Vascular Disorders.docx
- 2. 2 Сerebrovascular diseases - 3 place on death rate - leading cause of disability - 30% of stroke sufferers die in the course of the first month from the moment of stroke - 45-48% of patients die by the end of the year
- 3. 3 Cerebrovascular diseases Clinical classification I. Acute 1.Transient strokes - Transient ischemic attack (TIA) - Cerebral hypertensive crises - Acute hypertensive encephalopathy 2. Permanent strokes - Cerebral infarction (85%) - Subarachnoid haemorrhage (1-5%) - Intracerebral haemorrhage (10-12%) II. Chronic diseases
- 4. 4 Cerebrovascular diseases Classification (ICD-10): I60 Subarachnoid haemorrhage I61 Intracerebral haemorrhage I62 Other nontraumatic intracranial haemorrhage I63 Cerebral infarction I64 Stroke, not specified as haemorrhage or infarction G45 Transient cerebral ischemic attacks and related syndromes
- 5. 5 Transient strokes Transient ischemic attack (TIA) ― is an acute episode of temporary neurologic dysfunction resulting from focal cerebral ischemia not associated with permanent cerebral infarction and lasting less than 24h. • TIA is caused by a temporary blockage of one of the arteries that supply the brain.
- 6. 6 Symptoms of TIA in carotid arteries • hemiparesis • hemihypesthesia • aphasia and apraxia (in damage of the dominant hemisphere) • anosognosia • blindness or decreased vision in one eye • central paresis of the facial nerve
- 7. 7 Symptoms of TIA in in vertebral and basilar arteries - dizziness - nausea and vomiting - double vision - dysarthria and dysphagia - ataxia - amnesia - cortical blindness - tetraparesis - hearing loss - peripheral paresis of the facial nerve
- 8. 8 Cerebral hypertensive crises are associated with hypertensive diseases and accompanied by symptoms of increased intracranial pressure. Symptoms: occipital headache and visual disorders (photopsy); hyperhydrosis; hyperemia of face; a sharp headache; a nausea; vomiting; nonsystemic vertigo; epileptic attacks.
- 9. 9 Acute hypertensive encephalopathy is typically associated with hypertensive renal disease Symptoms: -elevated blood pressure, -psychomotor agitation, -nausea, vomiting, -visual and sensitive disorders, -impairment of consciousness, -symptoms of increased intracranial pressure, -meningeal symptoms,
- 10. 10 -local symptoms and epileptic attacks are probable. Permanent strokes Ischemic Stroke is a syndrome characterized by a sudden loss of brain function caused by the interruption of cerebral blood flow and lasting more than 24 hours. Etiology / risk factors 1. Atherosclerosis 2. Arterial hypertension
- 11. 11 4. Heart diseases (atrial fibrillation, myocardial infarction, left ventricular aneurysm,artificial heart valve, rheumatic disease of the heart valves, myocardiopathy, bacterial endocarditis)). 5. Vasculitis 6. Diabetes Etiology / risk factors 6. Hematological diseases (erythremia, sickle cell anemia, thrombocytosis, leukemia) 7. Immunological disorders (antiphospholipid syndrome)
- 12. 12 8. Venous thrombosis 9. Dissection of the precerebral or cerebral arteries 10. Migraine 11. In women - taking oral contraceptives 12. Smoking Pathogenesis of the Ischemic Stroke - thrombosis - Embolism - decreased perfusion Pathogenetic types: - aterotrombotic (15-20%)
- 13. 13 - cardioembolic (15-20%) - hemodynamic (5-10%) - lacunar (infarct size ≤1.5 cm) (15-20%) - hemorheologic - cryptogenic (20-30%)
- 14. 14 Pathogenesis of the Ischemic Stroke
- 15. 15 Metabolic changes in reply to the acute focal ischemia of the brain: 1.Decrease of cerebral blood flow below 55 ml (100 g/min) causes deceleration of proteins’ synthesis in neurons. 2. Decrease of the cerebral blood flow below 35 ml (100 g/min) stimulates anaerobic glycolysis. 3. Decrease of the cerebral blood flow below 20 ml leads to redundant
