HEMORRHAGE

STROKE

Penyusun :
Rachmania Budiati
Risky Pratiwi Pulungsari

Advisor : dr. Eva Delsi, Sp.EM

 WHO Definition of Stroke
“Rapidly developing clinical signs of focal (or global)
disturbance of cerebral function, lasting more than 24
hours or leading to death with no apparent cause
other then that of vascular origin.”

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

• According to estimates by the WHO, stroke

accounted for 5.7 million deaths and 16 million
first-time events in 2005 and these numbers may
reach 7.8 million and 23 million by 2030,
respectively.

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

Age After the age of 55 years

Sex 24% to 30% higher in men; however, absolute annual number of women
experiencing stroke is higher because women outlive men

Race 2- to 4-fold higher among African Americans

ethnicity
2-fold higher among Hispanics

Higher among Chinese

Heredity Almost 2-fold higher among first-degree relatives. Chromosome 9p21

(proximal to genes CDKN2A and CDKN2B) has been linked to ischemic stroke
risk
 Epidemiology

Stroke is the second leading cause of

preventable death worldwide and the fourth
leading cause of lost productivity, as measured by
disability-adjusted life years.

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

Onset Minute/hour 1-2 minutes Slowly (hour/day)

Headache Severe Very severe Mild

Rare, except if the
Vomittus Often Often lesion in brain
stem
Hypertension Always Rare Often
Loss of
+ + -
consciousness
Neck stifness rare + -

Hemiparese + - (in early onset) +

Speech disorder + rare +

HEMORRHAGE STROKE
 Are all hemorrhagic strokes the same?

• INTRACEREBRAL HEMORRHAGES (most common type of

hemorrhagic stroke):
 Occur when a blood vessel bleeds or ruptures into the tissue deep
within the brain.
 Are most often caused by chronically high blood pressure or aging
blood vessels.
 Are sometimes caused by an arteriovenous malformation (AVM).
 Are all hemorrhagic strokes the same?

• 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

• Where does the blood come from?

– An aneursym on a blood vessel in the subarachnoid space has ruptured (~70%)

– Unknown (~15%)

– AVM (~10%)

– Rare causes (e.g. tumour) (~5%)

• Where does the blood go?

– Anywhere where CSF goes, may get hydrocephalus if into ventricle & causes obstruction of
CSF circulation
 Subarachnoid hemorrhage
(SAH)

• Incidence = 1/7000 people

• Higher chance if:
– Female
– 3rd trimester of pregnancy
– Middle-aged
– Abuse of stimulant drugs
– Connective tissue disorder
– Family history
– Polycystic Kidney Disease (PCKD) subarachnoid
Subarachnoid hemorrhage
(SAH)
 Subarachnoid hemorrhage
(SAH)

Clinical Manifestations of Cerebral Aneurysm Rupture.

 Subarachnoid hemorrhage
(SAH)
• DIAGNOSTIC APPROACH
– The clinical diagnosis of SAH is best confirmed with brain CT.
– Its sensitivity is highest in the first 24 hours after headache
onset.
 Subarachnoid hemorrhage
(SAH)
CT GRADING SYSTEM OF FISHER

Grade CT Scan findings

No subarachnoid blood
1
detected

Diffuse or vertical layers < 1

2
mm thick

Localized clot and/or vertical

3
layer > 1 mm

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)

Gross specimen, coronal section of brain, large

subcortical hypertensive ICH
 Integral Components Of The History, Physical Examination &
Work Up Of The ICH Patient in The Emergency Department

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
Physical Examination
Vital signs
A general physical exam focusing on the head, heart,
lungs, abdomen, and extremities.
A thorough but time urgent neurologic exam
Comments
Fever is associated with early neurologic
deterioration.19
Higher initial blood pressure is associated with early
neurologic deterioration and increased mortality.216
A structured exam such as the National Institutes of
Health Stroke Scale (NIHSS) can be completed in
minutes and provides a quantification that allows
easy communication of the severity of the event to
other caregivers. Glasgow Coma Score (GCS) is
similarly well known, easily computed, and the initial
GCS is a strong predictor of long term outcome. 167,
215 These can be supplemented as needed.
© 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
Serum and Urine Tests
Complete blood count, electrolytes, blood urea
nitrogen and creatinine, and Glucose
Prothrombin time (PT) or international normalized
ratio (INR) and an activated partial thromboplastin
time (aPTT)
Toxicology screen in young or middle-aged patients
to detect cocaine and other sympathomimetic drugs
of abuse
Urinalysis and urine culture and a pregnancy test in
a woman of childbearing age.
Comments
Higher creatinine is associated with hematoma
expansion. Higher serum glucose is associated with
hematoma expansion and worse outcome (although
there are no data to suggest that normalization
improves outcome).216, 217
Warfarin-related hemorrhages are associated with
an increased hematoma volume, greater risk of
expansion, and increased morbidity and mortality. 17,
197, 218
Cocaine and other sympathomimetic drugs are
associated with ICH
© 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

