Initial diagnosis and management of acute stroke

1. Acute stroke
• Dr LNR González
• Robert Mangaliso Sobukwe Hospital(Kimberley Hospital)

2. Epidemiology
Exact incidence of stroke in South Africa is not
known. Maredza et al. (2015) put the incidence rate
of stroke in rural South Africa at 244 per 100 000.
The SANBD study (2000) listed stroke as the 3rd
most common cause of mortality for both males and
females after HIV/AIDS and IHD.
Stroke is the 2nd leading cause of death in the wolrd.

3. Epidemiology
Black women had the highest mortality rate (160 per
100 000), while white men had the lowest (72 per 100
000).
More stroke deaths occur in the elderly than in young
patients and is the most common cause of death in
people over the age of 50.

4. Epidemiology
The SA
Comparative Risk Assessment Collaborating Group
estimated the
contribution of 8 risk factors to stroke:
hypertension (52%),
tobacco use (24%),
excess body weight (18%),
high cholesterol (15%),
physical
inactivity (12%),
low fruit and vegetable intake (12%),
diabetes (8%)
alcohol consumption (8%)

5. Definition
Stroke as defined by the WHO: “A stroke is caused by
the interruption of the blood supply to the brain,
usually because a blood vessel bursts or is blocked by
a clot. This cuts off the supply of oxygen and
nutrients, causing damage to the brain tissue.”

6. Definition
Transient Ischemic Attack
In the past, defined as focal cerebral ischemic event with symptoms
lasting < 24 hours
Newer proposed definition (2002):
Brief episode of neurological dysfunction caused by focal brain or
retinal ischemia, with clinical symptoms typically lasting less than one
hour, and without evidence of acute infarction
15% of strokes are preceded by TIA
Between 2-10% of patients with TIA will have a stroke within 2 days,
up to 17% will have a stroke at 3 months

7. Definition
Stroke subtypes include:
Ischaemic stroke/cerebral infarction
Intracerebral haemorrhage
Subarachnoid haemorrhage

8. Definition
Stroke is classified into 2 major types:
1. Brain ischaemia
2. Brain haemorrhage

9. Definition
Acute ischaemic stroke may be secondary to
atherosclerosis, thrombosis, embolism or systemic
hypoperfusion.
Blood disorders causing coagulopathy are an
uncommon primary cause of stroke.

10. Risk Factors for Ischemic Stroke
MODIFIABLE
• Hypertension
• Tobacco Use
• Diabetes
• Dyslipidemia
• Coronary Artery Disease
• Atrial fibrillation
• Obstructive Sleep Apnea
• Substance abuse
• OCP/Hormone Use

11. Risk Factors for Ischemic Stroke
NON-MODIFIABLE
• Age
• Gender
• Race / Ethnicity
• Genetic predisposition
• Hypercoagulable states
• Malignancy

12. Clinical presentation
Anterior Circulation
• Aphasia – difficulty with
language
• Neglect / inattention
• Visual field cut
• Monocular vision loss
• Hemiparesis
• Face, arm, leg on same side
• Hemisensory loss
• Face, arm, leg on same side
• Dysarthria – difficulty with
speech

13. Clinical presentation
Posterior Circulation
• Vertigo
• Ataxia
• Double vision
• Dysarthria
• Visual field cut
• Hemiparesis and
hemisensory loss
• Facial involvement may be
contralateral to arm and leg
weakness/ sensory loss

14. Clinical presentation
Clinical Examination
Should be brief but thorough.
The NIHSS can be used as a
prognostic tool and used to
assess severity.

15. Special Investigations
All patients
To exclude conditions that may mimic a
stroke.
• blood glucose
• full blood count
• urea, creatinine, electrolytes
• ESR or CRP
• ECG
• chest X-ray
• oxygen saturation

16. Special Investigations
Investigations that may be
required on selected patients
based on patient history and
clinical suspicion.
• INR if patient suspected or known to be on
warfarin
• fasting serum lipids
• serological test for syphilis (RPR or VDRL)
• lumbar puncture
• echocardiogram: transthoracic or
transoesophageal
• 24-hour cardiac Holter
ETC

17. Brain imaging
Brain imaging distinguishes
ischaemic stroke from intracranial
haemorrhage.
Haemorrhage v. infarct cannot be
reliably predicted on clinical
grounds, and management differs.
Ideally, possible stroke patients
should be evaluated and have a CT
brain scan within 30 minutes of
arrival in the emergency unit

18. Brain imaging
Indications for URGENT CT scan include:
(i) depressed level
of consciousness for which the cause is uncertain;
(ii) suspected
subarachnoid haemorrhage or cerebellar haematoma;
(iii) if the
diagnosis is in doubt – to exclude treatable causes e.g.
subdural
haematoma, space-occupying lesion or other mimics of
stroke;
(iv)
if anticoagulants (e.g. patient in atrial fibrillation) or
thrombolytic
therapy are planned – for immediate detection of
intracerebral
haematoma or haemorrhagic infarct;
(v) worsening neurological
deficits;
(vi) history or clinical findings suggestive of trauma; and
(vii) ongoing seizures.

