Dr. H Syafruddin Arl, Sppd-Kgeh Mars

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PENATALAKSANAAN

PENDARAHAN SCBA NONVARISEAL


HSAR Lelosutan
Sekretaris Jenderal PB PEGI.
Sub SMF GEH Departemen Penyakit
Dalam RSPAD Gatot Soebroto
Ditkesad
Jakarta, 2012.

PENDARAHAN
SCBA

PENDARAHAN
GASTROINTESTINAL
PENDARAHAN
SCBB

PENDARAHAN SCBA
BATASAN
SCBA = Saluran Cerna Bagian Atas.
Pendarahan SCBA

Kehilangan darah dalam lumen


Saluran cerna mulai dari superior
Ligamentum Treitz, yakni :
=
=
=
=

Jejunum proksimal
Duodenum
Gaster
Esofagus

Marcellus SK. Comprehensive Management of Non-variceal Upper Gastrointestinal Bleed


Astra-Zeneca and PEGI Joint Symposium. IDDW 2007.

PENDARAHAN SCBA
PATOFISIOLOGI

PATOLOGI ANATOMI

1. HEMATEMESIS
2. MELENA
3. ANEMIA - Upper COGI blood loss
PSCBA VARISEAL PSCBA NON-VARISEAL
PVE
PVF

ETIOLOGI

SH
Hipertensi Portal
PHG

GERD ERD grade C/D


Ulkus gaster (GU)
Ulkus stress (SU)
Ulkus duodeni (UD)
Ektasis
Malignansi
NSAIDs, Jamu,
Alkohol, Radiasi
Critical ill, AP
HP, ARD

Patofisiologi Pendarahan SCBA Nonvariceal

DASAR
PATOLOGI
ANATOMI :
Mucosal
DASAR
damages
ETIOLOGI :
Deeping
Gangguan
submucosal
Keseimbangan damages
Faktor Agresif /

acidity level Microvasculair


Ketahanan
damages and
Mukosa /
mucosal barrier rupture
Aggregation
system
of Clotting

DASAR
PATOFISIOLOG
I:
pH < 4
Aktivitas
Pepsin
meningkat
dlm mencerna
protein
(proteolityc
enzymes)
Irritabilitas
faktor
pembekuan
darah
Disagregasi

Manifestasi Klinis Pendarahan SCBA


1. Gejala Subyektif
-

Syncope
Presyncope
Dyspepsia
Epigastric pain
Diffuse abdominal pain
Wight loss
Jaundice

KEKERAPAN
14%
43%
18%
41%
10%
12%
5%

2. Tanda Obyektif
- Haematemesis (coffee
ground emesis)
- Melaena
- Haematochezia (red or
maroon stool)

40 50%
70 80%
15 20%

www.patient.co.uk/doctor/Upper-Gastrointestinal-Bleeding.htm
Copyright 2011

pH

> 4 memegang peranan penting


dalam aktivitas pepsin

Aktivitas maksimum pepsin (%)

100
80
60
40
20
0
1

Berstad A. Scand J Gastroenterol 1970;5:343-8

pH asam lambung

pH 6 - 6.5 merupakan target pH untuk


menghentikan
perdarahan saluran cerna
Agregasi
(%)
ADP

(Data percobaan in-vitro dan pada hewan)

0
pH=6,0
Disagregasi=77%

20
40
Buffer

60

pH=6,4
Disagregasi=16%

80

pH=7,3
Disagregasi=0%

100
0

2
3
Waktu (menit)

Green FW, et al. Gastroenterology 1978;74:3843

ADP, adenosine diphosphate.

Pengontrolan asam lambung


Mengapa perlu ditingkatkan sampai pH > 6,0 ?

Penelitian Green et al :
- membuktikan bahwa kondisi asam
lambung sangat mempengaruhi
kestabilan bekuan darah yang terbentuk
- bekuan darah stabil bila pH asam
lambung dipertahankan diatas 6
(dalam suasana basa).

Green FW, et al. Gastroenterology


1978;74:3843

KOMPLIKASI
1. PENDARAHAN PERSISTEN

(Re-bleeding)
3.SYOK HIPOVOLEMIK
4.ASPIRASI PNEUMON IA
5.GGA
6.SINDROMA HEPATORENAL
7.KOMA HEPATIKUM
8.ANEMIA BERAT
2. PENDARAHAN BERULANG

INDIKATOR Re-bleeding
PSCBA
1.Rockall Numerical Risk Scoring
System
2.Blatchford Score
3.High-risk Endoscopic finding
4.Co-morbidity

Rockall Numerical Risk Scoring System

Initial ROCKALL Score Crciteria (Prior to GASTROSCOPY )


Score-point
1. Age (y.o) :

2. Shock :
< 100/min.

< 60

60 79

> 80

No Shock SBP > 100 mmHg, pulse

Tachycardia SBP > 100 mmHg,


pulse > 100/min.
Hypotension SBP < 100 mmHg.
3. Co-morbidity :

No major co-morbidity
Cardiac failure, IHD or any

co-morbidity

0
1
2

0
2
3

Renal or Liver failure,


Disseminated malignancy
Initial Rockall Score = ./7
INTERPRETATION :

0 = consider for discharge / OPFU


> 0 = should have an EARLY ENDOSCOPY
which will calculation of their FULL

Rockall Numerical Risk Scoring System

FULL ROCKALL Score Additional Crciteria


Score-point
(After GASTROSCOPY)
4. Diagnosis :
nor SRH

Mallory-Weis Tear, no lesion seen

All other diagnoses

Malignancy of UGIT

5. Major Stigmata of Recent Haemorrhage


(SRH) :
None or dark spot only
Blood in UGIT, adherent clot, visible or spurting
vessel

0
2

Rockall TA, Logan RF, Devlin HB, et al. Risk assessment after acute upper
Full Rockall Score = ./11
gastrointestinal haemorrhage.
INTERPRETATION
: > 8 = Worse
prognosis
Gut.
1996 Mar; 38(3):316-21.
1996 BMJ
Publishing Group Limited.

