Stroke

Pembimbing : Dr. Maula Nurrudin Gaharu, Sp.S

Definisi Stroke :

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/c
hapters/ok/gordon.ppt

Ischemic
Stroke

Intracerebral
Hemorrhage

Subarachnoid
Hemorrhage

Clot occluding
artery
85%

Bleeding
into brain
10%

Bleeding around
brain
5%

http://www.phillystroke.org/cont
ent/learn_about_stroke/act_fast.
asp

NIHSS (National Institute of Health Stroke Scale)

Stroke Scale

Stroke Severity

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:

Virchows 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
Brocas
Expressive aphasia
Left posterior inferior
frontal gyrus
Wernickes
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

PATOLOGI
1. Zona Oedematosa 6 hari 10
hari
2. Zona Degenerasi 6 8 bulan
3. Zona Nekratik > 8 bulan
Zona
Oedematosa
Placcid 1 2
minggu

Zona
Degenerasi
Recovery 6 8 bulan

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)

Zona Nekrotik
Residual lebih 6
bulan / permanen
tahunan

32 1

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

Causes of ICH

http://spinwarp.ucsd.edu/neuro
web/Text/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
Non- contrast CTH remains the
gold standard as it is superior
for showing IVH and ICH
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

MRI
Superior for showing underlying
structural lesions
Contraindications

www.acponline.org/about_acp/c
hapters/ok/gordon.ppt

Acute (4 hours)
Infarction

Subtle blurring of gray-white

junction & sulcal effacement

Subacute (4 days)
Infarction
L
R

Obvious dark changes &

mass effect (e.g.,
ventricle compression)

tPa
Fast Facts
Tissue plasminogen activator
clot buster
IV tpa window 3 hours
IA tpa window 4.5 hours
Disability risk 30% despite
~5% symptomatic ICH risk

Contraindications

Hemorrhage
SBP > 185 or DBP > 110
Recent surgery, trauma or
stroke
Coagulopathy
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
BP increase is due to
arterial occlusion (i.e.,
an effort to perfuse
penumbra)
Failure to recanalize (w/
or w/o thrombolytic
therapy) results in high
BP and poor neuro
outcomes
Lowering BP starves
Clot in
penumbra, worsens
Artery
outcomes

www.acponline.org/about_acp/c
hapters/ok/gordon.ppt

Penumbra

Core

www.acponline.org/about_acp/c
hapters/ok/gordon.ppt

Save the Penumbra!!

Normal
function

20
15
10

PENUMBRA

CORE
1

Neuronal
dysfunctio
n

CBF
8-18

Neuronal
death

CBF
<8

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

Hyperthermia
Treat fevers!
Evidence shows that fevers > 37.5 C that persists for > 24 hrs
correlates with ventricular extension and is found in 83% of
patients with poor outcomes