KULIAH
GASTROENTEROLOGI
SUKENDRO SENDJAJA
NYERI ABDOMEN
 Nyeri visceral
NYERI ABDOMEN
 Nyeri tekan pada abdomen
KULIAH GASTROENTEROLOGI
Penyakit Saluran Cerna Atas
 Disfagia
 Dispepsia
 Helicobacter pylori
 Tukak peptik
 Penyakit refluks gastroesofageal (GERD)
Penyakit saluran Cerna Bawah
GANGGUAN ESOFAGUS DAN GASTER
•D I S F A G I A
•D I S P E P S I A
•P E N Y A K I T R E F L U K S G A S T R O E S O F A G U S ( G E R D )
•P E N Y A K I T U L K U S P E P T I K U M
•P E R D A R A H A N G A S T R O I N T E S T I N A L
DISFAGIA
Definisi
 Sensasi gangguan pasase makanan dari mulut ke lambung.
Harus dibedakan dengan odinofagia (rasa sakit waktu
menelan).
Diagnostik
 Barium meal (esofagografi).
 Esofagogastroduodenoskopi (EGD).
 Pemantauan pH esofagus atau manometri esofagus.
DISFAGIA
 Etiologi
DISPEPSIA
 Dispepsia adalah keluhan nyeri (“abdominal pain”) atau
perasaan tak enak (“abdominal discomfort”) yang bersifat
menetap atau berulang, di daerah epigastrium.
 Keluhan ini dapat disertai rasa pedih, panas, kembung, mual,
muntah, cepat kenyang, tak suka makan dan pengeluaran gas
yang berlebihan (bersendawa) (Roma II)
 Dispepsia bukanlah suatu penyakit tetapi suatu sindrom yang
harus dicari penyebabnya.
PEMBAGIAN
1. Kelainan patologi
2. Keluhan pasien(Roma II)
1.1. Dispepsia fungsional
2.1. Tipe tukak (“ulcer-like”)
1.2. Dispepsia organik
2.2. Tipe dismotilitas (“dysmotility-like”)
2.3. Tipe nonspesifik (“unspecified”)
DISPEPSIA FUNGSIONAL
(ROMA III – 2006)
B1. Dispepsia Fungsional
•B1a: Sindroma Distres Pasca-makan
(Postprandial Distress Syndrome = PDS).
•B1b: Sindroma Nyeri Epigastrium
(Epigastric Pain Syndrome = EPS).
DISPEPSIA NON-TUKAK
 Dyspepsia
non
tukak
(“non-ulcer
dyspepsia”)
atau
dispepsia fungsional : bila pada pemeriksaan tidak
ditemukan kelainan organik, baik : klinik, endoskopik,
biokimia, maupun ultrasonografi (mis : tukak peptik,
refluks gastro-esofageal, pankreatitis, dsb), minimal selama
3 bulan dalam 6 bulan terakhir (Kriteria Roma III – 2006).
 Gastritis dengan/tanpa infeksi kuman Helicobacter pylori
termasuk dispepsia non tukak.
Activity of secretory cells of the gastric mucosa
PATOGENESIS DISPEPSIA
Mekanisme yang menimbulkan keluhan dispepsia masih belum jelas.
Beberapa teori :
1.
Asam lambung
2.
Motilitas
3.
Gangguan fungsi sensoris
4.
Kejiwaan
5.
Post-infeksi kuman H. pylori
6.
Duodenitis
7.
Diit dan lingkungan
PATOGENESIS
1. Asam lambung
 Peka terhadap asam lambung.

Gastric Releasing Peptide (GRP) pada NUD dg HP (+)
> orang sehat dg HP (+).

Tipe tukak (ulcer-like dyspepsia).
2. Motilitas
 40% NUD terdapat keterlambatan pengosongan



lambung untuk makanan padat.
25-50% hipomotilitas antrum post prandial.
Tipe dismotilitas (dysmotility-like dyspepsia).
Penyebab : kuman H.pylory, refluks gastroduodenal,
hormonal (DM), stress.
PATOGENESIS
3. Gangguan fungsi sensoris

Pada NUD : “decreased sensory threshold”.

Lesi organik sistem syaraf afferent visceral.
4. Kejiwaan

Tak ada hubungan dengan kepribadian.

Stress yang berlangsung lama.
PATOGENESIS
5. Post infeksi kuman Helicobacter pylori
 40-80% pasien dispepsia : kuman H. pylori (+).
 Tidak semua Hp (+), dispepsia (+).
 Chronic inflammation  visceral hyperalgesia.
6. Duodenitis
 14-83% pasien dispepsia : PA (+) duodenitis.
 Tidak semua End (+), PA (+) gastro-duodenitis.
 Kelainan PA tidak selalu = keluhan.
PATOGENESIS
7. Diet dan lingkungan
 Dispepsia akut : pemakai aspirin, NSAID.
 Dispepsia juga (+) : rokok, kopi.
 50% berhubungan dengan makanan : fatty, kopi,
merokok, alkohol, pedas, asam, panas, soda, dll.
KLASIFIKASI DISPEPSIA
(Roma II – 1999)
1. Tipe ulkus (“ulcer like”)
2. Tipe dismotilitas (“dysmotility like”)
3. Tipe tidak spesifik (“unspecified”)
Klasifikasi dispepsia berdasarkan keluhan yang dominan ini
sebenarnya kurang berarti dalam klinik, karena masingmasing saling tumpang tindih. Namun mungkin berguna
untuk pilihan pengobatan bagi pasien.
Kriteria Diagnostik Roma III
DISPEPSIA FUNGSIONAL
 Paling sedikit 3 bulan, dengan serangan minimal selama 6
bulan sebelumnya, salah satu atau lebih keluhan berikut ini :
- Rasa penuh yang mengganggu sehabis makan.
- Cepat kenyang.
- Nyeri epigastrium.
- Rasa terbakar di epigastrium dan
 Tidak ada bukti adanya kelainan struktur atau anatomi
(termasuk pemeriksaan gastroskopi) yang dapat menjelaskan
keluhan tersebut.
DIAGNOSIS
1.
Anamnesis : sangat penting.
2. Pemeriksaan fisik : tak banyak membantu.
3. Laboratorium : kuman Helicobacter pylori.
4. Foto Barium Saluran Cerna Atas (UGI).
5. Endoskopi : menyingkirkan kelainan organik.
Alarms atau ‘Red Flags’ dimana
Endoskopi sebaiknya segera
dikerjakan pada dispepsia
1. Anemia
2. Perdarahan gastrointestinal
3. Sering muntah
4. Anoreksia dengan BB menurun
5. Teraba masa atau benjolan
6. Upper GI photo menunjukkan kelainan yang
mencurigakan.
DIAGNOSIS BANDING
1.
Penyakit refluks gastro-esofageal (GERD).
2.
Irritable bowel syndrome (IBS).
3.
Penyakit saluran empedu (batu).
4.
Pankreatitis kronik.
5.
Dispepsia karena obat
6.
Kelainan jiwa.
7.
Lain-lain.
PENGOBATAN DISPEPSIA
70% pasien membaik dengan plasebo, mudah kambuh, kadangkadang membangkang.
1.
2.
3.
4.
5.
6.
7.
8.
Penghambat asam :
- Penyekat reseptor H-2 (PRH-2).
- Penyekat pompa proton (PPP).
Antibiotika/anti H. pylori.
Prokinetik : metoklopramide, domperidon, cisapride.
Antimuntah : antihistamin, fenotiasin, ondansetron.
Sitoprotektor : bismuth, sukralfat, setraksat.
Anti-depresan ringan : tricyclic.
Antasida.
Antispasmodik/antikolinergik.
HELICOBACTER PYLORI

