stroke in children

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Stroke is an emergency and a leading c/of death; a BV in brain has a blockage (90%) or bursts (adults). No Rx.: brain cells quickly die: serious disability/death

90%

Stroke is sudden onset of focal neuro-deficit due to occlusion of blood supply or hemorrhage in the brain causing SS lasting >24h

SS: symptoms and signs. BE: both eyes

Definition

Bangladesh Scenario

• Stroke is the 3rd leading c/of death• WHO: Bangladesh at mortality from stroke ranks 84• Prevalence: 0.3%. HTN is the main cause of IS and HS• Disability-Adjusted Life-Years from stroke: 485/10k• GoB needs to emphasize healthcare development to cope

with stroke

• Hemorrhagic strokes – 11.4%• Ischemic strokes – 88.6%

Prothrombotic states – 38.7% Cardiac disease – 19.3% Hyperlipidemia – 16.0% Homocysteinuria – 14.6%

99 Adult Pts. at AIIMS, New Delhi

Typical SS: Sudden numbness/weakness, esp. on 1 side, sudden vision changes in 1/BE, dysphagia; sudden: severe HA, dizziness, confusion, problem walking,

balance, speaking/understanding

Test: F.A.S.T.: Face: smile: 1 side droops? Raise Arms: does 1 side drift down? Speech. Can s/he repeat a simple sentence? Trouble talking, slur words? Time

STROKEIN CHILDREN

• Not exactly known; 3-13/100k/y• In INDIA: 13-33/100k/y • USA: 2.52/100k/y –14y– 1.89– hemorrhagic– 0.65- ischemic

• Children & Young adults: <5% of all strokes• Occurs in all age groups (NB-teenagers)• It may even occur before birth• 1/2,300 – 5k/NB have a stroke

NB: newborn. LB: live born

Incidence in Children

• Stroke is the 6th c/of death in children while in adult it is 3rd, ranking behind HD & cancer

• As common as brain tumors

• Impacts of strokes– Mortality 6-40% (hemorrhagic: x2)– Morbidity• Neurological d – 60%• Seizures – 15%• HA

Risk Factors Childhood Stroke (USA)• Cardiac D 19%• Coagulation D 14%• Dehydration 11%• Vasculitis 7%• Infection 6%• Dissection 5%• Neoplasm 4%• Metabolic D 3%• Moyamoya, SCD, Perinatal

Complication, andOthers: each 2%

Multiple risk factors are often present& predict worse outcome

Congenital

Aortic Stenosis, MS VSD, PDA Cyanotic CHD involving R-L shunt Inherited con. tissue d: Marfan, Ehlers-Danlos syn

Acquired Endocarditis, cardiomyopathy Arrthymia, Rh F Psoriatic HD

Cardiac Causes

Diagonal earlobe crease

• Disorder of RBC: SCD, Polycythemia• D. of WBC: Leukemia, lymphoma• D. of Platelets: Thrombocytosis, -penia

• D. of clotting: Protein C, S deficiency Factor V, antithrombin III deficiency Paroxysmal noc. Hb.nuria IBD, lupus anticoagulants Neonatal & childhood CSVT

Hematological Causes

SCD– 25 % develop stroke by 45y. Recurrent in 67%– IS predominantly in childhood– Hemorrhagic with steroid and HTN– Sinovenous thrombosis, posterior leukoencephalopathy,

watershed ischemia– Silent infarcts; more in the frontal lobe (17% under14)– HS (ICH/SAH) in adults– High WBC in inf. and anemia can precipitate

IS: ischaemic stroke. HS: hemorrhagic stroke

Moya –Moya AV malformations Aneurysm Sturge Weber syn Fibromuscular dysplasia

VASCULAR DISEASE

Normal lateral projection angiogram with injection of IC artery

Suzuki grades I to II with narrowing of IC artery before dev. of extensive collateral vessels

• Infection Meningitis HIV encephalopathy Local head & neck inf.

• Autoimmune d. SLE, Takayasu arteritis, PA nodosa Sarcoidosis Mixed CT D

INFLAMMATORY DISORDERS

METABOLIC DISORDERS

• Homocystinuria• Pseudoxanthoma elasticum• Fabry disease• Mitochondrial encephalopathies:

MELAS Leigh syn

Drug induced Amphetamines, cocaine

• Trauma• Child abuses• Placental embolism• ECMO therapy• Post varicella

Misc. Causes

Thrombosis occludes anterior, middle, posterior basilar, vertebral & internal carotid arteries. Arterial thrombosis more

common at atheromatous plaques or stenosis of arteries

Thrombi embolise to distal region

Causing intracranial ischemia & infarction

Intracranial Thrombosis

Emboli arise mainly from atheromata

within great vessel or from heart

Intracranial Embolism

Pathophysiology of Hemorrhage

20 % strokes are from rupture of IC aneurysmChacot – Bouchard aneurysms are usually due to chr. HTN

They usually involve small penetrating (0.8-1.0 mm) lenticulostriate br. of MCA in the basal ganglia, brainstem and midbrain. Cause IC hge.

