Copy Of Cva(3)


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  • Spelt Ischemia not ’Ischimia’
    5min or less? If there is less the brain might be fine... Transient Ischemic Attacks (TIA) can last for up to 30min, but the clot reducing blood flow breaks up or is dislodged. These often result in temporary demage that disapates leaving no lasting damage. Matthew Gavin (s)RN
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  • Figure 2. Most Common Sites and Sources of Intracerebral Hemorrhage. Intracerebral hemorrhages most commonly involve cerebral lobes, originating from penetrating cortical branches of the anterior, middle, or posterior cerebral arteries (A); basal ganglia, originating from ascending lenticulostriate branches of the middle cerebral artery (B); the thalamus, originating from ascending thalmogeniculate branches of the posterior cerebral artery (C); the pons, originating from paramedian branches of the basilar artery (D); and the cerebellum, originating from penetrating branches of the posterior inferior, anterior inferior, or superior cerebellar arteries (E).
  • Copy Of Cva(3)

    1. 1. Cerebro vascular accidents PRESENTED BY JOMI JOSEPH E GIKKU ALIAS BENNY
    2. 2. prayer <ul><li>“ Ragadi rogan sathathanu shakthan </li></ul><ul><li>Asheshakayaprasruthanasheshan </li></ul><ul><li>Outhusukya mohaarathithan jakkana </li></ul><ul><li>Yo apoorva vaidya namosthu thasmaii” </li></ul>
    3. 3. contents <ul><li>Definition of CVA </li></ul><ul><li>Blood supply of cerebral hemispheres </li></ul><ul><li>Classification </li></ul><ul><li>Stroke </li></ul><ul><li>Ischemia & infarction </li></ul><ul><li>Haemorrhages </li></ul><ul><li>Stroke in old age </li></ul><ul><li>Stroke in children </li></ul><ul><li>Examination </li></ul><ul><li>Investigation </li></ul><ul><li>Differential diagnosis </li></ul><ul><li>Management </li></ul><ul><li>Conclusion. </li></ul>
    4. 4. definition <ul><li>A cerebrovascular accident (CVA) is an ischemic attack of brain tissue or ultimately an infarction of brain tissue caused by an interruption in cerebral blood flow. This results from damage to an artery supplying blood to the brain. Ischimia of brain tissue lasting five minutes or less will cause permanent damage because neural tissue is incapable of regeneration </li></ul>
    5. 5. Causes of CVAs <ul><ul><li>cardiac disease </li></ul></ul><ul><ul><li>trauma </li></ul></ul><ul><ul><li>infection </li></ul></ul><ul><ul><li>neoplasm (tumor) </li></ul></ul><ul><ul><li>exogenous toxins </li></ul></ul><ul><ul><li>arterio-venous malformations (AVMs) </li></ul></ul>
    6. 6. Blood Supply of Brain <ul><li>Internal Carotid Arteries :transfer oxygen- ated blood from the common carotid arteries of the neck to the circle of Willis. </li></ul><ul><li>Circle of Willis : transfers oxygenated blood from incoming arteries to deep internal arteries of the brain. </li></ul>
    7. 7. <ul><li>Vertebral Arteries : transfer oxygen-ated blood from the subclavian arteries, up through the transverse foraminae of the cervical vertebrae and to the basilar artery of the brain. </li></ul><ul><li>Basilar Artery : transfers oxygenated blood from the vertebral arteries to the circle of Willis of thebrain. </li></ul>
    8. 8. Principle Brain Arteries
    9. 9. <ul><li>aortic arch </li></ul><ul><li>external carotid </li></ul><ul><li>Posterior cerebral </li></ul><ul><li>basilar </li></ul><ul><li>vertebral </li></ul><ul><li>internal carotid </li></ul><ul><li>middle cerebral </li></ul><ul><li>anterior cerebral </li></ul>
    10. 10. The major types of cerebrovascular accident <ul><li>Stroke </li></ul><ul><li>Cerebral ischaemia and infarction </li></ul><ul><li>Transient Ischemic Attacks </li></ul><ul><li>Atherosclerotic thrombosis </li></ul><ul><li>Lacunes </li></ul><ul><li>Embolism </li></ul><ul><li>Hemorrhage </li></ul>
