Stroke epidemiology

By: Dr. Michael B. Fawale

1. Epidemiology and Aetiology of Stroke Dr Michael B. Fawale Medicine Department, OAU , Ile-Ife [email protected]

2. Stroke remains a leading cause of death and long-term disability worldwide Global estimates suggest sub-Saharan Africa has the highest incidence, prevalence & case fatality Low-income and middle-income countries in Africa have scant resources for acute stroke care and rehabilitation Background

3. Background Stroke is associated with greater loss of productivity and wage-earning years in the younger age group While health systems strengthening is critical, prevention remains the most plausible strategy

4. Concepts & definitions Types & Subtypes Epidemiology Risk factors Clinical features Stroke Mimics Outline

5. Cerebrovascular Disease (CVD) Designates any abnormality of the brain resulting from a pathologic process of the blood vessels Includes CVA (Stroke); TIA ; cerebral angioma ; Subdural hematoma, Aneurysms; Vascular malformations; Small vessel disease (arteriosclerosis); Cerebral Amyloid angiopathy ; Cerebral Angitis ; Fibromuscular dysplasia; Moyamoya disease Concepts & Definitions

6. Stroke (Lay definition): Sudden loss of brain function due to sudden sustained interruption of blood flow and oxygen supply. This interruption may be due to an occlusion (Ischemic stroke) or rupture (Hemorrhagic stroke) of a vessel. Concepts & Definitions

7. Acute reduction or cessation of cerebral blood flow T emporary Sustained TIA CI Concepts & Definitions TIA Transient ischaemic attack, CI Cerebral infarct

8. The definitions of stroke and TIA are evolving Old Concepts: TIA: Any focal cerebral ischemic event with symptoms lasting < 24 hours Stroke: A rapidly developed focal/global cerebral dysfunction of vascular origin lasting >24 hrs or leading to death - (WHO 1988) Included in this definition are CI, ICH, SAH . Concepts & Definitions

9. Old Concepts: Misclassifies up to 1/3 of patients Most (90%) TIAs last 10 mins ; resolve in 30 mins . If symptoms last > I hr, chances of resolution:15% Can impede administration of acute stroke therapies Does not suggest medical emergency Does not take into cognizance the use of thrombolytics within 270 mins (4 ½ hrs) in CI or Recombinant activated factor VII within 4 hours in ICH Concepts & Definitions

10. New Concepts: TIA: focal brain or retinal ischemia, with clinical symptoms typically lasting < 1 hour, and without evidence of acute infarction Stroke Time-based - > 1 hr Tissue based – sudden global or focal neurological dysfunction resulting from spontaneous haemorrhage or infarction of the CNS, irrespective of the duration of the symptoms Concepts & Definitions

11. Stroke

12. Stroke Types & Subtypes

13. Stroke Types & Subtypes

14. Cardiogenic Arteroembolic Paradoxic embolism Ischemic Stroke Subtypes

15. Stroke - Epidemiology

16. The most common cause of adult disability . 2 nd most common cause of dementia.  2 nd leading cause of death in LIC, MIC, HIC . If no urgent action, deaths from stroke will increase over the next decade by: 12 % globally 20 % in resource-limited countries. Stroke impairs QOL, constitutes huge economic cost and burden to caregivers, family and society. The global burden of stroke

17. Incidence: 100-300/100,000 in most countries 15 million cases annually (2/3 in developing world) 5.5 million deaths yearly, 5 million disabled, 5 million recover Stroke incidence over the past 4 decades 42% ↓ in High Income Countries and 100%↑ in Low/Middle Income Countries. Stroke the leading cause of neurological admission in most centers in Nigeria Prevalence : Nigeria: 58-114 (West: 400-700)/100,000 The global burden of stroke

18. USA: 30 day stroke mortality - 28% CI - 19%, ICH-30-50%, SAH-45% 1-year survival (Ischemic Stroke) - 77% Nigeria: 30 day stroke mortality – 36.1–60.4% ( *1 in 6 people will have a stroke in their lifetime *6 million deaths yearly *Every 6 seconds, someone somewhere dies from stroke) Profile of Stroke Mortality

19. Global Deaths by Causes - WHO 2011

20. 20 Source: WHO 2005 Projected Global Deaths by Causes (All ages)

21. “We cannot afford to say, ’we must tackle other diseases first -HIV/AIDS, malaria, TB- then we will deal with chronic diseases later -Stroke, heart disease and cancers ’. If we wait even ten years, we will find that the problem is even larger and more expensive to address.” -President Olusegun Obasanjo (foreword to a 2005 WHO publication on Preventing CHRONIC DISEASES: a vital investment) 21

