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Penyakit dan

Kelainan pada
Esofagus dan
Easter
Oleh :
Yunia Annisa, dr, SpPD,
MKes
1

Pendahuluan
Tujuan :
Mahasiswa mampu memahami dan
menjelaskan dan melakukan diagnosis,
penatalaksanaan terhadap penyakit
sistim digestive (esofagus dan gaster)

Dyspepsia

Definisi
acute,

chronic, or recurrent pain or


discomfort centered in the upper
abdomen.

Dyspepsia

Etiologi
Food or Drug Intolerance
Functional Dyspepsia (common cause)
Luminal Gastrointestinal Tract Dysfunction
Helicobacter pylori Infection
Pancreatic Disease
Biliary Tract Disease
Other cause (Diabetes mellitus, thyroid
disease, chronic kidney disease, myocardial
ischemia, intra-abdominal malignancy, gastric
volvulus or paraesophageal hernia, chronic
gastric or intestinal ischemia, and pregnancy)

Dyspepsia

Sign & Symptops


Discomfort

(epigastric pain or burning, early


satiety, postprandial fullness, bloating, nausea,
or vomiting).
Concomitant weight loss, persistent vomiting,
constant or severe pain,
dysphagia,hematemesis, or melena warrants
endoscopy or abdominal imaging
Symptoms does not differentiate between
functional dyspepsia and organic gastrointestinal
disorders (primary care clinicians misdiagnose
nearly half of patients with peptic ulcers or
gastroesophageal reflux and have < 25%
accuracy in diagnosing functional dyspepsia)

Dyspepsia

Diagnosis

Lab:

blood count,
electrolytes,
liver enzymes,
calcium,
thyroid function tests
Age < 55yononinvasive test for H pylori

Upper Endoscopy (Age>55yo/ no


responds after4-8 week treatment/
frequent symptom relapse occurs)
Other Tests (USG, CTScan)

Dyspepsia

Penatalaksanaan
Empiric

Therapy (< 55 years and who


have no alarm features)
Treatment of Functional Dyspepsia

General measures
Pharmacologic agents
Anti-H pylori treatment
Alternative therapies

Nausea & Vomiting

Definisi
Nausea

is a vague, intensely disagreeable


sensation of sicknessor queasiness and is
distinguished from anorexia.
Vomiting often follows, as does retching
(spasmodic respiratory and abdominal
movements).
Vomiting should be distinguished from
regurgitation, the effortless reflux of liquid
or food stomach contents; and from
rumination, the chewing and swallowing of
food that is regurgitated volitionallyafter
meals.

Nausea & Vomiting

Tanda dan Gejala


Acute

symptoms without abdominal pain are typicallycaused by food


poisoning, infectious gastroenteritis, drugs, or systemic illness.
The acute onset of severe pain and vomiting suggests peritoneal
irritation, acute gastric or intestinal obstruction, or pan
Persistent vomiting suggests pregnancy, gastric outlet obstruction,
gastroparesis, intestinal dysmotility, psychogenic disorders, and central
nervous system or systemic disorders.creaticobiliary disease.
Vomiting that occurs in the morning before breakfast is common with
pregnancy, uremia, alcohol intake, and increased intracranial pressure.
Vomiting immediately after meals strongly suggests bulimia or
psychogenic causes.
Vomiting of undigested food one to several hours after meals is
characteristic of gastroparesis or a gastric outlet obstruction; physical
examination may reveal a succussion splash
Patients with acute or chronic symptoms should be asked about
neurologic symptoms (eg, headache, stiff neck, vertigo, and focal
paresthesias or weakness) that suggest a central nervous system
cause.

10

Nausea & Vomiting

Pemeriksaan Khusus
With vomiting that is severe or protracted:
serum electrolytes should be obtained
to
CT Scan
Endoscopy
MRI
USG

11

Nausea & Vomiting

Komplikasi
dehydration,
hypokalemia,
Metabolic

alkalosis,
aspiration,
rupture of the esophagus (Boerhaave
syndrome),
bleeding secondary to a mucosal tear at
the gastroesophageal junction (MalloryWeiss syndrome)

12

Nausea & Vomiting

Penatalaksanaan
Most causes of acute vomiting are mild, selflimited, and require no specific treatment.
Ingest clear liquids (broths, tea, soups,
carbonated beverages) and small quantities of dry
foods (soda crackers).
severe acute vomiting hospitalization
DehydratedHypokalemi+metabolic
alkalosisntravenous 0.45% saline solution with
20 mEq/L of potassium chloride maintain
hydration
nasogastric suction tube for gastric or mechanical
small bowel obstruction improves patient comfort
and permits monitoring of fluid loss.

