PENYAKIT SEREBROVASKULER

1.
2.
3.
4.

Definisi
Etiologi
Jenis-jenis penyakitnya
Patogenesis

STROKE
1. Definisi
2. Epidemiologi
Prevalence in the US: 550/100,000
Predominant age: Risk increases >45, and is highest in the 7th and 8th
decades.
Predominant sex: Male > Female (3:1), but equalizes after menopause

Hypertension is the most important risk factor for ischemic and hemorrhagic stroke. The
incidence of stroke increases directly in relation to the degree of elevation of systolic and
diastolic arterial blood pressure above threshold values. More important, there has been
conclusive evidence for more than 30 years that control of hypertension prevents strokes. Metaanalyses of randomized controlled trials confirm an approximate 30 to 40% reduction in stroke
risk with lowering of blood pressure.
Approximately 7 to 10% of men and 5 to 7% of women older than 65 years have asymptomatic
carotid stenosis of greater than 50%. Epidemiologic studies suggest that the rate of unheralded
stroke ipsilateral to a stenosis is about 1 to 2% annually.
Nonvalvar atrial fibrillation carries a 3 to 5% annual risk for stroke, with the risk becoming
even higher in the presence of advanced age, previous TIA or stroke, hypertension, impaired left
ventricular function, and diabetes mellitus.
In epidemiologic studies, the risk for stroke in smokers is almost double that in nonsmokers,
but the risk becomes essentially identical to that of nonsmokers by 2 to 5 years after quitting.
The relative risk for stroke is two to six times greater for patients with insulin-dependent
diabetes. Patients with sickle cell disease have a markedly increased risk for stroke.
Hyperlipidemia also increases the risk for stroke, and reduction of low-density lipoprotein
cholesterol levels with statins reduces this risk. Some evidence suggests that abdominal obesity
in men and obesity and weight gain in women are independent risk factors for stroke. Weight
reduction in overweight people is recommended, but weight loss has not been proved to reduce
the risk for stroke.
Epidemiologic studies have found that consumption of fruits and vegetables is associated with a
lower risk for stroke, but no randomized trials have proved the value of changing dietary habits.
Heavy alcohol consumption may be a risk factor for ischemic and hemorrhagic stroke.
Postmenopausal hormone replacement therapy has been shown to increase the risk for stroke.
The absolute risk for stroke remains low, however, in otherwise healthy, low-risk patients. Metaanalysis suggests an increase in the relative risk for stroke in women taking oral contraceptives,
but the absolute risk for stroke is small. Women who smoke, are hypertensive or diabetic, have
migraine headaches, or have previously suffered thromboembolic events may be at increased risk
for stroke when taking oral contraceptives.
GOLDMAN - CECIL MEDICINE. 23RD EDITION. LEE GOLDMAN.
SAUNDERS. 2007
3. Etiologi

NEUROLOGY.MARK MUMENTHALERS. THIEME. 2004

4. Klasifikasi

Table 641. Classification and Etiology of Cerebrovascular Accidents (CVA; Stroke).

Ischemic
Cerebral infarction
Nonocclusive
Cerebral arterial thrombosis
Cerebral embolism
Transient ischemic attack
Hypertensive encephalopathy with vasospasm
Venous occlusion in hypercoagulable states, infection
Arteritis: polyarteritis nodosa, giant cell arteritis
Dissecting aneurysm of the aorta
Carotid injury
Hemorrhagic
Intracerebral hemorrhage: hypertensive
Subarachnoid hemorrhage: berry aneurysms
Associated with vascular malformations and neoplasms
Associated with bleeding diatheses such as coagulation disorders, thrombocytopenia;
anticoagulant therapy
Mycotic aneurysm

