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MANAGEMENT OF STROKE
Abdul Gofir
Neurology Department of
Medical Faculty
Gadjah Mada University
Stroke: Definition
Stroke is clinically defined as a
neurologic syndrome characterized
by acute disruption of blood flow to
an area of the brain and
corresponding onset of neurologic
deficits related to the concerned
area of the brain
Causes of Stroke
Almost 80% of
strokes are from
an emboli or a
thrombus
Embolic &
Thrombotic
strokes are
ISCHEMIC
< 15% of strokes
are from
hemorrhage, with
an even smaller
percentage
caused by
hypoperfusion
Ischemic
Injury
Apoptotic
Cell Death
Necrotic
Cell Death
Dr.J.Husada 11-2003
Causes of Ischaemic
STROKE
Blockade of blood flow by ateroma, emboli,
and ateroscelerotic
Embolic
Once in your
brain, the
embolus
eventually travels
to a blood vessel
small enough to
block its passage
The embolus
lodges there,
blocking the
blood vessel and
causing a stroke
ion
Smoking
Diabetes
Hyperlipidemia
Atrial
fibrillation
(non-valvular)
Risk
reduction with
treatment
30% - 40%
50%
reduction in hypertensive
diabetics with tight blood pressure
control
20-30% with statins in patients
with known coronary heart disease
68%
21%
(warfarin)
(aspirin)
Stroke: Classification
Ischemic stroke : Account for 80%. Results from
occlusion in the blood vessel supplying the brain
Thrombotic : Occlusion due to
atherothrombosis of small/large vessels
supplying the brain
Embolic : Occlusion due to embolus arising
either from heart (e.g. atrial fibrillation,
valvular disease) or blood vessel
Classification (cont.)
Hemorrhagic stroke : Account for 20%. Results from
rupture of blood vessels leading to bleeding in
brain
Intracerebral: Bleeding within the brain due to
rupture of small blood vessels. Occurs mainly
due to high blood pressure
Subarachnoid: Bleeding around the brain;
commonest cause is rupture of aneurysm.
Other causes: Head injury
Obesity
Smoking
Atrial fibrillation
Sedentary lifestyle
Drug abuse (e.g.
cocaine use)
Hormone
replacement therapy
Oral contraceptive
Modifiable Risk
Factors for Stroke6
Hypertension
Diabetes
Smoking
Hyperlipidemia
Carotid stenosis
Atrial fibrillation
Stroke: Symptoms
Onset
of stroke symptoms
varies as per type of stroke:
Thrombotic stroke: Develop
more gradually
Embolic stroke: Hits suddenly
Hemorrhagic stroke: Hits
suddenly and continues to worsen
Stroke: Symptoms
(cont.)
Dizziness
Confusion
Loss of balance/coordination
Nausea/vomiting
Numbness/weakness on one side of the body
Seizure
Severe headache
Movement disorder/speech disorder/blindness etc
(depending on the area of brain affected)
Mini stroke
Stroke symptoms last for less than 24 hours
(usually 10 to 15 mins)
Result as a brief interruption in blood flow to
brain
Every TIA is an emergency
TIA may be a warning sign of a larger stroke
Patients with possible TIA should be evaluated
by a physician
< 1 hour
Head CT
Ischemic Stroke
Cortical
syndrome
ECG
Echo
CARDIAC
EMBOLISM
Lacunar syndrome
Doppler
MRA
Angiogram
MRI
CT
Vasculopathy
Coagulopathy
LARGE ARTERY
SMALL
OTHER DETERMINED
ATHEROSCLEROSIS VESSEL DISEASE
CAUSE
CRYPTOGENIC
STROKE
Acute
Treatment
r-TPA
Intravenous Thrombolysis
Intravenous rtPA (0.9 mg/kg, maximum
dose 90 mg) is recommended for selected
patients who may be treated within 3
hours of onset of ischemic stroke (Class I,
Level of Evidence A).
Besides bleeding complications, physicians
should be aware of the potential side
effect of angioedema that may cause
partial airway obstruction (Class I, Level of
Evidence C).
Heparin
There is no large clinical trial in the
literature comparing i.v. heparin as
traditionally administered to placebo
International Stroke Trial: compared s.q.
heparin at comparable doses to asa and
neither in 19435 patients: result: heparin
was not beneficial
Lancet.
1997;349:1569-81
Heparinoids
TOAST trial: indicated no benefit for a
LMW heparinoid in stroke (ORG 10172)
Stroke.
1998;29:286
Management of acute
ischemic stroke
Management of acute
ischemic stroke (contd.)
Management of acute
ischemic stroke (contd.)
UPDATE ON MANAGEMENT OF
ICH (Pouratian 2003)
Medical interventions
- Cardiopulmonary optimization
(ABCSS)
- Blood pressure control
- ICP reduction
- Ultra-early hemostatic therapy
Surgical interventions
Labetolol: 5-100 mg/h by intermittent bolus doses of 10-40 mg or continuous drip (2-8
mg/min).