Bizzozero, 1893 : kuman spiral dalam lambung mamalia.

Waren & Marshal, 1983 : Campylobacter-like organism dalam
lambung penderita gastritis kronik & tukak peptik.

Goddwin dkk., 1989 : Helicobacter pylori.

Kuman gram negatif, bulat lonjong, spiral, flagela.

Hidup antara lapisan mukus dan epitel lambung.

Hanya berkoloni di sel epitel lambung, terutama korpus dan
antrum.
Helicobacter pylori
HELICOBACTER PYLORI
Epidemiologi
Prevalensi lebih tinggi di :

Negara berkembang.

Sosio-ekonomi rendah.

Lingkungan berjubel semasa anak.

Ras/etnik dan genetik tertentu.
Pada penyakit saluran makan :

Tukak duodenum
: 95 – 100%

Gastritis kronik
: 90 – 95%

Tukak lambung
: 85 – 90%

Dispepsia non tukak
: 7 – 72%
HELICOBACTER PYLORI
(HP)
1. Efek sitotoksik : merusak mukosa lambung.
2. Respons
imunologik,
mukosa.
3. Reaksi inflamasi kronik.
menekan
resistensi
Suerbaum & Micheti, NEJM 2002;347:1175-1186
HELICOBACTER PYLORI
Memegang peranan penting dalam patogenesis beberapa penyakit:

Gastritis akut,

Gastritis kronik atrofikans,

Penyakit tukak peptik,

Metaplasia intestinal,

Kanker lambung, dan

“Mucosal associated lymphoid tissue (MALT) lymphoma”.
HELICOBACTER PYLORI
(HP)
In 1994
“IARC (the International Agency for
Research on Cancer)” – a working party of the
WHO
–
designated
H.
(“definitive”) carcinogen.
pylori
as
class
1

Urea breath test
Pasien diberi pil berisi urea
dengan atom karbon yang
diberi label 14C& 13C
Bila ada H.pylori, maka akan
ditemukan CO2 dengan label
13 atau 14 pada saat pasien
bernafas
Pemeriksaan H.pylori
Maastricht 3–2006
• Uji imunologi / serologi
Digunakan secara luas, uji non-invasif yang tidak
mahal
Akurasi diagnostik rendah (80-84%)
Disarankan untuk evaluasi ke arah infeksi H.pylori
pada pasien dengan ulkus yang berdarah dan keadaan
yang berkaitan dengan densitas bakteri yang rendah

