Cerebrovascular accidents

Terms Stroke TIA: Transient ischemic attack Progressive stroke/ stroke in evolution Completed stroke Definition The abrupt onset of focal neurological deficit which lasts > 24 hours. The abrupt onset of focal neurological deficit which resolves within 24 hours without any radiological abnormalities. A stroke in which the focal neurological deficit worsens >6 hrs after the patient first presents. Such worsening may be due to increasing volume of infarction, haemorrhage or related oedema. This describes a stroke in which the focal deficit persists and is not progressing within 6 hrs

Etiology:
Common causes A. Thrombosis 1. Lacunar stroke (small vessel) 2. Large vessel thrombosis 3. Dehydration B. Embolic occlusion 1. Artery-to-artery a) Carotid bifurcation atherosclerotic plaque b) Aortic arch c) Arterial dissection-thrombus-embolism 2. Cardioembolic a) Atrial fibrillation b) Rheumatic heart disease c) Mural thrombus d) Myocardial infarction e) Dilated cardiomyopathy f) Valvular lesions i. Mitral stenosis ii. Mechanical valve iii. Bacterial endocarditis g) Paradoxical embolus i. Atrial septal defect ii. Patent foramen ovale iii. Atrial septal aneurysm h) Spontaneous echo contrast Uncommon causes A. Hypercoagulable disorders Protein C deficiency Protein S deficiency Antithrombin III deficiency Polycythemia vera Systemic lupus erythematosus Thrombotic thrombocytopenic purpura Disseminated intravascular coagulation Nephrotic syndrome Inflammatory bowel disease Oral contraceptives b B. Venous sinous thrombosis C. Fibromuscular dysplasia D. Vasculitis Systemic vasculitis (PAN, Wegener's, Takayasu's, giant cell arteritis) Primary CNS vasculitis Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster) E. Cardiogenic Mitral valve calcification Atrial myxoma Intracardiac tumor Marantic endocarditis Libman-Sacks endocarditis F. Subarachnoid hemorrhage vasospasm G. Drugs: cocaine, amphetamine H. Moyamoya disease I. Eclampsia

Location of Stroke
ACA MCA

Signs and Symptoms

Contralateral & sensory loss in the leg, cognitive and personality change CHANG: Contralateral paresis and sensory loss in face and arm, Homonymous hemianopia, Aphagia (dominant), Neglect (nondominant), Gaze preference towards the lesion site. 4 Ds: Diplopia, Dizziness, Dysphagia, Dysarthria Focal motor or sensory deficits, loss of coordination, difficulty speaking Coma, locked-in syndrome, cranial nerve palsies, apnea, visual symptoms, dysphagia, dysarthria, vertigo, cross weakness and sensory loss affecting ipsilateral face & contralateral body, Syndromes: Webers syndrome, claudes syndrome, lateral medullary syndrome/ Wallenbergs syndrome, medial medullary syndrome

Fixed
1. Age; M>45yr, F>55yr 2. Gender (male > female, except in 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

the very young and very old)

3. Race (Afro-Caribbean > Asian >

European)
4. Heredity 5. Previous vascular event, e.g.

PCA

myocardial infarction, stroke or peripheral embolism 6. High fibrinogen

Modifiable High blood pressure Heart disease (atrial fibrillation, heart failure, endocarditis) Diabetes mellitus Hyperlipidaemia Atheromatous plaque causing stenosis Obesity Smoking Excess alcohol consumption Polycythaemia Oral contraceptives, hormone replacement therapy Social deprivation

