Stroke

Definisi Stroke :
manifestasi klinis dari gangguan fungsi otak, baik fokal
maupun global (menyeluruh), yang berlangsung cepat, berlangsung
lebih dari 24 jam atau sampai menyebabkan kematian, tanpa
penyebab lain selain gangguan vaskuler
Vaskularisasi Otak

1. Sistem Karotis Sinistra dan Dextra

- Masuk Cavum Cranii
Carotis Interna  Carotis Cerebre Media
2. Sistem Vertebra Basilaris
3. Sistem Vaskularisasi Yang Terganggu Menentukan Topis
Lesi
Menurut Penyebab Stroke dibagi :

1. Stroke Hemoragik
a. Intra cerebral hemoragik (ICH)
: Hypertensi, Aneurysma dan arterioveneus Malformasi
(AVM)
b. Sub Arachnoid Hemoragik (SAH)
 diagnosis medis : CT brain scan
2. Stroke Non Hemoragik (Iskemik)
Arteriosklerosis & sering dikaitkan dengan :
DM, Hypercolesterolemia, Asam urat, hyperagregasi trombosit

3. Emboli  Sumber dari tronkus di arteria carotis communis di

jantung  Lepas  trombus embolus  otak.
 www.acponline.org/about_acp/chapter
s/ok/gordon.ppt

Ischemic Intracerebral Subarachnoid

Stroke Hemorrhage Hemorrhage

Clot occluding Bleeding Bleeding around

artery into brain brain
85% 10% 5%
http://www.phillystroke.org/content/le
arn_about_stroke/act_fast.asp
NIHSS (National Institute of Health
Stroke Scale)
Stroke Scale Stroke Severity

0 No Stroke

1-4 Minor Stroke

5-15 Moderate Stroke

15-20 Moderate/Severe Stroke

21-42 Severe Stroke

NIHSS below 12-14 will have an 80% good or excellent outcome

NIHSS above 20-26 will have less than a 20% good or excellent
outcome
Lacunar infarct patients had the best outcomes
Etiology of Ischemic Strokes

LARGE VESSEL THROMBOTIC:

Virchow’s Triad….
 Blood vessel injury
- HTN, Atherosclerosis, Vasculitis
 Stasis/turbulent blood flow
- Atherosclerosis, A. fib., Valve disorders
 Hypercoagulable state
- Increased number of platelets
- Deficiency of anti-coagulation factors
- Presence of pro-coagulation factors
- Cancer
Etiology Of Ischemic Stroke:

LARGE VESSEL EMBOLIC:

 The Heart
 Valve diseases, A. Fib, Dilated cardiomyopathy, Myxoma

 Arterial Circulation (artery to artery emboli)

 Atherosclerosis of carotid, Arterial dissection, Vasculitis

 The Venous Circulation

 PFO w/R to L shunt, Emboli
Determining the Location

 Large Vessel:
 Look for cortical signs

 Small Vessel:
 No cortical signs on exam

 Posterior Circulation:
 Crossed signs
 Cranial nerve findings

 Watershed:
 Look at watershed and borderzone areas
 Hypo-perfusion
Cortical Signs

RIGHT BRAIN: LEFT BRAIN:

- Right gaze preference - Left gaze preference

- Neglect - Aphasia

If present, think LARGE VESSEL stroke

Large Vessel Stroke Syndromes

 MCA:
 Arm>leg weakness
 LMCA cognitive: Aphasia
 RMCA cognitive: Neglect,, topographical difficulty, apraxia, constructional
impairment
 ACA:
 Leg>arm weakness, grasp
 Cognitive: muteness, perseveration, abulia, disinhibition
 PCA:
 Hemianopia
 Cognitive: memory loss/confusion, alexia
 Cerebellum:
 Ipsilateral ataxia
Aphasia
 Broca’s
 Expressive aphasia
 Left posterior inferior
frontal gyrus

