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.


Cardiac causes of IS.High risk AF – MS –AMI – recent IE – NVAF-

dilated cardiomyopathy.Moderate risk Remote MI – PFO – TR – hypertrophic

myopathy- aterial myxoma


AF


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.


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.


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


Amaurosis fugax is the sole feature that distinguishes the carotid artery syndrome from a middle cerebral artery (MCA)


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.


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.


Top of the basilar syndrome (characterized by visual, oculomotor, and behavioral abnormalities, often without significant motor dysfunction)


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

MRI & MRA

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).

ischaemic stroke

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