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| * stroke..ISCHEMIC,EMBOLIC,LACUNAR,HEMORRHAGIC |
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im so confused ...help me here..forever,spartans1,the_dumb
its a very imp topic..and i have exam in few days |
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| * Re:stroke..ISCHEMIC,EMBOLIC,LACUNAR,HEMORRHAGIC |
| #2187757 |
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STROKE:
blood supply of the brain:
1. Anterior circulation: comprised of the internal carotid artery and its branches, esp. the paired anterior and middle cerebral arteries.
2. Posterior circulation: comprised of the paired vertebral arteries, which unites to form the basilar artery, which further divides into the paired posterior cerebral arteries.
TRANSIENT ISCHEMIC ATTACK:
Present as acute, focal neurologic deficits that resolve within 24 hours. A CT scan can be normal in this time, since ischemic strokes are not always visible on the CT scan within the first 24 hours of
presentation.
There are 3 subtypes of TIA:
1. Embolic (artery‐artery or cardio aortic)
2. Large vessel atherothromboic (large artery low flow TIA)
3. Small vessel atherothrombotic (lacunar flow TIA)
Atherothrombotic TIA’s are recurrent, stereotyped, and short in duration. MRI or CT angiography shows the site of stenosis. Normal MRI or CT angiography makes the diagnosis of large vessel low flow TIA unlikely
The tx of TIA includes
• Avoidance or correction of modifiable risk factors, such as smoking, HTN, and
hypercholesterolinemia.
• All pts with atherothrombotic TIA should receive an antiplatelet agent if there is no
contraindication to its use. It has been shown to reduce the incidence of stroke and other
vascular events. Aspirin is the initial agent of choice for this purpose.
• Clopidogrel (2nd line) is used when the pt is intolerant to aspirin.
• Ticlopidine (3rd line) is used when the pt is intolerant to both clopidogrel and aspirin
• Aspirin is used in combination with dipyridamole when the pt still develops a TIA despite being on aspirin.
• Anticoagulation (with warfarin, heparin) is considered when the TIA was caused by emboli from the heart. EKG may show evidence of a‐fib or MI. TEE usually reveals evidence of embolism from the aorta or heart.
There are 3 underlying causes of TIA:
1. Blood vessel abnormality (i.e. atherosclerosis, inflammation, dissection, venous thrombosis,
developmental malformation)
2. Embolic source (i.e. heart, extra cranial artery)
3. Inadequate cerebral blood flow (due to decreased perfusion or increased blood viscosity)
Reversible ischemic neurologic deficit (RIND) is characterized by a transient ischemic episode, followed by resolution of the associated focal symptoms in 24 hours to 1 week.
In the ELDERLY, atherosclerosis and emboli are the MCC. Carotid Doppler US is usually performed to check for these
In YOUNGER pts, atherosclerosis is very UNLIKELY and the more common causes are emboli,
vasculitis, dissection, etc. When you suspect emboli, a TTE can be performed. If it is normal, do a further work up for possible hypercoagulable conditions (ie factor V leiden, hyperhomocystenimea, lupus anticoagulant, prothrombin gene mutation, etc).
Strokes can be subdivided into: Ischemic and hemorrhagic
1‐ ISCHEMIC STROKE: are usually accompanied by a hx of previous TIA. Pts with ischemic stroke
usually don’t have headache or impaired consciousness.
1‐EMBOLIC:
Majority of embolic strokes are from mural thrombi of heart that develop as a result of Afib.
‐ Atheroembolic stroke (gradual onset usually)
Mechanism: obesity, hyperchol, HTN, DM atherosclerosis thrombosis and embolism of small
vessels ischemia cerebral edema Increased ICP pailledema, asymmetric pupils etc.
* Migration of emboli from areas more prone to atherosclerosis e.g. aortic arch, carotid bifurcation and intracranial vessels. These emboli migrate and obstruct the small cerebral vessels. These atheroembolic
strokes occur at rest and have a gradual onset. Pts often experience successive strokes with increasing frequency.