    11. 11. Definition Of Stroke <ul><li>“ Rapidly developed clinical sign of focal disturbance of cerebral function of presumed vascular origin and of more than 24 hours” ( WHO) </li></ul><ul><li>TIA (Transient Ischaemic Attack) recovery is complete within 24 hours. 10% of patients will go on to have a stroke. </li></ul>
    12. 12. Sub-types Of Stroke <ul><li>Ischaemic – obstruction to one of major cerebral arteries, brainstem strokes are less common. </li></ul><ul><li>Haemorrhage – 9% are caused by haemorrhage to the deep parts of the brain. Patients are usually hypertensive. </li></ul>
    13. 13. classification <ul><li>Based on duration </li></ul><ul><li>-Stroke </li></ul><ul><li>-Transiant ischaemic attack </li></ul><ul><li>-Minor stroke </li></ul><ul><li>Based on pathology of underlying focal -brain injury </li></ul><ul><li>-Infarction </li></ul><ul><li>-Haemorrhage. </li></ul>
    14. 14. Clinical classification <ul><li>Transient ischemic attack (TIA) :lasting less than 24hrs. </li></ul><ul><li>Evolving stroke:gradual step wise developmentof stroke. </li></ul><ul><li>Reversible ischemic neurological deficit (RIND):resolve within 1-3 weeks. </li></ul><ul><li>Completed stroke:rapid in onset,doesn’t progress beyond 96hrs </li></ul>
    15. 16. Etiology <ul><li>Complication of several disorders </li></ul><ul><li>Atherosclerosis – most common. </li></ul><ul><li>Hypertension, smoking, diabetes. </li></ul><ul><li>Heart disease – Atrial fibrillation. </li></ul><ul><li>Other: </li></ul><ul><ul><li>Trauma – fat embolism </li></ul></ul><ul><ul><li>Tumor, Infection </li></ul></ul><ul><ul><li>Caissons disease </li></ul></ul>
    16. 17. Risk factors <ul><li>Non modifiable </li></ul><ul><li>Age </li></ul><ul><li>Male sex </li></ul><ul><li>Race </li></ul><ul><li>Heredity </li></ul><ul><li>Modifiable </li></ul><ul><li>Hypertension </li></ul><ul><li>Diabetes </li></ul><ul><li>Smoking </li></ul><ul><li>Hyperlipidemia </li></ul><ul><li>Excess Alcohol* </li></ul><ul><li>Heart disease (AF) Oral contraceptives </li></ul><ul><li>Hypercoagulability </li></ul>
    17. 18. Complications of acute stroke <ul><li>Chest infection </li></ul><ul><li>Epileptic seizures </li></ul><ul><li>Deep venous thrombosis </li></ul><ul><li>Pulmonary embolisam </li></ul><ul><li>Painful sholder </li></ul><ul><li>Pressur sores </li></ul><ul><li>Urinary infection </li></ul><ul><li>Constipation </li></ul><ul><li>Depression & anxiety </li></ul>
    18. 19. Stroke: Ischemia <ul><li>Insufficiency of blood supply </li></ul><ul><ul><li>Glucose & O2 deprivation, build-up of wastes </li></ul></ul><ul><ul><li>NOT synonymous Anoxia: </li></ul></ul><ul><ul><ul><li>O2 deprivation only </li></ul></ul></ul><ul><li>Few seconds: little or no damage </li></ul><ul><li>6-8 minutes ---> Infarction </li></ul><ul><ul><li>neurons & other cells die </li></ul></ul>
    19. 20. A consequence of ischemia. Acute right hemispheric infarction with swelling leading to uncal herniation. This picture of the base of the <ul><li>A consequence of ischemia. Acute right hemispheric infarction with </li></ul><ul><li>swelling leading to uncal herniation. This picture of the base of the </li></ul><ul><li>brain shows the necrotic, herniated mesial temporal lobe (arrowhead). </li></ul>
    20. 21. Cerebral ischaemia and infarction <ul><li>The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it. </li></ul>
    21. 22. <ul><li>Occlusion leads to sudden severe ischaemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise to the clinical picture of a transient ischaemic attack . </li></ul><ul><li>When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischaemic neurological deficit ( RIND ) if it recovers completely in a few days, or a completed stroke if there is a persistent deficit. Sometimes recovery is very slow and incomplete . </li></ul>
