UPPER GI TRACT DISEASE

dr. Aritantri Darmayani, M.Sc, SpPD

 Digestive anatomy

• GI tract is conventionally divided into

upper (mouth to ileum) and lower
(cecum to anus).

• From the point of view of GI bleeding,

however, the demarcation between the
upper and lower GI tract is the
duodenojejunal (DJ) junction (ligament
of Treitz).

• Bleeding above the DJ junction is called

upper GI bleeding, and that below the
DJ junction is called lower GI bleeding.
Esophagus

 25-30 cm
 Tube from pharynx to stomach
 Upper esophageal sphincter (UES or cardiac
sphincter) closed except when swallowing
 Lower esophageal sphincter (LES) closes entrance to
stomach; prevents reflux of stomach contents back
into esophagus
 Normal Healthy
Esophagus
 Proximal 1/3
 Striated muscle
 Allows voluntary initiation of swallowing
 innvervated by spinal accessory nerve

 Middle 1/3
 Striated and smooth muscle
 Dorsal motor nerve of vagus

 Distal 1/3
 Smooth muscle
 Dorsal motor nerve of vagus
 Esophageal obstruction

 Foreign bodies
 Coins, food, batteries
 Anatomic anomalies
 Carcinoma
 Schiatzki’s ring
 Peptic / chemical stricture
 Extrinsic compression
 Thyroid enlargement
 Zenker’s diverticulum
 Aortic arch
 Anomalous right subclavian artery
 Bronchogenic carcinoma
 Esophageal obstruction diagnostic strategies

 Endoscopy
 Gold standard for diagnosis and treatment

 Plain radiographs
 If foreign body suspected
 Not seeing it does not rule it out

 Contrast studies
 Gastrograffin vs barium

 NB:radigraphs + contrast studies

 False negatives <20%
 False positives <1%

 CT scan
 Esophageal obstruction foreign body management

 Oropharyngeal
 Retrieve with Kelly / McGill forceps
 Esophageal
 Endoscopic removal
 Foley catheter (controversial)
 Lower esophagus
 Often food impaction
 Glucagon 1mg iv (maximum 2mg)
Relax sphincter enough to allow passage of food in 50%
of patients
Affects only smooth muscle, thus not useful for proximal
obstructions
Reflux esophagitis stricture

pizza

•Food impacted proximal

to stricture
Esophageal Strictures

I. Caustic stricture
• Narrowing of 2/3 of esophagus
due to caustic ingestion years ago
• Accidental in children
• Suicide
II. Radiation stricture
• Smooth midesophageal stricture
 ACHALASIA

• Achalasia is a primary esophageal

motility disorder characterized by an
inability of the lower esophageal
sphincter to relax and is constantly
contracted

• Food accumulates in the upper part of

the esophagus, which gradually dilates,

• Food is degraded bacteria and

occasionally there is a regurgitation
 Achalasia
 Incomplete relaxation of LES (resting pressure >30mm Hg)
 etiology
 idiopathic - most common
 Chagas disease - Latin America
 secondary to cancer (esophagus, stomach)

 Respiratory
 aspiration
 bronchiectasis
 lung abscesses
 GI
 malnutrition
 increased risk of esophageal cancer
Achalasia – Diagnosis - Treatment
 CXR
 absent air in stomach
 dilated fluid filled esophagus
 barium esophagogram
 prominent esophagus with “bird’s beak”
 esophageal motility study
 required for definitive diagnosis

 Nitrates, CCBs
 balloon dilatation of LES
 50% successful
 5% perforation
 Surgery
 Heller myotomy
 Achalasia
Manometry

•Failure of LES
relaxation
•Failure of
peristaltic
conduction to
LES
 GASTROESOPHAGEAL REFLUX DISEASE (GERD)
ü Gastroesophageal reflux disease
(GERD)
is the reflux of acid and pepsin from
the stomach to the esophagus that
causes esophagitis.

