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Transcript of Ischaemic stroke
ISCHAEMIC STROKEOsama RagabLecturer of Neurology
Tanta University2016
Definition
Stroke is defined as an episode of focal neurologic (brain, retina, spinal cord) dysfunction (even if less than 24 hours in duration) in which the autopsy, computed tomography (CT) brain scan, or magnetic resonance imaging (MRI) brain scan shows features consistent with focal brain infarction or hemorrhage .
Ischaemic stroke is responsible for about 80% of all strokes, intracerebral haemorrhage for 15%, and subarachnoid haemorrhage for 5%
Risk Factors for Stroke
classified as modifiable and unmodifiable risk for ischemic stroke
- Nonmodifiable risk factors for stroke include older age, male gender, ethnicity, family history, and prior history of stroke.
- Modifiable risk factors may be subdivided into lifestyle and behavioral risk factors and non-lifestyle factors,
modifiable lifestyle risk factors include cigarette consumption and illicit drug use,
Non-lifestyle risk factors include low socioeconomic status, arterial hypertension, dyslipidemia, heart disease, and asymptomatic carotid artery disease.
Risk Factors for Stroke
Cardiac causes of IS.High risk AF – MS –AMI – recent IE – NVAF-
dilated cardiomyopathy.Moderate risk Remote MI – PFO – TR – hypertrophic
myopathy- aterial myxoma
Risk Factors for Stroke
AF
Risk Factors for Stroke
arterial hypertension, reduction in SBP of 10 to 12 mm Hg and 5 to 6 mm Hg diastolic is associated with a 38% reduction in stroke incidence. Type 2 DM, Diabetic persons with retinopathy and autonomic neuropathy have high risk for ischemic stroke. High total cholesterol and high LDL
concentration:patients at risk for stroke or who have had a cerebral infarction should be treated to a goal LDL level of below 70 mg/dL.
Risk Factors for Stroke
Heredity and Risk of Stroke Nonatherosclerotic vasculopathies Familial atrial myxomas, hereditary
cardiomyopathies . Deficiencies of protein C and S or
antithrombin (AT). Inherited metabolic disorders that can
cause stroke include mitochondrial encephalopathy and homocystinuria.
Risk Factors for Stroke
Brain blood supply
Brain blood supply
Brain blood supply
Pathophysiology of Cerebral Ischemia
Normal cerebral blood flow at rest in the normal adult brain is approximately 50 to 55 mL/100 g/min.
When blood flow decreases to 18 mL/100 g/min, the brain reaches a threshold for electrical failure.
when blood flow decreases to 8 mL/100 g/min. Cell death can result.
These thresholds mark the upper and lower blood-flow limits of the ischemic penumbra.
Pathophysiology of Cerebral Ischemia
Clinical Syndromes of Cerebral Ischemia
Transient Ischemic AttacksTIA is a temporary and “non-marching” neurological deficit of sudden onset; attributed to focal ischemia of the brain, retina, or cochlea; and lasting less than 1 hours with free DW MRI.
ABCD2 ≥ 4 moderate to high stroke risk & in need for hospital admission.
Clinical Syndromes of Cerebral Ischemia
MCA occlusion Motor & sensory deficit (Face > UL >LL) homonymous hemianopia Gaze preference Dominant hemisphere: aphasia Non dominant hemisphere : neglect
Carotid Artery System Syndromes
ACA occlusion Motor +/- Sensory deficit (LL>> Face,
UL) Primitive reflexes grasp, sucking reflexes Gait apraxia Abulia , akinetic mutism, paratonia
Carotid Artery System Syndromes
Amaurosis fugax is the sole feature that distinguishes the carotid artery syndrome from a middle cerebral artery (MCA)
Carotid Artery System Syndromes
Alexia with agraphia may occur with left-sided angular gyrus involvement.
Gerstmann syndrome, which consists of finger agnosia, acalculia, right-left disorientation, and agraphia, may be seen with dominant-hemisphere parietal lesions.
Anosognosia, the denial of hemiparesis, is most commonly associated with right hemispheric strokes.
Nondominant infarction may cause hemi-inattention, tactile extinction, visual extinction, anosognosia, apraxia, impaired prosody, and (rarely) acute confusion and agitated delirium.
Carotid Artery System Syndromes
Lacunar SyndromesThe five best recognized
syndromes are: (1) pure motor hemiparesis(2) pure sensory stroke.(3) sensory motor stroke.(4) ataxic hemiparesis.(5) dysarthria–clumsy hand syndrome:
Vertebrobasilar System Syndromes
PCA cclusion Dominant hemisphere can create the interesting
phenomenon of alexia without agraphia. Bilateral occipital lobe damage can lead to
cortical blindness with denial of deficits and confabulation (Anton syndrome)
More extensive bilateral PCA infarctions affecting the posterior parietal lobes cause oculomotor apraxia, optic ataxia ,and simultagnosia a condition known as Balint syndrome .