22. Exercise Answer T or F Ischaemic stroke is more common than haemorrhagic stroke Thrombotic and embolic strokes are sugtypes of haemorrhagic stroke Stroke is the leading cause of adult disability globally Deaths due to stroke are more than deaths due to malaria, HIV and TB combined Stroke incidence is declining in high-income countries and rising in resource-limited countries

23. Stroke - Risk Factors

24. Stroke Risk Factors Risk factors = attributes or exposures associated with increased probability of disease but are not necessarily causal They directly increase disease probability and if absent or removed reduce disease probability Stroke risk factors Non-modifiable Modifiable Well-documented Less well-documented

25. Non-modifiable risk factors Age: The risk of stroke increases with age Stroke risk increased by 9%/y in men and 10%/y in women (Data from 8 European countries) The risk of ischemic stroke and ICH doubles for each successive decade after age 55

26. Non-modifiable risk factors Age The mean age at stroke occurrence is decreasing In the SIREN study, 39% of ICH and 16% of CI were > 65 yrs Although the younger age groups are at lower stroke risk, the public health burden is higher - relatively greater loss of productivity and wage-earning years

27. Non-modifiable risk factors Sex: generally, M>F Race : Blacks 38% > whites Family history of stroke increases risk by ~ 30% Father x 2.4, mother x 1.4 Low birth weight The odds of stroke in 2500 g > 2 x that of 4000 g

28. Modifiable risk factors Hypertension Remains the most important well-documented, modifiable risk factor for stroke The relationship between BP and stroke risk is strong, continuous, graded, consistent, independent, predictive, and etiologically significant Even within normal limits, higher BP confers higher stroke risk The risk of stroke begins at 115/75mmHg & doubles with each increment of 20/10mmHg

29. Modifiable risk factors Hypertension Stroke Investigative Research and Education Network (SIREN) Study Prevalence of hypertension in stroke: Indigenous Africans – 92.8% African Americans – 82.4% European Americans – 62.0% Stroke had an OR & PAR of 19·36 and 90·8% for hypertension

30. Hypertension and Stroke Rodgers et al, BMJ 1996

31. Hypertension and Stroke Mensah G. Epidemiology of stroke and high blood pressure in Africa, BMJ 2008

32. Blood Pressure Classification 2017 AHA/ACC Classification of Blood Pressure

33. Blood Pressure Classification 2018 ESC/ESH Guidelines for the management of arterial hypertension

34. Hypertension and Cardiovascular Risk The overall global prevalence of hypertension (HT) in adults is ~ 30 - 45 % HT becomes progressively more common with advancing age, with a prevalence of >60% in people aged >60 years As populations age, adopt more sedentary lifestyles , and increase their body weight, the prevalence of HT will continue to rise.

35. Hypertension and Cardiovascular Risk It is estimated that the number of people with HT will increase by 15–20% by 2025, reaching close to 1.5 billion SBP ≥ 140 mmHg accounts for most of the mortality and disability burden (70 %) globally T he largest number of SBP-related deaths/year are due to ischaemic heart disease, haemorrhagic stroke and ischaemic stroke HT has continuous and independent association with myocardial infarction, stroke, sudden death , heart failure, peripheral artery disease & end-stage renal disease.

36. Modifiable risk factors Smoking Has a strong graded linear association with all strokes RR – 1.9 for CI, 2.9 for SAH Smoking + OCP use (RR=7.2) Stroke risks: 18% current smokers 6% former smokers 12% environmental tobacco smoke exposure -Bonita,1999; Kurth , 2003 Contributes to 12% to 14% of all stroke deaths

37. Modifiable risk factors Diabetes I ndependently increases the risk of ischemic stroke (RR = 1.8-6) Prevalence of self-reported stroke - 9% among persons with diabetes ≥ 35 years Dyslipidemia 25% increase in ischemic stroke rates for every 1 mmol /L (38.7 mg/ dL ) increase in total cholesterol High total (RR- 1.5, low HDL-2.0) Inverse relationship with hemorrhagic stroke

38. Modifiable risk factors Diet/nutrition

39. Modifiable risk factors Diet/nutrition Salt High dietary sodium and low potassium increase the risk of stroke Na intake > 2300 mg, K intake < 4700 mg Vegetables , Fruits & Fish An inverse dose-relationship between intake of fruits, vegetables & boiled or baked fish and stroke occurrence

40. Modifiable risk factors Physical Inactivity Poor exercise and sedentary lifestyle increase the risk of ischemic stroke - ( Kurth et al., 2005). Physically active men and women generally have a 25% to 30% lower stroke or death risk