*The emboli from carotid artery can be cholesterol or thrombotic emboli.
‐ Cardioembolic stroke (sudden onset usually)
Mechanism: Preexisting cardiac disease e.g. AFib, MI, mural thrombus, dilated cardiomyopathy,
infective endocarditis causing septic emboli red thrombus in left side of heart large cerebral artery
stroke ischemia and so on.
*Most common site of obstruction lateral striate arteries (penetrating arteries of MCA). These arteries
supply internal capsule, caudate nucleus, putamen and globus pallidus.
*Also higher risk of transforming into a hemorrhagic stroke
Septic emboli suspect in an IV drug user. Mx ECHO and then IV antibiotics
2‐THROMBOTIC:
Lacunar strokes:
• The MC site for a lacunar infarct is the posterior internal capsule, producing a pure motor
stroke (the posterior internal capsule carries corticospinal and corticobulbar motor fibers). HTN
and DM are 2 major risk factors. Also caused by polycythemia.
• These occur secondary to occlusion of a single, deep penetrating artery in the brain. It is
thought to be a combination of microatheroma and lipohyalinosis. They are rarely embolic.
They comprise a good percentage of ischemic strokes. Because of their small size, lacunar
strokes are not often seen on non‐contrast CT scans.
• The principal cause is HTN, which induces lipohyalinotic thickening of the small vessels. Lacunae
are formed as a result of thrombotic occlusion of penetrating vessels, which are usually 0.5 to
0.8 cm in diameter. The area of ischemic damage in the brain tissue is relatively small, thus
explaining why the neurologic deficit is typically not prominent. There are several classic
syndromes:
Pure motor hemi paresis: due to lacunar infarction in the posterior limb of the internal
capsule. You see unilateral motor deficit (face,a rm, and to a lesser extent, leg); mild dysarthria; no
sensory, visual or higher cortical dysfunction.
Pure sensory stroke: stroke in the VPL nucleus of the thalamus. See unilateral numbness,
paresthesias, and hemisensory deficit involving the face, arm, trunk, and leg.
Ataxic‐hemi paresis: lacunar infarction in the posterior limb of the internal capsule. Weakness that is
more prominent in the LE, along with ipsilateral arm and leg incoordination.
Dysarthria‐clumsy hand syndrome. Lacunar stroke at the basis pontis hand weakness, mild motor
aphasia, NO sensory abnormalities.
3‐HYPOPERFUSION either systemic or local.
• Cocaine and metamphetamine drug induced vasospasm stroke
STROKE SYNDROMES OCCURING DUE TO ISCHEMIA:
ACA occlusion:
• Contralateral motor and/or sensory deficits which are more pronounced in the lower limb than
the upper limb.
• Sphincter incontinence
• Gait apraxia
• primitive reflexes (ie grasp and suckling)
• Emotional disturbances, abulia, akinetic mutism
• Deviation of head and eyes towards the side of lesion
MCA occlusion:
• Contralateral motor and/or sensory deficits (more pronounced in the upper limb than lower
limb)
• Homonymous hemianopia.
• If the dominant lobe (left) is involved, the pt may have aphasia
• if the non‐dominant lobe (right) is involved, the pt may have neglect and/or anosognosia.
• Conjugate eye deviation towards the side of lesion
Occlusion of the internal carotid artery results in signs and symptoms generally of MCA occlusion, along
with visual symptoms, such as amaurosis fugax (temporary monocular blindness).
PCA occlusion:
• Homonymous hemianopia
• Alexia without agraphia (dominant hemisphere)
• visual hallucinations (calcarine cortex)
• 3rd nerve palsy with paresis of vertical eye movement
• motor deficits (cerebral peduncle, midbrain).
• sensory symptoms (thalamus)
Thalamic stroke (dejerine‐roussy syndrome).
