Stroke (Cerebrovascular Accident – CVA)

Stroke (Cerebrovascular Accident – CVA)

1. General Information about Stroke:

• Stroke occurs when the blood supply to a part of the brain is interrupted or severely reduced, causing the brain tissue to be deprived of oxygen and nutrients. Within minutes, brain cells begin to die.

• Consequences: Deficits in brain function, sudden/simultaneous, without head trauma.

• Recognition Signs (FAST):

• F: Face – Facial: One side of the face droops, difficulty smiling

• A: Arm – Arm: Arm weakness or numbness

• S: Speech – Speech: Difficulty speaking or slurred speech

• T: Time – Time: Act quickly

• Medical Emergency: Early and timely management to minimize brain damage and complications, sequelae.

• Occurs Anytime: At any time, in any season.

• Leading Cause of Death:

• In developed countries, third leading cause after cancer and cardiovascular disease.

• In low and middle-income countries, accounts for 69%.

• Risk Groups: Men > Women, Age > 40.

• Age of Stroke Patients:

• Patients with stroke due to THA, NMCT, XVĐM are older than patients with stroke due to heart valve disease, VNTMNK.

2. Causes and Pathogenesis of Stroke:

• Pathology caused by damage to blood vessels in the brain:

• 1. Cerebral Infarction:

• Causes:

• Cardiovascular disease: Dilated cardiomyopathy, VNTMNK, RN, BMV…

• Atherosclerosis

• Hypertension

• Arteritis

• Diabetes

• Bayliss Mechanism of Cerebral Blood Flow Regulation:

• When there is a lot of blood flow to the brain: Cerebral arteries contract.

• When there is little blood flow to the brain: The blood vessels dilate.

• Cerebral blood flow is always constant at 50ml/100g brain/minute.

• Cerebral infarction due to embolism (cerebral infarction is more common due to the heart than due to atherosclerosis):

• Embolus with main component of platelets: Not stable, easily dissolved, can cause temporary focal cerebral ischemia, usually resolves within 24 hours.

• Embolus with main component of red blood cells: Stable, difficult to dissolve, causing permanent focal cerebral ischemia.

• Focal cerebral ischemia due to embolism or thrombosis has 2 zones:

• Central zone:

• Blood flow < 10ml/100g brain/minute

• Necrosis within a few hours

• No recovery.

• Peripheral zone with blood flow from 20-30ml/100g brain/minute:

• Zone of “twilight zone”.

• If collateral circulation is good or treated promptly, this area may recover.

• Recovery potential of cells: Occurs within a few hours and then turns into necrosis.

• 2. Cerebral Hemorrhage:

• Causes:

• Hypertension

• Coagulation disorders and the use of anticoagulants

• Extensive cerebral infarction

• Brain tumor

• Cerebral vascular malformation

• Cerebral amyloid angiopathy

• Head trauma

• Factors causing cerebral hemorrhage: Increased blood vessel pressure, Vessel wall, Coagulation disorder

• Cerebral Hemorrhage Hypotheses:

• Charrcot’s Theory:

• Blood vessel rupture due to microaneurysms formed when arteries degenerate due to hypertension.

• Location: Deep branches of the middle cerebral artery.

• Ruochuox’s Theory:

• Cerebral infarction occurs before cerebral hemorrhage.

• Infarcted area: Ischemia and necrosis.

• Surge in hypertension: Converts cerebral infarction into hemorrhage or ruptured blood vessels leading to hemorrhage.

• Conclusion: There are two factors causing stroke: Vessel wall damage and hypertension.

3. Classification of Stroke:

• 1. Cerebral Hemorrhage:

• Intracerebral hemorrhage (blood into brain parenchyma)

• Subarachnoid hemorrhage (into subarachnoid space)

• Cerebral-meningeal hemorrhage (combination of 2 types)

• 2. Cerebral Infarction:

• Due to atherosclerotic plaque: Large blood vessels; Plaque; Thrombosis.

• Due to emboli from a distance: Small blood vessels, usually the middle cerebral artery; Origin from the heart: Atrial fibrillation, VNTMNK, mitral stenosis.

