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stroke ( ischemic stroke )
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D.A.B.M
Nov. 21, 2016 • 38 likes • 3,846 views
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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
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! stroke ( ischemic stroke )
1. DONE BY : MUSTAFA KHALIL IBRAHIM TBILISI STATE MEDICAL UNIVERSITY 4th year, 2st semester, 1nd group
2.
Epidemiology
Treatments
3.
Introduction
Prevention
Pathophysiology
Rehabilitation
Risk factors
Prognosis
Etiology
Signs and symptoms
stroke-5 million die and 5 million are permanently disabled .
blocked.
Annually, 15 million worldwide su!er a
WHO estimates a stroke occurs every 5 seconds.
One American dies from a stroke every 4 minutes, on average
Americans each year, that’s 1 of every 20 deaths.
Diagnosis
References
Stroke is the 5th leading cause of death in the US and is a major cause of disability.
people in the US have a stroke each year.
Complications
adult ~ 800,000
killing nearly 130,000
About 87% of all strokes are ischemic stroke , when blood flow to the brain is
Stroke costs the United States an estimated 34 -40$ billion each year
Total cost of stroke has been estimated at $65.5
billion in 2008.
4. highest death rates from stroke are in the southeastern United States
5.
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.
6. 12%
7.
A transient ischemic attack (TIA) is sometimes called a "mini- stroke." It is di!erent 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
embolic, thrombotic or hemodynamic vascular mechanisms.
caused by
Some transient episodes last longer than 24 hours, yet patients
recover completely – reversible ischaemic neurological deficits.
8.
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.
9.
It can occur in the carotid artery of the neck as well as other arteries.
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.
10.
A thrombotic stroke is caused by a blood clot that forms inside one of the arteries supplying blood to the brain.
stroke is usually seen in people with and
This type of
Two types of blood clots can cause thrombotic stroke: and 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.
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.
11. 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 su!icient 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.
12. 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
13.
Functional alteration of endothelial cell layer
Denuding of endothelium
Superficial intimal injury
Deep intimal & media
damage with marked platelet aggregation and mural thrombosis
14.
Cardiogenic emboli lodge in the middle cerebral artery or its branches in 80% of cases,
branches 10% of the time,
in the posterior cerebral artery or its
and in the vertebral artery or its branches in the remaining 10% of cases.
15. • Geographic location- southeastern 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 .
16. • 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 • βThalassemia • 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 Lacunar stroke (small vessel) Large vessel
thrombosis Dehydration 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
17.
Contralateral paresis and sensory loss in the leg.
Cognitive or personality changes. The symptoms last more than 24 hours
or lead to death. Symptoms and signs of arterial infarcts depend on the vascular territory a!ected .
18.
Pneumonic: “CHANGes” ontralateral paresis and sensory loss in the face and the arm. omonymous emianopsia. phasia.
eglect. aze preference toward the side of the lesion.
19. POSTERIOR CEREBRAL ARTERY
Pneumonic: The 4 ’s iplopia izziness ysphagia ysarthria
20.
Pure motor or sensory stroke.
Dysarthria-clumsy hand syndrome, ataxic hemiparesis.
21.
Coma
Vertigo
“Locked-In” Syndrome
Cranial Nerve Palsies
Apnea
Visual Symptoms
Drop Attacks
Dysphagia
Dysarthria
“Crossed” weakness and sensory loss a!ecting the ipsilateral face and contralateral body.
22. occurs as a result of not being able to move as a result of the stroke. - can occur as a result of having a foley catheter . common
in larger strokes. very common a"er stroke or may be worsened in someone who had depression before the stroke.
23.
Heart rate .
Blood pressure.
Breathing.
Temperature.
BMI.
extremity, radial, or carotid) - favors atherosclerosis with thrombosis
O2 saturation
Patient history
Sudden onset of cold, blue limb- favors embolism.
Occlusion of common carotid artery in the neck neck with bruit - occlusive extracranial disease
arteries irregular and with dilatation, tender, pulseless
enlargement) - favor cardiac-origin embolism.
reactive, retinal ischemia
Absent pulses (inferior
Temporal arteritis- temporal
Cardiac findings(especially atrial fibrillation, murmurs,cardiac
Carotid artery occlusion –iris speckled, ipsilateral pupil dilated and poorly
Fundus - cholesterol crystal, white platelet-fibrin, or red clot emboli. Subhyaloid hemorrhage in brain
or subarachnoid hemorrhage.