    22. 24. Neurological symptoms and signs <ul><li>The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process </li></ul>
    23. 25. Clinical Categories <ul><li>Global Ischemia. </li></ul><ul><ul><li>Hypoxemic encephalopathy </li></ul></ul><ul><ul><li>Hypotension, hypoxemia, anemia. </li></ul></ul><ul><li>Focal Ischemia. </li></ul><ul><ul><li>Obstruction to blood supply to focal area. </li></ul></ul><ul><ul><li>Thrombosis, embolism or hemorrhage </li></ul></ul>
    24. 26. Global Ischemia <ul><li>Etiology: </li></ul><ul><ul><li>Impaired blood supply -Lung & Heart disorders. </li></ul></ul><ul><ul><li>Impaired O2 carrying – Anemia/Blood dis. </li></ul></ul><ul><li>Morphology : </li></ul><ul><ul><li>Laminar necrosis, Hippocampus, Purkinje cells. </li></ul></ul><ul><ul><li>Border zone infarcts – “Watershed” </li></ul></ul><ul><ul><li>Sickle shaped band of necrosis on cortex. </li></ul></ul><ul><li>Clinical Features : </li></ul><ul><ul><li>Mild transient confusion state to </li></ul></ul><ul><ul><li>Severe irreversible brain death. Flat EEG, Vegetative state. Coma. </li></ul></ul>
    25. 27. Focal Ischemia <ul><li>Thrombosis: </li></ul><ul><ul><li>Progressive, recurrent, </li></ul></ul><ul><ul><li>Pale or ischemic infarct. </li></ul></ul><ul><ul><li>Eg. Lacunar infarct </li></ul></ul><ul><li>Embolism / Hemorrhage: </li></ul><ul><ul><li>Sudden. </li></ul></ul><ul><ul><li>Red or hemorrhagic infarct. </li></ul></ul><ul><ul><li>Atherosclerosis – rupture/embolism </li></ul></ul>
    26. 28. Transient Ischemic Attacks(TIA) <ul><ul><li>Definition of term </li></ul></ul><ul><li>Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischaemic neurologic disturbance, Consensus has been that their duration should be less than 24 h. </li></ul>
    27. 29. Pathogenesis <ul><li>Pathogenesis of Ischemic neuronal death </li></ul><ul><li>Ischemia </li></ul><ul><li>↓ </li></ul><ul><li>Excitatory amino acid receptors </li></ul><ul><li>↓ </li></ul><ul><li>Borderzone or penumbra ↓ </li></ul><ul><li>Programmed cell death </li></ul>
    28. 30. Different types of TIA <ul><li>LOW FLOW TIA- Brief, recurrent,sterrotyped associated with atheroscleroticlesion at ICA,MCA STEM junction of veretabral &basilar arteries. </li></ul><ul><li>embolicTIA-discrete,single,prolonged,it lasts for less than 24 hrs,it idicates infarct has occuered. </li></ul><ul><li>Lacunar/penetrating vessel TIA-occlusion of small vessels as a result of lipohyalinosis in response to HTN </li></ul>
    29. 31. Clinical picture <ul><li>Transient Ischaemic Attacks can reflect the involvement of any cerebral artery. The loss of function entirely depends on the influenced artery. It may last a few seconds or up to 12 to 24 h, Most of them last 2 to 15 min. There are only a few attacks or several hundred. Between attacks, the neurologic examination may disclose no abnormalities. A stroke may occur after numerous attacks have occurred over a period of weeks or months. </li></ul>
    30. 32. Brain infarction <ul><li>Blood supply to brain is interupted </li></ul><ul><li>For 30 sec. Brain metabolism altered </li></ul><ul><li>For 1 mte neuronal function may cease </li></ul><ul><li>For 5 mte anoxia initiates. </li></ul>
    31. 33. local vaso dilation stasis of blood colum segmentation of blood cells oedema necrosis of brain tissue
    32. 34. Infarct Pathogenesis <ul><li>Reduced blood supply – hypoxia/anoxia. </li></ul><ul><li>Altered metabolism  Na/K pump block. </li></ul><ul><li>Glutamate receptor act.  calcium influx. </li></ul><ul><li>1-6 min – ischemic injury – vacuolation. </li></ul><ul><li>>6 min – cell death. </li></ul>