Other Routine Tests Comments

EKG To assess for active coronary ischemia

or prior cardiac injury that may indicate
poor cardiac function, and to obtain a
baseline in the event of cardiopulmonary
issues during hospitalization.
Neuroimaging As described in the text

© 2010 American Heart

Association, Inc. All rights
reserved. Unauthorized use
prohibited.
NEUROLOGIC FINDINGS
Neuroimaging of ICH
 Neuroimaging of ICH

Computed tomography (CT)

scan showing Left hemisphere
intracerebral hemorrhage
(ICH) with intraventricular
extravasation

Large left intraparenchymal

hematoma (ICH)
COMMON SITES OF ICH
COMMON SITES OF ICH
COMMON SITES OF ICH
 INTRACRANIAL PRESSURE (ICP)

• Normal Brain
physiology as relates
to IICP
– Brain surrounded by
ridged bone and
meninges
– Falx cerebri
– Tentorium cerebelli
 INTRACRANIAL PRESSURE (ICP)

Factors influence ICP :

• Arterial/venous pressure
• Intraabdominal & intrathoracic
pressure
• Posture
• Temperature
• Blood gasses (CO2)
 INTRACRANIAL PRESSURE (ICP)

The major causes of increased intracranial

pressure include:
• Intracranial mass lesions (eg, tumor, hematoma)
• Cerebral edema (such as in acute hypoxic ischemic
encephalopathy, large cerebral infarction, severe traumatic brain
injury)
• ↑ cerebrospinal fluid (CSF) production, eg, choroid plexus
papilloma
• ↓ CSF absorption, eg, arachnoid granulation adhesions after
bacterial meningitis
• Obstructive hydrocephalus
 INTRACRANIAL PRESSURE (ICP)

• Mechanisms of IICP:
– Caused by any space
occupying lesion;
cerebral edema; brain
inflammation;
metabolic changes
– Herniation syndromes
INTRACRANIAL PRESSURE (ICP)

Normal (adults < 20 cmH2O or 15 mmHg)

Cushing’s Triad:
• Hypertension
• Bradycardia
• Respiration low
Headache
Altered mental status
Seizures
Nausea and vomiting
Papiledema (engorgement and elevation of optic disc)
Visual loss
Diplopia
 INTRACRANIAL PRESSURE (ICP)

Brain Herniation
INTRACRANIAL PRESSURE (ICP)
Brain Herniation
Brain Herniation

Late Diencephalon Stage

 Brain Herniation
Midbrain-Upper Pons Stage
 INTRACRANIAL PRESSURE (ICP)

Invasive Measurement of ICP

 INTRACRANIAL PRESSURE (ICP)
MANAGEMENT

Resuscitation — The urgent assessment and support of

oxygenation, blood pressure, and end-organ perfusion.
Standard resuscitation technique :
• Head elevation 30o
• Hyperventilation to a PCO2 of 26 to 30 mmHg
• Intravenous mannitol (1 to 1.5 g/kg)

Aggressive evaluation of the underlying diagnosis, including neuroimaging,

detailed neurologic examination, and history gathering.
Hyperventilation may be contraindicated in the setting of traumatic brain
injury and acute stroke
 INTRACRANIAL PRESSURE (ICP)

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)

Blood pressure control — BP should be

sufficient to maintain CPP >60 mmHg.
Hypertension should generally only be treated
when CPP >120 mmHg and ICP >20 mmHg

CPP = MAP - ICP

 INTRACRANIAL PRESSURE (ICP)

• Position — Head elevated above the heart

(usually 30 degrees) to increase venous outflow.
 MANAGEMENT
STROKE HEMORRHAGE
 TREATMENT
• Keep the ABC stable
• Airway
– Give the patient O2 (look condition)
– O2 non re-breathing mask 12 lpm
– OPA or NPA if needed
– Laryngeal mask airway and endotracheal tube (if needed)
– Suction if gargling (+), head tilt and chin lift if snoring (+)
• Breating
– Evaluate the respiratory rate
– Oxygen saturation
• Circulation
– Make iv access, give isotonic fluid (don’t forget to take some
blood for laboratory checking)
– Blood pressure
– Pulse
 Cont…
• Disability
– Check and evaluate GCS
– GDS stick
• Exposure
Check temperature
 Management of Intracerebral
Hemorrhage Acute

