The document discusses stroke management, focusing on transient ischemic attacks and the classification of strokes based on symptom duration and progression. It outlines clinical features, investigative modalities, and supportive care strategies aimed at minimizing brain damage while preventing complications and recurrent vascular events. Additionally, it covers thrombolytic therapy, antiplatelet and anticoagulant treatments, as well as management of risk factors for ischemic and hemorrhagic strokes.
Overview of stroke and the presentation's objectives focusing on management modalities.
Definition and classification of strokes: TIA, progressing stroke, and completed stroke.
Detailed explanation of SRIRAJ and GREEK scoring systems for assessing stroke type and severity.Discussion on fixed and modifiable risk factors that contribute to stroke occurrences.
Investigation methods including CT scans and routine blood tests for accurate diagnosis of stroke.
Care strategies aimed at reducing brain damage and managing complications post-stroke.
Guidelines on blood pressure management for stroke patients, especially around thrombolytic therapy.
Thrombolysis guidelines including timing, dosage of rtPA, and monitoring for side effects post-treatment.
Approaches to using antiplatelet and anticoagulant therapy in stroke patients, discussing benefits and risks.
Long-term management strategies to mitigate risk factors and prevent recurrences of stroke.
List of references used for compiling the information in the presentation on stroke.
• Transient ischaemicattack (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.
7.
Variable Clinical FeaturesScore
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
INVESTIGATION
• Most acuteischemic 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
18.
SUPPORTIVE CARE
• Managementis 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: Ifdysphagia 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: Fluidsparentally 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 approvedthe 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)
24.
THROMBOLYSIS
• The decisionshould 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
• Contraindicatedin 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
• Extensivelyused (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
29.
REFERENCES
• Tintinallis EmergencyMedicine, 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
#8 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