Stroke is a leading cause of death and disability globally. The presentation summarizes key aspects of stroke management. It describes the epidemiology, pathophysiology, clinical features, diagnosis and management of both ischemic and hemorrhagic strokes. Prevention of initial and recurrent strokes is emphasized through control of risk factors and use of anticoagulants or antiplatelets depending on the patient's risk profile. Early diagnosis and treatment including thrombolysis are important to minimize brain damage from acute strokes.

1. Management of
Stroke.
28° NOVEMBER 2018
Maseno University
George Wanjau

2. •Presenters
•George kariuki
•Lily Cheronoh
•Peter Nyakwaka
•OlubayoTimothy.
• Moderator.
• Professor Jowi.

3. outline
• Introduction
• Epidemiology
• Pathophsiology
• Clinical features
• Diagnosis
• Management.

4. Introduction.
• WHO Definition of stroke
Clinical syndrome of presumed vascular origin characterized by rapid
development of neurological signs[focal or global] lasting more than 24 hours or
fatal.
• Other definitions
Demonstration of acute brain lesion(ischemic/hemorrhagic) by imaging
techniques[MRI superior] in patients with symptoms <24 hours

5. Introduction.
• Progressing stroke (or stroke in evolution). This describes a stroke
in which the focal neurological deficit worsens after the patient first
presents.
• Completed stroke.This describes a stroke in which the focal deficit
persists and is not progressing.
• Types of stroke,
Ischemic stroke
Hemorrhagic stroke

6. Introduction.
• Transient ischemic attack
A transient episode of neurological dysfunction caused by
focal brain, spinal cord or retinal ischemia without acute
infarction . (AHA)
• THE PRESENCEOF INFARCTION ISTHE MAIN DISTINCTION
BETWEENTIA and STROKE.

7. Epidemiology.
• Each year 15-20 million persons suffer from stroke globally. 5-8
million die!!
• 2/3 of those who suffer from stroke are from LMICs
• Burden of stroke is reducing in the developed countries while
increasing in developing countries.
• Stroke is the 3rd leading cause of mortality and 2nd leading
causing of disability in Sub-Saharan Africa.

8. Epidemiology.

9. Blood supply to the brain.

10. Anterior cerebral artery.
• The ACA extends upward and forward
from the ICA.
• It supplies frontal lobes, parts of the
brain that control logical thought,
personality, and voluntary movement,
especially the legs.
• Stroke results in opposite leg
weakness. If both ACA territories are
affected, profound mental symptoms
may result (akinetic mutism).

11. Middle cerebral artery.
• The MCA is the largest branch of the ICA.
• The artery supplies part of the frontal
lobe, lateral surfaces of the temporal and
parietal lobes, including the primary
motor and sensory areas of the face,
throat, hand and arm and in the
dominant hemisphere, the areas for
speech.
• The middle cerebral artery is the artery
most often occluded in stroke.

12. Posterior cerebral artery.
• The PCA supplies the temporal and
occipital lobes. PCA stroke is usually
secondary to embolism from
segments of the vertebral basilar
system or heart.
• Clinical symptoms depend on site of
occlusion.The most common finding
is occipital lobe infarction leading to
an opposite visual field defect

13. Lenticulostriate arteries.
• Small, deep penetrating arteries
known as the lenticulostriate arteries
branch from the middle cerebral
artery.
• Occlusions of these vessels or
penetrating branches of the circle of
Willis or vertebral or basilar arteries
are referred to as lacunar strokes.
About 20% of all stokes are lacunar

16. Risk factors.
• The global stroke studies showed that hypertension is the most
significant risk factor for stroke.
• Local studies have shown that 80% of the patients with stroke had
hypertension and 34% had diabetes mellitus.

17. Pathophysiology.

18. Ischemic stroke.
• Cerebral infarction is mostly due to thromboembolic disease
secondary to atherosclerosis in the major extracranial arteries
(carotid artery and aortic arch).
• About 20% of infarctions are due to embolism from the heart
• 20% are due to intrinsic disease of small perforating vessels
(lenticulostriate arteries), producing so-called ‘lacunar’ infarctions.
• About 5% are due to rare causes, including vasculitis, endocarditis
and cerebral venous disease.

