Stroke medina........................pptx

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1. Stroke Dr Medina Fedlu ( MD,Neurologist )

2. Definition Epidemiology Risk factors Stroke sub types Clinical features Management

3. Stroke -Sudden onset of neurologic deficit lasting for more than 24 hrs which is vascular in origin. Transient Ischemic Attack(TIA) -Is a temporary and “non-marching” neurological deficit of sudden onset; attributed to focal ischemia of the brain, retina, or cochlea ; and lasting less than 24 hours . -“ tissue-based” modification of the TIA -Transient episode, regardless of duration, associated with a clinically appropriate imaging lesion defined as a stroke.

4. Epidemiology Is the third leading cause of death Major leading cause of disability Occur at any age but risk increases with age Approximately 88% of these strokes are ischemic and 8%–12% of ischemic strokes result in death within 30 days.

5. Strokes types Ischemic stroke (may transform in to hemorrhagic) -85-88% -Thrombotic -embolic -cryptogenic Hemorrhagic (subarachnoid, intra cerebral)-12-15% -ICH -SAH -IVH

6. RFs of ischemic stroke NONMODIFIABLE Gender Family history Age Race/ethnicity MODIFIABLE Arterial HTN TIA/Prior stroke Atrial fibrillation C arotid a. stenosis/disease DM/dyslipidemia Smoking Excessive alcohol high fibrinogen high homocysteine Low folate Anti- cardiolipin Ab OCP Obesity 6

7. Approach to the diagnosis of stroke History obtained from close observer or relative Time of occurrence, circumstances and progression Previous TIA, Stroke History of fever, head ache, nuchal pain Palpitation, SOB, chest pain, leg swelling History of HTN, DM, Seizure, Collagen vascular disease, STD, Cardiac disease, Coagulopathies , malignancy History of drug abuse, alcohol abuse, cigarette History of trauma Use of medications like OCP, anticoagulants Family history of stroke, sudden cardiac death

8. General Examination Do rapid evaluation of the patient Attend Neck/ A ir way / Br eating / C irculation Vital signs   Blood pressure Rises acutely in 70-80% Returns to baseline in few days

9. Temperature Common in the first 24 hours <38.2 Might be a sign of infection after 24h Should be controlled Pulse rate Low pulse rate with high BP might be assign of increased ICP ( Cushings Reflex) Regularity (arrhythmia ) Respiratory rate Rate and pattern should be noted  

10. Fundi Papilledema sign of increased ICP Neck Neck stiffness should be checked Stiffness (subarachnoid hemorrhage)(Meningitis) Look for carotid bruit Heart Murmurs/arrhythmia Lungs Aspiration pneumonia

11. Neurologic Examination Mental status Level of consciousness and orientation Reduced (brain stem or extensive hemispheric injury) Fluctuating in thalamic hemorrhage/ subdural hematoma May worsen 3-5 days after stroke due to extension of Edema Memory Short term anteromedial thalamus/medial temporal lobe   Language Aphasia Cortical lesion in dominant hemisphere Thalamus / caudate/ Alzheimer disease Spatial attention Hemineglect extinction : cortical lésion nondominant hémisphère

12. Cranial nerves Pupil size symmetry and reaction to light Visual acuity Abducent nerve palsy poor localizing sign / ICP increase F acial deviation/facial nerve palsy supra or infra nuclear Visual field defects Homonymous hemianopia in primary visual cortex Homonymous quadrantanopia -optic radiation S ectoranopia lateral geniculate body lesions Gaze palsy Dorsolateral frotal lobe- gaze deviation to opposite side of hemiparesis Lateral pons - gaze deviation to the same side of the hemi paresis.  