13

Nausea & Vomiting

Penatalaksanaan
Antiemetic Medications
Serotonin 5-HT3-receptor antagonistsOndansetron, granisetron,
dolasetron, and palonosetron, preventing chemotherapy- and radiationinduced emesis when initiated prior to treatment
Corticosteroids Corticosteroids (eg, dexamethasone)have antiemetic
properties, but the basis for these effects is unknown.
Neurokinin receptor antagonists Aprepitant and fosaprepitant are
highly selective antagonists for NK1- receptors in the area postrema.
combination +corticosteroids and serotonin antagonists acute and
delayed nausea and vomiting with highly emetogenic chemotherapy
regimens.
Dopamine antagonists The phenothiazines, butyrophenones, and
substituted benzamides have antiemetic properties that are due to
dopaminergic blockade as well as to their sedative effects.
Antihistamines and anticholinergics(eg, meclizine, dimenhydrinate,
transdermal scopolamine) prevention of vomiting arising from
stimulation of the labyrinth, ie, motion sickness, vertigo, and migraines.
Cannabinoids

14

Hiccups (Singultus)

Definisi
Though usually a benign and self-limited annoyance,
hiccups may be persistent and a sign of serious
underlying illness.
In patients on mechanical ventilation, hiccups can
trigger a full respiratory cycle and result in respiratory
alkalosis.
Causes of benign, self-limited hiccups include gastric
distention (carbonated beverages, air swallowing,
overeating), sudden temperature changes (hot then
cold liquids, hot then cold shower), alcohol ingestion,
and states of heightened emotion (excitement, stress,
laughing). There are over 100 causes of recurrent or
persistent hiccups due to gastrointestinal, central
nervous system, cardiovascular, and thoracic disorders.

15

Hiccups (Singultus)

Diagnosis
Patient with persistent hiccups should include:
detailed neurologic examination, serum
creatinine,
liver chemistry tests,
a chest radiograph.
When the cause remains unclear:
CT or
MRI of the head, chest, and abdomen,
echocardiography,
upper endoscopy

16

Hiccups (Singultus)

Terapi
Simple Treatment
Irritation of the nasopharynx by tongue traction, lifting the uvula with a
spoon, catheter stimulation of the nasopharynx, or eating 1 teaspoon of
dry granulated sugar.
Interruption of the respiratory cycle by breath holding, Valsalva
maneuver, sneezing, gasping (fright stimulus), or rebreathing into a
bag.
Stimulation of the vagus by carotid massage.
Irritation of the diaphragm by holding knees to chest or by continuous
positive airway pressure during mechanical ventilation.
Relief of gastric distention by belching or insertion of a nasogastric tube.
Drugs medication
Chlorpromazine, 2550 mg orally or intramuscularly, is most commonly
used
Other agents reported to be effective include anticonvulsant (phenytoin,
carbamazepine), benzodiazepines (lorazepam, diazepam),
metoclopramide, baclofen, gabapentin, and occasionally general
anesthesia

17 Zollinger-Ellison

syndrome

Definisi
Peptic

ulcer diseaseGastric acid


hypersecretionmay be severe and
atypical.

18 Zollinger-Ellison

syndrome

Definisi
Peptic ulcer disease caused by gastrin-secreting
gutneuroendocrine tumors
(gastrinomas)hypergastrinemia and Gastric acid
hypersecretionmay be severe and atypical.
Primary gastrinomas may arise in the pancreas (25%),
duodenal wall (45%), or lymph nodes (515%), and in
other locations or of unknown primary in 20%.
Approximately 80% arise within the gastrinoma
triangle bounded by the porta hepatis, the neck of the
pancreas, and the third portion of the duodenum.
Most gastrinomas are solitary or multifocal nodules that
arepotentially resectable.
Over two-thirds of gastrinomas are malignant, and onethird have already metastasized to the liver at initial
presentation.

