STRESS ULCER DITINJAU

DARI ASPEK PATOFISIOLOGI

DAN TREATMENT

1895LEPINESTROKE
1955DOIG & SHAFARSTROKE

PSMBA

PENYAKIT KRITIS STRESS ULCER

STRESS ULCER / SRMD (STRESS RELATED

MUCOSAL DISEASE)

STRESOR

KELAINAN MUKOSA AKUT

PADA LAMBUNG

FISIK, KIMIA, PSIKIS, TRAUMA BERAT &

PENYAKIT BERAT

DEFENISI

TUKAK STRES / STRESS ULCER

(SRMD)

KERUSAKAN MUKOSA LAMBUNG AKUT

AKIBAT PADA PENDERITA CRITICAL ILL / ICU

SRMD

STRESS RELATED INJURY

DIFFUSE, SUPERFICIAL MUCOSAL
DAMAGE
STRESS ULCER DEEP FOCAL
PENETRATE SUB MUCOSAL

EPIDEMOLOGI
KEMUNGKINAN (24 JAM I ) DI ICU + 75 % - 100 %
2 % - 6 % PENDERITA DI ICU (CRITICAL ILL)

ETIOLOGI
MULTIFAKTORIAL & BELUM SELURUHNYA
DAPAT DITERANGKAN.

ISCHEMIA REPERFUSIONRUSAK FAKTOR DEFENSES

MUCOSAL INJURY & ULCERATION

FACTOR SRMD :
BLOOD FLOW MICROCIRCULATION
MUCOSAL ISCHEMIA ELIMINASI H+, OX RAD
HYPOPERFUSION NO OX RAD
REPERFUSION INJURY CELL DEATH, INFLAM,
DISMOTILITY

PATOFISIOLOGI
- DIKTUM SCHWARTZ 1910 : NO ACID NO ULCER
- ERA THN 80 TEORI KESEIMBANGAN
FAKTOR DEFENSIF DAN AGRESIF

FAKTOR AGRESIF

FAKTOR DEFENSIF

- ASAM LAMBUNG

- ALIRAN DARAH MUKOSA

(MIKROSIRKULASI)

- PEPSIN

- SEL EPITEL PERMUKAAN

- REFLUKS C.EMPEDU
- NIKOTIN
- ALKOHOL
- NSAID
- KORTIKOSTEROID
-

HELIKOBACTER PYLORI

- PROSTAGLANDIN
- FOSFOLIPID/SURFACTANS
- MUCIN
- BIKARBONAT
- MOTILITAS

EMOTIONAL MOTOR SYSTEM (EMS) PATHWAYS

LIFE
EVENTS

STRESS
EXTEROCEP
TIVE

al
n
re
Ad

AUTONOMIC
RESPONSE

in e

VIGILANCE
AROUSAL

EMOTIONAL
FEELINGS

EMS

STRESS
INTEROCEP
TIVE

Co
rtis

SENSORY
MODULATION

ol

NEUROENDO
CRINE
RESPONSE

GI PATHOPHYSIOLOGY
SYMPTOMS

es
n
ki
o
t
Cy

RISK FACTOR FOR STRESS ULCER

ACUTE :

MECHANICAL VENTILATION ( > 48 hours)

COAGULOPATHY
RENAL FAILURE
HYPOPERFUSION ( SEPSIS, SHOCK)
HIGH-DOSE CORTICOSTEROID (> 250 mg/day )
BRAIN / SPINAL CORD INJURY
SIGNIFICANT BURN INJURY (> 35 %)

POTENTIAL:
CONCOMITANT NSAID
CONCOMITANT CORTICOSTEROID
HISTORY GASTRIC BLEEDING, PEPTIC ULCER,

STRESS ULCER PROPHYLAXIS

Consider stress
ulcer prophylaxis

Are any acute risk

factors present ?

Yes
No

No therapy Indicated

Yes

Is patient on home
proton pump inhibitor
therapy ?

No
Initiate enteral or Parenteral
H2 blocker therapy
or surcralfate

Yes

Initiate enteral or Parenteral

Proton pump inhibitor
No
Is patient tolerating
H2 RA therapy ?

RECOMMENDATION :
LEVEL 1

ACUTE RISK FACTORS (+) H2RA

(ORAL / IV)
ACUTE RISK FACTORS (-) H2RA
(STOP)

LEVEL 2

ACUTE RISK FACTORS (+)

ALTERNATIF H2RA & SUCRALFATE
BILA H2RA & SUCRALFATE X
PPI

LEVEL 3

POTENTIAL RISK FACTORS H2RA

(ORAL / IV)

TREATMENT FOR BLEEDING

STRESS ULCER
ENDOSCOPIC THERAPEUTIC
THERMAL COAGULATION
MULTIPOLAR ELECTROCOAGULATION,
HEATER PROBE, LASER THERAPY, CLIPPING
INJECTION THERAPY
EPINEPHRINE, ALCOHOL
COMBINATION THERAPY ; THERMAL COAGULATION
AND INJECTION

MEDICAL TREATMENT
- MAINTAIN pH > 6 ( 3 - 4 days )
- PPI (OMEPRAZOLE,PANTOPRAZOLE :80mg IV BOLUS
CONTINUOUS INFUSION OF 8 mg/h

KESIMPULAN
PEMAHAMAN PATOFISIOLOGI DARI
STRESS RELATED MUCOSAL DISEASE ,
DAN PENDARAHAN SALURAN CERNA
ATAS
DAN
PENGGUNAAN
OBAT
PENEKAN
SEKRESI
ASAM
UNTUK
MENCEGAH PERDARAHAN, MEMBERI
PEGANGAN
PENATALAKSANAAN
PENDERITA
GAWAT
DARURAT
/
CRITICALLY ILL DI ICU.