By: Dr. Michael B. Fawale

1. Epidemiology and Aetiology of Stroke
Dr Michael B. Fawale
Medicine Department, OAU, Ile-Ife
bimbofawale@live.com

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
Temporary 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
Stroke
Ischaemic
Thrombotic Embolic Lacunar
Haemody
namic
Haemorrhagic
Intracerebral Subarachnoid

13. Osuntokun et al, 1977
ICH
15.7%
SAH
11.3%
CI
48.8%
Ill-defined
24.2%
USA
ICH, 15%
SAH, 5%
CI, 80%
Stroke Types & Subtypes

14. •Cardiogenic
•Arteroembolic
•Paradoxic embolism
Ischemic Stroke Subtypes

15. Stroke - Epidemiology

16. • The most common cause of adult disability.
• 2nd most common cause of dementia.
• 2nd 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. 0.0%
2.0%
4.0%
6.0%
8.0%
10.0%
12.0%
14.0%
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
A. Ischaemic stroke is more common than
haemorrhagic stroke
B. Thrombotic and embolic strokes are sugtypes of
haemorrhagic stroke
C. Stroke is the leading cause of adult disability globally
D. Deaths due to stroke are more than deaths due to
malaria, HIV and TB combined
E. 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
• The 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
– Independently 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/m2 between BMI
and stroke mortality
– The risk of stroke increases by 1.04
per unit increase in BMI

42. Measures of Adiposity
BMI (kg/m2) 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. • Data 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- 10 & 20, 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
A. Hypertension
B. Sickle cell disease
C. Asymptomatic carotid disease
D. Atrial fibrillation
E. 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 vs 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

68. Emergency Evaluation & Management

69. 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)

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

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

72. Highlights of Acute Stroke
Management
• Organized protocol
• Acute stroke team
• Oral ASA within 24-48
hrs of stroke onset 1st
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

73. 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)

74. 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)

75. Time is Brain!

77. Time is Brain!

78. 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)

79. Management

81. 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

82. Management
Step 1: Immediate General Assessment (<10
minutes)
• ABC Management
• Full vital signs including pulse oxymetry
– Deliver O2 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

83. 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 O2 by nasal cannula if SAO2 < 94%,
maintain SAO2 >94%
• Utility of hyperbaric oxygen is not established

84. Patient Positioning
ICP-Volume Curve

85. 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

86. 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

87. 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)

88. 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.

89. Emergency Evaluation & Treatment
• CVS
– Irregular pulse
– Feeble pulse
– 3rd 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)

90. 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

91. Brain Computerized Tomography
CI ICH SAH

92. Common sites of ICH

93. back

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

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

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

97. 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!

99. 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

100. 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

101. 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

102. 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

103. 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

104. 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

105. 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

106. 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

107. 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
– Ticlopidine, clopidogrel, or dipyridamole – not
recommended
• Dysphagia - timely swallow assessment
– Nasogastric, nasoduodenal, or PEG feedings for
Patients who cannot take orally

108. 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

109. 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

110. 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

111. 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

112. 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

113. 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

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

115. 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

116. 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

117. 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

118. 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.

119. Transient Ischemic Attack

120. 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

121. Transient Ischemic Attack
• Controversy 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

122. 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

123. Risk Stratification – ABCD2
• Age ≥ 60 years (1)
• Blood pressure 140/ 90 mm Hg on first
evaluation (1)
• Clinical symptoms of focal weakness with the
spell (2) or speech impairment without
weakness (1)
• Duration ≥ 60 minutes (2) or 10 to 59 minutes
(1)
• Diabetes (1).

124. Risk Stratification – ABCD2
• 2-day risk of stroke
– 0% for scores of 0 or 1
– 1.3% for 2 or 3
– 4.1% for 4 or 5
– 8.1% for 6 or 7

125. Decision to Admit
• If presents within 72 hours, hospitalize if:
– ABCD2 score of 3
– ABCD2 score of 0 to 2 and uncertainty that
diagnostic workup can be completed within 2 days
as an outpatient
– ABCD2 score of 0 to 2 and other evidence that
indicates the patient's event was caused by focal
ischemia
- AHA

126. 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

127. 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)

128. 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

129. Stroke Prevention

130. 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

131. 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

132. 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

133. 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

134. 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

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

136. Weight Control
• No clinical trial has tested the effects of
weight reduction on stroke risk
• An average weight lossof 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

137. 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

138. 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

139. <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

140. Healthy
Eating
Pyramid

141. 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)

143. 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

144. 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 HealthProfessionals’ Follow-Up Study
• Vegetables- to be taken in abundance, every
meal, every day.
• Fruits (2-3 times a day)

149. 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

150. 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

151. Thank You