• 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

– When SBP<180 mmHg and DBP<105 mmHg, delay

the administration of antihypertensive.
 Management of Intracerebral
Hemorrhage Acute (cont…)

• 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)

Improvement in memory function

improvement in motoric function,

cognition and psychic as well
obtained shortening times time of
hospitalization at patient
 Secondary Prevention

Lifestyle modification

Blood pressure lowering

• DOC: ACE-I and diuretic

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

Jenis kelamin Perempuan

Usia/ Tanggal lahir 58 tahun/ 1 Juli 1957

Alamat Pringtutul rt4/rw2, Rowokele

Pekerjaan Ibu rumah tangga

Pendidikan -

Datang ke RS 15 Januari 2018

Agama Islam

Status JKN
 TRIAGE

Airway Paten, Clear

Nafas spontan, RR 22x/menit,

Breathing SDV(+/+), ronkhi (+/+), wheezing
(-/-)

Akral hangat, Nadi 66bpm

Circulation reguler, SaO2 99% room air, TD
259/129

GCS E2V1M3

GDS 255 mg/dl

Triage P1
 Anamnesis
(Alloanamnesis dengan keluarga pasien dan autoanamnesis
pada 15 Januari 2018)

• Pasien datang dengan tidak sadarkan diri sejak 2 jam SMRS.

• Sebelumnya, pasien sedang di dapur menata-nata kayu bakar.

• Setelah itu tetangga sebelah pasien, mendengar pasien berteriak minta

tolong.

• Saat tetangga datang, pasien sudah terduduk bersandar kemudian

mengeluh pusing dan muntah-muntah.

• Setelah itu tetangga pasien memberi minum the hangat, lalu pasien
mulai tidak bisa diajak berkomunikasi.

• Riwayat hipertensi (+) tidak rutin kontrol. Pasien beberapa kali

dirawat dengan tensi tinggi diatas 200 namun tidak pernah kontrol.
 Anamnesis
(Alloanamnesis dengan keluarga pasien dan autoanamnesis pada 15
Januari 2018)

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

Anamnesis • Sistem Serebrospinal: Demam (-), Kejang (-),

Sistem Sakit kepala (+), Hemiparese (sde), Sulit bicara
(+)
• Sistem Kardiovaskuler: Jantung berdebar (-),
Nyeri dada (-), Hipertensi (-)
• Sistem Pernapasan: Batuk (-), Pilek (-), Sesak
napas (-)
• Sistem Gastrointestinal: Mual (-), Diare (-), Perut
kaku (-), Sulit BAB (-), Sulit menelan (-)
• Sistem Urogenital: BAK darah (-), BAB darah (-)
 Pemeriksaan Fisik
(Dilakukan di IGD pada 15 Januari 2018)

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

Legs Pulsasi A.dorsalis pedis teraba, scar (-)

Other Urin initial  100cc, temperature chart  normal

Lateralisasi : Ke kiri
R.Fisiologis : +2 +2 R.Patologis: -
+2 +2
 Pemeriksaan Nervus Cranialis
N I olfaktorius Tde
Kanan Kiri
N II optikus
Ketajaman penglihatan sde Sde

Menilai warna Sde sde

Funduskopi Tidak dilakukan Tidak dilakukan

Papil Tidak dilakukan Tidak dilakukan

Retina Tidak dilakukan Tidak dilakukan

Medan penglihatan sde Sde

Kanan Kiri
N III
Ptosis - -

Gerakan mata ke medial sde Sde

Gerakan mata ke atas sde Sde

Gerakan mata ke bawah sde Sde

Bentuk Pupil Bulat, isokor 2mm Bulat,isokor 2mm

Reflek Cahaya Langsung + +

Reflek Cahaya Tidak Langsung + +

 Pemeriksaan Nervus Cranialis
N IV troklearis Kanan Kiri
Gerakan mata ke lateral sde Sde