Invasif
• Endoskopi dengan biopsi lambung untuk uji urease cepat
(rapid urease test)
Malfertheiner P et al. Gut 2007;56:772-781
Colony of H pylori in anthral gland
PENGOBATAN
Anti Helicobacter pylori :
1. Monotherapy
: ARH-2 atau PPP.
2. Dual therapy
: ARH-2/PPP+ampicillin/
clarithromycin.
3. Triple therapy
: PPP+ampicillin+clarithromycin/
metronidazole.
4. Quadruple therapy : PPP+clarithromycin+metronidazol
+bismuth
PENGOBATAN
Pengobatan sangat dianjurkan pada :
 Tukak duodenum/tukak lambung (baik aktif atau tidak, termasuk tukak
peptik dengan komplikasi).
 MALT Lymphoma (Limfoma “Mucosal Associated Lymphoid Tissues”)
 Gastritis atrofikans.
 Pasca reseksi kanker lambung.
 Pasien yang mempunyai saudara kandung atau orang tua kandung dengan
kanker lambung.
 Keinginan pasien sendiri (setelah diberi penjelasan selengkapnya oleh
dokter).
TUKAK PEPTIK
BATASAN
 Tukak peptik adalah kerusakan jaringan mulai dari
mukosa, submukosa, sampai dengan muskularis
mukosa dari saluran makan bagian atas, dengan
batas yang jelas, akibat pengaruh asam lambung dan
pepsin.
TUKAK PEPTIK
PATOFISIOLOGI
 Patofisiologi terjadinya tukak peptik sangat kompleks.
 Asam
bukan satu-satunya faktor penyebab, masih
banyak faktor lain.
 Penting adanya keseimbangan antara :
Faktor agresif asam-pepsin dengan
Faktor defensif mukosa lambung dan usus.
HCL Pepsin pH 2.0
Mucus
pH 7.0
HCO3
pH 7.0
H+
Sensory nerve
7
Mucus HCO3
HCO3
3
M
Muscularis Mucosa
Mucus
Bicarbonat
Mucosal cell renewal
5
Microvessels
2
Surface epithelial cells
1
6
4
“Alkaline tide”
Prostaglandin E2
& prostacyclin
H+
M
M
Submucosal Artery
Submucosal Vein
Nerve
Figure . Mucosal defence mechanisms*
Tarnawski A, Eerickson R: Eur J Gastroenterol Hepatol, 1991.
TUKAK PEPTIK
PATOFISIOLOGI
Pertahanan mukosa menurun bila timbul :
 Kerusakan mukosa
 Penurunan sekresi mukus
 Penurunan sekresi bikarbonat
 Penurunan aliran darah mukosa (mikrosirkulasi)
Agresivitas asam lambung ditentukan oleh :
 Sekresi asam malam hari (nocturnal secretion)
 pH intraluminer yang tetap rendah
 Pembersihan asam dalam lambung
Pathogenesis of gastric mucosal injuri
NO ULCER
DEFENSIVE FACTORS:
Mucous membrane barrier
Mucus
Bicarbonante ion
Blood flow in gastric mucosa
Proliferating factors
Prostaglandin in gastric mucosa
ULCER
Inflammation
(Response to
cell injury)
Gastric acid
(Terano A , 2001)
TUKAK PEPTIK
PATOFISIOLOGI
 Tukak lambung  faktor defensif
 Tukak duodenum  faktor agresif
TUKAK PEPTIK
DIAGNOSIS
1.
Anamnesis : sangat penting untuk diagnosis, tak selalu
spesifik, datang dengan komplikasi dispepsia kronik, nyeri 
epigastrium (“Rhythmicity” : hunger pain food relieve,
“Chronicity” : sudah lama, “Periodicity” : malam hari)
2.
Pemeriksaan fisik : tak banyak membantu.
3.
Laboratorium : kuman H. pylori.
4.
Foto barium SCBA (saluran cerna bagian atas).
5.
Endoskopi + biopsi.
TUKAK PEPTIK
KOMPLIKASI
1. Perdarahan : hematemesis – melena
2. Perforasi lambung
3. Striktur pilorus
TUKAK PEPTIK
PENGOBATAN
Tujuan pengobatan :
1. Menghilangkan keluhan.
2. Menyembuhkan tukak.
3. Mencegah kekambuhan & komplikasi.
TUKAK PEPTIK
PENGOBATAN
1.
Diet (diet ketat tak dianjurkan lagi, hindari makanan yg
memperberat keluhan asam, pedas, panas, banyak lemak,
khususnya makan teratur dan hindarkan makan sebelum tidur).
2.
Stop merokok.
3.
Hindari alkohol terutama dalam lambung kosong.
4.
Hindari ASA/NSAID/Steroid.
5.
Banyak istirahat, hindari stress.
6.
Obat anti tukak.
TUKAK PEPTIK
PENGOBATAN
Obat anti tukak :
1. Penghambat sekresi asam lambung.
2. Sitoprotektif.
3. Prokinetik.
4. Anti H. Pylori.
TUKAK PEPTIK
Pengobatan :
1. Penghambat sekresi asam :
1.1. Antagonist reseptor H-2 (ARH-2) :
-Cimetidine
-Famotidine
-Nizatidine
-Ranitidine
-Roxatidine
1.2. Antikholinergik :
-Atropine
-Propantheline bromide
-Gastrozepine
1.3. Penyekat pompa proton (PPP)
-Omeprazole
-Pantoprazole
-Esomeprazole
-Lansoprozole
-Rabeprazole
TUKAK PEPTIK
Pengobatan :
2. Obat sitoprotektif :
2.1. Prostaglandin sintetik
-Misoprostol
2.2. Koloidal bismuth
2.3. Sucralphate
2.4. Cetraxate
2.5. Treprenone
2.6. Rebamipide
-Enprostil
TUKAK PEPTIK
Pengobatan :
3. Obat prokinetik :
1. Domperidon
2. Metoclopramide
3. Clebopride
4. Cisapride.
TUKAK PEPTIK
Pengobatan :
4. Anti Helicobacter pylori :
1. Monotherapy
: ARH-2 atau PPP.
2. Dual therapy
: ARH-2/PPP+ampicillin/
clarithromycin.
3. Triple therapy
: PPP+ampicillin+clarithromycin/
metronidazole.
4. Quadruple therapy : PPP+clarithromycin+metronidazol
+bismuth
PENYAKIT REFLUKS GASTROESOFAGEAL
(GERD)
Kelainan patologi yang disebabkan oleh usaha
untuk mengeluarkan isi lambung ke dalam
esofagus, yang dapat menyangkut kelainan
(keluhan maupun gejala) dari esofagus,
farings, larings, maupun saluran nafas.
Gastroesophageal Reflux Disease (GERD)
Pathophysiology of GERD
Impaired
mucosal
defence
peristaltic
salivary HCO3
esophageal clearance
of acid (lying flat,
alcohol, coffee)
Impaired LES
– transient LES
relaxations (TLESR)
– hypotensive LES
acid output
(smoking, coffee)
H. pylori
H+
Hiatus hernia
Bile and
pancreatic
enzymes
Pepsin
intragastric pressure
(obesity, lying flat)
gastric emptying (fat)
bile reflux
de Caestecker, BMJ 2001; 323:736–9.
Johanson, Am J Med 2000; 108(Suppl 4A): S99–103.
PENYAKIT REFLUKS GASTROESOFAGEAL
(GERD)
KLINIK :
1. Keluhan khas (“typical”) :
Nyeri epigastrium (perih atau rasa panas), menjalar ke atas, ke
arah retrosternal dan leher (“heartburn”), regurgitasi asam
(rasa asam di mulut), sekresi ludah berlebihan, hematemesis.
2.
Tidak khas (“atypical”) : disfagia, nyeri dada (“chestpain”),
nyeri telan.
3.
Ekstra-esofagus :
Batuk-batuk lama, suara parau, sesak nafas.
PENYAKIT REFLUKS GASTROESOFAGEAL
(GERD)
TIGA SPEKTRUM PENYAKIT :
1.
NERD (Non Erosive Reflux Disease) :
“Heartburn”, regurgitasi asam, tak ada kelainan esofagus pada
pemeriksaan endoskopi.
2.
GERD (Gastro Esophageal Reflux Disease) :
Keluhan “heartburn”, regurgitasi asam, esofagitis derajat
ringan sampai berat pada endoskopi.
3.
Esofagus BARET :
Kelainan khas pada pemeriksaan endoskopi.
PENYAKIT REFLUKS GASTROESOFAGEAL
(GERD)
DIAGNOSIS :
1.
Gambaran klinik
2. Acid suppresion test (PPP test)
3. Tes perfusi Bernstein
4. Endoskopi : esofagitis
5. Monitoring pH esofagus selama 24 jam
6. Manometri
PENYAKIT REFLUKS GASTROESOFAGEAL
(GERD)
Tergantung spektrum penyakit
A. NERD : berjalan jinak, tak memberi komplikasi serius.
B. ESOFAGUS “BARET” : adeno-carcinoma esofagus.
C. GERD :
1. Tukak esofagus
2. Striktur esofagus
3. Perdarahan SMBA
PENYAKIT REFLUKS GASTROESOFAGEAL
(GERD)
PENGOBATAN :
A.
Umum
Turunkan BB, tidur ½ duduk, tunggu perut kosong.
Hindari rokok, kopi, coklat, alkohol, pedas, lemak.
Pakaian longgar.
Hindari obat tertentu : theofilin, caffein, dst.
B.
Khusus
PPP, prokinetik, sitoprotektif, antasida.
Bedah bila obat gagal.
GASTROINTESTINAL TRACT
BLEEDING


