The GI Endoscopy Atlas:

New Bowel Imageing

(NBI)-6th edition
The GI Endoscopy Atlas:
New Bowel Imageing
(NBI)-6th edition
Edited by
Pradermchai Kongkam
Rapat Pittayanon
Rungsun Rerknimitr
Satimai Aniwan
Sombat Treeprasertsuk

6th edition
Thai Association for Gastrointestinal Endoscopy (TAGE)

First published 2014

ISBN: 978-616-91971-0-2

All endoscopic pictures in this New Bowel image (NBI) atlas.()6th edition were taken
by staffs of Excellent Center for GI Endoscopy (ECGE), Division of Gastroenterology,
Faculty of Medicine, Chulalongkorn University, Rama 4 road, Patumwan, Bangkok
10330 Thailand Tel: 662-256-4265, Fax: 662-252-7839, 662-652-4219.

All rights of pictures and contents reserved.

Graphic design @Sangsue Co., Ltd, 17/118 Soi Pradiphat 1, Pradiphat Road, Samsen
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 Preface

Dear Passionate Endoscopists,

Image-enhanced endoscopy has been developed far beyond our expectation.
It seems that the quotation by Albert Einstein “imagination is more important than
knowledge” is also true for GI Endoscopy. This latest book series of “Atlas in GI
Endoscopy” by TAGE provides a case series of GI Endoscopy from top to bottom (upper
GI, HPB, and lower GI Endoscopy). It includes many fantastic images with high quality
obtained by EVIS EXERA III-190 HD (Olympus Medical). This case series provide not
only the advancement in the Art and Knowledge of GI Endoscopy but also all the
related radiology and pathology.

I would like to take this opportunity to express my deeply thanks to the editors,
Professor Rungsun Rerknimitr, Associated Professor Sombat Treeprasertsuk, Dr.Linda
Pantongrag-Brown and colleagues who contribute their great efforts to make this
important 6th edition of the GI Endoscopy atlas available under the TAGE support.

Last but not least, I hope that you will enjoy learning and reading this book and
this in turn will ultimately help your daily practice at certain level.

Dr. Thawee Ratanachu-Ek, M.D.

TAGE President
From Editors

Gastro-intestinal endoscopy knowledge and technologies have significantly

changed over the last few decades. Many new endoscopic findings has been discovered
and effectively used for both diagnostic and the treatment purpose. Nevertheless, it
is still difficult for beginners to learn about these endoscopic findings within a short
period of time. Especially, in uncommon diseases, trainees may have never seen those
lesions during their training time. A helpful endoscopic atlas with a brief summary
of the case followed by a practical discussion is an invaluable resource for learners
including gastroenterologists, surgeons, internists, nurses and all GI paramedics.

This book was written by our faculties of the excellence center of GI Endoscopy,
Chulalongkorn University. This version is the sixth edition and consists of 4 section
including upper GI endoscopy, lower GI endoscopy, ERCP, and EUS. It comes in a
package of interesting presentations. Each case will be displayed with an intriguing
image findings and followed by the literature review of such case. Systematic indexing
of all case scenarios will help the readers to search for the most appropriate cases
within a few minutes. However, reading through all cases probably the most valuable
way.

We hope that the book will help our readers to improve the practice and clinical
knowledge and all readers would enjoy the content of this New Bowel image (NBI)
atlas.
Contributors

1. Kessarin Thanapirom 7. Phonthep Angsuwatcharakon

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

2. Kittiyod Poovorawan 8. Piyapan Prueksapanich

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

3. Narisorn Lakananurak 9. Pradermchai Kongkam

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

4. Naruemon Wisedopas-Klaikeaw 10. Rapat Pittayanon

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

5. Nopavut Geratikornsupuk 11. Rungsun Rerknimitr

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

6. Nopporn Anukulkarnkusol 12. Satimai Aniwan

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand
13. Sombat Treeprasertsuk 21. Piyachai Orkoonsawat, M.D.
- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

14. Tanassanee Soontornmanokul 22. Puth Muangpaisarn, M.D.

- Division of Gastroenterology, Department - Division of Gastroenterology, Department
of Medicine, Chulalongkorn University, of Medicine, Chulalongkorn University,
Bangkok, Thailand Bangkok, Thailand

15. Vichai Viriyautsahakul 23. Yuthana Sattawatthamrong, M.D.

- Department of Medicine, King - Division of Gastroenterology, Department
Chulalongkorn Memorial Hospital, Thai of Medicine, Chulalongkorn University,
Red Cross Society Bangkok, Thailand

16. Wiriyaporn Ridtitid 24. Sukprasert Jutaghokiat, M.D., M.Sc.

- Division of Gastroenterology, Department - Division of Gastroenterology, Vejthani
of Medicine, Chulalongkorn University, Hospital, Bangkok, Thailand
Bangkok, Thailand
25. Khin San Aye, M.D.
17. Sasipim Sallapant, M.D. - Division of Gastroenterology, Department
- Division of Gastroenterology, Department of Medicine, Chulalongkorn University,
of Medicine, Chulalongkorn University, Bangkok, Thailand
Bangkok, Thailand
26. Tanyaporn Chantarojanasiri, M.D.
18. Suppakorn Malikhao, M.D. - Division of Gastroenterology, Department
- Division of Gastroenterology, Department of Medicine, Police General Hospital,
of Medicine, Chulalongkorn University, Bangkok, Thailand
Bangkok, Thailand
27. Sutep Gonlachanvit, M.D., M.Sc.
19. Boonlert Imraporn, M.D.,M.Sc. - Division of Gastroenterology, Department
- Division of Gastroenterology, Department of Medicine, Chulalongkorn University,
of Medicine, Chulalongkorn University, Bangkok, Thailand
Bangkok, Thailand Vejthani Hospital,
Bangkok, Thailand 28. Linda Pantongrag-Brown
- AIMC, Ramathibodi Hospital, Bangkok,
20. Sayamon Kimtrakool, M.D. Thailand
- Division of Gastroenterology, Department
of Medicine, Chulalongkorn University,
Bangkok, Thailand
Content

Preface
From Editors
Contributors
Upper 1
Lower 81
ERCP 150
EUS 171
Index 223
 1 Upper

Piyapan Prueksapanich, M.D.

