ISCHEMIC CVA

INTRODUCTION Stroke = any vascular injury that reduces CBF to a specific region of the brain, causing neurologic impairment 80% ischemic, 20% hemorrhagic ISCHEMIC STROKES Thrombosis (1/3) or embolic (2/3) (carotid or heart) Large vessel thrombosis Cerebral branch points common, esp in ICA More common in men Plaque rupture and thrombosis as per MI Can shed emboli down stream Small vessel thrombosis (Lacunar Infarcts) Small, terminal sections of vessels Common in HTN, DM Commonly affect subcortical areas Infarcts are few mm to 2cm Most common in internal capsule, BG, thalamus, pons Lacunar syndromes: 20 have been described but most common are... Pure motor Pure sensory Ataxic hemiparesis Clumpsy hand syndrome Clues to Lacunar infarct No cognitive deficits No language deficit No LOC NO simultaneous motor and sensory findings No visual loss???? (could hit thalami) No loss of cortical sensory function (graphesthesia, stereognosis) Embolization Cardioembolic in 25% of all strokes Atrial fib is MCC 20% have Afib on admission ECG Afib: more like to be big, large vessel CVA and higher mortality Mural thrombi also seen with severe LV dysfunction: post MI (1-2% will have CVA), cardiomyopathy, CHF, myocarditis Carotid artery source of emboli also common CVA in the young person Hypercoagulable states: APC-resistance, Prot C def, Prot S def, antiphospholipid Ab syndrome, oral contraceptives, SLE Polycythemia DVT/PE with PFO Vasculitis Fibromuscular hyperplasia of cerebral vessel Prolonged vasoconstriction from Migraine Transient Ischemic Attack

Neurologic deficit completely resolves in 24hrs Important WARNING sign of impending CVA Majority last less than 30 min Crscendo TIAs = three or more TIA w/i 72hrs Anterior circulation TIA: 50% will have carotid disease on angio, others wont Clinical deficits RESOLVED at 24hrs but 60% have CT and 80% have MR findings of infarction First TIA > 65yo: 50% have evidence of previous infarct on MR --------> silent infarcts are common PROGNOSIS: see Johsons article in JAMA

Risk Factors for Ischemic CVA Modifiable: HTN, smoking, TIAs, heard disease, DM, hypercoagulopathy, carotid bruit, sickle cell anemia, polycythemia, hypercholesterolemia, inactivity Nonmodifiable: age, sex, race, prior stroke, fhx, previous MI

PATHOPHYSIOLOGY Review anatomy of circulation Ischemic brain cells become neurologically silent and thus lose function Ischemic penumbra is the area surrounding the primary injury where small amounts of blood flow are maintained by collateral circulation Natural collateral flow is important in determining deficit Time of vessel occlusion is KEY to determining < 2hrs usually reversible 2 - 6 hrs may or may not be reversible > 6 hrs definately NOT reversible

CLINICAL FEATURES General Classically sudden onset but can be stuttering or gradual onset Deficit depends on collateral supply Stroke in evolution = focal deficits worsen over the course of minutes to hours (20% of anterior and 405 of posterior circulation strokes have evidence of progression; anterior progress over 24hrs, posterior can progress over 3 days) Completed stroke = neurologic deficit persists longer than 3 weeks even if some improvement has occurred

Anterior Circulation Stroke Carotid ---------> ACA and MCA territories Rarely present with loss of consciousness (can occur if patient has had many previous strokes) Anterior Cerebral Artery Rare b/c of collateral supply Frontal Lobe function

