Kurikulum Vitae

• Nama : Dr. Amie Vidyani,SpPD

• Tgl Lahir : Pasuruan, 28 Januari,1980
• Jabatan : Staf Pengajar Departemen Ilmu Penyakit Dalam, Divisi
Gastroentero -Hepatologi, FK UNAIR-RSUD Dr.SOETOMO Surabaya
• Pendidikan :
Lulus Dokter FK UNAIR 2005
Lulus Dokter Spesialis Peny.Dalam FK-UNAIR 2013
Sub Spesialis Gastroenterologi-Hepatologi FK-UNAIR
(2016- sekarang)
Pendidikan Tambahan :
Pelatihan Pelatih Hepatitis B dan C (Jakarta, 2014)
Pelatihan Penatalaksanaan Hepatitis bagi Petugas
Pelaksana PNPK Hepatitis (Jakarta, 2014)
Fellowship observational in gastroenterology (University of
Santo Tomas, Manila, Filiphina, 2015)
Training program for Asian Young Endoscopist Award
(Kosin University, Gospel Hospital, Busan, Korea Selatan,
2016)
Preceptorship programme of Hepatology (National
University of Health System, Singapore, 2017)
Organisasi : Anggota IDI (2005-Sekarang)
Anggota PAPDI (2008-sekarang)
Anggota gabungan PGI-PEGI-PPHI (2013-sekarang)
 EMERGENCY
IN
GASTROENTEROLOGY

Amie Vidyani

Gastroenterology and Hepatology Center

Dr.Soetomo Hospital - Airlangga University
Surabaya, 2017
 OUTLINE
 Acute Gastrointestinal Bleeding
 Acute Abdominal Pain
ACUTE GASTROINTESTINAL
BLEEDING
ACUTE UPPER GASTROINTESTINAL
BLEEDING
 Hematemesis : Vomiting of bright red blood,
which suggests recent or ongoing bleeding, and
dark material (coffee-ground emesis), which
suggests bleeding that stopped some time ago.

 Melena : black tarry stool and results from

degradation of blood to hematin or other
hemochromes by intestinal bacteria. Generally
occurs when 50 to 100 mL or more of blood is
delivered into the GI tract (usually the upper
tract), with passage of characteristic stool
occurring several hours after the bleeding event

Savides & Jensen, 2016

Hematochezia : bright red blood per
rectum and suggests active UGI (Massive
UGI bleeding, > 1000 Ml) or small bowel
bleeding or distal colonic or anorectal
bleeding

Savides & Jensen, 2016

 Causes of Esophago-Gastro-
Duodenal Bleeding
Varices
Mallory Weiss
Esophagitis
Gastric Ulcer NSAID’s/
Aspirin

Neoplasm

Duodenal Acute
Ulcer Gastritis
Arterio-Venous
Malformation
 UGI
BLEEDING

VARICEAL NON-
BLEEDING VARICEAL
BLEEDING
Epidemiology of upper GI Bleeding

 Dr.Soetomo Hospital:
- 1990 : Esophageal varices is the most common
cause of upper GI bleeding

- 2006-2007 : >> Esophageal Varices

- 2008-now : >> Erosive gastritis due to NSAID

 Initial Evaluation

 Characteristics of bleeding
 Hematemesis blood
 Melena
 Hematochezia
 History
 Liver disease, alcoholism, coagulopathy
 NSAID, antiplatelet or anticoagulant use
 Abdominal Surgeries
 ↓ BW
Savides & Jensen, 2016
Savides & Jensen, 2016
Savides & Jensen, 2016
Examination
 Vitals
 Tachycardia, hypotension,
consciousness
 Sign of Liver Disease (jaundice, spider
nevi, erytema palmaris, ascites,
collateral vein, caput medusa)
 Rectal examination: melena, rectal mass
 Skin examination
Diagnostic Evaluation
 Hgb/Hct, plt count, coag studies
 LFTs, albumin, BUN and creatinine
 Type and screen /type and cross
 ECG
 Abdominal US
 Endoscopy
 Emergent Management
 Closely monitor airway, clinical status, vital
signs, cardiac rhythm
 two large bore IV lines (16 gauge or larger)
 bolus infusions of isotonic crystalloid
 Transfusion
 pRBCs – Hgb <7, hemodynamic instability
 FFP, platelets – coagulopathy, plt <50 or plt
dysfunction
 Triage – ICU vs Wards
 Hemodynamic instability or active bleeding > ICU
 Immediate GI consult
 NGT (Naso-Gastric Tube)