19 Zollinger-Ellison

syndrome

Gejala dan Tanda


90% of patients with Zollinger-Ellison syndrome
develop peptic ulcers. In most cases, the
symptoms are indistinguishable from other causes
of peptic ulcer disease and therefore the syndrome
may go undetected for years.
Isolated gastric ulcers do not occur
Gastroesophageal reflux symptoms occur often.
Diarrhea
In some cases theres absence of peptic symptoms
Gastric acid hypersecretion can cause direct
intestinal mucosal injury and pancreatic enzyme
inactivation, resulting in diarrhea, steatorrhea, and
weight loss

20 Zollinger-Ellison

syndrome

Screening
Fasting gastrin levels should be obtained in patients
with ulcers that are refractory to standard
therapies, giant ulcers (> 2 cm), ulcers located
distal to the duodenal bulb, multiple duodenal
ulcers, frequent ulcer recurrences, ulcers associated
with diarrhea, ulcers occurring after ulcer surgery,
and patients with ulcer complications.
Ulcer patients with hypercalcemia or family
histories of ulcers (suggesting MEN 1) should also
be screened.
patients with peptic ulcers who are H pylori
negative and who are not taking NSAIDs should be
screened.

21 Zollinger-Ellison

syndrome

Diagnosis
The most sensitive and specific method for identifying Zollinger-Ellison
syndrome is demonstration of an increased fasting serum gastrin
concentration (> 150 pg/mL [> 150 ng/L]).
Levels should be obtained with patients not taking H2-receptor
antagonists for 24 hours or proton pump inhibitors for 6 days.
Withdrawal of the proton pump inhibitor may be accompanied by massive
gastric hypersecretion with serious consequences and should be closely
monitored.
The median gastrin level is 500700 pg/ mL (500700 ng/L), and 60% of
patients have levels < 1000 pg/mL (< 1000 ng/L).
Hypochlorhydria with increased gastric pH is a much more common cause
of hypergastrinemia than is gastrinoma. Therefore, a measurement of
gastric pH (and, where available, gastric secretory studies) is performed in
patients with fasting hypergastrinemia.
Most patients have a basal acid output of over 15 mEq/h.
A gastric pH of > 3.0 implies hypochlorhydria and excludes gastrinoma.
In a patient with a serum gastrin level of > 1000 pg/mL (> 1000 ng/L) and
acid hypersecretion, the diagnosis of Zollinger-Ellison syndrome is
established.

22 Zollinger-Ellison

syndrome

Diagnosis
CT

Scan
MRI
Somatostatin receptor scintigraphy
(SRS) with single photon emission
computed tomography (SPECT)
endoscopic ultrasonography

23 Zollinger-Ellison

syndrome

Terapi
Metastatic

The most important predictor of survival is the presence of hepatic


metastases.
In patients with multiple hepatic metastases, initial therapy should be
directed at controlling hypersecretion.
Oral proton pump inhibitors (omeprazole, esomeprazole, rabeprazole,
pantoprazole, or lansoprazole) are given at a dose of 40120 mg/d, titrated
to achieve a basal acid output of < 10 mEq/h. At this level, there is
complete symptomatic relief and ulcer healing.

Localized

Disease

Disease

Cure can be achieved only if the gastrinoma can be resected before


hepatic metastatic spread has occurred. Lymph node metastases do not
adversely affect prognosis.
Laparotomy should be considered in all patients in whom preoperative
studies fail to demonstrate hepatic or other distant metastases.
A combination of preoperative studies, duodenotomy with careful duodenal
inspection, and intraoperative palpation and sonography allows successful
localization and resection in the majority of cases. The 15-year survival of
patients who do not have liver metastases at initial presentation is over
95%. Surgery usually is not recommended in patients with MEN 1 due to
the presence of multifocal tumors and long-term survival in the absence of
surgery in most patients.

