Download Free Medical Pediatric Stroke PowerPoint Presentation

Pediatric Stroke PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Pediatrics, which is titled "Pediatric Stroke", to know about Pediatric Stroke.

Tags : Pediatrics, Pediatric Stroke

Published on : Aug 02, 2021 | Views : 2730 | Downloads : 25

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Pediatric Stroke By: Dr. Himanshu Dave
Slide 2-

DEFINITION Acute disturbance of cerebral functions Vascular origin Disability of more than 24 hours or death within 24 hours Transient Ischemic Attack : Disability < 24 hours. (Latest concept < 1 hour)
Slide 3-

TYPES OF STROKE * Vascular Occlusive Arterial Ischemic stroke (AIS) Sinovenous thrombosis (SVT) * Vascular rupture (Haemorrhagic)
Slide 4-

DIFFERENCE FROM STROKE IN ADULT Childhood Stroke Stroke in children is relatively rare and frequently results in lack of recognition and delay in diagnosis . Stroke due to vascular rupture is as common as due to vascular occlusion (55% ischemic, 45% hemorrhagic).
Slide 5-

• Permanent aphasia is rare in children below 4 yrs, even with involvement of dominant hemisphere. • Neurodeficit is mild because collateral blood flow is better than adults.
Slide 6-

EPIDEMIOLOGY • • Incidence world over varies between 1.2 per lakh to 2.7 per lakh. In India hospital based studies indicate incidence of stroke in less than 1 percent of all pediatric admission (According to N.I.M.H.A.N.S. the incidence of stroke in children is 0.70% of pediatric hospitalization). • Slightly male preponderance.
Slide 7-

CAUSES OF STROKE IN CHILDREN • I. Cardiac Disease Congenital Heart Disease – – – – Ventricular / artrial septal defect Aortic or mitral stenosis Coarctation PDA • Acquired Heart Disease – – – – – – Prosthetic Heart Disease Rheumatic Heart Disease Endocarditis Cardio myopathy / myocarditis Atrial myxoma Arrhythmia
Slide 8-

CAUSES OF STROKE IN CHILDREN II. Hematologic Abnormalities • • • • • Sickle cell anemia. Polycythemia Thrombocytopenia / Thrombocytosis Leukemia, lymphoma Disorders of coagulation Protein C and S deficiency Antithrombin III deficiency Lupus Anticoagulant DIC Paroxysmal nocturnal hemoglobinuria.
Slide 9-

CAUSES OF STROKE IN CHILDREN III. Inflammatory Disorder • • • • Meningitis : Viral, bacterial or tuberculosis Systemic : Viremia, Bacteremia Autoimmune diseases Drug induced inflammation Amphetamine Cocaine
Slide 10-

CAUSES OF STROKE IN CHILDREN IV. Metabolic disease – – – – – – Homocysteinuria Fabry’s disease Pseudoxanthoma elasticum Hyperlipidemia MELAS Leigh syndrome V. Intracerebral vascular processes – – – – – – Rupture aneurysm Arteriovenous malformation Firbomuscular dysplasia Moyamoya disease Migrane headache Carotid artery dissection
Slide 11-

CAUSES OF STROKE IN CHILDREN Trauma and other causes Child abuse Neck / heat trauma Dehydration Fat or air embolism
Slide 12-

NEONATAL STROKE Hypoxic ischemic injury Placental infarction Sepsis Trauma Hypercoagulable conditions Thromboembolism Vitamin K deficiency
Slide 13-

ARTERIAL ISCHEMIC STROKE Arterial Circulation Two principal systems are anterior circulation and posterior circulation. Anterior circulation has paired carotid arteries and its major branches anterior and middle cerebral arteries. Posterior circulation has vertebro-basilar system with posterior cerebral arteries as its major branches. • •
Slide 14-

• Anterior and posterior circulation are linked by ACA and PCA to form the circle of Willis. Small perforator or lenticulostriate branches arise from the stems of anterior, middle and posterior cerebral arteries. •
Slide 15-

ppt slide no 15 content not found
Slide 16-

PATHOPHYSIOLOGY Severity of cerebral tissue damage and the resultant neurological impairment depend upon – – – – The duration of ischemia Size and location of brain structure involved Availability of collateral blood supply Metabolic demands of brain.
Slide 17-

