Documente Academic
Documente Profesional
Documente Cultură
2017
Stroke Subtypes
Stroke
•Much rarer
•The classic presentation is proximal
arm/leg weakness with present of
distal strength, the so-called “man in
a barrel”
Middle Cerebral Artery
Posterior
Cerebellar artery
Superior
Cerebellar artery
(necrosis)
Dr.J.Husada 11-2003
Ischemic Stroke
Incidency : 70-85%
Classification :
1. TIA (transient ischemic attack) : < 24 hours
2. RIND (Reversible Ischemic Neurological
Deficits) normal between 24 – 48 hours.
Prolonge-RIND normal in max. 3 – 4 days.
3. Stroke in evolution : worsen stroke ( > 48
hours)
4. Stroke complete : permanent neurologic
deficit
2 process in ischemic stroke:
1. Vascular : Aterosclerotic process
2. Biochemistry change /cellular
chemist
Aterosclerotic is a normal response to arterial
endotel injury
Aterosclerotic plaque forming, start in young
Clinical manifestation : acute and tent to occur one
time because sudden plaque rupture
Ischemic Stroke Infarct
• When a stroke
occurs, it kills brain
cells in that
immediate area
• This area of dead
cells is called an
infarct
• These cells usually
die within minutes to
a few hours after the
stroke starts
Definition of Ischemic 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
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
Thrombotic
• A thrombotic
stroke is when a
blood clot forms
in one of the
arteries in the
brain, or
supplying the
brain, and grows
and grows until it
is large enough
to block blood
flow.
Proses Aterosklerosis
Mediate area are insuficiently supplied with blood, and they die
Etiology %
Ruptured AVM 29,1%
Arterial hypertension 15,3%
Sympathomimetic drug abuse 9,7%
Tumor* 6,9%
Acute EtOH intoxication 4,2%
Pre-eclampsia/eclampsia 2,8%
Superior sagittal sinus 1,4%
thrombosis
Moyamoya 1,4%
Cryoglobulinemia 1,4%
Undetermined 23,6%
Definition:
• Intracerebral
hemorrhage (ICH)
results from the rupture
of an intracerebral
vessel leading to the
development of a
hematoma in the
substance of the brain.
Epidemilogy
Incidence
• USA
– ICH represents 10-15 percent of all strokes (approximately
70,000 new cases each year)1.
• Internationally
– Asian countries >> incidence of ICH (30%) 2
• It is twice as common as subarachnoid hemorrhage and carries an
equally poor prognosis 3
• .
1 Stroke. 1999; 30: 2523-2528.
2 Strokr.2003;34:2091-2096
Functionally indipendence
– At 1 month: 10%
– At 6 months: 20%
Primary Secondary
Hypertension Aneurysms
Amyloid angiopathy Arteriovenous malformations
Neoplasms
Trauma
Anticoagulation
Use of thrombolytics
Hemorrhagic conversion of
ischemic stroke
Haemorrhage
Effects of blood Release
Increase Vasoconstrictor agen
toxic Intracranial press Serotonin, Prostaglandin,
Global ischemic
Influks Ca+
Necrosis
Focal Ischemic
Neuron
Vasospasme Process on Haemorrhage
Vasospasme
Lumen stronge
vasculer Vasospasme
• Vasogenic :
– kerusakan vaskuler endotel kapiler, gangguan
tight junction, permeabilitas meningkat
• Cytotoxic :
– gangguan pompa Na, K, ATP ase, Na intrasel
meningkat
• Interstisial :
– Transudasi
Akibat Vasospasme
Fungsi bagian otak yg disuplai arteri vasospasme akan
terganggu
Disekitar hematoma dpt terjadi vasospasme lokal pd
arteri yg utuh (tidak pecah)
Ada kemungkinan vasospasme lokal di dekat sumber
perdarahan berubah menjadi vasospasme difus
Subarachnoid Hemorrhage
Seminar 1
• Incidence
• Genetic Factors
• Diagnosis
• Natural History
What causes aneurysms to
rupture?
• The probability of rupture is related to the tension on the
aneurysm wall
Autopsy Series
Total # Percentage
Author #of Series of Cases with aneurysms Rupt’d Unrupt’d
Jellinger 12 87,772 1.6 (0.2 to 9) 1
0.6
Bannerman 8 51,360 1.43 1.09
0.34
OVERVIEW
• Highest mortality occurs immediately after the
hemorrhage and then decreases rapidly
• Rebleeding is estimated to occur in 50% of
ruptured aneurysms within 6 months of the
first hemorrhage, and afterwards at 3% per
year
• 50-60% of patients die after rebleeding and
25% are left disabled
Probably the best natural history data
come from S Pakarinen: (Incidence, aetiology, and
prognosis of primary subarachnoid hemorrhage: a study based on 589 cases
diagnosed in a defined urban population during a defined period. Neurol Scand
(Suppl) 1967; 29:1-128)
• Reduced consciousness
• Meningism
– Vomiting
– Neck stiffness
– Photophobia
• Seizures
SAH of Unknown Etiology
(Subarachnoid Hemorrhage of Unknown Etiology. AH Friedman. Chapter 235 in Neurosurgery,
2nd Ed., Vol II, Edited by RH Wilkins and SS Rengachary, McGraw-Hill, 1966)
• 142 patients with 181 unruptured aneurysms, followed from the 1950’s until
death, SAH or 1997-98 (mean 19.7 yrs). No surgical selection.