13. Reflexes Asymmetry of tendon reflexes Plantar reflex   Motor function Tone Hypotonia early after stroke / pasticity after several days   Subtle weakness Flattened nasolabial fold Wide palpaberal fissure Pronator drift Slow alternating movements Decreased arm swinging in walking  

14. VASCULAR ANATOMY Anterior circulation Internal carotid artery arises from common carotid artery Branches–Anterior cerebral artery(ACA),Anterior communicating artery, middle cerebral artery(MCA) and Posterior communicating artery. Posterior circulation vertebral artery Arises from subclavian artery Merges to form basilar artery at the base of pones Branches-Posterior cerebral artery, superior cerebellar , PICA and AICA

15. 7/19/2021 Cerebrovascular Disease- STROKES 15

16. Stroke syndromes Divided in to: Large vessel stroke within the anterior circulation Large vessel stroke within the posterior circulation Small vessel disease of either vascular bed

17. Stroke with in the anterior circulation The internal carotid artery and its branches (MCA,ACA) comprises of the anterior circulation of the brain. ACA Stroke MCA Stroke -contra lateral face, arm and leg weakness leg>>arm and face. -contra lateral sensory loss in the leg -urinary incontinence -gait abnormality. - contralateral face, arm, and leg weakness face and arm>>leg. - contralateral hemi sensory loss. -Hemi neglect (non dominant) -Aphasia(dominant ). - contralateral visual field defect.

18. Stroke with in the posterior circulation Posterior circulation is composed of paired vertebral arteries, basilar and paired posterior cerebral arteries. PCA Stroke vertebro basilar artery stroke - con tralateral homonymous hemianopia . -memory deficit -cortical blindness(bilateral lesion) -Thalamic syndrome -contra lateral hemiparesis - Diplopia,Nystagmus,Vertigo - Dysartria,Dysphegia and Ataxia. -Hemi facial sensory deficit -Facial Weakness. -contra lateral Hemiparesis

19. Lacunar strokes Due to occlusion of small arteries by lipohayalinosis or micro thrombi. Hypertension and Dm are the main risk factors Lacunar stroke syndromes Clinical features Localization -Pure motor hemiparesis -Pure sensory stroke -Ataxic hemiparesis -Clumsy hand – Dysartria - Contralateral face,arm and leg weakness - Contralateral face,arm and leg sensory loss - Ipsilateral hemi ataxia with contralateral hemiparesis . - Contralateral face and hand weakness with dysartria . Internal capsule,Corona radiata and basis pontis -Thalamus - Contralateral post limb of internal capsule or basis pontis . -Basis Pontis

20. Principles of management for ischemic stroke Medical Support and Rx of acute complication IV Thrombolysis Endovascular techniques Anti thrombotic treatment Rehabilitation

21. 1) Medical Support 21 T o Optimize cerebral perfusion to the ischemic penumbra. T o Prevent/Treat complications of bed ridden pts General supports I) Maintain airway & oxygenation: Airway support and ventilatory assistance are recommended for the treatment of patients with acute stroke who have decreased consciousness or who have bulbar dysfunction that causes compromise of the airway. (class I , LOE C ) Target oxygen saturation is >94% ( Class IC). II) Adequate hydration MF (Isotonic solutions )

22. General support cont… III) Hypoglycemia (blood glucose level <60 mg/ dL ) Treat with slow IV push of 25 mL of 50% dextrose . IV) Hyperglycemia (RBS>180mg/dl) Treat with insulin Target is 140-180mg/dl (ADA recommendation) V) Sources of hyperthermia (temp>38°C) should be identified and treated, and antipyretic medications should be administered to lower temperature in hyperthermic patients with stroke (Class I, LOE C) VI) Cardiac monitoring : for the first 24hrs to screen for AF & other serious arrythmias (class 1 B)

23. General support cont… VII) Blood pressure should be lowered if there is: M alignant hypertension concomitant MI, If BP is >185/110 mmHg and Thrombolytic therapy is anticipated. In patients with markedly elevated blood pressure (SBP >220mm Hg or the DBP >120 mm Hg ) who do not receive fibrinolysis, goal is to lower blood pressure by 15% during the first 24 hours after onset of stroke . (Class I, LOE C)

24. General support cont… VIII) Preventing the common complications of bed ridden patients: infections (pneumonia, urinary, and skin) and DVT with PTE. Medical: heparin ( UFH < LMWH )is safe and can be used concomitantly. Mechanical : Use of pneumatic compression stockings is of proven benefit in reducing risk of DVT and is a safe alternative to heparin . Prevent cerebral edema & brain hernation ( mannitol , hemicraniectomy ) Treat seizures GI prophylaxi s