Brain stem infarctionDistubed conc level.Crossed hemiparesis.Lower motor cranial neuropathy.Diplopia -dysphagia- dysartheria.AtaxiaHorner syndrome.
Vertebrobasilar System Syndromes
Top of the basilar syndrome (characterized by visual, oculomotor, and behavioral abnormalities, often without significant motor dysfunction)
Vertebrobasilar System Syndromes
Differential diagnosis Seizure Migraine Encephalitis- Abcess Gliomas Demylination Hypoglycaemia Conversion Metabolic encephalopathy
Work upNeuro – imaging
CT and CTA MRI – MRA Carotid duplex and TCD
CT & CTA HDMCA sign
Insular ribbon sign
CT & CTA
Sulci effacement
CT & CTA
Lentiform obscuration
CT & CTA
CT & CTA
CT & CTA
CT & CTA
CT & CTA
MRI & MRA
MRI & MRA
MRI & MRA
MRI & MRA
MRI & MRA
MRI & MRA
TCD
aetiology investigtion Echo –cardiography. Extra and intracranial duplex. CTA & MRA. Lipid profile Coagulation profile ESR and vasculitic work up Homocystien – APLS- Anti thrombin –
sickle cell
management assess the patient’s airway, breathing,
and circulation (ABCs); stabilize the patient as necessary; and complete initial evaluation and assessment, including imaging and laboratory studies, within 60 minutes of patient arrival.
The central goal of therapy in acute ischemic stroke is to preserve tissue in the ischemic penumbra.
Oxygen supplementation Supplemental oxygen is recommended when the
patient has a documented oxygen requirement (ie, oxygen saturation < 95%).
In the small proportion of patients with stroke who are relatively hypotensive, administration of IV fluid, vasopressor therapy, or both may improve flow through critical stenoses.
Hypoglycemia and hyperglycemia Hypoglycemia needs to be identified and treated
early in the evaluation
management
Blood pressure: optimal management of blood pressure in acute stroke is uncertain. Blood pressure is often elevated on admission, but tends to decrease spontaneously during the first few days, while existing antihypertensive therapy should be continued.
Cerebral autoregulation is disturbed after stroke, so lower levels of hypertension should probably not be treated in the acute phase, except in patients with coexistent hypertensive encephalopathy, aortic dissection, acute myocardial infarction or severe left ventricular failure
management
Patient otherwise eligible for acute reperfusion therapy, except that BP is >185/110 mmHg
If heart rate >55 beats per minute:
– Labetalol 10–20 mg IV over 1–2 minutes; may repeat one time
or
– Metoprolol 5 mg IV over 3–5 minutes; may repeat in 5 minutes, two times, if necessary
or
• Nicardipine 5 mg/hr IV; titrate up by 2.5 mg/hr every 5–15 minutes, maximum 5 mg/hr; when desired BP reached, adjust to maintain proper BP limits
or
• Hydralazine 5 mg IV over 1 minute; may repeat 5 mg IV bolus in 5 minutes
– If systolic BP still >180 mmHg, give 10 mg IV bolus every 5 minutes until target systolic BP reached
– Increase to 20 mg bolus if required
– Maximum hydralazine dose = 240 mg
or
• Other agents (e.g. enalaprilat) may be considered when appropriate
Management of BP during and after r-tPA or other acute reperfusion therapy to maintain BP at or below 180/105 mmHg:
Monitor BP every 15 minutes for 2 hours from the start of r-tPA therapy, then every 30 minutes for 6 hours, and then every hour for 16 hours.
If systolic BP>180–230 mmHg or diastolic BP >105–120 mmHg:
– Labetalol 10 mg IV followed by continuous IV infusion 2–8 mg/min
Fibrinolytic Therapy
Thrombolysis with intravenous r tPA, alteplase, should be considered in all patients with a definite disabling ischemic stroke who can be treated within 4.5 hours of onset of focal neurologic symptoms that have been present for at least 30 minutes without significant improvement.