• Asymptomatic incidental aneurysms - 5 patients
Symptomatic intact aneurysms - 6 patients
SAH from another repaired aneurysm - 131 patients
(How did they determine the rupture site pre-CT? WST comment)
• In 2575 person-years of FU, 33 first-time episodes of SAH from previously
unruptured aneurysms for an average annual incidence of 1.3%. SAH fatal in
17 cases.
• The cumulative rate of bleeding was 10.5% at 10 yrs, 23% at 20 yrs and
30.3% at 30 yrs.
• Risk factors:
– Diameter of the aneurysm
– Patient age at diagnosis (inverse)
– Active smoking status at the time of diagnosis
Treatment
• Walter Dandy
Operative microscope
•
Complications with SAH
1. Re-bleeding
2. Hydrocephalus
3. Vasospasm
4. Hyponatraemia
5. Seizures
6. VTE
Complications with SAH
• Re-bleeding
– 80% mortality if re-bleed
– Communicating
• Due to blood blocking reabsorption of CSF through the
arachnoid granules
– Greatest risk of vasospasm is days 4-7 but significant risk for first
3 weeks after bleed, therefore will use preventative measures for
at least 3 weeks
Complications with SAH
• Hyponatraemia
– Susceptible due to being fluid loaded & cerebral salt
wasting
– TEDS
3. Age:
Younger patients had more good outcomes and lower mortality.
The mean age for good outcome was 46 and for death, 58
years.
4. Initial systolic blood pressure:
When categorized by initial systolic BP (<141, 141-180, >180),
patients with higher systolic BP were less likely to have a good
outcome and had a higher mortality rate (P<0.05)
5. Aneurysm size:
A bad outcome was seen in 72% of patients with aneurysm
diameter >21 mm and 56% with aneurysm diameter 4-6 mm
Non Neurological:
Infection : Respiratory, Urinary, Septicaemia
Metabolic : Dehydration, Electrolyte Disturbance,
Hypoglycaemia
Drugs : Major and Minor Tranquillizers, Baclofen,
Lithium Toxicity, Antiemetics
Hypoxia : Pulmonary Embolism, Chronic Pulmonary
Disease, Pulmonary Oedema
Hypercapnoea: Chronic Pulmonary Disease
Others : Limb or Bowel Ischaemia in Patients
with a Cardiac or Aortic Arch Source of
Embolism
Neurological:
• Progression/completion of the stroke
• Extension/early recurrence
• Hemorrhagic transformation of an infarct
• Development of oedema around the infarct or hemorrhage
• Obstructive hydrocephalus in patients with stroke in the posterior
fossa, or after subarachnoid hemorrhage
• Epileptic seizures
• Delayed ischaemia (in subarachnoid hemorrhage)
• Incorrect diagnosis :
– Cerebral Tumor - Cerebral abscess
– Encephalitis - Chronic Subdural Haematoma
– Subdural empyema
• Conscious level, i.e. Glasgow Coma Scale
• Pupillary Responses
• Eye Movements
• Limb Movements
• Temperature
• Pulse Rate
• Blood Pressure
• Respiratory Rate
• Pulse Oximetry
• Fluid Balance
• Fever
• Agitation
• Purulent Urine
• Tender Abdomen
INDICATIONS FOR CT & MRI IN
STROKE
DIAGNOSTIC
1. Types of stroke (etiopathology)
2. Topical localisation (Anatomy)
3. Size & extension
4. Diff. Diag. to SOL, etc.
5. Monitoring : follow up, assesment of
treatment
(PERDOSSI, 1999)
Time sequence of histology and CT in infarction
Density : Hypodens < 40 ( 0 - 35 HU)
Isodens
Time CT Finding
1st 3 hours Normal (isodense)
3rd - 6th hour ILL-Defined hypodense
Area (Infarct. edema begins)
6th - 24 th hour Hypodensity ↑
Sharper demarct. infarct
24th - 48th hour SD-Effect & Intensity ↑
2nd - 7th day Max.So-effect of edema
7th day weeks Cystic defect + scar
• Balloon angioplasty/stenting
• Carotid endarterectomy/Bypass
• Decompressive surgery
Purpose of Rehabilitation
• EUSI Recommendations
1. Rehabilitation should be initiated early after
stroke (Level I)
2. Every patient should have access to
evaluation for rehabilitation (Level III)
3. Rehabilitation services should be provided by
a multidisciplinary team (Level III)
Rehabilitation Program:
Physical therapy :
Speech Therapy :
• Mobilization
•Disorders of language
• Walking
•Disorders of articulation
• Major motor or sensory impairment
of the limbs •Disorders of swallowing
• Prescription of devices, such as a
cane or walker
Occupational Therapy :
• Fine movements of the hand
• Arm function
• Utilization of tools
• Assistive devices
• Ability to function independently
Factors that Influence the
Successfully of Rehabilitation
• Cause of stroke
• Severity of stroke
• Location
• Age
• Self motivation
• Premorbide personality and mood
• Family
• Social economy
• Specific deficit neurology
• Onset, duration and intensity
• Rehabilitation team