• This condition is caused by a stroke involving ventral postero‐lateral nucleus of the thalamus,
which transmits sensory information from the contralateral part of the body.
• The classic presentation involves contralateral hemianesthesia that can be accompanied by
transient hemiparesis, athetosis, or ballistic movements.
• Dysesthesia of the area affected by the sensory loss is characteristic and is called thalamic pain syndrome.
Occlusion of vertebrobasilar arteries
• Infarction of the vermis(medial) of the cerebellum can cause severe vertigo and nystagmus.
• Lateral cerebellar infarction causes dizziness, ataxia, weakness, and a tendency to sway towards
the side of the lesion.
2‐ HEMORRHAGIC STROKE:
Subarachnoid hemorrhage is usually accompanied by a sudden dramatic onset of a severe headache.
• If you plan to do a LP when suspecting subarachnoid hemorrhage, you still do a CT scan of the
head first to prevent herniation.
• Pts are at risk for subsequent vasospasm of the arteries of the brain. In affected pts, the signs of
ischemia usually appear in about 7 days after the SAH. Calcium channel blockers, ie nimodipine
are used to prevent vasospasm in pts.
• Pts may have “cerebral salt‐wasting syndrome”, which involves
1. Inappropriate secretion of vasopressin, which causes water retention
2. An increased secretion of atrial/brain natriuretic peptide.
These changes cause hyponatremia, which usually resolves within 1‐2 weeks. SIADH is also commonly
seen in pts with intracranial hemorrhage. It results in hyponatremia, for which water restriction is the
initial tx of choice.
Intracerebral hemorrhage:
• Characterized by focal neurological signs that develop suddenly and gradually worsen over
minutes or hours
• MCC HTN crisis
• Other causes Transformed cardioembolic stroke, AV malformation, amyloid angiopathy and
coagulation disorders . Anticoagulation therapy is the MC bleeding disorder responsible for
brain hemorrhage. As INR increases, the risk of bleeding increases.
*INR 9: stop warfarin, give oral vitamin K
*If the pt has a seroius intracranial bleed, they should have rapid correction of excess anticoagulation,
with a target INR of less than 1.5. FFP reverses the action of warfarin, works immediately, and lasts for a
few hours, so it should be administered immediately.
• MC affected structures: putamen > cerebellum
• Neurologic symptoms d/t mass effect of blood (headache, vomiting, altered mental status)
These occur when the hemorrhage expands.
Pontine hemorrhage: pts present with a deep coma and paraplegia that develops within minutes. The
pupils are pinpoint and reactive to light. There is decerebrate rigidity. There are NO horizontal eye
movements.
Putamen hemorrhage: the internal capsule lies adjacent to the putamen and is almost always involved
and thereby leads to hemi paresis. You also have hemi sensory loss, homonymous hemianopsia, stupor,
and coma. The eyes are deviated away from the paralytic side i.e towards the lesion.
Cerebellar hemorrhage:
• Small hemorrhage usually only acute onset occipital headache, repeated vomiting, and gait
ataxia.
• Larger hemorrhage may manifest with 6th nerve paralysis, conjugate deviation, and
blepharospasm. Pts with large hemorrhages often becomes stuporous in a few hours.
• Immediate evacuation of the hematoma is required and life‐saving for these pts.
• Neurological recovery in pts who survive is usually near complete
MANAGEMENT:
The first step in all pts suspected with a stroke is CT scan without contrast. This distinguishes
between the 3 subtypes of stroke. Ischemic changes may not appear in the CT in the first 24 hrs.
Hemorrhages are seen as hyper dense areas on CT scan, while infarcts characteristically have
hypodense parenchyma areas on CT scan.
If hemorrhage is ruled out, we think of ischemic, carotid Doppler(atheroembolic ) and TEE
(cardioembolic)are performed to evaluate the possible source of embolism.
Give tPA if hemorrhage ruled out on CT and pt. presents within 3 hrs of the stroke onset.
