stroke ( ischemic stroke )

10,525 views 59 slides Nov 21, 2016
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About This Presentation

 Is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke.
It can occur
in the caroti...


Slide Content

Ischemic stroke DONE BY : MUSTAFA KHALIL IBRAHIM TBILISI STATE MEDICAL UNIVERSITY 4 th year, 2 st semester, 1 nd group Neurology department

GUIDELINES Epidemiology Introduction Pathophysiology Risk factors Etiology Signs and symptoms Complications Diagnosis Treatments Prevention Rehabilitation Prognosis References

1- Heart disease: 614,348 2- Cancer : 591,699 3- Chronic lower respiratory diseases: 147,101 4-Accidents (unintentional injuries): 136,053 5- Stroke (cerebrovascular diseases): 133,103 6-Alzheimer's disease: 93,541 7-Diabetes : 76,488 8-Influenza and pneumonia: 55,227 9-Nephritis , nephrotic syndrome, and nephrosis : 48,146 10- Intentional self-harm (suicide): 42,773 Number of deaths for leading : causes of death

Stroke is the 5th leading cause of death in the US and is a major cause of disability. Annually, 15 million worldwide suffer a stroke-5 million die and 5 million are permanently disabled . WHO estimates a stroke occurs every 5 seconds. adult ~  800,000 people in the US have a stroke each year. One American dies from a stroke every 4 minutes, on average killing nearly 130,000 Americans each year, that’s 1 of every 20 deaths . About 87% of all strokes are  ischemic stroke , when blood flow to the brain is blocked. Stroke costs the United States an estimated  34 -40$ b illion  each year Total cost of stroke has been estimated at $65.5 billion in 2008. EPIDIMOLOGY

 highest death rates from stroke are in the southeastern United States

Annual Economic Costs of Stroke (All Types) In The US  

INTRODUCTION Stroke is a syndrome consisting of rapidly developing (usually seconds or minutes) symptoms and/or signs of loss of focal (or sometimes global) CNS function. The symptoms last more than 24 hours or lead to death .  Although the brain makes up only 2% of our body weight, it uses 20% of the oxygen you breathe.

Classification of Stroke 12%

A transient ischemic attack (TIA) is sometimes called a "mini-stroke." It is different from the major types of stroke because blood flow to the brain is blocked for only a short time. lasting less than 24 hours - usually no more than 5 minutes caused by embolic, thrombotic or hemodynamic vascular mechanisms . Some transient episodes last longer than 24 hours, yet patients recover completely – reversible ischaemic neurological deficits . Transient ischemic attack (TIA ) :

  Is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke. It can occur in the carotid artery of the neck as well as other arteries. Ischemic stroke

In an embolic stroke, a blood clot or plaque fragment forms somewhere in the body (usually the heart) and travels to the brain. Once in the brain, the clot travels to a blood vessel small enough to block its passage. The clot lodges there, blocking the blood vessel and causing a stroke. About 15% of embolic strokes occur in people with atrial fibrillation ( Afib ). The medical word for this type of blood clot is embolus . : 1- Embolic stroke

A thrombotic stroke is caused by a blood clot that forms inside one of the arteries supplying blood to the brain.   This type of stroke is usually seen in people with high cholesterol levels and atherosclerosis. Two types of blood clots can cause thrombotic stroke: large vessel thrombosis and small vessel disease.   Large Vessel Thrombosis The most common form of thrombotic stroke (large vessel thrombosis) occurs in the brain’s larger arteries. In most cases it is caused by long-term atherosclerosis in combination with rapid blood clot formation. High cholesterol is a common risk factor for this type of stroke. Small Vessel Disease Another form of thrombotic stroke happens when blood flow is blocked to a very small arterial vessel (small vessel disease or lacunar infarction). Little is known about the causes of this type of stroke, but it is closely linked to high blood pressure. 2- Thrombotic stroke

