1. Stroke is the third leading cause of death in the United States and the most common cause of long-term disability.
2. Completed stroke and transient ischemic attack (TIA) have the same pathophysiology and are distinguished mainly by the duration of ischemia and resultant infarction.
3. TIA had been arbitrarily defined as focal brain ischemia with symptoms resolving completely within 24 hours. Neuroimaging has revealed that a large number of events with symptoms lasting hours before complete resolution are, in fact, cerebral infarctions. This has led to revised definitions of TIA that take imaging data into account.
1. The onset of stroke is typically sudden, and symptoms vary according to the site of the ischemia.
2. The history is directed at distinguishing stroke and TIA from other causes of sudden focal deficits such as migraine and focal seizures.
3. Underlying factors in the history that suggest the cause of stroke are
a. Heart disease, including atrial fibrillation, and peripheral arterial disease.
b. Atherosclerotic risk factors (hypertension, diabetes, hypercholesterolemia, smoking, sedentary lifestyle, family history of stroke and atherosclerotic disease).
c. History suggesting thrombophilia, cranial or cervical trauma, or neck, face, and head pain that suggest arterial dissection; history of fever, chills, cardiac symptoms, or drug abuse that suggest endocarditis.
4. When acute thrombolytic therapies are being considered, the precise time of symptom onset and problems that contraindicate such therapy should be determined.
1. Most cases of focal cerebral ischemia are caused by blockage of a cerebral artery. The most common causes of occlusion are
a. Embolism of thrombotic material from the heart chambers or valves or from another source such as the aorta
b. Atherosclerosis in a large or medium artery, particularly the carotid arteries, causes either stenosis with reduction of distal blood flow, or local thrombosis that causes artery-to-artery embolism to a cerebral vessel
c. Hypertrophy and ultimately luminal stenosis of small cerebral vessels, the result of chronic exposure to hypertension (HTN), diabetes mellitus (DM), and hyperlipidemia
2. Less common causes of vascular occlusion include cervical arterial dissection; arteritis (vasculitis of large or small vessels); vasospasm; thrombophilia; and rarely embolism of material other than thrombus, such as fat, air, tumor, amniotic fluid, or intravascular medical devices. The main disorders underlying stroke are listed in Table 12-1, but most are infrequent in comparison to cardiac-source embolism and large vessel atherosclerosis or small vessel disease.
1. The examiner should note the temperature, blood pressure (BP), and cardiac rhythm, the quality of carotid pulses and the presence of bruits, and the quality of heart sounds and presence of murmur and any findings that might suggest a special mechanism, such as splinter hemorrhages (endocarditis) or petechiae (thrombotic thrombocytopenic purpura).
2. The neurologic examination should define the localization and clinical stroke syndrome. This allows prediction of the vessel involved and the mechanism of vascular occlusion.
1. Middle cerebral artery (MCA) territory syndrome: Contralateral gaze paresis, hemiparesis, and hemisensory loss, often with contralateral visual field loss, and cortical signs (aphasia with left hemispheric lesions; neglect with right).
2. MCA branch (partial) syndromes: Nonfluent aphasia (Broca aphasia if perisylvian and transcortical motor aphasia if sparing the perisylvian area) if involving
anterior division branches and fluent aphasia (Wernicke aphasia if perisylvian and transcortical sensory aphasia if sparing the perisylvian area) if involving posterior division branches of the left MCA.
TABLE 12-1 Main Causes of Stroke
Atherosclerotic disease of large and medium arteries: Hyperlipidemia, HTN, DM, hyperhomocysteinemia, radiotherapy, pseudoxanthoma elasticum
Nonatherosclerotic disease of large and medium arteries: Arterial dissection, fibromuscular dysplasia, moyamoya disease, sarcoidosis, fungal and tuberculous vasculitis, varicella zoster vasculitis, systemic vasculitic syndromes, isolated CNS angiitis
Lipohyalinosis, atherosclerosis, infections (syphilis, TB, cryptococcosis), vasculitis
HTN, atrial fibrillation, valvular heart disease, cardiomyopathy, paradoxical embolism, left atrial thrombus, ventricular mural thrombus after MI, bacterial endocarditis, nonbacterial thrombotic endocarditis (cancer, antiphospholipid antibody syndrome), left atrial myxoma
Oral contraceptives, pregnancy and the puerperium, antiphospholipid antibody syndrome, sickle cell disease, cancer, polycythemia vera, essential thrombocytosis, TTP, DIC, markedly elevated prothrombotic factors, deficiency or dysfunction of protein C, protein S, or antithrombin III, activated protein C resistance (factor V Leiden genotype or acquired), factor IIG20210A mutation, dysfibrinogenemias, disorders of fibrinolysis
Vasospasm, vasculitis, cardiac arrhythmias, endocarditis, mycotic aneurysm, injection of infected or thrombogenic material
CADASIL, Fabry disease, Sneddon syndrome, MELAS
TPP, thrombotic thrombocytopenic purpura; DIC, disseminated intravascular coagulation; CADASIL, cerebral autosomal dominant angiopathy with subcortical infarcts and leukoencephalopathy; MELAS, mitochondrial encephalopathy with lactic acidosis and stroke like episodes; CNS, central nervous system; TB, tuberculosis; MI, myocardial infarction; HTN, hypertension; DM, diabetes mellitus.