41. Modifiable risk factors Obesity and Body Fat Distribution Increased adiposity is associated with increased risk of stroke. There is a progressive, direct, dose-response relationship above 25 kg/m 2 between BMI and stroke mortality The risk of stroke increases by 1.04 per unit increase in BMI

42. Measures of Adiposity BMI (kg/m 2 ) Risk of Disease <18.5 Underweight 18.5–24.9 Healthy weight 25.0–29.9 Overweight Increased 30.0–34.9 Obesity High 35.0–39.9 Obesity Very high ≥ 40 Extreme Obesity Extremely high Sex Waist Circumference Men >94 cm (37 in) Women >80 cm (31.5 in)

43. Modifiable risk factors Sickle cell disease (RR = 200–400) Prevalence of stroke by age 20 is at least 11% Majority occur in homozygous SCD A substantial number have “silent” strokes on brain MRI The highest stroke rates occur in early childhood (1%/year) Patients with Transcranial Doppler (TCD) evidence of high cerebral blood flow velocities (time-averaged mean velocity 200 cm/s) have a stroke rate of 10% per year

44. Modifiable risk factors Past history of stroke/TIA Atrial fibrillation is associated with a 4-5-fold increased risk of ischemic stroke due to embolism of stasis-induced thrombi forming in the left atrial appendage Asymptomatic carotid stenosis (RR = 2.0) Oral Contraceptive use: (RR = 2.3) Postmenopausal hormone therapy (RR = 1.4)

45. D ata obtained from Nigerian and Ghana indicate that 98.2 % (95% CI 97.2–99.0) of adjusted PAR of stroke was associated with 11 potentially modifiable risk factors The Lancet Global Health . 6(4): e436-e446.

46. Risk Factor Odds Ratio (OR) Population Attributable Ratio (PAR) Hypertension 19·36 90·8% Dyslipidaemia 1・85 35・8% Regular meat consumption 1・59 31・1% Elevated waist-to-hip ratio 1・48 26・5% Diabetes 2 ・ 58 22 ・ 1% Low green leafy vegetable consumption 2・43 18・2% Stress (psychosocial) 1・89 11・6% Added salt at the table 2・14 5・3% Cardiac disease 1・65 4・3% Physical inactivity 2・13 2・4% Current cigarette smoking 4・42 2・3% The Lancet Global Health . 6(4): e436-e446.

47. Less Well-Documented Risk Factors Migraine with aura Metabolic syndrome Alcohol consumption Drug abuse Sleep-Disordered Breathing Hyper- homocysteinemia High Lipoprotein(a) Hypercoagulability Inflammatory processes Periodontal disease Infections HIV/AIDS Psychosocial stress

48. Other Risk Factors for ICH Hemorrhagic transformation of CI Amyloid angiopathy Metastatic brain tumor Coagulopathy Drugs - Cocaine, amphetamine Arteriovenous malformation Aneurysms

49. New Risk Factors MELAS: Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like episodes CADACIL: Cerebral Autosomal Dominant Arteropathy with Subcortical Infarcts and Leucoencephalopathy Chromosome 19q13. mutated gene – Notch 3 gene

50. Risk Factors for SAH Saccular aneurysm AVM Mycotic aneurysm: 2-3% of aneu . rupture Intracranial arterial dissection Coagulation disorders Benign perimesencephalic SAH Drugs - cocaine and amphetamine Brain neoplasm- 1 & 2 , SCD Pituitary apoplexy, Vasculitis Cortical thrombosis, Angioma Click

51. Risk Factors for Aneurysmal Rupture Hypertension Cigarette smoking Excessive alcohol consumption SAH in a first degree relative. Past history

52. Exercise The following are modifiable risk factors for stroke except Hypertension Sickle cell disease Asymptomatic carotid disease Atrial fibrillation Low birth weight

53. Exercise Answer T or F > 90% of stroke risk is modifiable Hypertension is the most important modifiable risk factor for stroke Up to 1/3 of the world’s adult population has hypertension As populations age, adopt more sedentary lifestyles, and increase their body weight, the prevalence of HT will continue to rise

54. Clinical Features

55. Whanganui District Health Board supports new FAST stroke awareness campaign

56. SUDDEN!

57. The neurologic deficits of stroke reflect the area of the brain typically involved Frontal Lobe Reasoning, planning, problem solving speech, movement, emotions, Parietal Lobe Sensation, orientation, recognition Occipital Lobe vision Temporal Lobe Hearing, memory, understanding. Cerebellum Coordination of movement, balance Brain stem reathing, heartbeat, & blood pressure

58. Common Clinical Features of CI & ICH Abrupt-onset of Hemi, mono, quadri -paresis Hemisensory deficits Monocular or binocular visual loss Visual field deficits Diplopia Dysarthria Ataxia Vertigo Aphasia Altered level of consciousness They are more likely to occur in combination

