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

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Presentation on theme: "CEREBRAL VASCULAR ACCIDENTS Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta."— Presentation transcript:

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

2 2 Objectives Epidemiology Risk factors Catergories Treatments

3 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 4 Epidemiology Increased awareness & reporting Improved imagings Better survival of underlying diseases

5 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% Dehydration11% Vasculitis 7% Infection 6% Dissection 5% Neoplasm 4% Metabolic Disorder 3% Moyamoya 2% Sickle Cell Anemia 2% Perinatal Complication 2% Other 2% Multiple risk factors are often present & predict worse outcome Lamthier et al. (2000) Neurology

7 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 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 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 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 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>90 th percentile –Abnormality of angiotensinogen gene: 4X increase in risk of strokes in SCD

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

13 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) 14

15 Pediatric Arterial Ischemic Strokes (AIS) 15

16 Pediatric Arterial Ischemic Strokes (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 16

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20 Pediatric Arterial Ischemic Strokes (AIS) 20

21 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 21

22 Pediatric Arterial Ischemic Strokes (AIS) Moyamoya –Bil. severe stenosis of end ICA with collaterals 22

23 23 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

24 24 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

25 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 25

26 Pediatric Arterial Ischemic Strokes (AIS) Vein of Galen Malformation –Male predominance –Embryonic choroidal AVM –Presentation: high output heart failure, hydrocephalus, sz 26

27 PEDIATRIC AIS 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.

28 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 28

29 Cerebral sinovenous thrombosis (CSVT) 29

30 Cerebral sinovenous thrombosis (CSVT) 30

31 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 31

32 CSVT Signs/symptoms –Severe HA associated with vomiting, sleepiness, double vision –Visual disturbances –Severe dizziness or unsteadiness –Sz activity 32

33 CSVT 33

34 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 34

35 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 35

36 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 36

37 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 37

38 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 38

39 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) 39

40 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 40

41 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 41

42 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 42

43 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 43

44 Intracranial Hemorrhage Risk factors –AV malformation25% –Hematologic anomalies10-13% –Brain tumors –Cavernous Hemangiomas –Vasculopathy –Vasculitis –Infection –Illicit drug uses 44

45 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 45

46 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 46

47 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 47

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