Esmolol: 500 g/kg as a load, maintenance use, 50-200 g/kg/min.
Hydralazine: 10-20 mg Q 4-6 h
Enalapril: 0.625-1.2 mg Q 6 h as needed.
Management of Acute
hemorrhagic stroke
RECOMMENDATIONS FOR
SURGICAL TREATMENT OF ICH
(Broderick 1999)
PREDICTORS OF EARLY
NEUROLOGIC
DETERIORATION IN ICH (Leira
2004)
Early neurologic deterioration (END) occurred in 22.9 % patients.
On admission:
Body temperature > 37.5 C (37.3 0.7 vs 36.4 0.5)
Neutrophil count by 1000-unit increase (10.8 2.9 vs 6.3 4.3)
Serum fibrinogen > 525 mg/dL (546 126 vs 396 119)
Within 48 hours:
Early ICH growth (48.2 vs 20.7)
Intraventricular bleeding (46.4 vs 29.5)
High systolic blood pressure (192 21 vs 179 27)
Source : Neurology 2004; 63: 461-467
Back
Brain Edema
Perdarahan
Efek toksik
darah
Peningkatan
TIK
Pelepasan agen
vasokonstriktor
Serotonin, Prostaglandin, darah
Iskemia
global
Influks Ca+
Nekrosis
Neuron
Influks Ca+
Vasospsme
Iskemia Fokal
Vasospasme
Influks Ca
Lumen
vasa darah
Vasospasme
kuat
Cerebral Ischaemia
pH
Na+
Reperfusion
(4)
Cl-
cytokines
Neuron depolarisation
molecules
adhesion
Glutamate release
(1)
VGCC open
Intracellular Ca
PLA2
Activation
Leukocyte
adhesion
(2)
++
mitochondria
(3)
NOS
Oxidative
stress
Organelle
damage
Neuronal death
(5)
Tissue
response
inflammation
Agents stroke iskemik :
1. NMDA & AMPA receptor antagonists,
Mg+
2. Ca A
3. NOS inhibitors
4. Anti-oxidants
5. Adhesion molecule antibodies
VGCC: Voltage gated calcium channels
PLA2 : Fosfolipase A2
Epidemiology of SAH
Incidence about 10/100,000/yr
Mean age of onset 51 years
55% women
men predominate until age 50, then
more women
Risk factors
cigarette smoking
hypertension
family history
Diagnostic approach to
SAH
Wide range of symptoms and
signs
CT scanning
Limited role of lumbar puncture
Angiography
conventional vs. spiral CT vs. MRA
identification of multiple aneurysms
SAH without aneurysm
Diagnostic approach to
SAH
Screening of certain hight risk
populations for unruptured
aneurysms is of uncertain value.
Digital Subtraction angiography
(DSA) remains the gold standard
for diagnosis for Unruptured
aneurysms. (Class II b, Leve;l of
Evidence B)
More subtle
subarachnoid
hemorrhage
Interhemispheric
fissure
Sylvian
fissure
Complications of SAH
rebleeding
cerebral
vasospasm
volume
disturbances
osmolar
disturbances
seizures
arrhythmias
and other
cardiovascula
r
complications
CNS
infections
other
complications
of critical
Antifibrinolytic therapy
may be useful between presentation and early
surgery
Analgesia
Minimal or no sedation to allow examination
Class I Recommendations
Blood pressure should be monitored and
controlled to balance the risk of strokes,
hypertension-related re-bleeding, and
maintenance of cerebral perfusion
pressure (LOE B)
Class II Recommendations
Bed rest alone is not enough to prevent rebleeding after SAH. It may be considered
as a component of a broader treatment
strategy along with more definitive
11/04/15 2009, American
measures (LOE B)Heart Association. All rights
reserved.
Class II Recommendations
Recent evidence suggests that early
treatment with antifibrinolytic
agents, when combined with a
program of early aneurysm treatment
followed by discontinuation of the
antifibrinolytic and prophylaxis
against hypovolemia and vasospasm
11/04/15 2009, American
Heart Association. All rights
reserved.
(LOE B)
Class I Recommendations
Surgical clipping or endovascular coiling is
strongly recommended to reduce the rate
of rebleeding after aneurysmal SAH (LOE
B)
Wrapped or coated aneurysms as well as
incompletely clipped or coiled aneurysms
have an increased risk of re-hemorrhage
compared to those completely occluded
and therefore require long-term follow-up
angiography. Complete obliteration
of the
11/04/15 2009, American
Association. All rights
aneurysm is recommendedHeart
whenever
reserved.
possible (LOE B)
Class I Recommendations
For patients with ruptured aneurysms
judgedby an experienced teamof
cerebrovascular surgeons and
endovascular practitioners to be
technically amenable to both endovascular
coiling and neurosurgical clipping,
endovascular coiling can be beneficial (LOE
B)
Class II Recommendations
Individual characteristics of the patient
and the aneurysm must be considered in
deciding the best means of repair,
and
11/04/15 2009,
American
Heart Association. All rights
management of patients in centers
offering
reserved.
both techniques is probably recommended
Class II Recommendations
Although previous studies showed that
overall outcome was not different for early
versus delayed surgery after SAH, early
treatment reduces the risk of rebleeding
after SAH, and newer methods may
increase the effectiveness of early
aneurysm treatment. Early aneurysm
treatment is reasonable and is probably
11/04/15 2009, American
indicated in the majority of cases
(LOEAllB)
Heart Association.
rights
reserved.
