Stroke [uncensored] - by MHR Corporation

Stroke + soalan

1. STROKE & CEREBROVASCULAR ACCIDENT MOHD HANAFI RAMLEE

2. Definition Transient Ischaemic Attack (TIA) – an acute focal neurological deficit resulting from cerebrovascular disease with resolution of signs and symptoms within 24 hours. Reversible Ischaemic Neurological Deficit (RIND) – attack lasting longer than 24 hours but with complete clearance of signs and symptoms within 7 days. Completed Stroke – neurological deficit lasts longer than 7 days.

3. HOW YOU GIVE THE DIAGNOSIS? The diagnosis should provide answers to the following questions: 1. What is the neurological deficit? 2. Where is the lesion? 3. What is the lesion? 4. Why has the lesion occurred? 5. What are the potential complications and prognosis?

4. What Artery Involved? Aphasia (dominant hemisphere) Hemiparesis / plegia Hemisensory loss/disturbance Homonymous hemianopia Parietal lobe dysfunction, e.g. astereognosis , agraphaesthesia , impaired two-point discrimination , sensory and visual inattention, left-right dissociation and acalculia

5. What Artery Involved? Weakness of lower limb more than upper limb

6. What Artery Involved? Homonymous hemianopia Cortical blindness Ataxia Dizziness or vertigo Dysarthria Diplopia Dysphagia Horner’s syndrome Hemiparesis or hemisensory loss contralateral to the cranial nerves palsy Cerebellar signs

7. SO… BASIC IS IMPORTANT!!!!!!!!

8. Brain Blood Supply Features: High oxygen requirement. Brain 2% of body weight - 15% of cardiac output 20% of total body oxygen. Continuous oxygen requirement Few minutes of ischemia - irreversible injury. Neurons - Predominantly aerobic. Sensitive areas: Adults -Hippocampus, 3,5th & 6th layer of cortex, Purkinje cells. Border zone (watershed areas) Brain stem nuclei in infants.

9. Anatomy – Stroke.

10. Brodman’s Cortical Map:

11. Frontal [f* ck – motor] Lobe Functions: High level cognitive functions. i.e reasoning, abstraction, concentration Storage of information – memory Control of voluntary eye movement Motor control of speech in the dominant hemisphere. Motor Cortex – Motor control of the contralateral side of the body Urinary continence Emotion and personality

12. Parietal [p- sx – sensory] Lobe Functions: Sensory cortex – sensory input is interpreted to define size, weight, texture and consistency (contralateral) Sensation is localised, and modalities of touch, pressure and position are identified. Awareness of the parts of body Non-dominant – processes visuospatial information and controls spatial orientation Dominant is involved in ideomotor praxis (ability to perform learned motor tasks

13. Temporal [t- telinga ] Lobe Functions: Primary auditory receptive areas In dominant ability to comprehend speech ( wernicke’s ) – reception Interpretive area – area at the junction of the temporal, parietal and occipital lobes. Plays an important role in visual, auditory and olfactory perception Important role in learning; memory and emotional affect .

14. Occipital [O-optic] Lobe Functions: Primary visual cortex Visual association areas Visual perception Some visual reflexes (i.e. visual fixation) Involuntary smooth eye movement

15. Diencephalon Functions: Brain Stem: Midbrain, Pons & Medulla 10 of the 12 ranial nerves arise from the brainstem ( ipsilateral signs) Cortical pathway decussation contralateral signs. Some major functions: eye movement, swallowing, breathing, blood pressure, heat beat, consciousness Cerebellum: movement – Balance & coordination

16. Motor & Sensory Cortex:

17. Diencephalon & Brain stem:

18. Cranial Nerves:

19. Stroke Types: Clinical Transient Ischemic Attack –TIA resolve <24h Evolving stroke – increasing >24h. – Thromb . Recurrent / multiple stroke – sec. factors. Completed stroke – no change… embolic. Pathological Focal / Global Ischemic & hemorrhagic (chronic/acute) Venous infarcts. (young, infections)

20. Common Types and Incidence: Infarction: Incidence 80% - mortality 20% 50% - Thrombotic – atherosclerosis Large-vessel 30% (carotid, middle cerebral) Small vessel 20% (lacunar stroke) 30% Embolic (heart dis / atherosclerosis) Young, rapid, extensive. Venous thromboembolism (rare) Hemorrhage: Incidence 20% - mortality 80% Berry aneurysm, Microaneurysm , Atheroma. Intracerebral or subarachnoid.