Case 1 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 58-year-old male with a history of stage I squamous cell carcinoma of

the oral cavity for a year underwent an esophagogastroduodenoscopy (EGD) for
esophageal cancer surviellance. He reported no upper GI symptom. The EGD showed
an ill-defined salmon-colored patch at the proximal esophagus just below the upper
esophageal sphincter. The narrow band imaging (NBI) showed a well-defined pink
patch with a clear margin separated from the normal surrounding greenish NBI based
mucosa (Figures 1 and 2). Probe-based confocal laser endomicroscopy (pCLE) revealed
a columnar epithelium without goblet cells (Figure 3). Biopsy was done and the
pathological study showed an area of gastric mucosa (Figure 4) compatible with the
diagnosis of an inlet patch.

Figures 1 and 2 NBI showed a well-defined pink patch surrounded by normal

esophageal mucosa.

1
 Figure 3 pCLE revealed columnar Figure 4 Histology confirmed the
epithelium without goblet cell. columnar epithelium as gastric
mucosa.

Diagnosis:
Inlet patch of the esophagus

Discussion:
The inlet patch of the esophagus is a congenital anomaly consisting of ectopic
gastric mucosa locates mainly in the upper part of the esophagus or just below the
upper esophageal sphincter. The incidence was reported as 1%-20% in routine upper
endoscopies. The inlet patches are usually asymptomatic and incidentally detected by
EGD.1,2 However, the inlet patch can rarely be associated with some complications
such as bleeding, perforation, stricture or malignancy.1,2

References
1. Tang P, McKinley MJ, Sporrer M, et al. Inlet patch: prevalence, histologic type,
and association with esophagitis, Barrett esophagus, and antritis. Arch pathol
lab Med 2004;128:444-7.
2. Chong VH. Clinical significance of heterotopic gastric mucosal patch of the
proximal esophagus. World J Gastroenterol 2013;19:331-8.

2
 Kessarin Thanapirom, M.D.
Case 2 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 66-year-old female presented with melena for 3 weeks. She had a history of
NSAIDs usage for knee pain. EGD revealed a 1.5 cm, oval-shaped, well-circumscribed,
clean-based esophageal ulcer at mid esophagus without active bleeding (short arrow).
The location was adjacent to the aortic arch (long arrow) (Figure1).

Figure 1 A clean-based ulcer at mid esophagus.

3
 Diagnosis:
Pill-induced esophageal ulcer

Discussion:
Various drugs such as NSAIDs, tetracycline, penicillin, potassium chloride
tablet, alendronate and quinidine were the common medicine causing pill-induced
esophageal injury. The symptom onset may occur from a few hours to one month after
ingestion of the drug.1 Common symptoms are odynophagia (72%), chest pain (59%),
vomiting (58%), dysphagia (33%), and hematemesis (15%).2
Endoscopic findings of pill-induced esophagitis included acute superficial
erythema (83%), esophageal erosion (58%), esophageal ulcer with exudates (27%),
esophageal ulcer with bleeding (19%), kissing ulcer with bleeding (8%), and
denudation of esophageal mucosa (3%).2 The important clinical clues for diagnosis
of NSIADs- induced esophageal injury are a history of drug usage, a shallow, discrete
ulcer at mid esophagus near aortic arch with normal surrounding mucosa.3 The
differential diagnoses are foreign body induce ulcer, esophageal carcinoma, and
infection, especially herpes esophagitis.

References
1. Zografos GN, Georgiadou D, Thomas D, et al. Drug-induced esophagitis. Dis
Esophagus 2009;22:633-7.
2. Abid S, Mumtaz K, Jafri W, et al. Pill-induced esophageal injury: endoscopic
features and clinical outcomes. Endoscopy 2005;37:740-4.
3. Sugawa C, Takekuma Y, Lucas CE, et al. Bleeding esophageal ulcers caused by
NSAIDs. Surg Endosc 1997;11:143-6.

4
 Piyapan Prueksapanich, M.D.
Case 3 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 65-year-old male with a history of stage II squamous cell carcinoma of the
hard palate diagnosed 4 years ago underwent NBI-protocol EGD for esophageal cancer
surveillance. He was asymptomatic and confirmed to be in a complete remission of his
hard palate cancer. EGD showed a nodular appearance of the esophageal mucosa. The
6-8 raised whitish nodules sized 2-5 mm were scatterly detected along the esophagus
more predominantly at the distal esophagus (Figure 1). Dual focus NBI showed white
and red strips (Figure 2) representing the extended intrapapillary capillary loops1. Under
Lugol chromoendoscopy, the lesions were heavily stained (Figure 3). The finding was
compatible with esophageal glycogenic acanthosis. Biopsy was done and pathology
confirmed the diagnosis of glycogenic acanthosis.

