CVA PRESENTATION.pptxkkkkkkkkkkkkkkkkkkkkkkkkkkk

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1. PEDIATRIC PRESENTER KELFALA HASSAN DAWOH I.D 22019 LECTURE: DR JALLOH CEREBRO VASCULAR ACCIDENT / STROKE

2. DEFINATION Cerebro vascular accident is the sudden death of brain cells due to lack of oxygen, caused by blockage of blood flow or rupture of an artery to the brain. CVA or stroke is a term used to describe the neurologic changes caused by an interruption in the blood supply to a part of the brain.

3. According to WHO “stroke is a focal neurological deficit due to local disruption in blood supply to brain. Its onset is usually abrupt but may extend over a few hours or longer” If neurological deficits exists for > 24 hours, only then it is termed as STROKE or CVA. If neurological deficits exist < 24 hours, it is called as Transient Ischaemic Stroke (TIA)

4. Vascular Occlusive Vascular rupture ( Haemorrhagic) Arterial Ischemic stroke (AIS) Sinovenous thrombosis (SVT)

5. DIFFERENCE FROM STROKE IN ADULT Stroke in child is relatively rare and frequently result is lack of recognition and delay in diagnosis Stroke in due to vascular rupture is as common as due to vascular occlusion (55% ischemic 45% haemorrhagic )

6. EPIDEMIOLOGY In India hospital based studies indicate incidence of stroke is less rhan 1 percent of all paediatric admission (According to N.I.M.H.A.N.S. the incidence of stroke in child is 0.70% of slight male paediatric hospital) Slight male preponderance

7. CAUSES OF STROKE IN CHILDREN 1 CARDIC DISEASES Congenital heart disease ventricular / artrial stenosis Aortic or mitral stenosis PDA Acquired heart disease prosthetic heart disease rheumatic heart disease cardio myopathy / myocarditis

8. CAUSES OF STROKE IN CHILDREN 2 HEAMTOLOGIC ABNORMALITIES Sickle cell anemia thrombocytopenia/ thrombocytosis leukemia, lymphoma DISORDER OF COAGULATION Protein C and S deficiency Antithrombin (3) deficiency DIC Paroxysmal nocturnal hemoglobinuria

9. CAUSES OF STROKE IN CHILDREN 3 INFLAMMATORY DISORDER Meningitis : Viral, bacterial or tuberculosis Systemic : Viremia , Bacteremia Autoimmune diseases Drug induced inflammation

10. CAUSES OF STROKE IN CHILDREN 4 . INTRACEREBRAL VASCULAR PROCESSES Rupture aneurysm Arteriovenous malformation Firbomuscular dysplasia Migraine headache Carotid artery dissection

11. NEONATAL STROKE Hypoxic ischemic injury Placental infarction Sepsis Trauma Hypercoagulable conditions Thromboembolism Vitamin K deficiency

12. 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.

13. Anterior and posterior circulation are linked by ACA and PCA to form the circle of Willis .

14. 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

15. 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

16. CLINICAL FEATURES

17. 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.

18. 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.

19. NEUROLOGICAL DEFICIT Motor function abnormalities Involuntary movement Cranial nerve function Sensory loss

20. RADIOGRAPHIC FEATURES CT Scan MIR Angiography X-RAY

21. 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

22. 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)

23. Indication of heparin and LMWH Arterial dissection Hypercoagulable states High risk of embolism Progressive neurological deficits not caused by cerebral haemorrhage .

24. Aspirin : It inhibits TXA 2 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

25. 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

26. 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.

27. Sinovenous Thrombosis (SVT) Sinovenous thrombosis, also known as cerebral venous sinus thrombosis (CVST ), is a rare but serious condition characterized by the formation of a thrombus (blood clot) in the cerebral venous sinuses. These sinuses are responsible for draining blood from the brain back to the heart. When a thrombus forms in these vessels, it can lead to increased intracranial pressure, hemorrhagic stroke, and other neurological complications.

28. PATHOPHYSIOLOGY sinovenous thrombosis involves several factors that contribute to the formation of clots within the venous system of the brain. The condition can be precipitated by various risk factors including

29. Coagulation Disorders Infections Trauma Dehydration

30. 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.

31. CT Scan MRI Ultrasonogram Angiography ( GOLD STANDARD )

32. 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.

33. 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

34. 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

35. 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 .

36. Damage is due to Mechanical disruption of neuronal structure Cerebral edema Mass effect particularly in posterior fossa

37. Subarachnoid hemorrhage Pathophysiology Rupture of aneurysm or from AV malformation arteries at the circle of Willis . Vasospasm in cerebral arteries causing secondary ischemic infarction .

38. Diagnosis Radiological features CT MRI Conventional angiography

39. MANAGEMENT Hypertension should be avoided and if present, treated Bed rest Anti- emetics and sedation Analgesia for headache Control of seizure Monitor ICP Do not use antifibrinolytic agents

40. 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.

41. 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 .

42. References: Piyush Gupta PG text book of Pediatrics Pediatric Neurology by: Veena Kalra

43. THANK YOU BY DAWOH JNR