21. Stroke location and incidence: Cause % Clinical presentation 30day mort(%) Pathogenesis Cerebral infarction 85 Slowly / sudden evolving signs and symptoms 15-45 Cerebral hypoperfusion Embolism Thrombosis Intracerebral hemaemorrhage 10 Sudden onset of stroke with raised intracranial pressure 80 Rupture of micro-aneurysm or arteriole Subarachnoid haemorrhage 5 Sudden headache with meningism 45 Rupture of saccular aneurysm on circle of Willis

22. Clinical Categories: Global Ischemia. Hypoxemic encephalopathy Hypotension, hypoxemia, anemia. Focal Ischemia. Obstruction to blood supply to focal area. Thrombosis, embolism or hemorrhage.

23. GLOBAL ISCHAEMIA

24. Global Ischemia: Etiology: Impaired blood supply - Lung & Heart disorders. Impaired O2 carrying – Anemia/Blood dis. Impaired O2 utilization – Cyanide poisoning. Morphology : 3rd, 5th and 6th layers of the cortex, hippocampus and in the Purkinje cells in the cerebellum Laminar necrosis, Hippocampus, Purkinje cells. Border zone infarcts – “ Watershed ” Sickle shaped band of necrosis on cortex. Clinical Features : Mild transient confusion state to Severe irreversible brain death. Flat EEG, Vegetative state. Coma.

25. Morphology in Global Ischemia Watershed zone (Acute - ACA-MCA) Laminar necrosis - (chronic- short penetrating arteries) Sommer sector of hippocampus. Purkinje cells of cerebellum.

26. Watershed/Boundary zone infarcts: Carotid thrombosis

27. Lamellar necrosis in global ischemia. Chronic

28. Local infarction: Cell death ~ 6min central infarct area or umbra , surrounded by a penumbra of ischemic tissue that may recover

29. Infarct Pathogenesis: Reduced blood supply – hypoxia/anoxia. Altered metabolism  Na/K pump block. Glutamate receptor act.  calcium influx. ischemic injury – Red neuron, vacuolation . cell death, karyorrhexis . Inflammation – edema. Macrophages - > 5d. Liquifaction cavity – >1wk Glial proliferation – >1wk. (astrocytes) Hours 1-day 3-day 1 wk. >4wk

30. Infarct Stages: Immediate – <24 hours No Change gross, micro  Na/K loss, Ca+ influx. Acute stage – < 1week Oedema , loss of grey/white matter border. Inflammation , Red neurons, necrosis, neutrophils Intermediate stage – 1- 4 weeks. Clear demarcation, soft friable tissue, cysts Macrophages, liquifactive necrosis Late stage – > 4 weeks. Removal of tissue by macrophages Fluid filled cysts with dark grey margin ( gliosis ) Gliosis – proliferation of glia at periphery.

31. FOCAL ISCHAEMIA

32. Brain Stem Stroke: Common Pattern Pure Motor - Weakness of face and limbs on one side of the body without abnormalities of higher brain function, sensation, or vision ( MCA /ACA) Pure Sensory - Decreased sensation of face and limbs on one side of the body without abnormalities of higher brain function, motor function, or vision   (PCA).

33. MCA [most common] Features: Paralysis of the contralateral face, arm and leg Sensory impairment over the contralateral face, arm & leg Homonymous hemi or quadranton opia Paralysis of gaze to the opposite side Aphasia (dominant) and dysarthria [ broca / wernicke ] Penetrating - contralateral hemiplegia/paresis, slurred speech. Impaired spatial perception

34. MCA stroke.

35. MCA stroke. Wikipedia: GNU Free Documentation license

36. MCA stroke. Wikipedia: GNU Free Documentation license

37. ACA stroke. Paralysis of contralateral foot and leg Sensory loss over toes, foot and leg Impairment of gait and stance Abulia (slowness and prolonged delays to perform acts) Flat affect , lack of spontaneity, slowness, distractibility Cognitive impairment , such as perseveration and amnesia Urinary incontinence Wikipedia: GNU Free Documentation license

38. PCA stroke. Peripheral (cortical) Homonymous hemianopia Memory deficits Perseveration Several visual deficits (cortical blindness, lack of depth perception, hallucinations) Central (penetrating) Thalamus - contralateral sensory loss , spontaneous pain, mild hemi Cerebral peduncle - CN III palsy with contralateral hemiplegia Brain stem - CN palsies, nystagmus , pupillary abnormalities Wikipedia: GNU Free Documentation license