59. Common Clinical Features Raised ICP Nausea Vomiting Headache Altered level of consciousness Seizures More common with ICH and large CI Neckache/neck stiffness – ventricular extension of an ICH or SAH Not enough to distinguish ischemic from hemorrhagic

60. Ischemic v s Hemorrhagic Clinical Variables Activity at onset Hemiparesis Hemisensory symptoms Headache Vomiting Loss of consciousness Time to maximum disability Changes in deficit after maximum disability

61. Ischemic vs Hemorrhagic

62. Temporal profiles Embolic Stroke abrupt in onset, with more rapid resolution tend to cause smaller deficits than a thrombotic stroke Thrombotic Strokes – may demonstrate gradual, stuttering, or stepwise evolution 1/3-1/2 may be preceded by TIA Hemorrhagic Strokes (ICH & SAH) devastating events of abrupt onset accompanied by a significant headache and other signs of raised ICP

63. Clinical Features of SAH Asymptomatic –> sudden death Headache Severe, sudden onset "thunderclap headache" Sentinel headache: 50-60%, lasts days – 1wk Hours - months, median - 2 wks, b/f rupture. Meningism > 75% of SAH many take several hours to develop. Nausea / Vomiting : ICP

64. Clinical Features of SAH LOC: From sudden rise in ICP Transient/persistent – 50% at onset. Seizures: ICP / cortical irritation – 20-25% Occurs close to onset Focal neurological deficits: 10-15%, may antedate rupture, Reflect mass effect of an., ICH, SDH, large SA clot, vasospasm, CI –intraaneurysmal thrombi.

65. Thank you

66. Emergency Evaluation & Management

67. Aims of Management Rx underlying disease process if possible Protect ischemic brain tissue from necrosis attempt to reverse/limit the degree of brain dysfunction Prevent and treat complications Rehabilitate the disabled patient physio / occupational/speech/swallow therapy Prevent recurrence (Cardiovascular risk modification)

68. Comprehensive Stroke Care Acute management Secondary prevention Early mobilization Rehabilitation Nursing care Speech therapy ( lagopaedics ) Swallow therapy

69. Phases of Contemporary Stroke Management Phase Period from onset Activities Prefered location 1Acute ( emmergency ) care 1 st -7 th day a)Assessment b)Early supportive care Hospital 2 Early sub-acute(supportive) care 2 nd -4 th week a)prevention and treatment of complications Hospital 3 Late sub-acute(maintanance) care 2 nd -6 th month a)Rehabilitation b)Psychological support c)Prevent recurrence Hospital/Community 4.Long-term (chronic) care 7 th month onwards a)Rehabilitation b)Psychological support c)Social support d)Prevent recurrence Community

70. Highlights of Acute Stroke Management Organized protocol Acute stroke team Oral ASA within 24-48 hrs of stroke onset 1 st dose 325mg Long term anticoagulation for patients in AF (INR of 2-3); or other high risk cardiac conditions Prophylactic anticoagulation: only to prevent DVT. BP management principle; lower by 15% if DBP>120,SBP>220 Early mobilization and rehab. Treat blood glucose >140mg/dl Thrombolytic: IV or IA recombinant Tissue Plasminogen Activator Carotid endarterectomy Treat co-morbidity

71. Emergency Evaluation History Take a brief History Generally, History tells you what it is, examination tells you where it is. A history of sudden onset neurological deficit is suggestive Quick, Targeted Physical Examination Corroborative, acaization, severity General, systemic, neurologic (+ GCS)

72. Time is Brain! If history is suggestive, ACT FAST Every minute counts, time lost is brain lost! There are ~200 billion neurons in the brain The brain ages by 3.6 years per hour of hypoxia Lost with each hour of stroke (per minute) 120 million neurons (1.9 m neurons) 830 billion synapses (14 billion synapses) 714 kilometers of myelinated fibres (12 km fibres )

73. Time is Brain!

74. Time is Brain!

75. Time is Neuron! Normal Cerebral Blood Flow = 55ml/100g/min <25ml – diffuse EEG slowing <15ml – electrical activity ceases Function ceases ( Penumbra ) “functionally impaired but structurally still viable tissue” “at risk but still salvageable” <10ml - irreversible Cell death ensue ( Umbra )

76. Management

77. Management Admit every patients with a Diagnosis of acute stroke Use of comprehensive specialized stroke care (stroke units) improves outcome Standardized stroke care order improves outcome The goal of management is to stabilize the patient and to complete initial evaluation and assessment, including imaging and laboratory studies, within 60 minutes of patient arrival