- 16. 16 release of the excitatory neurotransmitters and to the energy metabolism disorders. 4. Anoxic cell membrane depolarization ― apoptosis (death of neuron cells) occurs due to reduction of the cerebral blood flow below 10 ml. Сentral zone of the Cerebral infarction («nucleus») is formed in 6-8 minutes after acute focal ischemia development. In the course of several hours cerebral infarction
- 17. 17 «nucleus» is surrounded by a zone of «ischemic penumbra». Penumbra is an area of dynamic metabolic changes, in which brain bloodflow is reduced to 20-40 ml (100 g/min) and only functional changes take place. Duration of penumbra existence defines time period called «a therapeutic window»
- 18. 18 ― the period when medical actions are most perspective and can limit cerebral infarction area. The great mass of cerebral infarction is formed in 3-6 h after the first clinical symptoms occurrence, and its formation comes to the end in 48-56 h. Periods of the stroke: • up to 6 hours; • acute (from 1 day to 1 month);
- 19. 19 • early rehabilitation period (up to 3 months); • late rehabilitation period (from 3 months to 1 year); • sequelas of stroke (from a year and more). Symptoms of Cerebral infarction in MCA: • contralateral hemiparesis, hemihypesthesia, homonymous hemianopsia
- 20. 20 • paresis of gaze • motor and/or sensory aphasia • autotopagnosia, anosognosia (neglect)
- 21. 21 • MCA Superior Division Infarction
- 22. 22 • MCA Inferior Division Infarction
- 23. 23 • Bilateral MCA proximal main stem terriotry infarct.
- 24. 24 • MCA cortical branch Infarction
- 25. 25 Symptoms of Cerebral infarction in ACA: • contralateral paresis of the legs, less significant paresis of the arm • contralateral hemianesthesia, mainly in the leg • urinary incontinence • contralateral grasping reflex, sucking reflex • abulic-akinetic syndrome, akinetic mutism • apraxia of walking; apraxia in the extremities • emotional lability, euphoria
- 26. 26 • Anterior Cerebral Artery Infarction
- 27. 27 Symptoms of Cerebral infarction in PCA: • contralateral homonymous hemianopsia; bilateral lesions can lead to cortical blindness • Occlusion of the PCA in the dominant hemisphere can cause amnestic aphasia, alexia, agraphia, or amnesia • Blockage of the thalamoperforating arteries can cause depression of consciousness, paresis of the gaze up; contralateral hemianesthesia, ataxia, transient hemiparesis, choreoathetosis, pain and paresthesia.
- 28. 28 • Posterior Cerebral Artery Infarction
- 29. 29 Symptoms of Cerebral infarction in vertebral, basilar arteries: • bilateral hemiparesis, hemihypesthesia • cerebellar ataxia and nystagmus • classical alternating syndromes • impaired consciousness and vital functions • cortical blindness, oculomotor disorders, hyperkinesis, sleep disorders, hallucinations, amnesia • Bulbar syndrome
- 30. 30 • Obstruction of the artery of the labyrinth may manifest as dizziness and sudden unilateral deafness. • Multiple Lacunar State Lateral Medullary Infarction
- 32. 32 Diagnostics of CI - emergency examination of the patient with a diagnosis within 45 min from the time of delivery
- 33. 33 -assessment of neurological deficit according to NIHSS - general analysis of blood and urine; blood chemistry (+lipid profile); coagulogram - blood pressure monitoring • ECG; chest x-ray • CT or MRI of the brain (+with angioprogram) Diagnostics of CI • Ultrasound of the heart • Ultrasound of the precebral arteries • lumbar puncture in the absence of contraindications
