stroke onset
The vast majority of patients with stroke are safely managed in a stroke unit setting.
However, some patients require a level of care and monitoring that cannot be provided
on a stroke unit. In part due to a more aggressive approach to management, an
increasing number of patients with stroke are being referred and subsequently
admitted to intensive care. Appropriate triage and the decision to admit a patient to the
ICU can best be achieved through the collaboration of neurologists/stroke physicians
and intensivists.
A useful schematic of the ICU management principles for acute ischaemic stroke is
shown below (Figure 6).
Figure 6: Schematic outlining the general
principles of the endovascular and intensive care
management of acute ischemic stroke ...
 
Figure 6: Schematic outlining the general principles of the endovascular and intensive
care management of acute ischemic stroke.Abbreviations: ABG, arterial blood gas;
https://collaboration.esicm.org/dl866?display
AIS, acute ischemic stroke; ASPECTS, Alberta Stroke Program Early Computed
Tomography Score; BG, blood glucose; BP, blood pressure; CPP, cerebral perfusion
pressure; EEG, electroencephalography; ECG, electrocardiography; FFP, fresh frozen
plasma; ICP, intracranial pressure; ICU, intensive care unit; IPCC, intermittent
pneumatic calf compression; IV, intravenous; MCA, middle cerebral artery; PCC,
prothrombin complex concentrate; PiCCO, pulse contour continuous cardiac output;
Resp, respiratory; rFVII, recombinant factor VII; rt-PA, recombinant tissue plasminogen
activator; SIADH, syndrome of inappropriate anti-diuretic hormone secretion; TCD,
transcranial Doppler; VTE, venous thromboembolism.
4. 1. Reperfusion therapy
Reperfusion therapy, including intravenous thrombolysis, intra-arterial thrombolysis,
mechanical clot-removing devices, and angioplasty/stenting are important treatment
options in the acute stroke patient.

What is the purpose of recanalisation treatment in acute ischaemic
stroke when brain tissue is known to be irreversibly damaged
within 5-10 minutes of cessation of blood flow?
COMPLETE TASK THEN CLICK TO REVEAL THE ANSWER
 Administration of thrombolytic therapy in stroke is based on the
concept that early restoration of circulation in the affected territory by
recanalisation of an occluded intracranial artery preserves reversibly
damaged neuronal tissue in the penumbra and thereby enhances
recovery of neuronal function, reducing clinical neurological disability.
4. 1. 1. Thrombolysis
There is class I evidence supporting the use of intravenous rt-PA as soon as possible
but within 4.5 hour of stroke onset, after excluding a haemorrhagic stroke by imaging.
There are several factors to consider when evaluating a patient’s eligibility for
thrombolysis, including:
National Institutes of Health Stroke Scale score
Blood pressure lability
Pre-existing anticoagulant/antiplatelet use and/or presence of bleeding diathesis
Presence of seizures
Recent major surgery
History of previous stroke, intracranial haemorrhage, vascular malformation or
tumour
 Warning
 
Time is brain. A pooled analysis of four trials confirmed that the odds ratio of a
favourable three-month outcome decreases as time to thrombolysis increases.
This emphasises the importance of early treatment.
4. 1. 2. Endovascular treatment
Five recent randomised controlled trials have confirmed that, compared to standard
care (usually intravenous rt-PA), patients with proximal cerebral artery occlusions in
the anterior cerebral circulation who are given endovascular treatment combined with
standard care have improved:
Reperfusion rates
Early neurological recovery
Functional outcomes
 
With regards to specific types of endovascular treatment and their relative efficacy,
mechanical thrombectomy has been shown to be superior to endovascular
thrombolysis, and stent retrievers superior to first-generation mechanical
thrombectomy.
One of the trials recruited patients up to 12 hours following symptom onset and still
noted clinical benefit from endovascular treatment. Only one trial showed a difference
in mortality between the intervention and control arms, and the rates of symptomatic
intracranial haemorrhage were no different between the two groups in any of the trials.
To date there are no widely accepted and adopted eligibility criteria for endovascular
therapy. Furthermore, as these trials focused on anterior circulation strokes. For
posterior circulation stroke, there is no class 1 evidence to guide treatment but it is
known that intravenous thrombolysis is rarely effective in large vessel occlusions, and
acute basilar occlusions are generally treated through endovascular means.
 Warning
If the patient shows neurological deterioration following thrombolytic treatment,
you should immediately initiate a follow-up cranial CT to exclude complications
e.g. haemorrhage.