39. Posterior Cerebral Artery Visual disturbances contralateral homonymous hemianopsia (central vision is often spared) L. Hemi: lesions alexia (with or without agraphia ) Bilateral lesions: cortical blindness patients unaware they cannot see (Anton's syndrome) Memory impairment if temporal lobe is affected ~ Proximal occlusion contralateral hemisensory loss, spontaneous pain and dysesthesia if thalamus affected (thalamic pain syndrome) contralateral severe proximal chorea (hemiballism) ~

40. Haemorrhagic - Arterial embolus Embolic stroke: sudden, pin point hemorrhages over a triangular area.

41. Infarct with Punctate hemorrhage

42. Cerebral Infarction - Late

43. Cerebral Infarction - Late

44. Hypertensive CVD Intraerebral /Subarachnoid Hemorrhage Microaneurysm hemorrhages – Basal ganglia. Putamen(60%), thalamus, ventricles. Berry aneurysm hemorrhages – subarachnoid. Chronic Hypertension : (dementia) Slit hemorrhages. Microhemorrhages heal as slit with pigment. Lacunar infarcts: Brain stem - pale infarcts. A.sclerosis Hypertensive encephalopathy-Malignant . Headache, confusion, vomiting – Raised ICP .

45. Central Pontine Hemorrhage - Herniation

46. Subarachnoid Hemorrhage:

47. Ruptured Berry Aneurism

48. Fusiform atherosclerotic aneurysm

49. Saccular(berry) Aneurysm:

50. Intracerebral Hemorrhage:

51. Lacunar Infarct in pons

52. Left (Dominant) Hemisphere Stroke: Clinical Aphasia Right hemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze Dysarthria Difficulty reading, writing, or calculating Diagnosis: Recent cerebral infarction in left MCA distribution. Left cerebral hemisphere shows swelling with compression of the lateral ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral Artery (MCA) distribution. The brain in the MCA area shows discoloration of the cortex and also blurring between the cortex and white matter. L affect R

53. Right (Non-dominant) - Hemisphere Stroke: Defect of left visual field Extinction of left-sided stimuli Left hemiparesis Left-sided sensory loss Left visual field defect Poor left conjugate gaze Dysarthria Spatial disorientation R affect L

54. CNS AV Malformations: Many types: AV Malformation * Cavernous angioma Telangiectasia Venous angioma Cause of Seizure disorders & hemorrhage. Most common congenital vascular malformation. Typically located in the outer cerebral cortex underlying white matter.

55. Pathological Review: Stroke: Ischemic / Thrombotic / Hemorrhagic Acute neurological deficit - Clinical Cerebro Vascular Accident – Pathology. Etiology: Thrombosis, Embolism, Hemorrhage. Risk factors: AS, Hypertension, Smoking. Global – Systemic Hypoxia – Watershed & lamellar infarct Focal – Basal ganglia, Putamen, Int. capsule (MCA) Pathogenesis: Infarction  Liquifaction necrosis  Cyst formation with peripheral gliosis. (loss of neural function) Hypertension & CVA: Atherosclerosis - Thrombosis Haemorrhage (Intra/subarachnoid), chronic benign: Lacunar infarcts & slit hemorrhages. Hypertensive Encephalopathy,

56. Stroke – Risk Factors Modifiable Hypertension Tobacco use Excess Alcohol Hx of TIA’s Heart Disease Diabetes Mellitus Hypercoagulopathy Pregnancy, cancer, etc. Sickle Cell and increased RBC Hx of carotid Bruit Unmodifiable Age Gender Race Previous CVA Heredity

57. Stroke – Signs and Symptoms Ischemic Carotid Circulation Unilateral paralysis (opposite side) Numbness (opposite side) Language disturbance Aphasia – difficult comprehension, nonsense, difficult reading/writing Dysarthria – slurred speech, abnormal pronunciation. Visual disturbance (opposite side) Monocular blindness (same side)

58. Stroke – Signs and Symptoms Ischemic Vertebrobasilar Circulation Vertigo Visual disturbance Both eyes simultaneously Diplopia Ocular palsy – inability to move to one side Dysconjugate gaze – asynchronous movement Paralysis Numbness Dysarthria Ataxia

59. Stroke – Signs and Symptoms Hemorrhagic Subarachnoid hemorrhage Sudden severe HA Transient LOC Nausea/Vomiting Neck pain Intolerance of noise/light AMS Intracerebral hemorrhage Focal sx w/ LOC, N/V

60. History Detailed history from relative or friend or patient if he is able to speak. Rapidity of onset – sudden onset of a focal neurological deficit. Time course of symptoms – maximum deficit over seconds or minutes before starting to improve. Headache, coma at onset and vomiting at onset are more common in haemorrhage but also occur with infarction. Sudden onset of severe generalised headache associated with neck stiffness – subarachnoid haemorrhage. Specific record should be made about the presence of vascular risk factors.