 Wernicke’s
 Receptive aphasia
 Posterior part of the superior temporal gyrus
 Located on the dominant side (left) of the brain
Secara Klinis Infark Di Otak
1. TIA (Trenssient Ischemic Attack)  Gejala dan tanda
hilang dalam waktu beberapa detik sampai dengan 24
jam. Difisit neurologis dapat berupa hemiparise,
monoparise, gangguan penglihatan, sulit bicara.
2. RIND (Reversible Ischemic Neurological Deficit )  Tanda
dan gejala hilang dalam beberapa hari dampa dengan
minggu.
3. Stroke in evolution atau progressive Stroke  defisit
neurologis bersifat fluktuatif, progresif kearah jelek,
biasanya disertai penyakit penyerta (DM, Gangguan fungsi
jantung, gangguan fungsi ginjal, dll)
4. Completed Stroke (Stroke Komplit)  Defisit neurologis
bersifat permanen
 PATOLOGI
1. Zona Oedematosa  6 hari – 10 hari
2. Zona Degenerasi  6 – 8 bulan
3. Zona Nekratik  > 8 bulan

Zona Oedematosa Zona Degenerasi Zona Nekrotik

Placcid 1 – 2 minggu Recovery 6 – 8 bulan Residual lebih 6 bulan /
permanen tahunan
Neurological Improvement
1. Area Degenerasi (Bersifat iriversibel
permanen = Zona nekratik) Disebut
area umbra
2. Area degenerasi riversibel (area
penumbra = Zona degenerasi)
3. Area Oedematosa (Bersifat riversibel
= Zona Oedematosa)
GEJALA DAN TANDA
Tergantung pada : Topis Lesi
Derajat lesi (Luas Infark)

1. Gangguan Motoris
 Abnomelitas Tonus
(Placcid atau Spastik)
 Parese/plegia
(mono/ hemi)
Topis Lesi & Lenticulo Striata
 Hemiplegia/ hemiparese
typica nn. Cranial VII & XII
2. Gangguan Sensoris
1) Hemidisesthesia
2) Hemikinesthesia
Pada kondisi tertentu kelainan sensoris terjadi tanpa kelainan
motoris
Contoh : Pada gambaran angiografi terjadi :
Obstruksi dan penyempitan lumen
a. Carotis communis
a. Cerebre Media kiri didaerah siphon di basis cranii
terjadi keluhan hemiastesia sisi dextra tanpa adanya parese.

3) Central Pain ( Lesi pda kortex sensoris)

3. Gangguan Saraf Otonom dan Fungsi Luhur

1) Gangguan vasomotor (vasokontruksi, vasodilatasi pembuluh darah)

2) Gangguan aktivasi kelenjar sudorivera ( keringat berlebihan)
3) Fungsi luhur (aphasia motoris dan sensoris)

Gangguan lain yang berkaitan dengan fungsi kognitif dan memori serta
fungsi psikiatrik dan emosi.
Karakteristik gangguan tersebut diatas tergantung topis lesi dan derajat
lesi
Intracranial Hemorrhages
Etiology of ICH

 Traumatic
 Spontaneous
 Hypertensive
 Amyloid angiopathy
 Aneurysmal rupture
 Arteriovenous malformation rupture
 Bleeding into tumor
 Cocaine and amphetamine use
 http://spinwarp.ucsd.edu/neuroweb/T

Causes of ICH ext/non-trauma-ER.htm

Hypertensive ICH
 Spontaneous rupture of a small artery deep in the brain
 Typical sites
 Basal Ganglia
 Cerebellum
 Pons
 Typical clinical presentation
 Patient typically awake and often stressed, then
abrupt onset of symptoms with acute
decompensation
Ganglionic Bleed

 Contralateral hemiparesis
 Hemisensory loss
 Homonymous hemianopia
 Conjugate deviation of eyes toward the side of the
bleed or downward
 AMS (stupor, coma)
Cerebellar Hemorrhage

 Vomiting (more common in

ICH than SAH or Ischemic
CVA)
 Ataxia
 Eye deviation toward the
opposite side of the bleed
 Small sluggish pupils
 AMS
Pontine Hemorrhage