Lacunar arteries Basilar artery

Management:
Supportive Protection of airway; can aspirate Investigations Head elevation at 45o (propped up position) 1. Emergent head CT without contrast: to differentiate NG tube if cant feed own-self ischemic from hemorrhagic and to identify the potential Prevention of stress (to control ICP) candidate for thrombolytic therapy a) Catheterization 2. MRI & MRA b) Cough suppression 3. ECG and Echocardiogram if embolic stroke is suspected c) Avoid constipation 4. Blood profile: CBC, Hb, TC, DC, Electrolytes, BUN, cardiac 5. Careful nursing regular turning (every 2 hr) to avoid bed sore, cleaning of skin markers 6. Physiotherapy to prevent joint contracture, to clear chest secretion 5. Carotid artery and vertebral artery Doppler ultrasound 7. Speech and occupational therapy 6. Thrombophilia profile(<35 yr patients): PT, APTT, 8. Education of patient party about stroke Acute treatment of ischemic stroke: 1. Thrombolytic therapy within 3 hr of onset and no contraindications (i.e., evidence of hemorrhage on CT, recent surgery, anticoagulant use, recent hemorrhage, blood pressure >185/110 mm Hg) exist Drugs: Alteplase Aspirin/atorvastatin Cardioembolic: warfarin 2. Antiplatelet therapy should be started within 48 hr of the event to prevent additional strokes 3. Heparin or low molecular weight heparin (LMWH) may be considered in patients suspected of having progressive thromboembolism causing worsening symptoms 4. Lipid-lowering drugs should be started after the acute stages of stroke in addition to optimization of blood pressure control 1. 2. 3. 4. To prevent the secondary injuries: 1. Hypertension: Lower the BP 220/120 mmHg 2. Hypotension: 3. Control Blood sugar: 4. Treat fever: 5. Prevent ICP to rise: 6. Prevent & treat post-stroke complications such as aspiration pneumonia, UTI, DVT: Prevention of stroke: 1. TIA: find out the cause and treat; prophylaxis of aspirin or aspirin+ clopidogrel 2. Decrease the cardiovascular risk factors 3. Aspirin, clopidogrel: If stroke is 2 to small vessel disease or thrombosis, or if anticoagulation is contraindicated. 4. Carotid endarterectomy: If stenosis is > 70% in symptomatic patients or > 60% in asymptomatic patients (contraindicated in 100% occlusion). 5. Anticoagulation: In new AF or hypercoagulable states, the target INR is 23. In cases involving a prosthetic valve, the target INR is 34 or add an antiplatelet agent. 6. Management of hypertension, hypercholesterolemia, and diabetes (hypertension is the single greatest risk factor for stroke). Surgical
If ICP is raised then decompressive craniostomy / ventriculostomy / evacuation of ischemic part

Medical

Hemorrhagic stroke

Causes 1. 2. 3. 4. 5. Hypertension Cerebral amyloid angiopathy Cocaine Head injury Bleeding disorder(leukemia, aplastic anemia, thrombocytopenia) 6. Anticoagulant therapy 7. Brain tumor(Choriocarcinoma, malignant melanoma, renal cell carcinoma, and bronchogenic carcinoma are among the most common metastatic tumors) 8. A-V malformation (aneurysm) 9. Vasculitis 10. Sepsis

Clinical features almost always occur while the patient is awake and sometimes when stressed abrupt onset of focal neurologic deficit focal deficit typically worsens steadily over 3090 min and is associated with a diminishing level of consciousness and signs of increased ICP, such as headache and vomiting altered sensoriumconfusion, stupor, coma. Common site for hypertensive hemorrhage: 1. Putamen 2. Thalamus 3. Pons 4. Cerebellum

Investigations 1. Non-contrast CT: can show hemorrhage very early 2. Bleeding profile: PT, APTT 3. Echo: 4. <40 yr: Cerebral Angiogram 5. >40 yr: Angiogram, only if hemorrhage isnt in the typical site of hemorrhage (Putamen, Thalamus, Pons, Cerebellum)

Management Medical 0 1. Head elevation at 45 2. Avoid stresses catheterization, cough suppression, prevention of constipation 3. Treat hypertension: if systolic BP >180 or Mean arterial pressure >130 mmHg. 4. Avoid secondary brain injury by hypoxia, hypertension Surgical Indications: 1. Bleeding site is >2cm inside the brain 2. Clogging of ventricular system hydrocephalus (but do not take clot out) 3. >3cm bleeding & symptomatic (drowsy, GCS, bleeding in cerebellum, rapidly increasing th ICP & compression of 4 ventricle)- emergency surgery Options: 1. Carotid endarterectomy: for symptomatic(recent TIA or stroke) patient with severe carotid stenosis 2. Decompressive craniotomy & infarct / hemorrhage evacuation: for posterior fossa hemorrhage or ischemia

Prognostic factor: Supratentorial hematoma with <30ml=good; 30-60ml=intermediate; >60ml=poor Extension into ventricular system Advanced age, hemorrhage into posterior fossa, depressed level of consciousness at initial presentation