Figure 1 A nodular appearance at Figure 2 NBI with magnification

mid esophagus. showed white and red strops on
top of the nodules.

5
 Figure 3 Lugol chromoendoscopy
showed heavily stained nodule by
iodine.

Diagnosis:
Glycogenic acanthosis of the esophagus

Discussion:
Glycogenic acanthosis is a benign esophageal lesion with an unclear
pathogenesis. Its association with aging, gastroesophageal reflux, Cowden’s syndrome
or celiac disease has been reported in the literatures.2,3 Glycogenic acanthosis itself
is asymptomatic and can be found in 20-40% of the endoscopy which are more
prominent in the lower esophagus than in the upper esophagus.2

References
1. Norimura D, Isomoto H, Fukuda E, et al. Cowden’s disease manifested by
esophageal polyposis with characteristic appearance on magnifying endoscopy
using narrow band imaging. Endoscopy 2013;45 Suppl 2:E298.
2. Lee JK, Kum J, Ghosh P. Education and imaging. Gastrointestinal: glycogenic
acanthosis. J Gastroenterol Hepatol 2007;22:1550.
3. Nazligul Y, Aslan M, Esen R, et al. Benign glycogenic acanthosis lesions of the
esophagus. Turk J Gastroenterol 2012;23:199-202.

6
 Sasipim Sallapant, M.D.
Case 4 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 50-year-old male with previously healthy admitted in the surgical department
due to gastric ulcer perforation. He underwent exploratory laparotomy with simple
suture and omental patch. One week after operation, he developed acute hematemesis
with postural hypotension. Emergency EGD was performed and showed multiple long
linear esophageal ulcers and erosions with bridging of mucosal folds extending from
mid esophagus to gastroesophageal junction (Figure 1). There are moderate amount of
blood clot in the esophagus. The stomach and duodenum revealed neither erosion nor
ulcer.
He was treated with NPO, intravenous fluid, high dose proton pump inhibitors
as well as a head elevation. After a few days of treatment, the symptom improved and
the enteral feeding was initiated. He had no recurrent upper GI bleeding.

Figure 1 Severe reflux esophagitis

7
 Diagnosis:
Upper GI bleeding from severe reflux esophagitis, LA classification grade C

Discussion:
Bleeding reflux esophagitis is usually associated with deep esophageal ulcers or
severe esophagitis (LA classification grades C and D).1 Clinical presentation can ranges
from active GI bleeding to iron deficiency anemia. Clinically important hemorrhage
has been reported in 7% to 18% of GERD patients.2
A history of reflux esophagitis or heartburn was noted in only 28% or 37% of
the patients with bleeding reflux esophagitis. Severe bleeding from reflux esophagitis
is treated medically with a proton pump inhibitor (PPI). The patient should be treated
with a minimum 8-week course. Head of bed elevation and avoidance of meals 2–3
hours before bedtime are recommended.3
EGD is critical for diagnosis of the bleeding etiology, but endoscopic treatment
generally has not been required in this setting unless a focal ulcer with a stigma of
recent hemorrhage was found.4 Repeat endoscopy should be performed in patients
with severe erosive reflux disease after a course of PPI therapy to exclude underlying
Barrett’s esophagus.3

References
1. Higuchi D, Sagawa C, Shab SH, et al. Etiology, treatment and outcome of
esophageal ulcers: A 10 year experience in an urban emergency hospital. J
Gastrointest Surg 2003;7:836-42.
2. Costa ND, Cadiot G, Merle C, et al. Bleeding reflux esophagitis: a prospective
1-year study in a university hospital. Am J Gastroenterol 2001;96:47-51.
3. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of
gastroesophageal reflux disease. Am J Gastroenterol 2013;108:308-284.
4. Wang JH, Fisher DA, Ben-Menachem T, et al. The role of endoscopy in the
management of acute non-variceal upper GI bleeding. Gastrointest Endosc
2012;75:1132-8.

8
 Kessarin Thanapirom, M.D.
Case 5 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 28-year-old male presented with hematemesis after vomiting and retching
for one day after an overnight heavy alcohol drinking. Physical examination showed
tachycardia and mild pale mucosa. He had no sign of chronic liver stigmata. EGD was
performed and revealed one linear clean-based ulcer at the esophagogastric junction
(EGJ).

Figure 1 One linear clean-based ulcer, 1.5 cm

longed without visible vessel at EGJ (arrow).

9
 Diagnosis:
Mallory-Weiss syndrome

Discussion:
Three percent of patients with acute non-variceal upper gastrointestinal bleeding
is due to Mallory-Weiss syndrome (MWS).1 Mostly, bleeding from MWS is mild and
self-limited, and the patient can be safe only by a conservative medical treatment.
However, in certain patients such as patients with the overt stigmata of recent bleeding,
or with unstable vital signs or with severe co-morbid diseases, the hemostatic procedure
may be required.1 Endoscopic treatment is currently recommended as the first-line
therapy for active bleeding of Mallory–Weiss syndrome. Many endoscopic hemostatic
techniques including local adrenaline injection, hemoclipping, band ligation, and
electrocoagulation achieved a high rate of primary hemostasis (90%).1-3 Mechanical
hemostatic method is more effective than local adrenaline injection in patients with
active bleeding stigmata since re-bleeding rate was reportedly lower.2

References
1. Yin A, Li Y, Jiang Y, et al. Mallory-Weiss syndrome: clinical and endoscopic
characteristics. Eur J Intern Med 2012;23:e92-6.
2. Chung IK, Kim EJ, Hwang KY, et al. Evaluation of endoscopic hemostasis in
upper gastrointestinal bleeding related to Mallory-Weiss syndrome. Endoscopy
2002;34:474-9.
3. Park CH, Min SW, Sohn YH, et al. A prospective, randomized trial of endoscopic
band ligation vs. epinephrine injection for actively bleeding Mallory-Weiss
syndrome. Gastrointest Endosc 2004;60:22-7.

