This document discusses identifying and managing acute stroke. It begins by outlining stroke, including defining ischemic stroke and transient ischemic attack. It then discusses the classification, epidemiology and data from Malaysia on stroke. Risk factors like hyperhomocysteinemia and depression post-stroke are mentioned. The management of acute ischemic stroke is summarized, including thrombolysis guidelines. General investigations and imaging for acute stroke are provided. The document concludes by discussing secondary prevention strategies post-stroke.
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Managing Acute Stroke
1. Identifying and managing
Acute stroke
Dr Ahmad Shahir Mawardi,
Neurology registrar,
Neurology Department
HKL
20th
May 2015
2. Outline
• Identifying acute stroke
• Type of stroke
• Classification of stroke
• Management of acute stroke
– Ischaemic stroke
• Acute thrombolysis
3. Epidemiology
• Annually 15 million people worldwide
suffer a stroke
–5 million die
–5 million are left permanently disabled.
• Top 4 leading causes of death in ASEAN
countries,
– death rate :
• 10.9/100 000 (Thailand)
• 54.2/100 000 (Singapore).
5. • In Kelantan, 158 stroke patients were admitted to HUSM
between January 1997 and December 1998.
– 56·3% ischemic stroke
– 36·1% primary intracerebral hemorrhage
– 7·6% subarachnoid hemorrhage.
• 246 stroke patients admitted to Penang Hospital from
December 1998 to November 1999
– 74·8% ischemic stroke
– 25·2% hemorrhagic stroke
Malaysia's data
6. • 163 ischemic stroke patients were admitted to HUKM
from June 2000 until January 2001
– 62·6% lacunar infarct
– 26·4% middle cerebral infarct
– 11·0% other manifestations
– The mortality rate: 11·7%, with a mean age of 62·2 years
• UMMC 83 ischemic stroke patients were admitted
between June 2000 and November 2000
– hyperhomocysteinemia was found to be a risk factor for ischemic
stroke (odds ratio 5·3)
– Depression was reported in (66%) 3-6 months poststroke
• It has been reported that six new stroke cases occur in
Malaysia every hour
Malaysia's data
9. Stroke
• Clinical syndrome characterized by rapidly developing
clinical symptoms and/or signs of focal, and at times
global, loss of cerebral function, with symptoms lasting
more than 24 hours or leading to death, with no apparent
cause other than that of vascular origin”.
10. Transient Ischaemic Attack
• A Clinical syndrome characterized by an acute loss of
focal cerebral or monocular function with symptoms
lasting less than 24 hours and which is thought to be due
to inadequate cerebral or ocular blood supply as a result
of arterial thrombosis or embolism”.
11. Acute Stroke
• sudden non-convulsive, focal neurological
deficit resulting from vascular disease
• could be divided into
» Acute ischemia infarction
» Intraparenchymal hemorrhage
» Subarachnoid hemorrhage
**a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke
Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention
12. Transient Ischemic Attack
• Old definition - (Clinically-based)
– brief episode of neurologic dysfunction
< 24 hours resulting from focal temporary
cerebral ischemia
• New definition - (Tissue-based)
– transient episode of neurologic dysfunction
caused by focal brain, spinal cord, or
retinal ischemia, without acute infarction*
**a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke
Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention
13. Classification
Purpose:
1.Immediate stroke supportive care and rehabilitation,
2.Prognostic purposes
3.Guides cost effective investigations
4.Aids decisions for therapy and secondary stroke
prevention strategies.
5.Setting up stroke registries/ data banks/
epidemiological studies.
14. 1. WHO classification: hemorrhagic (intraparenchymal,
subarachnoid), ischemic or Transient Ischemic Attack TIA.
2. Oxfordshire Community Stroke Project (OCSP)
classification for ischemic stroke – TACI, PACI, POCI, LACI),
and unclassified.
3. Trial of ORG 10172 in Acute Stroke Treatment (TOAST)
classification – large artery, small vessels, cardioembolic,
stroke of determined cause, stroke of undetermined cause
4. Location of stroke – right hemisphere, left hemisphere,
brainstem, cerebellar.