CONCISE_PATHOLOGY. CLIVE R. TAYLOR. MCGRAW-HILL. 2006

5. Factor resiko
6. Patofisiologi

Vascular lesions causing ischaemia. A Thrombosis: initiated by either

abnormal flow (e.g. stasis, turbulence), damage to vessel wall (e.g.
denudation of endothelial lining) or abnormal blood constituents. B
Embolism. C Spasm: due to contraction of smooth muscle in media of
vessel, for example due to lack of nitric oxide from endothelium. D
Atheroma: occurs only in arteries and may in turn be complicated by
thrombosis and embolism. E Compression: veins are more susceptible
because of their thinner walls and lower intraluminal pressure. F Vasculitis:
inflammation of vessel wall narrows lumen and may be complicated by
superimposed thrombosis. G Vascular steal: for example, an artery may be
narrowed by atheroma but flow is still sufficient to maintain viability of
perfused territory; however, flow may be compromised by increased
demands of a neighbouring territory. H Hyperviscosity: increased viscosity,

in for example hypergammaglobulinaemia resulting from myeloma, causes

impaired flow and predisposes to thrombosis.
CONCISE_PATHOLOGY. CLIVE R. TAYLOR. MCGRAW-HILL. 2006
Mmmmmm

MECHANISM OF DISEASE. AN INTRODUCTION TO CINICAL SCIENCE.

2 EDITION. STEPHEN TOMLINSON. CAMBRIDGE UNIVERSITY PRESS.
2008
ND

Table 26-4. Comparison of the major causes of stroke

Cause

% Clinical

30-day

Pathogenesis

Predisposing factors

Cerebral
infarction

Intracerebral
haemorrhage

Subarachnoid
haemorrhage

presentation
85 Slowly evolving
signs and
symptoms

mortality
(%)
15-45

10 Sudden onset of
80
stroke with raised
intracranial
pressure
5 Sudden headache 45
with meningism

Cerebral
hypoperfusion
Embolism
Thrombosis

Heart disease (e.g.

infective endocarditis,
endocardial thrombus)
Hypertension
Atheroma Diabetes
mellitus

Rupture of microaneurysm or
arteriole

Hypertension Vascular
malformation

Rupture of saccular Hypertension Polycystic

aneurysm on circle renal disease
of Willis
Coarctation of the aorta

7. Manifestasi klinis

Effect of ischemia on the brain. Diagram of the effect of sudden total

deprivation of blood supply to the brain on tissue metabolism, consciousness,
the EEG, neuronal morphology, and tissue glucoseconcentration.

NEUROLOGY.MARK MUMENTHALERS. THIEME. 2004

COLOR ATLAS OF PATHOPHYSIOLOGY. STEFAN SILBERNAGL. THIEME. 2000

8. Diagnosis banding
Table 142-2 Differential Diagnosis of Acute
Stroke

Hypoglycemia
Postictal paralysis (Todd paralysis)
Bell's palsy
Hypertensive encephalopathy

Epidural or subdural hematoma

Brain tumor or abscess
Complicated migraine
Encephalitis
Diabetic ketoacidosis
Hyperosmotic coma
Meningoencephalitis
Wernicke encephalopathy
Multiple sclerosis
Meniere disease
Drug toxicity (lithium, phenytoin, carbamazepine)
EMERGENCY MEDICINE MANUAL. 6TH EDITION. O. JOHN. MA. THE
MCGRAW-HILL COMPANIES. 2007

9. Penegakan diagnosis

History

Vital Signs

Attempt
to
identify,
as
accurately as possible, the onset,
course, and type of symptoms, as
well as the patients activity at
onset.
Determine the patients stroke
risk
factors,
other
potential
causes
for
the
patients
symptoms,
and
any
contraindications to thrombolytics
or other agents.
Neurologic deficits that occur
abruptly, and are maximal at
onset, suggest an embolic stroke.
Stepwise, incremental deficits are
more indicative of thrombosis.
Hemorrhagic strokes often have
a rapid onset. Maximum deficit
may be present immediately but
worsening
may
occur.
Consciousness may be impaired.

Subarachnoid
hemorrhage
(SAH)
is
characterized
by
symptoms of variable onset and
progression; severe headache and
neck stiffness; and often impaired
consciousness.

