A slide presentation on Stroke made for medical students in Nigeria. It includes the definition, types, management and complications.

1. STROKE
Presentation by
Ogechi Grace Okoli
MBBS V
University of Jos, Nigeria.

2. OUTLINE
• Introduction
• Definition of terms
• Epidemiology
• Classification
• Aetiology
• Pathophysiology
• Management
• Prognosis
• Prevention
• Conclusion

3. INTRODUCTION
• Also known as cerebrovascular accidents (CVA)
• Too much blood? Or too little blood? Or both?
• A medical emergency!
• A leading cause of morbidity and mortality.

4. DEFINITION OF TERMS
• Stroke: a sudden focal neurological deficit of vascular origin
lasting >24 hours, or resulting in death.
• Transient Ischaemic Attack (TIA): when the neurologic deficit
lasts <24 hours.
• Stroke in evolution: when the focal neurologic deficit worsens
after patient first presents.
• Completed stroke: when focal neurologic deficits persists but
does not progress.
• Stroke in the young: stroke occurring in individuals <45 years
of age.

5. DEFINITION OF TERMS (contd.)
Current concepts in the definition include the following:
• 24 hours time frame is now outdated: confusing and misleading;
does not not suggest emergency; does not take into cognizance
the use of thrombolytics.
• TIA is not benign as
-10-20% develop stroke within 90 days.
- 50% in 24-48 hours

6. DEFINITION OF TERMS (contd.)
• Currently defined by Stroke Council of AHA/ASA (2013) as
• Stroke: FND of vascular origin with objective evidence of
infarction irrespective of duration of clinical symptoms.
• TIA: no objective evidence of acute infraction in the affected
region of the brain, spinal cord or retina.

7. EPIDEMIOLOGY
• leading cause of death and disability
• 1 in 4 adults will have a stroke in their lifetime
• 1 in 4 of stroke survivors will have another within 5 years.
• 2nd leading cause of death globally- 5.5 million deaths annually.
• 3rd common cause of death in developed countries after heart failure and cancers.
• Africa- annual incidence of 316 cases per 100,000 person-years.
• 3-year fatality rate in Africa >80%
• Nigeria- prevalence is 1.14 per 1000; 30-day case fatality rate is 40%
• JUTH- frequent cause of neurological admissions; 35% mortality rate, 76.2% within 1st week

8. EPIDEMIOLOGY
• Sex: commoner in males with 3:2
• Age:
• affects all ages including children
• risk increases with age especially >64 years (75% of all cases)
• commoner in the 6th and 7th decades
• Race: blacks

9. CLASSIFICATION
Based on mechanism,
1. Ischaemic stroke (85%)
a. Large vessel stroke
b. Small vessel stroke
c. Cardio-embolic stroke
d. Unclassified/Cryptogenic
2. Haemorrhagic stroke (10%)
a. Intracerebral
b. Subarachnoid
3. Others (5%)

10. CLASSIFICATION (contd.)

11. CLASSIFICATION (contd.)
Based on clinical picture,
1. TIA
2. Completed stroke
3. Stroke in evolution

12. AETIOLOGY
• Risk factors for stroke are:
1. Modifiable and
2. Non-modifiable

13. RISK FACTORS (contd.)
Non-modifiable risk factors
• Increasing age: 75% in people >64years
• Sex: M>F, M=F(post-menopausal)
• Race: afrocarribean > asian > caucasian
• Family history of TIA & stroke
• Previous vascular event eg MI, stroke, or peripheral embolism

14. RISK FACTORS (contd.)
Modifiable risk factors
• Uncontrolled hypertension
• Cardiogenic: atrial fibrillation, valvular heart disease, DVT
• DM
• Hyperlipidaemia
• Obesity
• Haematologic: polycythaemia, SCDx,
• Lifestyle: sedentary, cigarette smoking, alcohol consumption
• Infections: HIV, syphillis,
• Pregnancy
• Drugs: oral contraceptive pills; IV drug abuse eg cocaine, heroin
• Malignancy: leukemia
• Others

15. RISK FACTORS (contd.)
Specific risk factors for haemorrhagic stroke
• Bleeding disorders eg haemophilia; CLD
• Prolonged anticoagulant and antiplatelet use
• Pre-existing cerebral aneurysm
• Vascular malformation
• Trauma

16. Causes of stroke in the young
• Hereditary: CADASIL, CARASIL, MELAS, AVM, SCDx,
thrombophilia, homocystinuria, moya-moya, collagen disorders
• Acquired: Infections (HIV, syphilis), vasculitis, SLE, drug
abuse, trauma