3. Anterior cerebral artery (ACA) syndrome: Predominant leg weakness and sensory deficits, sparing of vision. Bilateral frontal signs suggest a common origin of the two anterior cerebral arteries.
4. Posterior cerebral artery (PCA) syndrome: Contralateral homonymous hemi- or quadrantanopsia, typically with intact motor and somatosensory function or with associated cortical deficits.
a. Memory loss from medial temporal infarction
b. Alexia without agraphia from dominant visual cortex and splenium of corpus callosum infarction
c. Agnosias, such as color naming and recognition disorders and prosopagnosia (facial recognition disorder), from infarction of the inferior temporo-occipital cortex
5. Mid-basilar artery syndrome implying atherosclerotic stenosis or occlusion of the mid-basilar artery with pontine (dysarthria, horizontal diplopia, vertigo, quadri-paresis) and cerebellar dysfunction.
6. Top-of-the-basilar syndrome implying embolic occlusion of the distal basilar artery with midbrain (decreased arousal; vertical and horizontal diplopia; bilateral ptosis; unequal and irregular poorly reactive pupils), thalamic, and occipital dysfunction.
7. Lacunar syndromes usually indicate occlusion of a small cerebral vessel (e.g., pure motor or pure sensory syndromes without visual loss or cortical findings [no aphasia or neglect]) or isolated hemiparesis with ataxia. Dysarthria is common when such lacunar infarcts are in the pons or the internal capsule.
8. Border-zone (watershed) infarcts occur when a region of the cerebrum is subject to reduced blood flow either from proximal vascular occlusion or from global reduction in perfusion due to systemic hypotension.
a. Anterior watershed stroke typically produces the “man-in-a-barrel” syndrome characterized by leg and proximal upper extremity weakness with relative sparing of the distal upper extremities from infarction of the ACA and MCA border zone in the high frontal convexity.
b. The posterior watershed stroke may produce Balint syndrome (astereognosis, optic ataxia, and ocular apraxia) from infarction of the MCA and PCA border zone in the parieto-occipital region.
1. The goals of neuroimaging acutely after the stroke are:
a. To define the site and location of an established infarct and the extent of ischemic tissue at risk
b. To identify the site of an acute vascular occlusion
c. To identify hemorrhage or unexpected lesions mimicking acute cerebral infarction
2. Computed tomography (CT) and CT angiography
a. Noncontrast CT dependably identifies acute hemorrhage. It is insensitive to infarction within hours of stroke onset. However, subtle changes are sometimes detected: “dense MCA sign” of thrombus in the MCA stem, sylvian fissure dot sign indicating thrombus in the more distal MCA branches, or hypodensity, loss of gray-white differentiation, and sulcal effacement all of which indicate early infarction. Loss of gray-white differentiation is most commonly seen in the basal ganglia-capsular region and insula (“insular ribbon sign”).
b. CT angiography allows evaluation of the patency of cerebral vessels from the aortic arch through the neck and for large intracranial vessels at least to the first branching beyond the circle of Willis.
c. CT perfusion techniques give acute information about the size of established infarct and of hypoperfused tissue at risk of infarction.
3. MRI and MRA
a. The diffusion-weighted imaging (DWI) sequence of MRI is far more sensitive than CT for detecting early infarction. Acute infarction becomes bright on this sequence within minutes of tissue infarction. Correlation with low signal on apparent diffusion coefficient (ADC) images differentiate acute infarction from other causes of bright signal on DWI.
b. MRA defines flow in the cerebral vessels from the aortic arch to the intracranial arteries but conventionally use methods that may overestimate the degree of stenosis.
c. MRI perfusion techniques can give information about the size of established infarct and of hypoperfused tissue at risk.
4. Conventional angiography
a. It is more sensitive and specific than either CTA or MRA and, remains the gold standard for diagnostic vascular imaging; however, it is infrequently required acutely except as part of interventional therapy.
5. Carotid duplex ultrasound
a. It includes Doppler assessment of blood flow velocities and anatomic imaging by gray scale and color flow techniques.
b. It is widely available, noninvasive, and, in good hands, reliably defines and quantifies most proximal atherosclerotic carotid lesions.
c. Doppler waveforms can also give indirect information about upstream and downstream stenoses that are outside of the field of carotid ultrasound.