- 34. 34 • EEG, consultation of a cardiologist, angiosurgeon according to indications • Occluded middle cerebral artery on CT angiography
- 35. 35 Occluded middle cerebral artery on CT angiography Carotid ultrasound
- 37. 37 Treatment of CI • treatment in intensive care unit • ALV, installation of a nasogastric tube, urinary catheter according to indications • raising the head end of the bed by 30⁰ • blood pressure correction is performed on the first day if systolic blood pressure is ˃220 mm Hg, diastolic blood pressure is ˃120 mm Hg • If necessary, blood pressure is reduced by no more than 15% from the initial level within
- 38. 38 24 hours (urapidil iv, ACE inhibitors, angiotensin receptor antagonists) Treatment • maintaining normovolemia • neuroprotective therapy: glycine, magnesium sulfate • parasympathomimetic drugs: ipidacrine, choline alfoscerate • In presence of cerebral edema: osmotic diuretics + furosemide • In big cerebellar infarction- consultation of a neurosurgeon
- 39. 39 • Antiplatelet agents (acetylsalicylic acid) and anticoagulants if indicated • In hyperlipidemia: atorvastatin, rosuvastatin Treatment of CI • in vomiting: domperidone, metoclopramide • in epileptic syndrome: phenytoin, carbomazepine, valproic acid • in spastic syndrome: baclofen, tolperisone • in dizziness: betahistine • in extrapyramidal syndrome: amantadine • in psychomotor agitation: tofisopam, diazepam, chlorprotixen
- 40. 40 • Early rehabilitation of patients in a stable state, physiotherapy, exercise therapy, speech therapist Systemic thrombolysis ALTEPLAZA 0.9 mg / kg (maximum dose 90 mg) -10% of the entire dose i/v in a bolus for 1 min, the remaining dose is administered in i/v infusion for 1 hour Conditions: 1. absence of hemorrhagic changes on brain CT 2. BP less than 180/105 mm Hg
- 41. 41 3. age 18-80 years 4. the onset of symptoms less than 4.5 hours before treatment Systemic thrombolysis Contraindications: - Hemorrhage on CT or signs of cerebral infarction with size more than 1/3 of the cerebral hemisphere; - minimal symptoms of CI - suspicion of SAH - internal bleeding in the last 3 weeks - hemorrhagic diseases - intracranial surgery or head injury last 3 months - major surgical interventions last 14 days
- 42. 42 - lumbar puncture last 7 days - intracranial hemorrhage, aneurysm, AVM in anamnesis - CI + epileptic seizures - myocardial infarction last 3 months Emergency endovascular procedures • Intra-arterial thrombolysis: medications delivered directly to the brain. • Removing the clot with a stent retriever
- 43. 43 (thrombectomy, thrombaspiration) Carotid endarterectomy Angioplasty and stents
- 44. 44 Intracerebral hemorrhage is a clinical form of stroke,
- 45. 45 caused by blood vessel rupture causing blood penetration into cerebral parenchyma. Сauses - arterial hypertension and rupture of microaneurysms - vascular malformations - saccular cerebral aneurysms - coagulopathies (hemorrhagic diathesis) - use of anticoagulants - vasculitis -brain tumors
- 46. 46 -amyloid angiopathy -alcohol, cocaine usage Symptoms of intracranial hemorrhage : • abrupt onset during physical or emotional stress; • sharp headache, nausea, vomiting • epileptic seizures are possible • impaired consciousness (from stunning to coma) • autonomic disorders: the skin is hyperemic, hyperhidrosis, tense pulse, increased blood pressure, hyperthermia
- 47. 47 • meningeal symptoms; • retinal edema and hemorrhages on the eye-ground; • Severe focal neurological signs.
- 49. 49 The subarachnoid hemorrhage in most cases (to 80%) occurs owing to: • ruptured cerebral aneurysm; • arteriovenous malformation; • systemic connective tissue disorders; • blood disorders; • hypertensive diseases and cerebral atherosclerosis.
