2. LEARNING OBJECTIVES
At the end of this session, we should be able to;
• Describe Cerebrovascular Accident
• Describe pathogenesis of CVA
• Explain clinical features of CVA
• Explain complications of CVA
• Describe management CVA
• Provide measures to prevent and control CVA
3. INTRODUCTION
Cerebral vascular accident is a sudden death of
some brain cells due to lack of oxygen when
the blood flow to the brain is impaired by
blockage or rupture of an artery to the brain.
CVA is also known as Stroke
Types of Cerebrovascular Accident
• Ischemic
• Haemorrhagic
4. Stroke is the third most common cause of
death in the developed world after cancer and
ischaemic heart disease, and is the most
common cause of severe physical disability.
It is the most frequent clinical manifestation of
diseases of the cerebral blood vessels, although
cerebrovascular disease may present,
particularly in the elderly, as a dementia.
EPIDEMIOLOGY
5. Stroke is a common medical emergency with
an annual incidence of between 180 and 300
per 100,000 in UK.
The incidence rises with age and in developing
countries, the incidence is rising because of the
adoption of less healthy lifestyles.
1/5 of patients with acute stroke will die within
a month of the event and at least ½ of those
who survive will have physical disability.
6. ISCHAEMIC STROKE
Ischemic stroke accounts for 80 – 90% of
all stroke in developed countries.
Ischaemic stroke is further divided into:
• Thrombotic ischaemic stroke
• Embolic ischaemic stroke
• Systemic hypoperfusion ischaemic stroke
7.
8. Thrombotic ischemic stroke: Pathological
process cause thrombus formation in artery
resulting in stroke.
Systemic hypoperfusion ischemic stroke:
Caused by brain hypoperfusion due to a
systemic circulatory failure, eg in Shock,
congestive cardiac failure, cardiac arrest or
arrhythmia.
9. Embolic ischemic stroke: An emboli
originating elsewhere block arterial access to a
particular brain region.
Common causes of ischemic stroke: Heart
failure, valvular heart diseases, myocardial
infarction, Atrial fibrillation, Infective
endocarditis, Hypertension, Cigarette smoking,
pulmonary embolism, deep venous thrombosis.
10. HEMORRHAGIC STROKE
Haemorrhagic stroke is due to rupture of an
artery to the brain causing blood to leak.
It accounts for 10 – 20% of CVA in developed
countries.
It is more common in developing countries due
to unrecognized or poorly controlled HTN.
Divided into Intracerebral and Subarachnoid.
11.
12. Intracerebral haemorrhage (ICH): Derived
from arterioles or small arteries, the bleeding
is directed into the brain, forming a localized
haematoma, accumulation of blood occurs
over minutes or hours.
Subarachnoid haemorrhage (SAH):
Aneurysm rupture releases blood directly into
the CSF pathway under arterial pressure,
hence increases intracranial pressure.
13. Common causes of Haemorrhagic stroke:
Trauma, Hypertension, Amyloidosis,
Angiopathy, Vascular malformations,
Intracranial arterial dissection, Drug abuse
(mostly amphetamines and cocaine),
Vasculitis., brain tumours.
NB: Hypertension (Systolic blood pressure
of ≥ 220 mmHg) highly suggestive of
haemorrhagic stroke.
14. Based on duration stroke can be:
• Transient Ischemic attack is the focal neuralgic
deficit lasting < 24 hours confined to an area
of brain perfused by specific artery and
neurologic deficit resolves in < 24 hours.
• Reversible Ischemic neurologic deficit is the
sudden onset focal neurologic deficit which
lasts for > 24 hours, but the neurologic deficit
recovers or resolves.
15. • Stroke in evolution is the focal neurologic
deficit, the degree of which is progressing
over a couple of hours or days.
• Complete stroke is a sudden onset of focal
neurologic deficit, in which the deficit neither
improves nor gets worse over time, often
associated with infarction of part of the brain.
16. RISK FACTORS
• Males and old age
• Hypertension
• Smoking
• Diabetic Mellitus
• Hyperlipidemia
• Atrial fibrillation
• Myocardial infarction
• Atherosclerosis
• High Cholesterol
• Family Hx of Stroke
• Vasculitis
• Cocaine Consumption
• Congestive heart failure
• Acute alcohol abuse
17. CLINICAL FEATURES
Strokes damage only one side of the brain.
Nerves in the brain cross over to the other side
of the body sign appear on the other side of the
body opposite to the damaged side of brain.
Signs and symptoms depend on the area of the
brain affected, include change in alertness
(consciousness), lethargy, drowsiness, stupor
or coma.
