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STROKE- DISCUSSION AND MANAGEMENT
Stroke- Discussion
• About 15 million people suffer from stroke every year worldwide
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Ischaemic stroke (85%)
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Non traumatic SAH (< 5%)
Clinical:
Oxfordshire Community Stroke Project criteria (Appendix A)
1
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Partial anterior circulation stroke (PACS)
3
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Posterior circulation stroke (POCS)
Aetiological: TOAST Classification
1
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Cardiogenic embolism
3
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Stroke of other determined aetiology
5
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Diagnosis
Stroke is a medical emergency
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Every patient suspected of acute stroke should under go NCCT brain
to exclude ICH (hyper dense)
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But ischaemia might take time to appear in NCCT
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This region
is very sensitive to ischaemia as it’s the furthest from collateral flow
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But it’s not cost
effective -> not routinely done
DW is positive at acute phase & then become brighter up to 7th day
ADC will be of low signal intensity with maximum at 24 hours & then increase signal intensity, finally
become bright in chronic stage
T2W doesn’t show early infarct
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When compared to T2W in chronic phase, DWI will show
more affected brain volume -> salvageable brain tissue

Haemorrhagic stroke
Non modifiable: age, male,
amyloid angiopathy (in elderly)
Modifiable: HTN (main factor)
Otherantiplatelet & anticoagulant,
alcohol excess, substance abuse
(cocaine)

This concept of salvageable brain tissue (penumbra) is the basis of acute management
Penumbra: clinically symptomatic area, but if reperfused, can be reversed
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Area is temporarily
supported by leptomeningeal collateral flow
Future: There are new scans (CT perfusion scans or MRI DWI & FLARE, MRI mismatch ratio)
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Aim of management
Achieve recanalization & reperfusion of ischaemic penumbra in appropriately selected patients to
salvage ischaemic, but viable brain tissue
Ideally managed in a acute stroke units where a stroke specific multi disciplinary team is working

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5 hours (ideally < 3 hrs)
Thrombectomy- up to 6 hours
(But in both, earlier intervention ensures better outcomes)
• Mechanical thrombectomy is beneficial in proximal large artery occlusions in anterior circulation
• Once NCCT brain done, if facilities for thrombectomy available & clinically a large artery occlusion
is suspected a CT angiogram of neck & intracerebral vessels performed
• RBS, ECG, FBC and INR/APTT and other relevant blood investigations done
• However, thrombolysis should not be delayed until investigation results are available except RBS
• Eligibility criteria for thrombolysis should be checked (Appendix B)
• NIHSS score should be calculated and documented (Appendix C)
Patient should have a fixed, measurable neurological deficit to undergo thrombolysis
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This deficit shouldn’t be rapidly recovering (that can be a TIA)
• Informed consent in writing for thrombolysis & thrombectomy (if patient can’t give consent, take
consent by proxy
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Tenecteplase better)
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9mg/kg (maximum 90mg)
with 10% administered as a bolus over 1 minute & remainder as an infusion over an hour
• Door to needle time < 1 hour (maximum 90 minutes)
• Blood pressure
BP ≤ 185/110 mmHg before administering rtPA
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Mechanical thrombectomy treatment should be started
as quickly as possible, should not be delayed to assess response to IV rtPA
Patients with ischaemic stroke who are not thrombolysed
• Aspirin 300 mg loading dose immediately followed by 75 to 150 mg daily thereafter (2 weeks)
• If not thrombolysed, BP is not treated acutely unless extreme (>220/120 mmHg), or patient has
ACS, HF, aortic dissection, hypertensive encephalopathy, ARF or preeclampsia/eclampsia