    33. 35. Causes of infarcts <ul><li>Thrombosis/occlusion </li></ul><ul><li>Decreased blood flow: </li></ul><ul><li>- hypotension </li></ul><ul><li>- vascular stenosis </li></ul><ul><li>- increase in vascular permeability </li></ul><ul><li>Emboli </li></ul><ul><li>- artery to artery ( arterial territory ) </li></ul><ul><li>- cardioembolic </li></ul>
    34. 36. Infarct Stages <ul><li>Immediate – 6 hours </li></ul><ul><ul><li>No Change both gross & micro </li></ul></ul><ul><li>Acute stage – 2 days </li></ul><ul><ul><li>Oedema, loss of grey/white matter border. </li></ul></ul><ul><ul><li>Inflammation, Red neurons, neutrophils </li></ul></ul><ul><li>Intermediate stage – 2 weeks. </li></ul><ul><ul><li>Demarcation, soft friable tissue, cysts </li></ul></ul><ul><ul><li>Macrophages, liquifactive necrosis </li></ul></ul><ul><li>Late stage – After 4 weeks. </li></ul><ul><ul><li>Fluid filled cysts with dark grey margin (gliosis) </li></ul></ul><ul><ul><li>Removal of tissue by macrophages </li></ul></ul><ul><ul><li>Gliosis – proliferation of glia, loss of architecture </li></ul></ul>
    35. 37. types <ul><li>Atherosclerottic infarction </li></ul><ul><li>Cardiac embolisam </li></ul><ul><li>Small vessel lacunar infarction </li></ul><ul><li>Cryptogenic infarction. </li></ul>
    36. 38. Atherosclerotic infarction <ul><li>Atherosclerotic plaque at the bifurcation or curve in one of the large vessels </li></ul><ul><li>Leads to progressive stenosis with final large artery occlusion </li></ul><ul><li>Caused by trombosis of narrowed lumen. </li></ul>
    37. 40. Embolic infarction <ul><li>This is one of the most common cause of stroke. In most cases of cerebral embolism, the embolic material consists of a fragment that has broken away from a thrombus within the heart. Embolism due to fat, tumor cells, fibrocartilage, amniotic fluid, or air is a rare occurrence and seldom enters into the differential diagnosis of stroke. </li></ul>
    38. 41. Clinical Picture <ul><li>Of all strokes, those due to cerebral embolism develop most rapidly. The embolus strikes at any time of the day or night. Getting up to go to the bathroom is a time of danger. The neurologic picture will depend on the artery involved and the site of obstruction. </li></ul>
    39. 42. <ul><li>It is important to repeat that an embolus may produce a severe neurologic deficit that is only temporary; symptoms disappear as the embolus fragments. In other words , embolism is a common cause of a single evanescent stroke that may reasonably be called a prolonged TIA. Also as already pointed out, several emboli can give rise to two or three transient attacks of differing pattern or , rarely , of almost identical pattern. </li></ul>
    40. 43. Course and prognosis <ul><li>Most patients survive the initial insult, and in many the neurologic deficit may recede relatively rapidly, as indicated above. The eventual prognosis is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis and so on. </li></ul>
    41. 44. Embolism formation
    42. 45. Cerebral thrombosis <ul><li>Most cerebrovascular disease can be attributed to atheroscleroses and chronic hypertension; until ways are found to prevent or control them, vascular disease of the brain will continue to be a major cause of morbidity </li></ul>
    43. 46. Embolism
    44. 47. Clinical picture <ul><li>In more than half of patients, the main part of the stroke is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction. The final stroke may be preceded by one or two attacks or a hundred or more brief TIAs, and stroke may follow the onset of the attacks by hours, weeks, or, rarely, months. </li></ul><ul><li>The most occurrence of the thrombotic stroke is during sleep.The patient awakens paralyzed. Either during the night or in the morning. </li></ul><ul><li>Unaware of any difficulty, he may arise and fall helplessly to the floor with the first step </li></ul>