10
 Piyapan Prueksapanich, M.D.

Case 6
Rapat Pittayanon, M.D., M.Sc.
Nareumon Wisedopas, M.D.
Rungsun Rerknimitr, M.D.

A 63-year-old male with a history of complete remission of stage III supraglottic

squamous cell carcinoma for one year underwent a surveillance EGD for esophageal
cancer. He was asymptomatic, EGD showed a flat and irregular boarder lesion at
20-30 cm from the incisor with fungating mass sized 1.5 cm on-top (Figure 1). NBI
confirmed as a well-defined brownish lesion (Figure 2) with abnormal intrapapillary
capillary loops (IPCLs). The IPCLs characters showed tortuous, dilated, irregular caliber,
and various in shapes of capillary loops with some avascular area (Figure 3). The NBI
finding of the IPCLs was compatible with carcinoma in situ according to the Inoue’s
classification.
After Lugol solution staining, the lesion was unstained and the border was more
clearly defined (Figure 4). The lesion was biopsied with the biopsy forceps. Pathology
showed well-differentiated squamous cell carcinoma with no basement membrane
penetration which was compatible with Tis staging (carcinoma insitu) (Figure 5).

Figure 1 EGD showed a flat and

irregular boarder lesion at 20-30 cm
from the incisor with a fungating
mass sized 1.5 cm on-top.

11
 Figure 2 With NBI mode, the lesion Figure 3 The IPCLs pattern showed
was seen as a well-defined brownish tortuous, dilated, irregular caliber and
lesion. various in shapes of capillaries with
some avascular area.

Figure 4 After a Lugol solution Figure 5 Pathology demonstrated

staining, the lesion was unstained well-differentiated squamous cell
and the border was well demarcated carcinoma with no basement mem-
(arrow). brane penetration compatible.

12
Diagnosis:
Esophageal squamous cell carcinoma in situ

Discussion:
The metachronous squamous cell carcinoma of esophagus can be developed in
the patient with history of head and neck cancer according to the “field cancerization”
hypothesis.1 Early detection of the second primary esophageal cancer in these patients
was a key to improve the prognosis. Chromoendoscopy with Lugol’s solution has an
excellent sensitivity to detect the early esophageal cancer in this group of patients.2
Narrow band imaging has comparable performance with additional ability to
charactereize the lesion by the IPCLs pattern.3

References
1. Slaughter DP, Southwick HW, Smejkal W. Field cancerization in oral stratified
squamous epithelium; clinical implications of multicentric origin. Cancer
1953;6:963-8.
2. Hashimoto CL, Iriya K, Baba ER, et al. Lugol’s dye spray chromoendoscopy
establishes early diagnosis of esophageal cancer in patients with primary head
and neck cancer. Am J Gastroenterol 2005;100:275-82.
3. Uedo N, Fujishiro M, Goda K,et al. Role of narrow band imaging for diagnosis
of early-stage esophagogastric cancer: current consensus of experienced
endoscopists in Asia-Pacific region. Dig Endosc 2011;23 Suppl 1:58-71.

13
 Suppakorn Malikhao, M.D.

Case 7
Boonlert Imraporn, M.D.
Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 70-year-old male presented with a longstanding history of heartburn,

regurgitation and dyspeptic symptoms. EGD found a lower esophageal ring at
the esophagogastric junction with a sliding hiatal hernia. This esophageal ring is
characterized by thin concentric protrusions covered proximally by normal esophageal
epithelium and on the distal side of the membrane was covered by gastric epithelium
(Figure 1).

Figure 1 EGD showed a lower esophageal

ring at the esophagogastric junction.

14
Diagnosis:
Schatzki´s ring

Discussion:
Schatzki´s ring, B type esophageal ring, is the most common esophageal ring
found on either barium radiographs or endoscopy. The pathogenesis and etiology
remain controversial.1 Although most of Schatzki´s rings are asymptomatic, they can
be the cause of episodic dysphagia for solids and food impaction regarding to the
narrowing esophageal lumen if the diameter is less than 13 mm in diameter.2 In those
symptomatic patients, esophageal dilatation is the mainstay of therapy.1

References
1. Advances in GERD: Current Developments in the Management of Acid-Related
GI Disorders. Gastroenterol Hepatol (N Y) 2010;6:297-9.
2. Muller M, Gockel I, Hedwig P, et al. Is the Schatzki ring a unique esophageal
entity? World J Gastroenterol 2011;17:2838-43.

15
 Sayamon Kimtrakool, M.D.
Case 8 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 54-year-old Thai male with underlying alcoholic cirrhosis child B was

transferred to the emergency room due to hematemesis for 4 hours. An emergency EGD
revealed a pulsatile bleeding from a small esophageal varix at the distal esophagus.
Endoscopic variceal ligation (EVL) was not successfully able to control the bleeding
at the first attempt due to a small size of varix on the post EVL scar. Then, N-butyl-
2-cyanoacrylate (Histoacryl) 0.5 ml mixed with Lipiodol 0.8 ml was injected at the
bleeding point and eventually bleeding stopped. At four days after the procedure, EGD
was repeated as a second-look EGD. It revealed only a superficial solitary ulcer with
necrotic area, representing the healing process from previous glue injection. After a
few days of supportive treatments, his hematocrit was stabilized and finally discharged
from the hospital.