All patients should undergo repeat cranial imaging 24 hours after reperfusion therapy,
to evaluate for haemorrhagic transformation.
Taken together, these data suggest that eligible patients with anterior circulation stroke
should be offered the following treatment:
Presenting within 4.5 hours of symptom onset: intravenous rt-PA plus
endovascular therapy
Presenting after 4.5 hours but within 6 hours of symptom onset: endovascular
therapy alone
 
In text References
(Lees et al. 2010; Powers et al. 2015; Hacke et al. 2008; Goyal et al. 2015; Berkhemer
et al. 2015; Campbell et al. 2015; Saver et al. 2015; Jovin et al. 2015) 
 References
Lees KR, Bluhmki E, von Kummer R, Brott TG, Toni D, Grotta JC, Albers
GW, Kaste M, Marler JR, Hamilton SA, Tilley BC, Davis SM, Donnan GA,
Hacke W; ECASS, ATLANTIS, NINDS and EPITHET rt-PA Study Group,
Allen K, Mau J, Meier D, del Zoppo G, De Silva DA, Bu, Time to treatment
with intravenous alteplase and outcome in stroke: an updated pooled
analysis of ECASS, ATLANTIS, NINDS, and EPITHET trials., 2010,
PMID:20472172
Powers WJ, Derdeyn CP, Biller J, Coffey CS, Hoh BL, Jauch EC, Johnston
KC, Johnston SC, Khalessi AA, Kidwell CS, Meschia JF, Ovbiagele B,
Yavagal DR; American Heart Association Stroke Council., 2015 American
Heart Association/American Stroke Association Focused Update of the
2013 Guidelines for the Early Management of Patients With Acute Ischemic
Stroke Regarding Endovascular Treatment: A Guideline for Healthcare
Professionals From the American , 2015, PMID:26123479
Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, Larrue
V, Lees KR, Medeghri Z, Machnig T, Schneider D, von Kummer R,
Wahlgren N, Toni D; ECASS Investigators., Thrombolysis with alteplase 3to
4.5 hours after acute ischemic stroke., 2008, PMID:18815396
Goyal M, Demchuk AM, Menon BK, Eesa M, Rempel JL, Thornton J, Roy
D, Jovin TG, Willinsky RA, Sapkota BL, Dowlatshahi D, Frei DF, Kamal NR,
Montanera WJ, Poppe AY, Ryckborst KJ, Silver FL, Shuaib A, Tampieri D,
Williams D, Bang OY, Baxter BW, Burns PA, Cho, Randomized assessment
of rapid endovascular treatment of ischemic stroke., 2015, PMID:25671798
Berkhemer OA, Fransen PS, Beumer D, van den Berg LA, Lingsma HF, Yoo
AJ, Schonewille WJ, Vos JA, Nederkoorn PJ, Wermer MJ, van Walderveen
MA, Staals J, Hofmeijer J, van Oostayen JA, Lycklama à Nijeholt GJ, Boiten
J, Brouwer PA, Emmer BJ, de Bruijn SF, van, A randomized trial of
intraarterial treatment for acute ischemic stroke., 2015, PMID:25517348
Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L, Yassi N, Yan
B, Dowling RJ, Parsons MW, Oxley TJ, Wu TY, Brooks M, Simpson MA,
Miteff F, Levi CR, Krause M, Harrington TJ, Faulder KC, Steinfort BS,
https://www.ncbi.nlm.nih.gov/pubmed/20472172
https://www.ncbi.nlm.nih.gov/pubmed/26123479
https://www.ncbi.nlm.nih.gov/pubmed/18815396
https://www.ncbi.nlm.nih.gov/pubmed/25671798
https://www.ncbi.nlm.nih.gov/pubmed/25517348
https://www.ncbi.nlm.nih.gov/pubmed/25671797
Priglinger M, Ang T, Scroop R, Barber PA, McGu, Endovascular therapy for
ischemic stroke with perfusion-imaging selection., 2015, PMID:25671797
Saver JL, Goyal M, Bonafe A, Diener HC, Levy EI, Pereira VM, Albers GW,
Cognard C, Cohen DJ, Hacke W, Jansen O, Jovin TG, Mattle HP, Nogueira
RG, Siddiqui AH, Yavagal DR, Baxter BW, Devlin TG, Lopes DK, Reddy
VK, du Mesnil de Rochemont R, Singer OC, Jahan, Stent-retriever
thrombectomy after intravenous t-PA vs. t-PA alone in stroke., 2015,
PMID:25882376
Jovin TG, Chamorro A, Cobo E, de Miquel MA, Molina CA, Rovira A, San
Román L, Serena J, Abilleira S, Ribó M, Millán M, Urra X, Cardona P,
López-Cancio E, Tomasello A, Castaño C, Blasco J, Aja L, Dorado L,
Quesada H, Rubiera M, Hernandez-Pérez M, Goyal M, , Thrombectomy
within 8 hours after symptom onset in ischemic stroke., 2015,
PMID:25882510
4. 2. Which stroke patients should be admitted to the ICU?
