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Cva 2018
- 1. APPROACH TO A PATIENTWITH STROKE WILSON E. MTWANA MBCHB VI
- 4. DEFINITIONS • STROKE • ACLINICAL SYNDROME CONSISTING OF RAPIDLY DEVELOPING CLINICAL SIGNS OF FOCAL (OR GLOBAL IN CASE OF COMA) DISTURBANCE OF CEREBRAL FUNCTION LASTING MORE THAN 24 HOURS OR LEADING TO DEATH WITH NO APPARENT CAUSE OTHER THAN A VASCULAR ORIGIN. • TRANSIENT ISCHEMIC ATTACK (TIA) • CLINICAL SYNDROME OF RAPID ONSET OF FOCAL DEFICITS OF BRAIN FUNCTION WHICH RESOLVES WITHIN 24 HOURS, WITHOUT RADIOLOGICAL EVIDENCE. • A TRANSIENT EPISODE OF NEUROLOGIC DYSFUNCTION CAUSED BY FOCAL BRAIN, SPINAL CORD OR RETINAL ISCHEMIA WITHOUT ACUTE INFARCTION.
- 5. DEFINITIONS • PROGRESSIVE STROKE •A STROKE IN WHICH THE FOCAL NEUROLOGICAL DEFICITS WORSEN WITH TIME • ALSO CALLED STROKE IN EVOLUTION • COMPLETED STROKE • A STROKE IN WHICH THE FOCAL NEUROLOGICAL DEFICITS PERSIST AND DO NOT WORSEN WITH TIME
- 6. EPIDEMIOLOGY • THIRD MOSTCOMMON CAUSE OF DEATH AFTER CANCER AND ISCHEMIC HEART DISEASE • MOST COMMON CAUSE OF SEVERE PHYSICAL DISABILITY • IN KENYA, IN HOSPITAL STROKE AUDITS REPORT A STROKE PREVALENCE 3042/100,000 ADMISSIONS WITH A MEAN AGE OF STROKE OCCURRENCE OF 61 YEARS WHICH IS 10 YEARS YOUNGER COMPARED TO STUDIES IN THE UNITED STATES OF AMERICA AND EUROPEAN COUNTRIES. • INCIDENCE AND PREVALENCE OF STROKE IS ON THE RISE DUE TO INCREASING ADOPTION OF UNHEALTHY LIFESTYLE & AN INCREASING LIFE EXPECTANCY
- 7. STROKE RISK FACTORS •FIXED • AGE • GENDER (MALE>FEMALE) • RACE (AFRO- CARIBBEAN>ASIAN>EUROPE AN) • HEREDITY • PREVIOUS VASCULAR EVENT EG. MI, PERIPHERAL EMBOLISM • HIGH FIBRINOGEN • MODIFIABLE • HYPERTENSION • HEART DISEASE (ATRIAL FIBRILLATION, ENDOCARDITIS) • DIABETES MELLITUS • HYPERLIPIDAEMIA • SMOKING • EXCESS ALCOHOL CONSUMPTION • ORAL CONTRACEPTIVES
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- 12. CLASSIFICATION & ETIOLOGY STROKEIS CLASSIFIED INTO TWO MAJOR TYPES: BRAIN ISCHEMIA: DUE TO THROMBOSIS, EMBOLISM, OR SYSTEMIC HYPOPERFUSION BRAIN HEMORRHAGE: DUE TO • INTRACEREBRAL HEMORRHAGE OR • SUBARACHNOID HEMORRHAGE APPROXIMATELY 80 PERCENT OF STROKES ARE DUE TO ISCHEMIC CEREBRAL INFARCTION AND 20 PERCENT TO BRAIN HEMORRHAGE
- 13. TYPES OF STROKE •ISCHEMIC • HEMORRHAGIC
- 14. ISCHEMIC STROKE • 80%OF STROKES • ARTERIAL OCCLUSION OF AN INTRACRANIAL VESSEL LEADS TO HYPOPERFUSION OF THE BRAIN REGION IT SUPPLIES • THREE ETIOLOGICAL TYPES • THROMBOTIC • EMBOLIC • SYSTEMIC HYPOPERFUSION