Arterial ischemic stroke (AIS) Cerebral SinoVenous thrombosis (CSVT) IC hemorrhage

Types of Stroke Syn.

SIGNS &

SYMPTOMS

Seizures

Extreme sleepiness

A tendency to use only 1 side of body

Newborns and Infants

CN: cranial nerve. HA: headache. V: vomiting

Weakness/numbness of face, arm/leg,usually on 1 side

Trouble walking (weakness/trouble moving 1 side, or incoordination)

Problem speaking/understanding: slurred speech, or difficulty in understanding simple directions

Severe HA especially with V and sleepiness

Children and Teenagers

Trouble seeing clearly in 1 or both eyes

Severe dizziness/incoordination: losing balance/falling

New seizures, especially if affecting 1 side of body and followed by paralysis on the side of the seizure activity

Progressively worsening non-stop HA with drowsiness and repetitive V, lasting days without relief

Complaint of acute onset of the "worst HA of my life"

Contd….

Lesion can be divided in 2 groups based of CN palsy as :

CN palsy on same side as that of hemiplegia

CN palsy on opposite to that of hemiplegia

Localization of Lesion in Hemiplegia

• Lesion above the level of brain stem (Ipsilateral hemiplegia); at the level of either

Cortex Sub cortical region Internal capsule

CN Palsy on Same Side as that of H..

Lobes of the Cerebrum

Parietal Lobe

Temporal Lobe

Frontal Lobe

Limbic Lobe

Occipital Lobe

• Hemiparesis or Monoparesis• Involvement: Upper limb > LL or vice versa• Altered sensorium, convulsion

• Cortical sensory loss: asteriognosis, agraphesthesia • Aphasia (If dominant cortex)

Cortical Lesion

Frontal Lobe

is responsible for higher cognitive functions:

• Problem solving• Spontaneity• Memory• Language• Motivation• Judgment• Impulse control• Social/sexual behavior

• Altered behavior• Upper limb> LL• Motor aphasia• Convulsions• Bladder & bowel involvement• Persistent neonatal reflexes on opposite side

Frontal Lobe Involvement

Parietal Lobea role in our sensations of touch, smell, taste. It also processes sensory and spatial awareness,

and is a key component in eye-hand

co-ordination and arm movement

It also contains a specialized area

called Wernicke area that is responsible

for matching written words with the sound of

spoken speech

–Cortical sensory loss–Astereognosis

Parietal Lobe Involvement

Temporal Lobe

plays a role in emotions, and is also responsible for smelling, tasting, perception, memory, music, aggressiveness, sexual behavior

It also contains the language area

• TL epilepsy• Sensory aphasia• Memory loss

Temporal Lobe Involvement

Occipital Lobe

controls vision and recognition

OCCIPITAL LOBE INVOLVEMENT

Homonymous hemianopia

INTERNAL CAPSULE LESION

Dense hemiplegiaHemianaesthesiaHomonymous hemianopiaDysarthria

SUB CORTICAL LESION

Similar to cortical lesion except loss of cortical sensation & convulsions

• Lesion at/below the level of brain stem (Contra lateral hemiplegia). Lesion can be either of

Midbrain Pons Medulla Spinal cord ( b/w C 1 – C4 )

CN Palsy on Opposite Side to that of …

• Weber Syn.: CN3 palsy + contra lateral hemiplegia• Benedict Syn.: CN3 palsy + contra lateral H + red nucleus

affection( tremor, rigidity & ataxia on opposite side)

H: hemiplegia

Mid brain lesion

The Pons

The pons lies between the midbrain and medulla. Pons means “bridge”

Pons connects cerebellum to the rest of the brain and modify the respiratory output of medulla

The pons is the origin of several CNs

• Millard Gubbler Syn.: CN7 palsy + contra lateral H• Foville Syn.: CN6&7 palsy+ contra lateral hemiplegia

Pons lesion

• Jackson Syn.: CN12 palsy + contra lateral hemiplegia

Medullary lesion

• Brown Sequard Syn.: Hemiplegia + CN palsy + differential sensory loss (loss of vibration & joint sense on same side & pain ,touch & temp. on opposite