Glasgow-Blatchford
Bleeding Score (GBS)
Stratifies GI bleeding patients who are "low-

risk" and candidates for outpatient


management.
Hemoglobin
g/dL
BUN
mg/dL
Initial Systolic Blood Pressure mm Hg

Low risk = Score of 0.


Any score higher than 0 is "high risk" for needing a medical
intervention of transfusion, endoscopy, or surgery.
mdcalc.com Glasgow-Blatchford Bleeding Score (GBS)_files

SCORING VALUE
In the validation group, scores of 6 or more

were associated with a greater than 50% risk


of needing an intervention.
Score is equal to "0" if the following are all

present:
Hemoglobinlevel >12.9 g/dL (men) or >11.9
g/dL (women)
Systolic blood pressure>109mm Hg
Pulse<100/minute
Blood urea nitrogen level <18.2mg/dL
Nomelenaorsyncope

Score points
Is patient female?

Yes
Heart Rate 100
Yes+1
Does the patient have melena?
Yes+1
Did the patient have syncope?
Yes+2
Does the patient have hepatic disease?
Yes+2
Does the patient have heart failure?
Yes+2
Score

points

Hemoglobin Score
Hemoglobin (g/L) for men

12.0 <13.0
1
10.0 <12.0
3
<10.0
6
Hemoglobin (g/L) for women
10.0 <12.0
1
<10.0
6

Blood Urea Score


65 <80

80 <100
100 <250 4
25

Hemodinamic Related Status


100109

9099

2
<90
3
Pulse 100 (per min)
1
Presentation with melaena
Presentation with syncope
Hepatic disease
2
Cardiac failure
2

1
2

PENATALAKSANAAN PSCBA
DIAGNOSTIK :

Pemeriksaan Penunjang

TERAPEUTIK :

Non-farmakologis : - Transfusi PRC


- Plasma / Kristalloid
- Interventional Radiology
- Surgery

Farmakologis : EDUKASIONAL :

Medikamentosa

Mencegah / Menghambat proses Re-bleedin

MEDIKAMENTOSA

STERILISASI
1. LAKTULOSA
2. NEOMISIN
3. PROBIOTIK

PENDARAHAN VARISEAL :
1. INJEKSI VIT. K
2. SOMATOSTATIN
3. OCTREOTIDE
4. BETABLOKER
5. ISDN/ISMN
GIT :6. ANTIEMESIS
7. HEMOSTATIK LAINNYA

PENDARAHAN NON-VARISEAL
1. H2RA

PPIs
3. SITOPROTEKTOR
2.

Medikamentosa
- Reduksi produksi HCl dan Pepsin
- Menghambat kerja pompa proton
(H+/K+ ATPase pump system)
S block H+ secretion
Proton Pump Inhibitors

PPI

GASTER : CHIEF (Parietal) Cells

Produksi : Gastric acid (HCl), Pep

Pompa Proton : is the terminal stage in gastric acid secretion


to gastric lumen and increased acidity level

PPIs

PPIS
1.ESOMEPRAZOL

2.Omeprazol
3.Lansoprazol
4.Pantoprazol

OMEPRAZOL
Three days of IV PPI therapy
reduced rebleeding for up to 30
days but did not affect mortality.
J. Stephen Bohan, MD, MS, FACP, FACEP
Published in Journal Watch Emergency Medicine May 1, 2009

PENELITIAN DR. Dr. Ch. Manan, Sp.PD-KGEH


patients with high-risk endoscopic signs
with high-dose (80 mg omeprazole IV
followed by 8mg/hour IV infusion for 72
hours) PPI treatment also showed a
mortality benefit

Gut doi:10.1136/gut.2010.230292
Guidelines
Asia-Pacific Working Group consensus on
non-variceal upper gastrointestinal bleeding
Published Online First 6 April 2011
1. A pre-endoscopy proton pump inhibitor (PPI) is recommended as
a stop-gap treatment when endoscopy within 24h is not available.
2. An adherent clot on a peptic ulcer should be treated with
endoscopy combined with a PPI if the clot cannot be removed.
Routine repeated endoscopy is not recommended.
3. High-dose intravenous and oral PPIs are recommended but lowdose intravenous PPIs should be avoided.
4. COX-2 selective non-steroidal anti-inflammatory drugs combined
with a PPI are recommended for patients with very high risk of
UGIB.
5. Aspirin should be resumed soon after stabilisation and
clopidogrel alone is no safer than aspirin plus a PPI.
6. When dual antiplatelet agents are used, prophylactic use of a PPI
reduces the risk of adverse gastrointestinal events

Alasan penggunaan PPI iv pada


pasien
rawat inap
Spektrum
Penggunaan

Jumlah
Pasien(%)
PPI
iv di

Perdarahan saluran cerna atas

27

Profilaksis pada saat masuk di ICU

23

Perdarahan varises esofagus dan


perdarahan karsinoma esofagus

Peptic ulcer disease

10

Gastritis

Perdarahan saluran cerna bawah

Lain-lain (bowel obstruction, ischaemic


bowel, pankreatitis, dll)

30

55% diresepkan pada saat


Slattery Ekondisi
, et al. Europeankritis
Journal Gastroenterology and
Hepatology. 2007;19:461-464

RS

Terimakasih..

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