Classification
15.
16. • NO cortical sign
• Common site:
– Putamen 37%
– Thalamus 14%
– Caudate 10%
– Pons 16%
– Int capsule, post limb 10%
• less common ant limbs, cerebellum
• 5 subtypes
1. Pure motor
2. Pure sensory
3. Ataxic Hemiparesis
4. Dysarthria-clumsy hand syndrome
5. Mixed motor sensory
Lacunar infarction
17. Cortical signs
• Aphasia
• Neglect (may be spatial, sensory, visual,
auditory)
• Alteration of consciousness
• Visual field cut
18. Time course of lacunar infarction
Percentage
offunction%
See you
See traditional medicine
19. Diagnosis/ Identifying
• Stroke is a clinical diagnosis
• History is of utmost importance
– obtain information from the patient, family members, friends, or
witnesses.
• The diagnosis should provide answers to the following
questions:
1. What is the neurological deficit?
2. Where is the lesion?
3. What is the lesion?
4. Why has the lesion occurred?
5. What are the potential complications and prognosis?
20. • The signs and symptoms of a stroke depend on the type,
location and the extent of the affected brain tissue.
• Sudden or rapid onset within minutes to an hour.
– however, a stepwise or gradual worsening or waxing and waning
symptoms.
• 1/3 of all strokes occur during night sleep
– Further imaging is needed to detect mismatch of penumbra
and infarcted area
Diagnosis/ Identifying
26. 1. Atherothromboembolism (50%)
2. Intracranial small vessel disease (penetrating artery
disease) (25%)
3. Cardiogenic embolism (20%)
4. Others
– arterial dissection, trauma, vasculitis (primary/secondary),
metabolic disorders, congenital disorders
– less common causes such as migraine, pregnancy, oral
contraceptives, etc.
Etiology
27. Investigations
1. Confirm the diagnosis
2. Determine the stroke mechanism
3. Risk stratification and prognostication
4. Identify potentially treatable large obstructive
lesions of the cerebrovascular circulation
28. • ON ADMISSION
– FBC, RP, LFT, RBS, Coag*
• NEXT DAY
– FBS, FSL
• OPTIONAL TESTS
– VDRL, Autoimmune, Thrombophilia, LA,
Homocystein, CRP
• ECG/Holter
Blood investigations
29. Imaging
CXR madatory
CT brain
haemorrhage from infarction
Confirms site of lesion, cause of lesion, extent of brain affected
ECHO suspected cardioembolism, assess cardiac function
MRI
Sensitive
Useful tool to select patients for thrombolysis where available
Carotid duplex extracranial vessel disease
TCD
Identifies intracranial vessel disease with prognostic and
therapeutic implications
MRA
Non invasive tool to assess intra- and extra-cerebral circulation
Objective assessment of vessel stenosis
CT angiography Non invasive tool to assess intra- and extra-cerebral circulation.
MR venography In suspected cerebral venous thrombosis
Contrast
angiogram
Gold standard assessment of cerebral vasculature
35. Reperfusion therapy
• Intravenous rt-PA can be given only if the following is
available:
1. A physician with expertise in the diagnosis and mx of stroke.
2. Appropriate neuroimaging tests are available 24 hours a day
3. Capability to manage the complications of thrombolysis,
particularly intracranial haemorrhage.
• Onset:
– 4.5 hours
– 3 hours ( >80 y.o with DM)
• NIHSS 6-22 (some centre 4-22)
36. Tips to know the exact onset
• The exact time of “last seen well”
• What is the patient doing during the onset?
• Where does the patient stay?
• Challenge the eye witness regarding the time
37.
38. Candidate for thrombolysis
1. Diagnosis of ischaemic stroke causing measurable
neurological deficit.
2. The neurological signs should not be clearing
spontaneously.
3. The neurological signs should not be minor and isolated.
4. Caution should be exercised in treating a patient with
major deficits.