There are several indications for ICU admission, including:
A requirement for intubation and/or mechanical ventilation
Impaired level of consciousness (GCS ≤8) and/or evidence of brainstem
dysfunction and/or any other cause of a compromised airway
To prevent aspiration pneumonia in any of the above
As an adjunct therapy for elevated ICP and/or in the presence of significant
cerebral oedema
Acute respiratory failure e.g. due to neurogenic or cardiogenic pulmonary
oedema
Generalized tonic-clonic seizures or status epilepticus
Episodes of apnoea
Severe stroke (National Institutes of Health Stroke Scale (NIHSS) Score >17)
Reperfusion therapy (intravenous or intraarterial), in the presence of multiorgan
failure and/or to manage the complications of therapy (e.g. haemorrhagic
transformation), and in those undergoing local intraarterial therapy
Large middle cerebral artery infarct volume (>145cm ), which predicts a malignant
course
Uncontrolled derangements of blood pressure that are difficult to manage in a
ward setting
Organ support, including renal replacement therapy, noninvasive ventilation,
and/or cardiac dysfunction
Postoperative monitoring and management following decompressive craniectomy
Management of patients with massive stroke and high mortality risk in whom
organ retrieval/harvesting is planned
3
https://www.ncbi.nlm.nih.gov/pubmed/25671797
https://www.ncbi.nlm.nih.gov/pubmed/25882376
https://www.ncbi.nlm.nih.gov/pubmed/25882510
 
Crucial to the decision-making process about whether or not to admit to intensive care
is an assessment of the likely neurological prognosis of the patient, the presence or
absence of non-neurological organ compromise, comorbidities, and patient and/or
relative wishes. It is important to exclude and correct reversible causes of neurological
impairment prior to this assessment.
In text References
(Kirkman, Citerio and Smith. 2014) 
 References
Kirkman MA, Citerio G, Smith M., The intensive care management of acute
ischemic stroke: an overview., 2014, PMID:24658914
4. 3. Managing the critically ill patient with stroke
The ICU management of stroke focuses on the monitoring and optimisation of
systemic physiological homeostasis, and the monitoring and management of
intracranial complications. Once the patient has been transferred to the ICU,
monitoring (e.g. ECG, blood pressure, pulse oximetry, and where available, other
methods such as transcranial Doppler and end-tidal CO2) and global treatment (such
as insertion of cannulae and intubation, if necessary) should be initiated according to
local ICU protocols.
4. 3. 1. Basic measures and principles
Some routine techniques in intensive care must be applied with caution in stroke
patients, especially if elevated ICP is present or suspected:
Keep the head in the midline and slightly elevated at approximately 20– 30°. The
midline position is of special importance since it influences venous drainage.
Placement of a jugular vein catheter may be hazardous due to the need for neck
rotation, which may impede cerebral venous drainage and increase ICP. If
required, consider femoral or subclavian catheters.
If analgosedation is indicated, ensure adequate, deep sedation and analgesia.
Otherwise, stimuli may increase ICP by evoking motor responses such as
coughing and Valsalva manoeuvres. 
Laryngoscopy and intubation: consider the risk of further haemodynamic
impairment, especially in those with carotid artery stenosis, keep blood pressure
stable and ensure normocapnia (modified rapid sequence intubation
recommended) during these procedures.
https://www.ncbi.nlm.nih.gov/pubmed/24658914
For intubation, short acting anaesthetic agents are recommended. Consider
propofol (2–4 mg/kg) or etomidate (0.15–0.3 mg/kg) in conjunction with a non-
depolarising neuromuscular blocking agent such as rocuronium (1.0 mg/kg given
in a rapid sequence) if indicated. One must be cognisant of the increased risk of
vomiting and aspiration in patients with stroke.
Note that high PEEP levels may exacerbate intracranial hypertension, although
this effect may be less significant than previously thought (see references).