    45. 48. Clinical picture <ul><li>Associated symptoms </li></ul><ul><ul><li>Seizures accompany the onset of stroke in a small number of cases (10-50%); in other instances, they follow the stroke by weeks to years. The presence of seizures does not definitively distinguish embolic from thrombotic strokes, but seizure at the onset of stroke may be more common with embolus. </li></ul></ul>
    46. 49. Clinical picture <ul><li>Associated symptoms </li></ul><ul><ul><li>Headache occurs in about 25% of patients with ischaemic stroke, possibly because of the acute dilation of collateral vessels. </li></ul></ul>
    47. 50. Course and Prognosis <ul><li>When the patient is seen early in the cerebral thrombosis, it is difficult to give an accurate prognosis. </li></ul><ul><li>As for the eventual or long-term prognosis of the neurologic deficit , there are many possibilities. </li></ul><ul><li>It must be mentioned that having had one thrombotic stroke, the patient is at risk in the ensuing months and years of having a stroke at the same or another site, especially if there is hypertension or diabetes mellitus </li></ul>
    48. 51. <ul><li>Normal blood flow </li></ul><ul><li>Thrombosis </li></ul><ul><li>Artery </li></ul><ul><li>Blood supply </li></ul><ul><li>Blood clot </li></ul>Oxygen starved brain tissue
    49. 52. Lacunar infarct <ul><li>small penetrating branches of the cerebral arteries may become occluded, and the resulting infarcts may be so small or so situated as to cause no symptoms whatever. As the softened tissue is removed, it leaves a small cavity, or lacune. </li></ul>
    50. 53. Lacunar infarct <ul><li>In our clinical and pathologic material, there has always been a strong correlation of the lacunar state with a combination of hypertension and atherosclerosis and, to a lesser degree, with diabetes. In all the cases of lacunar infarction, the diagnosis depends essentially on the occurrence of the certain unique stroke syndromes of limited proportions. </li></ul>
    51. 54. Lacunar infarct <ul><li>Recognition of lacunar stroke is important </li></ul><ul><li>Future lacunar stroke can be reduced by </li></ul><ul><li>treating HTN </li></ul><ul><li>Anticoagulation is not indicated ( No evidence) </li></ul><ul><li>Aspirin is also of uncertanty </li></ul>
    52. 55. Lacunar Infarct in pons
    53. 56. Cryptogenic infarction <ul><li>Infarct of undetermind cause. </li></ul>
    54. 57. Cerebral hemorrhage <ul><li>“ Neurologic symptoms from mass effect on neural structures or from toxic effects of blood itself.” </li></ul>
    55. 58. types <ul><li>Intracranial </li></ul><ul><li>Intracerebral </li></ul><ul><li>Sub arachnoid </li></ul>
    56. 59. Intracranial Hemorrhage <ul><li>This is the common, well-known “spontaneous” brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries.Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema. </li></ul>
    57. 60. <ul><li>Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually caused by arterial bleeding. </li></ul>
    58. 61. <ul><ul><li>The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues . Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death. </li></ul></ul>
    59. 63. Intraventricular Hemorrhage
    60. 64. Intracerebral Hemorrhage <ul><li>Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic.It has been given its own name, “apoplexy”. </li></ul>
    61. 65. Clinical Picture <ul><li>With smaller hemorrhages, the clinical picture conforms more closely to the usual temporal profile of a stroke, i.e, an abrupt onset of symptoms that evolve gradually and steadily over minutes, hours, or a day or two, depending on the size of the ruptured artery and the speed of bleeding. </li></ul><ul><li>Headache and vomiting are cardinal features.Very small hemorrhages in “silent” regions of the brain may escape clinical detection. </li></ul>
