CVA lecture for medical students

1. APPROACH TO A
PATIENT WITH
STROKE
WILSON E. MTWANA
MBCHB VI

4. DEFINITIONS
• STROKE
• A CLINICAL 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 MOST COMMON 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

8. Anterior Circulation
Posterior Circulation

9. Middle Cerebral Artery

10. Anterior Cerebral Artery

11. Posterior Cerebral Artery

12. CLASSIFICATION & ETIOLOGY
STROKE IS 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 ISCHEMIC STROKE
• 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
• ATHEROSCLEROSIS IS 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
• LACUNAR STROKE
• 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
 CARDIOEMBOLIC STROKE
 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 ischemic stroke

21. PATHOPHYSIOLOGY OF ISCHEMIC STROKE
• 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
• TISSUE SURROUNDING 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 of Na+/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
• TWO TYPES
• INTRACEREBRAL
HEMORRHAGE(ICH)
• SUBARACHNOID
HEMORRHAGE(SAH)
• HIGHER MORTALITY RATES
WHEN COMPARED TO
ISCHEMIC STROKE

25. INTRACEREBRAL HEMORRHAGE
• RESULT OF 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
• MOST COMMON 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

28. CLINICAL FEATURES

29. HISTORY
• ASK FOR ONSET 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 OF SEIZURES & 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 A STROKE
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 A STROKE
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
• MOST CEREBROVASCULAR 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
• STROKE SYNDROMES 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 THE ANTERIOR
CIRCULATION

36. POSTERIOR CIRCULATION

38. CLASSICAL PRESENTATIONS
THROMBOTIC
• H/O TIA
• 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

39. TIA TO STROKE

40. DIFFERENTIAL DIAGNOSIS
• SPACE OCCUPYING LESION(TUMOR)
• SEIZURE
• MIGRAINE
• SUBDURAL HAEMATOMA
• METABOLIC DISTURBANCE

41. HYPOGLYCEMIA
• TRANSIENT HYPOGLYCEMIA MAY
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 POST ICTAL
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 MAY ACTUALLY 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 ONSET FOCAL DEFICIT OF BRAIN FUNCTION
CONFIRMS STROKE
• ONSET AND PROGRESSION WILL DECIDE THE AETIOLOGY
• PRECISE HISTORY OF DEFICIT WILL DECIDE THE SITE OF
LESION

46. MANAGEMENT
OF STROKE

47. INVESTIGATION OBJECTIVES
• TO CONFIRM 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
• CT SCAN
• MRI SCAN
• MR ANGIOGRAPHY
• DOPPLER ULTRASOUND
• EEG
• PET
• SPECT
INVASIVE
• LUMBAR PUNCTURE
• CONTRAST ANGIOGRAPHY
(CEREBRAL
ARTERIOGRAPHY)
• CT ANGIOGRAPHY

49. CT SCAN
• MANDATORY INITIAL 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

50. HAEMORRHAGIC LESION

51. ISCHAEMIC LESION

52. STROKE PATIENT
CT SCAN/MRI
VASCULAR NATURE
CONFIRMED
HAEMORRHAGE ISCHAEMIA
Cont’d…

53. SEARCH FOR
SOURCE
CEREBRAL
ARTERIOGRAPHY
MRA/CTA DOPPLER PET/SPECT
SEARCH FOR SOURCE
Cont’d…

54. NORMAL CT
SCAN
HAEMORRHAGE
SUSPECTED
LUMBAR
PUNCTURE
CSF WITH BLOOD/
XANTHOCHROMIA
HAEMORRHAGE CONFIRMED

55. UNDERLYING DISEASE
• CEREBRAL VASCULATURE
• 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
• SERUM LIPIDS 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. MINIMIZE VOLUME OF BRAIN IRREVERSIBLY
DAMAGED
2. PREVENT COMPLICATIONS
3. REHABILITATION
4. REDUCE RISK OF RECCURENCE

59. MANAGEMENT OF A
TRANSIENT ISCHAEMIC
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 A TRANSIENT
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
ACUTE EPISODE 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
ACUTE EPISODE 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
• THROMBOLYTICS AND 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
• CONTROL OF 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
• SPEECH THERAPY
• IMPROVE QUALITY OF LIFE
WITH MOTOR AIDS
• -LEG BRACE, TOE SPRING ,
CANE , WALKING STICK

70. STROKE UNITS –
A MULTIDISCIPLINARY
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
• BLOOD PRESSURE 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 TO CORTICAL BRAIN INJURY(IMMEDIATE)
- EPILEPSY/SEIZURES
- CEREBRAL OEDEMA
• RESIDUAL DEFICITS FROM STROKE
- PARALYSIS
- APHASIA

73. COMPLICATIONS –
CONT’D
• DUE TO IMMOBILITY
- CHEST INFECTIONS
- PRESSURE SORES
- DEEP VEIN THROMBOSIS /
PULMONARY EMBOLISM
- PAINFUL SHOULDER
- URINARY INFECTION/CONSTIPATION
- DEPRESSION AND ANXIETY

74. PROGNOSIS
ISCHAEMIC STROKE
• MORTALITY RATE 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
INTRACEREBRAL HAEMORRHAGE
• 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 .

77. THANK YOU 