- 15. ETIOLOGY OF ISCHEMICSTROKE • THROMBOTIC • LACUNAR STROKE • LARGE VESSEL THROMBOSIS • HYPERCOAGULABLE DISORDERS • EMBOLIC • ARTERY TO ARTERY • CAROTID BIFURCATION • AORTIC ARCH • CARDIOEMBOLIC • ATRIAL FIBRILLATION • MYOCARDIAL INFARCTION • MURAL THROMBUS • BACTERIAL ENDOCARDITIS • MITRAL STENOSIS • PARADOXICAL EMBOLUS
- 16. THROMBOTIC STROKE • ATHEROSCLEROSISIS THE MOST COMMON PATHOLOGY LEADING TO THROMBOTIC OCCLUSION OF BLOOD VESSELS • HYPERCOAGULABLE DISORDERS – UNCOMMON CAUSE • ANTIPHOSPHOLIPID SYNDROME • SICKLE CELL ANEMIA • POLYCYTHEMIA VERA • HOMOCYSTEINEMIA • VASCULITIS: PAN, WEGENER’S GRANULOMATOSIS, GIANT CELL ARTERITIS
- 17. THROMBOTIC STROKE • LACUNARSTROKE • ACCOUNTS FOR 20% OF ALL STROKES • RESULTS FROM OCCLUSION OF SMALL DEEP PENETRATING ARTERIES OF THE BRAIN • PATHOLOGY: • LIPOHYALINOSIS :-A LIPID HYALINE BUILD-UP DISTALLY SECONDARY TO HYPERTENSION) AND FIBRINOID DEGENERATION • MICROATHEROMA :- DEGENERATION OF THE WALLS OF THE ARTERIES CAUSED BY ACCUMULATED FATTY DEPOSITS AND SCAR TISSUE, AND LEADING TO RESTRICTION OF THE CIRCULATION AND A RISK OF THROMBOSIS • THROMBOSIS LEADS TO SMALL INFARCTS KNOWN AS LACUNES • CLINICALLY MANIFESTED AS LACUNAR SYNDROMES
- 19. EMBOLIC STROKE CARDIOEMBOLICSTROKE EMBOLUS FROM THE HEART GETS LODGED IN INTRACRANIAL VESSELS MCA MOST COMMONLY AFFECTED ATRIAL FIBRILLATION IS THE MOST COMMON CAUSE OTHERS: MI, PROSTHETIC VALVES, RHEUMATIC HEART DISEASE ARTERY TO ARTERY EMBOLISM THROMBUS FORMED ON ATHEROSCLEROTIC PLAQUES GETS EMBOLIZED TO INTRACRANIAL VESSELS CAROTID BIFURCATION ATHEROSCLEROSIS IS THE MOST COMMON SOURCE OTHERS: AORTIC ARCH, VERTEBRAL ARTERIES ETC.
- 20. Etiology of ischemicstroke
- 21. PATHOPHYSIOLOGY OF ISCHEMICSTROKE • BLOOD SUPPLY TO THE BRAIN IS AUTO REGULATED • BLOOD FLOW • IF ZERO LEADS TO DEATH OF BRAIN TISSUE WITHIN 4-10MIN • <16-18ML/100G TISSUE/MIN INFARCTION WITHIN AN HOUR • ISCHEMIA LEADS TO DEVELOPMENT OF AN ISCHEMIC CORE AND AN ISCHEMIC PENUMBRA
- 22. ISCHEMIC PENUMBRA • TISSUESURROUNDING THE CORE REGION OF INFARCTION WHICH IS ISCHEMIC BUT REVERSIBLY DYSFUNCTIONAL • MAINTAINED BY COLLATERALS • CAN BE SALVAGED IF REPERFUSED IN TIME • PRIMARY GOAL OF REVASCURALIZATION THERAPIES
- 23. ATP depletion Hypoperfusion Failure ofNa+/K+ ATPase membrane ionic pump Calcium entry Glutamate release Activation of lipid peroxidases, proteases & NO synthase Destruction of intracellular organelles, cell membrane & release of free radicals Free fatty acid release Activation of pro- coagulant pathways Liquefactive necrosis Thrombus/embol us Membrane depolarization & cytotoxic cellular edema