19. Brain imaging
Non-contrast CT scan of the brain
distinguishes reliably between
haemorrhagic and ischaemic stroke
and is the most cost-effective
strategy for imaging acute stroke
patients.
Non-haemorrhagic
infarcts (ischaemic strokes) may
not be apparent on CT scan
within the first 6 hours of onset.

20. Brain imaging
Anterior cerebral artery (ACA)
infarct
Radiographic features
The features are those of cerebral
infarction in the anterior cerebral artery
vascular territory:
paramedian frontoparietal cerebral cortex
anterior corpus callosum
anterior limb of the internal capsule
inferior portion of the caudate head

21. Brain imaging
Posterior circulation infarction
(POCI)
Radiographic features
CT, which is the main brain imaging
modality in hyperacute stroke,
unfortunately, has a known limited
sensitivity to assess strokes involving the
posterior circulation, especially in the
posterior fossa structures

22. Brain imaging
Haemorrhagic stroke
Radiographic features
The sensitivity of CT to the presence of
subarachnoid blood is strongly influenced
by both the amount of blood and the time
since the haemorrhage.
The diagnosis is suspected when a
hyperattenuating material is seen filling
the subarachnoid space. Most commonly
this is apparent around the circle of
Willis, on account of the majority of berry
aneurysms occurring in this region
(~65%), or in the Sylvian fissure (~30%)

23. Management
General supportive treatment to maintain
homeostasis and treatment of
complications:
Monitoring
4-hourly observations for the first 72 hours after stroke
Airway protection and pulmonary function
Common causes of hypoxia are partial airway
obstruction, hypoventilation, aspiration pneumonia and
atelectasis
Patients with decreased level of consciousness or signs of
brainstem dysfunction are at greatest risk of airway
compromise because of impaired oropharyngeal mobility
and loss of protective reflexes
Fluid balance
Many stroke patients are dehydrated on admission to
hospital; this is associated with poor outcome.
Patients should remain nil per mouth, and fluids
provided through intravenous line until their swallowing
is formally assessed.
Normal saline (0.9%) is recommended for fluid
replacement during the first 24 hours after stroke.

24. Management
Blood pressure
Blood pressure is elevated in many patients with acute
stroke and often drops spontaneously during the first
days after stroke, even without specific medical
treatment.
Blood flow in the critical ischaemic penumbra of the brain
(brain tissue that is potentially salvageable following
stroke) is passively dependent on the mean arterial
pressure, and lowering the mean arterial pressure may
damage this area.
It is common practice in many centres to begin cautious
blood pressure reduction when levels exceed 220 mmHg
systolic and 120 mmHg diastolic.
Glucose metabolism
Hyperglycaemia after acute stroke is associated with
larger infarct volumes and poor functional outcome.
Hypoglycaemia (<2.8 mmol/l) may mimic an acute
ischaemic infarction, and should be treated by
intravenous dextrose bolus or infusion of 10 - 20%
glucose.

25. Management
Body temperature
Fever is associated with poorer neurological outcome
after stroke.
It is common practice to treat fever (and its cause) when
temperature ≥37.5°C
Swallowing and nutrition
Nil per mouth until assessment of ability to swallow (as a
matter of routine) because of high risk of aspiration.
All patients have their swallowing assessed before
receiving aspirin. Aspirin could be delayed for 24 hours,
so it is not necessary to put a nasogastric tube into every
patient

26. Management
Specific treatment
Intravenous thrombolytic therapy with recombinant
tissue plasminogen activator (tPA) is an accepted
therapy for acute ischaemic stroke within 4.5 hours
of onset.
Intravenous tPA (0.9 mg/kg body weight, maximum
90 mg, with 10% of the dose given as a bolus and the
remainder given by a 60-minute infusion) given
within 3 hours after ischaemic stroke onset,
significantly improves outcome.
Imaging of the brain (CT scan or MRI) must be done
prior to treatment with tPA

28. Management
Specific treatment
Endovascular therapy
There are no RCTs comparing intra-arterial tPA with
intravenous tPA, which is the presently accepted
standard of care.
The limited trials (intra-arterial route) available are
often characterised by inadequate controls, no good
outcome studies, and small sample sizes.

29. Management
Specific treatment
Early antiplatelet treatment after acute ischaemic
stroke
Aspirin started within 48 hours of ischaemic stroke
is safe and effective, resulting in a modest net
benefit with significantly fewer recurrent strokes.
Aspirin was tested in large RCTs in acute (<48
hours) stroke, and a significant reduction was seen
in death and dependency and recurrence of stroke (9
fewer deaths or non-fatal strokes per 1 000 in the
first few weeks, and 13 fewer dead or dependent per
1 000 after some weeks’ or months’ follow-up).

30. Management
Specific treatment
Anticoagulation for acute ischaemic stroke
Results of recent trials show that early
administration of either heparin or low-molecular-
weight heparin fail to show net benefit and are
associated with an increased risk of bleeding
complications.

31. Preguntas por favor