{"id":5126,"date":"2011-09-06T15:55:29","date_gmt":"2011-09-06T15:55:29","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5126.htm\/"},"modified":"2018-11-10T17:46:28","modified_gmt":"2018-11-10T22:46:28","slug":"ischemic-stroke","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/ischemic-stroke.htm\/","title":{"rendered":"Ischemic Stroke (CVA)"},"content":{"rendered":"
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<\/a><\/p>\n <\/p>\n Lacunar\/small vessel strokes-usually eithe risolated sensory or isolated motor<\/p>\n Cortical\/large vessel=alterations of cosciousness, thinking, language<\/p>\n Ant=leg, Arm\/face=MCA, Homonymous hemianopsia=PCA<\/p>\n Must, must do sensory exam inthese patients, often times they will not complain fo sensory c\/o<\/p>\n <\/p>\n <\/a><\/p>\n <\/p>\n from Michael Liao<\/p>\n NINDSNNT 6 (42.7% vs 26.5%)NNH 17 (6.4% vs 0.6%)ECASSIIINNT 14 (52.4% vs 45.2%)NNH 47 (2.4% vs 0.2%)…. 23 (7.9% vs 3.5% with NINDS definitions)NNT is based on mRS <= 1 at 3 moNNH is based on symptomatic ICHI use all the NINDS data as it appears they skewed both part 1 andpart 2 (artificially(?)) to have approx half of the patients in the0-90min time windows. I find NINDS a bit trickier to piece back together than ECASS3.<\/p>\n —<\/p>\n <\/p>\n Expansion of TPA window to 4.5 hours by AHA (Stroke 2009;40:)<\/p>\n ECASS III<\/p>\n Table 1 ECASS III Exclusion Criteria<\/strong><\/p>\n The Evidence <\/strong>Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke, N Engl J Med 2008; 359: 1317-1329.<\/a>\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 t-PA\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Placebo\u00a0\u00a0\u00a0 NNT\u00a0\u00a0\u00a0 NNHGood Recovery at 90 Days\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0<\/strong>\u00a0\u00a0\u00a0 52.4%\u00a0\u00a0\u00a0\u00a0 45.2%\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 14\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 N\/A Symptomatic ICH\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong>2.4%\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 0.3%\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 N\/A\u00a0\u00a0\u00a0\u00a0 47Death\u00a0\u00a0\u00a0\u00a0<\/strong>\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 7.7%\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 8.4%\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 N\/A\u00a0\u00a0\u00a0\u00a0 N\/A<\/p>\n Tenecteplase vs. Alteplase-New inclusion criteria, manufacturer supported, (N Engl J Med 2012;366:1099-107.)<\/p>\n <\/p>\n Acute Stroke with NIHSS Score of 0<\/strong><\/p>\n <\/p>\n Physicians rely on the National Institutes of Health Stroke Scale (NIHSS) to evaluate patients with suspected acute stroke and to make decisions about acute treatment. The NIHSS correlates with infarct size, clinical severity, and long-term outcome. It is important to recognize, however, that ischemic stroke may cause symptoms that are not captured by the NIHSS scale.<\/p>\n The NIHSS scale is highly weighted toward deficits caused by anterior circulation strokes, whereas deficits caused by posterior circulation strokes receive fewer points (1-3).\u00a0 Within the anterior circulation, the scale underestimates the degree of right versus left hemisphere injury (1,4). It is possible that some patients with persistent symptoms on arrival to ED and an NIHSS score of 0 still have an infarct (1).<\/p>\n In a recent study, stroke patients with an NIHSS score of 0 most commonly presented with nausea, vomiting, and headache, all of which are associated with posterior circulation ischemia (1). Midline lesions of the cerebellum cause truncal ataxia, which is not part of the NIHSS.\u00a0 In addition, decreased visual acuity, Horner’s syndrome, and memory impairments are neurologic deficits not captured by the NIHSS.\u00a0 Subtle limb weakness (4\/5) in an upper motor neuron pattern (extensors of the arms or flexors of the legs) may not be observed on the motor component of the NIHSS.<\/p>\n These data reinforce that the NIHSS cannot replace history and a thorough neurologic exam to diagnose acute stroke and that the NIHSS alone cannot be used to rule out a stroke in patients with acute persistent symptoms.<\/p>\n References:<\/em><\/p>\n (1) Martin-Schild S, et al.\u00a0\u00a0 Zero on the NIHSS Does Not Equal the Absence of Stroke Ann Emerg Med<\/em> 2010 Sep 8. [Epub ahead of print]<\/p>\n (2) Libman RB, et al. Differences between anterior and posterior circulation stroke in TOAST Cerebrovasc Dis<\/em> 2001;11:311\u0096316.<\/p>\n (3) Sato S, et al. Baseline NIH stroke scale score predicting outcome in anterior and posterior circulation strokes Neurology<\/em> 2008;70:2371\u00962377.