24

GERD

Definisi
Suatu

keadaan patologis sebagai akibat


refluks kandungan lambung ke dalam
esofagus, dengan berbagai gejala yang
timbul akibat keterlibatan esofagus,
faring, laring dan saluran nafas.
Dapat menimbulkan berbagai gejala di
esofagus maupun ekstraesofagus
Dapat menyebabkan komplikasi berat
seperti striktur, Barrets Esophagus
bahkan adeno karsinoma di kardia dan
esofagus

25

GERD

Etiologi
Nikotin
Alkohol
Aspirin
Kelainan pada lambung (dilatasi lambung,
obstruksi gastrik outlet, delayed gastric
emptying)
Infeksi H.Pylori
Hiatus hernia
Obat2an antikolinergik, beta adrenegik,
theofilin, opiat, dll
Hipersensitivitas viseral

26

GERD

Gejala
Nyeri/ rasa tidak enak pada epigastrum atau
retrosternal bagian bawah dideskripsikan
sebagai heartburn
Disfagia (pada makanan padat striktur atau
keganasan yg berkembang dari Barrets
esophagus
Mual/regurgitasi
Rasa pahit di lidah
Odinofagiaa bisa timbul ulserasi esofagus berat
Kadang timbul rasa tidak enak retrosernal
Bisa muncul juga gejala ekstra esofageal (nyeri
dada non kardiak, suara serak, laringitis, batuk
karena aspirasi, bronkiektasis, asma)

27

GERD

Diagnosis

Endoskopi standar baku


Klasifikasi Los Angeles& klasifikasi Savarry-Miller

Esofagografi dengan barium kurang peka pada


esofagitis ringan lebih efektif dari endoskopi pada
stenosis esofagus derajat ringan akibat esofagitis
peptik dengan gejala disfagia dan hiatus hernia
Pemantauan pH 24 jam (+) pH<4 jarak 5 cm dari LES
Tes Bernstein pelengkap pemantauan pH
Manometri esofagusjika pada pasien dengan gejala
nyeri epi gastrium dan regurgitasi yang nyata didapati
esofagografi barium dan endoskopi yang normal.
Sintigrafi gastroesofageal Tes ini masih diragukan
Tes penghambat pompa proton/ Tes supresi asam jika
tidak terdapat modalitas diagnostik seperti endoskopi,
pH metri dll

28

GERD

Penatalaksanaan
Modifikasi
Terapi
Terapi
Terapi
Terapi

Gaya Hidup
Medikamentosa
terhadap komplikasi
Bedah
Endoskopi

29

GERD

Penatalaksanaan
Modifikasi

Gaya Hidup

Meninggikan posisi kepala pada saat tidur,


menghindari makan sebelum tidur
Berhenti merokok dan mengkonsumsi alkohol
Mengurangi konsumsi lemat, mengurangi
jumlah makanan yg dimakan
Menurunkan berat badan&menghindari
pakaian ketat
Menghindari makanan seperti coklat, the,
peppermint, kopi, minuman bersoda
Menghindari obat2an yg dapat menurunkan
tonus LES anti kolinergik, teofilin, diazepam,
opiat, antagonis kalsium, agonist beta
adrenergik, progesteron

30

GERD

Penatalaksanaan
Terapi

Medikamentosa

Antasid
Antagonis reseptor H2
Sukralafat (Alumunium
hidroksida+sukrosa oktasulfat)
Penghambat Pompa Proton ( PPI)

31

GERD

Penatalaksanaan
Terapi

terhadap komplikasi

Striktur Esofagus
Jika

pasien mengeluh disfagia dengan


diameter < 13 mm dilatasi busi (Hurst
bougie, Maloney bougie, Savarry bougie,
Pneumatic Bougie), jika gagal operasi

Esofagus Barret

32

GERD

Penatalaksanaan
Terapi

Bedah jika terapi


medikamentosa gagal/ pasien GERD
dengan striktur berulang

33

GERD

Penatalaksanaan
Terapi

Endoskopi

Penggunaan energi radiofrekuensi


Plikasi gastrik endoluminal
Implantasi endoskopis menyuntikkan
zat implandi bawah mukosa esofagus
bagian distal.

