Vivien Puspitasari, dr, SpS

Faculty of Medicine
Pelita Harapan University

 Anatomy

& Brain circulation

Stroke definition
Types of stroke
Pathophysiology
Sign and symptom
Diagnosis
Treatment

Stroke

is clinical syndrome characterised by

an acute loss of focal brain function lasting more
than 24 hours or leading to death, which is
thought to be due to either spontaneous
haemorrhage into or over the brain substance
(primary intracerebral haemorrhage or
subarachnoid haemorrhage respectivelyhaemorrhagic stroke) or inadequate blood supply
to a part of the brain as a result of flow,
thrombosis or embolism associated with diseases
of the blood vessel, heart or blood (ischemic
stroke/cerebral infarction)

Transient Ischemic Attack

clinical syndrome characterised by the
acute loss of focal brain or monocular
function lasting less than 24 haours, due
to inadequate blood supply to a part of
the brain or eyes as a result of low blood
flow, thrombosis or embolism associated
with diseases of the blood veseels, heart
or blood.

 Infarction: Incidence 80% - mortality 40%

50% - Thrombotic atherosclerosis
Large-vessel 30% (carotid, middle cerebral)
Small vessel 20% (lacunar stroke)
30% Embolic (heart disease/ atherosclerosis)
Cardioembolic
Artery-to-artery

Hemorrhage: Incidence 20% - mortality

60%
Intracerebral or subarachnoid
hypertension, aneurysm, AVM

Based on stadium / course

a. TIA, RIND
b. stroke in evolution
c. completed stroke
Based on vascular system
a. Carotid system = anterior
b. Vertebrobasilar = posterior
Bamford Classification
TACI, PACI, LACI, POCI

Atheroma
important factor in embolic & thrombotic
stroke
Commonly rises at the junctions of arteries
ex.carotis bifurcation
Risk factors: Hypertension, Diabetes,
smoking, family history,Cholesterol, excess
alcohol intake
Cardioemboli
AF

AUTOREGULATION
Normally : CPP 70 100 mmHg (CPP=MAP ICP) ; CBF =
CPP/CVR
To maintaine CBF 50 ml/100mg/menit needs CPP 40 - 140
mm Hg

ISCHEMIC CORE
the lowest CBF ,Neuron degeneration, blood
vessel dilatated , High lactic acid , low Po2
nekrosis
PENUMBRA around ischemic core higher CBF
loss cell function , saveable
Around penumbrahyperemia & edema.
Dilatated blood vessel high CBFhyper
perfusion

Usually due to hypertension or ruptered

aneurysm/ AVM, bleeding disorders
Hypertension Lipohyalinosis &
microaneurysm (Charcot-Bouchard
aneurysm) of small penetrating arteries
within the brain
Ganglia basal (50%), lobar white matter
(20%), pons (10%), cerebellum (10%)

ANEURYSM

HYPERTENSION

Ruptured saccular aneurysm

a. komunikans anterior, a. serebri media,
anterior, a. komunikans posterior
Symptom: sudden severe headache = like being
hit by a baseball bat = thunder clap; neck
stiffness
Complication : hydrocephalus

 History taking
Physical & neurologic examination
Supportive examination
Treatment

Stroke
Stroke like

No

Yes
Location
-Brain : hemiphere , brain stem
-Vascular system : Carotid
Vertebrobasilar
Etiopathology
Ischemi, infarct :

- trombosis
- emboli
Hemorrhagic : - intracranial
- Subarachnoid
(SAH)
Stadium
Stroke in evolution
Completed stroke
TIA : < 24 hours
RIND : < 2 weeks

Carotis system symptom

Facial, extremities pareses (contralateral lesion)
Deficit of sensibilities
Afasia
Dysartria
Vertebrobasilar system
Visual disturbance : diplopia, cortical blindness
Ataksia
Vertigo
Tetraparesis
Dysphagia

The presence of any of the following should alert

the physician
to consider conditions other than stroke:
- Gradual progressive course and insidious onset
- Pure hemifacial weakness including forehead
(Bells palsy)
- Trauma
- Fever prior to onset of symptoms
- Recurrent seizures
- Weakness with atrophy
- Recurrent headaches (migrain)

Score system: Gajah Mada score, Siriraj score

SIRIRAJ STROKE SCORE
(2,5xconcious)+(2x vomiting)+ (2xheadache)
+ (0,1xdiastolic)-(3xateroma)-12

Score >1 haemorrhage

Score <1 infarct
Consciousness: CM=0 , drowsy/stupor=1, semi coma/coma=2
Vomiting & headache within 2 h : no=0, yes=1
Ateroma diabetic history
none=0
- angina
one/more=1
- claudicatio

Sensitivity : 89.3% and 93.2%

Specificity : 90.3%.

