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Stroke in children
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Stroke in children






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Stroke in children Presentation Transcript

  • 2. WHO Definition 2004
    “A clinical syndrome typified by rapidly developing signs of focal or global disturbance of cerebral functions, lasting more than 24 hours or leading to death, with no apparent causes other than of vascular origin”
    “Brain imaging is mandatory for accurate diagnosis, subsequent referral and, in particular, to exclude conditions requiring urgent neurosurgical intervention”
    Stroke in adult - chronic vascular injury.
    Obesity, cigarette smoking, arterial hypertension, diabetes mellitus, sedentary lifestyle.
    Children with stroke-chronic lifestyle factors make little contribution.
    Developmental, genetic, environmental factors are all possible contributors to vascular injury .
  • 4. Stroke in Children Differs …..
    Rare, subtle presentation, wide differential diagnosis.
    Coagulation, vascular & neurological systems differ.
    Risk factors: multiple, age-related, poorly understood.
    No established treatments.
  • 6.
  • 7. Premature and Term Neonates
    Higher risk than older children.
    ICH-germinal matrix prone to rupture with increases in BP.
    ICH-1 in 100 term neonates -Gradnitzer et al.
    Ischaemic stroke- 1 in 4000 and 1 in 5600 term births( Lynch et al).
    CVT-0.67 cases per 100,000 children per year, with neonates making up 4 3% of cases.
    Increased awareness and reporting.
    Improvement in radiographic diagnosis.
    Increasing survival in previously lethal diseases that predispose to stroke.
    Congenital heart disease
  • 9. Impact of Ped.Stroke
    Mortality - up to 10%
    Risk of recurrence of arterial stroke -20 to 30%
    Neonates-recurrence - 4%
    Risk of death, disability, reduced quality of life-50%
    Seizures (15%).
    Headache disorders (30%).
    Neurologic deficits (60%) -Motor, Memory, Visual.
  • 10. High-Risk Subgroups
    Vascular malformations
    Bleeding disorders
    Sickle cell anemia
    Complex congenital heart disease
    Children with cancer
    Syndromes- Down, NF- 1, Marfan's, EDS, moyamoya, homocystinuria , Fabry's ,
    familial hyperlipedemias.
    Apnea, irritability, jitteriness, lethargy, bulging fontanel.
    Hemiparesis may not be apparent
    until a child > 6 months of age.
  • 12. Children > 6 months
    Seizures or focal signs similar to those seen in adult stroke with hemiparesis, ataxia, or aphasia.
    Severe headaches with ICH.
    Developmental delay(17% - sickle disease).
  • 13.
  • 14. Hematological Causes
    Vit. K deficiency.
    Deficiencies of coag. factor VIII ,factor IX ,VWF.
    Deficiencies of protein C, protein S, and antithrombin III .
    Low platelet count.
    Sickled cells, polycythemia, chronic hypoxia.
  • 15.
  • 16.
  • 17. Trauma
    Trauma injure vessels directly, leading to hmge from torn vessels and thrombosis in damaged intima.
    Subdural hmges, subarachnoid hmges, and ischemic infarctions occur in accidental and non accidental head injury.
    Bony abnormalities of the vertebrae, or abnormalities of vessel walls resulting from collagen vascular disease or metabolic disease may predispose to cervicocephalic arterial dissection after mild trauma.
    Child abuse and neglect.
  • 18. Infection
    Bacterial meningitis - DIC and vascular inflammation, subsequent arterial or venous thrombosis .
    Group B streptococcus, gram-negative enteric bacilli, and Listeriamonocytogenes.
    After 2 months of age, Streptococcus pneumoniae and Neisseriameningitidis.
    Haemophilusinfluenzal type B vaccination at 2 months of age has led drop in HIB meningitis.
    In immunosuppressed children with cancer or AIDS- Aspergillus species may lead to vasculitis and infarction.
    Tuberculosis leads -vasculitis and infarction.
    Lyme disease - infectious vasculitis and aneurysm formation.
    Varicella-zoster virus - vasculitis by direct infection of the arterial wall or by a postinfectious inflammatory reaction that manifests weeks to months after the primary infection.
  • 19.
  • 20. Cardiac Causes
    Complex congenital heart disease may lead to thrombosis and ischemic stroke .
    Abnormal cardiac anatomy or arrhythmias- abnormal flow - predispose to the formation of intracardiac thrombi.
    Septal defects may lead to R-L shunts -venous thrombi cross to the arterial side and cause infarction.
    Surgery and cardiac catheterization disrupt the endothelium and to thrombosis.
    An abnormal heart valve serve as a nidus for bacterial vegetations that cause cardioembolic stroke.
    Chronic hypoxemia in severe cases of congenital heart disease lead to polycythemia, and the increased blood viscosity- promote thrombosis.
    PFO -arterial infarction in both children and adults, R-to L shunting.
  • 21. Combinations of Multiple Factors
    Some children >1 factor contributing to the cause of their stroke.
    Hemorrhages in children with hemophilia are often precipitated by trauma.
    Children with ischemic stroke may have multiple prothrombotic abnormalities.
    Children with congenital heart disease or with leukemia may be at higher risk for developing thrombotic complications during hospitalization if they also have a prothrombotic abnormality.
  • 22.
  • 23. Differential Diagnosis
    postictal Todd's paresis.
    Alternating hemiplegia of childhood.
    Edema, bleeding, or shifting of brain tumor.
    Encephalitis or meningoencephalitis.
    ADEM, multiple sclerosis.
  • 24.