34

Striktus Esofagus

Definisi
Penyempitan

lumen esofagus, dapat


karena tumor atau penyebab lain
Jarang ditemui

35

Striktus Esofagus

Patogenesis dan Patofisiologi


Kebanyakan

akibat esofagitis karena


refluks gastroesofageal
Faktor yang berperan pada Striktur
Esofagus:

Disfungsi sfingter esofagus bawah


Gangguan motilitas yang menyebabkan
memburuknya kemampuan pembersihan
esofagus
Faktor lain yang mungkin berperan
( hernia hiatal, sekresi asam dan pepsin
dan gangguan pengosongan lambung)

36

Striktus Esofagus

Gejala dan Tanda


Disfagia

pada makanan padat

Heartburn
Rasa

tidak enak didada


Ada yang mengganjal substernal
wwaktu makan
Mual dan Muntah
Bila makin berat malnutrisi

37

Striktus Esofagus

Etiologi
Penyakit

intrinsik yang menyempitkan


lumen esofagus melalui inflamasi,
fibrosis atau neoplasia
Penyakit ekstrinsik yang menyempitkan
lumen esofagus melalui invasi langsung
atau pembesaran kelenjar limfe
Penyakit-penyakit yang merusak
peristaltik esofagus dan/atau fungsi
sfingter esofagus bawah (LES) melalui
efek penyakit pada otot polos esofagus
dan persarafannya

38

Striktus Esofagus

Diagnosis
Anamnesis
Gangguan menelan makanan

39

Ulkus peptik

Definisi
Suatu

gambaran bulat atau semi


bulat/oval, ukuran > 5mm kedalaman
sub ukosal pada muosa lambung akibat
terputusnya kontinuitas/ integritas
mukosa lambung
Disebut juga tukak gaster

40

Ulkus peptik

Etiologi
Gangguan

keseimbangan antara faktor


agresif/ asam dan pepsin dengan
defensif ( mukus, bikarbonat, aliran
darah, PG)
Helycobacter Pylori

41

Ulkus peptik

Gambaran Klinis
Mengeluh dispepsia
Nyeri ulu hati
Rasa tidak nyaman disertai muntah
Rasa sakit timbul saat pasien lapar, terasa di
sebelah kanan, bisa membangunkan pasien
tengah malam, rasa sakit hilang setelah
makan atau minum obat antasida (tukak
duodeni)
Rasa sakisa disebelah kirit timbul setelah
makan, terasa di sebelah kiri, terasa mulanya
pada satu titik dan menyebar sampai ke
punggung (tukak gaster)

42

Ulkus peptik

Diagnosis
Pemeriksaan Fisisk
Rasa nyeri ulu hati
Penurunan berat badan
Nyeri teka4-5 jam setelahjumpain perut
Perut diam tanpa terdengar peristaltik
Goncangan perut 4-5 jam setelah
makan disertai muntah-muntah

43

Ulkus peptik

Diagnosis
Pemeriksaan penunjang
Radiologi dengan barium meal kontras
ganda
Endoskopi
Biopsi

44

Ulkus peptik

Komplikasi
Perdarahan
Perforasi,

rasa sakit tiba-tiba


Stenosis pilorik/ gastric Outlet
obstruction

45

Ulkus peptik

Terapi
Non

medikamentosa

Istirahat
Diet
Menghindari obat2an OAINS

Medikamentosa

Antasida
Obat penangkal kerusakan mukus
Koloid

bismuth
Sukralafat
Prostaglandin
Antagonis reseptor H2/ARH2
PPI
Operasi

46

Akalasia

Definisi
Suatu

keadaan khas yang ditandai


dengan tidak adanya peristaltik korpus
esofagus bagian bawah dan sfingter
esofagus bagian bawah (SEB) yang
hipertonik sehingga tidak bisa
mengadakan rlaksasi secara sempurna
pada wakt menelan makanan.

47

Akalasia

Etiologi
Akalasia

Tidak diketahui, diduga akibat virus


neurotropik

Akalasia

Primer

Sekunder

Infeksi
Tumor intraluminer
Obat antikolinergik
Pasca vogotomi

48

Akalasia

Manifestasi Klinis

Disfagia
Regurgitasi
Penurunan berat badan
Nyeri dada

49

Akalasia

Diagnosis

Radiologi (esofagogram)
Endoskopi

50

Akalasia

Penatalaksanaan
Medikamentosa

Nitrat (isosorbid dinitrat)


Calcium Channel blockers

Dilatasi/

Peregangan SEB
Operasi (esofagomiotomi)

51

Mallory Weiss Syndrome

Definisi
Mallory-Weiss

syndrome is characterized
by a nonpenetrating mucosal tear at the
gastroesophageal junction that is
hypothesized to arise from events that
suddenly raise transabdominal pressure,
such as lifting, retching, or vomiting.
Alcoholism is a strong predisposing
factor.