Plain CT scan of the head is the initial neuroimaging study of

choice in
acute stroke. The main objective is to exclude hemorrhagic
stroke and
stroke mimickers.
CT scan is 100% sensitive in documenting intracranial hemorrhage
(ICH)
and 96% sensitive in documenting subarachnoid hemorrhage (SAH).
Cerebral infarcts are often not documented within 3 hours from stroke
onset. However, 60% have early infarct signs when viewed very
closely:
1. Dense MCA sign
2. Obscuration of the lentiform nucleus
3. Loss of the gray-white interphase along the lateral insula (Insular
ribbon sign)
4. Effacement of the sulci

Obscuration of lentiform nucleus

Dense MCA sign

Insular ribbon sign

MRI has the technical advantage of documenting

small lesions or those located in the brainstem or
posterior fossa

MRI can detect early infarction as early as 90

minutes using Diffusion Weighted Imaging (DWI)

Despite the superior diagnostic yield of MRI over CT, MRI is

not
recommended as routine evaluation of patients with acute
ischemic
stroke. It is more expensive, time-consuming and less
readily available.

MRI
DIFFUSION

CT can accurately document the exact location of the

hemorrhage and the presence of mass effect, ventricular
extension and hydrocephalus.
In hypertensive ICH, a repeat plain CT scan after 24 hours is
recommended especially in cases showing clinical deterioration to
document hematoma enlargement and/or development of
hydrocephalus.
Computation of Hematoma Volume (Kothari method)
Hematoma volume (in cc) = ( A x B x C ) : 2

A= Largest diameter of hematoma (in cm)

B= Diameter perpendicular to A (in cm)
C= Number of slices on CT scan with hemorrhage X slice thickness
(in cm)

RADIOIAMAGING: CT SCAN
Ischemic stroke

Hemorrhagic stroke

MULTISLICES CT SCAN : CT
Angiography

Ascertain clinical diagnosis of stroke (history and physical exam are

very
important)
Exclude common stroke mimickers
Basic emergent supportive care (ABCs of resuscitation)
Neuro-vital signs, BP, MAP, RR, temperature, pupils
Perform stroke scales (NIHSS, GCS)
Monitor and manage BP; treat if SBP>220 or DBP>120 or MAP>130
Precaution: Avoid precipitous drop in BP (not >20% of baseline MAP)
Do not use rapid-acting sublingual agents; when needed use easily
titratable IV or oral antihypertensive medication.
Identify comorbidities (cardiac disease, diabetes, liver disease,
gastric
ulcer, etc.)
Recognize and treat early signs and symptoms of increased
ICP
Ensure appropriate hydration. If IVF is needed, use 0.9% NaCl

Allow permissive hypertension during the first week to

ensure adequate CPP but ascertain cardiac and renal
protection
a. Treat if SBP>220 or DBP>120 or MAP>130
b. Defer emergency BP therapy if MAP is within 110-130 or
SBP=185-220
mmHg or DBP=105-120 mmHg, unless in the presence of:
Acute MI
Congestive heart failure
Aortic dissection
Acute pulmonary edema
Acute renal failure
Hypertensive encephalopath y

Thrombolytic therapy

If within 3 hours of stroke onset, consider IV

recombinant tissue plasminogen activator (rtPA)
-----at least 30% more likely to have minimal or no
disability at 3 months.
Dose of rtPA is 0.9 mg/kg (maximum 90 mg). 10% of
total dose is given as IV bolus, the rest as infusion
over 60 minutes.
If within 6 hours of stroke onset and in specialized
centers,
consider intra-arterial (IA) thrombolysis
Streptokinase has no role in acute thrombolysis for
ischemic stroke .

Antithrombotic therapy

Stroke non-cardioembolic : Aspirin 160-325 mg/day start

as early as
possible and continue for 14 days

Anticoagulation

Stroke cardioembolic
If source of embolism can be demonstrated, consider early
anticoagulation with IV heparin or low
molecular-weight heparin (LMWH)
or
Aspirin 160-325 mg/day (if anticoagulation is not possible
or contraindicated)

Neuroprotection
Neuroprotective Interventions: The 5
H
Principle
Avoid hypotension, hypoxemia,
hyperglycemia or hypoglycemia and
hyperthermia (fever) during acute
stroke in an effort to "salvage the
ischemic penumbra

Neuroprotectans
Protect against excitotoxins and prolong
neuronal survival
Block the release of glutamate, free
radicals, inflammatory cytokines, and the
accumulation of intracellular calcium
cations.
CITICHOLINE / CDPcholine
helps increase phosphatidylcholine synthesis and inhibition
of
phospholipase A2 within the injured brain during ischemia

Medical Treatment for all ICH:

1. The goals are to prevent complications and careful manage
BP.
2. Maintain MAP <130, but not lower than 110 mmHg
3. Manage increased ICP
4. Start anticonvulsants only if with seizures
5. Prevent and treat respiratory complications.
6. Prevent and treat infections.
7. Maintain adequate nutrition.
8. Ensure proper fluid and electrolyte balance; maintain
normothermia and normoglycemia.
9. Rehabilitate early once stable.
10.Practice bedsore precautions.
11.Deep-vein thrombosis and pulmonary embolism
prophylaxis

Non-surgical candidates
Patients with small hemorrhages
(<10 mL) or minimal neurological
deficits
Patients with GCS<5 except those
who have cerebellar hemorrhage and
brainstem compression
Patients with hematoma volume >
85 mL

Candidates for immediate surgery

Patients with cerebellar hemorrhage >3 cm who are
neurologically deteriorating or have brainstem compression
and hydrocephalus from ventricular obstruction
Patients with bleed associated with a structural lesion such
as an aneurysm, AV malformation or cavernous angioma if
there is a chance for good outcome and the vascular lesion
is surgically accessible
Clinically deteriorating young patients with moderate or
large lobar hemorrhage.
Ventricular drainage for patients with intraventricular
hemorrhage with moderate to severe hydrocephalus.

All other patients may benefit from

surgery
Patients with basal ganglia or
thalamic hemorrhage
Patients with GCS >4
Patients with supratentorial
hematoma with volume >30 cc

Signs and symptoms of increased ICP

1. Deteriorating level of sensorium
2. Cushings triad
i. Hypertension
ii. Bradycardia
iii. Irregular respiration

3. Anisocoria
4. Headache, vomit

1. Control agitation and pain with short-acting medications,

such as NSAIDS
and opioids.
2. Control fever. Avoid hyperthermia.
3. Control seizures if present. May treat with phenytoin with a
loading dose of 18-20 mg/kg IV then maintained at 3-5
mg/kg. Status epilepticus should be managed accordingly.
4. Strict glucose control between 80-110 mg/dL
5. No dextrose-containing IVF. Hyperglycemia may extend
ischemic zone (penumbra) and further cause cerebral
edema
6. Use stool softeners to prevent straining.

Elevate the head at 30 to 45 degrees to assist venous drainage.

Give osmotic diuretics: Mannitol 20% loading dose at 1 g/kg,
maintenance dose at 0.5-0.75 mg/kg) to decrease intravascular
volume and free water.
Lost fluids must be replaced. Hypertonic saline is an option and has
the
advantage of maintaining an effective serum gradient for a prolonged
period with lower incidence of rebound intracranial hypertension. Aim
for
serum osmolarity=310 mOsm/L. (Serum osmolarity = 2 (Na) +
Glucose/18
+ BUN /2.8)
Hyperventilate only in impending herniation by adjusting tidal volume
and pCO2 between 25 to 30. This maneuver is usually effective only
for
approximately 6 hours. Otherwise maintain normal pCO2 between 35
and 40.

Carefully intubate patients with GCS 8 or less, or those

unable to protect
the airway.
Do CSF drainage in patients with intraventricular
hemorrhage (IVH) or
hydrocephalus.
Use barbiturates if all other measures fail. Available locally
is thiopental
(loading dose=10 mg/kg, maintenance dose titrated at 112 mg/kg/hour
continuous infusion)
Consider surgical evacuation for mass lesions.
Consider decompressive hemicraniectomy in cases of
malignant middle
cerebral artery infarcts

NIHSS was developed to quantify neurological

deficits status in stroke patients based on a scale
originally devised at the university of Cincinnati
Stroke Center (Brott et all,1989;Goldstein et al
1989)
NIHSS is a 0 24 point scale (11 item)
Score :
* higher than 15 points major stroke
* a score of 4 15 points moderate stroke
* less than 4 points mild stroke
NIHSS is performed during the bedside neurological
evaluation (twice exam : 24 hours and discharge)
Disadvantage of NIHSS scale is
* not good for posterior circulation stroke,
* and who have mainly brainstem features
scores less severe despite significant deficits

Grade 0
No symptoms at all
Grade 1
No significant disability despite
symptoms: able to carry out usual duties and
activities
Grade 2
Slight disability: unable to carry
out all previous activities but able to look
after own affairs without assistance
Grade 3
Moderate disability: requiring
some help, but able to walk without
assistance
Grade 4
Moderate severe disability:
unable to walk without assistance, and
unable to attend to own bodily needs
Grade 5
Severe disability: bedridden,
incontinent, and requiring constant nursing
care and attention
Grade 6
Deceased

Control of risk factors

Antiplatelets (aspirin, ticlopidine, dipyridamole,
extended-release dipyridamole + aspirin
combination, clopidogrel,
cilostazol)
Anticoagulation ----for cardioembolic
Carotid ultrasound ---carotid stent
TCD (Trancranial dopler)

 Long-term

strict BP control and

monitoring
Consider CT angiography, MRA,or 4vessel
angiography in suspected cases of
aneurysm, AV malformation or
vasculitis

THANK YOU