61. Examination General Examination BP – should be taken in both arms. Stroke may cause an acute rise in BP and therefore hypertension should not be diagnosed in the first few days after a stroke unless left ventricular hypertrophy of fundal changes are present . Pulse – for arrhythmias particularly atrial fibrillation. Peripheral pulses. Auscultation for a carotid bruit. Heart – for valvular heart disease especially mitral stenosis . Neck stiffness – subarachnoid haemorrhage or meningitis. Identify the anatomical localization of the lesion and record the degree of disability.

62. Oxfordshire Community Stroke Project Classification OCSP

63. Causes of ischaemic stroke

64. Causes of ischaemic stroke 2

65. Causes of ischaemic stroke 3

66. Causes of intracranial haemorrhage

67. Subarachnoid haemorrhage Initial headache or coma – sudden rise in intracranial pressure. Focal symptoms if aneurysm ruptures into underlying brain. Cerebral vasospasm causes delayed cerebral infarction 4-14 days after onset in 30% of patients. Recurrent haemorrhage and hydrocephalus are other complications.

68. Intracerebral Haemorrhage Sudden rupture of microaneurysms caused by hypertensive vascular disease. Characteristically occurs in the basal ganglia, pons and cerebellum. Elderly patients – cerebral amyloid angiopathy, a degenerative disorder affecting the walls of the artey – subcortical haematomas. Cryptic av malformations are suspect especially in younger patients < 40 yrs and when the haemotoma is Lobar (frontal, temporal, parieto-occipital).

69. Investigations Confirm the diagnosis CT Scan To establish the site, size and pathological diagnosis by showing infarction or haemorrhage. To exclude other conditions that may mimic stroke like subdural haematoma, intracranial tumour.

70. There is doubt about the diagnosis. Symptoms progress or fluctuate. Conscious level is depressed or patient is in coma. If thrombolytic therapy or anticoagulant treatment is considered. Neck stiffness is present. Has severe headache. Deteriorates unexpectedly . Haemorrhage can be seen within a few minutes as an area of increased attenuation. Infarction as a low density lesion which conforms to a vascular territory usually wedge shaped. It is not immediately visible on CT but in most patients becomes apparent in 4-7 days. Y CT Scan?

71. MRI Scan Posterior circulation strokes are more readily identified than by CT.

72. General Investigations identify conditions which may predispose towards premature cerebrovasculardisease. Full blood count – polycythemia, thrombocytopoenia. Blood glucose – diabetes mellitus. Serum lipids – hypercholesterolemia. Blood cultures – SBE.

73. General Investigations II HIV screen – AIDS. Syphilis serology – VDRL. Clotting Screen. Thrombophilia Screen – Protein C, Protein S, Antithrombin III. Anticardolipin antibodies – SLE. Lumbar Puncture – subarachnoid haemorrhage.

74. DD Stroke Differential Diagnosis of Stroke Head/Cervical trauma Meningitis/encephalitis Hypertensive encephalopathy Intracranial mass Tumor Sub/epi dural hematoma Todd’s paralysis Migraine w/ neuro sx Metabolic Hyper/hypo glycemia Post arrest ischemia Drug OD

75. Differential Diagnosis Space occupying lesion 5% of people with stroke like symptoms have a subdural haematoma, tumour or cerebral abscess. Distinction is readily made on CT or MRI. If there is any doubt repeat the scan after 6 weeks.

76. Differential Diagnosis II Multiple sclerosis May present with hemiparesis, sensory impairment or brainstem symptoms that mimic stroke. Symptoms occur gradually over a few days. Hypoglycaemia May cause hemiparesis. Migraine

77. Complications I Cerebral oedema Should be suspected in a patient with a large infarct or haemorrhage experiences a lucid interval of 24-48 hours and then shows a decline in consciousness.

78. Complication II Haemorrhagic transformation Can occur as a result of thrombolysis. Pneumonia In patients with swallowing difficulties as a result of aspiration. Pressure sores Develop rapidly and may be exacerbated because of incontinence. Oedema of Weak Limbs Is common and has a partially autonomic basis.