Inclusion criteria
Diagnosis of ischemic stroke causing measurable neurological deficit Onset of symptoms <3 hours before beginning treatment Aged ≥18 years
Exclusion criteria
Significant head trauma or prior stroke in previous 3 months Symptoms suggest subarachnoid hemorrhage Arterial puncture at noncompressible site in previous 7 days History of previous intracranial hemorrhage Intracranial neoplasm, arteriovenous malformation, or aneurysm Recent intracranial or intraspinal surgery Elevated blood pressure (systolic >185 mm Hg or diastolic >110 mm Hg) Active internal bleeding Acute bleeding diathesis, including but not limited to Platelet count <100 000/mm3 Heparin received within 48 hours, resulting in abnormally elevated aPTT
greater than the upper limit of normal Current use of anticoagulant with INR >1.7 or PT >15 seconds Current use of direct thrombin inhibitors or direct factor Xa inhibitors with
elevated sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT; TT; or appropriate factor Xa activity assays)
Blood glucose concentration <50 mg/dL (2.7 mmol/L) CT demonstrates multilobar infarction (hypodensity >1/3 cerebral
hemisphere)
Relative exclusion criteria
Only minor or rapidly improving stroke symptoms (clearing spontaneously)
Pregnancy Seizure at onset with postictal residual neurological impairments Major surgery or serious trauma within previous 14 days Recent gastrointestinal or urinary tract hemorrhage (within previous 21
days) Recent acute myocardial infarction (within previous 3 months)
Intra-arterial thrombolysis requires specialized facilities and experienced neuroradiologists, limiting its widespread applicability. Moreover, the need to establish arterial access increases the delay to treatment compared with the intravenous route .
There are therefore studies in progress investigating the benefits of arterial thrombolysis following an initial intravenous dose of alteplase, to determine if this combination results in superior outcomes in patients who do not initially benefit from an intravenous agent. Intra-arterial thrombolysis may also have a particular role in patients with basilar artery thrombosis, possibly up to 12 hours after onset, particularly if infarction in the posterior circulation has not yet developed (Furlan et al., 2015).
Fibrinolytic Therapy
Mechanical recanalization
A number of devices are being developed to extract or break up thrombus occluding the larger intracranial blood vessels following acute ischaemic stroke, using microcatheters
Antiplatelet therapy with aspirin/ acetylsalicylic acid
All acute stroke patients not already on an antiplatelet agent should be given at least 160 mg of aspirin immediately as a one time loading dose (evidence level A). In patients treated with r tPA, aspirin should be delayed until after the 24 hour post thrombolysis scan has excluded intracranial hemorrhage (evidence level B).In patients already on aspirin prior to ischemic stroke or transient ischemic attack, clopidigrel may be considered as an alternative (evidence level B). If patients have a recent (within the past 24 hours) TIA or minor ischemic stroke, clopidogrel may be added to aspirin for the first 21–90 days (evidence level B)
Anticoagulation therapy
The data do not support the routine use of any of the currently available anticoagulants in acute ischemic stroke to prevent early recurrent stroke.
Early mobilization and adequate hydration should be encouraged for all acute stroke patients (evidence level C).
Patients at high risk of venous thromboembolism should be started on venous thromboembolism prophylaxis immediately (evidence level A).
LMWH should be considered for patients with acute ischemic stroke at high risk of venous thromboembolism; or UFH for patients with renal failure (evidence level B).
Sub-acute care.
Neuroprotection Currently, data are inadequate to justify the
routine use of heparin or other anticoagulants in the acute management of ischemic stroke.[126] Patients with embolic stroke who have another indication for anticoagulation (eg, atrial fibrillation) may be placed on anticoagulation therapy nonemergently, with the goal of preventing further embolic disease; however, the potential benefits of that intervention must be weighed against the risk of hemorrhagic transformation.[1] For more information
Stroke Prevention
Carotid revascularization CEA should be performed by a surgeon
with a known perioperative morbidity and mortality of less than 6% (evidence level A).
Secondary prevention guidelines
All patients with ischemic stroke or TIA should be prescribed antiplatelet therapy immediately for secondary (evidence level A).
Aspirin, combined aspirin (25 mg) and ER dipyridamole (200 mg), or clopidogrel (75 mg) are all appropriate options (evidence level A).
Long term concurrent use of aspirin and clopidogrel is not recommended for secondary stroke prevention unless there is a compelling indication (evidence level B).
prevention of recurrent ischemic stroke of cardiac origin Patients with TIA and AF should begin oral anticoagulation
(warfarin, dabigatran, rivaroxaban, or apixaban) immediately after brain imaging has excluded intracranial hemorrhage or large infarct (evidence level B).
For patients presenting with acute ischemic stroke and AF, the immediate use of heparin/heparinoid anticoagulation is not recommended (evidence level A).
The optimal timing of oral anticoagulation following acute stroke for patients in AF is unclear; it is common practice to wait 2–14 days and repeat brain imaging (CT or MRI) to rule out asymptomatic intracranial hemorrhage before starting warfarin (evidence level C).