bawah
Strabismus konvergen sde Sde
Diplopia Sde Sde

N V Trigeminus Bagian Motorik

Menggigit Sde

Membuka mulut Sde

Bagian Sensorik
Ophtalmik Tde
Maxilla Sde

Mandibula Sde

Reflek Kornea Tde

 Pemeriksaan Nervus Cranialis
Nervus VI Abdusen Kanan Kiri

Gerakan mata ke lateral sde Sde

Strabismus konvergen sde Sde

Diplopia sde sde

Nervus VII Fasialis Kanan Kiri

Fungsi Motorik

Mengerutkan dahi sde Sde

Mengangkat alis Sde Sde

Memejamkan mata Sde Sde

Menyeringai Sde Sde

Mengembungkan pipi Sde Sde

Mencucurkan bibir Sde sde

Fungsi Pengecapan

2/3 depan lidah tde

 Pemeriksaan Nervus Cranialis
Nervus VIII Vestibulokoklearis tde

Nervus IX dan X tde

Glossofaringeus dan Vagus

Nervus XI Aksesorius Mengangkat bahu & Menoleh

Kanan Sde

Kiri Sde

Nervus XII Hipoglosus Menjulurkan lidah Sde

Atrofi Sde

Artikulasi Sde

Tremor Sde
Pemeriksaan Penunjang

Laboratorium (15 Januari 2018)

AL 16120
AE 4.31
Hb 12.8
AT 289000
Hct 39.6
Bas 0.1 %
Eos 0.4 %
Neu 83.5 %
Lim 13.3 %
Mono 2.7 %
Ur 19
Cr 0.65
OT 23
PT 15
Na 138.5
K 3.11
 SHIRIRAJ SCORE
No. Sign/Symptom Score Index Score
1 Awareness (0) Compos mentis X 2,5
(1) Somnolen
(2) Semi coma/coma
2 Vommiting (0) No X2
(1) Yes
3 Headache (0) No X2
(1) Yes
4 Blood pressure Diastolic X 10%
5 Aterome X (-3)
DM (0) No
Angina pectoris (1) Yes
Claudicatio intermittent
6 Constanta -12 -12
SSS > 1 Stroke Hemorrhage
SSS < -1 Stroke Non Hemorrhage
 Diagnosis
• AMS e.c SH (ICH, IVH)
Tatalaksana di IGD

• 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…)

Konsul dr.Asri, SpS. Advice:

• Injeksi citicolin 500mg/12 jam
• Injeksi ranitidine 50mg/12 jam
• Injeksi manitol 4x125cc
• Injeksi kalnex 500mg/8 jam
• Nikardipin lanjut target 150/90
• Rawat ICU
 Monitoring

Jam Tensi Nadi RR Suhu GCS Pupil Urin SiO2

11.40 259/129 78 20 36.5 E2V1M3 2/2 100cc 100%

(172)

12.00 246/125 82 20 36.5 E2V1M3 2/2 300cc 100%

(165)

12.30 229/111 87 20 36.5 E2V1M3 2/2 500cc 100%

(150)

13.00 208/97 92 22 36.5 E2V1M3 2/2 1000cc 100%

(134)
FOLLOW UP
 15/1/2018
Subjektif Objektif Asessment Terapi dan Plan

Penurunan KU : lemah, GCS: E2V1M2 -Penurunan kesadaran - IVFD asering 16 tpm

kesadaran dengan lateralisasi dx ec IVH, - Injeksi manitol 4x125cc
TD : 196/105
ICH - Injeksi ceftriaxone
HR : 90x/menit
-Hiperglikemia 1gr/12jam
RR : 20x
-HT emergency - Nicardipin 7.5 cc/jam target
T : 37
150/90
- Injeksi kalnex 500mg/8jam
Mata: CA (-/-), SI (-/-), isokor (3/3) - Amlodipin 10 mg 0-0-1
Pulmo: SDV (+/+), ST (-/-) - Irbesartan 300 mg 1-0-0
Cor: BJ I-II regular, intensitas - Injeksi paracetamol 1gr bila
normal, bising (-) demam
Abdomen: Supel, NT (-), BU (+)
Ext: Akral Hangat
Kekuatan: sde, kesan lateralisasi
dextra
R.Fisiologis dbn
R.Patologis (+)
Clonus (-)

Nn.craniales: sde
 16/1/2018
Subjektif Objektif Asessment Terapi dan Plan

Penurunan KU : lemah, GCS: E2V4M2 -Penurunan kesadaran - IVFD asering 16 tpm

kesadaran dengan lateralisasi dx ec IVH, - Injeksi manitol 4x125cc
TD : 181/98
ICH - Injeksi ceftriaxone
HR : 86x/menit
-Hiperglikemia 1gr/12jam
RR : 22x
-HT emergency - Nicardipin 9 cc/jam target
T : 36
150/90
- Injeksi kalnex 500mg/8jam
Mata: CA (-/-), SI (-/-), isokor (3/3) - Amlodipin 10 mg 0-0-1
Pulmo: SDV (+/+), ST (-/-) - Irbesartan 300 mg 1-0-0
Cor: BJ I-II regular, intensitas - RI 4-4-4
normal, bising (-) - Injeksi paracetamol 1gr bila
Abdomen: Supel, NT (-), BU (+) demam
Ext: Akral Hangat
Kekuatan: sde, kesan lateralisasi
dextra
R.Fisiologis dbn
R.Patologis (+)
Clonus (-)