- 50. 50
- 51. 51 Symptoms: • sudden sharp headache, nausea, vomiting • epileptic seizures are possible • impaired consciousness (from stunning to coma) • psychomotor agitation • main syndrome is meningeal • autonomic disorders: hyperemia of the skin, change in heart rate, increased blood pressure, hyperthermia, changes in the ECG
- 52. 52 • focal neurological symptoms are usually absent, but possible
- 53. 53
- 54. 54 Diagnostics of SAH - general analysis of blood and urine; blood chemistry; coagulogram • ECG; chest x-ray X-ray of the skull (if head injury is suspected) • CT or MRI of the brain with angioprogram • digital subtraction angiography • transcranial dopplerography • lumbar puncture in the absence of contraindications • neurosurgeon consultation
- 55. 55 • consultation of an ophthalmologist and therapist subarachnoid hemorrhage
- 56. 56 A: Digital subtraction angiography of the cerebral vessels, demonstrating an aneurysm (black arrow) at the junction of the A1
- 57. 57 and A2 segments of the right ACA. B: Complete embolization of the aneurysm sac after coiling. Magnetic Resonance Angiography (MRA) Treatment of ICH and SAH • treatment in intensive care unit
- 58. 58 • ALV, installation of a nasogastric tube, urinary catheter according to indications • raising the head end of the bed by 30⁰ • maintaining blood pressure not more than 150 mm Hg (to reduce BP - urapidil) • For the prevention and treatment of vasospasm: nimodipine orally or i/v • maintaining normovolemia • analgesia and sedation during all manipulations
- 59. Treatment • neuroprotective therapy: emoxipin, mexibel, magnesium sulfate • in hypertensive hemorrhages by the type of hemorrhagic impregnation: vitamin K, and etamzilat • In presence of cerebral edema: osmotic diuretics + furosemide • in psychomotor agitation: tofisopam, diazepam, chlorprotixen
- 60. 60 • in pain and hyperthermia: analgin, paracetamol, diclofenac, ketoprofen, ketorolac, meloxicam, ibuprofen, tramadol59 Treatment • in vomiting: domperidone, metoclopramide • in epileptic syndrome: phenytoin, carbomazepine, valproic acid • in spastic syndrome: baclofen, tolperisone • in dizziness: betahistine • in extrapyramidal syndrome: amantadine
- 61. 61 • IN ICH early rehabilitation of patients in a stable state, physiotherapy, exercise therapy • Surgical treatment according to indications Indications for Surgical treatment in ICH 1.Increase of intracranial pressure in patients with putamenny and subcortical hematomas with a volume of more than 40 cm³ and cerebellar hematomas more than 15 cm³
- 62. 62 2.Hemispheric hematoma with a volume of 30- 40 cm³ and the absence of the effect of treatment for 3-5 days 3.Thalamus hemorrhage + ventricular tamponade and / or occlusive hydrocephalus Contraindications for Surgical treatment in ICH Relative contraindication: age older than 70 years; somatic pathology in the stage of subcompensation or decompensation; hemorrhage in brainstem and thalamus
- 63. 63 Absolute contraindications: coma (GCS ≤7). In acute occlusive hydrocephalus - installation of external ventricular drainage Chronic cerebral ischemia ― discirculatory encephalopathy 3 stages: First stage. Subjective patient complains of headaches, weakness, fatigability, emotional lability, memory and
- 64. 64 attention decrease, dizziness, instability at walking, sleep disturbance. Second stage. Patient’ s complaints are similar to the first stage, but they degrade. The focal signs progress:
- 65. 65 - coordination and oculomotor disorders; - pyramidal insufficiency; - amyostatic syndrome; - - memory and emotional disorders. Third stage. The quantity of complaints decreases.
- 66. 66 Neurological symptoms : coordination disorders, pyramidal, bulbar, pseudobulbar, amyostatic, psychoorganic syndromes. Patients are invalid; social and communal maladjustment is observed.