Spinal Cord Lesion

Focal cerebral ischemia IC hemorrhage Cerebral abscess, encephalitis (HSV) Brain tumor Alternating hemiplegia of infancy MS Malingering/conversion disorder Epilepsy: Todd's paralysis or a focal inhibitory seizure Complicated migraine

Differential Diagnosis

Seizures

Raised IC tension

Hypertension

Aphasia

Skeletal deformities

Complications

• FIRST LINE: Performed within 48h of admission • SECOND LINE: Performed within first week • THRID LINE: Performed as per need

Diagnostic Evaluation

CBC FilmBlood sugar, BUN, S electrolytes ( Na, K, Ca, Mg, Phos.) AST, ALT, S. lipid profile CXR, CT brain, MRI brain & MR angiography Ultrasonography ANA ECG

FIRST LINE

CT: rapid disappearance of IC hge. from R b. ganglia

Echo- (transthoracic) with saline contrast Transcranial and/or carotid dopplers MR angiogram, EEG Rh. Factor, S. amino a., urine for organic a. Blood culture. Hb. electrophoresis Complement profile, VDRL Lactate/pyruvate, ammonia CSF: cell count, protein, glucose, lactate

SECOND LINE

Antithrombin III Protein C (activity and antigen) Factor V Leiden mutation Antiphospholipid antibody; Lupus-anticoagulant Anticardiolipin

Hypercoagulable Evaluation

HIV Lyme, Mycoplasma, Cat-scratch titers Cardiac MRI Echocardiogram (transesophageal) Muscle Biopsy DNA testing for MELAS Cerebral angiogram (transfemoral) Leptomeningeal biopsy Serum homocysteine after methionine load

THIRD LINE

MANAGEMENT

Time = Brain Damage: every second counts. Hypoxia kills brain cells within mins. Clot-busting drugs can curb damage, if used in 3h of attack. Stroke is a top c/of long-term

disability

• 1st step is to DD ischemic & HS• Anticoagulant Rx is contraindicated in HS• Hyperglycemia & HTN worsen the stroke• Multidisciplinary approach

General Consideration before Rx

Rx primarily is directed towards stabilizing systemic factors & management of the underlying causes

Arterial Ischemic Stroke (AIS)

Intracranial tension:1. Fluid restriction2. Mannitol3. Steroids

4. Shunt surgery ( In special case)

Hypertension: by appropriate antihypertensive

Supportive Care

Fluid balance Hyperglycemia Hyperthermia Seizures with AED ABT to prevent secondary inf.

AED: antiepileptic drugs, ABT: antibiotic

Contd…..

HEPARIN: -

•28U/kg/h in infants,

•20U/kg/h in >1y

•18U/kg/h in older children for 5-10d

•LMW Heparin: 0.5-1U/ml

Loading dose 75- 100 /kg iv over 10 min followed by

maintenance dose :

Antithrombotic Rx

Antiplatelet: -Aspirin 3-5mg/kg/d Clopidrogel

Oral anticoagulants: Wafarin for secondary prevention of stroke if aspirin Fails. Congenital or acquired HD, severe coagulable states, arterial dissection & recurrent AIS or TIA while on aspirin

Thrombolytic agents: streptokinase & urokinase to dissolve the existing thrombus

Contd….

Physiotherapy

Occupational therapy

Psychological therapy

Rehabilitation Therapy

Surgical repair of Fallot T

Regular phlebotomy for thrombosis in Polycythemia

BT to prevent future episodes of stroke in SCD

Surgery for AVM & aneurysm

Steroids & immunosuppressants in autoimmune d.

Specific Rx

Variable. Mostly dependent upon underlying cause80% survived 10y after an IS, most with residual

hemiparesisPoor prognosis with seizures during infancy, and with an

angiographic pattern of Moyamoya disease

HS have higher mortality than IS Pts. with HS & coma have higher mortality

Prognosis

Persistence of hemi paresis one month after the stroke

cortical location

Moyamoya pattern on angiography

Risk Factors for Poor Outcome

Early Dx and intervention for children with stroke in order to improve their recovery rate and prevent recurrence

Early Dx and close monitoring of children at high risk for stroke

Education and support for families of children with strokes

Education about childhood stroke for HCP

Education for the general public about childhood strokes

Ongoing research into the causes of childhood stroke and effective Rx and prevention strategies

GOAL

Amiakum falls, Bandarban!

THANKYOU