• HCl, pepsin and bile - induce

mucosal inflammation, erosion and
ulceration

• It is a consequence of weaken function of the lower esophageal

sphincter, delayed gastric emptying with an increase in the pressure
of its content and weaken clearing function of the esophagus (lack
of saliva, poor esophageal peristalsis, and decreased production of
the esophageal mucosal glands).
Anatomy of Esophagus and Hiatal
Hernia
Clinical manifestation:
− heartburn, chronic cough, asthma attacks
− abdominal pain (within 1 hour after meals,
repeating)
− symptoms may worsen if the individual lies down,
or in the case of increasing intra-abdominal
pressure (as a result of coughing, vomiting, or of
hard stool)
− symptoms may be present even if the acid is not
present in the esophagus

− heartburn can be seen as chest pain, which requires the exclusion of

cardiac ischemia
− alcohol or foods that contain acid (citrus fruits) can cause discomfort
and worsen the syptoms
Diagnosis of GERD

 Empirically, via symptoms (symptoms don’t always correlate with the

degree of damage)
 Endoscopy – to confirm Barrett’s Esophagus and dysplasia (a negative
endoscopy does not rule out the presence of GERD)
 Ambulatory reflux monitoring

DeVault KR and Castell DO. Updated guidelines for the

diagnosis and treatment of Gastroesophageal Reflux disease.
Am J. Gastroenterol 2005;100:190-200
Ambulatory Reflux Monitoring
 Nutrition Prescription for GERD

 Initiate weight-reduction program if overweight

 Initiate smoking cessation (lowers LES pressure)
 Improve clearing of materials from esophagus
 Remain upright after eating
 Avoid eating within 3 hours of bedtime
 Wear loose-fitting clothing
 Raise the head of bed for sleeping

ADA Nutrition Care Manual, accessed 4-06

 Nutrition Prescription for GERD
Reduce gastric acidity by eliminating the following:
 Black and red pepper
 Coffee (caffeinated and decaffeinated)
 Alcohol

Substitute smaller more frequent meals

Restrict foods that lessen lower esophageal sphincter pressure by eliminating the
following:
 Chocolate
 Mint
 Foods with a high fat content.
 Spicy, acidic foods may be irritating if esophagitis is present
 Limitation of these foods should be based on individual tolerance

ADA Nutrition Care Manual, accessed 4-06

Surgical Treatment of GERD
 Fundoplication: Fundus of stomach is wrapped around lower
esophagus to limit reflux
Complications of GERD
 Esophagitis, stricture or ulcer
 Barrett’s Esophagus (premalignant state)
Barrett’s Esophagus

I. Barrett’s esophagus – ulceration of posterolateral wall

II. Midesophageal stricture from healed Barrett’s ulcer
III. Adenocarcinoma secondary to Barrett’s esophagus
DYSPEPSIA
 Definisi
 Dispepsia yang telah diinvestigasi terdiri dari dispepsia organik dan fungsional.
 Dispepsia merupakan rasa tidak nyaman yang berasal dari daerah abdomen
bagian atas.
 Berupa salah satu atau beberapa gejala berikut yaitu: nyeri epigastrium, rasa
terbakar di epigastrium, rasa penuh setelah makan, cepat kenyang, rasa
kembung pada saluran cerna atas, mual, muntah, dan sendawa.
 Dispepsia organik terdiri dari ulkus gaster, ulkus duodenum, gastritis erosi, gastritis,
duodenitis dan proses keganasan.
 Untuk dispepsia fungsional, keluhan harus berlangsung setidaknya
selama tiga bulan terakhir dengan awitan gejala enam bulan sebelum
diagnosis ditegakkan.

 Dispepsia fungsional disebabkan oleh beberapa faktor utama, antara

lain gangguan motilitas gastroduodenal, infeksi Hp, asam lambung,
hipersensitivitas viseral, dan faktor psikologis.

 Faktor-faktor lainnya yang dapat berperan adalah genetik, gaya hidup,

lingkungan, diet dan riwayat infeksi gastrointestinal sebelumnya
 PEPTIC ULCER

- is a result of imbalance between

the mucosal defense
mechanisms in the esophagus,
stomach and duodenum, and
gastric mucosa-damaging
mechanisms

- relates to digestion of mucous

membrane and lower parts of
the stomach, duodenum, and
lower esophagus by HCl and
pepsin
Risk factors for peptic ulcer
disease:
• genetic predisposition
• H.pylori infection of the
gastric mucosa
• age greater than 65 years
• psychologic stress
(mechanism unknown)
• excessive use of alcohol
• smoking
• acute pancreatitis
• chronic obstructive
pulmonary disease
• obesity
• cirrhosis
PEPTIC ULCER
PEPTIC ULCER
EPITHELIAL GASTRODUODENAL BARRIER
• Mucus-bicarbonate barrier
− smooth adhesive mucus layer
− pH gradient (lumen – epithelial surfice)
− bicarbonate secretion by epithelial cells