79. Complication III Anxiety and Depression Common reactions to stroke but depression may have an organic basis related to damage of the frontal and limbic systems. Emotional Lability Precipitated by minor emotional stimuli.

80. Management I Has the following aims Confirmation of the diagnosis, anatomical site of the lesion, pathology and aetiology . Acute care. Rehabilitation of persistent disability and handicap. Prevention of recurrence.

81. Management II Acute Care Treatment aims Prevent progression of present event. Prevent immediate complication. Prevent the development of subsequent events. To rehabilitate the patient.

82. Management III General Measures Around the edge of the infarct, ischaemic tissue is at risk, but is potentially recoverable. This must be protected by ensuring a good supply of glucose and oxygen. Maintain hydration, oxygenation and blood pressure.

83. Specific Measures Medical Treatment Anticoagulation Patient with high risk of developing deep vein thrombosis. Thromboembolic stroke - started as soon as possible, except in large infarcts where it may be wise to delay anticoagulation for 2 weeks. Stroke in a patient with myocardial infarct - due to mural thrombus. Stroke in evolution. Exclude a haemorrhage by doing a CT scan first.

84. Medical Treatment II Antiplatelet Agents Especially in TIA. Thrombolysis I/V thrombolysis espcially recombinant tissue plasminogen activator rTPA to be given only within the first 3 hours after onset to those patients who have not developed CT abnormalities especially in patients with basilar artery occlusion. Risk – haemorrhage.

85. Hypertension Treated cautiously in acute stroke. A reduction in blood pressure may lower cerebral blood flow in the regions surrounding the infarct below a critical level at which further ischaemic brain damage will occur. Mild to moderate elevations in BP – no treatment unless they are maintained for several days after admission.

86. If stroke associated with hypertensive encephalopathy or if diastolic BP is persistently above 120 mm Hg. The BP should be lowered cautiously using oral agents. Sudden precipitious fall in BP should be avoided. Hypertension II

87. Medical Treatment Calcium Antagonist Nimodipine prevents ischaemic brain damage and reduces the number of patients remaining disabled after subarachnoid haemorrhage . Prescribed as soon as diagnosis is made (within 12 hours).

88. Neurosurgery Should be considered in subaracnoid and intracerebral haemorrhage. Evacuation of cerebellar haematoma. Evacuation of supratentorial haematomas should only be considered in younger patients with superficial cortical haematomas causing mass effect with a deteriorating level of conciousness.

89. Nursing Care and Rehabilitation Physiotherapy, proper positioning and early mobilization – prevent pressure sores. Support stockings – prevent deep vein thrombosis and pulmonary embolism. Swallowing difficulties. Lead to silent aspiration – aspiration pneuomonia. Nasogastric tube feeding. Percutanious endoscopic gastrostomy.

90. Rehabilitation Physiotherapy, occupational therapy, speech therapy and psychology input – multidisciplinary stroke rehabilitation team. Home visit by occupational therapist to plan adaptations to home before discharge.

91. Secondary Preventation Control hypertension and diabetes mellitus. Correct lipid abnormality. Stop cigarette smoking. Stop thrombogenic drugs e.g. oral contraceptives.

92. Give platlet antiaggregation drugs to reduce the rate of reinfarction. Low dose aspirin (75 mg – 150 mg), if patient allergic or has gastrointestinal side effects give ticlopidine. Regular blood tests because of a small risk of neutropoenia. Remove or treat embolic source (long term anticoagulation in atrial fibrillation). Treat inflammatory or vascular inflammatory diseases. Secondary Preventation II

93. Carotid Endarterectomy – preventing stroke in symptomatic patients with recent TIA and stroke and severe stenosis of the internal carotid artery (at least 70%). Secondary Preventation III

94. Chain of Survival Stroke Stroke Chain of Survival Detection Early sx recognition Dispatch Prompt EMS response Delivery Transport, approp, prehospital care, prearrival notification Door ER Triage Data ER evaluation incl, CT, etc. Decision Appropriate therapies Drug/Therapy

95. Detect & Dispatch Detection: Early Recognition Public education of Stroke sx Early access to medical care Dispatch: Early EMS and PDI’s Caller triage EMD recognition of Stroke sx

96. How to detect? Delivery: Pre-hospital Transport and Management How we scale the pre-hospital management of the patient?