Figures 1 and 2 EGD showed a superficial solitary ulcer with

necrotic area resulting from the prior glue injection (arrow).

16
Diagnosis:
Glue injection-associated esophageal ulcer

Discussion:
Cyanoacrylate becomes polymerized rapidly after contacting with blood (just
a few minute after injection into the varix). This effect results in rapid hemostasis.
Moreover, it also provide the secondary change such as perivascular inflammation,
vessel-wall necrosis, sloughing of mucosa, and tissue adhesion.1 Consequently, the
ulceration from cyanoacrylate injection has been reported as an asymptomatic finding
during second-look EGD.1, 2 However, the treatment of symptomatic glue injection-
associated ulcer can be successfully management by supportive treatment.1

References
1. Krige JE, Bornman PC, Shaw JM, et al. Complications of endoscopic variceal
therapy. S Afr J Surg 2005;43:177-88.
2. Noophun P, Kongkam P, Gonlachanvit S, et al. Bleeding gastric varices: results
of endoscopic injection with cyanoacrylate at King Chulalongkorn Memorial
Hospital. World J Gastroenterol 2005;11:7531-5.

17
 Piyachai Orkoonsawat, M.D.
Case 9 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 70-year-old male with a history of stage I squamous cell carcinoma of the
oral cavity for a year came for esophageal cancer surveillance. He reported no upper
GI symptom. EGD exam was unremarkable under the white light mode. After Lugol’s
iodine staining, a well-demarcated depressed mucosa was observed at the proximal
esophagus. Under NBI exam, it showed a 1x3 cm, well-demarcated purplish area
(Figure 1). Under magnifying NBI, the abnormal pattern of the intraepithelial papillary
capillary loop (IPCL) was clearly demonstrated including dilatation, tortuosity, variation
in the shape and caliber of IPCL which were compatible with neoplasia (Figure 2).
Biopsy was done and pathology showed a high grade dysplasia. Subsequently, an
endoscopic mucosal resection (EMR) was carried on. Cap-assisted esophageal EMR
was done by using a crescent (Duck bill) snare (Figure 3). No active bleeding developed
after the procedure (Figure 4).

Figure 1 NBI showed a 1x3 cm,

well-demarcated with puplish
color of the unstained lugol area.

18
 Figure 2 Figure 3

Figure 2 Magnifying NBI showed

dilatation, tortuosity, variation in the
shape and calibre of the intrae-pithelial
papillary capillary loop (IPCL) (arrow).

Figure 3 Cap-assisted esophageal EMR

was done by using a crescent (Duck
bill) snare.

Figure 4 Post cap-assisted esophageal

EMR without active bleeding.
Figure 4

Diagnosis:
High grade dysplasia of the second primary esophageal squamous cell neoplasm
treated with an endoscopic mucosal resection (EMR)

Discussion:
Head and neck squamous cell carcinomas patients have a high risk of
developing other neoplasms either simultaneously or subsequently. The incidence of
second primary esophageal squamous cell carcinoma (ESCC) was reported as 9%-
44%.1 The treatment for early ESCC including high grade dysplasia when it is limited
to the superficial layers of the mucosa and also measures less than 2 cm in extension
with involvement less than 1/3 of the circumference is EMR. With a complete en-bloc
resection, the 5-year survival rate is up to 95%.2, 3

19
 References
1. Priante AV, Castilho EC, Kowalski LP. Second primary tumors in patients with
head and neck cancer. Curr Oncol Rep 2011;13:132-7.
2. Mannath J, Ragunath K. Endoscopic mucosal resection: who and how? Therap
Adv Gastroenterol 2011;4:275-82.
3. Shimizu M, Zaninotto G, Nagata K, et al. Esophageal squamous cell carcinoma
with special reference to its early stage. Best Pract Res Clin Gastroenterol
2013;27:171-86.

20
 Suppakorn Malikhao, M.D.
Case 10 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 56-year-old male with a history of heavy alcohol drinking, has complaint about
dysphagia and retrosternal pain during swallowing for 3 months. EGD demonstrated
confluent, linear, yellowish elevated plaques covering on the erythematous mucosa
throughout the esophagus (Figure 1). His anti-HIV result was non-reactive.

Figure 1 EGD revealed confluent, linear,

yellowish elevated plaques covering on
the erythematous mucosa throughout the
esophagus.

21
 Diagnosis:
Esophageal candidiasis (EC)

Discussion:
Esophageal candidiasis (EC) is the most common infectious disease of esophagus
in patients with human immunodeficiency vi­rus (HIV) infection and other conditions
that impaired cellular immunity, but a rare condition among healthy people. Half
of those with EC are asymptomatic. The risk factors of EC healthy individu­als are
prolonged use of antibiotics, corticosteroids, heavy drinking and herb medica­tion.1, 2
Endoscopy is essential for the diagnosis, not only for evaluation by the gross
appearance but also it can enable tissue biopsy. Systemic antifungal therapy with oral
fluconazole remains the mainstay of treatment.3

References
1. Nishimura S, Nagata N, Shimbo T, et al. Factors associated with esophageal
candidiasis and its endoscopic severity in the era of antiretroviral therapy. PLoS
One 2013;8:e58217.
2. Choi JH, Lee CG, Lim YJ, et al. Prevalence and risk factors of esophageal
candidiasis in healthy individuals: a single center experience in Korea. Yonsei
Med J 2013;54:160-5.
3. Asayama N, Nagata N, Shimbo T, et al. Relationship between clinical factors
and severity of esophageal candidiasis according to Kodsi’s classification. Dis
Esophagus 2013.