25. Indications Contraindication Clinical Dx of ischemic stroke Sustained BP > 185/110 despite Rx Onset of ssx to time of drug adm 3hrs-4.5hrs Plt < 100k, HCT < 25%, RBS <50, >400 CT showing no h’ge Use of Heparin within 48h & pro PTT, or ↑ INR Age ≥ 18 Rapidly improving Consent by pt or surrogate Prior stroke, HI within 3m, ICH, major surgery past 14dys GIB in 21 dys, recent MI 2 ) Thrombolysis - improve clinical outcomes

26. 3) Endovascular revascularization Surgical recanalization of intracranial and extracranial vessels. Ischemic stroke from large-vessel intracranial occlusion ( MCA , Carotid aa and basilar aa ) result in high rates of mortality and morbidity. Intra-arterial fibrinolysis Mechanical thrombectomy (<8hrs)

27. 4)Anti-thrombotic Agents Anti-Platelet Agents ASA is the only drug studied approved for primary Acute ichemic stroke . ASA reduced both recurrence and mortality minimally. Start ASA (initial dose is 325 mg) loading dose within 24 to 48 hrs after stroke onset for treatment of most patients (Class I; LOE A). Delay aspirin for at least 24 hours after rtPA . Anti-Coagulation Role in atherothrombotic stroke is uncertain Several Trials showed no better benefit than ASA rather increased risk of bleeding. Used in crescendo TIA… (heparin) Role in embolic stroke Useful both for primary and secondary prevention. If low risk hemorrhage, high risk of recurrence , initiate anticoagulation. Target INR : 2 (1.6-2.5) if age >75 yrs 27

28. 5) Rehabilitation 28 Improves neurologic outcome and reduces mortality Proper rehabilitation of the stroke patient includes: Early physical, occupational, and speech therapy . Prevention of complications of immobility

29. Classification of stroke

30. Hemorrhagic stroke Causes include Hypertension Ruptured aneurysm Ruptured AV malformation Bleeding in to prior stroke Bleeding in to the tumor Coagulopaty Medications- cocane ,Amphetamine Head trauma Amyloid angiopathy

31. Intra- parenchymal hemorrhage Most common form of intracranial hemorrhage. Accounts for 10% of all strokes. Associated with 50% case fatality rate. Mostly due to hypertension ,trauma and cerebral amyloid angiopathy . Advanced age and alcohol consumption increase the risk. Cochane and metamphithamine use is important cause in the young. Pts typically present with an acute onset of a FND that corresponds to the part of the brain affected

32. Hypertensive hemorrhage Due to rupture of arteries deep in the brain. Most common sites of bleeding 1-basal ganglia (especially putamen ) 2-lobar 3-Thalamus 3- Cerebellum 4- Pones

33. HTNsive ICH.. Acute BP elevation may also be the immediate precipitating cause Occur in the territory of penetrating arteries that branch off major intracranial arteries, often at 90 degrees Most occur during routine activity Neurologic symptoms increase gradually over minutes or few hours Headache, vomiting, and a decreased LOC develop as hematoma enlarges and other ssx of ↑ ICP Seizures in the 1 st days occur in up to 1/3 rd of pts (more common in lobar haemorrhage) Neurologic signs vary depending on the location of the h’ge

34. Putamen hemorrhage Most common site Adjacent internal capsule is invariably involved Contralateral hemiparesis & facial palsy, slurred speech, eye deviation away from hemiparesis If large, ↑ ICP and brainstem compression Depressed LOC , deep, irregular, or intermittent respiration, a dilated and fixed ipsilateral pupil, and decerebrate rigidity →coma

35. Thalamic hemorrhage Contralateral hemiparesis due to pressure effect on i/capsule with prominent sensory deficit of all modalities Aphasia (dominant) Visual field defect due to extension to upper midbrain Downward and inward looking eyes Ocular disturbances (midbrain compression) Homonymous hemianopia Unequal and nonreactive pupils Nystagmus Ipsilateral Horner’s syndrome Dejerine-Roussy Syndrome- chronic, contralateral pain syndrome