• Due to reduced cerebral blood flow: Narrowed blood vessels; Ischemia in distant areas, Classic example is the watershed area between the anterior cerebral artery and the middle cerebral artery due to narrowing of the internal carotid artery after hypotension.

• Rare:

• Cerebral artery dissection: Often occurs in the internal carotid artery or vertebral artery.

• Cerebral vasculitis

• Cerebral vein thrombosis

• 3. Transient Ischemic Attack (TIA):

• Transient cerebral ischemia, these signs regress completely within 24 hours.

• Due to blockage of a cerebral artery.

• The clot dissolves on its own.

4. Predicting the Location of Brain Artery Damage:

• Aphasia + Hemiplegia: Middle cerebral artery.

• Weakness on one side of the body and/or loss of sensation on one side of the body: Lacunar stroke.

• Leg weakness more than arm, urinary incontinence, personality changes: Anterior cerebral artery.

• Homonymous hemianopia: Posterior cerebral artery.

• Weakness in all limbs, cranial nerve palsy, ataxia: Basilar artery.

5. Three Main Causes of Cerebral Infarction:

• Atherosclerotic plaque

• Emboli from a distance

• Reduced cerebral blood flow.

• Other rare causes include: Cerebral artery dissection, vasculitis, and cerebral vein thrombosis.

6. History and Physical Examination of Stroke Patients:

• To preliminarily determine the area of brain artery damage and the cause of stroke, ask:

• Does the patient have:

• Aphasia

• Right hemiplegia

• Suggests damage to the right middle cerebral artery, usually due to embolism from the carotid artery or of arterial origin.

• Weakness of the face, arm and leg without other signs: Suggests lacunar stroke ->due to blockage of small vessels deep in the brain.

• It is not possible to accurately differentiate CEREBRAL INFARCTION and CEREBRAL HEMORRHAGE clinically:

• Cerebral hemorrhage: Sudden onset, accompanied by meningeal signs, CSF has non-coagulating blood when there is cerebral-meningeal hemorrhage…

• Cerebral infarction: There are preceding symptoms, common in patients with hypertension.

• Risk factors for stroke: Hypertension, diabetes, heart disease, TIA, BP, Alcohol abuse, smoking, dyslipidemia, hyperuricemia.

7. Important Risk Factors for Stroke:

• Hypertension

• Diabetes mellitus

• Heart disease (mitral valve disease, atrial fibrillation, infective endocarditis, dilated cardiomyopathy, myocardial infarction…)

• Transient ischemic attack

• Obesity, alcohol abuse, smoking, dyslipidemia, hyperuricemia

8. Diagnosis and Assessment of Stroke:

• Clinical:

• Diverse, atypical.

• There may be warning signs but they are not characteristic and are easily overlooked such as: Headache, dizziness, tinnitus… Especially headache.

• Hemiplegia/± meningeal syndrome/cerebellum/depending on the lobe of the brain that is damaged.

• There may be impaired consciousness, coma.

• Systemic signs.

• Patient with aphasia, ask family members carefully.

• Comprehensive cardiovascular and neurological examination including auscultation of the carotid arteries bilaterally and blood pressure measurement in both arms.

• Neurological examination includes assessment of consciousness, speech, cranial nerves, motor, cerebellum, ataxia, sensation, and deep tendon reflexes.

• Paraclinical:

• Complete blood count:

• Blood sugar.

• Electrolytes: Magnesium and calcium: Can cause symptoms similar to stroke.

• Blood creatinine.

• Quick time, PT ratio and aPTT.

• Electrocardiogram.

• Chest X-ray: General assessment of cardiovascular disease and pneumonia due to aspiration.

• Urinalysis (if red blood cells are seen in the urine, it is necessary to look for causes of renal artery blockage).

• CT Scan: In the early stages.

• Blurred bean nucleus

• Ribbon sign of the insular cortex

• Blurry Sylvian fissure

• Blurred cerebral cortical sulci

• Decreased parenchymal density

• Lacunar infarction: In elderly patients, hypertension, atherosclerosis.