 Pin-point but reactive pupils

 Abrupt onset of coma
 Decerebrate posturing or
flaccidity
 Ataxic breathing pattern
Subarachnoid Hemorrhage

 “Worst headache of my life”

 AMS
 Photophobia
 Nuchal rigidity
 Seizures
 Nausea and vomiting
Management
Airway

 Most likely related to decreased level of consciousness

(LOC), dysarthria, dysphagia
 GCS < 8 - INTUBATE
 Avoid Hyperventilation or Hypoventilation
 NPO until swallow assessment completed- high
aspiration risk
 Begin mobilization as soon as clinically safe
 Keep HOB greater than 30 degrees
Stroke
Algorithm
1. Computerized Tomography Scanning (CT scan)
1) Infark  lesi hipodens (lesi dengan densitas rendah) tampak lebih
hitam dibanding jaringan otak disekitarnya.
2) Perdarahan  Lesi hiperdens (lesi dengan densitas tinggi) tampak
lebih putih dibanding jaringan otak disekitarnya.
2. MRI & MRA ( Magnetic Resonance Imaging & Magnetic Resonace
Angiography)
untuk mengetahui topis kebocoran pembuluh darah di otak
3. PET Scan ( Positron Emision Tomography Scan)
 Imaging
CT scan
MRI
 Non- contrast CTH remains the
 Superior for showing underlying
gold standard as it is superior
structural lesions
for showing IVH and ICH
 Contraindications
 CT with contrast may help
identify aneurysms, AVMs, or
tumors but is not required to
determine whether or not the
patient is a tPa candidate
 www.acponline.org/about_acp/chapter
s/ok/gordon.ppt

Acute (4 hours) Subacute (4 days)

Infarction Infarction
R L R L

Subtle blurring of gray-white Obvious dark changes &

junction & sulcal effacement “mass effect” (e.g.,
ventricle compression)
tPa
Contraindications
Fast Facts
 Tissue plasminogen activator  Hemorrhage
 “clot buster”  SBP > 185 or DBP > 110
 IV tpa window 3 hours  Recent surgery, trauma or
 IA tpa window 4.5 hours stroke
 Disability risk  30% despite  Coagulopathy
~5% symptomatic ICH risk  Seizure at onset of
symptoms
 NIHSS >21
 Age?
 Glucose < 50
Mechanical Thrombolysis

 Often used in adjunct with tPa

 MERCI (Mechanical Embolus Removal in Cerebral Ischemia)
Retrieval System is a corkscrew-like apparatus designed to
remove clots from vessels
 PENUMBRA system aspirates the clot
Blood Pressure Management

BP Management
 The goal is to maintain cerebral perfusion!!
 CPP = MAP – ICP (needs to be at least 70)
 Higher BP goals with Ischemic stroke
 Lower BP goals with Hemorrhagic stroke (avoid
hemorrhagic expansion, especially in AVMs and
aneurysms)
BP-AIS Relationship www.acponline.org/about_acp/chapter
s/ok/gordon.ppt

 BP increase is due to Penumbra

arterial occlusion (i.e., an

effort to perfuse Core
penumbra)
 Failure to recanalize (w/ or
w/o thrombolytic therapy)
results in high BP and
poor neuro outcomes
 Lowering BP starves
penumbra, worsens
outcomes Clot in
Artery
 www.acponline.org/about_acp/chapter
s/ok/gordon.ppt

Save the Penumbra!!

Normal
20 function

15
Neuronal CBF
PENUMBRA dysfunction 8-18
10

5 Neuronal CBF
CORE death <8

1 2 3
TIME (hours) CEREBRAL
BLOOD
FLOW
(ml/100g/min)
Supportive Therapy
 Glucose Management
 Infarction size and edema increase with acute and chronic
hyperglycemia
 Hyperglycemia is an independent risk factor for
hemorrhage when stroke is treated with t-PA
 Antiepileptic Drugs
 Seizures are common after hemorrhagic CVAs
 ICH related seizures are generally non-convulsive and are
associated to with higher NIHSS scores, a midline shift,
and tend to predict poorer outcomes