Gastrointestinal tract bleeding divided into two
groups :
1. Upper gastrointestinal bleeding
2. Lower gastrointestinal bleeding
How to differentiate ???
 the source of bleeding
1. Upper GI bleeding : Upper GI bleeding
originates in the first part of the GI tract-the
esophagus, stomach, or duodenum (first part
of the intestine).
2. Lower GI bleeding : Lower GI bleeding
originates in the portions of the GI tract
farther down the digestive system-the
segment of the small intestine farther from
the stomach, large intestine, rectum, and
anus.
Upper GI Bleeding


The major causes of UGIB are duodenal ulcer
hemorrhage (25%), gastric ulcer hemorrhage
(20%), mucosal tears of the esophagus or
fundus (Mallory-Weiss tear), esophageal
varices, erosive gastritis, erosive esophagitis,
Dieulafoy lesion, gastric varices, gastric
cancer, and ulcerated gastric leiomyoma.
Rare causes of UGIB include aortoenteric
fistula, gastric antral vascular ectasia,
angiectasias, and Osler-Weber-Rendu
syndrome.
Lower GI Bleeding

Lower gastrointestinal bleeding (LGIB) accounts for 2033% of episodes of gastrointestinal hemorrhage. LGIB that
requires hospitalization represents less than 1% of all
hospital admissions in the United States. The leading
causes of significant LGIB are diverticulosis and
angiodysplasia. Diverticulosis accounts for 30-50% of the
cases of hemodynamically significant LGIB, while
angiodysplasia accounts for 20-30% of cases. Some
experts believe that angiodysplasia is the most frequent
cause of LGIB in patients older than 65 years.
Hemorrhoids are the most common cause of LGIB in
patients younger than 50 years, but bleeding is usually
minor and is rarely the cause of significant LGIB. According
to a review of 7 series of patients with LGIB, the most
common cause of LGIB was diverticulosis, accounting for
33% of cases, followed by cancer and polyps, which
accounted for 19% of cases.

Common causes of LGIB include
diverticular bleeding, angiodysplasia,
ischemic colitis, radiation-induced colitis,
and other vascular causes. Neoplasms,
infectious colitis, idiopathic colitis,
anorectal abnormalities, as well as other
entities can also cause LGIB.
Diagnostic Approach
History and physical examination
 Focused history to identify risk factors (e.g., NSAID or alcohol
use) and to evaluate likely source of bleeding
Physical examination
 Evaluate hemodynamic stability by measurement of heart rate
and blood pressure.
 Search for signs of an underlying disorder (e.g., liver disease).
 Rectal examination is usually indicated; consider anoscopy if
appropriate.
Laboratory evaluation
 Degree of anemia
Diagnostic procedures
 Upper endoscopy in patients with suspected upper GI bleeding
 Colonoscopy in patients with suspected lower GI bleeding
Other imaging studies, when indicated
Diagnosis of Upper GI Bleeding
Imaging Studies
 Chest radiographs should be ordered to exclude aspiration
pneumonia, effusion, and esophageal perforation; abdominal
scout and upright films should be ordered to exclude perforated
viscus and ileus.
 Barium contrast studies are not usually helpful and can make
endoscopic procedures more difficult (ie, white barium obscuring
the view) and dangerous (ie, risk of aspiration).
 CT scan and ultrasonography may be indicated to evaluate liver
disease with cirrhosis, cholecystitis with hemorrhage, pancreatitis
with pseudocyst and hemorrhage, aortoenteric fistula, and other
unusual causes of upper gastrointestinal hemorrhage.
 Nuclear medicine scans may be useful to determine the area of
active hemorrhage.
 Angiography may be useful if bleeding persists and endoscopy
fails to identify a bleeding site. As salvage therapy, embolization
of the bleeding vessel can be as successful as emergent surgery
in patients who have failed a second attempt of endoscopic
therapy.
Diagnosis of Lower GI Bleeding