Altered mentation Impaired judgement and insight Presence of primitive reflexes (suckle, grasp) Bowel and bladder incontinence Weakness and sensory loss of LEG > ARM is characteristic (contralateral side; shouldnt involve arm unless MCA involved) Apraxia or gait clumsiness can occur Middle Cerebral Artery Contralateral weakness and sensory loss in FACE/ARM > LEG is characteristic Weakness may be fairly focal in a part of the face or arm but is almost always accompanied by sensory loss in the area of wknes Ipsilateral (??) Hemianopsia is common Agnosia common (inability to recognize previously known subjects) Gaze preference TOWARD the lesion (distruption of the cortical lateral gaze centers): a stroke looks TOWARD the lesion, a seizure looks AWAY from the lesion Neglect if involves nondominant hemiphere Aphasia common if affects the dominant hemisphere Aphasia = disturbance in language function (comprehension, repetition, naming, fluency) Dysphasia = Aphasia Dysphagia = difficulty swallowing Dysarthria = normal language function but slurred speech due motor deficit of muscles involved in speech Wernickes aphasia = receptive aphasia Brocas aphasia = expressive aphasia Posterior Circulation Stroke Vertebrobasillar system Can present with loss of consciousness b/c RAS is in brain stem Nausea and vomiting common b/c of emesis center in BS Parietal lobes: neglect, visual neglect, visual agnosia (unable to recognize known objects), alexia (unable to understand writing) Occipital lobes: homonomous hemianopsia Cranial nerves of BS: diplopia, IIIrd nerve palsy, vertigo, nystagmus, facial droop, dysphagia Cerebellum: ataxia Sensory and motor deficits Crossed deficits = disruption of sensation/power on one side of face but opposite side of body

DDX OF ISCHEMIC STROKE Vascular ICH Vasculitis: GCA, PAN AVM

Carotid dissection Vertebral dissection Infectious Brain abscess Meningitis/Encephalitis Neoplastic Brain tumor Traumatic EDH SDH SAH Contusion/hemorrhage Seizure Migraine Metabolic (hyperglycemia, hypoglycemia, wernikes encephalopathy (DOA), Air embolism (diving, during procedures) Peripheral vertigo

DIAGNOSTIC STRATEGIES Chemstrip ECG R/O MI and Afib Be aware of ECG changes with CNS event (cannot clinically distinguish ST elevation or ischemic changes due to ACS vs CNS event -> to cath lab) Labs Thrombocytosis or thrombocytopenia Polycythemia Coags CT head MAIN reason = r/o hemorrhagic stroke, tumor, AVM, SDH, EDH Sensitivity 100% for ICH and 95% for SAH Early findings in 1/3 (w/i 3hrs) Localized Hypodensity Loss of Grey - White differentiation Hyperdense MCA sign Dissapearing Basal Ganglia sign Sulcal effacement (due to edema) Loss of insular ribbon Mass effect (due to edema) Majority do not have findings until 6 - 12 - 24hrs Contrast CT is not indicated unless noncontrast is abnormal and you want contrast to look for tumor, abscess, AVM Echocardiogram Mural thrombus, tumor, PFO, valvular dz, valvular veggies, Consider in all patients < 65 with no obvious source of CVA

Carotid Dopplers Known or suspected lesions in carotids May identify candidates for heparin or emergency carotid endarterectomy May require angiography to further delineate lesion Other Angiography MRA: identifies large vessel occlusions well, may miss small vessel occlusion; is replacing angiography for identifying occlusion or stenosis in selected pts New MRI techniques: diffusion-weighted imaging (DWI) and perfusionweighted imaging (PWI) may be able to differentiate reversible lesions CTA MRI Better for early detection Better for posterior circulation infarcts/lesions

