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STROKE
Prepared by: Anish Dhakal (Aryan)
PAHS MBBS 5th Batch
OBJECTIVES
• To discuss about stroke focusing on its management
modalities
• Transient ischaemic attack (TIA). Describes a stroke in which
symptoms resolve within 24 hours-an arbitrary cutoff which
has little value in practice
AHA defines TIA as: ‘A transient episode of neurological
dysfunction caused by focal brain, spinal cord or retinal
ischemia without acute infarction.’
• Stroke.
• Stroke is the term used to describe episodes of focal brain
dysfunction due to focal ischaemia or haemorrhage
• This is the term reserved for those events in which symptoms
last more than 24 hours.
• Progressing stroke (or stroke in evolution). This describes a
stroke in which the focal neurological deficit worsens after
the patient first presents. Such worsening may be due to
increasing volume of infarction, haemorrhagic
transformation or increasing oedema.
• Completed stroke. This describes a stroke in which the focal
deficit persists and is not progressing.
Variable Clinical Features Score
Consciousness Alert
Drowsy, Stupor
Semicoma, Coma
+0 x 2.5
+1 x 2.5
+2 x 2.5
Vomiting No
Yes
+0 x 2
+1 x 2
Headache [within 2 hrs] No
Yes
+0 x 2
+1 x 2
Diastolic BP ____mm of Hg +__ x 0.1
Atheroma Markers
[DM, Angina,
Intermittent Claudication]
None
One or More
-0 x 3
-1 x 3
Constant -12
SRIRAJ SCORING
• <-1 Ischemic stroke
• -1 to +1 Equivocal
• >+1 Hemorrhagic stroke
• Formula:
(2.5 * consciousness) + ( 2 * vomiting) + ( 2 * headache) + (
0.1* DBP) – ( 3 * atheroma) – 12
SRIRAJ SCORING
• <=3 Infarction
• 3-11 Equivocal
• >=11 Hemorrhage
GREEK SCORING
Sign/ Symptoms Points
Neurological detoriation within 3 hours of admission 6
Vomiting 4
White cell count >12000 4
Decreased level of consciousness 3
RISK FACTORS
Fixed
• Age
• Gender (male > female, except in
the very young and very old)
• Race (Afro-Caribbean > Asian >
European)
• Heredity
• Previous vascular event, e.g.
myocardial infarction, stroke or
peripheral embolism
• High fibrinogen
Modifiable
• High Blood pressure
• Heart disease (atrial fibrillation,
heart failure, endocarditis)
• Diabetes mellitus
• Hyperlipidaemia
• Smoking
• Excess alcohol consumption
• Polycythaemia
• Oral contraceptives
CLINICAL FEATURES
INVESTIGATION
• Most acute ischemic strokes are not visualized by
noncontrast CT in early hours but it helps to exclude
intracranial bleeding, abscess, tumor and other
stroke mimics
• Within 48 hours, CT identifies all parenchymal
hemorrhages >1cm in diameter and up to 95% of
subarachnoid hemorrhage.
• Routine bloods (CBC, ESR, blood glucose, clotting
studies, lipid profile)
• Chest X-ray
• ECG, Echo
• Doppler ultrasound, MR/CT angiography
SUPPORTIVE CARE
• Management is aimed at minimizing the volume of brain that
is irreversibly damaged, preventing complications, reducing
the patient’s disability and handicap and to reduce recurrent
stroke risk and other vascular events
• Neurological signs may worsen over time due to lacunar
infarcts, extension of infarction, haemorrhagic transformation
or development of oedema with consequent mass effect
• Airway: Detect dysphagia early. NPO if swallowing unsafe or
risk of aspiration
• Breathing/Hypoxia: Routine oxygen administration does
not improve survival. Give oxygen if saturation <95%
ASA/AHA guidelines recommend oxygen therapy only as
necessary to maintain saturation ≥92%
• Nutrition: If dysphagia persists for >48 hours start feeding by
nasogastric tube
• Pressure areas: Treat infection, pressure relieving mattress,
mobilize bedridden patients
• Incontinence: Avoid catheterization unless patient is in acute
urinary retention or incontinence is threatening pressure areas
• Coagulation abnormalities should be reversed asap
• Hyperpyrexia: Treat underlying cause and symptoms
• Hyperglycaemia: Treat when ≥200 mg/dL
Higher brain temperature and higher blood glucose both have been
reported to increase volume of infarction for a certain amount of
reduction in cerebral perfusion
• Hydration: Fluids parentally or by nasogastric tube.