Hypotension
may
be
the
underlying cause of a stroke;
markedly elevated blood pressure
is suggestive but not diagnostic
of a hemorrhagic stroke.
An irregular cardiac rhythm may
indicate chronic or new-onset
atrial fibrillation and an embolic
source.

Increased
ICP
may
be
accompanied by bradycardia.
Focus on searching for an
underlying
systemic
cause,
especially a treatable one.
HEENT

Physical
Examination

Note any signs of trauma.

Palpate the temporal arteries.
Fundoscopic exam may reveal
evidence
of
embolization.
Papilledema indicates increased
ICP. Retinal hemorrhages may
be noted in SAH.
Determine patency of the
airway and ensure the airway is
protected.
Neck: evaluate the carotid
pulses and check for carotid
bruits, Neck stiffness may or may
not be present in SAH.

Cardiac
exam:
note
any
arrhythmias
or
evidence
of
valvular disease (i.e., murmurs).
Neurologic exam
The initial neurologic exam
should be a brief search for
signs of increased ICP or
impending
transtentorial
herniation (e.g., dilated pupil,
depressed consciousness,
or
posturing).
Neurologic deficits that do not
conform to the distribution of
any
single
cerebral
artery
suggest a hemorrhagic or mass
lesion.

Assess
the
level
of
consciousness
and
mental
status. Determine whether the
patient has aphasia (expressive
or receptive?) or dysarthria.
Evaluate cranial nerve function,
with special attention paid to
pupils, extraocular
movements, visual fields, facial
symmetry,
gag
reflex
and
corneal reflex.
The presence of a gaze palsy
may help localize the lesion. A
patient with a cerebral
hemispheric stroke will typically
gaze toward the side of the
insult; a brainstem
infarct will cause the patient to
gaze away from the side of the
lesion.
Motor exam: the most sensitive
indicator of upper extremity
weakness is the
presence of a pronator drift.
Whenever
possible,
lower
extremity strength should
be assessed by observing the
patients gait.

Sensory
exam:
peripheral
sensation (light touch, pinprick,
and vibration/position
sense).
Double
simultaneous
stimulation: assess sensation on
both sides of
the
body
simultaneously;
patients with cortical infarcts
will only notice the unaffected

Evaluation

side.
Cerebellar exam: look for
nystagmus, ataxia, or poor
coordination.
Reflexes: recent stroke is
accompanied by hyporeflexia
(and
flaccidity). Search for
pathologic
reflexes
(e.g.,
presence of a Babinski reflex
indicates
an
upper
motor
neuron disorder).
Pulse Oximetry
Rapid determination of oxygen
saturation
may
reveal
impending respiratory failure
and the need for mechanical
ventilation.
Supplemental
oxygen may suffice.
Laboratory
Bedside glucose testing is
crucial to exclude hypoglycemia
as a cause of focal neurologic
deficits.
A complete blood count may
reveal
an
underlying
hematologic disorder presenting
as a stroke.
Prothrombin time (PT) and
partial
thromboplastin
time
(PTT) are helpful in excluding
coagulopathy.
Baseline serum electrolytes are
recommended.
An elevated ESR may suggest
giant cell arteritis or other
vasculitis.
Blood for type and cross match
(patients with SAH)
Consider a toxicology screen in
patients suspected of drug
abuse (although the results
seldom change the patients
acute management).
Pregnancy test in females of
child-bearing age.
Lumbar puncture (LP) is
indicated when CNS infection or
SAH is suspected. In the case of
SAH, LP is performed after a
negative CT scan. LP may also
suggest a venous or sinus
thrombosis (CSF pressure is
typically
increased
and
pleocytosis
may
occur),
or
granulomatous
angiitis
(CSF
pleocytosis occurs).
EKG
May detect cardiac ischemia, or
cardiac
arrhythmias
which
predispose to stroke (e.g., atrial
fibrillation).
In
addition,
multiple
abnormalities
are
described
in
patients
with
subarachnoid
hemorrhage,
including peaked or symmetric,
deeply
inverted
T
waves;
shortened PR intervals; and tall