ISCHEMIC STROKE MANAGEMENT Prehopital Time is brain ABCs O2 - iv General Time is brain :. stroke protocols Avoid overhydration b/c it increased edema Airway isnt usually an issue unless posterior circulation or vomiting Avoid glucose solutions for iv hydration (hyperglycemia worsens outcomes) Chemstrip is sixth vital sign Determining TIMING of ONSET critical to determine eligibility for TPA ED Approach Triage to monitored bed ABCDEF, adjunts, secondary survey, adjunts Dont forget to check chemstrip Monitors - iv - 02 ECG, labs Quick neuro and general exam To CT Pearls of History History of previous CVA, risk factors Migraine: History of headache, migraines, aura, visual features Brain abscess: Fever, travel, dental work, neurosurgery, penetrating trauma Endocarditis: valvular lesions, IVDA, fevers Seizure activity Cocaine, amphetamine use Chest pain: dissection, MI Trauma: vascular dissection, EDH/SDH Pearls of Physical Examination Dont forget temp and chemstrip Peripheral manifestations of endocarditis Pulse differences, ischemic leg to suggest dissection

Carotid bruits Fundoscopy: papilledema, preretinal hemorrhage, HTN retinopathy BP Management with ischemic CVA or TIA Controversial b/c of limited data More aggressive control if getting tPA (table 95-5) Generally leave BP alone b/c brain does a better job of autoregulation Labetolol or nitroprusside iv favored (avoid nifedipine b/c big drops in BP) Leave BP alone unless (i) severe HTN (>220/120) (ii) getting tPA or (iii) has one of the following.... Aortic dissection Hypertensive encephalopathy Acute MI Severe CHF

ACUTE DRUG THERAPY Targets with tPA Door to doctor 10 min Door to CT 25 min Door to CT interp 45 min Door to tPA 60 min Intravenous tPA NINDS and Clevland data Must be initiated in 3hrs Dose = 0.9 mg/kg (max 90mg): 10% of dose as bolus and the rest over 60 min Onset MUST be clearly known Caution with CT findings of large infarcts (early hypodensity/hyperdense MCA signs) b/c increased risk of hemorrhage Not shown to be effective > 3hrs (being studied) Intraarterial tPA PROACT II May extend time window to 6hrs Bleeding rates still 10%

Patients receiving tPA st Restrict central venous access and arterial puncture during 1 24hrs Avoid placement of bladder catheter during infusion and until 30min a/f st Avoid NG tube if possible during 1 24hrs st Should NOT receive asa, heparin, warfarin, ticlopiding, etc w/i 1 24hrs People who have taken asa ARE eligible for tPA
ASA Being studied NNT is 100 for prevention of death or non-fatal recurrence in first few weeks NNT is 100 for prevention of death or dependance at 6 months Should not be given with tPA in first 24hrs (increased bleeding rates)

Heparin

Often given for ischemic strokes but benefit UNPROVEN No data has established the efficacy of anticoagulation Net balance of further thrombosis/embolism versus hemorrhagic transformation Consider for use: crescendo TIAs, cardioembolic source, high-grade carotid lesion, posterior circulation TIA, evolving strokes LMWH: benefit shown by Kay 1995 but not reproducible by larger study Neuroprotection Antioxidants, CCBs, NMDA inhibitors, glycine, glutamine antagonists None have been effective in human trials None have FDA approval

MANAGEMENT OF TRANSIENT ISCHEMIC ATTACK Same approach as per ischemic CVA ABCs, ECG, Labs, CT head Labs CBC, lytes, Cr, gluc, cholesterol PTT, INR ESR, syphylis serology?? Hypercoagulable w/u if: < 50yo and no cause, hx of prior venous thrombosis, hx of hypercoaguable state CT head Should be done for all TIAs 1% will reveal non-vascular mimic (tumor, AVM, abscess, etc) 20% show hypodensities Carotid Dopplers Arrange if bruit heard Echo Yield low (<3%) without evidence of heart disease Known heart disease: do TTE or TEE TEE for ... Young No cause No major risk factors Counselling Modify risk factors Risk of subsequent CVA Do NOT d/c HRT D/C oral contraceptive Antiplatelet Therapy Aspirin Proven benefit in preventing subsequent CVA NO difference has been demonstrated in dosing ECASA 80 - 325 mg/day Plavix (clopidogrel) CAPRIE trial: plavix vs ASA Showed plavix to be slightly better than ASA (relative risk reduction of 8% - NOT absolute RR) Ticlid (ticlopidine) Shown to be effective by CATS trial