• H+ disposal in gastric wall

− mucoid barrier damage
− back diffusion of H+ into the wall
− mucosal blood flow

• Proliferation and epithelial repair

− mitosis and cell migration along the basal membrane
− mucoid cap after epithelial damage
• Mucus - bicarbonate layer
- protects the mucosa from autodigestion
- on the surface of the mucosa -> layer of mucus – non-permeable layer
for acid and pepsin -> and prevent the intake of the hydrogen ion (H+)
to the mucosal tissue which causes damage to the cells and subsequent
digestion with pepsin
- in mucosa itself, a large amount of bicarbonate ions (HCO3-) is
produced - buffering H+ ions that penetrate mucosa
- good blood flow
EPITHELIAL GASTRODUODENAL BARRIER

• Mucoid cap
- mechanisms associated with rapid repairing of the damage area
- mucus with fibrin - form "fibrin cap" - strongly adhere to erosion - gives
the condition of regeneration of the epithelium under it (preventing
further penetration of aggressive agents)
 EPITHELIAL GASTRODUODENAL BARRIER

• Mitosis and the cell migration along the basal layer

Disorders of the GIT – PEPTIC ULCER
üPrevalensi infeksi Hp pada pasien dispepsia yang
menjalani pemeriksaan endoskopik di berbagai rumah
sakit pendidikan kedokteran di Indonesia (2003-2004)
ditemukan sebesar 10.2%.

üPrevalensi yang cukup tinggi ditemui di Makasar tahun

2011 (55%), Solo tahun 2008 (51,8%), Yogyakarta (30.6%)
dan Surabaya tahun 2013 (23,5%), serta prevalensi
terendah di Jakarta (8%).
üPPI yang digunakan antara lain rabeprazole 20 mg, lansoprazole 30
mg,omeprazole 20 mg, pantoprazole 40 mg, esomeprazole 40 mg.

üCatatan : Terapi sekuensial (dapat diberikan sebagai lini pertama

apabila tidak ada data resistensi klaritromisin) : PPI + amoxicillin selama
5 hari diikuti PPI + klaritromisin dan nitroimidazole (tinidazole) selama 5
hari.

ü Penggunaan prokinetik seperti metoklopramid, domperidon,

cisaprid, itoprid dan lain sebagainya dapat memberikan
perbaikan gejala pada beberapa pasien dengan dispepsia
fungsional.

ü Hal ini terkait dengan perlambatan pengosongan lambung

sebagai salah satu patofisiologi dispepsia fungsional.
Kewaspadaan harus diterapkan pada penggunaan cisaprid oleh
karena potensi komplikasi kardiovaskular.
üApabila ditemukan lesi mukosa (mucosal damage) sesuai hasil
endoskopi, terapi dilakukan berdasarkan kelainan yang ditemukan.

üKelainan yang termasuk ke dalam kelompok dispepsia organik antara

lain gastritis, gastritis hemoragik, duodenitis, ulkus gaster, ulkus
duodenum, atau proses keganasan.

üPada ulkus peptikum (ulkus gaster dan/ atau ulkus duodenum), obat
yang diberikan antara lain kombinasi PPI, misal rabeprazole 2x20 mg/
lanzoprazole 2x30 mg dengan mukoprotektor, misalnya rebamipide
3x100 mg.
 HEMATEMESIS MELENA

Bleeding in the upper GIT Bleeding in the lower GIT

(esophagus, stomach, duodenum) (jejunum, ileum, colon, rectum)

ü esophageal varices ü inflammation

ü hemorrhagic gastritis ü tumors

ü gastric and duodenal ulcers ü hemorrhoids

Definisi :
Perdarahan dari saluran cerna, mulai dari esofagus
sampai dengan duodenum (Lig Treitz)
- Hematemesis : Muntah darah
- Melena : Bab yang lembek dengan warna
hitam pekat seperti ter (aspal)
- sudden and intense bleeding in the GIT is life threatening and
manifests the presence of blood in the stool or vomit

Signs of bleeding in GIT

ü Hematemesis presence of blood in vomit, in the form
of fresh blood or blood precipitates
ü blood in vomit in the blood flows more slowly in the stomach
form of "coffee grounds" - it's time for him to digest it -
hemoglobin converts to acidic hematin
(black)
ü Melena dark stool caused by digested blood

