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CEREBRAL VASCULAR ACCIDENTS

CEREBRAL VASCULAR ACCIDENTS. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. Objectives. Epidemiology Risk factors Catergories Treatments. Epidemiology. 2.52/100,000/yr – children thru 14 yrs 1.89/100,000/yr – hemorrhagic 0.65/100,000/yr - ischemic

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CEREBRAL VASCULAR ACCIDENTS

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  1. CEREBRAL VASCULAR ACCIDENTS Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta

  2. Objectives • Epidemiology • Risk factors • Catergories • Treatments

  3. Epidemiology • 2.52/100,000/yr – children thru 14 yrs • 1.89/100,000/yr – hemorrhagic • 0.65/100,000/yr - ischemic • As common as brain tumors • Neonatal strokes 28/100,000 live births

  4. Epidemiology • Increased awareness & reporting • Improved imagings • Better survival of underlying diseases

  5. Epidemiology • Impacts of strokes • Mortality 6-40% (hemorrhagic 2x ischemic) • Morbidity • Neurological disability – 60% • Seizures – 15% • Headaches

  6. Risk Factors • Cardiac Disease 19% • Coagulation Disorders 14% • Dehydration 11% • Vasculitis 7% • Infection 6% • Dissection 5% • Neoplasm 4% • Metabolic Disorder 3% • Moyamoya 2% • Sickle Cell Anemia 2% • Perinatal Complication 2% • Other 2% Lamthier et al. (2000) Neurology Multiple risk factors are often present & predict worse outcome

  7. Risk factors • Congenital Heart Disease • Asymptomatic aortic valvular disease • Associated with dissection • Undiagnosed cardiac disease (PFO)- rare • Inherited connective tissue diseases • Marfan • Erlos-Danlos

  8. Risk factors • Coagulation disorders • Factor V Leiden • common in Caucasian • most common cause of activated Protein C resistance • Prothrombin 20210 mutation • Neonatal & childhood CSVT • Infection, Inflammation, Immune Deficiency • 1/3 cases associated with infection (esp vacicella within the previous year) • High WBC (in association with SCD) increase recurrence • Inflammation: harmful effects on the endothelium

  9. Risk factors • Sickle Cell Disease • 25 % with stroke by the age 45 • Ischemic stroke predominantly in childhood • Hemorrhagic with steroid and Hypertension • Sinovenous thrombosis, posterior leukoencephalopathy, watershed ischemia • Silent infarcts • Hemorrhagic (ICH or SAH) in adult secondary to aneurysm • High WBC associated with infection can precipitate CVD – indicate chronic infection

  10. Risk factors • Anemias • Hemolytic anemias: thalassemia, hereditary spherocytosis & paroxysmal nocturnal hemoglobinuria • Metabolic disorders • Homocysteinemia: predispose to vessel abn. • Lipid abnormality: • Elevation in Cholesterol (9%), TG (31%), Lipoprotein (22%) • Apolipoprotein abnormality

  11. Risk factors • Vascular abnormality • Vascular adhesion • Adhesion of WBC, RBC, platelets causing endothelial damage • Hypertension • Highest risk in young adult & elderly • Largely ignored in pediatric population • ½ strokes with SBP>90th percentile • Abnormality of angiotensinogen gene: 4X increase in risk of strokes in SCD

  12. Pediatric Arterial Ischemic Strokes (AIS) • Primary Hemiparesis: new focal deficits • Ataxic gait • Chorea • Vertigo • Speech and visual disturbance • Headaches with neurological deficits

  13. Pediatric Arterial Ischemic Strokes (AIS) • Median presentation of 5.6 hrs after AIS symptoms onset • ½ presented within the first 6 hrs • ½ presented >24 hrs • Main factor in delayed presentation: was the failure of parents to recognize that a child was having neurologic symptoms

  14. Pediatric Arterial Ischemic Strokes (AIS)

  15. Pediatric Arterial Ischemic Strokes (AIS)

  16. Pediatric Arterial Ischemic Stroke s (AIS) • Ischemic • Mortality 6-20% • 30% recurrence risks • 5 yr survival • 1.2% after perinatal • 19% after child hood • Median time 2.7 months • 60% recurrence if associated with vasc. abn • Hemorrhagic • Mortality 8-40% • 10-20% recurrence rate but associated with higher mortality • Recurrence is higher with struct. abn. • Girls>boys (16% vs 3%) excluding trauma • Lower neurological morbidity