PATHOPHYSIOLOGY When an artery is acutely occluded by thrombus or embolus, the area of the CNS supplied by it will undergo infarction if there is no adequate collateral blood supply. Surrounding a central necrotic zone, an ‘ ischemic penumbra ’ remains viable for a time, i.e. it may recover function if blood flow is restored. CNS ischemia may be accompanied by swelling for two reasons: ● cytotoxic oedema – accumulation of water in damaged glial cells and neurones , ● vasogenic oedema – extracellular fluid accumulation as a result of breakdown of the blood–brain barrier . In the brain, this swelling may be sufficient to produce clinical deterioration in the days following a major stroke, as a result of a rise in intracranial pressure and compression of adjacent structures .

ATHEROSCLEROSIS AND THROMBOSIS Atherosclerosis: decades-long process; progression favored by hypercholesterolemia, HTN, cigarette smoking Fatty streak : yellowish discoloration on intimal surface of blood Focal plaques : eccentric thickening at bifurcations; addition of massive extracellular lipids that displaced normal cells and matrix Complicated fibrous plaques: central a cellular area of lipid covered by a cap of smooth muscle cells and collagen

Atherosclerosis and Thrombus Formation: Arterial Wall Injury Functional alteration of endothelial cell layer Denuding of endothelium Superficial intimal injury Deep intimal & media damage with marked platelet aggregation and mural thrombosis

Thromboembolism

Cardiogenic Emboli Cardiogenic emboli lodge in the middle cerebral artery or its branches in 80% of cases , in the posterior cerebral artery or its branches 10% of the time , and in the vertebral artery or its branches in the remaining 10% of cases.

THE ISCHEMIC PENUMBRA

less well documented Can be changed, treatable, controlled : Cannot Be Changed: Geographic location- s outheastern US > other areas.  so-called "stroke belt" states. Socioeconomic factors- some evidence strokes among low-income people > people with high -income . Alcohol abuse. Drug abuse. Acute infection* High blood pressure. Cigarette smoking. Diabetes mellitus  —Many people with DM have high BP, dyslipidemia and overweight.  Carotid or other artery disease .    Peripheral artery disease. Atrial fibrillation  ~ 15% of embolic strokes occur in people with Afib . Other heart disease - CAD or HF … etc Transient ischemic attacks (TIA). Sickle cell disease. High blood cholesterol . Poor diet. Physical inactivity and obesity   Increased age . Being male . Race (e.g., African-Americans) . Diabetes mellitus . Prior stroke/transient. ischemic attacks . Family history of stroke Asymptomatic carotid bruit. Genetic disorders . RISK FACTORS

UNCOMMON CAUSES COMMON CAUSES Hypercoagulable disorders Protein C deficiency Protein S deficiency Antithrombin III deficiency Antiphospholipid syndrome Factor V Leiden mutation a Prothrombin G20210 Mutation a Systemic malignancy Sickle cell anemia β- Thalassemia Polycythemia vera Systemic lupus erythematosus Homocysteinemia Thrombotic thrombocytopenic purpura Disseminated intravascular coagulation Dysproteinemias Nephrotic syndrome Inflammatory bowel disease Oral contraceptives Venous sinus thrombosis b Fibromuscular dysplasia Vasculitis Thrombosis: Lacunar stroke (small vessel) Large vessel thrombosis Dehydration Embolic occlusion : Artery-to-artery Carotid bifurcation Aortic arch Arterial dissection Cardioembolic Atrial fibrillation Mural thrombus Myocardial infarction Dilated cardiomyopathy Valvular lesions Mitral stenosis Mechanical valve Bacterial endocarditis Paradoxical embolus Atrial septal defect Patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast ETIOLOGY

ANTERIOR CEREBRAL ARTERY Contralateral paresis and sensory loss in the leg . Cognitive or personality changes. SIGNS & SYMPTOMS The symptoms last more than 24 hours or lead to death. Symptoms and signs of arterial infarcts depend on the vascular territory affected .