22
 Narisorn Lakananurak, M.D.
Case 11 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 67-year-old Thai monk presented with 2 episodes of melena within 3 months.

He refused any history of hematemesis or dysphagia. EGD showed a deep, linear,
friable ulcerative mass with elevated and irregular border, measured as 10 cm in length
(Figures 1 and 2). This lesion was near the esophagogastric junction (EGJ) (Figure 3).
Biopsy at the edge of ulcerative mass was done and histology showed squamous cell
carcinoma.

Figure 1 Figure 2

Figures 1 and 2 Deep, linear,

friable ulcerative mass with
elevated and irregular border
with easily contact bleeding.

Figure 3 The lesion did not

involve EGJ.

Figure 3

23
 Diagnosis:
Squamous cell carcinoma of the esophagus

Discussion:
Esophageal squamous cell carcinoma (ESCC) is one of the two most common
types of esophageal cancer. The incidence of ESCC is varying widely. It is accounting
for 50-90% of esophageal cancer in developing countries but the incidence was lower
by time.1 The risk factors of ESCC include tobacco and alcohol drinking, achalasia,
caustic injury and dietary such as drinking very hot beverages, aromatic hydrocarbon,
and N-nitroso compound.1,2 Symptoms of esophageal cancer depend on the stage
of disease that usually asymptomatic but may present with melena as in this case.
Others symptoms are dysphagia, weight loss, odynophagia, and fistula in advance
stage.3 Endoscopic findings of ESCC include fungating, friable, ulcerated mass lesions
occupying some or the entire luminal circumference, usually with unclear margins.
The middle esophagus is the most common involved location.4

References
1. Blot WJ. Esophageal cancer trends and risk factors. Semin Oncol 1994;21:403-
10.
2. Vaughan TL, Davis S, Kristal A, et al. Obesity, alcohol, and tobacco as risk
factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus
squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev 1995;4:85-92.
3. Ojala K, Sorri M, Jokinen K, et al. Symptoms of carcinoma of the oesophagus.
Med J Aust 1982;1:384-5.
4. Higuchi K, Koizumi W, Tanabe S, et al. Current management of esophageal
squamous-cell carcinoma in Japan and other countries. Gastrointest Cancer
Res 2009;3:153-61.

24
 Sasipim Sallapant, M.D.
Case 12 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 17-year-old female without previous medical illness, presented with chronic
esophageal dysphagia with significant weight loss for 3 years. EGD was performed and
showed proximal esophageal dilatation with tight gastroesophageal junction (EGJ).
However, scope can pass through EGJ and revealed no lesion at the gastric cardia.
Barium meal was compatible with non-sigmoid type achalasia cardia. Esophageal
manometry also confirmed as achalasia cardia.
Peroral endoscopic myotomy (POEM) was performed as the treatment. The
procedure was successfully done without complication. The submucosal tunnel length
was 10 cm and the total myotomy was 8 cm in length (5 cm above and 3 cm below
lower esophageal sphincter) (Figures 1-6). The patient was safely discharge at day 3
after the procedure the resolution of dysphagia.

25
 Figures 1-6 Endoscopic images illustrating POEM. (1) Submucosal lifting by glycerol
and indigo carmine injection followed by a 2-cm long mucosal incision. (2) A long
submucosal tunnel extended 2 cm beyond the EGJ was created. (3) Myotomy of
the circular muscle started from 5 cm above lower esophageal sphincter (LES). (4)
Scope can pass through EGJ without any difficulty. (5 and 6) clips closure were
placed at the mucosal incision site.

Diagnosis:
POEM for achalasia cardia

Discussion:
Achalasia cardia is a motility disorder of the esophagus of unknown etiology
and the important feature is the failure of LES relaxation after swallowing.1 Diagnosis
is confirmed by manometric, endoscopic, and radiographic investigations.
The mainstay of treatment is either pneumatic balloon dilatation or laparoscopic
myotomy which demonstrate a similar short term outcome.2 Endoscopic and surgical
therapy are focused disrupting the LES rather than correcting the motility abnormalities.
POEM is a new paradigm shift in achalasia therapy. It is convenient and less
invasive than surgery.3 Recent studies have demonstrated the excellence in efficacy
and safety of this procedure.3,4 The treatment success rate was greater than 90% and
similar to the initial treatment success rate of laparoscopic Heller myotomy (LHM).4

References
1. O’Neill OM, Johnston BT, Coleman HG. Achalasia: A review of clinical
diagnosis, epidemiology, treatment and outcomes. World J Gastroenterol
2013;19:5806-5812.
2. Wu JC. Pneumatic Dilation versus Laparoscopic Heller’s Myotomy for Idiopathic
Achalasia. J Neurogastroenterol Motil 2011;17:324-6.
3. Stavropoulos SN, Modayil R, Friedel D. Achalasia. Gastrointest Endosc Clin N
Am 2013;23:53-75.
4. Campos GM, Vittinghoff E, Rabl C, et al. Endoscopic and surgical treatments for
achalasia: a systematic review and meta-analysis. Ann Surg 2009;249:45-57.