19. Ischemic stroke.
• After the occlusion of an artery, infarction may be forestalled by ;
• opening of anastomotic channels
• Compensatory homeostatic changes that maintain tissue oxygenation
• When these homeostatic mechanisms fail, the process of ischemia starts and
ultimately lead to infarction unless vascular supply is restored.
• If the blood flow increases again, function returns and the patient will have had a
TIA.

20. Cont…
• As the cerebral blood flow declines, different neuronal functions fail at various
thresholds leading to neurological deficits.
• Hypoxia leads to an inadequate supply of ATP, which in turn leads to failure of
membrane pumps,
• This allows influx of sodium and water into the cell (cytotoxic oedema) and the
release of the excitatory neurotransmitter glutamate into the extracellular fluid.
• Glutamate opens membrane channels, allowing the influx of calcium and more
sodium into the neurons.
• Calcium entering the neurons activates intracellular enzymes that complete the
destructive process.
• The release of inflammatory mediators by microglia and astrocytes produces
death of all cell types in the area of maximum ischemia.
• The infarction process is worsened by the anaerobic production of lactic acid

21. Cont…
• Subsequent restoration of blood flow may cause hemorrhage into
the infarcted area (‘hemorrhagic transformation’).
• This is particularly likely to occur in patients given antithrombotic or
thrombolytic drugs, and in patients with larger infarcts.

22. Hemorrhagic stroke.
• This usually results from rupture of a blood vessel within the brain parenchyma
but may also occur in a patient with a subarachnoid haemorrhage.
• The explosive entry of blood into the brain parenchyma causes immediate
cessation of function in that area as neurons are structurally disrupted and
white matter fibre tracts are split apart.
• The haemorrhage itself may expand over the first minutes or hours, or it may
be associated with a rim of cerebral oedema, which, along with the
haematoma,acts like a mass lesion to cause progression of the neurological
deficit.
• If big enough, this can cause shift of the intracranial contents, producing
transtentorial coning and sometimes rapid death.
• If the patient survives, the haematoma is gradually absorbed, leaving a
haemosiderin-lined slit in the brain parenchyma.

23. Clinical presentation
• Clinical presentation of stroke depends upon which arterial territory
is involved and the size of the lesion.
• unilateral motor deficit, a higher cerebral function deficit such as
aphasia or neglect, or a visual field defect-cerebral hemisphere
• Ataxia, diplopia, vertigo and/or bilateral weakness-lesion in the brain
stem or cerebellum.
• Reduced conscious level usually indicates a large volume lesion in the
cerebral hemisphere but may result from a lesion in the brain stem or
complications such as obstructive hydrocephalus, hypoxia or severe
systemic infection.

24. Cincinnati prehospital stroke scale.
• If any one of the three tests
shows abnormal findings, the
patient may be having a
stroke.
• Patients with 1 of these 3
findings -as a new event - have
a 72% probability of an
ischemic stroke.
• If all 3 findings are present the
probability of an acute stroke is
more than 85%

25. Investigations.
• Confirm the vascular nature of the lesion
• Distinguish cerebral infarction from hemorrhage
• Identify the underlying vascular disease and risk factors.

26. Investigations.
• ImmediateCT scan is essential
• MRI diffusion weighted imaging (DWI) can detect ischaemia earlier than
CT
• MR angiography (MRA) or CT angiography .
• reserved for patients in whom non-invasive methods have
provided
• contradictory picture
• yielded incomplete information,
• Details needed-delineate a saccular aneurysm, an arteriovenous
malformation or vasculitis
• Cardiac exam-ECG,TRANSESOPHAGEAL ECHO
• OTHERS-RBS,U/E/CS, FHG, Lipid profiles

27. Hypodense area:
• Ischemic area with edema,
swelling
• Indicates >3 hours old
• No fibrinolytics!

29. Management of acute stroke

30. Goals of management
• Minimizing volume of brain that is irreversibly damaged,
• Preventing complications
• Reducing the patient's disability and handicap through rehabilitation
• Reducing the risk of recurrent episodes