- 24. HEMORRHAGIC STROKE • TWOTYPES • INTRACEREBRAL HEMORRHAGE(ICH) • SUBARACHNOID HEMORRHAGE(SAH) • HIGHER MORTALITY RATES WHEN COMPARED TO ISCHEMIC STROKE
- 25. INTRACEREBRAL HEMORRHAGE • RESULTOF CHRONIC HYPERTENSION • SMALL ARTERIES ARE DAMAGED DUE TO HYPERTENSION • IN ADVANCED STAGES VESSEL WALL IS DISRUPTED AND LEADS TO LEAKAGE • OTHER CAUSES: AMYLOID ANGIOPATHY, ANTICOAGULANT THERAPY, CAVERNOUS HEMANGIOMA, COCAINE, AMPHETAMINES
- 26. SUBARACHNOID HEMORRHAGE • MOSTCOMMON CAUSE IS RUPTURE OF SACCULAR OR BERRY ANEURYSMS • OTHER CAUSES INCLUDE ARTERIOVENOUS MALFORMATIONS, ANGIOMAS, MYCOTIC ANEURYSMAL RUPTURE ETC. • ASSOCIATED WITH EXTREMELY SEVERE HEADACHE
- 27. PATHOPHYSIOLOGY OF HEMORRHAGIC STROKE •EXPLOSIVE ENTRY OF BLOOD INTO THE BRAIN PARENCHYMA STRUCTURALLY DISRUPTS NEURONS • WHITE MATTER FIBRE TRACTS ARE SPLIT • IMMEDIATE CESSATION OF NEURONAL FUNCTION • EXPANDING HEMORRHAGE CAN ACT AS A MASS LESION AND CAUSE FURTHER PROGRESSION OF NEUROLOGICAL DEFICITS • LARGE HEMORRHAGES CAN CAUSE TRANSTENTORIAL CONING AND RAPID DEATH
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- 29. HISTORY • ASK FORONSET AND PROGRESSION OF NEUROLOGICAL SYMPTOMS – COMPLETED STROKE OR STROKE IN EVOLUTION • HISTORY OF PREVIOUS TIAS & AMAUROSIS FUGAX • HISTORY OF HYPERTENSION & DIABETES MELLITUS • HISTORY OF HEART CONDITIONS LIKE ARRHYTHMIAS, RHD & PROSTHETIC VALVES
- 30. HISTORY • HISTORY OFSEIZURES & MIGRAINE • HISTORY OF ANTICOAGULANT THERAPY • HISTORY OF ORAL CONTRACEPTIVE USE • HISTORY OF ANY HYPERCOAGULABLE DISORDERS LIKE SICKLE CELL ANEMIA & POLYCYTHEMIA VERA • SUBSTANCE ABUSE: COCAINE, AMPHETAMINES
- 31. EXAMINATION OF ASTROKE PATIENT • THE NEUROLOGICAL EXAMINATION IS HIGHLY VARIABLE AND DEPENDS ON THE LOCATION OF THE VASCULAR LESION. • SKIN: LOOK FOR XANTHELASMA,RASHES (ARTERITIS,SPLINTER HAEMORRHAGES,LIVEDO RETICULARIS),LIMB ISCHEMIA(DVT) • EYES:LOOK FOR DIABETIC CHANGES,RETINAL EMBOLI,HYPERTENSIVE CHANGES,ARCUS SENILIS
- 32. EXAMINATION OF ASTROKE PATIENT • CVS: HYPER/HYPOTENSION, ABNORMAL RHYTHM(ATRIAL FIBRILLATION),MURMURS(VALVULAR ANOMALY),RAISED JVP(HEART FAILURE),PERIPHERAL PULSES AND BRUITS(GENERALISED ARTERIOPATHY) • RESPIRATORY SYSTEM: PULMONARY EDEMA, INFECTION • ABDOMEN: URINARY RETENTION • LOCOMOTOR SYSTEM: INJURIES SUSTAINED DURING COLLAPSE WITH STROKE, COMORBITIES WHICH INFLUENCE FUNCTIONAL ABILITIES.
- 33. GENERAL FEATURE • MOSTCEREBROVASCULAR DISEASES ARE MANIFEST BY THE ABRUPT ONSET OF A FOCAL NEUROLOGIC DEFICIT, AS IF THE PATIENT WAS "STRUCK BY THE HAND OF GOD.” • THE CLINICAL MANIFESTATIONS OF STROKE ARE HIGHLY VARIABLE BECAUSE OF THE COMPLEX ANATOMY OF THE BRAIN AND ITS VASCULATURE.