PATTERN OF ARTERIAL ISCHEMIC STROKE Transient ischemic attacks (TIA) • Clinical deficit is usually extremely brief < 24 hours usually < 1 hour. • Also called mini, warning or transient stroke.
Slide 18-

• Deficit is focal and confined to an area of brain perfused by a specific artery. This excludes pre-syncope and syncope, which are due to diffuse and not focal cerebral ischemia. • Mechanism Low flow in an artery due to tight stenosis or occlusion Embolism
Slide 19-

PATTERN OF ARTERIAL ISCHEMIC STROKE Reversible ischemic neurological deficit (RIND) An ischemic event in which the deficit usually recovers over a 24-72 hour period but which may take as long as one week to resolve (24 hours – 1 week) •
Slide 20-

Completed stroke • • Typically evolves to maximal deficit within a few hours Two zones – – Central core zone (irreversible damage) Penumbra zone (potential viable zone)
Slide 21-

CLINICAL FEATURES
Slide 22-

AGE OF ONSET Varies with specific cause Cerebral vascular occlusive disease associated with cyanotic CHD : during first two years of life. Trauma and bacterial infections : pre-school years Most children are symptomatic before six years of age with largest number before three years. • •
Slide 23-

MODE OF ONSET • Abrupt – most common mode With seizures Febrile reaction of 101-103ºF Coma Hemiplegia Acute Onset Sudden onset without any seizure activity Altered sensorium Intermittent Seen in some cases of carotid arterial thrombosis. • •
Slide 24-

NEUROLOGICAL DEFICIT According to vascular territory affected Motor function abnormalities – Hemiparesis : It is the most common manifestation : also called acute infantile hemiplegia, infantile acquired hemipelgia, Marie Strumpell encephalitis or Hemiconvulsion-Hemiplegia syndrome (H.H. Syndrome).
Slide 25-

Maximal at onset Upper extremity more severely affected It may disappear rapidly, slowly regress over a period of time or persist indefinitely. 50% of affected children have some residual neurological deficit.
Slide 26-

• Spasticity appears about 2-3 weeks after the onset & contractures 1-3 months later. Persistent weakness 2-3 weeks after the onset indicates residual motor deficit in later life. • Involuntary movements • • • Athetosis, dystonia and choreiform movements Implies basal ganglia involvement Imitative or mirror movements.
Slide 27-

Deep Tendon Reflexes Absent or hypotonic during flaccid phase • Exaggerated in spastic phase • Babinski response : soon after onset and persists for indefinite time
Slide 28-

Cranial Nerve Function Eye deficit – homonymous hemianopia, strabismus, amblyopia, severe myopia. Facial paralysis Bulbar – Psuedobulbar paralysis • • Sensory loss • • Superficial modalities (touch and pain) may be intact Stereognosis, position sense discrimination are often impaired Hemi-atrophy and two point •
Slide 29-

Speech deficit : Dependent upon the age of child at onset and hemisphere involved * >4 years dysphasia common if dominant hemisphere is involved * <4 year : relatively rare . Never seen in <2 years of age. * Normal speech pattern returns after 2-21 days.
Slide 30-

Vasomotor function During acute stage, involved extremity may be warmer, edematous and skin may be erythematous. Development of spasticity causes affected extremity to to be cold.
Slide 31-

Epilepsy 50% of children with acute hemiplegia subsequently develop recurrent seizures. • More common if onset <2 years of age or multiple seizures at the time of onset. .
Slide 32-

Defects in learning, behavior and intellect • Usually mild intellectual deficit is present. Approximately 25% are mentally retarded. • Severe intellectual impairment is most common observed when the hemiplegia is complicated by seizures refractory to anticonvulsants
Slide 33-

• Learning defects are due to motor deficits, perceptual disturbances, visiospatial problems and spatial orientation. • Behavioral problems are typically a child with hyperkinetic behavior with short attention span, impulsivity and distractibility. • Child may be passive or underactive, particularly for the initial 1-5 months.
Slide 34-