97. CINCINNATI STROKE SCALE

98. CINCINNATI STROKE SCALE Identifies patients with strokes. It evaluates three major physical findings. Facial droop Motor arm weakness Speech abnormalities

99. CSS - Facial Droop Have the patient show their teeth or smile. Normal – both sides of the face move equally well Abnormal – one side of the face does not move as well as the other side

100. Arm Drift Have the patient close his/her eyes and hold both arms out. Normal – both arms move the same way, or both arms do not move at all. Abnormal – one arm does not move or one arm drifts down compared to the other arm. Other findings such as pronator grip, may be helpful

101. Speech Have the patient say “You can’t teach an old dog new tricks .” – “ Perlambagaan Malaysia” Normal – patient uses correct words with no slurring. Abnormal – patient slurs words, uses inappropriate words, or is unable to speak

102. “You can’t teach an old dog new tricks.”

103. Cincinnati Prehospital Stroke Scale Patients with 1 of these 3 findings - as a new event - have a 72% probability of an ischemic stroke. If all 3 findings are present the probability of an acute stroke is more than 85% Immediately contact medical control and the destination ED and provide prearrival notification.

104. Stroke – Management In Review: Prehospital Critical Actions Assess and support cardiorespiratory function Assess and support blood glucose Assess and support oxygenation and ventilation Assess neurologic function Determine precise time of symptom onset Determine essential medical information Provide rapid emergent transport to ED Notify ED that a possible stroke patient is en route

105. Stroke - Management Door: ER Triage Stroke evaluation targets for stroke patients who are thrombolytic candidates Door-to–doctor first sees patient …….………… 10 min Door-to–CT completed …….………………….. 25 min Door-to–CT read ...…………..………………… 45 min Door-to–fibrinolytic therapy starts …………….. 60 min Neurologic expertise available* …..…………… 15 min Neurosurgical expertise available* …………… 2 hours Admitted to monitored bed ..……...…………… 3 hours *By phone or in person

106. Stroke - Management Data: ER Evaluation and Management Assessment Goal : in first 10 minutes Assess ABCs, vital signs Provide oxygen by nasal cannula Obtain IV access; obtain blood samples (CBC, ’lytes, coagulation studies) Obtain 12-lead ECG, check rhythm, place on monitor Check blood sugar; treat if indicated Alert Stroke Team: neurologist, radiologist, CT technician Perform general neurologic screening assessment

107. Stroke - Management Assessment Goal : in first 25 minutes Review patient history Establish symptom onset (<6 hours required for fibrinolytics) Perform physical examination Perform neurologic exam Determine level of consciousness (Glasgow Coma Scale) Determine level of stroke severity (NIHSS or Hunt and Hess Scale) Order urgent non-contrast CT scan/angiogram if non-hemorrhage (door-to–CT scan performed: goal <25 min from arrival) Read CT scan (door-to–CT read: goal <45 min from arrival) Perform lateral cervical spine x-ray (if patient comatose/trauma history)

108. Stroke - Management ER Diagnostic Studies CT scan – done w/in 25 mins, read w/in 45 mins r/o hemorrhage Often normal early in ischemic stroke Lumbar puncture EKG Changes may be caused by or cause of stroke MRA (Magnetic Resonance Angiography) Cerebral Angiography

109. Hypodense area: Ischemic area with edema, swelling Indicates >3 hours old No fibrinolytics !

110. (White areas indicate hyperdensity = blood) Large left frontal intracerebral hemorrhage. I ntraventricular bleeding is also present No fibrinolytics !

111. Acute subarachnoid hemorrhage Diffuse areas of white ( hyperdense ) images Blood visible in ventricles and multiple areas on surface of brain

112. Stroke - Management Decision: Specific Therapies General Care ABC’s, O 2 IV w/ BSS Treat hypotension Avoid over-hydration Monitor input/output Normalize BGL Manage Elevated BP?

113. Stroke - Management Indications for Antihypertensive therapy In general : Consider: absolute level of BP? If BP: >185/>110 mm Hg = fibrinolytic therapy contraindicated Consider: other than BP, is patient candidate for fibrinolytics? If patient is candidate for fibrinolytics: treat initial BP >185/>110 mm Hg Consider: response to initial efforts to lower BP in ED? If treatment brings BP down to <185/110 mm Hg: give fibrinolytics Consider: ischemic vs hemorrhagic stroke? Treat BP in the 180-230/110-140 mm Hg range the same The obvious: no fibrinolytics for hemorrhagic stroke

114. Stroke - Management Decision: Specific Therapies (cont.) Management of Seizures Benzodiazepines Long-acting anticonvulsants Management of Increased ICP Maintain PaCO 2 30mm Hg Mannitol/Diuretics Barbiturates Neurosurgical decompression

115. Stroke - Management Drugs: Thrombolytic Therapy Fibrinolytic Therapy Checklist Ischemic Stroke Candidates for Neurointerventional Therapy  Age 18 years or older  Acute signs and symptoms of CVA <6 hours onset.  No contraindications.

