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Childhood stroke ped neurology view



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  • BUT not go on with children because1- commonly have a brain infarction shown by brain imaging despite thetransient nature of their symptoms. 2- Children with cerebral venous sinus thrombosis (CVST) commonly present withheadache or seizures. 3- “Stroke-like episodes” without an obvious vascular cause may occur in migraine or metabolic disease but may require specific treatment. 4- Prior illness (eg, infection) or events (eg, head trauma) need not preclude a diagnosis of stroke
  • Adult risk factors: BP, DM, Obesity, atherosclerosis. Sedentary life20% hgic – 80% ischemic
  • This incidence rate of childhood stroke makes childhood stroke more common than pediatric brain tumors . Most under age of 2 ysHowever, recent research has led physicians to believe that pediatric stroke is about twice this common, affecting about 5 or 6 per 100,000 children 1/3 in newbornAlthough cerebrovascular disorders occur less often in children than in adults, recognition of stroke in children has probably increased because of the wide spread application of noninvasive diagnostic studies such as magnetic resonance imaging (MRI),magnetic resonance angiography (MRA), computed tomography (CT) and, in the neonate,cranial ultrasound studies.1-
  • Spontaneous Intraparenchymal and SAH non traumatic
  • Intrapaenchymal he might occur spontaneously
  • Pmt and neoenates with higher risk
  • Numbness or pins and needles of the face, arm or leg on one side of the body Slurring speech or difficulty finding words Brief loss of vision in one or both eyes. Children often experience different symptoms of stroke to adults, The signs and symptoms of a stroke vary depending on several factors, including the age of the child and the location and severity of the CVA. A child who is having a stroke generally experiences the same symptoms that an adult would The signs and symptoms of a stroke vary depending on several factors, including the age of the child and the location and severity of the CVA. A child who is having a stroke generally experiences the same symptoms that an adult would such as seizures, headache and fever. However, many of the symptoms of stroke in children are similar to those experienced by adults. Depending on the areas of the brain affected by stroke
  • Therefore a cascade occurs in which vwf promotes sickle red cell/endothelial cell adhesion( nidus for thrombus formation)
  • Breavment
  • Thalamic infarction
  • CT vesus MRI
  • urgent exchange transfusion should be undertaken to reduce HbS to <30% and raise hemoglobin to 10–12.5 g/dlII- if the patient has had a neurological event in the context of severe anemia (eg., splenic sequestration or aplastic crisis), or if exchange transfusion is going to be delayed for more than four hours, urgent top-up blood transfusion should be undertaken

Childhood stroke ped neurology view Presentation Transcript

  • 1. Stroke in Children: Clinical Guidelines Prof Dr Hussein AbdeldayemProf of Ped Neurology, Alex Univ
  • 2. CASE STUDY• 4 YS DS with TF• Sudden onset of hemiplegia
  • 3. WHO DEFINITION OF STROCK 2004• “A clinical syndrome in which there is 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”
  • 4. Definition• Transient ischaemic attacks (TIAs): ‘where the neurological deficit resolves within 1 hr (previously 24 hours).
  • 5. Differs from Adult Stroke• In adult: chronic risk factors• In children: 1- congenital and developmental risk factors 2- rare 3-subtle presentation* 4- wide DD 5- no established tt *Among neonates, signs of hemiparesis are generally not seen before the first six months to one year of life
  • 6. incidence-2.5 – 3.0 children out of 100,000 affected every year.-Newborn babies can develop a stroke 28/100,000- More in boys- Nearly half are hgic strokeOne of the top ten causes of childhood deaths world wide
  • 7. types• A hemorrhagic stroke: a ruptured blood vessel bleeding into the brain. with: headache, disturb consc, vomiting• An ischaemic stroke: +++ 51% isch, 49% hgic 80% isch and 20% hgic (adult)
  • 8. Hgic Stroke
  • 9. Types (cont. )• An ischaemic stroke : an embolism or thrombus blocks a blood vessel in the brain ++ EMBOLI: sec thrombus: minutes warning: TIA Arterial ischaemic stroke: ‘a clinical stroke syndrome due to cerebral infarction in an arterial distribution’.
