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STROKE
Penyusun :
Rachmania Budiati
Risky Pratiwi Pulungsari
By this definition, TIA which lasts <24 hours, and patients with stroke
symptoms caused by subdurah hemorrhage, tumors, poisoning, or
trauma are excluded.
WHO MONICA Project Investigators. The World Health Organization MONICA Project (Monitoring trends and
determinants in cardiovascular disease). J Clin Epidemiol 41, 105-114. 1988.
Epidemiology
Strong K, Mathers C, Bonita R. Preventing stroke: saving lives around the world. Lancet
Neurol. 2007;6(2):182–187
Epidemiology
• Approximately 800,000 primary (first-time) or secondary
(recurrent) strokes occur each year, with the majority
being primary strokes (roughly 600,000).
• Of these strokes, approximately
– 87% are ischemic infarctions
– 10% are primary hemorrhages
– 3% are subarachnoid hemorrhage
Strong K, Mathers C, Bonita R. Preventing stroke: saving lives around the world. Lancet
Neurol. 2007;6(2):182–187
Epidemiology
Nonmodifiable Risk Factors For Stroke
Sex 24% to 30% higher in men; however, absolute annual number of women
experiencing stroke is higher because women outlive men
WHO. The Global Burden of Disease: 2004 Update. Geneva, Switzerland: WHO; 2008
Epidemiology
Epidemiology and the Global Burden of Stroke
Epidemiology
Classification of Stroke
Sign & Intracereberal Subarachnoid Stroke Non
Symptoms hemorrhage hemorrhage Hemorrhage
Focal deficit Severe Mild Mild-severe
• SUBARACHNOID HEMORRHAGES
Occur when an aneurysm (a blood-filled pouch that balloons out from an artery)
Are often caused by high blood pressure.
In addition to high blood pressure, factors that increase the risk of hemorrhagic
strokes include:
cigarette smoking
use of oral contraceptives (particularly those with high estrogen content)
excessive alcohol intake
use of illegal drugs
Are all hemorrhagic strokes the same?
SUBARACHNOID
HEMORRHAGE
Subarachnoid hemorrhage
(SAH)
• What is it?
– Bleeding into the subarachnoid space (space between the pia & arachnoid meningeal layers)
where blood vessels lie & CSF flows
– Unknown (~15%)
– AVM (~10%)
No subarachnoid blood
1
detected
Intracerebral or
4 intraventricular clot with
diffuse or no SAH
Subarachnoid hemorrhage
(SAH)
• DIAGNOSTIC APPROACH
– Whenever the clinical suspicion of SAH exists but CT is
negative → A LUMBAR PUNCTURE MUST BE PERFORMED
Subarachnoid hemorrhage
(SAH)
• DIAGNOSTIC APPROACH
‒ The cause of the hemorrhage is best evaluated with a four-
vessel cerebral arteriogram.
‒ Aneurysms are detected as focal areas of outpouching or
dilatation of the arterial wall → within or near the circle of Willis.
ECG in Subarachnoid
Hemorrhage
• Raised ICP is associated with certain characteristic ECG changes:
– Widespread giant T-wave inversions (“cerebral T waves”).
– QT prolongation.
– Bradycardia (the Cushing reflex – indicates imminent brainstem
herniation).
• Other possible ECG changes that may be seen:
– ST segment elevation / depression — this may mimic myocardial
ischaemia or pericarditis.
– Increased U wave amplitude.
– Other rhythm disturbances: sinus tachycardia, junctional rhythms,
premature ventricular contractions, atrial fibrillation.
• In some cases, these ECG abnormalities may be associated with
echocardiographic evidence of regional ventricular wall motion
abnormality (so-called “neurogenic stunned myocardium”)
Subarachnoid Haemorrhage
Widespread, giant T-wave inversions (“cerebral T waves”) secondary to subarachnoid
haemorrhage.
The QT interval is also grossly prolonged (600 ms).
Another example of cerebral T-waves with marked QT prolongation
secondary to subarachnoid haemorrhage
Subarachnoid Haemorrhage
Widespread T-wave inversions with slight ST depression secondary to subarachnoid
haemorrhage.
The QT interval is prolonged (greater than half the R-R interval).
This ECG pattern could easily be mistaken for myocardial ischaemia as the T-wave
morphology is very similar, although obviously the clinical picture would be very different
(coma versus chest pain).