U waves.
Chest radiograph
In selected patients, chest Xray
(CXR)
may
reveal
an
infectious process, malignancy,
or evidence of heart failure. In
intubated patients, CXR is used
to confirm placement of the
endotracheal tube.
Imaging
Noncontrast CT scan is the
emergency radiologic study of
choice when evaluating patients
with suspected stroke, TIA, or
SAH. CT is able to distinguish
between
ischemic
and
hemorrhagic strokes, and will
detect blood in more than 90%
of cases of aneurysmal rupture.
In addition, early signs of
cerebral edema are identified
with noncontrast CT scanning.
When available, MRI is useful
for early ischemic infarcts. MRI
may also be more sensitive for
ischemic
strokes
in
the
brainstem or cerebellum, as well
as
in
detecting
thrombotic
occlusion of venous sinuses.
Electroencephalogram (EEG) is
rarely useful in the acute
evaluation of stroke. It may,
however, help to differentiate
between seizure disorder and
TIA, or between lacunar and
cortical infarcts.

EMERGENCY MEDICINE. SEAN. O. HANDERSON. LANDES BIOSCIENCE.

2006
10.Penatalaksanaan
General Management Issues

Oxygen

Blood Pressure Control

As with all emergent conditions,

evaluation of the patient with a
neurologic deficit begins with airway,
breathing, and circulation. Patients with
severely depressed mental status and
patients with an unprotected airway may
require
intubation
and
mechanical
ventilation.
All patients should be placed on
continuous pulse oximetry and cardiac
monitoring,
and
have
peripheral
intravenous access established.
Patients noted to have signs of
increased ICP should be aggressively
managed.
Supplemental oxygen may be required
to maintain oxygen saturation >95%.
However, in the absence of hypoxia,
supplemental oxygen has not been
shown to affect outcome.
In the first few hours following acute
stroke, mild to moderate hypertension is
commonly observed. Over the next few
hours to days, the blood pressure

Anticoagulants

Antiplatelet Agents

generally declines spontaneously. The

ischemic penumbra may be dependent
upon a moderately increased blood
pressure for adequate perfusion; thus,
use of antihypertensive agents may
exacerbate the patients condition.
Cautious blood pressure controlwith
easily titratable, short-acting parenteral
medicationsis recommended in the
following situations: (1) hypertensive
encephalopathy; (2) cardiac ischemia or
aortic
dissection;
(3)
intracerebral
hemorrhage; (4) when thrombolytic
therapy is considered (see exclusion
criteria below); and (5) the mean arterial
pressure (MAP) is >130, or the SBP is
>220.
Heparin has been shown to benefit
patients at risk for cardioembolic stroke
(especially patients with ischemic or
rheumatic heart disease). In addition,
patients with venous sinus occlusion
benefit from heparin use.
Aspirin has been shown to reduce the
rate of nonfatal recurrent stroke and
death
after
acute
stroke
(versus
placebo). Aspirin is recommended in
patients who are not candidates for
thrombolytics or other anticoagulants.
Ticlopidine inhibits the ADP pathway of
platelet aggregation; it also reduces
blood fibrinogen levels. In patients with
TIA or minor stroke, ticlopidine results in
significant risk reduction in stroke
recurrence or death versus aspirin.
However, the hematologic side effects
(TTP,
thrombocytopenia,
and
neutropenia)
have
limited
its
recommended use to patients who have
a contraindication to aspirin and who
can be closely monitored in this setting;
clopidogrel
is
preferred
by
many
practitioners.
Clopidogrel is similar in action and
effect to ticlopidine. It is recommended
for aspirin-intolerant patients and has a
significantly lower rate of TTP than
ticlopidine.

EMERGENCY MEDICINE. SEAN. O. HANDERSON. LANDES BIOSCIENCE.

2006
11.Rehabilitasi
12.Pencegahan
13.Prognosis
14.Komplikasi