  • 10. Ischemic Stroke
  • 11. types of stroke ischemic hemorrhagic I Ventricular Stenosisthrombosis embolus Spasm subarachnoid intraparenchymal arterial venous
  • 12. Fate• About 10% of childhood strokes are fatal.
  • 13. Fate• Recurrence ( 20-30%)• Motor impairment• Seizures (10-20%)• Language, Communication• Cognition• Headache (30%)• Social interaction• Learning
  • 14. Motor impairment• Hemiparesis/hemiplegia• Spasticity (?CP)• dystonia• a mixed pattern
  • 15. Language and communicationdefects• language input :(receptive aphasias)• language processing (word-finding problems, grammatical problems and other aphasias),• speech production ( dysarthria )• written language (dyslexia).• Mutism: problems of social interaction and the willingness to communicate
  • 16. Blood supply of brain
  • 17. pathophysiology• Blood supply of the brain
  • 18. • In children ischemic stroke has been most commonly reported in the distribution of the middle cerebral artery.
  • 19. Types of stroke (2)According to time of onset :1- prenatal2- perinatal2- pediatric
  • 20. Prenatal and Perinatal stroke• 17 times more common than pediatric stroke beyond the newborn period.• Arterial ischemia occurring during the 3 days surround birth is reported to be responsible for 50% to 70% of congenital hemiplegic cerebral palsy.• Germinal matrix hge : prone with increase BP
  • 21. Pathophysiology• Features of perinatal period that influence coagulation state – Presence of fetal hemoglobins – Fetal proteins – High hematocrit and blood viscosity – Concentrations of procoagulant and anticoagulant proteins change with gestational and postnatal age
  • 22. Risk Factors for Perinatal Arterial Stroke• Infants : Antiprothrombin factors• in the mothers, antiphospholipid antibodies : anticardiolipin (aCL) antibodies and lupus anticoagulant (LA).,
  • 23. Prenatal Stroke• Focal cerebral infarction (stroke) secondary to intrauterine or perinatal thromboembolism related to thrombophilic disorders, especially anticardiolipin antibodies, is an important cause of hemiplegic CP Nelson Textbook of Pediatrics 18th ed
  • 24. Prenatal Stroke• Family histories suggestive of thrombosis and inherited clotting disorders may be present and evaluation of the mother may provide information valuable for future pregnancies and other family members. Nelson Textbook of Pediatrics 18th ed
  • 25. Perinatal stroke and the risk of developingchildhood epilepsy.• Childhood epilepsy is frequent after perinatal stroke. Evidence of infarction on prenatal ultrasonography and a family history of epilepsy predict earlier onset of active seizures J Pediatr. 2007 Oct
  • 26. Stroke Awareness• Survival from risky disease : PMT, LK, Cyanotic CHD• Improving of radiography
  • 27. CPNeonates - <6 months• Seizures• Irritability, drowsiness, bulge AF, jitterness, apnea• Focal motor defect ( hemiparesis): >6 mo age
  • 28. CP> 6 months• As adult: focal motor, ataxia, aphasia sensation troubles• ICHge: severe headache• SAH: meningism• Developmental delay (17%- SCD)
  • 29. Potential signs• Motor Disorder• Sensory• Reflexes - focal weakness - initial hypotonia then spasticity - Abnormal plantar reflex ( Babinski’s)
  • 30. Aetiology Cong/Acq/ IdiopathicCONGENITAL: Cardiac, SCD, Coag abnACQUIRED:• 1- TRAUMA/ drug induced• 2-VASCULAR• 3-INFLAMMATORY/autoimmune• 4-NEOPLASM• 5-systemic: METABOLIC, DEHYDRATION DEGENERATIVE