• Small density-reducing lesions in the internal capsule and central gray matter or adjacent to the lateral ventricles.

• Size usually under 15mm, more common than lesions < 10mm, old lacunar lesions < 5mm.

• Lacunar lesions are too small to be seen on scans.

• CT scan can miss quite a lot (up to 50%) if taken within 12 hours of onset.

• CT is difficult to detect:

• Small infarcted areas,

• Infarction in the posterior fossa

• Lesions causing demyelination

• Magnetic resonance imaging (MRI): More detailed images than CT scan.

• Provides more information about the histopathological characteristics of lesions.

• Can choose the positions of the survey, sensitive to tissues, especially damaged tissues.

• Detecting various large and small blockages; less noise, clear images, especially differentiating infarction-hemorrhage images.

• Indications for MRI:

• Unclear CT results.

• Acute stroke.

• Small infarction (lacunar stroke).

• Infarction of the posterior fossa, or vascular malformations.

• Carotid artery ultrasound:

• Assessing damage at the bifurcation of the carotid arteries, the system of vertebral arteries.

• Transcranial Doppler ultrasound: Examining the flow (direction, velocity) of large arteries in the skull.

• 24, 48 hour Holter ECG: Paroxysmal RN or other rhythm disturbances.

• Cardiac Doppler ultrasound: Suspect stroke cause due to embolism from the heart.

• Cerebral angiography: The “gold standard” for diagnosing pathology in large brain vessels and small vessels in the skull.

• Indications:

• Stroke in young patients.

• Suspected cerebral artery dissection.

• Cerebral vasculitis.

• Before carotid endarterectomy surgery.

• Lumbar puncture and electroencephalography: When suspecting small subarachnoid hemorrhage.

• Investigation of hypercoagulability: In stroke patients under 45 years of age, with a history of arterial or venous thrombosis, history of spontaneous miscarriage, family history of young thromboembolism, unexplained stroke occurring in patients with autoimmune disease…

9. Differential Diagnosis of Stroke:

• Brain tumor

• Subdural/epidural hematoma

• Epilepsy

• Hysteria (functional neurological disorder)

10. Which of the following causes of cerebral infarction is most likely to cause secondary cerebral hemorrhage:

• A. Atherosclerosis causing small lacunar infarction

• B. Increased blood homocysteine

• C. Vasospasm

• D. Mitral stenosis

Answer: A

11. Treatment of Stroke:

• Preventing Complications:

• Recovering acute brain tissue damage.

• Preventing recurrent stroke.

• Preventing Complications:

• 1. Control cerebral edema: With hypertonic solutions:

• Mannitol: 0.51 g/kg over 20-30 minutes, then re-infuse 0.25-0.5 g/kg every 6 hours. If infusing for more than 48 hours: Gradually reduce mannitol dose to avoid re-edema.

• Should not be infused for more than 3 days.

• If you want to infuse longer: There is a break to eliminate the drug, avoiding the secondary effect of increasing intracranial pressure.

• Glycerol (1mg/kg over 120 minutes) Consider:

• Hypertonic saline

• Decompressive surgery

• Controlled hyperventilation for a short time, causing: Alkalosis, cerebral vasoconstriction and reduced brain volume significantly reducing intracranial pressure.

• Barbiturates: Reduce brain blood volume due to vasoconstriction.

• Dose 250-500 mg thiopental (bolus injection) then continue infusion at 5 mg/kg/h or bolus injection periodically.

• Complications: Severe hypotension causing reduced cerebral perfusion pressure.

• 2. Control arterial blood pressure:

• Do not lower blood pressure suddenly: K interferes with the mechanism of cerebral autoregulation, exacerbating the ischemia of the “border zone”, making clinical symptoms worse.

• Reducing the level of hypertension is mandatory in some cases:

• Severe heart disease,

• Malignant hypertension,

• Aortic dissection

• Patients treated with tPA.

• Maintain systolic blood pressure < 185 mmHg and diastolic blood pressure < 110 mmHg.