- 34. STROKE SYNDROMES • STROKESYNDROMES ARE DIVIDED INTO: • (1) LARGE-VESSEL STROKE WITHIN THE ANTERIOR CIRCULATION • (2) LARGE-VESSEL STROKE WITHIN THE POSTERIOR CIRCULATION AND • (3) SMALL-VESSEL DISEASE OF EITHER VASCULAR BED.
- 35. STROKE WITHIN THEANTERIOR CIRCULATION
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- 38. CLASSICAL PRESENTATIONS THROMBOTIC • H/OTIA • STROKE IN EVOLUTION • USUALLY HAPPENS EARLY MORNING EMBOLIC • PATIENTS WITH KNOWN HEART DISEASE LIKE IHD, VALVULAR HEART DISEASE • RAPID RECOVERY HAEMORRHAGIC STROKE IN HYPERTENSIVE PATIENTS ASSOCIATED WITH EMOTIONAL EXCITEMENT HEADACHE & VOMITING
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- 40. DIFFERENTIAL DIAGNOSIS • SPACEOCCUPYING LESION(TUMOR) • SEIZURE • MIGRAINE • SUBDURAL HAEMATOMA • METABOLIC DISTURBANCE
- 41. HYPOGLYCEMIA • TRANSIENT HYPOGLYCEMIAMAY PRODUCE A STROKE LIKE PICTURE WITH HEMIPLEGIA AND APHASIA. • THE HEMIPLEGIA MAY RESOLVE IMMEDIATELY WITH THE ADMINISTRATION OF INTRAVENOUS GLUCOSE BUT RESOLUTION OVER A HOURS IS ALSO REPORTED
- 42. SPACE OCCUPYING LESIONS •SUBACUTE OR CHRONIC DURATION OF SYMPTOMS, HOWEVER SOME PATIENTS MAY PRESENT WITH ACUTELY PROBABLY DUE TO BLEEDING INTO A TUMOUR • ASSOCIATED WITH DEEP SEATED BURSTING HEADACHE, PROJECTILE VOMITING DUE RAISED ICT
- 43. SEIZURES AND POSTICTAL STATES • TRADITIONAL THOUGHT IS THAT THESE POSTICTAL SYMPTOMS ARE MANIFESTATIONS OF SEIZURE-INDUCED ALTERATIONS IN NEURONAL FUNCTION THAT ARE REVERSIBLE; STRUCTURAL NEURONAL ALTERATIONS ARE NOT PRESENT. THE POSTICTAL WEAKNESS OR TODD’S PARALYSIS USUALLY FOLLOWS PARTIAL MOTOR SEIZURES BUT MAY FOLLOW GENERALIZED SEIZURES AS WELL. DURATION IS USUALLY BRIEF BUT MAY LAST 48 HOURS
- 44. MIGRAINE • MIGRAINE MAYACTUALLY PRECIPITATE A STROKE, BUT THERE IS ALSO A VARIANT OF MIGRAINE, HEMIPLEGIC MIGRAINE, WHERE UNILATERAL HEMIPARESIS OUTLASTS THE HEADACHE. THIS IS DIFFICULT IF NOT IMPOSSIBLE TO DIAGNOSE CORRECTLY AT FIRST PRESENTATION WHEN IT MUST BE REGARDED AS A DIAGNOSIS OF EXCLUSION; ONLY WITH RECURRENT, STEREOTYPIC ATTACKS CAN THIS BE SUSPECTED. CASES WITH ALTERNATING HEMIPLEGIA HAVE BEEN REPORTED. AT TIMES THIS DISORDER HAS BEEN SHOWN TO BE FAMILIAL.