Diagnosis for acute lower gastrointestinal
bleeding, it is colonoscopy, or arteriography if the
bleeding is too brisk. When bleeding cannot be
identified and controlled, intraoperative
enteroscopy or arteriography may help localize
the bleeding source, facilitating segmental
resection of the bowel. If no upper
gastrointestinal or large bowel source of bleeding
is identified, the small bowel can be investigated
using a barium-contrast upper gastrointestinal
series with small bowel follow-through,
enteroclysis, push enteroscopy, technetium-99mtagged red blood cell scan, arteriography, or a
Meckel's scan. These tests may be used alone or
in combination.
PENATALASANAAN AWAL
Anannesis & pemeriksaan fisis
Tanda vital, Jalan infus yg sangat besar
Selang nasogastrik Hb, Ht, trombosit,
hemostaisis
Hemodinamik stabil
Tidak ada perdarahan aktif
Hemodinamik tidak stabil
Perdarahan aktif
Pengobatan empirik
RESUSITASI
Cairan krostaloid, cairan koloid,
Transfusi darah, koreksi
faktor koagulasi
Hemodinamik stabil
Perdarahan berhenti
Hemodinamik stabil
Perdarahan tetap berlangsung
Perdarahan berhenti
Elektif
Endoskopi SCBA
Emergensi atau Dini
Endoskopi SCBA
Varises esophagus
lambung
Pengobatan
definitif
Obat Vasoaktif
Octreotide, Somat ostatin,
Vasopressin
Bedah
Jika
gagal
Skleroterapi
Atau ligasi
Atau “SB tube”
Tukak
Injeksi,
hemostatik
Atau bedah segera
Sumber perdarahan
Tak tervisualisasi
Radiologi, Intervensional
Diagnostik & terapeutik
Atau bedah segera
INITIAL ASSESSMENT
History & Physical Exam;vital sign;
large bore iv line;nasogastric tube;laboratory
examtasis;Hb, Ht, thrombocyte,hemostasis
Hemodynamic stable; No active bleeding
Hemodynamic instable; Active bleeding
Emperical treatment
RESUSCITATION
Crystalloid solution; Colloid solution
Blood Transfusion; Correction for
coagulation factors
Hemodynamic stable; Bleeding stop
Hemodynamic instable; Bleeding continued
Bleeding stop
EMERGENCY or EARLY UGI
endoscopy
ELECTIVE UGI endoscopy
Esophageal/gastric Varices
Sclerotherapy or Ligattion
Or SB tube
Ulcer
Hemostatic injection
Or urgent surgery
VASOACTIVE DRUGS
Ocreotide; Somatostatin
vasopressin
Bleeding site non-visualized
Interventional diagnostic
& therapeutic
radiology or urgent surgery
If fail
DEFINITIVE TREATMT
Surgery
Algoritma penatalaksanaan perdarahan varises di Rumah Sakit
Tipe A dan B, dimama tersedia fasilitas endoskopi.
INITIAL ASSESSMENT
History & Physical Exam; Vital sign;
Large bore iv line;nasogastric tube;laboratory
examtasis;Hb, Ht, thrombocyte,hemostasis
Hemodynamic stable; No active bleeding
Emperical treatment
Vit.K;Antisecretory
Drugs;Antacida;Sucralfate
Hemodynamic stable; Bleeding stop
BP.90/60 mmHg;pulse,100/m;
Hb>9g%;Tilt test (-)
Referral system for
Elective Evaluation
UGI Barium Radiography or
Referal for Upper GI Endoscopy
DEFINITIVE TREATMT
Hemodynamic instable; Active bleeding
RESUSCITATION
Crystalloid solution;Colloid solution; Transfusion: PRC +/- FFP
Hemodynamic instable; Bleeding
BP<90/60 mmH;Pulse>100/m;
Hb<9g%;Tilt test (+)
STABILIZATION
Fluid resuscitation; blood
Transfusion; Coagulation factors
REFERRAL in
Stable hemodynamic
VASO-ACTIVE DRUG
Octreotide;Somatostatin
vasopressin
Resuscitation
a. Mild or Moderate Bleed
* Pulse and blood pressure : N
* Hb > 10 mg/ml
* Without comorbidity
* Less than 60 years of age
b. Severe Bleed
Pulse > 100 beats/min
Sistolic blood pressure < 100
mmHg
Hb < 10 mg/ml
Aged > 60 years
Table 1. Hypovolaemic shock: symptoms, sign, and fluid replacement
Blood loss (ml)
Blood loss (%bv)
Pulse rate
Blood pressure
Pulse pressure
Respiratory rate
Urine output
Mental status
Fluid replacement
<750
<15%
<100
Norma
Normal or increased
14-20
>30
Slightly anxious
Crystalloid
750-1500
15-30%
>100
Norma
Decreased
20-30
20-30
Mildly anxious
Crystalloid
1500-2000
30-40%
>120
Decreased
Decreased
30-40
30-40
Anxious & confused
Crystalloid & blood
>2000
<40%
>140
Decreased
Decreased
>35
>35
Confused & letargic
Crystalloid blood
Adapted from Grenvick A, Ayres SM, Holbrook PR,
et al. Textbook of critical care. 4th edition. Philadelphia WB Saunders Company; 40-5
DIARRHEA
Diarrhea is a common symptom that
can range in severity from an acute,
self-limited annoyance to a severe,
life-threatening illness. Patients may
use the term "diarrhea" to refer to
increased frequency of bowel
movements, increased stool liquidity,
a sense of fecal urgency, or fecal
incontinence
Definition
• In the normal state, approximately 10 L of
fluid enter the duodenum daily, of which all
but 1.5 L are absorbed by the small
intestine. The colon absorbs most of the
remaining fluid, with only 100 mL lost in
the stool. From a medical standpoint,
diarrhea is defined as a stool weight of more
than 250 g/24 h
• The causes of diarrhea are myriad.
In clinical practice, it is helpful to
distinguish acute from chronic
diarrhea, as the evaluation and
treatment are entirely different
Causes of acute infectious
diarrhea
•
1.
2.
3.
Noninflammatory Diarrhea
Viral - Norwalk virus, Norwalk-like virus, Rotavirus
Protozoal - Giardia lamblia, Cryptosporidium
Bacterial - Preformed enterotoxin production
Staphylococcus aureus, Bacillus
cereus, Clostridium perfringens
Enterotoxin production; Enterotoxigenic E coli
(ETEC), Vibrio cholerae
Inflammatory Diarrhea
• Viral – Cytomegalovirus
• Protozoal - Entamoeba histolytica
• Bacterial - Cytotoxin productio;
Enterohemorrhagic E coli, Vibrio
parahaemolyticus, Clostridium difficile.
Mucosal invasion; Shigella, Campylobacter jejuni
Salmonella, Enteroinvasive E coli ,Aeromonas
Plesiomonas,Yersinia enterocolitica,Chlamydia
Neisseria gonorrhoeae, Listeria monocytogenes
Causes of chronic diarrhea
• Osmotic diarrhea
Stool volume decreases with fasting;
increased stool osmotic gap
1. Medications: antacids, lactulose, sorbitol
2. Disaccharidase deficiency: lactose
intolerance
3. Factitious diarrhea: magnesium (antacids,
laxatives)
CLUES:
Secretory diarrhea
• Large volume ( >1 L/d); little change with fasting;
normal stool osmotic gap
1. Hormonally mediated: VIPoma, carcinoid,
medullary carcinoma of thyroid (calcitonin),
Zollinger-Ellison syndrome (gastrin)
2. Factitious diarrhea (laxative abuse):
phenolphthalein, cascara, senna
3. Villous adenoma
4. Bile salt malabsorption (ileal resection; Crohn's