78. Management Step 1: Immediate General Assessment (<10 minutes) ABC Management Full vital signs including pulse oxymetry Deliver O 2 by nasal cannula if SAO2 < 92%, keep >92% Utility of hyperbaric oxygen is not established Obtain Intravenous Access Bedside Random Plasma Glucose Avoid urethral catheterization if no obstruction

79. Supplemental Oxygen Hypoxia (oxygen saturation <96% for >5 minutes) occurred in 63% within 48 hours of stroke onset Common causes of hypoxia partial airway obstruction, hypoventilation, aspiration, atelectasis , and pneumonia. Deliver O 2 by nasal cannula if SAO 2 < 94%, maintain SAO 2 >94% Utility of hyperbaric oxygen is not established

80. Patient Positioning ICP-Volume Curve

81. Patient Positioning 15° to 30° head-up if suspected elevated ICP, at risk for airway obstruction or aspiration When position is altered, close monitoring of the airway, oxygenation, and neurological status Nurse lying flat if non-hypoxic and able to tolerate

82. IV Fluid Management Volume: Euvolemic patients: maintenance IVF (apart from unusual losses) - 30 mL per kg body weight. Hypovolemic patients: Rapid fluid replacement, then maintenance Type: 0.9% saline Avoid hypotonic solutions – 5%DW etc

83. Management Labs to obtain in all patients ECG FBC, ESR E, U, Cr Lipid profile PT, PTTK, platelets Labs in selected patients Liver Function Tests Urine toxicology screen Blood Alcohol level Pregnancy Test Arterial Blood Gas Chest Xray - altered mx in only 3.8% of patients Step 1: Immediate General Assessment (<10 minutes)

84. Management Step 2: Immediate Neurologic Assessment (<25 minutes) Obtain history Determine onset of CVA symptoms Consider Thrombolytics within 3 hours of onset General physical examination Targeted neurologic examination Level of Consciousness (Glascow Coma Scale) Carotid bruit, CVS.

85. Emergency Evaluation & Treatment CVS Irregular pulse Feeble pulse 3 rd heart sound Chest Crepitations Calves Differential warmth, tenderness & swelling Skin stigmata of coagulopathies signs of trauma embolic lesions Janeway lesions Osler nodes Step 2: Immediate Neurologic Assessment (<25 minutes)

86. Management Step 3: Rule-out Hemorrhagic Stroke Imaging Urgent non-contrast Brain CT (<25 minutes) CT preferred over MRI - Fiebach (2004) Stroke 35(2): 502-6 CT read by radiologist (<45 minutes) Lateral Neck XRay – if trauma A negative CT suggests Ischemic stroke Consider Thrombolytic Therapy

87. Brain Computerized Tomography CI ICH SAH

88. Common sites of ICH

89. back

90. X-ray CT T2WI DWI PWI PET-CBF right left Multimodal Imaging Comparison of various imaging findings in a patient with right side focal signs

91. Question A 59-year-old woman with hypertension presents with sudden left-sided weakness What is the most obvious abnormality? List 4 other possible clinical features What is the Diagnosis?

92. Question Cranial CT of a 65 year old farmer What is the most obvious abnormality? List 5 risk factors What is the arterial territory involved?

93. Question Which of the following may be found on examination of this patient? Dysdiadokokinesia on the right Right hemichorea Past-pointing on the left Hypertonia on the left Intension tremor on the right A 62-year-old known hypertensive with a history of acute-onset ataxia and confusion

94. Ischaemic Stroke Management Step 4: Thrombolytic Therapy (if indicated in CI) Review Thrombolytic Contraindications Review risks and benefits of Thrombolytic therapy Review indications for Thrombolytic therapy IV < 3-4.5 hours, IA < 6hours The rate of thrombolytic therapy was < 6% in the US in 2009!

95. Management Step 4: Specific Medical Treatment of ICH Activated Factor VII No clear clinical benefit so not recommended in unselected patients Can limit the extent of hematoma expansion in non- coagulopathic ICH patients, there is an increase in thromboembolic risk Replacement therapy in coagupathies

96. Management Step 4: Specific Medical Treatment of SAH Antifibrinolytic therapy: Recent evidence of benefit with early, short course Epsilon aminocaproic acid (36 g/d) Tranexamic acid (6 to 12 g/d) Vasospasm: Preventin : Oral nimodipine 60mg 6hry x 21 days Rx - volume expansion, induction of hypertension, and hemodilution (triple-H therapy) cerebral angioplasty and/or selective intra-arterial vasodilator therapy