Anticoagulation therapy is of use ONLY if ischemic stroke of cardioembolic origin.
Oral aspirin prevents stroke in pts who have a Hx of atheroembolic TIAs, also given when he has
been ruled out via CT.
Though HTN can sometimes be most common in the early acute period of stroke, aggressive
control is not advised since this may impair the cerebral autoregulation and worsen neurological
outcome. Tx is indicated when the systolic BP is greater than 220mmHg or diastolic greater
than 130. HTN should be reduced over a period of several hours. The preferred drugs are CCBs
(ie nicardipine) and ACE inhibitors. IV nitroglyerine and nitroprusside iare NOT indicated.
CAROTID ATHEROSCLEROSIS:
• Blockage of 60 to 99% are considered to have a proven indication for CEA(carotid
endarterectomy)
• Blockage of > or = 60% CEA is the best tx for an irregular atherosclerotic lesion in the carotids
even in ASYMPTOMATIC individuals.
• Blockage of < 60% follow every 6‐12 months with duplex USG
• Blockage of > or = 70%, CEA is indicated and ASA is given after surgery for life.
• Complete occlusion (100% stenosis) is a contraindication to surgery.
Aspirin cannot regress the lesion, but can only prevent progression. It is more as a prophylactic agent to
prevent carotid artery |
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| * Re:stroke..ISCHEMIC,EMBOLIC,LACUNAR,HEMORRHAGIC |
| #2187759 |
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Strokes: caused by thrombosis or embolism, or due to a hemorrhage
20-30 % from cardiogenic thromboembolism and caused by several pathogenic factors.
--Most common: Atrial fibrillation and MI and endothelial abnormalities due to valvular disease
REST: 80% of strokes are due to ischemia; carotid occlusion, atherosclerosis the remainders are due to hemorrhage due to rupture of a blood vessel or an abnormal vascular structure
1-Ischemic stroke blood supply to part of the brain is decreased, leading to dysfunction-necrosis of the brain tissue area
*thrombosis (obstruction of a blood vessel by a blood clot forming locally), embolism (idem due to a blood clot from elsewhere in the body), systemic hypoperfusion (general decrease in blood supply, e.g. in shock) and venous thrombosis
2-Thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower
--Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis
--Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery
3-Embolic stroke ïƒ blockage of an artery by an embolus (fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria), arising from elsewhere and traveling particle or debris in the arterial bloodstream. Most commonly arise from the heart (especially in atrial fibrillation
4-By Systemic hypoperfusion
Reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries
5- Venous thrombosis ïƒ Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke
6-Hemorrhagic stroke
Accumulation of blood anywhere within the skull vault. Intracerebral, epidural hematoma, subdural hematoma¦
DX stroke:
* The diagnosis of stroke itself is clinical, with assistance from the imaging techniques * Neurological examination, CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriographyan angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation) **blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria
**For diagnosing ischemic stroke in the emergency setting
-CT scans (without contrast enhancements)
sensitivity= 16%
specificity= 96%
-MRI scan
sensitivity= 83%
specificity= 98%
**For diagnosing hemorrhagic stroke in the emergency setting: **For detecting hemorrhages, MRI scan is more sensitive***
-CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%
-MRI scan ***
sensitivity= 81%
specificity= 100%
***Stroke treatment
1-Ischemic stroke 1st step: Imaging¨ Hemorrhagic stroke must be ruled out with medical imaging
-ABCD if needed
-Medication (aspirin, clopidogrel, dipyridamole)
-Anticoagulant medication (warfarin-heparin)
tPA¨Thrombolysis within three hours of onset of symptoms and Contraindications (such as abnormal lab values, high blood pressure, or recent surgery).