Further analgosedation regimens should be individualised and depend on the brain
lesion, expected clinical time course and non-cerebral conditions of the patient. Agents
often involved in neurocritical analgosedation are sedatives such as midazolam or
propofol, with possible adjuncts such as clonidine or dexmedetomidine, in combination
with opioids (morphine, fentanyl, remifentanil, sufentanil) for analgesia. Use of these
drugs requires appropriate systemic and cerebral monitoring. Sedation scales are
recommended and (if available) continuous EEG monitoring.
In text References 
(Georgiadis et al. 2002; Georgiadis et al. 2001; Waldmann. 2008; Ropper. 1993) 
4. 3. 2. Oxygenation and ventilation
Hypoxaemia can exacerbate cerebral ischaemia and should be strictly avoided after
stroke. It is common following stroke and can result from:
Pulmonary infections
Aspiration
Acute lung injury/acute respiratory distress syndrome
Pulmonary embolism
Pulmonary oedema
Altered central regulation of respiration
Sleep apnoea
Respiratory muscle weakness
 
All patients with stroke on the ICU should undergo continuous monitoring of systemic
oxygenation through pulse oximetry. Routine oxygen supplementation does not
improve outcomes and in fact appears to be detrimental irrespective of the severity of
the stroke (see references). Oxygen supplementation should only be provided to
patients if SpO2 falls below 94%, and in such instances, arterial blood gas (ABG)
should be performed to confirm systemic oxygenation as SpO2 monitoring obtained
through pulse oximetry may not correlate with true SaO2.
Indications for intubation and mechanical ventilation are discussed in Which stroke
patients should be admitted to the ICU? . In patientswith imminent or established
hypoxia and who undergo mechanical ventilation, regular ABG monitoring should be
performed, aiming for an SaO of 94% or higher, as well as normocapnea. Primary,
elective tracheostomy should be considered in patients predicted to require prolonged
2
https://collaboration.esicm.org/Acute%20Ischaemic%20Stroke:%20GENERAL%20CRITICAL%20CARE%20AND%20STROKE%20TREATMENT:%20Which%20stroke%20patients%20should%20be%20admitted%20to%20the%20ICU??page_ref_id=2388
mechanical ventilation (>2 weeks), and in those with severe dysphagia and/or bulbar
palsies resulting from brainstem and large hemispheric infarction, if a reasonable
outcome is predicted. Optimal timing of the tracheostomy has been controversial,
although recent evidence from a small single-centre RCT suggests tracheostomy
within 3 days reduces ICU and six-month mortality with no effect on tracheostomy-
related complications (including bleeding) when compared to tracheostomy within 7-14
days (see references).
Dysphagia is common in patients with stroke and, given the association with aspiration
pneumonia, mandates a swallow assessment soon after admission. Patients should
remain nil by mouth until their swallow has been deemed safe. It is important that
patients with stroke receive adequate nutrition, but a recent Cochrane systematic
review found no difference in death or dependency between early and late feeding in
patients with acute and subacute stroke.
In text References 
(Bösel et al. 2013; Geeganage et al. 2012; Rønning and Guldvog. 1999; Rincon et al.
2014) 
4. 3. 3. Haemodynamic and fluid management
The majority of patients with stroke are hypertensive at presentation. The hypertension
may be associated with chronic hypertension, raised intracranial pressure, a stress
response, or a neuroendocrine response. All patients with stroke on the ICU should
undergo regular blood pressure monitoring (at least every 3 minutes during
endovascular therapy with subsequent frequency of monitoring on the ICU determined
by the results of this, otherwise BP should be monitored at least every 10-15 minutes
on the ICU for the first 24 hours, again with subsequent frequency of monitoring
determined by the results of this). Those with unstable blood pressure or who are
intubated and ventilated should have continuous monitoring via an arterial line.
There is a U-shaped relationship between blood pressure and outcome following
stroke, with both hyper- and hypotension having deleterious outcomes. Despite this,
there are no clear benefits of acutely lowering blood pressure in the hypertensive
stroke patient, and severe hypotension resulting from excessive overcorrection of
hypertension could result in compromised cerebral perfusion and potentially increased
infarct volumes. It is possible that patients with severe carotid stenosis could benefit
from blood pressure augmentation, but long-term outcome data are required to fully
evaluate this. European Stroke Organisation guidelines recommend that blood
pressure be lowered to <185/110 mmHg in those undergoing thrombolysis prior to
commencing treatment and for 24 hours after. In those not undergoing thrombolysis, a
more relaxed threshold of <220/120 mmHg can be used unless the patient has
significant comorbidities and in particular severe cardiac failure, aortic dissection, or
hypertensive encephalopathy. First line anti-hypertensive agents include intravenous
labetalol, nicardipine, urapidil, and clevedipine. Hypotension (dependent on the
patient’s normal blood pressure, but <90 mmHg is a reasonable threshold) should be
treated with intravenous fluids followed by vasoactive agents such as norepinephrine if
this is not successful.