26
 Suppakorn Malikhao, M.D.

Case 13
Rapat Pittayanon, M.D., M.Sc.
Naruemon Wisedopas, M.D.
Rungsun Rerknimitr, M.D.

A 80-year-old Thai female presented with dyspepsia. EGD found a solitary

elevated lesion (0-IIa), 2.0 cm in size with no ulceration at the lesser curvature of
gastric body (Figures 1 and 2). The biopsy was done and showed high grade dysplasia
of columnar epithelium.
Endoscopic submucosal dissection (ESD) was subsequently performed (Figures
3-8). The final histopathology was compatible with gastritis cystica profunda (GCP)
with low grade dysplasia (Figures 9-11).

Figure 1 and 2 EGD with Narrow band imaging (NBI) showed elevated
lesion (0-IIa).

27
 Figures 3-8 Demonstrated ESD technique starting by marking the area followed by
circumferential incision and dissection of the lesion.

Figures 9-11 Multiple cystic gastric glands located underneath low grade dysplastic
gastric epithlium.

Diagnosis:
Gastritis cystica profunda (GCP)

Discussion:
Gastritis cystica profunda (GCP) is a rare disorder characterized by polypoid
gastric mass typically located beneath a normal mucosa and histopathological
characteristics demonstrated by foveolar hyperplasia and cystic glands extend through
a disrupted muscularis mucosae into the submucosa.1,2 The pathophysiology is still

28
unclear but GCP may develop secondary to chronic inflammation, foreign body
reaction or ischemic injury.2 Prior gastric surgery is the most common occurrence in
several reported cases; nevertheless, GCP was described in non-surgical patient as
well.3,4
Clinical manifestations are typically nonspecific symptoms and seldom give
rise to the symptoms.1,5 GCP generally has a benign behavior; however, several reports
have documented accompanied by gastric carcinomas but the relationship between
the two conditions remains uncertain.
Endoscopic submucosal dissection (ESD) technique is an en-bloc endoscopic
tumor removal. It was developed for definite treatment of benign mucosal lesion with
more than 2 cm in size and early malignant lesion (with less than 3 cm in size without
ulcer or less than 2 cm in size with ulcer) in digestive tract. The outcome of ESD
showed complete resection in 73.9% and very low complication rate of bleeding and
perforation in 1.4% and 0.5%, respectively.6

References
1. Franzin G, Novelli P. Gastritis cystica profunda. Histopathology 1981;5:535-
47.
2. Fonde EC, Rodning CB. Gastritis cystica profunda. Am J Gastroenterol
1986;81:459-64.
3. Bechade D, Desrame J, Algayres JP. Gastritis cystica profunda in a patient with
no history of gastric surgery. Endoscopy 2007;39 Suppl 1:E80-1.
4. Moon SY, Kim KO, Park SH, et al. [Gastritis cystica profunda accompanied by
multiple early gastric cancers]. Korean J Gastroenterol 2010;55:325-30.
5. Kurland J, DuBois S, Behling C, et al. Severe upper-GI bleed caused by gastritis
cystica profunda. Gastrointestinal endoscopy 2006;63:716-7.6
6. Kojima T, Parra-Blanco A, Takahashi H, et al. Outcome of endoscopic mucosal
resection for early gastric cancer: review of the Japanese literature. Gastrointest
Endosc 1998;48:550-4

29
 Suppakorn Malikhao, M.D.
Case 14 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 69-year-old female presented with fatigue, dizziness, and melena for 1 month.
Laboratory investigation showed iron deficiency anemia. The endoscopy showed
multiple erythematous stripes of red tortuous ectatic vessels along longitudinal rugal
folds in the antrum converging toward the pylorus (Figures 1 and 2).

Figures 1 and 2 Multiple stripes of red tortuous ectatic vessels along

longitudinal folds of the antrum and converging toward the pylorus.

30
Diagnosis:
Gastric antral vascular ectasia (GAVE)

Discussion:
Gastric antral vascular ectasia (GAVE) accounted for 4% of non-variceal upper
GI bleeding and usually presented with iron deficiency anemia due to occult GI
bleeding.1 The most commonly proposed mechanisms of GAVE are mechanical stress
to gastric antral mucosa and locally high concentrations of vasoactive substance,
leading to the dilatation of the blood vessels.1, 2 The most common underlying chronic
illness is cirrhosis (30% of case.3, therefore, portal hypertensive gastropathy (PHG)
can be found in the same situation. GAVE is most commonly limited to the antrum,
while PHG predominantly located in the fundus and corpus, and with endoscopic
appearance of snake-skin mosaic pattern. Moreover, the severity of portal pressure is
not directly related to GAVE which is totally different from PHG.4
APC was considered as the effective endoscopic therapy for GAVE with the
success rate of 90%-100%5. Medical treatment has no benefit in GAVE-related
bleeding.5

References
1. Selinger CP, Ang YS. Gastric antral vascular ectasia (GAVE): an update on
clinical presentation, pathophysiology and treatment. Digestion 2008;77:131-
7.
2. Charneau J, Petit R, Cales P, et al. Antral motility in patients with cirrhosis with
or without gastric antral vascular ectasia. Gut 1995;37:488-92.
3. Spahr L, Villeneuve JP, Dufresne MP,et al. Gastric antral vascular ectasia in
cirrhotic patients: absence of relation with portal hypertension. Gut 1999;44:739-
42.
4. Ripoll C, Garcia-Tsao G. The management of portal hypertensive gastropathy
and gastric antral vascular ectasia. Dig Liver Dis 2011;43:345-51.
5. Fuccio L, Mussetto A, Laterza L, et al. Diagnosis and management of gastric
antral vascular ectasia. World J Gastrointest Endosc 2013;5:6-13.