-Workup: Blood tests, such as a full blood count, coagulation studies (PT/INR and APTT), and tests of electrolytes, renal function, liver function tests and glucose levels are carried out
-Protect brain:
-Ensuring that blood sugar is as normal as possible
-Stroke patient is receiving adequate oxygen and intravenous fluids
-Pt Positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have shown that this increases blood flow to the brain
-Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily), clopidogrel (75 mg daily), and combined aspirin and dipyridamole
**If studies show carotid stenosis >70% symptomatic, and the patient has residual function in the affected side, carotid endarterectomy
**Thrombectomy // In acute ischemic stroke  removal of the offending thrombus directly by catheter into the femoral artery
2-Embolic stroke Anticoagulation can prevent recurrent stroke
3-Hemorrhagic stroke ïƒ require neurosurgical evaluation to detect and treat the cause of the bleeding
Careful: Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage **Important: Care and rehabilitation and prevention!!!
**Thiamine deficiency.- from Korsakoff syndrome evidenced by amnesia  Be aware with Glucose admon (AVOID) because high dose glucose can precipitate symptoms
**The basal ganglia and thalamus are the classic sites of a acute hypertensive bleed
***Bleeding in the brain stem¨ due to hemorrhagic stroke, poor prognosis
***Bleeding in the ventriclesï¨ from subarachnoid hemorrhage in adults
**Bleeding in epidural space: epidural hematoma
**Bleeding bridging veins: subdural hematoma
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| * Re:stroke..ISCHEMIC,EMBOLIC,LACUNAR,HEMORRHAGIC |
| #2187772 |
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Anterior Spinal Artery Infarct: is when anterior spinal artery which supplies the anterior part of the spinal cord gets plugged up (infarct=clogged up). Anterior spinal artery is a branch of vertebral arteries. An infarct decrease in blood flow to the anterior part of the spinal cord.
Presentations: flaccid paralysis that leads to spastic paresis in days. Loss of pain and temperature sensations.
There is NO NO NO effect of vibratory and position sense b/c there supplied by posterior spinal artery.
Diag: MRI
Tx: cOumadin
Cerebrovascular Disease: brain can not get enough blood due to disease in blood vessels that supply the brain. Most common cause: hypertension- it damages the endothelium that lines the blood vessels- this causes collagen to get exposed, platelets aggregate at the site to fix the issue but it does not always get fixed completely. Sustained hypertension causes stiffening, narrowing, deformed and uneven vessels making them susceptible to damage.
Decrease in blood pressure during sleepïƒ decrease in blood flow ==ischemis stroke
Increase in blood pressure causes vessels to tear causing intracranial hemorrhage.
Common in elderly, diabetic, smokers, or those w/ ischemic heart disease have cerebrovascular disease.
Diag: CT of head to differenciate between hemorrhage vs stroke
Tx: - if pt comes within 3 hours of symptom onset= tissue plasminogen activator
Contraindications are: stroke, head trauma within 3 months, hemorrhage-GI or GU within 21days.
-Heparin in acute ischemic stroke reduces number of recurrent strokes.
-anti-platelet therapy-most effective to prevent secondary ischemic stroke. *Aspirin is 1st line tx for prevention*
-Carotid endarterectomy-if lesion is symptomatic and occlusion is 70% of arterial lumen.
6 arteries that are commonly affected: ACP, MCP, PCP, P-PCP, P-BA, PICA
-Anterior Cerebral Artery: centro-lateral weakness and sensory loss in legs more then upper extremities. Urinary incontinence, confusion, and behavior disturbance.
-Medial cerebral Artery- contra-lateral hemiplegia, hemisensory loss, homonymous hemi-anopia w/ eye deviation towards cortical lesion. IF dominant=aphasia , IF NOT dominant=apraxia, confusion
-Posterior cerebral artery- contralateral homonymous hemianopia, visual hallucination, agnosia
-Posterior Inferior cerebral artery- (Wallenberg syndrome) contralateral body sensory loss, ipisilateral facial sensory loss, , vertigo ataxia, dysarthria, dysphagia, Horner syndrome.
