TIA and Stroke

number one of stroke

# 1 HTN 50% cardio ,50 % vascular

Prognosis With TIA regarding risk for a stroke

1/3 will have a real stroke withing the next 5 years

Hypotension with stroke

100/70 and below--fluid resuscitation Goal MAP 110-130 to prevent vasospasm, improve O2 delivery

TIA time definition

<24h w/o any residual deficits--old definition.As endorsed by consensus statements from the American Heart Association and American Stroke Association (AHA/ASA), transient ischemic attack (TIA) is defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. Thus, the benign connotation of "TIA" has been replaced by an understanding that even relatively brief ischemia can cause permanent brain injury.

Q3. What lesion should be suspected if the eyes are tonically deviated to the left?

A frontal lobe lesion on the same side as the eye deviation, commonly a stroke or A pontine lesion on the opposite side to the eye deviation.

fibrinolytic Tx time frame with MI and stroke

According to the American Heart Association, you have a better chance of surviving and recovering from certain types of heart attacks if you receive a thrombolytic drug within 12 hours after the heart attack starts. Ideally, you should receive thrombolytic medications within the first 90 minutes after arriving at the hospital for treatment. Intravenous fibrinolytic therapy at the cerebral circulation dose within the first 3 hours of ischemic stroke onset offers substantial net benefits for virtually all patients with potentially disabling deficits. Intravenous fibrinolytic therapy at the cerebral circulation dose within 3-4.5 hours offers moderate net benefits when applied to all patients with potentially disabling deficits. MRI of the extent of the infarct core (already irreversibly injured tissue) and the penumbra (tissue at risk but still salvageable) can likely increase the therapeutic yield of lytic therapy, especially in the 3- to 9-hour window. Intra-arterial fibrinolytic therapy in the 3- to 6-hour window offers moderate net benefits when applied to all patients with potentially disabling deficits and large artery cerebral thrombotic occlusions.

amaurosis fugax

Amaurosis fugax is a painless transient monocular visual loss (i.e., loss of vision in one eye that is not permanent), that appears as a "curtain coming down vertically into the field of vision in one eye;", it is due to occlusion of ophtalmic artery. Other descriptions of this experience include a monocular blindness, dimming, fogging, or blurring.[

s/s of TIA originating from ipsilateral carotid atheroma

Anterior/carotid. A hallmark of TIA of the eye is amaurosis fugax, which manifests as severe monocular vision loss or blindness that occurs abruptly and resolves in less than five minutes. Occasionally, there is reported vision loss perceived as a curtain descending across the visual field. The patho-physiological correlation to amaurosis is a transient embolic occlusion of the central retinal or OA.6 Amaurosis/TMVL may coexist with other symptoms, such as contralateral hemiparesis and hemisensory deficit. However, it is unlikely that a patient would present to the office with amaurosis because of the short duration of the TIA.

position with stroke

Bed rest with HOB eleveated to decrease ICP and improve venous drain Studies have shown that cerebral perfusion pressure is maximized when patients are maintained in a supine position. However, lying flat may serve to increase ICP and thus is not recommended in cases of subarachnoid or other intracranial hemorrhage. Because prolonged immobilization may lead to its own complications, including deep venous thrombosis, pressure ulcer aspiration, and pneumonia, patients should not be kept flat for longer than 24 hours.

hemorrhagic stroke origin, cause and localisation

Bleeding around the brain is referred to as subarachnoid hemorrhage (SAH) and is often caused by rupture of an abnormal blood vessel (aneurysm) on the surface of the brain. Bleeding into the brain is called intracerebral hemorrhage (ICH) and is often caused by high blood pressure

CPP formula

CPP=MAP-ICP

first test with TIA and stroke, and other tests

CT to exclude hemorrhage MRI is better for ischemia Echo to exclude cardiogenic emoli Carotid doppler US cerebral angio

labs and tests for stroke

CT, Cerebral angiography, Lumbar puncture if aneurysm I or II grade to detect blood. LP contraind with large bleeds---herniation is possible

time for brain cells death in case of blockage

Depending on the severity of cerebral blood flow reduction, tissue death can occur in as little as four to 10 minutes The tissue immediately surrounding the actual infarct is called the "ischemic penumbra," and cellular death will eventually occur if blood flow is not restored.

