STROKE

Presentation by
Ogechi Grace Okoli
MBBS V
University of Jos, Nigeria.
 OUTLINE
• Introduction
• Definition of terms
• Epidemiology
• Classification
• Aetiology
• Pathophysiology
• Management
• Prognosis
• Prevention
• Conclusion
 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.
 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.
 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• 24 hours time frame is now outdated: confusing and misleading; does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
 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.
 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
 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
 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%)
CLASSIFICATION (contd.)
 CLASSIFICATION (contd.)

Based on clinical picture,

1. TIA
2. Completed stroke
3. Stroke in evolution
 AETIOLOGY

• Risk factors for stroke are:

1. Modifiable and
2. Non-modifiable
 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
 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
 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
 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
 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
 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
 Pathophysiology of Ischaemic Stroke
• Origin of emboli
 Pathophysiology: Cellular level

Occlusion

Hypoxia

Depletion of ATP

Depolarization of membranes

Influx of Ca+ and glutamates

Neuronal damage
 Pathophysiology of Ischaemic Stroke

Ischaemia

Infarction

Cellular edema

Ionic/Interstitial
edema

Vasogenic edema

Necrosis
 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
 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
Pathophysiology of Haemorrhagic stroke
Management
 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
 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.
• R/O stroke chameleon: trauma in the past, tumours
 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
 Management: Physical Examination

• CNS exam: GCS, swallow test, cn7 palsy,

• MSK
• CVS
• Resp
 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
 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 2 0 long standing
hypertension
 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
Fig 1: NCCT demonstrates cortical and
subcortical hypodensity involving the
right mid to anterior temporal lobe.
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.
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
• 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).
 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
 Difference btw haemorrhagic and ischaemic stroke

Variant Haemorrhagic stroke Ischaemic stroke

Preceeding activity + -

Preceeding headache + -

Convulsion + -

LOC + -

TIA - +

BP at presentation +++ ++

CSF appearance Xanthochromia; clear

haemorrhagic tap
 Treatment

Time is Brain!!!
• lost with each hour of stroke
-120 million neurones
-830 billion synapses
-714 kilometer of myelinated fibres
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
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
 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
 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)
Management of complications and 2o prevention of stroke
Acute/Early Complications
• Hyperglycemia
• Hyperthermia
• Seizures
• Cerebral edema
• Hydrocephalus
 Chronic/Late Complications
• Contractures
• Bed sores
• DVT
• UTI
• Pneumonia
• Dementia
• Psychosis
 Prevention

• Primary
• Secondary
• Tertiary
 Prevention
1. Lifestyle modification
2. Lower BP
3. Lower cholesterol levels
4. Surgery i.e. endarterectomy
 Rehabilitation
• Physiotherapy
• Speech therapy
• Occupational therapy
• Nutritional therapy
 Prognosis

Poor prognostic factors include:

• Accompanying fever
• Low GCS
• Hypotension
• Low O2 saturation
• Hyperglycemia
• Total anterior circulation stroke- 55% mortality
• Pontine haemorrhage
 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.
The End?
questions?
additions?
 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