18. • Difficulty speaking or understanding others
• Difficulty swallowing
• Difficulty writing or reading
• Headache
• Loss of coordination
• Loss of balance
• Movement changes usually on only one side
of the body.
19. • Nausea or vomiting
• Seizures
• Sensation changes usually on only one side of
the body.
• Sudden onset of confusion
• Vision changes
• Weakness or paralysis of one side of the body.
20. Embolisms usually occur suddenly when the
patient is awake, most often early in the
morning, giving maximum deficit at onset.
Hemorrhagic stokes occur suddenly while the
patient is awake, may be physically active or
straining, and progresses within min to hours.
Thrombosis occurs during sleep or upon arising
from bed progressing in a stepwise fashion.
21. EMBOLIC THROMBOTIC HAEMORRHAGIC
Onset Sudden
onset
with max
Deficit
Sudden,
Gradual,
Stepwise or
Stuttering
Sudden (deficit
Progresses over
minutes to hours)
Time of
Occurrence
Patient is
Awake.
When patient is
Asleep/Inactive
When the patient is
Awake and active
Warning
Sign (TIA)
None Usually None
Head, Vom Sometimes Sometimes Usually
LP Clear Clear Bloody
23. INVESTIGATIONS
• RBG R/O Hypoglycemia, FBP, ESR, VDRL
• Lipid Profile, HIV Test
• Coagulation Profile
• Lumbar Puncture
• CT Scan and MRI of the brain
• ECG to diagnose underlying heart disorders
• Echo to R/O blood clot from the heart
24. TREATMENT
Goal of Treatment:
• Interruption of further brain damage
• Prevention and management of complication
General Measures:
• Admit the patient in close follow up area
• Asses and manage the A, B, Cs
• Monitor vital signs (BP, Temp, Hydration)
25. • If the patient is comatose or has impaired
mental status, change the patients position
every 2 hours to avoid bed sores.
• Bladder and bowel care: Catheterize
• Infections such as aspiration pneumonia
should be treated with antibiotics.
26. For Ischemic Stroke:
• Thrombolytic therapy: rt–PA (Plasminogen
Activator), to patients present within 3 hours
of onset of stroke, helps to lyse the thrombus
and restore perfusion to the affected brain.
• Anticoagulants: Heparin and Warfarin is
controversial, low dose heparin can be given
for prevention of thromboembolism.
27. • Anti-platelet aggregation agents: Clopidogrel
or Aspirin 150 mg OD 1/12, reduces the
incidence and recurrence of stroke and
vascular mortality, NB: Don’t give Aspirin if
given rt-PA (Increase risk of ICH).
• BP should not be lowered in the first 48 hours
unless it is very severe (SBP > 200), After 48
hours use statin (Simvastatin 20mg) to lower
BP to a range of 140 – 160 of SBP.
28. • Start Ranitidine or PPI to prevent stress ulcers.
• Elevate the head to prevent aspiration.
• For Increased ICP use Mannitol.
For Haemorrhagic Stroke:
• Supportive therapy
• Control BP cautiously, rapid control may cause
another stroke to occur.
• Surgical to remove cerebellar hematoma.
29. Rehabilitation: Very important part of
management and should be started early
• Physiotherapy
• Occupational therapy
• Speech therapy
30. PREVENTION
• Control of hypertension
• Control blood sugar in diabetics
• Ceasation of smoking
• Physical activity and weight reduction
• Anticoagulation for atrial fibrillation
• ASA 75 mg PO daily in individuals older than
50 and have history of TIA
31. KEY POINTS
Stroke is a sudden death of some brain cells due
to lack of O2 when the blood flow to the brain
is impaired by blockage or rupture of artery.
Stroke can be Ischemic or Hemorrhagic.
In transient ischemic attacks symptoms resolve
within 24 hours.
Diagnosis is based on history, examination and
imaging studies.
32. Recovery after a stroke depends on location
and extent of damage, patient’s age and
presence of other disorders.
Controlling high blood pressure, high
cholesterol levels, and high blood sugar
levels and stop smoking help prevent strokes.
Control of HTN may prevent strokes.
33. EVALUATION
1. What do you understand the term CVA?
2. What are the risk factors for CVA?
3. What are the clinical features of CVA?
4. Explain the complications of
Cerebrovascular accident.
5. How can CVA be prevented?
34. REFERENCES
Davidson’s Principle & Practice of Medicine
20th Edition, Page 1200 – 1210.
Ministry of Health and Social Welfare,
United Republic of Tanzania, CMT 05211
Internal Medicine II, NTA Level 5 Semester
2, Student Manual, Page 185 – 189.
Ethiopia Public Health Training Initiative,
Internal Medicine, Lecture Notes for Health
Officers, 2006, Page 506 – 514.