52

Mallory Weiss Syndrome

Gejala dan Tanda


usually

present with hematemesis with


or without melena.
A history of retching, vomiting, or
straining

53

Mallory Weiss Syndrome

Diagnosis
Endoscopy

after resusitation

54

Mallory Weiss Syndrome

Penatalaksanaan
fluid

resuscitation
blood transfusions

55

Gastritis

Definisi
Proses

inflamasi pada mukosa dan sub


mukosa lambung
Termasuk paling sering dijumpai di klinik

56

Gastritis

Klasifikasi
Berdasarkan Update Sydney system:
Topografi
Mortologi
Etiologi
Klasifikasi umum:
Monahopik
Atropik
Bentuk khusus

57

Gastritis

Etiologi
plyori (HP) >90%
Penggunaan antibiotik infeksi paru
Ganguan fungsi imun
Virus enteric rotavirus dan calcivirus
JamurCandida Sp, Histoplasma
capsulatum dan Mukonaceae
Heliobacter

58

Gastritis

Gejala dan tanda


Asimptomatik
Keluhantidak

khas:

Nyeri panas dan pedih di ulu hati


Mual sampai muntah

59

Diagnosis

Endoskopi
Hispatologi
Biopsi (bila perlu)

Gastritis

60

Gastritis

Penatalaksanaan

Radikasi Kuman

61

Gastropati

Definisi
erosive

and hemorrhagic gastritis


The most common causes of erosive gastropathy
are medications (especially NSAIDs), alcohol,
stress due to severe medical or surgical illness,
and portal hypertension (portal gastropathy).
Major risk factors for stress gastritis include
mechanical ventilation, coagulopathy, trauma,
burns, shock, sepsis, central nervous system
injury, liver failure, kidney disease, and
multiorgan failure.
Uncommon causes of erosive gastropathy
include caustic ingestion and radiation.

62

Gastropati

Tanda dan Gejala


usually

asymptomatic.
When occur : anorexia, epigastric pain,
nausea, and vomiting.
There is poor correlation between symptoms
and the number or severity of endoscopic
abnormalities.
upper gastrointestinal bleeding, which
presents as hematemesis, coffee grounds
emesis, or bloody aspirate in a patient
receiving nasogastric suction, or as melena
hemodynamically significant bleeding is rare

63

Gastropati

Diagnosis
The

laboratory findings are nonspecific.


The hematocrit is low if significant
bleeding has occurred; iron deficiency
may be found.
Upper endoscopy is the most sensitive
method of diagnosis.

64

Gastropati

Klasifikasi
Berdasarkan penyebab
Stress Gastritis
NSAID Gastritis
Alcoholic Gastritis
Portal Hypertensive Gastropathy

65

Gastropati

Klasifikasi

Stress Gastritis

Prophylaxis Stress-related mucosal erosions and subepithelial


hemorrhages 72 hours in critically ill patients. Bleeding higher mortality
rate but is seldom the cause of death. Risk factors for bleeding are
coagulopathy (platelets < 50,000/mcL or INR > 1.5) and respiratory failure
with the need for mechanical ventilation for over 48 hours. Other risk factors
include traumatic brain injury, severe burns, sepsis, vasopressor therapy,
corticosteroid therapy, and prior history of peptic ulcer disease and
gastrointestinal bleeding. Early enteral tube feeding may decrease the risk of
significant bleeding. Prophylaxis should be routinely administered to critically
ill patients. Prophylactic suppression of gastric acid with intravenous H2receptor antagonists or proton pump inhibitors (oral or intravenous) reduce
the incidence and significant bleeding.
Treatment Once bleeding occurs, patients should receive continuous
infusions of a proton pump inhibitor (esomeprazole or pantoprazole, 80 mg
intravenous bolus, followed by 8 mg/h continuous infusion) as well as
sucralfate suspension, 1 g orally every 4 to 6 hours. Endoscopy should be
performed in patients with clinically significant bleeding to look for treatable
causes, especially stressrelated peptic ulcers with active bleeding or visible
vessels. When bleeding arises from diffuse gastritis, endoscopic hemostasis
techniques are not helpful.