 ACG, 2012: Nasogastric or orogastric lavage is not

required in patients with UGIB for diagnosis,
prognosis, visualization, or therapeutic effect
(Conditional recommendation)

 NGT for on going bleeding and hemodinamic

instability (Prevent aspiration, decompresion,
determine the source of bleeding) (ACG, 2012; PGI,
2012)
 NG-Lavage: for special condition, iced-saline is not
recommended
Medications (Non-Variceal Bleeding)

 Acid Suppression
 PPI (Proton Pump Inhibitor) (ACG, 2012)
 Omeprazol, Lansoprazol, Pantoprazol,
Esomeprazol, Lansoprazol, Rabeprazol
 Omeprazol, Pantoprazol: 80mg IV bolus, then
8mg/hr infusion
 Esomeprazole at the same dose
 Lansoprazol: 60 mg IV bolus, then 6 mg/hr
infusion
 Role of acid in haemostasis
Impairs clot formation
– Impairs platelet aggregation and causes
disaggregation

Accelerates clot lysis

- Predominantly acid-stimulated pepsin

May impair integrity of mucus/bicarbonate barrier

 Role of acid in haemostasis
Impairs clot formation
– Impairs platelet aggregation and causes
disaggregation

Accelerates clot lysis

- Predominantly acid-stimulated pepsin

May impair integrity of mucus/bicarbonate barrier

 Effect of PPI on gastric pH

Increase intragastric pH
 pH>6.0 for 84-99% of day

No reported tolerance

Continuous infusion (CI) superior to intermittent bolus

administration

Clinical improvements in rebleeding and/or surgery

with:
Bolus 80mg + CI 8mg/h
 Medications
Somatostatin and analogues (octreotide)

 a reduction in splanchnic and gastroduodenal

mucosal blood flow, a decrease in GI motility,
inhibition of gastric acid secretion, inhibition of
pepsin secretion, and gastric mucosal
cytoprotective effects (Savides & Jensen, 2016)

 It can not be considered for routine use

 It can be considered in patients with severe

ongoing bleeding who are not responsive to
endoscopic therapy, an intravenous PPI, or both,
and are not surgical candidates, although their
effectiveness in these patients is uncertain.
 Tranexamic acid, vit K??
 Endoscopy
 Surgery
 Variceal Bleeding

 Somatostatin and analogues (octreotide)

 Suspected variceal bleeding/cirrhosis
 selective splanchnic vasoconstriction and lower portal
pressure
 Octreotide 50mcg IV bolus, then 50mcg/hr infusion
 Somatostatin 250 mcg IV bolus, then 250mcg/hr infusion

 Antibiotics
 Suspected variceal bleeding/cirrhosis
 Most common regimen is Ceftriaxone (1 g/day) for seven
days
 Can switch to Norfloxacin PO upon discharge
 ..........Variceal Bleeding

 PPI ??
 Recombinant factor VIIa
 Tranexamic acid, vit K
 Endoscopic Treatment: Ligation,
schlerotherapy
 TIPS (Transjugular intrahepatic
portosystemic shunt)
 ..........Variceal Bleeding

 Propanolol: Primary and secondary

prophylaxis (after bleeding stop)
 ACUTE LOWER
GASTROINTESTINAL
BLEEDING
 Hematochezia : bright red blood per rectum and
suggests active UGI (Massive UGI bleeding, > 1000
Ml) or small bowel bleeding or distal colonic or
anorectal bleeding

 Occult GI bleeding refers to subacute bleeding

that is not clinically visible.

 Obscure GI bleeding is bleeding from a site that is

not apparent after routine endoscopic evaluation
with esophagogastroduodenoscopy (upper
endoscopy) and colonoscopy, and possibly small
bowel radiography

Savides & Jensen, 2016

Savides & Jensen, 2016
Savides & Jensen, 2016
Savides & Jensen, 2016
Acute Abdominal Pain
 ABDOMINAL PAIN
Acute abdominal pain accounts for 5% of all ED visits.
• Three categories
– Intra-abdominal
• 3G’s
– GI.
– GU.
– GYN.
• Vascular emergencies.
– Extra-abdominal
• Cardiopulmonary
• Abdominal wall.
• Toxic-metabolic
• Neurogenic
– Undifferentiated
Savides & Jensen, 2016
Savides & Jensen, 2016
Savides & Jensen, 2016
 ACUTE ABDOMINAL PAIN
• Three categories:
• Visceral
– Often poorly localized.
– Steady ache or dull.
– Vague discomfort or gaseous.
– Colicky or crampy.
– Can be excruciating.
• Parietal
– Sharper and more localized.
– Tenderness and guarding.
– Rigidity and rebound.
• Referred
 ABDOMINAL PAIN
• Visceral pain
– Often the earliest symptom .
– Caused by inflammation, distention, or ischemia of
nerve fibers innervating the walls or capsules of
hollow or solid organs.