17. Pathophysiology of Stroke
Cerebral blood flow
• Brain: 1350g, 2% of total body weight
• Normal CBF = 50-65 ml/100g of brain tissue/minute
• CBF for the entire brain = 750-900 ml/min, i.e. 15% of the cardiac
output.
• As CBF reduces, esp <30 ml/100g/min, dysfunction of brain tissue
begins.
• CBF <18ml/100g/min, penumbric brain tissue formation is seen.
• CBF <10ml/100g/min, irreversible damage

18. Pathophysiology of Stroke
• Cerebral perfusion pressure (CPP)
• CPP = MAP - ICP
• Hence, CPP is dependent on MAP and autoregulation
• Autoregulation by
-Collateral supply
-Vasodilation
-Increased O2 extraction
• Further reduction in perfusion results in
-Ischaemia
-Infarction

19. Pathophysiology of Ischaemic Stroke
• Origin of emboli

20. Pathophysiology: Cellular level
Occlusion
Hypoxia
Depletion of ATP
Depolarization of membranes
Influx of Ca+ and glutamates
Neuronal damage

21. Pathophysiology of Ischaemic Stroke
Ischaemia
Infarction
Cellular edema
Ionic/Interstitial
edema
Vasogenic edema
Necrosis

22. Pathophysiology of Ischaemic Stroke
• Haemorrhagic transformation
-Due to reperfusion of damaged vascular endothelium
-Seen in 5% of ischaemic stroke
-May be haematoma or petechial bleeds
-May be associated with neurologic decline

23. Pathophysiology of Haemorrhagic stroke
Intracerebral haemorrhage
• Spontaneous rupture of small, deep penetrating arteries
• common sites: basal ganglia, thalamus, crebellum, pons.
• Entry of blood into the parenchyma causes cessation of function
• Associated rim of cerebral edema
Subarachnoid haemorrhage
• Rupture of cerebral arteries into SA space

24. Pathophysiology of Haemorrhagic stroke

25. Management

27. Management
• It is a medical emergency
• multidisciplinary
• Stroke unit: reduces mortality by 20%
• Principles of management include:
a. Resuscitation
b. Treat precipitating factor(s) that will worsen the stroke.
c. Employ specific measures to treat ischaemic stroke.
d. Management of complications & secondary prevention of stroke.
e. Rehabilitation

28. Management: History
• Age
• Sex
• handedness of the patient? - right or left hemispheric stroke
• Sudden neurologic deficit- collapse, weakness, speech deficit or
blindness.
• Antecedent history of headache (thunderclap), vomiting, fainting -
?haemorrhagic
• location of the lesion
-ACA: contralateral hemiparesis more in LL mutism, incontinence,
disinhibition, gait apraxia
-MCA: contralateral hemiparesis, more in the face and UL, than in LL
-PCA: cortical blindness, impaired memory
• -SCDx, RVS, syphillis etc.

29. Management: History
• History suggestive of a risk factor
-previous TIA
-family history
-hypertension, DM, dyslipidaemia
-alcohol, cigarette
-heart disease: chest pain, shoulder tip pain, palpitation, dyspnea, cough etc
• Complications
• Care
• other parts of history

30. Management: Physical Examination
• CNS exam: GCS, swallow test, cn7 palsy,
• MSK
• CVS
• Resp

31. Differential Diagnoses of Stroke
• Subdural haematoma from trauma
• Cerebral abscess : fever, long progression
• Tumours: long progression
• Hypoglycemia: autonomic symptoms
• Hemiplegic migraine: resolves in <1 hour
• Todd's paralysis: with seizures
• Infections: TB, cryptococcosis, toxoplasmosis
• Meningitis
• Hysterical conversion

32. Making a diagnosis
• a clinical diagnosis
• type of stroke is confirmed by imaging
• must contain
-anatomical site of lesion
-location of clinical manifestation
-possible cause/precipitant
eg. Left hemispheric stroke with right-sided hemiplegia 20 long standing
hypertension

33. Investigations
To support diagnosis, and to find out cause
• Imaging
-MRI: gold standard
-Brain CT scan: hyperdense (haemorrhagic),
hypodense (ischaemic)
-Vascular imaging (doppler): large or small vessel
-Echo: valvular heart disease, mural thrombus

34. Fig 1: NCCT demonstrates cortical
and subcortical hypodensity
involving the right mid to anterior
temporal lobe.

35. Fig. 2: Axial non-contrast CT scan of the brain
demonstrates 2 areas of intracerebral
hemorrhage in the right lentiform nucleus with
surrounding edema and effacement of the
adjacent cortical sulci and right sylvian fissure.
Mass effect is present upon the frontal horn of
the right lateral ventricle with intraventricular
extension of hemorrhage.