66

Gastropati

Klasifikasi

NSAID Gastritis

Patients receiving NSAIDs in clinical trials, 2550% have


gastritis and 1020% have ulcers at endoscopy
Patients with alarm symptoms or signs, such as severe pain,
weight loss, vomiting, gastrointestinal bleeding, or anemia,
should undergo diagnostic upper endoscopy. For other patients,
symptoms may improve with discontinuation of the agent,
reduction to the lowest effective dose, or administration with
meals.
Proton pump inhibitors have demonstrated efficacy in controlled
trials for the treatment
an empiric 24 week trial of an oral proton pump inhibitor
(omeprazole, rabeprazole, or esomeprazole 2040 mg/d;
lansoprazole or dexlansoprazole, 30 mg/d; pantoprazole, 40
mg/d) is recommended for patients with NSAID-related
If symptoms do not improve, diagnostic upper endoscopy
should be conducted.

67

Gastropati

Klasifikasi
Alcohol

ic Gastritis

Excessive alcohol consumption may lead


to dyspepsia, nausea, emesis, and minor
hematemesisa condition sometimes
labeled alcoholic gastritis. However, it is
not proven that alcohol alone actually
causes significant erosive gastritis.
Therapy with H -receptor antagonists,
protonpump inhibitors, or sucralfate for 2
4 weeks often is empirically prescribed.
2

68

Gastropati

Klasifikasi

Portal hypertensive Gastritis

Portal hypertension commonly results in gastric


mucosal and submucosal congestion of capillaries and
venules, which is correlated with the severity of the
portal hypertension and underlying liver disease.
Usually asymptomatic, it may cause chronic
gastrointestinal bleeding in 10% of patients and, less
commonly, clinically significant bleeding with
hematemesis.
Treatment with propranolol or nadolol reduces the
incidence of recurrent acute bleeding by lowering
portal pressures.
Patients who fail propranolol therapy may be
successfully treated with portal decompressive
procedures

Pendarahan SCBA

Definisi
Manifestasi

pendarahan saluran cerna


bagian atas (SCBA) dapat dalam bentuk
hematemesis (muntah darah) dan atau
melena (buang air besar hitam)
Pada hematemesis darah segar atau
bercampur darah hitam yang berasal dari
zat hematin paparan darah pada asam
lambung
Pendarahan pada duodenum hanya
bermanifestasi hanya dalam bentuk melena

Pendarahan SCBA

Etiologi
Pecahnya

varises esofagus (terbanyak


di Indonesia 60-70%)
Tukak peptik
Gastritis karena obat aspirin/ anti
imflamasi non steroid
Gastropati hipertensi portal
Tumor
Angiodisplasia dan sebagainya

Pendarahan SCBA

Manifestasi Klinis
Kemungkinan pasien datang dengan:
Anemia defisiensi besi akibat
pendarahan tersembunyi yg
berlangsung lama
Hematemesis dan atau melena disertai
atau tanpa anemia. Dengan atau tanpa
gangguan hemodinamik; derajat
hipovolemi menentukan tingkat
kegawatan pasien

Pendarahan SCBA

Pendekatan Diagnostik
Anamnesis akuratidentifikasi faktor
pencetuspenyakit dasar yg ada
Bila perlu pemasangan pipa nasogastrik
utk diagnostik dan dekompresi
Pemeriksaan fisik yg teliti identifikasi
penyakit dasar& penyerta
Pemeriksaan
esofagogastroduodenoskopi sarana
diagnostik definitif

Pendarahan SCBA

Pendekatan Diagnostik
Anamnesis akuratidentifikasi faktor
pencetuspenyakit dasar yg ada
Bila perlu pemasangan pipa nasogastrik
utk diagnostik dan dekompresi
Pemeriksaan fisik yg teliti identifikasi
penyakit dasar& penyerta
Pemeriksaan
esofagogastroduodenoskopi sarana
diagnostik definitif