  17. Pediatric Arterial Ischemic Strokes (AIS)

  18. Pediatric Arterial Ischemic Strokes (AIS) • Dissection: • ICA>vertebral • Intracranial: anterior circulation 60% (ICA, MCA & anterior cerebral • Extracranial: 80% of posterior circulation with ½ located within the vertebral artery at C1=C2 • Trauma is common cause

  19. Pediatric Arterial Ischemic Strokes (AIS) • Moyamoya • Bil. severe stenosis of end ICA with collaterals

  20. Pediatric Arterial Ischemic Strokes (AIS) • Transient Cerebral arteriopathy • Inflammatory response to infection (varicell, Borrelia or tonsilitis • Multi-focal lesions • Most cases stabilize but some progress to recurrent strokes

  21. Pediatric Arterial Ischemic Strokes (AIS) • Sickle Cell Disease • Narrowing of distal ICA & proximal MCA, anterior cerebral arteries • Gradual progression to occlusion • Endothelial proliferation • Silent infarcts occur in MCA territory or in border zones • High recurrence rate • 25% with CVD by age 45 • Ischemic in children • Hemorrhagic in adults

  22. Pediatric Arterial Ischemic Strokes (AIS) • Vascular Malformation • 10-500/100,000 • Hi flow AV shunts without capillary bed • In children: hemorrhagic presentation, deep areas • Types • Capillary telaangioma • Venous angioma • ngiectasia • Cavernous Sturge-Weber syndrome: venous angioma of the leptomeninges, coroidal angioma and a facial capillary hemangioma

  23. Pediatric Arterial Ischemic Strokes (AIS) • Vein of Galen Malformation • Male predominance • Embryonic choroidal AVM • Presentation: high output heart failure, hydrocephalus, sz

  24. Aneurysm Acquired, rare in children <5% ¾ presented with ICH 10-15%: Post-traumatic 10-15%: mycotic Others: polycystic kidney dz, SCD, TS, Marfan, Ehlers-Danlos etc. PEDIATRIC AIS

  25. Cerebral sinovenous thrombosis (CSVT) • Superficial & Deep • Superficial: cortical veins superior sagittal sinus right lateral sinus • Deep: inferior sagittal sinus & paired internal cerebral veins, join to form v. of Galen & straight sinus • Flow is highly responsive to changes in MAP which can cause reversal of flow • Relative low thrombomodulin prothrombotic

  26. Cerebral sinovenous thrombosis (CSVT)

  27. Cerebral sinovenous thrombosis (CSVT)

  28. CSVT • Pathophysiology • Mechanical: birth trauma • Trauma, sepsis, underlying disease (malignancy, systemic inflamation) • Septic foci: inner ear, mastoid or air sinuses • Dehydration, anemia, coagulation disorders • Venous Infarction: venous HTN by outflow obstruction • Intracranial Hypertension: disruption of CSF absorption

  29. CSVT • Signs/symptoms • Severe HA associated with vomiting, sleepiness, double vision • Visual disturbances • Severe dizziness or unsteadiness • Sz activity

  30. CSVT

  31. Other Strokes Mimics • Posterior Circulation Arterial Strokes • Posterior infarction of cerebellum, brain stem • Boys>girls • Trauma, subluxation of cervical spines causing arterial dissection • Reversible Posterior Leukoencephalopathy • Sx: sz, AMS, disorder of consciousness, visual abn., HA • Predominant post. White matter abn. • Clinical condition: HTN encephalopathy, eclampsia, AC in SCD, immunosuppression • Acute hypotension (poor cardiac fxn/anemia) • Rapid resolution: vasogenic cerebral edema prob secondary to autoregulation & endothelial injury • Acute Disseminated Encephalomyelitis

  32. Other Strokes Mimics • Metabolic Strokes: Diabetes, inborn errors of metabolism • Vascular injury • Homocysteine: direct endothelial injury • Fabry: lysosomal storage with accumulation and deposition of glycosphingolipid in blood vessels endothelial cells • Menkes: deficiency in copper; obliteration of intracranial vasculature • Non-vascular injury: diabetes, organic acidemias, Urea cycle defects etc. • MILAS (mitochondrial dz with LA and stroke like sx): lacking of energy supply with generation of oxygen free radicals • Others: accumulation of toxic substances