ileitis; postcholecystectomy)
5. Medications
Inflammatory conditions
• Fever, hematochezia, abdominal pain
1. Ulcerative colitis
2. Crohn's disease
3. Microscopic colitis
4. Malignancy: lymphoma, adenocarcinoma
(with obstruction and pseudodiarrhea)
5. Radiation enteritis
Malabsorption syndromes
• Weight loss, abnormal laboratory values; fecal fat
> 7-10 g/24 h, tropical sprue, Whipple's disease,
eosinophilic gastroenteritis, Crohn's disease, small
bowel resection (short bowel syndrome)
2. Lymphatic obstruction: lymphoma, carcinoid,
infectious (TB, MAI), Kaposi's sarcoma,
sarcoidosis, retroperitoneal fibrosis
3. Pancreatic disease: chronic pancreatitis, pancreatic
carcinoma
4. Bacterial overgrowth: motility disorders (diabetes,
vagotomy, scleroderma), fistulas, small intestinal
diverticula
Motility disorders
• Systemic disease or prior abdominal surgery
1. Postsurgical: vagotomy, partial
gastrectomy, blind loop with bacterial
overgrowth
2. Systemic disorders: scleroderma, diabetes
mellitus, hyperthyroidism
3. Irritable bowel syndrome
Chronic infections
• Parasites: Giardia lamblia, Entamoeba
histolytica, Cyclospora
• AIDS-related:
• Viral: Cytomegalovirus, HIV infection (?)
• Bacterial: Clostridium difficile,
Mycobacterium avium complex
• Protozoal: Microsporida (Enterocytozoon
bieneusi ), Cryptosporidium, Isospora belli
ACUTE DIARRHEA
• Diarrhea that is acute in onset and
persists for less than 3 weeks is most
commonly caused by infectious agents,
bacterial toxins (either ingested
preformed in food or produced in the
gut), or drugs
• Recent ingestion of improperly stored or
prepared food implicates food poisoning,
especially if other people were similarly
affected. Exposure to unpurified water
(camping, swimming) may result in
infection with Giardia or Cryptosporidium
TRAVELER'S DIARRHEA
• Whenever a person travels from one
country to another—particularly if the
change involves a marked difference in
climate, social conditions, or sanitation
standards and facilities—diarrhea is likely
to develop within 2–10 days
• There may be up to ten or even more loose stools
per day, often accompanied by abdominal cramps,
nausea, occasionally vomiting, and rarely fever.
The stools do not usually contain mucus or blood,
and aside from weakness, dehydration, and
occasionally acidosis, there are no systemic
manifestations of infection. The illness usually
subsides spontaneously within 1–5 days, although
10% remain symptomatic for a week or longer,
and in 2% symptoms persist for longer than a
month
• Bacteria cause 80% of cases of traveler's diarrhea,
with enterotoxigenic E coli, Shigella species, and
Campylobacter jejuni being the most common
pathogens. Less common causative agents include
Aeromonas, Salmonella, noncholera vibrios,
Entamoeba histolytica, and Giardia lamblia.
Contributory causes may at times include unusual
food and drink, change in living habits, occasional
viral infections (adenoviruses or rotaviruses), and
change in bowel flora
• For most individuals, the affliction is short-lived,
and symptomatic therapy with opiates or
diphenoxylate with atropine is all that is required
provided the patient is not systemically ill (fever ł
39 °C) and does not have dysentery (bloody
stools), in which case antimotility agents should
be avoided. Packages of oral rehydration salts to
treat dehydration are available over the counter in
the USA and in many foreign countries
• Avoidance of fresh foods and water sources
that are likely to be contaminated is
recommended for travelers to developing
countries, where infectious diarrheal
illnesses are endemic. Prophylaxis is
recommended for those with significant
underlying disease (inflammatory bowel
disease, AIDS, diabetes, heart disease in the
elderly
• Prophylaxis is started upon entry into the destination
country and is continued for 1 or 2 days after leaving. For
stays of more than 3 weeks, prophylaxis is not
recommended because of the cost and increased toxicity.
For prophylaxis, bismuth subsalicylate is effective but
turns the tongue and the stools blue and can interfere with
doxycycline absorption, which may be needed for malaria
prophylaxis. Numerous antimicrobial regimens for oncedaily prophylaxis also are effective, such as norfloxacin
400 mg, ciprofloxacin 500 mg, ofloxacin 300 mg, or
trimethoprim-sulfamethoxazole 160/800 mg. daily for 5
days
• Because not all travelers will have diarrhea and because
most episodes are brief and self-limited, an alternative
approach that is currently recommended is to provide the
traveler with a 3- to 5-day supply of antimicrobials to be
taken if significant diarrhea occurs during the trip.
Commonly used regimens include ciprofloxacin 500 mg
twice daily, ofloxacin 300 mg twice daily, or norfloxacin
400 mg twice daily. Trimethoprim-sulfamethoxazole
160/800 mg twice daily can be used as an alternative
(especially in children), but resistance is common in many
areas. Aztreonam, a poorly absorbed monobactam with
activity against most bacterial enteropathogens, also is
efficacious when given orally in a dose of 100 mg three
times
Noninflammatory Diarrhea
• Watery, nonbloody diarrhea associated with
periumbilical cramps, bloating, nausea, or
vomiting (singly or in any combination) suggests
small bowel enteritis caused by either a toxinproducing bacterium (enterotoxigenic E coli
[ETEC], Staphylococcus aureus, Bacillus cereus,
C perfringens) or other agents (viruses, Giardia)
that disrupt the normal absorption and secretory
process in the small intestine.
• Prominent vomiting suggests viral enteritis or S
aureus food poisoning. Though typically mild, the
diarrhea (which originates in the small intestine)
may be voluminous (ranging from 10 to 200
mL/kg/24 h) and result in dehydration with
hypokalemia and metabolic acidosis due to loss of
HCO3– in the stool (eg, cholera). Because tissue
invasion does not occur, fecal leukocytes are not
present.
Inflammatory Diarrhea
• The presence of fever and bloody diarrhea
(dysentery) indicates colonic tissue damage caused
by invasion (shigellosis, salmonellosis,
Campylobacter or Yersinia infection, amebiasis)
or a toxin (C difficile, E coli O157:H7). Because
these organisms involve predominantly the colon,
the diarrhea is small in volume (< 1 L/d) and