31. The deterioriating stroke patient
• Identify cause of deteroriation and correct
• Most common with lacunar infarction patients,Others may be due to
extension of the area of infarction, haemorrhage into it or the
development of oedema with consequent mass effect.
• Deteriorating as a result of complications such as hypoxia, sepsis,
epileptic seizures should be reversed
• Hydrocephalus

32. ADMISSION CHECKLIST
AIRWAY •Is the patient able to protect his/her airway?
•Can the patient swallow without evidence of aspiration?
•Perform a swallow screen and keep patient nil by mouth if swallowing unsafe
BREATHING Is the patient breathing adequately?
Check oxygen saturation and give supplementary oxygen if oxygen saturation < 95%
CIRCULATION Are peripheral perfusion, pulse and blood pressure adequate?
Treat with fluid replacement, anti-arrhythmics and inotropic drugs as appropriate
HYDRATION Is the patient dehydrated or unable to swallow?
Give fluids parenterally or by nasogastric tube if swallow is unsafe

33. NUTRITION Assess nutritional status
Consider nutritional supplements
If dysphagia persists for a day or two, start feeding via a nasogastric tube
MEDICATION
If the patient is dysphagic, consider alternative routes for essential medications
BLOOD PRESSURE
Unless there is heart failure or renal failure,evidence of hypertensive encephalopathy or
aortic dissection, do not lower the blood pressure in the first week since it will often
return towards the patient's normal level within the first few days
•Early blood pressure reduction may decrease cerebral perfusion and increase area of
infarction .

34. BLOODGLUCOSE
•Is the blood glucose ≥11.1 mmol/l (200 mg/dl)?
•Hyperglycaemia may increase infarct volume, therefore use insulin (via infusion or
glucose/potassium/insulin (GKI)) to normalise levels but monitor closely to avoid
hypoglycaemia
TEMPERATURE •Is the patient pyrexial?
•Raised brain temperature may increase infarct volume
•Investigate and treat any cause but give antipyretics early
PRESSURE AREAS These should be formally assessed and measures taken to reduce the risk
Treat infection, maintain nutrition, provide a pressure-relieving mattress and turn
immobile patients regularly
INCONTINENCE Ensure the patient is not constipated or in urinary retention
Avoid urinary catheterisation unless the patient is in acute urinary retention or
incontinence is threatening pressure areas

35. SPECIFIC MEDICAL TREATMENT

37. Thrombolysis and other revascularisation
treatments
• Intravenous thrombolysis with recombinant tissue plasminogen
activator (rt-PA) increases the risk of haemorrhagic transformation of
the cerebral infarct with potentially fatal results. However, if given
within 3 hours of symptom onset to highly selected patients, the
haemorrhagic risk may be offset by an improvement in overall
outcome .
• Alternative methods of revascularisation may be used :including
intra-arterial thrombolysis, mechanical dissolution or removal of the
thrombus

38. Prevention.
38

39. prevention
• Primary stroke prevention refers to the treatment of individuals with
no history of stroke.
• Secondary stroke prevention refers to the treatment of individuals
who have already had a stroke or transient ischemic attack.
39

40. Prevention.
PRIMARY PREVENTION
• Optimise treatment for HTN,
DM, Dyslipidaemia
• Mitigate behavioral risk
factors. (smoking, alcohol)
• Screening for risk factor
conditions in the community
SECONDARY PREVENTION.
• A= anticoagualants or
antiplatelets
• B= blood pressure
• C= cessation of cigarette,
cholesterol, carotic
revascularization
• D= diet
• E= exercise.
40

41. Prevention of stroke in AF.
• Anticoagulant therapy has both risks (principally bleeding) and
benefits (a reduced risk of thrombosis)
• Scoring systems which estimate the risks of these outcomes have
been established

42. Risk of ischaemic stroke in AF(CHA2D2VaSC
score)

43. Bleeding risk scores.

44. TIA and Stroke
• The ABCD2 score is a simple clinical prediction tool for use in triaging
patients presenting with acuteTIA. Optimized to predict the 2-day
stroke risk
• Those who are at increased risk and may benefit from hospital
admission.

45. Conclusion.

46. References.
• MOH Kenya National Guidelines For Cardiovascular Diseases
Management
• Davidson 22nd edition