Management of TIA

Endarterectomy is indicated for >70 % -80% stenosis of diameter of vesses with s/s

Management of stroke with fibrinolitics

Fibrinolitics window up to 4.5 h of s/s onset blood evac craniotomy if needed MRI of the extent of the infarct core (already irreversibly injured tissue) and the penumbra (tissue at risk but still salvageable) can likely increase the therapeutic yield of lytic therapy, especially in the 3- to 9-hour window. Intra-arterial fibrinolytic therapy in the 3- to 6-hour window offers moderate net benefits when applied to all patients with potentially disabling deficits and large artery cerebral thrombotic occlusions.

BP control in case when no fibrinolisis is indicated

For patients who are not candidates for thrombolysis with recombinant t-PA (rt-PA) and who have a systolic blood pressure of less than 220 mm Hg and a diastolic blood pressure of less than 120 mm Hg in the absence of evidence of end-organ involvement (ie, pulmonary edema, aortic dissection, hypertensive encephalopathy), blood pressure should be monitored (without acute intervention) and stroke symptoms and complications (eg, increased ICP, seizures) should be treated.

Tx of HTN incase of fibrinolitic Tx

For patients who will be receiving rt-PA, systolic BP greater than 185 mm Hg and diastolic BP greater than 110 mm Hg require intervention. The initial drug of choice, labetalol (10-20 mg IV for 1-2 min), may be repeated (maximum dose 300 mg). One to 2 inches of transdermal nitropaste (see nitroglycerin topical) may also be used. As an alternative to these choices, nicardipine infusion at 5 mg/h, titrated up to a maximum dose of 15 mg/h, can be used. The goal is to reduce up to 15-25% in the first day, . If BP is 185-230 /110-120 labetalol is given at a dose of 10-20 mg IV over 1-2 minutes; the dose may be repeated every 10-20 minutes, up to 300 mg total, or an infusion rate of up to 2-8 mg/min may be used.[1] For systolic blood pressure of greater than 230 mm Hg or diastolic blood pressure of 121-140 mm Hg Labetalol can be used, but nicardipine infusion administered at a rate of 5 mg/h, to a maximum of 15 mg/h, might be a better first choice. For difficult-to-control blood pressure, sodium nitroprusside can be considered.

Treatment of HTN with stroke

For patients with a systolic blood pressure above 220 mm Hg or a diastolic blood pressure greater than 120 mm Hg, labetalol (10-20 mg IV for 1-2 min) should be the initial drug of choice, unless a contraindication to its use exists. Dosing may be repeated or doubled every 10 minutes to a maximum dose of 300 mg. Alternatively, nicardipine may be used for blood pressure control. Nicardipine is given intravenously at an initial rate of 5 mg/h and titrated to effect by increasing the infusion rate 2.5 mg/h every 5 minutes, to a maximum of 15 mg/h. Lastly, nitroprusside at 0.5 mcg/kg/min IV infusion may be used in the setting of continuous blood pressure monitoring. The goal of intervention is a reduction in blood pressure of 10-15%.

number one cause of stroke

HTN

homonimous hemianopsia

Homonymous hemianopsia, or homonymous hemianopia, is hemianopic visual field loss on the same side of both eyes. Homonymous hemianopsia occurs because the right half of the brain has visual pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for the right hemifield of both eyes. When one of these pathways is damaged, the corresponding visual field is lost. Transient homonymous hemianopsia does not necessarily mean stroke. For instance, it can constitute the aura phase of migraine

hyperventilation and ICP

Hyperventilation and decreased arterial pCO2 pCO2 of 32-36 mm ) leads to vasoconstriction, decreased perfusion and decreased ICP. Goal is 35 generally. It can be used only with imminent threat of herniation. Otherwise no hypervent.The normal level for PCO2 is between 35 to 45 mmHg

ICP goal with stroke

ICP is normally 7-15 mm Hg; ICP <20 is OK with stroke at >20-25 mm Hg, the upper limit of normal, treatment to reduce ICP may be needed.[2]

tongue deviation

If the right CN 12 is dysfunctional, the tongue will deviate to the right.