associated with left lower quadrant cramps,
urgency, and tenesmus.
• Fecal leukocytes are present in infections with
invasive organisms. E coli O157:H7 is a toxigenic,
noninvasive organisms that may be acquired from
contaminated meat or unpasteurized juice and has
resulted in several outbreaks of an acute, often
severe hemorrhagic colitis. In
immunocompromised and HIV-infected patients,
cytomegalovirus may result in intestinal ulceration
with watery or bloody diarrhea
Enteric Fever
• A severe systemic illness manifested
initially by prolonged high fevers,
prostration, confusion, respiratory
symptoms followed by abdominal
tenderness, diarrhea, and a rash is due to
infection with Salmonella typhi or
Salmonella paratyphi, which causes
bacteremia and multiorgan dysfunction
Evaluation
• In over 90% of patients with acute diarrhea, the
illness is mild and self-limited and responds
within 5 days to simple rehydration therapy or
antidiarrheal agents
• Patients with signs of inflammatory diarrhea
manifested by any of the following require prompt
medical attention: high fever (> 38.5 °C), bloody
diarrhea, abdominal pain, or diarrhea not
subsiding after 4–5 days. Similarly, patients with
symptoms of dehydration must be evaluated
(excessive thirst, dry mouth, decreased urination,
weakness, lethargy)
• Physical examination should note the patient's
general appearance, mental status, volume status,
and the presence of abdominal tenderness or
peritonitis
• Peritoneal findings may be present in C difficile
and enterohemorrhagic E coli. Hospitalization is
required in patients with severe dehydration,
toxicity, or marked abdominal pain. Stool
specimens should be sent in all cases for
examination for fecal leukocytes and bacterial
cultures
• The rate of positive bacterial cultures in patients with
dysentery is 60–75%. A wet mount examination of the
stool for amebiasis should also be performed in patients
with dysentery who have a history of recent travel to
endemic areas or those who are homosexuals. In patients
with a history of antibiotic exposure, a stool sample should
be sent for C difficile toxin. If E coli O157:H7 is
suspected, the laboratory must be alerted to do specific
serotyping. In patients with diarrhea that persists for more
than 10 days, three stool examinations for ova and
parasites also should be performed. Rectal swabs may be
sent for Chlamydia, Neisseria gonorrhoeae, and herpes
simplex virus in sexually active patients with severe
proctitis
Treatment
• Diet :The overwhelming majority of adults have
mild diarrhea that will not lead to dehydration
provided the patient takes adequate oral fluids
containing carbohydrates and electrolytes. Patients
will find it more comfortable to rest the bowel by
avoiding high-fiber foods, fats, milk products,
caffeine, and alcohol. Frequent feedings of fruit
drinks, tea, "flat" carbonated beverages, and soft,
easily digested foods (eg, soups, crackers) are
encouraged
Rehydration
• In more severe diarrhea, dehydration can
occur quickly, especially in children. Oral
rehydration with fluids containing glucose,
Na+, K+, Cl–, and bicarbonate or citrate is
preferred in most cases to intravenous fluids
because it is inexpensive, safe, and highly
effective in almost all awake patients
• An easy mixture is ˝ tsp salt (3.5 g), 1 tsp baking
soda (2.5 g NaHCO3), 8 tsp sugar (40 g), and 8 oz
orange juice (1.5 g KCl), diluted to 1 L with
water. Alternatively, oral electrolyte solutions (eg,
Pedialyte) are readily available. Fluids should be
given at rates of 50–200 mL/kg/24 h depending on
the hydration status. Intravenous fluids (lactated
Ringer's solution) are preferred acutely in patients
with severe dehydration.
Antidiarrheal Agents
• Loperamide is the preferred drug in a dosage of 4 mg
initially, followed by 2 mg after each loose stool
(maximum:16 mg/24 h
• Bismuth subsalicylate (Pepto-Bismol), two tablets or
30 mL four times daily, reduces symptoms in
patients with traveler's diarrhea by virtue of its antiinflammatory and antibacterial properties
• Anticholinergic agents are contraindicated in acute
diarrhea
Antibiotic Therapy
• Empiric treatment-fluoroquinolones (eg,
ciprofloxacin, 500 mg twice daily) for 5–7 days.
These agents provide good antibiotic coverage
against most invasive bacterial pathogens,
including Shigella, Salmonella, Campylobacter,
Yersinia, and Aeromonas. Alternative agents are
trimethoprim-sulfamethoxazole, 160/800 mg twice
daily, or erythromycin, 250–500 mg four times
daily
• Specific antimicrobial treatment- Antibiotics are
not generally recommended in patients with
nontyphoid Salmonella, Campylobacter, or
Yersinia infection except in severe or prolonged
disease because they have not been shown to
hasten recovery or reduce the period of fecal
bacterial excretion. The infectious diarrheas for
which treatment is clearly recommended are
shigellosis, cholera, extraintestinal salmonellosis,
"traveler's" diarrhea, C difficile infection,
giardiasis, amebiasis, and the sexually transmitted
infections (gonorrhea, syphilis, chlamydiosis, and
herpes simplex infection)
CHRONIC DIARRHEA
• Etiology
The causes of chronic diarrhea may
be grouped into six major
pathophysiologic categories
Osmotic Diarrheas
• As stool leaves the colon, fecal osmolality
is equal to the serum osmolality, ie,
approximately 290 mosm/kg. Under normal
circumstances, the major osmoles are Na+,
K+, Cl–, and HCO3–. The stool osmolality
may be estimated by multiplying the stool
(Na+ + K+) × 2 (multiplied by 2 to account
for the anions)
• The osmotic gap is the difference between
the measured osmolality of the stool (or
serum) and the estimated stool osmolality
and is normally less than 50 mosm/kg
• An increased osmotic gap implies that the
diarrhea is caused by ingestion or
malabsorption of an osmotically active
substance
• The most common causes of osmotic diarrhea are
disaccharidase deficiency (lactase deficiency),
laxative abuse, and malabsorption syndromes (see
below). Osmotic diarrheas resolve during fasting.
Osmotic diarrheas caused by malabsorbed
carbohydrates are characterized by abdominal
distention, bloating, and flatulence due to
increased colonic gas production.
Malabsorptive Conditions