24.
levels of cholesterol and sugar in your blood.
including platelets & ESR
electrocardiogram (ECG) .
Cardiac enzymes and troponin
Electrocardiogram
Electrolytes, urea nitrogen, creatinine
international normalized ratio (INR), Partial thromboplastin time
Oxygen saturation
Complete blood count
Prothrombin time and
Coagulation studies: May reveal a
coagulopathy and are useful when fibrinolytics or anticoagulants are to be used
25. Middle cerebral artery infarct Posterior cerebral artery infarct Strokes <6 hours old are usually NOT visible on CT scan.
26. acute middle carotid artery (MCA) stroke
27. CT SCAN MRI
28. MRA (Magnetic Resonance Angiography) CT Angiography
29.
Liver function tests
Toxicology screen
blood gas if hypoxia is suspected
Blood alcohol level
Pregnancy test in women of child-bearing potential
Electroencephalogram if seizures are suspected
30. Craniocerebral / cervical trauma Meningitis/encephalitis Intracranial mass
Tumor
persistent neurological signs Migraine with persistent neurological signs Metabolic
cardiac arrest ischemia
Arterial
Subdural hematoma Seizure with
Hyperglycemia
Hypoglycemia
Post-
Drug/narcotic overdose
31. ● Admission to a stroke unit . -Aspirin 300mg daily or Clopidogrel , modest benefit when given within 48 hours of onset,
Alteplase ( tissue plasminogen activator (tPA)) -IV Alteplase : within 3 hours of stroke symptom onset -IA Alteplase : within 6 hours.
(SBP<185 and SBP <110mmHg.) Warfarin, or Heparin Also :
Endotracheal intubation
Nasogastric tube
Iv fluid to prevent
dehydrated
32. *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).
33.
Reduce fever.
Regulate blood pressure. - if severe hypertension IV Labetalol or Nicardipine infusion.
Regulate blood glucose.
Manage cardiac arrhythmias.
34. Pneumonic: SAMPLE STAGES
PTT.
MI (recent).
Diastolic >110mmHg
Manage myocardial ischemia.
Stroke or head trauma within the last 3 months.
Prior Intracranial Haemorrhage.
Surgery in the past 14 days.
urinary bleeding in the past 21 days
Correct hypoxia.
Anticoagulation with INR>1.7 or prolonged
Low Platelet Count (<100,000/mm3 )
Elevated BP: Systolic>185 or
TIA (mild symptoms or rapid improvement of symptoms).
Elevated (>400mg/dl) or Decreased (<50mg/dl) Blood glucose.
Age<18
GI or
Seizures present at the
onset of stroke.
35.
Carotid Endarterectomy to remove blood clots and fatty deposits from one of the carotid arteries (but isn’t suitable for
everyone).
36.
If stenosis is >70% in symptomatic patients or >60% in asymptomatic patients (Contraindicated on 100% occlusion).
37.
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 a"er 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 a"er a
cerebral infarct. The initial dose of aspirin (300mg daily) can be reduced to 75mg daily a"er 4 weeks.
Anticoagulation with
warfarin is e!ective prophylaxis in the presence of atrial fibrillation and other cardiac sources of embolism.
38.
Anticoagulants (Heparin, Warfarin)
ARB (-sartan), or ACE inhibitor + HCTZ
Antiplatelets (aspirin, clopidogrel dipyridamole/ASA combination, ticlopidine)
Carotid endarterectomy if indicated
Carotid or intracranial stent.
Statin
Risk factor
control!!!
39.
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 a"erwards but you may
continue to improve for years.
40.
Hypotension
41. BOOKS :
Hyperglycemia
Hyperthermia
Infection
Harrisons Neurology in Clinical Medicine, 3rd Ed
http://www.cdc.gov/stroke/index.htm
Cerebral hypoperfusion
Ginsberg lecture notes neurology INTERNET :
http://www.who.int/topics/cerebrovascular_accident/en/
http://www.stroke.org/understand-stroke/what- stroke/ischemic-stroke
stroke/ischemic-stroke/
http://www.strokecenter.org/patients/about-
http://www.strokeassociation.org/STROKEORG/AboutStr oke/TypesofStroke/Types-of-
Stroke_UCM_308531_SubHomePage.jsp
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