Pendarahan SCBA

Langkah Praktis pengelolaan


perdarahan SCBA (PGI-PEGI-PPHI)
Pemeriksaan awal, penekanan pada evaluasi
status hemodinamik
Resusitasi, terutama utk stabilisasi hemodinamik
Melanjutkan anamnesis, pemeriksaan fisik dan
pemeriksaan lain yg diperlukan
Menegakkan diagnosis pasti penyebab
perdarahan
Terapi utk menghentikan perdarahan,
penyembuhan penyebab perdarahan, mencegah
perdarahan ulang

Pendarahan SCBA

Pemeriksaan awal

Tekanan

darah dan nadi posisi baring


Perubahan ortostatik tekanan darah dan nadi
Ada tidaknya vasokonstriksi tekanan darah dan nadi
Kelayakan napas
Tingkat kesadaran
Produksi urin
Pendarahan akut > 20% vol intravaskular ada kondisi hemodinamik tdk stabil:
Hipotensi (<90/60 mmHg, MAP < 70mmHg, HR >100/m)
Tekanan diastolik ortostatik turun > 10 mmHg/sistolik turun >20mmHg)
Frekuensi nadi ortostatik meningkat> 15/m
Akral dingin
Kesadaran menurun
Anuria atau oliguria (produksi urin < 30 ml/jam)
Juga bisa diperkirakan apabila ditemukan:
Hematemesis
Hematokesia
Darah segar pada aspirasi pipa nasogastrik dan dengan lavase tidak segeera
jernih
Hipotensi persisten
Dalam 24 jam menghabiskan tranfusi darah 800-1000 ml

Pendarahan SCBA

Stabilisasi Hemodinamika
Berikan

infus cairan kristaloid (ex garam fisiologis


tetesancepat2jarum diameter besar(min16G))
Biasanya tidak memerlukan cairaan koloid kecuali kondisi
hipoalbuminemia berat
Kirim pemeriksaan darah secepatnya (utk identifikasi darah)
Kecurigaan diatesis hemoragik tes Rumpel-Leede, pemeriksaan
waktu darah, waktu pembekuan, retraksi bekuan darah, PPT,aPPT
Kapan tranfusi darah pada SCBA?
Perdarahan dgn kondisi hemodinamik tdk stabil
Perdarahan baru/berlangsung dngan perkiraan 1L atau lebih
Perdarahan baru/berlangsung dgn Hb<10atau hematrokit< 30%
Ada tanda oksigenasi jaringan yg menurun
NB:
Jumlah hematrokit kurang akurat bila perdarahan baru/berlangsung
Proses hemodilusi dari cairan ekstra vaskuler selesai 24-72 jam
setelah onset perdarahan
Target pwncapaian hematrokit muda sehat (20-25%), usia lanjut
(30%), hipertensi portal (tidak boleh lebih 27-28%)

Pendarahan SCBA

Pemeriksaan Lanjutan

Anamnesis
Sejak kapan terjadi perdarahan & perkiraan darah keluar
Riwayat perdarahan sebelumnya
Riwayat perdarahan keluarga
Ada tidaknya perdarahan di bag tubuh lain
Penggunaan obat antiinflamasi non-steroid dan anti koagulan
Kebiasaaan minum alkohol
Mencari kemungkinan penyakit hati kronik, demam berdarah, demam tifoid,
CKD, DM, Hipertensi, Alergi obat
Riwayat tranfusi sebelumnya
PF
Stigmata penyakit hati kronik
Suhu badan dan perdarahan di tempat lain
Tanda-tanda kulit dan mukosa penyakit sistematik yg bisa disertai
perdarahan saluran makanan
Pemeriksaan pelengkap
EKG
BUN, kreatinin serum
Pemeriksaan elektrolit (Na, K Cl)
Pemeriksaan lain yg diperlukan

Pendarahan SCBA

Alur Penatalaksanaan P SCBA

Pendarahan SCBA

Pendarahan SCBA
Endoskopi

Contact thermal
Non contact thermal
Non thermal

Pendarahan SCBA
Terapi

Radiologi
Pembedahan

82

Daftar pustaka
Buku

Ajar penyakit Dalam Edisi 6.


Jakarta. Pusat penerbitan Departemen
Ilmu Penyakit Dalam
Harrissons Principles of Internal
medicine, Edisi ke 18. McGraw-Hill

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