    Questions about delivery and perinatal period, attainment of hand preference, and basic developmental milestones
    Past hx -Previous hemorrhages, abnormal bruising, petechiae, or thromboses, and other risk factors of stroke, such as complex congenital heart disease, renal failure, or sickle cell anemia.
    Family hx -abnormal bleeding in other family members, strokes or heart attacks before age 45, peripheral arteriopathy, or DVT.
  • 26. PE in the child with stroke
    Head circumference-
    Macrocephaly-Hydrocephalus caused by IVH, SDH, SAH, or vascular malformation.
    Microcephaly-Failure of brain growth resulting from stroke or genetic disorder.
  • 27. Eyes
    External/Iris Epicanthal folds, brushfield's spots-Down syndrome
    Horner's syndrome-Carotid dissection
    Pulsating exophthalmos-Carotid-cavernous fistula
    Lens subluxation-Marfan's syndrome, homocystinuria
    Angioid streaks-Pseudoxanthomaelasticum
    Xanthelasma on lids, corneal arcus-Hyperlipidemia
    Corneal opacity-Fabry's disease
    Papilledema-Increased ICP resulting from hydrocephalus, vascular malformation, or acute edema
    Hemorrhages-Trauma (consider child abuse), bleeding diathesis, ruptured aneurysm,collagen disease, emboli
    Vasculopathy-Systemic vasculitis
    Angioid streaks-Pseudoxanthomaelasticum. Paget's disease, sickle cell
    Angioma-Familial cavernous angiomatosis, von Hippel-l.indau disease
  • 28. SKIN
  • 29.
  • 30.
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  • 34.
  • 35.
  • 36.
  • 37.
  • 38.
  • 39. THERAPIES-The Acute Period
    Children with hemorrhagic stroke require close observation in the first hours.
    Children with hemophilia need immediate factor replacement and may require blood transfusion.
    Children with large hematomas with significant mass effect may need surgery.
    Any child presenting with unexplained or poorly explained intracranial hemorrhage should also be evaluated for child abuse and other sites of injury.
    Acute stroke is usually treated with exchange transfusion.
    Stroke Prevention in Sickle Cell Trial showed that in children with evidence of vasculopathy by transcranial Doppler ultrasound screening, treating with regular transfusions reduced the risk of recurrent stroke by 90% (Adams ).
    Chronic transfusions carry the risk of infection and cause increases in serum ferritin.
    Some require treatment with deferoxaminechelation to prevent iron overload.
  • 41. Chronic Therapy
    Patients with hemophilia and severe bleeding may require prophylaxis with regular factor transfusions.
    Young or ataxic children with hemophilia may need to wear protective helmets until their balance improves.
    Patients with genetic, chronic thrombotic abnormalities such as protein C or S deficiency, or with lupus anticoagulant, may require long-term care with LMWH or warfarin (Andrew et al).
    LMWH may be used for 3-6 months after cervicoccphalic arterial dissection or CVT.
    Warfarin or aspirin are used for long-term therapy.
    Families of children on aspirin are generally concerned about Reye's syndrome, but no cases have been reported in children taking aspirin for stroke prophylaxis.
  • 42.
  • 43. Few case reports describing children with IS treated with intra-arterial or intravenous tissue plasminogen activator.
    Few children present within the mandated 3 hours of infarct onset.
    No clear guidelines on using intravenous or intra-arterial thrombolytics in children.
    May not be helpful in neonates, who have lower levels of plasminogen than older children.
    Centers trying thrombolytic therapy in children should have stroke neurologists experienced in its use to assist in management, 24 hour access to a CT scanner to monitor for intracranial hemorrhage, and a pediatric neurosurgeon and operating room on-call in case of disastrous intracranial hemorrhagic complication.
  • 44. Recommendations for Thrombolytic Therapy for Childhood Stroke
    Class II Recommendation
    1. Thrombolytic therapy with tPA may be considered in selected children with CVST (Class IIb, Level of Evidence C).
    Class III Recommendation
    1. Until there are additional published safety and efficacy data, tPA generally is not recommended for children with AIS outside a clinical trial (Class III, Level of Evidence C). However, there was no consensus about the use of tPA in older adolescents who otherwise meet standard adult tPA eligibility criteria.
  • 45.
  • 46. Retrospective study that analyzes 20% of all community hospital admissions in the United States.
    Over a 4-year period, 2904 pediatric patients with stroke were included in the study, with 2% of them receiving intravenous or intra-arterial thrombolysis.
    firstly, no symptomatic intracranial hemorrhage was reported in the tPA group;
    secondly, mortality and dependency were more frequent in the tPA group at discharge, but the difference was not significant,
    thirdly, patients of the tPA group needed mechanical ventilation more frequently and their stay was longer.
    However, mortality, dependency, hospital stay and mechanical ventilation are related to the severity of the stroke, and this variable is not controlled in this study.
    In addition, no data about the National Institutes of Health Stroke Scale (NIHSS; before and after thrombolysis), the modified Rankin Scale and the Barthel Index scores are provided, because this register is retrospective.
    Finally, neither the therapeutic window, tPA doses, nor information about the vessel occluded are explained.
    Without these data no conclusion about efficacy of thrombolysis can be drawn.
  • 47. APPROACH
  • 48. OUTCOMES
    More than 85 percent of babies who have strokes live to adulthood.
    Between 50 and 80 percent of infants and children will have serious, long‐term challenges including: hemiplegia or hemiparesis seizures; and speech, visual, behavioral and learning difficulties.
    Many childhood stroke survivors require both acute and long‐term rehabilitation.
  • 49.
  • 50. Thank you