5. Onset of symptoms <4.5 hours before beginning
treatment.
39. Candidate for thrombolysis
6. No contraindication for thrombolytic therapy.
7. Blood pressure less than 185mm Hg systolic and/or less
than 110mm Hg diastolic.
8. Brain CT is normal or minimal change.
9. The patient or family understand the potential risks and
benefits from treatment.
*written consent
40. 1. Current use of oral anticoagulant or a promthrombin time (PT) > 15
seconds (INR > 1.7)
2. Use of heparin in the previous 48 hours and a prolonged partial
thromboplastin time (PTT)
3. A platelet count < 100,000/mm3
4. Another stroke or any serious head injury in the previous 3 months
5. Major surgery within the preceding 14 days
6. Arterial puncture at noncompressible site within the last 21 days
7. Pre-treatment systolic blood pressure > 185mmHg or diastolic blood
pressure > 110mmHg
Contraindication for thrombolysis (I)
41. 8. Neurological signs that are improving rapidly
9. Isolated mild neurological deficits, such as ataxia alone, sensory loss
alone, dysarthria alone or minimal weakness
10. Prior intracranial haemorrhage
11. A blood glucose < 2.7mmol/l or > 22.2mmol/l
12. Seizure at the onset of stroke
13. Gastrointestinal or urinary bleeding within the preceding 24 days
14. Recent myocardial infarction
Contraindication for thrombolysis (II)
46. Post thrombolysis care (I)
1. Admit to ICU or a stroke unit
2. Perform neurological assessments
• every 15 minutes during the infusion of rt-PA
• every 30 minutes for the next 6 hours
• every hour until 24 hours from treatment.
3. If the patient develops severe headache, acute hypertension,
nausea or vomiting --> discontinue the rt-PA, obtain a CT scan of
brain.
4. Measure blood pressure
• every 15 minutes for the first 2 hours
• every 30 minutes for the next 6 hours
• every hour until 24 hours from treatment.
47. Post thrombolysis care (I)
5. Increase blood pressure measurements if a systolic blood pressure
>180mmHg or diastolic blood pressure >105mmHg is recorded.
Administer anti-hypertensive
6. Delay placement of NG tube, CBD, arterial line.
7. Avoid antiplatelet drugs for the first 24 hours after rt-PA.
58. Question 1
A 50 year-old man presents to you with
right-sided hemiparesis upon waking up in
the morning. Urgent CT brain shows early
changes over the left MCA territory. What
is your next step?
A. order for MRI brain
B. order for CT Angiogram
C. order for CT perfusion C
D. start thrombolysis
E. Echocardiogram c
59. Question 2
What is the contraindication of IV
Alteplase in acute stroke?
A. BP > 180/90 mmHg
B. Major surgery within 3 months
C. Hypodensity > 1/3 of the cerebral
hemisphere
D. INR > 1.2
E. Age > 80
c
60. Question 3
• Which of the following is TRUE regarding NIHSS assessment?
A. While assessing question 1b, 2 point should be given if the
patient has severe dysarthria or is intubated
B. For sensory assessment, 1 point is given for quadriplegic patient
C. Limb ataxia should not be scored if the patient has dense
hemiplegia
D. Best language cannot be assessed in intubated patient
E. No points should be given for visual assessment if the patient
was blind before the stroke
c
61. Question 4
• Which of the following is NOT early changes of infarction on CT brain?
• A. Hypodensity
• B. Loss of sulcus
• C. Loss of insular ribbon
• D. Dot’s sign
• E. Poor grey-white differentiation
A
62. Question 5
• Regarding clinical features of stroke
• A. lower limb weakness is worse than upper limb weakness in MCA infarction
• B. Abulia in a common presentation in posterior circulation infarction
• C. Cortical signs are present in lacunar infarction
• D. The common sites of lacunar infarction include basal ganglia, internal
capsule, thalamus, cerebellum and pons
• E. Visual neglect is a feature of posterior circulation infarction
D