<\/p>\n (4) Fink JN, et al. Is the association of National Institutes of Health Stroke Scale scores and acute magnetic resonance imaging stroke volume equal for patients with right- and left-hemisphere ischemic stroke? Stroke<\/em> 2002;33:954\u0096958.<\/p>\n (Source Unknown Sorry!!!!!)<\/p>\n <\/p>\n <\/p>\n <\/p>\n Acute Stroke, Neuroimaging, and Thrombolysis<\/strong><\/p>\n Reference: <\/em>Latchaw RE,et al. Recommendations for imaging of acute ischemic stroke: a scientific statement from the American Heart Association Stroke<\/em> 2009;40(11):3646-78.<\/p>\n <\/p>\n _____<\/p>\n <\/p>\n <\/p>\n from emedhome<\/p>\n The NINDS Study found a 31% sensitivity for early signs of ischemic stroke on noncontrast CT within 3 hours of symptom onset. The rate of detection increased to 82% at 6 hours (1).<\/p>\n Early signs of cerebral ischemia on CT:<\/p>\n The sooner these signs become evident, the more profound is the degree of ischemia (1,2). Typically, at 6-12 hours sufficient edema is recruited into the stroke area to produce significant regional hypodensity on CT; a large hypodense area present within 3 hours of reported symptom onset should prompt careful review regarding the time of stroke symptom onset.<\/p>\n There is controversy as to whether early signs of infarct on CT are a contraindication to thrombolysis. The presence of CT evidence of infarction early in presentation has been associated with poor outcome and increased propensity for hemorrhagic transformation after thrombolytics in some studies (3,4).\u00a0 In the NINDS trial, there was no interaction between early infarction signs and tPA treatment for any clinical outcomes. Currently early signs of ischemia on CT are not generally considered to be a contraindication to use of tPA. \u00a0However, “frank hypointensity” on CT, particularly if it involves more than one third of an MCA territory, is a strong contraindication to treatment (1).<\/p>\n References:<\/p>\n (1 ) Latchaw et al.\u00a0 Recommendations for imaging acute ischemic stroke:\u00a0 A scientific statement from the American Heart Association \u00a0Stroke\u00a02009;40:3646-78.<\/p>\n (2) Patel SC, et al. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Lack of clinical significance of early ischemic changes on computed tomography in acute stroke\u00a0JAMA. 2001;286: 2830\u00962838.<\/p>\n (3) von Kummer R, et al. Acute stroke: usefulness of early CT findings before thrombolytic therapy\u00a0Radiology1997;205(2):327-33.<\/p>\n (4) Dzialowski I, et al. Extent of early ischemic changes on computed tomography (CT) before thrombolysis: prognostic value of the Alberta Stroke Program Early CT Score in ECASS II\u00a0Stroke\u00a02006;37(4):973-8.<\/p>\n <\/p>\n <\/p>\n <\/p>\n 80-85% of strokes<\/p>\n majority are thrombotic vs. embolic (Mitral Stenosis, MI, A-Fib)<\/p>\n Hallmark of stroke is sudden onset of focal neurological derangement in a vascular area<\/p>\n <\/p>\n Hemorrhage<\/strong> Migraine<\/strong> Hyperglycemia<\/strong> Carotid Dissection<\/strong> Todd’s Paralysis<\/strong> Bell’s<\/strong> Encephalitis\/Abscess<\/strong> Temporal Arteritis<\/strong> Hypoglycemia<\/strong> Hyponatremia<\/strong> Hypertensive Encephalopathy<\/strong> Air Embolism<\/strong> Multiple Sclerosis<\/strong> Dementia<\/strong><\/p>\n <\/p>\n Anterior Circulation<\/strong><\/p>\n Frontoparietal Lobes<\/p>\n Anterior Aspect of Temporal Lobes<\/p>\n Optic Nerve and Retina<\/p>\n Deep Gray Matter Structures<\/p>\n <\/p>\n Posterior Circulation<\/strong><\/p>\n Medial Aspect of Temporal Lobes<\/p>\n Visual Occipital Cortex<\/p>\n Thalamus<\/p>\n Brainstem<\/p>\n Upper Spinal Cord<\/p>\n Cerebellum<\/p>\n Auditory and Vestibular Aspects of the Ear<\/p>\n <\/p>\n Paralysis mainly of opposite leg and mild arm involvement<\/p>\n Sensory deficits paralleling paralysis<\/p>\n Altered mentation, confusion, judgment, and impaired insight<\/p>\n Gait apraxia (clumsiness)<\/p>\n Bowel and bladder incontinence<\/p>\n Paralysis of opposite side of body; arm and face worse than leg<\/p>\n Sensory deficits paralleling paralysis<\/p>\n Blindness in half of visual field (hemianopsia)<\/p>\n Aphasia (if dominant hemisphere involved, usually left)<\/p>\n Hemineglect (If non-dominant hemisphere, usually right)<\/p>\n Inability to recognize known objects (agnosia)<\/p>\n If Gaze preference, patients look towards the lesion<\/p>\n<\/span>NNT<\/span><\/h3>\n
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<\/span>2009 AHA Stroke Imaging Recs<\/span><\/h2>\n
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<\/span>Advanced Stroke Imaging References<\/span><\/h2>\n
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<\/span>Early CT Signs of Ischemic Stroke<\/span><\/h2>\n
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<\/span>Differential<\/span><\/h3>\n
<\/span>Common Major Stroke Syndromes<\/span><\/h3>\n
Anterior cerebral artery<\/h4>\n
Middle cerebral artery<\/h4>\n