36. Pontine Hemorrhage Rapidly progressing deep coma with quadriplegia Decererate rigidity and pin-point pupils reacting to light Absent horizontal eye movements and oculocephalic reflex Death often occurs in few hours but small hemorrhages are compatible with survival

37. Cerebellar Hemorrhage Develop over several hrs → occipital HA, vom, ataxia, dizziness or vertigo F orced deviation of the eyes to the opposite side, pupils are small and reactive As hrs pass pt becomes comatose due to brainstem compression or obstructive hydrocephalus If deep cerebellar nuclei are spared, full recovery is common

38. Lobar Hemorrhage V ary in their neurologic signs depending upon location Occipital hemorrhage – hemianopia Left temporal hemorrhage – aphasia and delirium Parietal hemorrhage – hemisensory loss Frontal hemorrhage – weakness Large hemorrhages - stupor or coma Associated with a higher incidence of seizures

39. Laboratory and imaging Evaluation CBC, blood chemistries and electrolytes Noncontrast head CT imaging Reliable at demonstrating the hematoma A contrast enhanced MRI To detect underlying cause (AV malformation, tumor, and cerebral amyloid angiopathy), should be done when these are suspected or the cause of ICH otherwise remains obscure Angiography (CT, MRI conventional x-ray) and coagulation profile When cause is uncertain, young or non hypertensive and for unusual site hematoma LP should be avoided as it may induce cerebral herniation

40. Management General management issues Fever should be controlled look for sources of fever and Rx it + antipyretic Hyperglycemia Insulin Rx if blood glucose > 185mg/dl DVT prophylaxis P neumatic compression (mainstay), LMWH, UFH, and IVC filter are options After documented cessation of bleeding, LMWH or UFH may be considered as early as 1 st day after onset and for high risk pts (48hrs)

41. Reverse if any coagulopathy Stop all anticoagulant and antiplatelet drugs for at least 2wks and anticoagulant effect should be reversed with appropriate agent Prothrombin complex concentrate (if not available FFP) and iv vit K for pt taking warfarin Pts with thrombocytopenia of < 50,000 should be transfused with platelet Protamine sulfate is recommended for urgent Rx of pts with heparin-associated ICH

42. Surgical intervention Indications vary with the site of the bleed Evacuation for supratentorial ICH is controversial Craniotomy only for lobar clots within 1 cm of the surface Evacuation for cerebellar h’ges is recommended > 3 cm in diameter + Deteriorating or Brainstem compression and or Hydrocephalus due to ventricular obstruction

43. BP Control Severe ↑ worsen hematoma expansion and hypotension may cause ischemia and worsening neurologic condition AHA/ASA guideline 1. For ICH patients presenting with SBP between 150 and 220 mm Hg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe (Class I; Level of Evidence A) and can be effective for improving functional outcome (Class IIa ; Level of Evidence B 2. For ICH patients presenting with SBP >220 mm Hg,it may be reasonable to consider aggressive reductionof BP with a continuous intravenous infusion and frequent BP monitoring (Class IIb ; Level of Evidence C). (New recommendation)

44. Management of complication Raised ICP Expanding hematoma and surrounding edema Simple measures Head elevate head of bed 30 degree Aggressive measures (GCS < 8, IVH ± hydrocephalus, evidence of herniation) Mannitol or hypertonic saline H yperventilation (PCo2 to 25-30 mm Hg) Ventriculostomy (obstructive hydrocephalus) S teroids are not recommend

45. Seizers ( 4.2 to 29%) More in lobar, often nonconvulsive Rx with appropriate iv AED to prevent recurrence (usually phenytoin) No benefit of prophylaxis Ventricular extension If hydrocephalus Rx with ventriculostomy and EVD