36. Fig 3: The non-contrast CT
(left image) demonstrates
diffuse, high-density
subarachnoid hemorrhage in
the basilar cisterns and both
Sylvian fissures. Diffuse loss
of gray-white differentiation is
present.
Right image is Fluid-
attenuated inversion recovery
(FLAIR) MRI which is more
sensitive for SAH

37. • 3 main stages are used to describe the CT
manifestations of stroke:
-Acute (less than 24 hours),
-Subacute (24 hours to 5 days) and
-Chronic (weeks).

39. Investigations
• Blood
-FBC: thrombocytopenia (haemorrhagic), -cytosis (ischaemic)
-FBG/RBG: DM
-Hb electrophoresis: SCDx
-Lipid profile: dyslipidaemia
-E/U/Cr
-Clotting profile
-ESR
-Protein C, S; anti-thrombin III; anti-phospholipid antibodies
• Lumbar puncture: haemorrhagic tap, xanthochromia
• Kidney scan
• Retroviral screening

40. Difference btw haemorrhagic and ischaemic stroke
Variant Haemorrhagic stroke Ischaemic stroke
Preceeding activity + -
Preceeding headache + -
Convulsion + -
LOC + -
TIA - +
BP at presentation +++ ++
CSF appearance Xanthochromia;
haemorrhagic tap
clear

41. Treatment
Time is Brain!!!
• lost with each hour of stroke
-120 million neurones
-830 billion synapses
-714 kilometer of myelinated fibres

42. Resuscitation
• Airway: suction, intubation, tracheostomy
• Breathing: give O2 if SPO2 <95%
• Circulation: hypertonic fluid (N/S), mannitol (+/- frusemide
cover)
• Position at 30o: cerebral edema, aspiration

43. Treat precipitating factors that can worsen symptoms- 5H's
• Hypo- / hyperglycemia: increases umbra
• Hypo- / hypertension: reduce only when MAP >145mmHg; or
SBP =/> 220mmHg or DBP =/> 120mmHg
Target is SBP </= 145 mmHg
• Hypoxia
• Hypovolemia
• Hyperthermia

44. Specific Treatment for Ischaemic stroke
• Tissue plasminogen activator (TPA) if patient presents within 5
hours of stroke
• Antiplatelet eg low dose aspirin (150-250mg) if patient presents
after 5 hours
• Antioxidants eg vit C, vit E
• Statins eg simvastatin

45. Other recommendations in management
• Cholesterol lowering with atorvastatin or simvastatin
• Lifestyle modifications
• Endovascular interventions: angioplasty, stenting, mechanical
clot disruption, clot extraction (mechanical embolus removal in
cerebral embolism)

46. Management of complications and 2o prevention of stroke
Acute/Early Complications
• Hyperglycemia
• Hyperthermia
• Seizures
• Cerebral edema
• Hydrocephalus

47. Chronic/Late Complications
• Contractures
• Bed sores
• DVT
• UTI
• Pneumonia
• Dementia
• Psychosis

48. Prevention
• Primary
• Secondary
• Tertiary

49. Prevention
1. Lifestyle modification
2. Lower BP
3. Lower cholesterol levels
4. Surgery i.e. endarterectomy

50. Rehabilitation
• Physiotherapy
• Speech therapy
• Occupational therapy
• Nutritional therapy

51. Prognosis
Poor prognostic factors include:
• Accompanying fever
• Low GCS
• Hypotension
• Low O2 saturation
• Hyperglycemia
• Total anterior circulation stroke- 55% mortality
• Pontine haemorrhage

52. Conclusion
• Stroke is a leading cause of death and disability
• Early recognition, classification and institution of treatment is
key to reducing mortality and morbidity
• It is better prevented than treated.

53. The End?

54. questions?
additions?

55. References
1. Kumar & Clark's Clinical Medicine 9th edition
2. Global burden of disease 2018: www.cdc.gov.org
3. Definition of stroke: American Heart Associtaion/American Stroke Association (AHA/ASA) 2010
4. Akinyemi 2021: Stroke in Africa: Profile, Progress, Prospects and Priorities.
5. KW Wahab 2008: Burden of Stroke in Nigeria.
6. B. Ekeh 2015: Stroke Mortality and its Predictors in a Nigerian Teaching Hospital.
7. Boon et al: Davidson's Principles and Practice of Medicine 20th edition -
www.studentconsult.com
8. Longo DL, et al.: Harrison's Principles of Internal Medicine, 18th edition
9. Schwartz DT. Emergency Radiology:Case Studies. McGraw Hill; 2008. pp. 501–522. [Google
Scholar]
10. Stroke Imaging: https://emedicine.medscape.com/article/338385-
overview?icd=login_success_email_match_norm
11. David S. Liebeskind and Joanna M. Wardlaw: Acute-on-Chronic Stroke ; Mar 2021;
https://doi.org/10.1161/STROKEAHA.121.033449Stroke. 2021;52:1486–1489