    62. 66. Clinical Picture <ul><li>Clinical features vary with the site of hemorrhage. </li></ul><ul><li>Deep cerebral hemorrhage The two most common sites of hypertensive hemorrhage are the putamen and the thalamus , which are separated by the posterior limb of the internal capsule. This segment of the internal capsule is traversed by descending motor fibers and ascending sensory fibers, including the optic radiations. </li></ul>
    63. 67. Clinical Picture <ul><li>Lobar hemorrhage Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temporal, and occipital lobes. Symptoms and signs vary according to the location. </li></ul>
    64. 68. <ul><li>Pontine hemorrhage With bleeding into the pons, coma occurs within seconds to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eye movements are absent or impaired, but vertical eye movements may be preserved. </li></ul><ul><li>Cerebellar hemorrhage The distinctive symptoms of cerebellar hemorrhage (headache, dizziness, vomiting, and the inability to stand or walk) begin suddenly, within minutes after onset of bleeding . </li></ul>
    65. 69. Clinical Picture <ul><li>Of all strokes, those due to cerebral embolism develop most rapidly. The embolus strikes at any time of the day or night. Getting up to go to the bathroom is a time of danger. The neurologic picture will depend on the artery involved and the site of obstruction. </li></ul>
    66. 70. Subarachnoid Hemorrhage <ul><li>This is the fourth most frequent cerebrovascular disorder following atherothrombosis, embolism, and primary intracerebral hemorrhage. Saccular aneurysms are also called berry” aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure. </li></ul><ul><li>Aneurysms are multiple in 20 percent of patients </li></ul>
    67. 71. <ul><li>In childhood , rupture of saccular aneurysms is rare, and they are seldom found at routine postmortem examination; beyond childhood, they gradually increase in frequency to reach their peak incidence between 35 and 65 years of age. </li></ul><ul><li>proximately 90 to 95 percent of saccular aneurysms lie on the anterior part of the circle of Willis </li></ul>
    68. 73. WHAT IS A STROKE?
    69. 74. Qureshi, A. I. et al. N Engl J Med 2001;344:1450-1460 Most Common Sites and Sources of Intracerebral Hemorrhage
    70. 75. Subarachnoid Hemorrhage
    71. 77. Stroke in old age <ul><li>Incidence:2/3 rd of stroke patients are aged over 60 yrs </li></ul><ul><li>Diagnosis:a clear history to be needed </li></ul><ul><li>Thrombolysis:few data avilable. </li></ul><ul><li>Carotid endarterectomy:benefits occur quickly after transiant stroke,it indicates age alone is nota contra indication. </li></ul><ul><li>Cormobiditis:IHD,cardiac failure,COPD,OA,& visual impairements. </li></ul>
    72. 78. Contd. <ul><li>Cognitive impairment : adversely affects outcome. </li></ul><ul><li>Diffuse small vessel CVD: very common & may present insidiously with gait abnormalities or significant memory impairment. </li></ul>
    73. 79. STROKE IN CHILDREN <ul><li>Stroke in children differs from that of adult by 3 ways </li></ul><ul><li>Predisposing factors:cyanotic heart disease. </li></ul><ul><li>Clinical evaluvation:stroke is often improved due to collateral cir culation. </li></ul><ul><li>Anatomical site:perferal bifurcation of cerebral of willis </li></ul><ul><li>Incidence:252/100000 children. </li></ul><ul><li>Cva complications-6-25%with sickle cell disease </li></ul><ul><li>67%untreated sickle cell disease. </li></ul>
    74. 80. General examination of stroke patients Eyes Diabetic changes Hypertensive changes Retinal emboli Arcus senilis Cardiovascular system Blood pressure Heart rhythm Murmurs Jugular venous pressure Peripheral pulses and bruits Respiratory system Pulmonary oedema Respiratory infection Abdomen Urinary retention