46. Resuming antithrombotic Rx Antiplatlets Aspirin is safe after the acute phase provided well controlled BP, and if there is strong indication (AF, large vessel stenosis, DCM and malignancy) 81mg/d after 1-2wks of ICH can be restarted Anticoagulation For pts at high risk of embolic events AHA/ASA recommendation Iv UFH may be safe than oral agents, and oral agents may be resumed 3-4wks later (maintain in the INR lower range)

47. Secondary prevention BP control to < 130/80 mm Hg is most important Life style change – stop smoking, avoid heavy smoking and cocaine abuse

48. Prognosis 50% of pts with HTN ICH die, but others have a good to complete recovery if they survive the initial h’ge ICH scoring system is useful for prediction of mortality and clinical outcome

49. ICH score .

50. 4. Subarachnoid Hemorrhage (SAH) Accounts for ~10% of hemorrhagic stroke, and causes include Saccular aneurysm (80%) Trauma AVM Extension from ICH

51. Saccular (Berry) Aneurysm. 2% of adults have intracranial aneurysms, of which 20-30% are multiple Accounts for 2 -5 % of all new strokes Incidence increases with age, mean age is 50 yrs, F > M About 85% of them are located in the anterior circulation Case fatality rate ~51%, and 50% of survivors will develop sequelae , especially cognitive abnormalities Annual risk of rupture of asymptomatic aneurysm is 0.1% for < 1cm, 0.5-1% for > 1cm, and 6% for > 2.5cm (giant) aneurysm

52. Common sites of saccular Aneurysm

53. Risk factors for rupture Cigarette smoking and/or cocaine use Heavy alcohol use Hypertension Family history of SAH Connective tissue diseases Fibromuscular dysplasia Size, site (>7 mm, located top of basilar a.)

54. Clinical Manifestation Unruptured aneurysms are usu asymptomatic, but prodromal symptoms can occur Worst HA (80%), and SZ (20%) N/V, neck stiffness, LOC, or FNDs may occur Minor h’ges occur within 2- 8 wks before overt SAH M isdiagnosis rate ~12%

55. Complications of SAH

56. Rerupture (Rebleeding) H ighest during the 1 st 72hrs, ~30% in 1 st month Sudden deterioration, new blood on CT Mortality – 60% Higher grade and large aneurysm, are risk factors of rebleeding

57. Hydrocephalus Occur within 72 hrs in 20%-30% of pts, often accompanied by intraventricular bleeding Treatment Spontaneous resolution in 50% of cases Ventricular drainage Chronic ventriculomegaly requiring permanent shunting

58. Vasospasm A t the base of the brain and causes and infarction in 30% Typical onset 3 - 5 dys after the h’ge, max narrowing at 5 -14 days, and a gradual resolution over 2-4 wks Risk factors- P oor clinical grade, age < 50 yrs and hyperglycemia Hypomagnesaemia appears to be common after SAH and associated with both poor outcome and vasospasm Presentation Deterioration clinical condition, FND in the vascular territory, ssx of raised ICP Diagnosis can be made by angiography and t ranscortical Doppler U/S

59. Hyponatremia Occur in about 30% of patients. Secondary to either CSW or SAIDH Associated with development of DCI P oor clinical outcome

60. Diagnosis of SAH Blood in the CSF is the hallmark In 95 % detected by CT within 72 hrs In negative CT scan – do LP and CSF analysis Xanthochromic CSF within 6-12 hrs, peaks in 48 hrs and stays for 1-4 wks Angiography (xy, CT), MRA

61. Medical Management ABC of life BP control to maintain adequate cerebral perfusion Rest, sedation, laxatives, analgesics, GI prophylaxis and nutrition Prophylactic AED Prevent DVT using pneumatic compression stockings, avoid heparin Antithrombotic Rx can be started or resumed after definitive Rx of the aneurysm

62. Manage hyponatremia Normal Saline Oral salt Hypertonic Saline vasospasm Nimodipine 60mg Q4hrs for 21 days Reduces poor outcome associated with vasospasm If no response Intraarterial Vasodilators Percutaneous t ransluminal angioplasty

63. Surgical Management Clipping Craniotomy and brain retraction needed Coiling Endovascular, through femoral artery L ess mortality and morbidity

64. Thank you!!!