Nn.craniales: sde
 17/1/2018
Subjektif Objektif Asessment Terapi dan Plan

Penurunan KU : lemah, GCS: E4V5M4 -Penurunan kesadaran - IVFD asering 16 tpm

kesadaran dengan lateralisasi dx ec IVH, - Injeksi manitol 4x125cc
TD : 170/90
ICH - Injeksi ceftriaxone
HR : 95x/menit
-HT emergency 1gr/12jam
RR : 22x
- Nicardipin 4.5 cc/jam target
T : 36
150/90
- Injeksi kalnex 500mg/8jam
Mata: CA (-/-), SI (-/-), isokor (3/3) - Amlodipin 10 mg 0-0-1
Pulmo: SDV (+/+), ST (-/-) - Irbesartan 300 mg 1-0-0
Cor: BJ I-II regular, intensitas - Injeksi paracetamol 1gr bila
normal, bising (-) demam
Abdomen: Supel, NT (-), BU (+) - Boleh perawatan ruangan
Ext: Akral Hangat biasa
Kekuatan: sde, kesan lateralisasi
dextra
R.Fisiologis dbn
R.Patologis (+)
Clonus (-)

Nn.craniales: sde
 18/1/2018
Subjektif Objektif Asessment Terapi dan Plan

- KU : - IWR Pasien dinyatakan iwr pada

pukul 04.30
TD : -
HR : -
RR : -
T :-

Keluarga pasien lapor perawat

ketika pasien sudah tidak
bergerak. Perawat datang sudah
kaku, biru, tidak ada napas dan
nadi. Setelah itu menghubungi
dokter. Dokter datang pasien
sudah ditutup selimut.
 THEORY Patient
Manifestation:
• Focal deficit Severe
• Onset Hours
• Headache Severe
• Vomittus +
• Hypertension +
• Loss of consciousness +
• Hemiparese Difficult to evaluate
• Speecdisorder Difficult to evaluate
 Approach to Patients
Clinical Presentation

THEORY
- Penurunan kesadaran
mendadak pada pasien dengan
stroke hemoragik
- Pupil
- Deviasi konjugat
- Meningeal sign
- R.fisiologis
- R.patologis
- Kekuatan motorik
- Lateralisasi
Patient
GCS E2V1M3
Pupil isokor
Deviasi konjugat (-)
Meningeal sign (-)
R.Fisiologis dbn
R.Patologis (-)
Kekuatan motorik s.d.e
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

SSS : 6.9 (>1) Stroke Hemorrhage

 Approach to Patients
Clinical Presentation

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

• Head up 30o Head up 30o

• Patients should be Inf. NS 0.9%

kept euvolemic
and normo- to
hyperosmolar
• Antihypertension Nicardipine 7.5 cc/h target 150/90

• Manitol Initial 200cc

Maintanance 4 x 125 cc
• Stroke is preventable, but public knowledge about the
risk factors for stroke is low.
• High blood pressure, the most important risk factor
for stroke, is significantly under-treated.
• Majority of strokes are ischemic compared to
hemorrhagic. Though hemorrhagic stroke have much
higher mortality.
• CT or MRI scans with high sensitivity for hemorrhage
stroke, are essential in diagnosis.
• But in rural areas, SSS seems quite useful, especially
when the price for radiological examinations is not
affordable or if transportation to the nearest CT scan
is high risk for the patient.
• The treatment goal is to restore cerebral perfusion
and to decrease the hypertension.
• The primary treatment of hemorrhagic stroke involves
supportive care and optimization of intracranial
hemodynamics.
• The ‘Cushing reflex’ has been reported as the
occurrence of hypertension, bradycardia and
apnoea following intracranial hypertension. Clinicians
use the occurrence of bradycardia and hypertension
as an indication of acute intracranial hypertension.
• It is important to treat strokes as quickly as possible.
With a hemorrhagic stroke, the first steps are to find the
cause of bleeding in the brain and then control it.
• Post stroke rehabilitation can help people overcome
disabilities caused by stroke damage.
Thankyou