97. Management Step 5: General Measures NPO acutely to lower the risk of aspiration Gentle IVF hydration only (avoid D5W) Normal saline or lactated ringers at 50 cc/hour Maintain normal body temperature Increased body temperature is associated with poor neurological outcome Treat sources of fever, give antipyretic – PCM Utility of hypothermia not established Consider Thiamine in Alcoholics and malnutrition

98. Management Step 6: Observe for and treat complications Blood Sugar Monitoring Treat Hypoglycemia: Bolus D50W (do not over correct) Treat Hyperglycemia (>180 mg/dl) – Insulin, GKI Seizures If seizures or electrographic seizures on EEG Evaluate with glucose and Serum Sodium Treat with Diazepam and Phenytoin

99. Step 6: Observe for and treat complications Blood Glucose Treat Hypoglycemia (<60mg/dl): Slow IV push of 25 mL of D50W (or as required) Do not over correct Treat Hyperglycemia (>180 mg/dl) Occurs in up to 40% of patients with CI Associated with worse clinical outcomes Insulin vs GKI (no difference in outcomes) feasibility and safety of rapid reductions have been demonstrated Goal: 140 to 180 mg/ dL

100. Management Step 6: Observe for and treat complications Blood Pressure Control Both elevated and low BPs are associated with poor outcome Elevated BP may be due to the stress of the event, full bladder, nausea, pain, hypoxia, raised ICP, so address these 1st Withhold antihypertensive unless CI: SBP >220 mm Hg or DBP > 120 mm Hg ~ 15% reduction during the first 24 hours ICH: SBP > 140 mm Hg DBP > 90 mmHg SAH : SBP > 140 mm Hg DBP > 90 mmHg End organ damage

101. Management Step 6: Observe for and treat complications Blood Pressure Control Aggressive treatment of BP may lead to neurological worsening CPP = MAP – ICP; MAP = DBP + 1/3 PP Mild to moderate strokes not at high risk for raised ICP may have their pre-stroke antihypertensives restarted ~ 24 hours Hypotension Find the cause and treat - hypovolemia , cardiac arrhythmias, vasopressive agents

102. Management Step 6: Observe for and treat complications Cerebral edema (peaks on day 3-5, duration 10/7 Intubate and hyperventilate to pCO2 of 35 mmHg Mannitol – 0.25-0.5g/kg/dose over 20 mins , q6hrs Neurosurgery consultation for decompression Corticosteroids are not indicated Other common complications SIADH, Pneumonia, UTI, Pulmonary Embolism

103. Management Step 7: Adjunctive Therapy Aspirin 325 mg stat within 24-48 hours then, 75mg daily Prevents CI recurrence Avoid in ICH & SAH until after several weeks T iclopidine , clopidogrel , or dipyridamole – not recommended Dysphagia - timely swallow assessment N asogastric , nasoduodenal , or PEG feedings for Patients who cannot take orally

104. Don’ts Avoid urethral catheterization in men if no obstruction (use Paul’s tube) Do not administer excessive IV fluids Do not administer dextrose-containing fluids in nonhypoglycemic patients Do not feed or administer medications by mouth (maintain NPO) Do not initiate interventions for hypertension in CI unless there is a compelling indication Do not delay consult, referral or transfer if indicated

105. Management Surgery : CI: Not sufficient data on the safety and effectiveness of carotid endarterectomy and other operations ICH: clot removal in cerebellar hemorrhage deteriorating neurologically, brainstem compression and/or, hydrocephalus from ventricular obstruction lobar clots >30 mL and within 1 cm of the surface might be considered

106. Management Surgery : SAH: Surgical clipping or endovascular coiling of aneurysm Temporary or permanent CSF diversion in symptomatic chronic hydrocephalus Ventriculostomy – ventriculomegaly and diminished level of consciousness after acute SAH

107. Management Endovascular interventions for CI : The usefulness of mechanical endovascular treatments is not established Prevention of DVT/PE SC anticoagulants – within 24hrs not advisable in CI, avoid in ICH & SAH Intermittent external compression devices + elastic stockings for patients who cannot receive anticoagulants

108. Management Neuroprotective Agents : Including Vits E & C No intervention with putative neuroprotective actions has been established to be effective Early mobilisation & rehabilitation within 24 hours of onset of symptoms Swallow test before oral intake Treatment of concomitant medical diseases and complications Prophylactic antibiotics not recommend

109. Nutrition Malnutrition may slow recovery Impairments of swallowing are associated with a high risk of pneumonia & death A preserved gag reflex may not indicate safety with swallowing NPO till swallowing assessment is performed 50 mls of water PO; impaired if cough, wet voice Early NG tube feeding, commence ASAP PEG for prolonged tube feeding

110. Bowel Care Constipation - associated with poor outcomes at 12 weeks Bowel management to avoid constipation, faecal impaction or diarrhoea