  • 31. Coagulopathies and Metabolic/syndromeHematologic DisordersRBC: SCD, polycythemia HomocystinuriaPlatelets: ITP-Thrombocytosis,Protein C deficiency Mitochondrial disordersProtein S deficiency Sulfite oxidaseFactor V (Laiden) mutation deficiencyAnticardiolipin antibodiesLupus anticoagulant antithrombin III Fabry’s syndromedeficiency DSCong coagulation defects 8-9-VWFDIC Ehler’s – DanlosLiver dysfunction with coagulation defects, -Moyamoya syndromeVit K defeciencyMalgnancy: Leukemia
  • 32. Hematologic causes• Sickle cell disease:Overt or silent strokes1-Occlusion of small vessels by deformed sickled cells2-Membranes of SRC are abnormal ,so have a pro coagulant activity3-VWF enhances adherence of sickle red cells to endothelium in cases of high rates of flow (linear sheer stress)
  • 33. Consequences of Arterial Occlusive Stroke in SickleCell DiseaseAge: 5 y (1-18y)1-disturbed learning and intellectual problems2 -Neovascularization occurs in the areas that are left underperfused by the stroke. The network of small, delicate vessels that appear as cloud-like puffs on an arteriogram are called "moyamoya
  • 34. Moyamoya disease Basal arterial occlusion with telangectasiaChronic , progressive, non inflammatory vasculopathyBilateral slowly progressive occlusion of ICAAs occlusion is slowly progressive multiple anastomosis between external & internal carotidNew vascular net work at the base of the braincomposed of collaterals(basillar meningeal& choroidal arteries)
  • 35. • It is not a disease but secondary to other disordersSickle cell anaemiaVSDDown syndromeTOFNFI
  • 36. MR angiography :telangectasis produces hazyappearance like a puff of smoke ( japanese word:moyamoya)
  • 37. Moyamoya disease in a 9-year-old boy.©1999 by Radiological Society of North America
  • 38. Disorders of coagulation:1- anticoagulant deficiencyProtein cProtein sAT III2- Factor v leiden3- prothrombin mutation
  • 39. Protein C, Protein S, AntithrombinIIIdeficiency• Protein C and protein S are inhibitors of factor V(Leiden) and antithrombin III opposes the normal procoagulant activity of factors II, IX, X, XI, and XII by promoting the irreversible formation of inactive complexes of these factors.• inherited or acquired
  • 40. Congenital Heart Acquired Heart DiseaseDisease Rheumatic heart diseaseVSD, Prosthetic heart valveASD, Libman-Sacks endocarditisPDA Bacterial endocarditisAortic stenosis CardiomyopathyMitral stenosis MyocarditisCoarctation Atrial myxomaCardiac rhabdomyoma ArrhythmiaComplex congenitalheart defects as FT
  • 41. Cardiac causesCyanotic heart disease (<2 years)1. Venus sinus thrombosis: polycythemia, dehydration ,viral illness and iron deficiency anaemia2. Embolic arterial occlusion in children due to vegetations or RT to LT shunt Cardiomyopathy , prothetic valve ,endocarditis, cardiac cath and surgical repair
  • 42. Vasculitis Systemic Vascular DiseaseMeningitis/encephalitisSystemic infection, Systemic hypertensionSLE Volume depletion orPolyarteritis nodosa systemic hypotensionGranulomatous angiitis HypernatremiaTakayasus arteritis Superior vena cavaRheumatoid arthritis syndromeDermatomyositis DiabetesIBD, HUSDrug abuse (cocaine,amphetamines),Drug induced