However volume expansion and hemodilution has
significantly improved outcomes in severely polycythaemia
stroke patients
• Blood Pressure: Unless heart or renal failure, evidence of
hypertensive encephalopathy or aortic dissection do not
lower blood pressure
• Several studies demonstrated correlation of poor outcomes
and hypertension. However poor outcomes also have been
repeatedly associated with active attempts to lower blood
pressure
BLOOD PRESSURE GUIDELNES
• AHA/ASA recommends
For patients who are not candidates for thrombolytics or
reperfusion methods, guidelines call for permissive
hypertension: No attempts to reduce bp unless systolic
and diastolic bp are greater than 220 and 120 mm Hg
For patients who are candidates for thrombolytic therapy
(rtPA) reduce blood pressure to acceptable limits (>185
mmHg systolic and >110 mmHg diastolic is CI to
Thrombolytic therapy)
THROMBOLYSIS
• FDA approved the use of IV rtPA in acute ischemic stroke
within 3 hours of stroke onset( European Stroke Guidelines
suggest for up to 4.5 hours)
• The time of symptom onset is defined as the last moment
the patient was known to be at baseline
• Intravenous thrombolysis with rtPA increases the risk of
haemorrhagic transformation of the cerebral infarct with
potentially fatal results ( In a double blind study by
National Institute of Health intracerebral haemorrhage
occurred in 6.4% with 45% mortality)
THROMBOLYSIS
• The decision should be individualized for thrombolytic
therapy.
• Do not wait for lab results unless pathologic or iatrogenic
coagulopathy is suspected.
• Total dose of rtPA is 0.9mg/kg (max. 90mg); 10% of the
dose as bolus, rest infused over 60 mins
• Blood pressure and neurologic checks every 15 minutes for 2
hours
• No anticoagulants or antiplatelet agents in initial 24
hours following treatment
ANTIPLATELET THERAPY
• Contraindicated in Acute hemorrhagic stroke
• Start 300 mg of aspirin daily if rtPA is not given( reduce
to 75mg/day after several days)
• If thrombolytic therapy is given withheld it for next 24 hours
• Meta analysis suggest combination antiplatelet therapy
is superior than monotherapy to prevent recurrent stroke
(mostly with dipyridamole)
• By rectal suppository or nasogastric tube in dysphagic
patients
ANTICOAGULANT THERAPY
• Extensively used (heparin) in past to decrease risk of
thromboembolism and early ischemic recurrence
• ASA recommends anticoagulant therapy not to be started in
ED but in the inpatient setting with warfarin in presence of
atrial fibrillation
• Heparin though seems helpful increases risk of both intracranial
and extra cranial haemorrhage in first 48 hours
• A Cochrane meta analysis of 8 randomized controlled trials
(22,125 patients) found no net benefit of anticoagulants in
acute stroke; so it cannot be recommended even in presence
of atrial fibrillation
• Still may be useful for some patients like those with MI
MANAGEMENT OF RISK
FACTORS
• Long term antiplatelet drugs therapy and statins to lower
cholesterol
• For patients in atrial fibrillation, risk can be reduced by about
60% with oral anticoagulation to archive INR of 2-3
• Blood pressure reduction also is helpful for both ischemic
and haemorrhagic stoke patients to prevent recurrence
• Surgical methods like carotid endarterectomy and
angioplasty may be considered in severe cases
REFERENCES
• Tintinallis Emergency Medicine, A Comprehensive Study
Guide 7th edition
• Harrison’s Principles of Internal Medicine, 19th edition
• Davidson’s Principles and Practice of Medicine, 22nd edition
Stroke (Cerebrovascular Accident)

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Stroke (Cerebrovascular Accident)

  • 1. STROKE Prepared by: Anish Dhakal (Aryan) PAHS MBBS 5th Batch
  • 2. OBJECTIVES • To discuss about stroke focusing on its management modalities
  • 3. • Transient ischaemic attack (TIA). Describes a stroke in which symptoms resolve within 24 hours-an arbitrary cutoff which has little value in practice AHA defines TIA as: ‘A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction.’ • Stroke. • Stroke is the term used to describe episodes of focal brain dysfunction due to focal ischaemia or haemorrhage • This is the term reserved for those events in which symptoms last more than 24 hours.