111. Infections Pneumonia and UTI – most common Appearance of fever should prompt a search for pneumonia or UTI Prophylactic antibiotics not useful Investigate and treat with appropriate antibiotics when suspected

112. Infections Pneumonia prevention Ventilation in a semirecumbent position Suctioning Early mobilization Shortened use of intubation Treat nausea and vomiting Exercise and deep breaths UTI prevention Avoid indwelling catheters if possible Assess for UTI if there is a change in level of consciousness Acidification of the urine may lessen the risk of infection

113. Management- Nursing 4/12/07 118 Observation How often Target Parameters SSS, GCS 3hrly first 12 hours, then 6 hrly GCS only if drowsy BP 6 hourly Target 160-180/90-100 in normotensives Target 180/100-105 in hypertensives Heart rate 6 hourly Cardiac monitoring for history of arrhythmias, unstable BP Temperature 6 hourly Keep below 37.5C Respiration 6 hourly Treat if saturation <92% Oxygen Saturation 6 hourly Treat if saturation <92% Glucose Daily (increase frequency if abnormal) Keep < 10mmol/L Hydration Use normal saline first 24hrs (preventing blood glucose increasing, EUSI 2003) Nutrition Introduce NG tube within 24 hours European Stroke Initiative 2003 ( http://eusi-stroke.com/recommendations ) unchanged November, 2007

114. Question A 54 year old School teacher presents in the emergency room with a 17 hour history of sudden weakness of the right side of the body. GCS is 11, BP 242/156mmHg and RBS 240mg/dl. Cranial CT done 30 minutes after presentation reveals a hypodense lesion in the deep left parietal lobe with significant cerebral edema . Discuss his acute management.

115. Transient Ischemic Attack

116. Transient Ischemic Attack The epidemiology essentially mirrors that of stroke > 10% of TIAs will develop CI within 90 days (4-8% of CI will recur within 90 days) 2.6% of TIAs will develop other major CV events within 90 days 10-15% of patients have a stroke within 3 months, with half occurring within 48 hours CF: Amaurosis fugax , transient stoke-like syndromes

117. Transient Ischemic Attack C ontroversy exists regarding the need for admission Admission to a "rapid evaluation unit" or "observation unit", dropped the 90-day stroke risk from 10 % to 4-5% No controversy regarding the need for urgent evaluation, risk stratification, and initiation of stroke prevention therapy

118. Initial Evaluation Level of consciousness and neurologic examination are usually at the patient's baseline. Initial assessment is aimed at excluding conditions that can mimic a TIA, eg , ICH, hypoglycemia , seizure. Laboratory studies- within 24 hours RPG, ECG, CT, FBC , coagulation studies, E,U.Cr . MRI preferred to CT Echo, carotid and vertebral doppler uss

119. Risk Stratification – ABCD 2 A ge ≥ 60 years (1 ) B lood pressure 140/ 90 mm Hg on first evaluation (1 ) C linical symptoms of focal weakness with the spell (2) or speech impairment without weakness (1 ) D uration ≥ 60 minutes (2) or 10 to 59 minutes (1 ) D iabetes (1).

120. Risk Stratification – ABCD 2 2-day risk of stroke % for scores of 0 or 1 1.3 % for 2 or 3 4.1 % for 4 or 5 8.1 % for 6 or 7

121. Decision to Admit If presents within 72 hours, hospitalize if: ABCD 2 score of 3 ABCD 2 score of 0 to 2 and uncertainty that diagnostic workup can be completed within 2 days as an outpatient ABCD 2 score of 0 to 2 and other evidence that indicates the patient's event was caused by focal ischemia - AHA

122. Management Admit for Restoration of Vital Signs Cardiac monitoring, pulse oximetry Intravenous access Management of hypertension, hyperglycemia etc Non- cardioembolic TIA Aspirin (50-325 mg/d), combination aspirin/extended-release dipyridamole , and clopidogrel

123. Management Cardioembolic TIA Atrial fibrillation, MI, DCM, RHD, After TIA, long-term anticoagulation with warfarin (goal INR, 2-3) is typically recommended. LMW heparin if warfarin is interrupted Aspirin , 325 mg/d Mechanical prosthetic valves, warfarin (goal INR 2.5-3.5), aspirin, 75-100 mg/d Bioprosthetic valves, warfarin (goal INR 2-3 )

124. Management Carotid Stenosis CEA if Ipsilateral severe (70% to 99 %) carotid stenosis Ipsilateral moderate (50% to 69%) stenosis depending on patient-specific factors - age, sex, and comorbidities (CAS – an alternative) Stenosis <50%, no indication for CEA/CAS CEA within 2 weeks is reasonable