6. Transcranial Doppler ultrasound (TCD)
a. TCD allows imaging of the flow of the major vessels of the circle of Willis, the proximal middle, anterior, and posterior cerebral arteries; the ophthalmic artery; and the vertebral and basilar arteries. Information about direction and velocity of flow allows identification of stenosis or intracranial vessels or vasospasm and to assess pathways of collateralization.
b. High flow velocities suggest vascular narrowing from stenosis or vasospasm, or elevated flow, as in generalized high flow states, such as arteriovenous malformations or collateral flow in the setting of stenosis or occlusion at another site. Because ultrasound is safe and noninvasive, it can be used serially for repeated examinations. Its most valuable application has been serial evaluation of the severity of cerebral vasospasm after subarachnoid hemorrhage (SAH).
1. Electrocardiogram (ECG), chest radiograph (CXR), glucose, electrolytes, blood urea nitrogen (BUN), creatinine, complete blood count (CBC) with platelets, and prothrombin time ([PT], international normalized ratio [INR]), and an activated partial thromboplastin time (aPTT) should be part of the initial evaluation to help determine the cause of the event and to provide information critical to the planning of acute therapy.
2. If fever or cardiac murmur is present, or if there are other reasons to suspect endocarditis, then C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR), blood cultures, and echocardiogram are important to pursue this diagnosis.
3. If there is reason to suspect drug abuse, toxicology screening is valuable.
4. In the postacute phase, echocardiography, cardiac rhythm monitoring, further definition of the cerebral vasculature and laboratory tests directed at stroke risk factors are indicated as follows:
a. Fasting serum glucose; total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol; and triglycerides.
b. High sensitivity CRP elevation and hyperhomocysteinemia have been identified as a modifiable risk factor for atherosclerosis.
c. Where aortic atheroma, valvular, or left atrial appendage visualization, or definition of a patent foramen ovale (PFO) will alter secondary preventive therapy, transesophageal echocardiography should be considered, because the sensitivity of transthoracic echocardiography is low for lesions at these sites.
1. Cerebral perfusion depends on the mean systemic arterial pressure (MAP) based on the basic hemodynamic relationship [CBF = (MAP – CVP)/CVR, where CBF = cerebral blood flow, CVP = cerebral venous pressure, and CVR = cerebrovascular resistance].
2. Areas of brain distal to narrowed or occluded arteries may be supplied by collateral vessels. When fully dilated (i.e., autoregulated to maximize CBF), flow in these vessels becomes passively dependent on the MAP. Therefore, it is desirable to maintain MAP high in the setting of acute stroke.
TABLE 12-2 Acute Antihypertensive Therapy for Administration of Intravenous Tissue Plasminogen Activator
Management of BP before treatment with IV tPA
For SBP > 185 mm Hg or DBP > 110 mm Hg
Give IV labetalol 10-20 mg over 1-2 min; may repeat once, or
Give nitropaste 1-2 in, or
Give nicardipine infusion 5 mg/hr; titrate up by 2.5 mg/hr at 5-15 min intervals; maximum dose 15 mg/hr; when desired BP attained, reduce to 3 mg/hr
If BP does not decline and remains >185/110, do not administer tPA
Management of BP during and after treatment with IV tPA
Monitor arterial BP during the first 24 hr after starting treatment: every 15 min during treatment and for the first 2 hr, then every 30 min for 6 hr, then every hour for 16 hr
If systolic BP is 180-230 mm Hg or diastolic BP 105-120 mm Hg for two or more readings 5-10 min apart:
Give labetalol 10 mg IV over 1-2 min. May repeat every 10-20 min; maximum dose 300 mg, or
Give labetalol 10 mg IV followed by an infusion of 2-8 mg/min
If systolic BP > 230 mm Hg or diastolic BP is 121-140 mm Hg for two or more readings 5-10 min apart:
Give labetalol 10 mg IV over 1-2 min. May repeat every 10-20 min; maximum dose 300 mg, or
Give labetalol 10 mg IV followed by an infusion of 2-8 mg/min, or
Give nicardipine infusion 5 mg/hr; titrate up to desired effect by increasing 2.5 mg/hr every 5 min to a maximum of 15 mg/hr
If BP is not controlled, consider sodium nitroprusside (starting at 0.5 μg/kg/min)
IV, intravenous; BP, blood pressure.
From Guidelines for early management of adults with ischemic stroke. Stroke. 2007; 38:1655.