major vessesl involved in stroke

It affects the carotid area in about 80% and the vertebrobasilar area in about 20%.

stroke at medulla and pons levels

Medulla/ pons --all cranial nerves . Ipsilateral facial sensory loss or motor weakness with contralateral body hemianesthesia or hemiparesis indicates a lesion at the pons or medulla. There are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain)

6 leading death among middle age/ old age in US

Middle age heart Accident Lung Ca ( smoking) Stroke Breast/Colon Ca COPD old age: heart CVA COPD Pneumonia Lung CA

modifiable and nonmodifiable risk factors for stroke

Risk factors: The following are the modifiable factors that contribute the most to increased risk of stroke: Hypertension Cigarette smoking!!!!!!!!!!!!!!!!!! Dyslipidemia Diabetes Abdominal obesity Alcoholism!!!!!!!!!!!!!!!!!!!!!!!!!!! Lack of physical activity!!!!!!!!!!!!!!!!!!!!!!!!! High-risk diet (eg, high in saturated fats, trans fats, and calories)!!!!!!!!!!!!!!!!!!!!! Psychosocial stress (eg, depression) !!!!!!!!!!!!!! Heart disorders (particularly disorders that predispose to emboli, such as acute MI, infective endocarditis, and atrial fibrillation) Hypercoagulability (thrombotic stroke only) Intracranial aneurysms (subarachnoid hemorrhage only) Use of certain drugs (eg, cocaine, amphetamines) Vasculitis Unmodifiable risk factors include the following: Prior stroke Older age Family history of stroke Male sex!!!!!!!!!!!!!!!!!!!!!!!!!!!!

R stroke

Spatial problems: Trouble knowing how far or near an object is to the body. Neglect of left side of the body, or not able to see things to the left of the body. Poor decision making, lack of insight into the changes in ability since the stroke, leading to safety concerns. Impulsiveness Short attention span and slowed learning of new things. Facial weakness, unclear speech, or problems swallowing. may not be able to move the left side misjudge distances leading to falls. The person may not be able to control the hand to pick up an object. problems making good decisions left-sided neglet causes the person to "forget" or "ignore" objects on the left side. short-term memory. Although the person may be able to tell you about an event that happened 20 years ago, they may not be able to tell you whom they spoke with that morning or what they had for breakfast

carotid region stroke s/s

Symptoms are usually unilateral and most often affect the motor area, causing unilateral weakness, affecting an arm, leg, or one side of the face. There may be dysarthria. There may be sensory symptoms in the same areas. If Broca's area is involved, there will also be difficulty with speech - called Broca's dysphasia. This produces inconsistent and unpredictable errors, usually substitution, with spontaneous speech containing fewer errors. This is a great simplification and the matter is discussed more fully in the separate article on Dysarthria and Dysphasia. There may be amaurosis fugax (fleeting loss of vision), a unilateral loss indicative of retinal ischaemia, usually associated with emboli or stenosis of the ipsilateral carotid artery.

general management of stroke T, diet , fluids

Table 2. General Management of Patients With Acute Stroke[1, 4] (Open Table in a new window) Blood glucose Treat hypoglycemia with D50 Treat hyperglycemia with insulin if serum glucose >200 mg/dL ( goal 90-140) Blood pressure See recommendations for thrombolysis candidates and noncandidates Continuous monitoring for ischemic changes or atrial fibrillation Intravenous fluids Avoid D5W and excessive fluid administration IV isotonic sodium chloride solution at 50 mL/h unless otherwise indicated. Patients with severe brain injury should be kept normovolaemic. Oral intake NPO initially; aspiration risk is great, avoid oral intake until swallowing assessed Oxygen Supplement if indicated (Sa02 < 94%) Temperature Avoid hyperthermia; use oral or rectal acetaminophen and cooling blankets as needed

leading death 1-24

The five leading causes of death for those aged 1-24 years include external causes (i.e., accidents, homicide, and suicide) followed by cancer and heart disease