125. Stroke Prevention

126. Prevention Stroke is best treated by prevention! Up to 90% of strokes are preventable Stroke prevention hinges on risk modification Treatment of cardiovascular risk diseases Lifestyle modification

127. Prevention Risk modification Hypertension Antihypertensive therapy reduces stroke risk by about 38% Reduction of diastolic BP by 6 mmHg reduces stroke risk by more than 33% Reduction of systolic BP by 3mmHg reduces risk by 8% Diabetes No demonstrated benefit in stroke reduction with tight glycemic control BP control and statins reduce stroke risk in DM

128. Prevention Aspirin - 25% risk reduction Carotid endarterectomy : symptomatic atherosclerotic stenosis of > 70% in the carotid artery High Blood Cholesterol Stroke risk reduction of 27% to 32% is achieved with statins 25% reduction in TIAs Smoking Cessation Reduces risk by 50% within 1 y; to baseline after 5 years

129. Prevention Avoid alcohol drinking Recommendation: No drinks at all Weight control An average weight loss of 5.1 kg reduced systolic BP by 4.4 mmHg and diastolic BP by 3.6 mmHg Exercise Recommendation: 30 minutes of moderate-intensity activity daily

130. Atrial fibrillation ( nonvalvular ) RR = 2.6 – 4.5 Warfarin vs control: 64% risk reduction Aspirin vs placebo: 19% risk reduction Warfarin vs aspirin: 39% risk reduction

131. Asymptomatic carotid stenosis RR = 2.0 50% reduction with endarterectomy Aggressive management of other identifiable vascular risk factors

132. Weight Control No clinical trial has tested the effects of weight reduction on stroke risk An average weight loss of 5.1 kg reduced systolic BP by 4.4 mmHg and diastolic BP by 3.6 mmHg Therefore, weight reduction is reasonable as a means of reducing stroke risk Don’t just advise, set SMART weight management goals

133. Physical Inactivity Mechanisms: BP, DM, weight, plasma fibrinogen, platelet activity & plasma tPA activity and HDL-cholesterol. Recommendation (The 2008 Physical Activity Guidelines for Americans ): At least 150 minutes per week of moderate intensity or 75 minutes per week of vigorous intensity aerobic physical activity or an equivalent combination of moderate and vigorous intensity aerobic activity

134. Prevention Sickle Cell Disease Screening with TCD starting at age 2 years Optimal interval not yet established, more frequently in younger children and with borderline abnormal TCD velocities Transfusion therapy (target reduction of Hb S from a baseline of >90% to <30 %) Reduced risk from 10% to 1% Hydroxyurea or bone marrow transplantation

135. < 15% Saturated fatty acids Polyunsaturated fatty acids Monounsaturated fatty acids 8%-10% < 10% Recommended Daily Nutrient Content Carbohydrate > 55% Protein 15% Fat < 30% Cholesterol: <300 mg/d Fiber: 20-30 g/d

136. Healthy Eating Pyramid

137. Prevention - Diet Carbohydrates Include at least one starchy food in each main meal Use refined carbohydrates sparingly Fats Low-fat dairy products and low saturated and total fat diets reduce BP and stroke risk Yoruba diet has lower mean cholesterol level (166mg/dl) compared to that of the African Americans (220mg/dl) (Ogunniyi et al ,2000)

138. Prevention - Diet Proteins Red Meat - Use Sparingly Fish, Poultry, and Eggs - 0-2 times a day Nuts and Legumes - 1- 3 times a day Nuts and legumes are an excellent source of protein, fiber, vitamins, and minerals. Examples: Brown beans, soya beans. Contain healthy fat, good for the heart . Milk A good source of calcium Try to stick to low or no fat milk

139. Fruits and Vegetables Increased fruit and vegetable consumption is associated with a reduced risk of stroke in a dose-response fashion For each 1-serving/day increment in fruit and vegetable intake, the risk of stroke was reduced by 6% - Nurses’ Health Study & the Health Professionals’ Follow-Up Study Vegetables - to be taken in abundance, every meal, every day. Fruits (2-3 times a day )

140. Prevention - Salt 75% of the salt we eat is already in food when we buy it Avoid foods high in salt Fast foods, canned foods, tomato ketchup, mayonnaise, roasted nuts, smoked meat and fish. No added salt at table Recommended daily intake of table salt for adults: not more than 6g a day: around one full teaspoon

141. Conclusion Stroke is a disease of major public health importance in Nigeria & mortality is still very high Recognition by patients and care providers that stroke is a medical emergency will change the current picture Stroke is preventable and prevention is the only affordable option for developing countries TIA is not benign

142. Thank You