  • 43. VasoSpastic Structural Anomalies of theDisorders Cerebrovascular SystemMigraine Arterial fibromuscular dysplasiaErgot poisoning Agenesis or hypoplasia of theVasospasm with internal carotid orsubarachnoid vertebral arterieshemorrhage Arteriovenous malformation AVM Hereditary hemorrhagic telangiectasia Sturge-Weber syndrome Intracranial aneurysm
  • 44. TraumaChild abuse Posttraumatic arterialFat or air embolism dissectionForeign body embolism ArteriographyCarotid ligation (e.g., Posttraumatic carotidECMO) cavernous fistulaVertebral occlusion Coagulation defect withfollowing abrupt cervical minor traumarotation Amniotic fluid/placentalBlunt cervical arterial embolismTrauma: Neck trauma, Penetrating intracranialintraoral trauma trauma
  • 45. Drugs:AmphetaminesCocaineSympathomimeticsL asparginase
  • 46. Inflammatory• Meningitis• Encephalitis (due to vasculitis, venous thrombosis orparenchymal necrosis)( bacterial & varicella)• Local head and neck infection Sebrie et al 1999
  • 47. MetabolicSystemic DisorderMetabolic MELAS• 1. Mitochondrial emcephalopathy, lactic acidosis, and stroke• 2. Point mutation of mitochondrial DNA• 3. Normal developmental milestones in first few years of life.• 4. Episodic vomiting, lactic acidosis, and proximal muscle weakness• 5. Stroke syndromes - migranous HA, seizures, or hemiplegia• 6. Encephalopathy/dementia are progressive.• 7. Hearing loss, visual defects, and short stature are typical
  • 48. • Mitochondrial disorder(MELAS):Mitochondrial accumulations and abnormalities in sm of intramuscular vessels , brain arterioles and in blood vessels of choroid plexus(mitochondrial angiopathy)
  • 49. • Fabry’s diseaseX-linked, defniciency of alpha-galactosidase angiokeratomas, corneal and lenticular opacities, and painful acroparesthesias ,hypohydrosis,Vascular complications:(renal failure, cerebral thrombosis.?
  • 50. Homocystinuria:Thromboembolic episodes involving both large and small vessels specially brainDamage to the vascular endothelium and increased platelet adhessivness 2ry to elevated homocystine level
  • 51. Metabolic Hyperhomocysteinemia• HC is a highly reactive amino acid toxic to vascular endothelium – Pro-atherogenic and pro-thrombotic effect on blood vessels• HC can potentiate the auto-oxidation of LDL• HC is emerging as a potentially modifiable risk factor for atherosclerosis
  • 52. prothrombin gene G20210A mutation• Prothrombin G20210A mutation is an important prothrombotic condition for venous thrombosis. Recently, some studies have also considered it to be a risk factor for arterial ischemic stroke in children. J Child Neurol 2007 Mar;22(3):329-31
  • 53. Clinical presentation• F:M = 3:2• Girl + headache+ bilateral UMNL signs1. Sudden hemiplegia of face and limbs associated with hemianopia ,hemianaesthesia and aphasia recovery may occur followed by new episodes of focal neurological findings on same or other side2-recurrent TIA with episodic hemiparesis for min or hrs with no loss of consciousness
  • 54. Scope of the guidelines• the diagnosis, investigation and management of acute arterial ischaemic stroke in children beyond the neonatal period
  • 55. Stroke Guidelines1st• Families/carers should be given actual information about their child’s condition as soon as possible after diagnosis . This should be simple and consistent, avoiding technical terms and jargon• Children should be given information about their condition at an appropriate level .