RADIOGRAPHIC FEATURES CT Scan May be normal within the first 12 hours of Arterial Ischaemic Stroke. Bland lesion infarct appears as low-density fitting a vascular territory. If hemorrhage occurs additive hyperdense area are seen. CT spiral angiography :It identifies the AV malformation and aneurysm. •
Slide 35-

RADIOGRAPHIC FEATURES MRI and MRA : MRI is better than CT scan as It is more sensitive than CT in detecting small and multiple infarcts. In posterior fossa, it is more sensitive than CT scan • • More sensitive at detecting hemorrhagic conversion of infarct. MRA can be performed at the same time. It is able to visualize the flow in major cerebral, vertebral and external carotid arteries. •
Slide 36-

ppt slide no 36 content not found
Slide 37-

RADIOGRAPHIC FEATURES Angiography It is the definite method of visualizing the extra and intracranial vasculature including the medium and small sized arteries, which are not seen in MRA. Other neuroimaging techniques Doppler imaging of carotid arteries and transcranial Doppler for detecting large vessel vasculopathy.
Slide 38-

RADIOGRAPHIC FEATURES X-ray skull Early X-ray are normal but after a period of years they may show Dyke-Davidoff-Mason (DDM) syndrome – thickening of cranial vault, overdevelopment of frontal and ethmoid sinuses and elevation of the petrous pyramid contralateral side of temporal bone on the due to cerebral hemiatrophy, specially if onset is at <3 years of age.
Slide 39-

TREATMENT OF AIS Non anti-thrombotic Anti thrombotic Anti thrombotic : Heparin – considered if there is high risk of recurrence and low risk of secondary hemorrhage. Nowadays It has been replaced by low molecular weight heparin
Slide 40-

TREATMENT OF AIS Protocol Loading dose : 75 u/kg IV over 10 minutes Initial maintenance dose : 28 U/kg/hr for <1 year / 20 U / kg / hr for > 1 year APTT should be kept between 60-85 seconds. Obtain blood for APTT 4 hours after administration of loading dose and four hours after each change in infusion rate. LMW Heparin : Its advantages are subcutaneous route, minimal monitoring and great safety and efficacy. Dose:1mg/kg sc (5to10days)
Slide 41-

TREATMENT OF AIS Indication of heparin and LMWH • • • • Arterial dissection Hypercoagulable states High risk of embolism Progressive neurological hemorrhage . deficits not caused by cerebral • Antifactor Xa is used for monitoring of LMWH(.5 to 1 unit/ml)
Slide 42-

• • • Aspirin : It inhibits TXA2 in platelets. It is indicated in secondary prevention of stroke recurrence Ex,. in cerebral artery stenosis . Dose : 3-5 mg/kg/day which may be switched to alternate day therapy. •
Slide 43-

TREAMENT OF AIS Warfarin • Indications Congenital or acquired heart disease (CHD) Severe hypercoagulable state Arterial dissection Recurrent AIS or TIA while on aspirin Dosing schedule Dose 1 : If base – line INR is 1-1.3, dose: 0.2 mg/kg
Slide 44-

TREATMENT OF AIS
Slide 45-

TREATMENT OF AIS • Target is INR 2-3 . In children with mechanical valves target INR is – 2.5 to 3.5 Long term •
Slide 46-

TREATMENT OF AIS Non antithrombotic Supportive care Monitor BP Fluid balance Aggressive use of AEDs(Antiepileptic Drugs) ideally with EEG monitoring in a comatose patient. Control raised ICT : Mannitol decreases ICT, maintains microcirculation and has anti-oxidant effect.
Slide 47-

TREATMENT OF AIS • Imunosuppressive agents and corticosteroids in proven or suspected vasculitis with documented progression of cerebral artery stenosis. • Transfusion therapy in sickle cell disease. • Rehabilitation:Physical therapy,Occupation therapy ,speech therapy • Neuroprotective agents • Interventional neuroradiological techniques
Slide 48-