DIAGNOSIS
1. CT scan
– 90% sensitivity to bleeding in the brain
2. Lumbar puncture
– For negative CT with clinical signs of SAH
3. Angiography
– Identifies location/characteristics of the
aneurysm
– Helps with treatment decision
– Detects vasospasm
INTRACEREBRAL
HEMORRHAGE
Intracerebral Hemorrhage (ICH)
History Comments
Time of symptom onset (or time the patient was
last normal)
Vascular risk factors Hypertension, diabetes, hypercholesterolemia, and
smoking
Medications Anticoagulants, antiplatelet agents, decongestants,
antihypertensive medications, stimulants (including
diet pills), sympathomimetics
Recent trauma or surgery Carotid endarterectomy or carotid stenting in
particular, as ICH may be related to hyperperfusion
after such procedures
Dementia Associated with amyloid angiopathy
Alcohol or illicit drug use Cocaine and other sympathomimetic drugs are
associated with ICH, stimulants
Seizures
Liver disease May be associated with coagulopathy
Cancer and hematologic disorders. May be associated with coagulopathy
© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
Integral Components Of The History, Physical Examination &
Work Up Of The ICH Patient in The Emergency Department
Toxicology screen in young or middle-aged patients Cocaine and other sympathomimetic drugs are
to detect cocaine and other sympathomimetic drugs associated with ICH
of abuse
Urinalysis and urine culture and a pregnancy test in
a woman of childbearing age.
• Normal Brain
physiology as relates
to IICP
– Brain surrounded by
ridged bone and
meninges
– Falx cerebri
– Tentorium cerebelli
INTRACRANIAL PRESSURE (ICP)
• Mechanisms of IICP:
– Caused by any space
occupying lesion;
cerebral edema; brain
inflammation;
metabolic changes
– Herniation syndromes
INTRACRANIAL PRESSURE (ICP)
Brain Herniation
INTRACRANIAL PRESSURE (ICP)
Brain Herniation
Brain Herniation
Fluid management
• Patients should be kept euvolemic and normo-
to hyperosmolar.
• Avoid all free water (including D5W, 0.45
percent (half normal) saline, and enteral free
water)
• Employ only isotonic fluids (such as 0.9
percent (normal) saline)
INTRACRANIAL PRESSURE (ICP)
• Antihypertensive
– When blood pressure is not accompanied by signs
and symptoms of increased intracranial pressure,
blood pressure is carefully lowered by continuous or
intermittent (decrease max.MAP 25% within the first
hour, and then cautiously to normal over the
following 24-48 hours) use of intravenous
antihypertensive drugs with monitoring blood
pressure every 15 minutes until MAP 110 mmHg or
blood pressure 160/90 mmHg
• Intracranial hypertensive
– Use manitol 20%
– Initial bolus of 0.25-1 g/kg (the higher dose for more
urgent reduction of ICP)
– Followed by 0.25-0.5 g/kg boluses repeated everi 2-6
hour as per requirement.
– Position — Head elevated above the heart (usually
30 degrees) to increase venous outflow.
Management of Subarrachnoid
hemorrhage
• Antihypertensive
– To prevent recurrent subarachnoid hemorrhage, in
patients with acute subarachnoid hemorrhage, blood
pressure is reduced to SBP 140-160 mmHg.
– Whereas SBP 160-180 mmHg is often used as a
target of SBP in preventing the risk of vasospasm.
– Calcium Channel Blocker (nimodipin) has been
recognized in various subarachnoid hemorrhage
management guidelines as it can improve the
functional of the patient if cerebral vasospasm has
occurred.
Choice of Antihypertensive
Management of Subarrachnoid
hemorrhage
• Citicoline (1g/day)
Lifestyle modification
Antiplatelet therapy
• Just for stroke ischemic (cilostazole, aspirin, clopidogrel)
Anticoagulant therapy
• For stroke ischemic with fibrillation/cardioembolic stoke
Cholesterol lowering
Surgical Recommendations On Brain
Parenchymal Bleeding
Surgical Indications:
1) Patients with GCS 6-8 with cerebral bleeding of the brain in
the frontal area or temporal with bleeding volume >20 cc,
with structural shift midline ≥5 mm and or compression on
the sisterna.
2) Brain parenchymal hemorrhage with bleeding volume >50
cc
3) Patients with brain parenchymal hemorrhage and signs of
neurologic deterioration which progressively corresponds
to the lesion, refractory intracranial hypertension with
medikamentosa, or signs of mass effect on CT scan
CASE REPORT
HAEMORRHAGE STROKE
IDENTITAS PASIEN
Nama Ny. A
Pendidikan -
Agama Islam
Status JKN
TRIAGE
GCS E2V1M3
Triage P1
Anamnesis
(Alloanamnesis dengan keluarga pasien dan autoanamnesis
pada 15 Januari 2018)
• Setelah itu tetangga pasien memberi minum the hangat, lalu pasien
mulai tidak bisa diajak berkomunikasi.
RPD
• Riwayat darah tinggi sebelumnya (+) tidak rutin kontrol
• Riwayat DM sebelumnya (+) tidak rutin kontrol
• Riwayat penyakit jantung disangkal
• Riwayat penyakit ginjal disangkal
• Alergi disangkal
RPK
• Riwayat darah tinggi pada keluarga disangkal
• Riwayat DM pada keluarga disangkal
• Riwayat penyakit jantung pada keluarga disangkal
• Riwayat penyakit ginjal pada keluarga disangkal
Anamnesis Sistem
Vital Sign
Keadaan Umum E2V1M3, moderately ill.