  • 56. Stroke Guidelines2ndPresentation and diagnosis• All children with acute stroke should be referred to, or have their management discussed with, a consultant paediatric neurologist
  • 57. Stroke Guidelines3rdBrain Imaging• Cross-sectional brain imaging is mandatory in children presenting with clinical stroke• Brain magnetic resonance imaging (MRI) is recommended for the investigation of children presenting with clinical stroke
  • 58. Stroke Guidelines 4th• If brain MRI will not be available within 48 hours, computed tomography (CT) is an acceptable initial alternative
  • 59. Stroke Guidelines5th Further Non-invasive cerebrovascular imaging :- M R Angiography- CT angiography- ultrasound with Doppler techniques- combination MRV (magnetic resonance venography)
  • 60. Stroke Guidelines6th• All children with clinical stroke should have regular assessment of conscious level and vital signs• Brain imaging should be undertaken urgently in children with clinical stroke who have a depressed level of consciousness at presentation or whose clinical status is deteriorating
  • 61. History Subsequent Lab
  • 62. Initial Lab• CBC (WBC, RBC*, Platelets)• Electrolytes• PT/PTT• Liver functions• Lipid profiles• ESR• Echocardiograph: Transthoracic cardiac echocardiography• * CSF examination *Hemoglobin electrophoresis
  • 63. Stroke Guidelines8th Echocardigram: - for congenital and acquired cardiac disease - Transthoracic cardiac echocardiography should be undertaken within 48 hours after presentation in all children with arterial ischaemic stroke
  • 64. A lumbar puncture• LP will screen for metabolic derangements and CNS inflammatory and infectious disorders.
  • 65. Subsequent Lab• Prothormbic tendency factors• Other relevant tests
  • 66. prothrombotic Factors• protein C deficiency• protein S deficiency• Antithrombin III• Factor V Leiden• antiphospholipid antibodies:anticardiolipin (aCL) antibodies and lupus anticoagulant (LA).,• activated protein C resistance• lipoprotein-associated phospholipase A2 (Lp-PLA2)*• high-sensitivity C-reactive protein (hs-CRP) *• increased plasma homocysteine ( & urine)• prothrombin G20210A and MTHFR TT677 mutations and A 1298C *FDA approved for stroke recurrence
  • 67. • homocysteine levels, levels of protein C,S,and antithromin III, Leiden factor V, RPR, C reactive protein/ESR,lipid panel, troponin, creatinine kinase, electrolytes, glucose, HbA1C, diffusion weighted and perfusion weighted MR, transesophageal echocariogram, EKG with rhythm strip, CBC with platelets, chest X ray?
  • 68. Other relevant tests• ANA• HIV• Lactic acid, pyruvic acid ( blood , CSF)
  • 69. Acute care• General measures• Specific measures• Prevention/prophylaxis Recovery after stroke depends on the severity of the stroke and the speed of treatment
  • 70. Acute caregeneral measuresStroke Guidelines9th• Hospital• ABCD care• Temperature should be maintained within normal limits• Oxygen saturation should be maintained within normal limits
  • 71. Acute caregeneral measures Stroke Guidelines10th• i - swallowing safety• ii-feeding and nutrition• iii-communication• Iv- pain• v-moving and handling requirements• vi- positioning requirements• vii- risk of pressure ulcers
  • 72. Acute caregeneral measuresPain:• Children affected by stroke should be assessed for the presence of pain using non verbal technique• All pain should be treated actively, using appropriate measures including positioning, handling, and medicationReduce intracranial tension : mannitol IV
  • 73. Specific treatment
  • 74. Acute carespecific medical treatments (cont.)If diagnosed within 3 hrs:• Thrombolytics: streptokinase, tissue plasminogen activator (tPA)
  • 75. Acute carespecific medical treatments• Aspirin (5 mg/kg/day)* should be given once there is radiological confirmation of arterial ischaemic stroke, except in patients with evidence of intracranial haemorrhage on imaging and those with sickle cell disease - LMWH (1 week) - Warfarin ( for 6 months)*max 300 mg
  • 76. SCD stroke1- exchange transfusion2- prevention: repeat transfusion 4-6 weeks to keep hemoglobin S <20- 30%
  • 77. • Neonate + noncardioembolic AIS do not use anticoagulant or aspirin• Neonate+cardioembolic AIS use anticoagulant therapy (UFH or LMWH ) for 3 months• Child+AIS treat with anticoagulant for 5-7 days or until cardio-embolic or vascular dissection has been excluded.Antithrombotic therapy in children: the Seventh ACCP Conference on Antithrombotic Chest 2004 Sep;126 (3 Suppl):645S-687S.