Sinovenous Thrombosis (SVT) .
Slide 49-

PATHOPHYSIOLOGY • Septic SVT : Spread of infection from sinuses- thrombophlebitis – thrombus formation. Non septic SVT : Slow blood flow, dehydration and pro-thrombotic states predispose. Occlusion of cerebral venous structure – increases the cerebral venous pressure – raised ICT. occlusion of blood flow – marked edema and infarction with or without hemorrhage. Superior saggital sinus thrombosis – communicating hydrocephalus – raised ICT. • • •
Slide 50-

Clinical Features • • Age at risk : particularly seen in neonates and young children. Clinical features are subtle and develop gradually over many hours / days / weeks. Diffuse neurological signs and seizures Focal neurologic signs and symptoms are not seen in neonates. • •
Slide 51-

Radiological Features • CT Scan – Occasionally suggests diagnosis of SVT • MRI and MRA : Diagnostic method of choice Absence of flow related signal and visualization of thrombus in a given vein Thrombus – increase signal on T1 weighted and T2 weighted images.
Slide 52-

• Ultrasonogram Can screen SVT in neonate with open AF. Regular cranial USG can monitor the presence and severity of ICH associated with SVT. Angiography Gold standard Diagnostic : Partial or complete lack of flow Suggestive Delayed venous emptying Reversal of flow Abnormal cortical veins •
Slide 53-

TREATMENT • Antithrombotic therapy : In infants heparin or LMWH is used for 10-14 days. If hemorrhage is associated, use is controversial. Thrombolytic therapy : limited use in cases with progressive thrombosis despite maximal systemic anticoagulation.
Slide 54-

Non Anti-thrombotic • Septic SVT Antibiotics Surgical removal and drainage of infected focus Raised ICT Repeated LP Acetazolamide Lumboperitoneal shunting Long term raised ICT – monitor optic fields
Slide 55-

HEMORRHAGIC STROKE • Hemorrhagic stroke : Rupture of normal cerebral blood vessels as in bleeding diathesis, or abnormal blood vessels as with aneurysms or vascular malformations. • Hemorrhagic stroke is as common in children as ischemic stroke. • Frequently requires neurosurgical intervention.
Slide 56-

Hemorrhagic stroke has two major types • • Intarcerebral hemorrhage Subarachnoid hemorrhage Intracerebral Hemorrhage Pathophysiology • Usually site of rupture is medium or small branches of the major cerebral arteries. Rupture of aneurysm in sub-arachnoid space.
Slide 57-

• Damage is due to Mechanical disruption of neuronal structure Cerebral edema Mass effect particularly in posterior fossa.
Slide 58-

Subarachnoid hemorrhage Pathophysiology Rupture of aneurysm or from AV malformation arteries at the circle of Willis. involving major Vasospasm in cerebral arteries causing secondary ischemic infarction.
Slide 59-

Diagnosis Radiological features • • • CT scan : Hyperdense areas MRI and MRA:More sensitive for posterior fossa lesions Conventional angiography CSF In case of SAH, CSF is blood stained and xanthochromic after six hours, but LP should never be performed on child presenting with suggestive of haemorrhage without prior CT scan.
Slide 60-

MANAGEMENT • • Hypertension should be avoided and if present, treated Straining at stool and anything producing Valsalva-like maneuver should be avoided. Bed rest Anti-emetics and sedation Analgesia for headache Control of seizure Monitor ICP Do not use antifibrinolytic agents • • • • • •
Slide 61-

• Neurosurgical intervention : In children who present with SAH or intracerebral bleed, due to an aneurysm or AV malformation surgery is management of choice. • If child is in coma, if angiography shows aneurysm is fusiform or if there is any question of a mycotic aneurysm then conservative medical management is indicated. • Overall prognosis for cerebral hemorrhage in childhood is poor with 50% mortality.
Slide 62-

PROGNOSIS • Mortality after stroke in children from 20-30% depending upon the location and underlying cause. • Hemorrhagic stroke has higher mortality • Residual neurological deficit is present in more than 50% of survivors and is more common after ischemic stroke.
Slide 63-

References: Piyush Gupta PG text book of Pediatrics Pediatric Neurology by: Veena Kalra
Slide 64-

THANK YOU