-Penetrating vells of the posterior cerebral artery- contralateral homonymous hemianopsia, visual hallucianation, agnosia
-Paramedian branch of Basilar artery- (locked in syndrome), quadric-paresis w/ intact vertical eye movments.
----Diag: CT of head to differenciate between hemorrhage and stroke
----TX: Acute Ischemis Stroke-if pt comes I within 3 hours of symptoms= Tissue Plasminogen Activator , contraindicated if pt has had stroke, sever head trauma in past 3 months, hemorrhage within 21 days, or surgery within 14 days hx of intracranial hemorrhage, Hypertensive ER etc..
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| * Re:stroke..ISCHEMIC,EMBOLIC,LACUNAR,HEMORRHAGIC |
| #2188274 |
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PLEASE STICK TO THIS BECAUSE THIS IS CLOSE TO KAPLAN NOTE
Anterior Spinal Artery Infarct: is when anterior spinal artery which supplies the anterior part of the spinal cord gets plugged up (infarct=clogged up). Anterior spinal artery is a branch of vertebral arteries. An infarct decrease in blood flow to the anterior part of the spinal cord.
Presentations: flaccid paralysis that leads to spastic paresis in days. Loss of pain and temperature sensations.
There is NO NO NO effect of vibratory and position sense b/c there supplied by posterior spinal artery.
Diag: MRI
Tx: cOumadin
Cerebrovascular Disease: brain can not get enough blood due to disease in blood vessels that supply the brain. Most common cause: hypertension- it damages the endothelium that lines the blood vessels- this causes collagen to get exposed, platelets aggregate at the site to fix the issue but it does not always get fixed completely. Sustained hypertension causes stiffening, narrowing, deformed and uneven vessels making them susceptible to damage.
Decrease in blood pressure during sleepïƒ decrease in blood flow ==ischemis stroke
Increase in blood pressure causes vessels to tear causing intracranial hemorrhage.
Common in elderly, diabetic, smokers, or those w/ ischemic heart disease have cerebrovascular disease.
Diag: CT of head to differenciate between hemorrhage vs stroke
Tx: - if pt comes within 3 hours of symptom onset= tissue plasminogen activator
Contraindications are: stroke, head trauma within 3 months, hemorrhage-GI or GU within 21days.
-Heparin in acute ischemic stroke reduces number of recurrent strokes.
-anti-platelet therapy-most effective to prevent secondary ischemic stroke. *Aspirin is 1st line tx for prevention*
-Carotid endarterectomy-if lesion is symptomatic and occlusion is 70% of arterial lumen.
6 arteries that are commonly affected: ACP, MCP, PCP, P-PCP, P-BA, PICA
-Anterior Cerebral Artery: centro-lateral weakness and sensory loss in legs more then upper extremities. Urinary incontinence, confusion, and behavior disturbance.
-Medial cerebral Artery- contra-lateral hemiplegia, hemisensory loss, homonymous hemi-anopia w/ eye deviation towards cortical lesion. IF dominant=aphasia , IF NOT dominant=apraxia, confusion
-Posterior cerebral artery- contralateral homonymous hemianopia, visual hallucination, agnosia
-Posterior Inferior cerebral artery- (Wallenberg syndrome) contralateral body sensory loss, ipisilateral facial sensory loss, , vertigo ataxia, dysarthria, dysphagia, Horner syndrome.
-Penetrating vells of the posterior cerebral artery- contralateral homonymous hemianopsia, visual hallucianation, agnosia
-Paramedian branch of Basilar artery- (locked in syndrome), quadric-paresis w/ intact vertical eye movments.
----Diag: CT of head to differenciate between hemorrhage and stroke
----TX: Acute Ischemis Stroke-if pt comes I within 3 hours of symptoms= Tissue Plasminogen Activator , contraindicated if pt has had stroke, sever head trauma in past 3 months, hemorrhage within 21 days, or surgery within 14 days hx of intracranial hemorrhage, Hypertensive ER etc..
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