  • 78. Acute carespecific medical treatments (cont.)• Treatment of underlying cause
  • 79. A Cardiac Source of Embolism and AIS• The decision to use anticoagulation should be discussed with a consultant paediatric cardiologist and paediatric neurologist
  • 80. 3- preventionStroke recurrence• Arterial ischaemic stroke recurs in between 6% and 20% of all children.• The risk of recurrence* is increased in children with multiple risk factors and in those with protein C deficiency, increased levels of lipoprotein (a) and vascular disease *(Lanthier et al2000)
  • 81. Stroke recurrence Stroke Guidelines11th1- Aspirin• Patients with cerebral arteriopathy other than arterial dissection or moyamoya syndrome or those with sickle cell disease should be treated with aspirin (1–3 mg/kg/day)
  • 82. Stroke recurrence prevention2- Anticoagulation• should be considered:1- until there is evidence of vessel healing, or for a maximum of six months, in patients with arterial dissection2- if there is recurrence of arterial ischaemic stroke despite treatment with aspirin3- in children with cardiac sources of embolism, following discussion with the cardiologist managing the patient4- until there is evidence of recanalisation or for a maximum of six months after cerebral venous sinus thrombosis
  • 83. Stroke recurrence In children withsickle cell disease:• should be considered:1- regular blood transfusion (every three to six weeks) should be undertaken to maintain the HbS% <30% and the Hb between 10–12.5 g/dl (C)2- transfusion may be stopped after two years in patients who experienced stroke in the context of a precipitating illness (eg aplastic crisis) and whose repeat vascular imaging is normal at this time (C)3- after three years a less intensive regime maintaining HbS <50% may be sufficient for stroke prevention(C)
  • 84. Stroke recurrence Stroke Guidelines12thmoyamoya syndrome• Children should be referred for evaluation to a centre with expertise in evaluating patients for surgical re-vascularisation
  • 85. Stroke recurrence• Advice should be offered regarding preventable risk factors for arterial disease in adult life, particularly smoking, exercise and diet• Blood pressure should be measured annually to screen for hypertension
  • 86. DD of stroke like events1- Alternating hemiplegia:2-18 month, intermittent episodes of hemiplegia from one side to the other associated with choreoathetosis and dystonia for min or weeks and then resolve ,occasionally associated with migrainProgressive MR and developmental disabilities , poor prognosisRadiology & lab are free
  • 87. • Todds paralysis• Stroke like episodes: migraine• Focal post viral encephalitis, ADAM, HIV• hyperlipidemia• Familial hemiplegic migraine
  • 88. RehabilitationUse of assessment measures• The assessment tools selected should be appropriate for the child’s age and developmental and functional level
  • 89. Goal of Rehabilitation• Help children with physical disabilities improve FUNCTION and PARTICIPATE more fully in family, social, educational and recreational activities.
  • 90. Rehabilitation Tools• Motor and cognitive exercises• Medications• Injections• Braces• Adaptive equipment• Referral to therapies• Referral to surgeries• Recreational involvement
  • 91. • Child +AIS+cardioembolic treat with anticoagulant 5-7 days followed by oral anticoagulant for 3-6 mon• ALL children +AIS TREAT WITH aspirin 2-5 mglkglday after the anticoagulant therapy
  • 92. - Prevention of recurrence:Low dose aspirin or oral anticoagulant for long term prophylaxis in certain conditions?
  • 93. 1. Cardiac emboli2. Disecting aneurysm3. Severe prothrombotic conditions4. High grade cerebral artery stenosis
  • 94. 3- treatment of underlying causea) For SCD: • Moyamoya: considerExchange transfusion revascularizationFrequent transfusion • ProthromboticBone marrow transplant :consider anticoagulantHydroxy urea • For others :low dose asprin
  • 95. • 4- rehabilitation therapy:Speech , physiotherapy, occupational &psychotherapy