Tekanan Darah 259/129 mmHg
Nadi 78 bpm regular
Respiratory 20 x/m
Rate
Temperature 36.5 C
SpO2 100% dengan NRM 12lpm
Akral Hangat
Pemeriksaan Fisik
Kepala-Leher Kepala : Mesosefal
Mata : pupil isokor 2mm/2mm, refleks cahaya (+/+), ptosis (-),
perdarahan konjungtiva (-), deviasi konjugat (-)
Mulut : mukosa basah, gusi berdarah (-), trismus (-), kesulitan
menelan (-)
Leher : JVP normal, pulsasi A. Karotis teraba kuat, paralisis otot
leher (-)
Tangan Pulsasi A.radialis kanan = kiri, reguler, teraba kuat, clubbing finger
(-), sianosis perifer (-).
Thorax Precordium :
Inspeksi : scars (-), deformitas (-), apex ICS V LMC, abnormal
pulse (-)
Palpasi : Apex ICS V LMCS , strong pulse, thrill (-), abnormal
impulse (-)
Auskultasi : Heart sounds I/II reguler, murmur (-), respiratory :
vesiculer +/+, ronchi -/-, wheezing -/-
Pemeriksaan Fisik
Back (sitting forward) Scars (-), deformitas (-)
Perkusi : pleural effusion (-)
Abdomen (lying flat) Inspeksi: Scar (-) distensi (-) Vena prominen (-) Striae (-) bruising (-)
massa (-)
Ausklutasi: BU (+) Normal, bruits (-)
Perkusi: Timpani (+) shifting dullness (-)
Palpasi: tenderness (-) rigiditiy (-)
Liver : normal on palpation,
femoral arteries : strong pulse
Kanan Kiri
N III
Ptosis - -
bawah
Strabismus konvergen sde Sde
Diplopia Sde Sde
Bagian Sensorik
Ophtalmik Tde
Maxilla Sde
Mandibula Sde
Fungsi Motorik
Fungsi Pengecapan
Kanan Sde
Kiri Sde
Atrofi Sde
Artikulasi Sde
Tremor Sde
Pemeriksaan Penunjang
• O2 NRM 12lpm
• Head up 30o
• IVFD NS 20 tpm
• Injeksi citicolin 500 mg
• Injeksi ranitidin 50 mg
• Injeksi ondancentron 4 mg
• Folley catheter
• Manitol 200cc/30 menit
• Injeksi kalnex 500 mg
• Injeksi nikardipin start 7.5 cc/jam
• NGT
Monitoring:
• KU, TTV
• GCS
Tatalaksana (cont…)
Nn.craniales: sde
16/1/2018
Subjektif Objektif Asessment Terapi dan Plan
Nn.craniales: sde
17/1/2018
Subjektif Objektif Asessment Terapi dan Plan
Nn.craniales: sde
18/1/2018
Subjektif Objektif Asessment Terapi dan Plan
THEORY Patient
- Penurunan kesadaran GCS E2V1M3
mendadak pada pasien dengan
stroke hemoragik
- Pupil Pupil isokor
- Deviasi konjugat Deviasi konjugat (-)
- Meningeal sign Meningeal sign (-)
- R.fisiologis R.Fisiologis dbn
- R.patologis R.Patologis (-)
- Kekuatan motorik Kekuatan motorik s.d.e
- Lateralisasi Lateralisasi sinistra
No. Sign/Symptom Score Index Score
1 Awareness (0) Compos mentis X 2,5 5
(1) Somnolen
(2) Semi coma/coma
2 Vommiting (0) No X2 2
(1) Yes
3 Headache (0) No X2 2
(1) Yes
4 Blood pressure Diastolic (259/129) X 10% 12.9
5 Aterome X (-3) -3
DM (0) No
Angina pectoris (1) Yes
Claudicatio intermittent
6 Constanta -12 -12
Ganglia
basalis
Ventrikel
lateralis
dx sn, 3, 4
Approach to Patients
Clinical Presentation
Intracereberal pressure (ICP)
Theory Patient
Cushing’s Triad:
Hypertension +
Bradycardia -
-
Respiration low
Headache +
Altered mental status +
Seizures -
Nausea and vomiting + Famili : Viperidae
Famili : Viperidae Famili : Viperidae
Calloselasma rhodostoma
Trimeresurus albolabris Trimeresurus albolabris
Papil edema Not
evaluated (ular tanah)
Nama jawa: ular gadung luwuk Nama jawa: ular gadung luwuk
Nama jawa: ular wedudak
Visual loss Difficult to evaluatemacan
Diplopia Difficult to evaluate
Approach to Patients
Clinical Presentation
THEORY PATIENT
• O2 O2 NRM 10 lpm