  33. Diagnosis – w/o SCD • First 24 hours • Angiogram • MRA • Blood cultures if febrile • Toxicology screen • 24-72 hours • Echo with bubble study • Limited initial pro-thrombotic evaluation • Lupus anticoagulants, antiphospholipid abs, lipid profile, lipoprotein A, Homocysteine, gene mutation • Systemic inflammatory disease evaluation: ANA, ESR, CRP, UA Rollins N, Dowling M, Booth T, Purdy P, AJNR, 2000substances

  34. Diagnosis – w/o SCD • After acute setting • Further prothrombotic evaluation • Protein C & S • Antithrombin • Factor VIII • Confirmation of early abnormal tests Rollins N, Dowling M, Booth T, Purdy P, AJNR, 2000substances

  35. Ischemic Stroke Treatments • General management • Normo-thermia • Normal oxygen saturation • Cerebral protection with the presence of increase ICP • Specific management • Early neurosurgery consult as indicated

  36. Stroke Treatments • Anticoagulation • Commonly use in: • AIS: Heparin or LMWH for 5-7 days until cardioembolic stroke and dissection are excluded • CSVT: 3-6 months of therapy reduced risk of recurrent systemic or cerebral thrombosis • High risk of embolism with underlying disease • Dissection: 3-6 months with extracranial dissection. • Known prothrombotic abnormalities • With cardiac embolism: controversial • Balance of risk with precipitate hemorrhage vs recurrence embolic event (lower risk in children for progression to hemorrhage)

  37. Stroke Treatments • Anticoagulation: • 115 w/ first AIS treated by standardized guidelines • Warfarin: 44 pts 2 (4.5%) major bleed (non-fatal) • Keep INR 2-3 • LMWH: 51 pts for 7-14 days no major bleed • ASA: 103 pts (3-5mg/kg/day) no major bleed, no Reye’s syndrome

  38. Stroke Treatments • Aspirin therapy • Efficacy and dose are unknown • Usual dose 5mg/lg/day • Long term prophylaxis dose may be lower • No report case of Rye’s syndrome • One case in adult when the pt increased ASA dosage with flu like sx

  39. Stroke Treatments • Thrombolytic agents: urokinase & streptokinase • No evidence to support efficacy- 203 (pooled literature) for non-cerebral thrombotic complication • 80% thrombus cleared • 54% minor bleeding (no transfusion needed) • 1 pt with intra-cranial hemorrhage • Toronto: 29 pts treated with tPA (0.5mg/kg) • 79% - clot was dissolved • ¼ of the pts had bleeding required transfusion • No good data regarding outcomes, therefore treatment is controversial

  40. Stroke Treatments - SCD • ½ will have another stroke • Urgent exchange transfusion (HbS <30% or HgB 10=12.5) • Top off transfusion if exchange transfusion is delayed or severe anemia • Chronic exchange transfusion • Keep HgS <50% • Relapse if stop even with period of symptoms free • Risk: iron overload treated with chelation • Use of hydroxyurea to prevent stroke • Induction of HbF • Generation of Nitric Oxide

  41. Intracranial Hemorrhage • Risk factors • AV malformation 25% • Hematologic anomalies 10-13% • Brain tumors • Cavernous Hemangiomas • Vasculopathy • Vasculitis • Infection • Illicit drug uses

  42. Intracranial Hemorrhage • Non traumatic SAH mostly caused by aneurysms • 10% are secondary to CSVT • Controversial in anti-coag of CSVT with hemorrhage • 25% mortality with 42% significant disability • No standard management and treatm

  43. Treatments: ICH • Treat ICP, cerebral protection • Reverse coagulopathy • Recombinant activated Factor VII within the first 4 hrs: limited growth of hematoma, reduced mortality, improved functional outcomes • Treat space occupying lesion • Treat associated vasospasm (SAH) with Triple H therapy • Supportive treatment

  44. Treatments: SAH • Vasospasm associated with 20-30% of aneurysmal SAH • Related to spasmogenic substances generated during lysis of subarachnoid blood clots • Present no earlier than day 3, peak day 7-8 • Triple-H therapy • Moderate hemodilution • Hypertension • Hypervolumia • Nimodipine: selective cerebral vessel Ca channel blocker, start within 4 days • Decrease morbidity and mortality • Potential for systemic effect causing severe hypotension

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