116. Stroke - Management Contraindications for Interventional Therapy Absolute  Evidence of intracranial hemorrhage on non-contrast head CT  Patient with early infarct signs on CT scan. Relative  Recent (w/in 2 mo’s) cranial or spinal surgery, trauma, or injury  Known bleeding disorder and/or risk of bleeding including: - Current anticoagulant therapy, prothrombin time >15 sec. - Heparin within 48 hrs of admission, PTT elevated - Platelet count <100,000/mm  Active internal bleeding w/in the previous 10 days  Known or suspected pregnancy  History of stroke w/in past 6 weeks

117. Stroke - Management Contraindications for Interventional Therapy (cont.) Relative  Patient comatose  >85 years old  Diabetic hemorrhagic retinopathy or other opthalmic hemorrhagic disorder  Advanced liver or kidney disease  Other pathology with a propensity for bleeding  Infectiouse endocarditis  Severe EKG disturbance, uncontrolled angina or acute MI

118. Stroke - Management Thrombolytic Agents TPA NINDS trial Streptokinase VEGGIE trial Anticoagulant Therapy Heparin ASA/Warfarin/Ticlodipine

119. Stroke - Management Management of Hemorrhagic Stroke Subarachnoid Neurosurgical intervention Nimodipine Intracerebral Management of ICP Neurosurgical decompression Cerebellar Surgical evacuation Often associated with good outcome Lobar Surgical evacuation

120. 141

121. THE END

122. If they come to you with stroke, what investigation what you like to do?

123. QUIZ ON STROKE MOHD HANAFI RAMLEE

124. ANSWER GILIR2 TAU

125. QUESTION 1 On the history of a patient with suspected or known stroke, what should you ask about?

126. ANSWER 1 Ask about the presenting symptoms of stroke initially, for example Unilateral weakness or clumsiness Difficulty understanding or expressing spoken language Altered sensation unilaterally Partial or complete loss of vision in one eye

127. ANSWER 1 Questions to focus on the causes of stroke Atherosclerosis, e.g. enquire about vascular risk factors (smoking, DM, hyperlipids , PVDs, etc…) History of heart disease, e.g. recent myocardial infarction, history of AF requiring anticoagulation, palpitations History of hypertension (lacunar infarcts due to arteriosclerosis of small penetrating arteries of the brain) Migraine Manipulation of neck (precipitating cause for dissection of carotid artery or vertebral artery) Any recent cessation of anticoagulation Family history of stroke History of connective tissue disease (e.g. SLE, vasculitis , etc …)

128. ANSWER 1 History of connective tissue disease (e.g. SLE, vasculitis , etc…) Medication history, esp. those that increase risk of stroke include oral contraceptives, some antihypertensives Ask about alcohol consumption and recent falls (may have caused an intracranial haemorrhage) Enquire about premorbid as well as the current level of independence and mobility If patient is incapacitated, ask about social support available at home Don’t forget to screen for depression

129. QUESTION 2 On examination, what features should you be looking for?

130. ANSWER 2 A complete examination of the neurological and cardiovascular systems is essential Check the fundi for evidence of emboli, hypertensive changes, diabetic changes and ischaemic neuropathy Test the visual fields for homonymous hemianopia Listen for bruit over the carotids and orbits (commonly heard in the side opposite the carotid occlusion, due to increased contralateral flow) Decide whether patient is in AF Assess BP and test for postural drop Listen for murmurs (e.g. AS, infective endocarditis, rheumatic heart disease or prosthetic valve) Note presence of electronic pace maker and assess whether it’s working Perform peripheral vascular examination Look for complications, e.g. pressure sores, limb contractures and disuse atrophy of the paralysed limbs See if patient has a percutaneous gastrostomy (PEG) feeding tube inserted and, if present, inspect for cellulitis or pus around the insertion site

131. QUESTION 3 What clinical features are suggestive of a carotid arterial stroke?

132. ANSWER 3 Transient aphasia Ipsilateral amaurosis fugax Contralateral hemiplegia/ monoplegia Contralateral hemi or monoparesis Carotid bruits ( a/w >50% stenosis)