  • 4. • Progressing stroke (or stroke in evolution). This describes a stroke in which the focal neurological deficit worsens after the patient first presents. Such worsening may be due to increasing volume of infarction, haemorrhagic transformation or increasing oedema. • Completed stroke. This describes a stroke in which the focal deficit persists and is not progressing.
  • 5.
  • 6.
  • 7. Variable Clinical Features Score Consciousness Alert Drowsy, Stupor Semicoma, Coma +0 x 2.5 +1 x 2.5 +2 x 2.5 Vomiting No Yes +0 x 2 +1 x 2 Headache [within 2 hrs] No Yes +0 x 2 +1 x 2 Diastolic BP ____mm of Hg +__ x 0.1 Atheroma Markers [DM, Angina, Intermittent Claudication] None One or More -0 x 3 -1 x 3 Constant -12 SRIRAJ SCORING
  • 8. • <-1 Ischemic stroke • -1 to +1 Equivocal • >+1 Hemorrhagic stroke • Formula: (2.5 * consciousness) + ( 2 * vomiting) + ( 2 * headache) + ( 0.1* DBP) – ( 3 * atheroma) – 12 SRIRAJ SCORING
  • 9. • <=3 Infarction • 3-11 Equivocal • >=11 Hemorrhage GREEK SCORING Sign/ Symptoms Points Neurological detoriation within 3 hours of admission 6 Vomiting 4 White cell count >12000 4 Decreased level of consciousness 3
  • 10. RISK FACTORS Fixed • Age • Gender (male > female, except in the very young and very old) • Race (Afro-Caribbean > Asian > European) • Heredity • Previous vascular event, e.g. myocardial infarction, stroke or peripheral embolism • High fibrinogen Modifiable • High Blood pressure • Heart disease (atrial fibrillation, heart failure, endocarditis) • Diabetes mellitus • Hyperlipidaemia • Smoking • Excess alcohol consumption • Polycythaemia • Oral contraceptives
  • 12.
  • 13.
  • 14.
  • 15.
  • 16. INVESTIGATION • Most acute ischemic strokes are not visualized by noncontrast CT in early hours but it helps to exclude intracranial bleeding, abscess, tumor and other stroke mimics • Within 48 hours, CT identifies all parenchymal hemorrhages >1cm in diameter and up to 95% of subarachnoid hemorrhage. • Routine bloods (CBC, ESR, blood glucose, clotting studies, lipid profile) • Chest X-ray • ECG, Echo • Doppler ultrasound, MR/CT angiography
  • 17.