 Other Disposition

Shown to be slightly better than ASA by TASS trial (20% relative risk reduction compared to ASA) Diarrhea, rash, neutropenia (1%) are problematic Disopyridamole Phosphodiesterase inhibitor Slightly better than ASA NO evidence for heparin routinely (consider with crescendo TIAs, carotid dissection, known severe carotid stenosis, antiphosholipid Ab syndrome) Warfarin being studied ED ----> start ASA (or plavix, or disopyridamole) No consensus of what to do if 2nd TIA when already on ASA Start antiplatelet therapy D/C and f/u with stroke prevention clinic or urgent neuro clinic Consider admission for high risk of early CVA (3 or more risk factors from Johnson article) age > 60 DM symptoms > 10 min weakness with episode speech impairment with episode

HEMORRHAGIC CVA
INTRODUCTION 10% of strokes 2Xs as common as SAH 30 day mortality 50% ( in 2 days) Etiologies: hypertensive hemorrhage, amyloid angiopathy, AVMs, hypertensive emergencies (sympathomimetics, pheo, cocaine), tumor bleed, anticoagulants Hypertensive hemorrhages Predominantly elderly Degenerative changes in small penetrating arteries leading to the formation of microaneurysms (MC in MCA territory) Most common sites..... Putamen 44% Other cortical areas 25% Thalamus 13% Cerebellum 9% Pons 9% Amyloid Angiopathy Tend to be lobar MC in whites Sudden increases in BP from any cause (drugs, etc) can lead to rupture of the abnormal vessel AVMs Can cause intraparenchymal or subarachnoid blood

More likely to bleed into the ventricles and subarachnoid space than are hypertensive ICHs and usually have a less disruptive impact on cerebral function

CLINICAL FEATURES Sudden onset headache, vomiting, HTN, focal neuro deficit Motor/sensory deficit contralateral to lesion Agitation, lethargy and may rapidly progress to coma 1/3 have significant growth of hemorrhage size in first hrs More likely to have precipitant like exertion, sex, valsalva, labor Airway more of a problem b/c of decreased LOC Cheyne-Stokes (deep and rapid then apnea) common with large ICH Irregular resp pattern with putamenal hemorrhages Normal resp pattern with CB hemorrhages Pontine hemorrhage: bilateral pinpoint pupils b/c of loss of sympathetics Dilated pupils: putamen Anisocoria, miosis, poor response with thalamic bleed Estimate volume of blood (ABC/2 method): see figure 95-1 DIFFERENTIAL DX OF HEMORRHAGIC CVA As per ischemic stroke DIAGNOSTIC STRATEGIES Labs, ECG, CT head Look for coagulopathy on labs Dysrhytmias and ECG changes MORE common than with ischemic CVAs CT head 95% sensitive for hemorrhagic Only misses very small lesions May appear isodense after days MANAGEMENT Essential you cant tell ischemic vs hemorrhagic until the CT ........THUS same approach as per ischemic CVA with more concern for ABCs b/c level of consciousness and arrythmia problems are more common RSI intubation: lidocaine and fentanyl for pretreatment, phenobarb for induction, succ not contraindicated in acute setting, ? contraindicated if recent CVA BP management Target BP is < 180/105 (some aim for < 160) Generally more aggressive Mx than with ischemic CVA Labetolol and nitroprusside iv are main options Management of complications Increased ICP: elevate head of bed, hyperventilation, mannitol for signs of worsening ICP or herniation (NOT used prophylactically) No role for steriods Seizures: dilantin prophylaxis considered for all pts (especially lobar ICH) Surgery Usually not beneficial Selected patients may benefit

Lobar hemorrhage with progressive deficit Deep hemorrhages: more damage done by surgery Cerebellar hemorrhages: more prone to operate b/c of high risk of sudden herniation/death