- 45. SUMMARY • RAPID ONSETFOCAL DEFICIT OF BRAIN FUNCTION CONFIRMS STROKE • ONSET AND PROGRESSION WILL DECIDE THE AETIOLOGY • PRECISE HISTORY OF DEFICIT WILL DECIDE THE SITE OF LESION
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- 47. INVESTIGATION OBJECTIVES • TOCONFIRM THE VASCULAR NATURE OF THE LESION • THE PATHOLOGICAL TYPE OF THE VASCULAR LESION • THE UNDERLYING VASCULAR DISEASE • RISK FACTORS PRESENT
- 48. INVESTIGATION MODALITIES: BRAIN NON-INVASIVE • CTSCAN • MRI SCAN • MR ANGIOGRAPHY • DOPPLER ULTRASOUND • EEG • PET • SPECT INVASIVE • LUMBAR PUNCTURE • CONTRAST ANGIOGRAPHY (CEREBRAL ARTERIOGRAPHY) • CT ANGIOGRAPHY
- 49. CT SCAN • MANDATORYINITIAL INVESTIGATION • HAEMORRHAGE APPEARS INSTANTLY AS A HYPERDENSE AREA • INFARCT APPEARS AS A HYPODENSE AREA • INFARCT MAY NOT APPEAR BEFORE 48 HRS • MRI MAY BE DONE INSTEAD BUT CT SCAN IS MORE SENSITIVE FOR DETECTING HAEMORRHAGE • DIFFUSION WEIGHTED MRI IS GOOD FOR IDENTIFYING ISCHAEMIC LESION
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- 52. STROKE PATIENT CT SCAN/MRI VASCULARNATURE CONFIRMED HAEMORRHAGE ISCHAEMIA Cont’d…
- 53. SEARCH FOR SOURCE CEREBRAL ARTERIOGRAPHY MRA/CTA DOPPLERPET/SPECT SEARCH FOR SOURCE Cont’d…
- 54. NORMAL CT SCAN HAEMORRHAGE SUSPECTED LUMBAR PUNCTURE CSF WITHBLOOD/ XANTHOCHROMIA HAEMORRHAGE CONFIRMED
- 55. UNDERLYING DISEASE • CEREBRALVASCULATURE • ABNORMALITIES LIKE ANEURYSMS OR • AV MALFORMATIONS • CEREBRAL ANGIOGRAPHY • VASCULAR IMAGING – MRA/CTA OR DOPPLER (NON INVASIVE)
- 56. UNDERLYING DISEASE CARDIOVASCULAR LIKE MI,ATRIAL FIBRILLATION, VALVULAR DISEASES ETC. • ELECTROCARDIOGRAM • CHEST X-RAY • ECHOCARDIOGRAPHY • TRANSESOPHAGEAL ULTRASOUND • HOLTER MONITORING(PAROXYSMAL NOCTURNAL ARRHYTHMIA) • BLOOD CULTURES
- 57. UNDERLYING DISEASE • SERUMLIPIDS FOR HYPERLIPIDEMIA • ANA FOR SLE • MR ANGIOGRAPHY FOR ARTERIAL DISSECTION • LUPUS ANTICOAGULANT FOR ANTIPHOSPHOLIPID ANTIBODY SYNDROME • ESR, CRP, ANCA FOR VASCULITIS • PT, APTT, PLATELET COUNT FOR BLEEDING DISORDERS • PROTEINS C & S FOR HYPERCOAGULABILITY
- 58. TREATMENT OBJECTIVES 1. MINIMIZEVOLUME OF BRAIN IRREVERSIBLY DAMAGED 2. PREVENT COMPLICATIONS 3. REHABILITATION 4. REDUCE RISK OF RECCURENCE
- 59. MANAGEMENT OF A TRANSIENTISCHAEMIC ATTACK (TIA)MEDICAL MANAGEMENT (IF DIFFUSE ATHEROSCLEROTIC DISEASE OR POOR OPERATIVE CANDIDATES) 1. STOP SMOKING 2. CONCURRENT MEDICAL PROBLEMS TO BE ADDRESSED: • EMBOLI FROM HEART AND OTHER PARTS OF CARDIOVASCULAR SYSTEM (A) ANTI COAGULANTS: HEPARIN(IV), WARFARIN(ORAL)
- 60. MANAGEMENT OF ATRANSIENT ISCHAEMIC ATTACK(TIA) – CONT’D SURGICAL MANAGEMENT • CAROTID AND CEREBRAL ARTERIOGRAPHY STENOSIS MILD TO MODERATE SEVERE REGULAR FOLLOW UP CAROTID ENDARTERECTOMY • ALL ABOVE CAN BE DONE ONLY IF THERE IS RELATIVELY LITTLE ATHEROSCLEROSIS ELSEWHERE IN CEREBROVASCULAR SYSTEM.