• Parietal or Somatic pain

– Irritation of fibers that innervate the parietal
peritoneum.
– Often initiated by chemical or bacterial
inflammation.

• Referred Pain
– Any pain felt in a cutaneous site distant from a
diseased organ.
 ABDOMINAL PAIN

• Epigastric pain hypochondriac

– Forgut organs
• Stomach
• Duodenum
• Biliary tract
• Periumbilical pain
– Midgut lumbar
• Most of small intestines
• Appendix
hypogastric
• Cecum
iliac
• Suprapubic or hypogastric pain
– Hindgut organs
• Most of colon including sigmoid.
• Intra-peritoneal portions of GU system.
– Kidney, Ureters and Bladder.
– Pelvic organs.
• History.
• Onset and Duration of Pain.
• Location, radiation and migration of Pain.
• Quality and Severity of Pain.
• Aggravating and relieving factors.
• Associated Symptoms.
– Past and Current Medical History.
– ____________________________(very important)
– Social History.
• Physical Exam.
– General Appearance and Vital Signs.
– Inspection, Auscultation, and Percussion.
– Palpation and Localization of Tenderness.
– Rectal and Pelvic Examination.
– Extra-abdominal Examination.
 Lab & imaging
• White Blood Cell Count.
• Urinalysis.
• Electrolytes.
• Renal function test.
• Tests for Pregnancy.
• Amylase and Lipase.
• LFTs.
• Plain abdominal films.
• Abdominal ultrasound.
• Abdominal CT scan.
 CHOLELITHIASIS

Cholecystitis
Choledocolitiasis
 Medical Treatment
Ursodeoxycholic acid (UDCA)
 Decreases cholesterol saturation of
bile and also appears to produce a
lamellar liquid crystalline phase in bile
that allows a dispersion of cholesterol
from stones by physical-chemical
means
 UDCA may also retard cholesterol
crystal nucleation

Harrison, 2012
Ursodeoxycholic acid (UDCA)
 A functioning gallbladder and with radiolucent
stones <10 mm in diameter
 For good results within a reasonable time
period, this therapy should be limited to
radiolucent stones smaller than 5 mm in
diameter
 10–15 mg/kg per day
 Stones larger than 15 mm in size rarely
dissolve

Harrison, 2012
 Cholecystectomy??
 The presence of symptoms that are frequent enough or severe
enough to interfere with the patient's general routine

 The presence of a prior complication of gallstone disease, i.e.,

history of acute cholecystitis, pancreatitis, gallstone fistula, etc.; or

 The presence of an underlying condition predisposing the patient

to increased risk of gallstone complications (e.g., calcified or
porcelain gallbladder and/or a previous attack of acute cholecystitis
regardless of current symptomatic status).

 Patients with very large gallstones (>3 cm in diameter) and

patients having gallstones in a congenitally anomalous gallbladder
might also be considered for prophylactic cholecystectomy.
Harrison, 2012
 Acute pancreatitis
• In the U.S. Cholelithiasis or alcohol
abuse accounts for 90% of all cases of
acute pancreatitis
 Clinical features
• Boring epigastric pain that radiates to
the back.
• Tachycardia
• Nausea and vomiting
• Abdominal distension
• Cullen’s sign
• Grey Turner’s sign
• Blood loss, refractory hypotension, and
respiratory failure may accompany more
severe forms.
 Diagnosis and differential
• Diagnosis is made by a suggestive
history and physical exam, associated
with elevated pancreatic enzymes.
• Amylase greater than 3x the upper limit
of normal has a specificity of 75% and a
sensitivity of 80-90%
• Lipase is more specific than amylase
and is the preferred test. At a cutoff of
2x the upper limit of normal, lipase is
90% sensitive and specific.
 Diagnosis and differential

• Ultrasound is helpful in the identification

of gallstones or dilatation of the biliary
tree.
• CT is the study of choice for
visualizing the pancreas, confirmation of
inflammation, and the identification of
phlegmons, abscesses, or pseudocyts.
It cannot be used to rule out Acute
Pancreatitis.
ACG, 2013
ACG, 2013
ACG, 2013
Kosin University, Gospel Hospital,
Busan, South Korea, 2016