    75. 81. Investigations <ul><li>Computed Tomographic Scans </li></ul><ul><ul><li>Usually demonstrates the lesion, more ever it is very useful to exclude hemorrhagic lesion. </li></ul></ul><ul><ul><li>In ischemic stroke, occasionally CT may be normal in first 24 hours. </li></ul></ul><ul><ul><li>Small posterior fossa or lacunar infarction may be easily missed by CT. </li></ul></ul><ul><li>Other imaging techniques (MRI, angiography, transcranial doppler) can be applied in selected cases. </li></ul><ul><li>Carotid doppler </li></ul><ul><li>ECG, echocardiogram in suspected Cardiac emboli </li></ul><ul><li>Assessment of the risk factors for stroke: blood sugar, serum lipids, polycythemia </li></ul>
    76. 82. Investigation of a patient with an acute stroke Diagnostic question investigation Is it a vascular lesion? CT/MRI Is it ischaemic or haemorrhage? CT Lumbaer puncture What is the un derlying vascular ECG cardiac ultra sound MRA Doppler ulrasound contrast angiography What are the risk facctors? Blood count cholesterol clotting/thrombopenia screen blood glucose Investigation of a patient with an acute stroke <ul><li>Diagnostic question investigation </li></ul><ul><li>Is it a vascular lesion? CT/MRI </li></ul><ul><li>Is it ischaemic or haemorrhage? CT </li></ul><ul><li>Lumbaer puncture </li></ul><ul><li>What is the underlying vascular disease? ECG </li></ul><ul><li>cardiac ultra sound </li></ul><ul><li>MRA </li></ul><ul><li>doppler ultra sound </li></ul><ul><li>contrast angiography </li></ul><ul><li>What are the risk facctors? Blood count </li></ul><ul><li>cholesterol </li></ul><ul><li>clotting/thrombopenia screen </li></ul><ul><li>blood glucose </li></ul>
    77. 83. Differential Diagnosis Of CVA <ul><li>Primary cerebral tumours </li></ul><ul><li>Metastatic cerebral tumours </li></ul><ul><li>Subdural heamatoma </li></ul><ul><li>Cerebral abscess </li></ul><ul><li>Demylination </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Encephalitis </li></ul><ul><li>Hysterical conversion </li></ul>
    78. 84. Management <ul><li>Supportive measures </li></ul><ul><li>Antiplatelet agents </li></ul><ul><li>Thrombolysis </li></ul><ul><li>Anticoagulation </li></ul><ul><li>Secondary prevention </li></ul>
    79. 85. <ul><li>Anti-platelet agents </li></ul><ul><ul><li>Aspirin 325 mg per day </li></ul></ul><ul><ul><li>Contraindicated in associated hemorrhage </li></ul></ul><ul><ul><li>Active bleeding lesion (e.g. bleeding peptic ulcer) </li></ul></ul><ul><li>Anticoagulation </li></ul><ul><ul><li>Indicated in cardiac emboli in presence of atrial fibrillation or thrombus in left ventricle </li></ul></ul><ul><ul><li>Start with heparin infusion continue with warfarin . </li></ul></ul><ul><ul><li>Complication : hemorrhagic transformation </li></ul></ul>
    80. 86. <ul><li>Thrombolysis </li></ul><ul><ul><li>Frequently associated with hemorrhagic transformation of ischemic stroke </li></ul></ul><ul><ul><li>Still can be tried if patients presents within 6 hours of onset, absence of hypertension, when CT does not show excessive low density, or there are no other obvious contraindication. </li></ul></ul><ul><ul><li>Drugs that can be used are streptokinase and Rt-PA. </li></ul></ul><ul><li>Secondary prevention </li></ul><ul><ul><li>Control of risk factors </li></ul></ul><ul><ul><li>Antiplatelet agent ( aspirin, ticlopidine, Dipyridamole, clopidogrel ) </li></ul></ul>
    81. 87. conclusion <ul><li>Thus we have gone through the basic pathology, clinical features, investigations and complications of cerebro -vascular accidents. cerebro -vascular accidents are those occuring due to impaired structure and function of various blood vessels suppling the brain.even a mild infarct or haemorrhage can create wide spread consequnce in the body.they are medical emergencies. </li></ul>
    82. 88. <ul><li>Thank You </li></ul>