Fluid balance should be carefully monitored and managed on an individualised basis
to maintain euvolaemia. Particular care is required in patients with an increased
vulnerability to fluid overload and those with conditions such as the syndrome of
inappropriate antidiuretic hormone secretion. Intentional haemodilution has been
shown in a meta-analysis of 18 trials not to improve outcomes. Major stroke guidelines
emphasise a preference for 0.9% saline, while dextrose-containing fluids should be
avoided unless the patient is hypoglycaemic, due to the risk of exacerbating cerebral
oedema. There are no apparent benefits in the use of 25% albumin over saline.
In text References
(Asplund 2002; European Stroke Organisation (ESO) Executive Committee; ESO
Writing. 2008; Ginsberg et al. 2013; Leonardi-Bee et al. 2002; Rordorf et al. 2001) 
4. 3. 4. Cardiovascular monitoring and myocardial complications
Cardiac abnormalities are common in patients with stroke, in particular dysrhythmias.
Elevated cardiac troponin levels and abnormal left ventricular function are also found
in patients with stroke. Sudden death after stroke is an important but under-recognised
phenomenon, thought to result from the interaction between cardiovascular and
neurological pathology. It may be related to impaired central autonomic control
particularly if the stroke involves the insular cortex.
All patients with stroke on the ICU should have continuous electrocardiography and
have echocardiography at least once during their admission. Cardiac troponin should
be measured in the presence of ECG changes and echocardiographic evidence of
ventricular function. Minimally-invasive monitors (e.g. PiCCO) may aid haemodynamic
and fluid management in patients with cardiovascular abnormalities.
In text References
(Norris, Froggatt and Hachinski. 1978; Kerr et al. 2009; Darki et al. 2013; Sörös and
Hachinski. 2012) 
4. 3. 5. Glycaemic control
Hyperglycaemia is present in over 40% of patients with stroke at admission. It is a
marker of illness severity and associated with, among other things, larger infarct
volumes and susceptibility to infection. Hyperglycaemia following stroke is
independently associated with increased morbidity and mortality at 90 days, and an
increased risk of intracerebral haemorrhage following thrombolysis. Importantly,
hyperglycaemia may attenuate the benefits of intraarterial thrombolysis.
For these reasons, regular serum glucose monitoring (at least every hour) and careful
glycaemic control for the patient with stroke in the ICU is essential. Tight glycaemic
control does not appear to result in deleterious outcomes, but no clinical benefit of
such an approach has been demonstrated either. Continuous intravenous infusion of
insulin is preferred over subcutaneous administration in the ICU setting. Different
stroke guidelines vary in their recommendations on serum glucose levels, but a
reasonable target advised by the American Stroke Association is 140-180 mg/dl (8.0-
10.0 mmol/l).
In text References
( et al. 2003; Southerland and Johnston. 2012; Kase et al. 2001; Leigh et al. 2004;
Bellolio, Gilmore and Ganti. 2014) 
4. 3. 6. Temperature control
Pyrexia is common after stroke, affecting up to one half of patients, and is an
independent predictor of a poor outcome. It may occur in the absence of infection, due
to a centrally-mediated inflammatory response. In all cases, an infective source should
be excluded or treated appropriately, and the fever should be treated aggressively. In
one randomised controlled trial, high-dose paracetamol (acetaminophen, 6 g daily)
within 12 hours of stroke onset did not have any overall significant benefits. Post hoc
analyses suggested improved functional outcomes in patients with admission
temperatures of 36.5 °C or higher, and the Paracetamol (acetaminophen) in Stroke 2
trial is evaluating this further.
There is no widely accepted optimal temperature target, but it is reasonable to treat
temperatures above 37.5 °C. First-line treatment is paracetamol (acetaminophen), and
second-line therapies include intravenous metamizole, rapid infusion of cold saline (4
°C), and deployment of automatic cooling systems.
There has been significant interest in the use of therapeutic hypothermia (TH) in a
range of acute brain injuries, and there