  • 18. SUPPORTIVE CARE • Management is aimed at minimizing the volume of brain that is irreversibly damaged, preventing complications, reducing the patient’s disability and handicap and to reduce recurrent stroke risk and other vascular events • Neurological signs may worsen over time due to lacunar infarcts, extension of infarction, haemorrhagic transformation or development of oedema with consequent mass effect • Airway: Detect dysphagia early. NPO if swallowing unsafe or risk of aspiration • Breathing/Hypoxia: Routine oxygen administration does not improve survival. Give oxygen if saturation <95% ASA/AHA guidelines recommend oxygen therapy only as necessary to maintain saturation ≥92%
  • 19. • Nutrition: If dysphagia persists for >48 hours start feeding by nasogastric tube • Pressure areas: Treat infection, pressure relieving mattress, mobilize bedridden patients • Incontinence: Avoid catheterization unless patient is in acute urinary retention or incontinence is threatening pressure areas • Coagulation abnormalities should be reversed asap • Hyperpyrexia: Treat underlying cause and symptoms • Hyperglycaemia: Treat when ≥200 mg/dL Higher brain temperature and higher blood glucose both have been reported to increase volume of infarction for a certain amount of reduction in cerebral perfusion
  • 20. • Hydration: Fluids parentally or by nasogastric tube. However volume expansion and hemodilution has significantly improved outcomes in severely polycythaemia stroke patients • Blood Pressure: Unless heart or renal failure, evidence of hypertensive encephalopathy or aortic dissection do not lower blood pressure • Several studies demonstrated correlation of poor outcomes and hypertension. However poor outcomes also have been repeatedly associated with active attempts to lower blood pressure
  • 21. BLOOD PRESSURE GUIDELNES • AHA/ASA recommends For patients who are not candidates for thrombolytics or reperfusion methods, guidelines call for permissive hypertension: No attempts to reduce bp unless systolic and diastolic bp are greater than 220 and 120 mm Hg For patients who are candidates for thrombolytic therapy (rtPA) reduce blood pressure to acceptable limits (>185 mmHg systolic and >110 mmHg diastolic is CI to Thrombolytic therapy)
  • 22. THROMBOLYSIS • FDA approved the use of IV rtPA in acute ischemic stroke within 3 hours of stroke onset( European Stroke Guidelines suggest for up to 4.5 hours) • The time of symptom onset is defined as the last moment the patient was known to be at baseline • Intravenous thrombolysis with rtPA increases the risk of haemorrhagic transformation of the cerebral infarct with potentially fatal results ( In a double blind study by National Institute of Health intracerebral haemorrhage occurred in 6.4% with 45% mortality)
  • 23.
  • 24. THROMBOLYSIS • The decision should be individualized for thrombolytic therapy. • Do not wait for lab results unless pathologic or iatrogenic coagulopathy is suspected. • Total dose of rtPA is 0.9mg/kg (max. 90mg); 10% of the dose as bolus, rest infused over 60 mins • Blood pressure and neurologic checks every 15 minutes for 2 hours • No anticoagulants or antiplatelet agents in initial 24 hours following treatment
  • 25. ANTIPLATELET THERAPY • Contraindicated in Acute hemorrhagic stroke • Start 300 mg of aspirin daily if rtPA is not given( reduce to 75mg/day after several days) • If thrombolytic therapy is given withheld it for next 24 hours • Meta analysis suggest combination antiplatelet therapy is superior than monotherapy to prevent recurrent stroke (mostly with dipyridamole) • By rectal suppository or nasogastric tube in dysphagic patients
  • 26. ANTICOAGULANT THERAPY • Extensively used (heparin) in past to decrease risk of thromboembolism and early ischemic recurrence • ASA recommends anticoagulant therapy not to be started in ED but in the inpatient setting with warfarin in presence of atrial fibrillation • Heparin though seems helpful increases risk of both intracranial and extra cranial haemorrhage in first 48 hours • A Cochrane meta analysis of 8 randomized controlled trials (22,125 patients) found no net benefit of anticoagulants in acute stroke; so it cannot be recommended even in presence of atrial fibrillation • Still may be useful for some patients like those with MI
  • 27. MANAGEMENT OF RISK FACTORS • Long term antiplatelet drugs therapy and statins to lower cholesterol • For patients in atrial fibrillation, risk can be reduced by about 60% with oral anticoagulation to archive INR of 2-3 • Blood pressure reduction also is helpful for both ischemic and haemorrhagic stoke patients to prevent recurrence • Surgical methods like carotid endarterectomy and angioplasty may be considered in severe cases
  • 28.
  • 29. REFERENCES • Tintinallis Emergency Medicine, A Comprehensive Study Guide 7th edition • Harrison’s Principles of Internal Medicine, 19th edition • Davidson’s Principles and Practice of Medicine, 22nd edition

Editor's Notes

  1. Iby poor circulation of the blood to the affected area. The poor blood flow is often a result of atherosclerotic blockages more proximal to the affected area;[3] individuals with intermittent claudication may have diabetes—often undiagnosed