• When treatment is indicated, cautious lowering of BP is recommended (if BP acutely reduced,
there’s risk of increasing size of infarction
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Keep it at 140/90 Hgmm)
Decompressive hemicraniectomy
Recommended in patients aged 60 years or younger with massive MCA territory infarction with:
o Infarct size >50% of MCA territory (or infarct volume > 145 cm3 on DW-MRI)
o Clinical deficit attributable to MCA infarct
o NIHSS score >15 associated with a decreased level of consciousness
o A pre-stroke modified Rankin Scale score of < 2
o If surgery can be initiated within 48 hours of stroke onset
For otherwise healthy patients who are older than 60 years or within 48 - 96 hours after malignant
MCA infarct onset, decompressive hemicraniectomy remains an option on a case-by-case basis
4
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Excess free water,
hypotonic fluids and 5% dextrose should be avoided
Glycaemic control
Both hyperglycaemia & hypoglycaemia augment brain injury
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Elevation of head of bed to 30o
may be necessary if at risk for increased ICP, aspiration or cardiopulmonary decompensation
Dysphagia
• Swallowing assessment done within first 24 hours & before feeding or administering drugs orally
• Nasogastric feeding initiated if dysphagia present & efforts are continued to improve swallowing
• Percutaneous endoscopic gastrostomy (PEG): if dysphagia is expected to persist for > 4 weeks
Body temperature control
• Fever may contribute to brain injury in acute stroke
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Effective rehabilitation needs coordinated
contribution of a MDT (neurologist/ physician, nurse/s, physiotherapists, occupational therapists,
speech & language therapists, mental health specialist and a social services officer)
Team members should meet at least once per week to discuss the progress of the patient and to set
goals for the oncoming week
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There is a risk of about similar magnitude for other vascular events such as myocardial
infarction
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So, it is important to start
secondary prevention strategies in all patients ASAP
Life style modifications
• Quit smoking & avid passive smoking
• Exercise (moderate intensity- sufficient to break a sweat or noticeable raise in HR) 150 mins/ week
• Modifications in diet
Pharmacological therapy
Hypertension
• Goal is to maintain BP < 140/ 90 Hgmm
• Start 10 days after stroke, in previously untreated patients whose BP is persistently elevated
Lipid lowering therapy
• High intensity statin therapy (atorvastatin 40-80 mg or rosuvastatin 20-40 mg)

• Expected to reduce LDL-C level by 50 %
• Use cautiously in patients with a PHx of ICH as there may be an increased risk of further ICH
Antiplatelet drugs
For ischaemic strokes;
• Aspirin 300 mg should be started in all patients within 48 hours to prevent early re-infarctions
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Vitamin K antagonist – warfarin is recommended for
valvular AF while warfarin or any one of the non-vitamin K antagonist newer oral anticoagulants
(NOACs: dabigatran, apixaban, rivaroxaban and edoxaban) is recommended for non-valvular AF
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recently symptomatic carotid stenosis of 70 to 99 %
b
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Diagnosis & evaluation
• Prompt recognition of symptoms of TIA
Sudden onset transient focal neurological signs: hemiparesis, dysphasia, dysarthria, amaurosis
fugax, hemianopia, diplopia
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Medical management
• Clopidogrel 300 mg stat & 75 mg daily + aspirin 300 mg stat & 150 mg daily for 21 days
• Clopidogrel or aspirin alone should be continued indefinitely after 21 days
Spontaneous intracerebral haemorrhage
1
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Timing of 2nd imaging is based on patient’s clinical progress
Aetiology
Hypertension
Amyloid angiopathy

Nature of haemorrhage
Supra-tentorial: internal capsule, basal ganglia
Infra-tentorial: cerebellar, pontine haemorrhage
Entire lobe haemorrhage or small, multiple haemorrhage

2
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Acute management
Monitoring
• Vital parameters, Body temperature, Level of consciousness, Blood glucose, Oximetry
Anticoagulation related ICH

Goal is to normalize INR in those whose INR is elevated due to Vitamin K antagonist (VKA)
• Withhold VKA
• Fresh frozen plasma (FFP), Vitamin K intravenously)
However, high doses of vit
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General management
Same as ischaemic stroke
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Others survive because a clot or vasospasms have occluded
aneurysmal bleeding
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So, aim is to prevent re bleeds
Risk factors
• Non-modifiable: Female sex, increasing age (mean age 50 years), Family history of SAH, hx of
aneurysm in 1st degree relatives (specially in 2 or more), Genetic (AD PCKD, type IV Ehlers Danlos xn)
• Modifiable: Hypertension, cigarette smoking, heavy alcohol use, sympathomimetic drugs (cocaine)
Clinical presentation
• Sudden onset severe/ worst-ever/ thunderclap headache or unexplained loss of consciousness
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Focal neurological signs and seizures may occur in some
Predictive factors of prognosis
Depends on neurologic grade on admission, age & amount of blood on initial cranial CT
World Federation of Neurological Surgeons (WFNS) grading system is widely used for neurologic
grading of patients with SAH (Appendix F)
Diagnosis of SAH
• NNCCT head as early as possible
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CSF is
centrifuged & supernatant be visually examined for xanthochromia
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Hyponatremia, in
particular, is common; sodium levels should be checked at least daily
• Patients should be given stool softeners, kept at strict bedrest & given analgesia (short acting
opiates) to diminish haemodynamic fluctuations & lower the risk of rebleeding
• Plasma glucose & body temperature regularly monitored & maintained within normal limits
• All anticoagulants and antiplatelet agents should be discontinued
• Deep venous thrombosis prophylaxis with pneumatic compression stockings
• MAP ≤ 110 mmHg or SBP < 160mmHg is maintained
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IV labetalol preferred
Nimodipine 60 mg every four hours should be commenced within four days of SAH and continued for
21 days

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