3. It is common for patients with acute stroke to have acute BP elevations on presentation.
a. In general, BP should not be lowered unless
1) BP lowering is necessary to fulfill criteria for safe thrombolysis (see the section on Intravenous Thrombolysis and Tables 12-2 and 12-3), or unless acute medical issues demand it:
a) Acute myocardial infarction
b) Aortic dissection
c) Hypertensive crisis with end-organ involvement (congestive heart failure, acute renal failure, hypertensive encephalopathy)
b. A threshold above which BP should be treated acutely has not been established outside of these complications; however, consensus guidelines from the American Stroke Association suggest that therapy should be withheld unless diastolic BP is above 120 mm Hg or systolic BP is above 220 mm Hg.
c. Patients with excessive BP elevation who are otherwise suitable for tissue plasminogen activator (tPA) should be treated acutely to achieve tolerable BP for therapy (systolic BP ≤ 185, diastolic BP ≤ 110). The antihypertensive goals and regimen modeled after the practice in the National Institute of Neurological Disorders and Stroke (NINDS) trial of intravenous (IV) tPA and recommended by the American Stroke Association are shown in Table 12-2.
1. Patients should be monitored with pulse oximetry and given supplemental oxygen for desaturation to less than 95%.
2. Both hyperthermia and hyperglycemia may increase the size of the ultimate infarct; therefore, patients should generally receive antipyretic medications and external cooling, if needed, to maintain normal body temperature and insulin to avoid excessive glucose elevation.
1. All patients who present within 3 hours of onset of stroke symptoms should be considered for IV thrombolytic therapy with tPA.
2. Patients who can be treated within 3 to 4.5 hours should be considered for IV tPA therapy if they do not meet these added exclusion criteria: Older than 80 years, NIHSS more than 25, taking oral anticoagulants, history of prior stroke, or DM.1
3. Indications and contraindications for IV thrombolysis are listed in Table 12-3.
4. For suitable patients, IV tPA should be given as soon as the essential evaluation can be completed. The dose of tPA is 0.9 mg/kg to a maximum total dose of 90 mg. Ten percent of this dose is given as a bolus over about 1 to 2 minutes. The remainder is infused over 1 hour. It is advised that emergency departments establish protocols for administration to speed up preparation and minimize errors.
5. BP should be controlled within recommended parameters for 24 hours after administration (see Table 12-2), and patients should be closely monitored for evidence of hemorrhage with serial neurologic examinations and follow-up CT scanning.
6. No adjunctive antiplatelet or anticoagulant medication should be given for 24 hours after IV thrombolysis.
1. Where adequate facilities and expertise are available, emergency angiography allows for mechanical clot removal and delivery of intra-arterial thrombolytic agents in patients who present after 3 to 4.5 hours or who will not safely tolerate systemic treatment. Such therapies have been shown to promote early recanalization of occluded arteries, which correlates with favorable outcomes. One controlled study of patients with proximal MCA occlusion demonstrated clinical benefit of intra-arterial thrombolysis when applied within 6 hours of symptom onset. However, the status of intravascular approaches to acute strokes is still being evaluated. Conventional IV thrombolysis should not be delayed in anticipation of intravascular treatment.
2. Proper concurrent use of heparins, antiplatelet agents, and induced HTN have not been established by systematic study, and at this time are based on institutional protocols.
1. Acute administration of aspirin and other antiplatelet agents has not been shown to decrease stroke size, although in large trials, early institution of low-dose aspirin has slightly improved outcome, possibly by reducing the incidence of early recurrent events within approximately 2 weeks.
2. Early use of unfractionated heparin and low-molecular-weight heparins has been studied with variable results.
3. There appears to be some benefit in preventing early recurrent events in patients with carotid stenosis and atrial fibrillation.
4. Patients with prosthetic heart valves requiring anticoagulation and other cardiac lesions representing clear embolic risks are best placed back on anticoagulants as early as judged to be safe.
TABLE 12-3 Indications and Contraindications for Intravenous Tissue Plasminogen Activator for Acute Ischemic Stroke
Acute ischemic stroke with disabling deficit
Onset time within 3 hr (and within 3-4.5 hr with the added exclusion criteria noted below under “Absolute contraindications, item 4.”)a
Head CT without well-established infarct, hemorrhage, or alternative explanation for focal neurologic deficit
Hemorrhage on head CT; well-established infarct, or other diagnosis that contraindicates treatment (tumor, abscess, etc.)
Known CNS vascular malformation or tumor
Mild or rapidly improving deficit
For 3-4.5 hr window only: >80 yr old; NIHSS > 25, taking oral anticoagulants, history of both prior stroke and diabetes mellitus
Significant trauma within 3 mo
Stroke within 3 mo
History of intracranial hemorrhage or symptoms suspicious for SAH
Major surgery within past 14 d or minor surgery within past 10 d, including liver and kidney biopsy, thoracocentesis, lumbar puncture
Arterial puncture at noncompressible site within 7 d
Gastrointestinal, urologic, or pulmonary hemorrhage within 21 d
Known bleeding diathesis or hemodialysis
PTT > 40 s: INR > 1.5; platelet count < 100,000 mm3
SBP > 185 or DBP > 110 despite therapy to lower BP acutely
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