MIDDLE CEREBRAL ARTERY Pneumonic: “ CHANG es” C ontralateral paresis and sensory loss in the face and the arm. H omonymous H emianopsia . A phasia . N eglect . G aze preference toward the side of the lesion.

POSTERIOR CEREBRAL ARTERY Pneumonic: The 4 D ’s D iplopia D izziness D ysphagia D ysarthria

BASAL GANGLIA LACUNAR Pure motor or sensory stroke. Dysarthria-clumsy hand syndrome, ataxic hemiparesis.

BASILAR ARTERY Coma “Locked-In” Syndrome Cranial Nerve Palsies Apnea Visual Symptoms Drop Attacks Dysphagia Dysarthria Vertigo “Crossed” weakness and sensory loss affecting the ipsilateral face and contralateral body.

COMPLICATIONS Brain edema. Pneumonia- occurs as a result of not being able to move as a result of the stroke. Urinary tract infection (UTI) - can occur as a result of having a foley catheter . Seizures - common in larger strokes. Clinical depression - very common after stroke or may be worsened in someone who had depression before the stroke. Bedsores . Limb contractures . Deep venous thrombosis (DVT ). myocardial infarction, arrhythmias and heart failure. fluid imbalance. spasticity , with pain, contractures and frozen shoulder,

Vital signs  Heart rate . Blood pressure. Breathing. Temperature. BMI. O2 saturation Patient history DIAGNOSIS Physical examination Absent pulses (inferior extremity, radial, or carotid) - favors atherosclerosis with thrombosis Sudden onset of cold, blue limb- favors embolism. Occlusion of common carotid artery in the neck neck with bruit -occlusive extracranial disease Temporal arteritis- temporal arteries irregular and with dilatation, tender, pulseless Cardiac findings(especially atrial fibrillation, murmurs,cardiac enlargement) - favor cardiac-origin embolism. Carotid artery occlusion –iris speckled, ipsilateral pupil dilated and poorly reactive, retinal ischemia  Fundus - cholesterol crystal, white platelet-fibrin, or red clot emboli. Subhyaloid hemorrhage in brain or subarachnoid hemorrhage . 

DIAGNOSIS levels of cholesterol and sugar in your blood. electrocardiogram ( ECG ) . Electrocardiogram Complete blood count including platelets & ESR Cardiac enzymes and troponin Electrolytes, urea nitrogen, creatinine Prothrombin time and international normalized ratio (INR), Partial thromboplastin time Oxygen saturation Coagulation studies : May reveal a coagulopathy and are useful when fibrinolytics or anticoagulants are to be used

CT Scan Middle cerebral artery infarct Posterior cerebral artery infarct Strokes <6 hours old are usually NOT visible on CT scan.

MRI acute middle carotid artery (MCA) stroke

CT SCAN MRI

Carotid Duplex (Ultrasound)

Transcranial Doppler

MRA (Magnetic Resonance Angiography) CT Angiography Conventional Angiography

Liver function tests Toxicology screen Blood alcohol level Pregnancy test in women of child-bearing potential Arterial blood gas if hypoxia is suspected Electroencephalogram if seizures are suspected Appropriate in selected patients

Differential Diagnosis of Stroke Craniocerebral / cervical trauma Meningitis/encephalitis Intracranial mass Tumor Subdural hematoma Seizure with persistent neurological signs Migraine with persistent neurological signs Metabolic Hyperglycemia Hypoglycemia Post-cardiac arrest ischemia Drug/narcotic overdose   

MANAGEMENT

● Admission to a stroke unit . ● Antiplatelet agents: - Aspirin 300mg daily or Clopidogrel , modest benefit when given within 48 hours of onset, ● Thrombolysis: Alteplase (  tissue plasminogen activator ( tPA ) ) -IV Alteplase : within 3 hours of stroke symptom onset -IA Alteplase : within 6 hours. (SBP <185 and SBP <110mmHg.) ● anticoagulant: Warfarin, or Heparin Also : Endotracheal intubation Nasogastric tube Iv fluid to prevent dehydrated The acute management of ischemic stroke

Management of Cerebral Edema, Increased : Intracranial Pressure and Hydrocephalus *Brain edema peaks at 3-5 days 1 . IV Mannitol ( 0.25 mg/kg over 20 minutes). 2. hyperventilation (lower PCO2 ). 3 . osmotic diuretics. 4. drainage of CSF (ventriculostomy ). 5. surgery (lobectomy ).