- 61. MANAGEMENT OF AN ACUTEEPISODE OF STROKE• AIRWAY - MAINTAIN AIRWAY, PREVENT ASPIRATION, KEEP NIL PER ORAL • BREATHING - MAINTAIN OXYGEN SATURATION > 97% - SUPPLEMENTARY OXYGEN • CIRCULATION - ADEQUACY OF PULSE AND BP - FLUID, ANTI ARRHYTHMICS, IONOTROPES • HYDRATION - PREVENT DEHYDRATION ; GIVE ADEQUATE FLUIDS - PARENTERAL OR VIA NASOGASTRIC TUBE • NUTRITION - NUTRITIONAL SUPPLEMENTS AND NASOGATRIC FEEDING • MEDICATION - ADMINISTER MEDICATION ALSO BY ROUTES OTHER THAN ORAL
- 62. MANAGEMENT OF AN ACUTEEPISODE OF STROKE CONT’D • BLOOD PRESSURE - UNLESS INDICATED (HEART OR RENAL FAILURE,HYPERTENSIVE ENCEPHALOPATHY OR AORTIC DISSECTION) IT SHOULD NOT BE LOWERED FOR THE FEAR OF EXPANSION OF INFARCT. ISCHAEMIC STROKE - MAINTAIN 180/110 MM HG HAEMORRHAGIC STROKE – KEEP MAP <115 MM HG • BLOOD GLUCOSE - INSULIN TO TREAT HYPERGLYCAEMIA(CAN INCREASE INFARCT SIZE) - MAINTAIN < 200MG% • TEMPERATURE - EARLY USE OF ANTIPYRETICS • PRESSURE AREAS – TO PREVENT OCCURRENCE OF DECUBITUS ULCERS • INCONTINENCE
- 63. ISCHAEMIC STROKE • THROMBOLYTICSAND REVASCULARISATION - - TPA (ALTEPLASE)-0.9MG/KG(MAX 90MG) 10% OF DOSE – INITIAL IV BOLUS REMAINDER INFUSED OVER ONE HOUR - TO BE USED < 3 HRS OF ONSET OF SYMPTOMS (FOR MAXIMUM EFFICACY) - HAEMORRHAGE TO BE RULED OUT • NEUROPROTECTIVE AGENTS:-AC-11,ACETYL-L-
- 64. ANTI PLATELET THERAPY •ASPRIN, CLOPIDOGREL - ACT BY INHIBITING PLATELET AGGREGATION AND ADHESION. - ASPIRIN 300MG SINGLE DOSE TO BE GIVEN IMMEDIATELY FOLLOWING DIAGNOSIS. - IF ALTEPLASE GIVEN IT CAN BE WITH HELD FOR 24 HRS. - LATER ASPIRIN AT A DOSE OF 75 MG IN COMBINATION WITH CLOPIDOGREL 75 MG DAILY FOR ABOUT ONE YEAR DURATION.