ü Occult bleeding chronically recurrent losses of small

amounts of blood that usually results in
anemia due to iron losses
 Penyebab / sumber perdarahan :
Perdarahan SCBA
vVarises v Non varises
– Varises esofagus – Esofagitis
– Varises fundus – Tukak peptik
– Stress ulcer
– Mallory-Weiss tear
– Duodenitis / esofagitis
– Tumor / Carcinoma
– Telengectasia
herediter
– Hemostatic defect
– Angiodisplasia
– dll
 PATOGENESIS
 Varises esofagus / gastropati kongestif  Mallory Weiss
- hipertensi portal - laserasi mukosa esofagogastric
 NSAID junction
- efek topikal langsung - ok muntah-muntah
- jalur hambatan prostaglandin  Esofagitis
 Tukak peptik - refluk
- Hp
- aspirin / NSAID
- hipersekresi asam lambung
- iskemia mukosa
 Gambaran Klinis

vSinkop : takikardia, kepala pusing, melayang

v Syok : - tekanan darah turun

(sistolik < 100 mmHg)
nadi cepat (> 100x/ mnt)
- muka (kulit, mukosa) pucat
- acral dingin
 Postural Signs :
vPrinsip : Kehilangan darah = kehilangan volume
intravaskuler :
– Kardiak output & tekanan darah menurun
– Nadi menjadi cepat
– Perdarahan > 1000 cc kompensasi postural tekanan darah dan nadi
tidak cukup

v Cara : Pasien tidur terlentang (ukur tensi & nadi) dudukkan (ukur tensi & nadi)
– Jika nadi meningkat > 20 / mnt atau TDS turun > 10 mmHg Kehilangan darah
sekitar 20 % (1 Ltr)
 DIAGNOSIS

 Anamnesis : aspirin / NSAID

riwayat tukak peptik
obat tradisional penghilang nyeri
 Pemeriksaan fisik : RT
stigmata peny hati kronis
diatesis hemoragik
 NGT
 Laboratorium
 Ba meal
 Endoskopi
Karsinoma esofagus
Perdarahan varises
Acute peptic ulcer

Ulcer

Freytag et al., Atlas of gastrointestinal endoscopy. www.home.t-

online.de/home/afreytag/indexe.htm
Bleeding gastric ulcer

Martin & Lyons, The Atlas of Gastrointestinal Endoscopy.

www.mindspring.com/~atlsouthgastro/stul01.html
Duodenal ulcer

Freytag et al., Atlas of gastrointestinal endoscopy. www.home.t-

online.de/home/afreytag/indexe.htm
Bleeding duodenal ulcer

Freytag et al., Atlas of gastrointestinal endoscopy. www.home.t-

online.de/home/afreytag/indexe.htm
NSAIDs administration
?
Virulence
Host
Environment
PENATALAKSANAAN UMUM

 Penilaian hemodinamik + resusitasi cairan

 Penilaian onset dan derajat perdarahan
 Usaha menghentikan perdarahan
 Identifikasi sumber perdarahan
 Mengatasi sumber perdarahan secara defenitif
 Meminimalisasi komplikasi
 Mencegah perdarahan ulang
PENATALAKSANAAN
Perdarahan SCBA non varises

 Penatalaksanaan medis
- non farmakologis
- farmakologis
H2RA / PPI, obat hemostatik
sitoprotektor, antibiotika
- penatalaksanaan khusus
terapi hemostatik perendoskopik
somatostatin jangka pendek
embolisasi arteri daerah ulkus
 Penatalaksanaan bedah / operasi
 Tukak peptik

Risiko perdarahan rendah Perdarahan aktif / risiko tinggi

Perdarahan (syok/visible vessel)

Terapi endoskopi
Monitor

Perdarahan ulang Tidak dapat mengontrol

perdarahan

Perdarahan berhenti Ulang terapi endoskopi

Operasi / bedah
Perdarahan ulang

Penatalaksanaan perdarahan tukak peptik berdarah

 PENATALAKSANAN
Perdarahan SCBA oleh varises

 Penatalaksanaan umum
 Vasoaktif (vasopresin, somatostatin, octreotide)
 Antibiotika
 Pengobatan komplikasi
 Pengobatan defenitif : SB tube, STE, LVE, TIPS,
 Profilaksis sekunder : beta bloker, ISMN