• Blood pressure too high (systolic blood pressure ≥ 220 mmHg, diastolic blood pressure ≥ 120 mmHg):

• Must lower blood pressure immediately.

• Gradually reduce systolic blood pressure: 170-180 mmHg and diastolic blood pressure: 95-100 mmHg.

• Do not use sublingual Nifedipine to lower blood pressure acutely in stroke because:

• Blood pressure drops too quickly.

• Its effect on cerebral blood flow regulation will make the stroke worse.

• AVOID using antihypertensives that can increase intracranial pressure such as:

• Direct vasodilators (Sodium Nitroprusside, Nitroglycerin, Hydralazine)

• Calcium channel blockers

• 3. Preventing deep vein thrombosis and pulmonary embolism.

• 4. Preventing pneumonia due to aspiration or reflux.

• 5. Control blood sugar:

• Blood sugar < 170 mg/dl (< 9.5 mmol/l),

• Insulin injection/infusion intravenously if needed.

• 6. Control body temperature:

• Reduce body temperature from mild to moderate:

• Limit secondary brain damage spread,

• Reduce intracranial pressure

• Reduce mortality rate.

• 7. Craniotomy or ventriculostomy.

• Recovering acute brain tissue damage:

• Thrombolytic drugs:

• rtPA 0.9mg/kg given within 3 hours of onset.

• Intravenous bolus injection of 10%, then infuse the rest over 1 hour, maximum dose 90 mg.

• Indications for rtPA:

• Ischemic stroke.

• The time of onset can be clearly determined.

• rtPA can be given immediately within 3 hours of onset.

• CT scan shows no cerebral hemorrhage or other serious brain diseases.

• Age ≥ 18.

• Heparin: Intravenous heparin:

• Does not reduce the severity of stroke when it has occurred,

• Increases the risk of converting cerebral infarction to hemorrhage by increasing blood flow to the infarcted area.

• Contraindication to using heparin within 24 hours if the patient has been treated with rtPA.

• Indications for Heparin: To prevent progression or recurrence of cerebral infarction including:

• Progressive cerebral infarction.

• Stroke due to cardiac thrombosis (if infarcted area is small or moderate).

• Vertebral artery thrombosis.

• Cerebral artery dissection.

• Moving emboli from artery to brain artery.

• Progressive TIA.

• Cerebral vein thrombosis.

• Some hypercoagulable conditions.

• Aspirin (160-300 mg/day): Given immediately in the acute stage.

• Neuroprotective drugs:

• Inhibit aa receptors in the postsynaptic region

• Inhibit Glutamate release enzymes

• Limit calcium and free radical activity

• Inhibit NO formation

• Preventing Recurrent Stroke:

• Control and treat risk factors well:

• Hypertension

• Organic heart disease

• Diabetes

• Smoking…

• Need to treat heart valve disease completely.

• Stenosis >70% of the internal carotid artery or common carotid artery: Carotid endarterectomy or stent placement

12. Which of the following is not a characteristic of damage to the superficial branch of the middle cerebral artery:

• A. Most common

• B. Hemiplegia dominant in the right hand

• C. Contralateral hemiparesis

• D. Proportional hemiplegia

Answer: D

13. Which of the following is not a sign of stroke in the deep branches of the middle cerebral artery:

• A. Disproportionate paralysis between the right leg and hand

• B. No hemiparesis

• C. No sensory disturbance on the side of the body with paralysis

• D. Wernicke’s aphasia

Answer: C

14. Which of the following does not worsen cerebral infarction in the first 3 days:

• A. Electrolyte disturbance

• B. Infarct expansion

• C. Secondary hemorrhage

• D. Ulceration

Answer: D

15. In severe cerebral hemorrhage, which of the following signs is not consistent:

• A. Coma

• B. Severe headache beforehand

• C. Vomiting

• D. No vegetative disturbance

Answer: D

16. The golden hour in stroke is?

Answer: 4 hours

Note: This article is for general information about stroke only. For more detailed information, you should consult a specialist.