133. QUESTION 4 What clinical features are suggestive of vertebrobasilar insufficiency?

134. ANSWER 4 All the Ds Dizziness (vertigo and ataxia) Diplopia +/- blindness Dysphagia Dysarthria ‘Demi-anaesthesia’ – ipsilateral face, contralateral limb Quadraparesis – indicates basilar artery involvement  

135. QUESTION 5 What clinical features are suggestive of a middle cerebral artery stroke?

136. ANSWER 5 Contralateral hemiplegia, hemiparesis, homonymous hemianopia UMN face, arm > leg, eyes deviated to side of lesion Aphasia (if dominant lobe) Expressive dysphasia, arm + leg involvement – anterior MCA Receptive dysphasia, visual fields defects – posterior MCA If non-dominant – speech + comprehension intact

137. QUESTION 6 What clinical features are suggestive of a posterior cerebral artery stroke?

138. ANSWER 6 Homonymous hemianopia (complete) Cortical blindness Hemisensory loss Ipsilateral III nerve palsy

139. QUESTION 7 What clinical features are suggestive of an anterior cerebral artery stroke?

140. ANSWER 7 Contralateral monoplegia (UMN) Confusion, behaviour disturbance Grasp reflex Urinary incontinence

141. QUESTION 8 What clinical features are suggestive of a lacunar syndrome?

142. ANSWER 8 Clumsy hand/dysarthria syndrome – lesion in mid pons Leg paresis + ataxia – pons or internal capsule Pure sensory stroke – usually thalamic Pure motor stroke (arm>leg) - pons or internal capsule

143. QUESTION 9 What investigations would you perform in a stroke patient ? – MAINLY TO DIAGNOSE ANY STROKE….

144. ANSWER 9 CT or MRI of the head, looking for ischaemic infarcts, haemorrhage, or mass lesions

145. QUESTION 10 What investigations would you perform in a stroke patient ? MAINLY TO FIND THE CAUSE OF STROKE

146. ANSWER 10 Doppler scan of the carotid arteries – if duplex scan suggest significant carotid stenosis, esp. in patients <75, ask for results of carotid angiography, carotid digital substraction angiography or MR angiography If patient is in AF, ask for results of transoesophageal echo, looking for thrombus or spontaneous atheromatous plaques in ascending aorta and arch of aorta that may have contributed to stroke ECG for AMI and AF FBE, looking at Hb (to exclude polycythemia ) and platelet count (rarely, essential thrombocytopenia can contribute to stroke) ESR (to exclude an inflammatory arteritic / vasculitic process CXR (for cardiomegaly/neoplasm) Urea, creatinine and electrolytes

147. QUESTION 11 What investigations would you perform in a stroke patient? MAINLY IN YOUNGER PATIENT?

148. QUESTION 11 Drug screen, looking for narcotic agents Vasculitic screen (if there are features of vasculitis ) Blood cultures and cardiac imaging if endocarditis is suspected Cardiac event monitor looking for paroxysmal AF and Thrombophilic screen

149. What 3 specific strategies in the management of acute stroke that have been proven to improve outcomes ? The 3 main strategies are Administration of iv tissue plasminogen activator ( tPA ) within 3hrs of stroke onset Giving aspirin (100mg) within first 48hrs of ischaemic stroke Managing patient in a stroke unit Note that tPA and aspirin are never given before brain imaging to exclude intracranial haemorrhage

150. What are the strategies for secondary prevention of stroke ? There are now at least 4 early strategies for secondary prevention in improving long term outcomes after TIAs or stoke Antiplatelet therapy, e.g. aspirin, clopidogrel , aspirin with dipyridamole Blood pressure lowering Warfarin (indicated for patients with AF) Carotid endarterectomy (indicated when stenosis >70%) Lipids lowering is the fifth strategy to consider

151. A patient just had a stroke, what criteria do you look for to select this patient for rehab. Patients must be medically stable (i.e. no aspiration pneumonia, AMI, DVT, etc…) They have a functional disability They have the intellectual capability to learn There are defined goals to be achieved There are non or minimal co-morbidities, e.g. recurrent stroke, AMI, COAD, etc… They are not clinically depressed (this can affect motivation to rehabilitate) They didn’t suffer from a dense stroke or ones that causes hemi-neglect (e.g. a right hemisphere stroke)

152. What are some of the common predictors of poor functional outcome after a stroke ? A dense stroke, a recurrent stroke, or a stroke resulting in hemi-neglect Impairment of bladder and bowel function Depression or cognitive deficits Delayed acute medical care or delayed rehabilitation Co-morbidities and poor social support