Reduce fever. Regulate blood pressure . - if severe hypertension IV Labetalol or Nicardipine infusion. Correct hypoxia. Regulate blood glucose. Manage cardiac arrhythmias. Manage myocardial ischemia. Other treatment

CONTRAINDICATIONS TO ALTEPLASE THERAPY Pneumonic: SAMPLE STAGES S troke or head trauma within the last 3 months. A nticoagulation with INR>1.7 or prolonged PTT. M I (recent). P rior Intracranial Haemorrhage. L ow Platelet Count (<100,000/mm 3 ) E levated BP: Systolic>185 or Diastolic >110mmHg S urgery in the past 14 days. T IA (mild symptoms or rapid improvement of symptoms). A ge<18 G I or urinary bleeding in the past 21 days E levated (>400mg/dl) or Decreased (<50mg/dl) Blood glucose. S eizures present at the onset of stroke.

SURGERY Carotid E ndarterectomy to remove blood clots and fatty deposits from one of the carotid arteries (but isn’t suitable for everyone).

CAROTID ENDARTERECTOMY If stenosis is >70% in symptomatic patients or >60% in asymptomatic patients (Contraindicated on 100% occlusion).

Some patients with cerebellar infarction may require urgent posterior fossa decompression and ventricular drainage if swelling caused by the infarct is leading to brainstem compression and obstruction to CSF flow Surgery

PREVENTIONS Stopping smoking. Healthy diet (low animal fat, low salt, avoiding excess alcohol) and prescribing cholesterol-lowering agents, i.e. statins. In the long term , control of blood pressure is also important. For the first 2 weeks after an ischaemic stroke, however, patients should not receive antihypertensive therapy beyond their pre-existing treatment unless there is evidence of malignant hypertension. This is because too rapid lowering of blood pressure may worsen ischaemia in a region where the cerebral circulation is already compromised. Lifelong antiplatelet treatment is indicated, commencing as soon as possible after a cerebral infarct . The initial dose of aspirin (300mg daily) can be reduced to 75mg daily after 4 weeks. Anticoagulation with warfarin is effective prophylaxis in the presence of atrial fibrillation and other cardiac sources of embolism.

Stroke Prevention Anticoagulants (Heparin, Warfarin ) Antiplatelets (aspirin, clopidogrel dipyridamole /ASA combination, ticlopidine ) Statin ARB (- sartan ), or ACE inhibitor + HCTZ Carotid endarterectomy if indicated Carotid or intracranial stent. Risk factor control !!!

REHABILITATION A multidisciplinary team of health professionals will work out a rehabilitation programme for you that’s designed around your particular needs. Rehabilitation aims to help you stay as independent as possible and get back to your usual activities, or adapt to new ways of doing things. You may make most of your recovery in the early weeks and months afterwards but you may continue to improve for years.

Factors That Cause Stroke Progression Hypotension Hyperglycemia Hyperthermia Infection Cerebral hypoperfusion

BOOKS : Harrisons Neurology in Clinical Medicine, 3rd Ed Ginsberg lecture notes neurology INTERNET : http:// www.cdc.gov/stroke/index.htm http://www.who.int/topics/cerebrovascular_accident/en / http:// www.stroke.org/understand-stroke/what-stroke/ischemic-stroke http://www.strokecenter.org/patients/about-stroke/ischemic-stroke / http:// www.strokeassociation.org/STROKEORG/AboutStroke/TypesofStroke/Types-of-Stroke_UCM_308531_SubHomePage.jsp REFERENCES