Stroke Definition Appearance sudden neurological deficit of vascular origin Manifestations Etiology varied varied Etiopathogenic classification Ischemic

Atherothrombotic cardioembolic lacunar Atrial atrial myocardial infarction Rheumatic Valvular Classification Hemorrhagic For other causes Vasculitis (LES) carotid dissection Hematoma Hemorrhagic Hypercoagulability

subarachnoid hemorrhage intraparenchymal For Time Evolution Ischemia Transient cerebral ischemic neurologic deficit reversible l infarction or progressive set Approach Diagnosis syndromic and differential with other causes of focal neurological deficit of or igin Diagnosing vascular lesion location Etiologic diagnosis severity rati ng Initial Assessment A third of patients who are having a stroke are unaware Contact emergency medica l service in recognition of airway Assessment, circulation and respiration Risk Factors Ischemic Age Hemorrhagic Age Using HAS > 65 Being male maternal family history of stroke DM 2 Smoking Alcohol Atrial fibrillation Carotid stenosis Hyperlipidemia evolving myocardia

drug Cocaine Amphetamines In <45th infrequent Enf. Etiologies Systemic Coagulopathies Physical Exploration Carotid Palpation for murmurs temporal artery embolic signs of coronary atherosclero sis Signs Peripheral Fundus Neurological Exam Functions Language Memory Care higher Sensitivity Positional thermoalgesic Awareness Cerebellum March's Standing Pairs cranial reflexes Pathologic tendon Signs Meningeal Topographic diagnosis Supratentorial Agnosia Aphasia Infratentorial Ataxia visual field cerebellar Diplopia Dysarthria Ageusia lingual dysmotility Muscle strength

Apraxia Deficit

Vascular Syndromes Location Internal Carotid Artery Contralateral hemiparesis or hemiplegia Deficit Hemihipoestesia homonymous hemianopia or hemi Aphasia or dysphasia Amaurosis fu gax Anosognosia Hemianosognosia crural paresis or sensory deficit or akinetic mu tism Apulia palmomentoniano March Reflection apraxic hemiparesis and sensory uri nary incontinence prevalence Homonymous hemianopia faciobraquial Aphasia, agraph

ia, alexia, acalculia, left-right confusion Apraxia clothing, anosognosia Ipsila teral nondominant hemisphere dominant hemisphere Contralateral Bilateral Anterio r Cerebral Middle Cerebral Contralateral Non-dominant hemisphere dominant hemisphere Vascular Syndromes A. Location Vertebrobasilar Artery Posterior cerebral deficit or quadrantanopia hemianopia with macular sparing, alexia without agraphia, agnosia for colors. He mihipoestesia, dysphasia, spatial disorientation, amnesia. Paralysis of cranial nerves III and IV neocerebellum Syndrome sixth nerve palsy, ageusia, deafness, t innitus, facial hypoesthesia dysphagia, dysphonia, loss of gag reflex ipsilatera l lingual hemiparesis, facial hypoesthesia, vertigo, nystagmus pure motor hemipa resis, pure hemisensitivo deficit, deficit pure motor sensory, ataxic hemiparesi s, dysarthria Lump Parkinsonism Mesencephalon Thalamus Bulb Lacunar Laboratory A all Children of 45th. BH QS Glycemia Serology Anti Luetic Immunologic Ac DNA. Antinuclear Ac. Studies coagulation pulse oximetry Antiphospholipid hypercoagulability studies Proteins CyS Antithrombin III Cabinet Electrocardiogram x E Creatinine Electrolytes

Chest CT scan MRI Eco-Doppler of supra-aortic trunks arteriography chocardiogram Lumbar Puncture Electroencephalogram Skull CT Conduct

Urgent cases In 24-48 hours in all altered consciousness signs of intracranial hypertension Suspected subarachn oid hemorrhage or CNS infection severe neurological deficit If anticoagulati on treatment is expected Skull CT Ischemia hypodensity of the affected territory Bruising In Normal or mass effect in the early hours

acute phase are all as hyperdense areas Hemorrhage It subarachnoid 85% of them are in the first week 50 min. Skull CT 3 hours. 25 hs. Skull CT Repeat

In chronic phase and hypodense areas

during evolution if complications are suspected Edema cerebral herniation and hemorrhagic transformation halus onset of new neurological deficits Magnetic Resonance Only if Suspected uncommon causes in young patients with borderline clinical t concordant with clinical findings Echo-Doppler In ACV's of carotid origin gent carotid surgery If Except for those with contraindication to further Ur normal TAC TAC no Development of hydrocep

carotid dissection is suspected

In progressive stroke recurrence in ICT

Arteriography Conduct in subarachnoid hemorrhage Best method for diagnosing Aneurysms Malformations arteriovenous Also extracranial carotid stenosis Echocardiogram Conduct > 45th. in No risk factors Signs and symptoms heart unexplained syncope systemic embolism clinical picture of embolic etiology If the normal transthoracic, transesophageal do Lumbar Puncture High clinical suspicion of SAH and the CT scan is normal (15% of cases) or meninges In fever Systemic Complications Hypoventilation Aspiration Pneumonia arrhythmias sis Ulcer venous heart Pulmonary embolism deep decubitus Neurological Complications Edema cerebral Home cause of death in the first week Decreased level of consciousness ntracranial hypertension or herniation Asymmetry signs of i Malnutrition Contractures IAM HAS Thrombo History of

pupillary paresis VI bilateral extensor plantar reflex Papilledema headach e or vomiting decerebración Pose Neurological Complications Hydrocephalus Infarct

or cerebellar hematomas that open the 4th ventricle intraventricular hemorrhage Crisis Hemorrhagic Transformation seizures Prognosis Grave Alteration awareness of incontinence Paresis 0-2/5 Hemianopsia phasia Ataxia Prognosis Moderate Limitation Mild Deficit independence and self care Food Control that does not interfere with the independence Diplopia Paresis Paresis facial Wandering sphincter Communication paresis (3-4/5) Dysphagia extensive parenchymal injury A

oculocephalic deviation asomatognosia anesthesia

Minimum (4 + / 5) quadrantanopia Treatment Prevention and treatment of complications General Measures Rest bed head elevation to 30 ° airway patency Sidebars Liquid parenteral b lood glucose monitoring Nutrition Prophylaxis of deep vein thrombosis and pu lmonary embolism General Measures Treatment of hypertension reflection of the TA that lasts 3-4 days TA ↓ Avoid sudden hypoperfusion not t o produce the area of necrosis Pharmacological treatment if TAS > 220 or DBP> 120 No treatment has demonstrated efficacy

Download only known in hypertensive H Avoid drugs sublingual Treatment of Cerebral Edema Measures General Elevation header 30 ° Avoiding fluid overload and hypoosmolarity apnia and hyperthermia Avoid using sodium nitroprusside Mannitol Monitor Avoid hypoxia, hyperc 185/105 down to 150/90 in patients without prior SA

Use furosemide electrolytes if concomitant heart disease or heart failure Intravenous Thrombolysis Activator Best Tissue plasminogen activator (tPA) neurological recovery Increased risk of hemorrhage mortality in placebo and treated as should be treated as soon as possible Streptokinase Studies suspended early excess mortality