Ca channel blockers with stroke

The use of sublingual nifedipine to lower blood pressure in the ED is discouraged, since extreme hypotension may result. Trials of nimodipine, initially thought to be beneficial given its vasodilatory effect as a calcium-channel blocker, have failed to demonstrate any beneficial outcome in comparison with placebo

cerebral circulation

There is a dual blood supply to the brain that allows for both anterior and posterior circulation. The two main arterial systems that supply cerebral blood are the carotid (anterior) and the vertebrobasilar (posterior). Both systems are joined at the base of the brain. At the neck, the carotid arteries bifurcate into the external carotid (ECA) and internal carotid (ICA), and this is often the site of atheromatous disease. The vertebral arteries, which supply the lower brainstem and cerebellum, join to form the basilar artery; the basilar artery supplies the upper brainstem and cerebellum. The basilar artery's terminal branch is the posterior cerebral artery (PCA), and it supplies the occipital lobe and visual cortex

L sided stroke

Trouble speaking or understanding words said or written (aphasia Slow, careful movements. Not able to see things on the right side of the body. Facial weakness, unclear speech, or problems with swallowing may not be able to move the right side of the body, (hemiplegia) or may be very weak in the right arm or leg (hemiparesis). trouble remembering or learning new things.

visual changes with stroke

Unilateral infarction produces homonymous hemianopia. R stroke---R optic nerve lesion----R blindness a person who has a lesion of the right optic tract will no longer see objects on his left side. Similarly, a person who has a stroke to the right occipital lobe visual cortex.

vertebral region stroke s/s

Vertigo, ataxia, dizziness, visual fields If the ophthalmic cortex is involved there will be a homonymous hemianopia that may present purely as ignoring one side of the visual field. There may be bilateral visual impairment ( occipital region) There may be hemiparesis, hemisensory symptoms, diplopia, vertigo, vomiting, dysarthria, dysphagia, or ataxia. a drooping face, gait, confusion, dysarthria, loss of memory or abnormal behaviour. Fleeting symptoms may be more obvious to those around than to the patient.

autoregulation limits by MAP

When the MAP is less than 65 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate

general management of stroke

able 1. NINDS* and ACLS** Recommended Stroke Evaluation Time Benchmarks for Potential Thrombolysis Candidate (Open Table in a new window) Time Interval Time Target Door to doctor 10 min Access to neurologic expertise 15 min Door to CT scan completion 25 min Door to CT scan interpretation 45 min Door to treatment 60 min Admission to stroke unit or ICU 3 h

General s/s of TIA

altered vision ( ophtalmic nerve) altered speech: aphasia ( the Broca area in the frontal lobe (usually the left) or Wernicke's aphasia, also referred to as fluent or receptive aphasia, you may have serious comprehension difficulties and be unable to grasp the meaning of spoken words. Yet you may be able to produce fluent, connected speech. What you say, however, is in most cases a series of meaningless words that sound like sentences, strokes above medulla--->cotralateral motor and sensory, hemilateral sensrory face

Causes of TIA

atherosclerosis, thrombus, arterial occlusion, emboli, hemmorhage MI, endocarditis, valve diseaseEmbolic travel to the carotid terminal branches, particularly the MCA, is most often responsible for stroke. Although thrombotic carotid disease is usually implicated, cardiogenic embolism is the cause of 20% of TIAs and stroke.

s/s with ischemic

change LOC, VS, visual, speech

bruit with complete and partial occlusion of carotid

complete-no bruit partial-bruit

DD b/w ischemic presentation and hemorrhagic

hemorrhagic is more acute in onset and more focal

% of infarcts to hemorrhages

infarcts > hemorrhages infarcts 80%, hemorrhages 20%

s/s of TIA

ipsilateral monocular blindness ( amaurosis fugax)

sedation with stroke

only if needed

s/s of hemorrhagic stroke

s/s of suddent increase in ICP (vomiting, HA, altered LOC) L. dominant hemisphere---> R. hemiparesis, aphasia ( Broka/Werniske ) diarthria, difficalty writing and reading R. non-dominant ---> L hemiparsis, R visual, spatial disorientation (not even remember how to get around their home any more).

speech impairment TIA or stroke?

stroke> then TIA