- 65. ANTI COAGULANTS • HEPARINS, WARFARIN -HEPARINS ACT BY ACCELERATING THE INHIBITION OF FACTOR II AND FACTOR X OF COAGULATION CASCADE -WARFARIN ANTAGONISES VITAMIN K TO PREVENT ACTIVATION OF CLOTTING FACTORS -DECREASE RISK OF RECURRENCE AND VENOUS THROMBOEMBOLISM -INTRA CRANIAL HAEMORRHAGE TO BE EXCLUDED BEFORE THERAPY -MORE USEFUL IF STROKE IS EVOLVING
- 66. ANTI COAGULANTS - CONT’D •HYPEROSMOLAR AGENTS - REDUCE CEREBRAL OEDEMA - 20% MANNITOL IV – 100ML TID - ORAL GLYCEROL IF SWALLOW IS NORMAL • CONCURRENT MEDICAL PROBLEMS SUCH AS ATRIAL FIBRILLATIONS TO BE TACKLED • OTHERS: - PENTOXIFYLLINE (HEMORRHEOLOGY MODIFIER) TO BE USED WITHIN 12 HRS -NEUROPROTECTIVE AGENTS
- 67. HAEMORRHAGIC STROKE • CONTROLOF HYPERTENSION • CONTROL COAGULATION ABNORMALITIES (ESP DUE TO ORAL ANTICOAGULANTS) • SURGICAL DECOMPRESSION • SURGERY FOR ANEURYSMS AND ARTERIO-VENOUS MALFORMATIONS • ANTI PLATELET AND ANTI COAGULANTS ARE CONTRAINDICATED
- 68. REHABILITATION • PHYSIOTHERAPY -AS EARLY AS POSSIBLE - INITIALLY PASSIVE MOMENTS - LATER ACTIVE MOVEMENTS - IN EVERY CASE EARLY MOBILIZATION - PREVENTS CONTRACTURES, SPASTICITY AND ATROPHY • OCCUPATIONAL THERAPY
- 69. REHABILITATION - CONT’D • SPEECHTHERAPY • IMPROVE QUALITY OF LIFE WITH MOTOR AIDS • -LEG BRACE, TOE SPRING , CANE , WALKING STICK
- 70. STROKE UNITS – AMULTIDISCIPLINARY APPROACH • IMMEDIATE RESUSCITATION , PREVENT COMPLICATIONS AND RECURRENCE • EMERGENCY 24 HR EVALUATION AND COMPREHENSIVE CARE • IMPROVES NEUROLOGICAL OUTCOME • REDUCES MORTALITY • 1000 PATIENTS ADMITTED TO STROKE UNITS SAVES THE LIVES OF ATLEAST 5O PATIENTS AT END OF 6 MONTHS
- 71. SECONDARY PREVENTION • BLOODPRESSURE CONTROL • DIABETES MANAGEMENT • LIPID MANAGEMENT • SMOKING CESSATION • ALCOHOL MODERATION • WEIGHT REDUCTION/PHYSICAL ACTIVITY • CAROTID ARTERY INTERVENTIONS • ANTI PLATELET AGENTS / ANTI COAGULANTS • STATINS • DIURETICS +/- ACE INHIBITORS
- 72. COMPLICATIONS • DUE TOCORTICAL BRAIN INJURY(IMMEDIATE) - EPILEPSY/SEIZURES - CEREBRAL OEDEMA • RESIDUAL DEFICITS FROM STROKE - PARALYSIS - APHASIA
- 73. COMPLICATIONS – CONT’D • DUETO IMMOBILITY - CHEST INFECTIONS - PRESSURE SORES - DEEP VEIN THROMBOSIS / PULMONARY EMBOLISM - PAINFUL SHOULDER - URINARY INFECTION/CONSTIPATION - DEPRESSION AND ANXIETY
- 74. PROGNOSIS ISCHAEMIC STROKE • MORTALITYRATE IN FIRST 30 DAYS IS 8-12% • CAN VARY DEPENDING UPON SIZE, LOCATION, SYMPTOMS OF STROKE • TIME THAT ELAPSES FROM THE EVENT TO MEDICAL INTERVENTION • FIRST 3 HRS AFTER STROKE - GOLDEN PERIOD
- 75. PROGNOSIS – CONT’D INTRACEREBRALHAEMORRHAGE • MORTALITY RATE IN FIRST 30 DAYS IS ALMOST 50% • SITE AND EXTENT OF HEMATOMA ALSO PLAYS A ROLE IN DETERMINING THE PROGNOSIS • HAMORRHAGIC STROKES HAVE A POOR PROGNOSIS COMPARED TO ISCHAEMIC TYPE .
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Editor's Notes
- #5 Amaurosis fugax is a painless temporary loss of vision in one or both eyes
- #7 In this study, most of the stroke cases were ischaemic (85%) while hemorrhagic stroke constituted 8 % of the stroke cases. Dr. Julius Okell Kenya Association of Physicians 2013 Prof. James Jowi
- #22 50 to 54
- #38 WALLENBERG..POSTERIOR INFERIOR CEREBELLAR ARTERY LOCKED IN BASILAR WEBER,,PCA
- #57 A Holter monitor is a battery-operated portable device that measures and records your heart's activity (ECG)
- #63 PERMISIVE HTN
- #68 NIMODIPINE.