• The major causes of malabsorption are
small mucosal intestinal diseases, intestinal
resections, lymphatic obstruction, small
intestinal bacterial overgrowth, and
pancreatic insufficiency
• In patients with suspected malabsorption,
quantification of fecal fat should be
performed
Secretory Conditions
• Increased intestinal secretion or decreased
absorption results in a watery diarrhea that may be
large in volume (1–10 L/d) but with a normal
osmotic gap
• here is little change in stool output during the
fasting state. In serious conditions, significant
dehydration and electrolyte imbalance may
develop. Major causes include endocrine tumors
(stimulating intestinal or pancreatic secretion), bile
salt malabsorption (stimulating colonic secretion),
and laxative abuse
Inflammatory Conditions
• Diarrhea is present in most patients with
inflammatory bowel disease (ulcerative
colitis, Crohn's disease, microscopic colitis).
A variety of other symptoms may be
present, including abdominal pain, fever,
weight loss, and hematochezia
Motility Disorders
• Abnormal intestinal motility secondary to
systemic disorders or surgery may result in
diarrhea due to rapid transit or to stasis of
intestinal contents with bacterial
overgrowth resulting in malabsorption
Chronic Infections
• Chronic parasitic infections may cause diarrhea through a
number of mechanisms. Although the list of parasitic
organisms is a long one, agents most commonly
associated with diarrhea include the protozoans Giardia,
E histolytica, Cyclospora, and the intestinal nematodes
• Immunocompromised patients, especially those with
AIDS, are susceptible to a number of infectious agents
that can cause acute or chronic diarrhea
Chronic diarrhea in AIDS is commonly caused by
Microsporida, Cryptosporidium, cytomegalovirus, Isospora
belli, Cyclospora, and Mycobacterium avium complex.
Factitial Diarrhea
• Approximately 15% of patients with
chronic diarrhea have factitial diarrhea
caused by surreptitious laxative abuse or
factitious dilution of stool
Evaluation
• Stool Analysis - Twenty-four-hour stool
collection for weight and quantitative fecal
fat–A stool weight of more than 300 g/24 h
confirms the presence of diarrhea, justifying
further workup. A weight greater than
1000–1500 g suggests a secretory process.
A fecal fat in excess of 10 g/24 h indicates a
malabsorptive process
• 2. Stool osmolality–An osmotic gap confirms
osmotic diarrhea. A stool osmolality less than the
serum osmolality implies that water or urine has
been added to the specimen (factitious diarrhea).
• 3. Stool laxative screen–In cases of suspected
laxative abuse, stool magnesium, phosphate, and
sulfate levels may be measured. Phenolphthalein,
senna, and cascara are indicated by the presence of
a bright-red color after alkalinization of the stool
or urine. Bisacodyl can be detected in the urine
4. Fecal leukocytes–The presence of
leukocytes in a stool sample implies an
underlying inflammatory diarrhea.
• 5. Stool for ova and parasites–The presence
of Giardia and E histolytica is detected in
routine wet mounts. Cryptosporidium and
Cyclospora are detected with modified acidfast staining.
Blood Tests
• Routine laboratory tests–CBC, serum electrolytes, liver
function tests, calcium, phosphorus, albumin, TSH,
total T4, beta-carotene, and prothrombin time should
be obtained. Anemia occurs in malabsorption
syndromes (vitamin B12, folate, iron) and
inflammatory conditions. Hypoalbuminemia is present
in malabsorption, protein-losing enteropathies, and
inflammatory diseases. Hyponatremia and non–anion
gap metabolic acidosis may occur in profound
secretory diarrheas. Malabsorption of fat-soluble
vitamins may result in an abnormal prothrombin time,
low serum calcium, low carotene, or abnormal serum
alkaline phosphatase
Other laboratory tests
• In patients with suspected secretory diarrhea,
serum VIP (VIPoma), gastrin (Zollinger-Ellison
syndrome), calcitonin (medullary thyroid
carcinoma), cortisol (Addison's disease), and
urinary 5-HIAA (carcinoid syndrome) levels
should be obtained
• Proctosigmoidoscopy With Mucosal Biopsy:
Examination may be helpful in detecting
inflammatory bowel disease (including
microscopic colitis) and melanosis coli, indicative
of chronic use of anthraquinone laxatives.
Imaging
• Calcification on a plain abdominal radiograph
confirms the diagnosis of chronic pancreatitis. An upper
gastrointestinal series or enteroclysis study is helpful in
evaluating Crohn's disease, lymphoma, or carcinoid
syndrome. Colonoscopy is helpful in evaluating colonic
inflammation due to inflammatory bowel disease. Upper
endoscopy with small bowel biopsy is useful in suspected
malabsorption due to mucosal diseases. Upper endoscopy
with a duodenal aspirate and small bowel biopsy is also
useful in patients with AIDS and to document
Cryptosporidium, Microsporida, and M aviumintracellulare infection. Abdominal CT is helpful to
detect chronic pancreatitis or pancreatic endocrine tumors.
Treatment
• A. Loperamide: 4 mg initially, then 2 mg after
each loose stool (maximum: 16 mg/d)
• Diphenoxylate With Atropine: One tablet three or
four times daily
• Codeine, Paregoric: Because of their addictive
potential, these drugs are generally avoided except
in cases of chronic, intractable diarrhea. Codeine
may be given in a dosage of 15–60 mg every 4
hours as needed; the dosage of paregoric is 4–8
mL after each liquid bowel movement
• Clonidine: a2-Adrenergic agonists inhibit
intestinal electrolyte secretion. A clonidine patch
that delivers 0.1–0.2 mg/d for 7 days may be
useful in some patients with secretory diarrheas,
cryptosporidiosis, and diabetes.
. Octreotide: This somatostatin analog stimulates
intestinal fluid and electrolyte absorption and
inhibits secretion. Furthermore, it inhibits the
release of gastrointestinal peptides. It is very
useful in treating secretory diarrheas due to
VIPomas and carcinoid tumors and in some cases
of diarrhea associated with AIDS. Effective doses
range from 50 mg to 250 mg subcutaneously three
times daily. A dosage of 4 g one to three times
daily is recommended
• Cholestyramine: This bile salt binding resin
may be useful in patients with bile saltinduced diarrhea secondary to intestinal
resection or ileal disease