Diagnosis
clinical
transcranial Doppler flow velocity
monitoring
electrophysiologic
radiologic
Vasospasm in acute
SAH
Initial angiogram
Repeat angiogram
showing vasospasm
(small arrows)
Hypertension/treatment
In general, antihypertensive drugs should be
withheld unless the calculated mean blood
pressure (the sum of the systolic pressure plus
double the diastolic pressure, divided by three) is
greater than 130 mm Hg or the systolic blood
pressure is greater than 220 mm Hg
Elevated blood pressure usually declines
spontaneously over the first 24 hours after stroke
onset and overzealous use of a calcium antagonist
and other antihypertensive drugs should be
avoided because they can further reduce cerebral
perfusion.
Antithypertensive
Treatment
Indicated for:
aortic dissection
acute myocardial infarction
heart failure
acute renal failure
hypertensive encephalopathy
thrombolytic therapy
Temperature
Increase temp increases percentage
of poor outcome in stroke
Increase cerebral oxygen/substrate
consumption
Lancet 1996:422
Fever
Fever: Treatment
Treat any temperature elevations
Data is not in as to whether hypothermia
may be protective
CEREBRAL EDEMA
Hypo-osmolar fluids, such as 5%
dextrose in water, may worsen edema.
1/2NS or NS recommended
Mannitol
Mannitol (0.25 to 0.5 g/kg IV) given over
20 minutes rapidly lowers intracranial
pressure and can be given every 6
hours.57 The usual maximum daily dose
is 2 g/kg.57
Mannitol
Dose: - 25 to 50 g I.v. q 3-5 hrs.
Maximal dose of 2 g /KG/D.
Furosemide I.v. 20 to 80 mg q 4 to 12
hours to supplement mannitol.
Replacement fluids to maintain the
calculated serum osmolality at 300 to
320 mOsm per kilogram of water.
Rehabilitation Program:
Physical therapy :
Mobilization
Walking
Major motor or sensory impairment of the
limbs
Prescription of devices, such as a cane or
walker
Occupational Therapy :
Dizziness
Prevalence
1 in 5 adults report dizziness in last month
Increases in elderly
Worsened by decreased visual acuity,
proprioception and vestibular input
Dizziness
Non-specific term
Different meanings to different people
Could mean
-
Vertigo
Weak
Anemia
- Syncope
- Giddiness
- Depression
- Presyncope
- Anxiety
- Unsteady
Cerebrovascular Disease
Epidemiology of Cerebrovascular
Disease
5,500,000 stroke survivors are alive today
700,000 each year
Incidence of Cerebrovascular
Disease
Increases with age
28% are less than 65 yrs old
80% of cerebrobvascular disease
are preventable
19% greater in men than women
Women > 65 have higher incidence
than men
Vertebrobasilar insufficiency
Dizziness, diplopia, dysarthria, gait
ataxia and bilateral sensory & motor
disturbance
Transient ischemia - low stroke risk
Anatomi
1- Posterior Cerebral
2- Superior Cerebellar
3- Pontine Branches of
Basilar
4- Anterior Inferior Cerebellar
5- Internal Auditory
6- Vertebral
7- Posterior Inferior
Cerebellar
8- Anterior Spinal
9- Basilar
Dizziness
Central causes
Peripheral causes
canalithiasis (BPPV)-50%
Cerebrovascular disease
(vertebrobasilar insufficiency)-50%
vestibular neuronitis
demyelinating (multiple sclerosis)
(labyrinthitis)-25%
Menieres disease-10%
drugs (anticonvulsants, alcohol,
hypnotics)
trauma
drugs (aminoglycosides)
positional changes
Time course
Associated symptoms
Vertebrobasilar disease / stroke: diplopia,
dysarthria, dysphagia, weakness, numbness
Menieres disease: aural fullness, deafness,
tinnitus
Psych/Panic attack: SOB, palpitations,
diaphoresis
Multiple sclerosis: vertigo preceded by other
neurologic dysfunction
Migraine
Hypertension, Diabetes Mellitus,
smoking, Peripheral Vascular Disease
Head injury
Psychiatric illness
Physical examination
Vestibular exam
Neurologic exam
Severity of postural instability
Hearing tests
Cont..
Management of TIA