31
 Piyapan Prueksapanich, M.D.
Case 15 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

An 86-year-old male with a history of hypertension and dyslipidemia presented

with melena and anemic symptom. Esophagogastroduodenoscopy (EGD) was done and
showed a large gastric ulcer at the gastric body. The ulcer was deep and had irregular
border (Figures 1 and 2). The microvascular pattern was clearly demonstrated by NBI
(Figure 3). Magnify NBI showed a focal abnormal area of absence in microsurface
pattern (MSP) and irregular microvascular pattern (MVP) at the border of the ulcer
(Figures 4). Biopsy taken from the area was compatible with adenocarcinoma.

Figures 1 and 2 White light endoscopy showed a large gastric ulcer at the
body of stomach. The ulcer was deep with irregular border.

32
 Figure 3 The microsurface pattern Figures 4 Magnifying NBI showed the
and microvascular pattern was clearly absence of microsurface pattern with
visible under the NBI mode. irregular microvascular pattern at the
focal area near ulcer border (arrow).

Diagnosis:
Adenocarcinoma of the stomach.

Discussion:
White light endoscopy has a limitation in differentiating malignant from benign
gastric ulcer and also in detecting the early malignant gastric lesion. Only certain
characteristics such as irregular shape, irregular and necrotic base, size larger than
2 cm and rigid border may suggest malignant lesions which yield a correct diagnosis
in only about two-third of lesions. Some gastric cancers may have benign appearance
with the reported rate of misclassification of 2-6%.1,2 With magnifying NBI, the
microstructure can be identified. In 2009, the new classification system was proposed
by Yao.3 The absence microsurface pattern (MSP) and irregular microvessel pattern
(MVP) (type IV) had 89.7% in accuracy to identify malignancy.4

33
 References
1. Bustamante M, Devesa F, Borghol A, et al. Accuracy of the initial endoscopic
diagnosis in the discrimination of gastric ulcers: is endoscopic follow-up study
always needed? J Clin Gastroenterol 2002;35:25-8.
2. Podolsky I, Storms PR, Richardson CT, et al. Gastric adenocarcinoma
masquerading endoscopically as benign gastric ulcer. A five-year experience.
Dig Dis Sci 1988;33:1057-63.
3. Yao K, Anagnostopoulos GK, Ragunath K. Magnifying endoscopy for diagnosing
and delineating early gastric cancer. Endoscopy 2009;41:462-7.
4. Mochizuki Y, Saito Y, Kobori A, et al. Magnifying endoscopy with narrow-band
imaging in the differential diagnosis of gastric adenoma and carcinoma and
identification of a simple indicator. J Gastrointestin Liver Dis 2012;21:383-90.

34
 Sasipim Sallapant, M.D.
Case 16 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 46-year-old female presented with chronic dyspepsia with partial response
to medical treatment. She denied weight loss or nausea/vomiting. Her past medical
history was not significant. She has no family history of gastrointestinal malignancy.
During EGD a 2 cm submucosal mass with central umbilication at the prepyloric
region was found (Figure 1). The esophagus and duodenum appeared normal.

Figure 1 A 2 cm well-defined submucosal

lesion with central umbilication at the
prepyloric area.

35
 Diagnosis:
Pancreatic rest (Heterotopic pancreas)

Discussion:
Pancreatic rest is a pancreatic tissue found outside the usual anatomical location
of the pancreas and thought to be a result of separation of fragments from the main
pancreatic mass due to the rotation of the foregut.1 The stomach is the most common
location (25 to 38%),2 mostly located within 3-4 cm of the pylorus and usually found
on posterior side.3 This remnant can migrate with the developing gastrointestinal tract
accounting for its various locations including duodenum, small bowel, gall bladder,
common bile duct, spleen, and mesentery.
Most patients are asymptomatic but they can present with nonspecific symptoms
such as abdominal pain, abdominal fullness, nausea, vomiting, anorexia, weight loss,
anemia, and melena.4 In terms of endoscopic characteristics, the pancreatic heterotopia
appears as smooth-walled, well circumscribed, and firm consistency submucosal
lesion. It is typically 1-4 cm in size. Its shape can be round, oval, or hemispherical. A
distinctive feature is the presence of central dimple that corresponding to the opening
of a duct. Microscopically and immunohistochemically, heterotopic pancreas contain
all features of a normal pancreas.5

References
1. Anca T, Eugen T, Mihai D, et al. Gastric Heterotopic Pancreas: an Unusual Case
and Review of the Literature. Gastrointestin Liver Dis 2012;21:209-12.
2. Chandan VS, Wang W. Pancreatic heterotopia in the gastric antrum. Arch Pathol
Lab Med 2004;128:111–2.
3. Ponsaing LG, Kiss K, Hansen MB. Classification of submucosal tumors in the
gastrointestinal tract. World J Gastroenterol 2007;13:3311-5.
4. Lai EC, Tompkins RK. Heterotopic pancreas. Review of a 26 year experience.
Am J Surg 1986;151:697-700.
5. Nickels J, Laasonen EM. Pancreatic heterotopia. Scand J Gastroenterol
1970;5:639-40.

36
 Kessarin Thanapirom, M.D.
Case 17 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A healthy 34-year-old male presented with coffee-ground vomiting after
frequent retching for one day. He admitted that he heavily consumed a large amount
of alcohol one day before this presentation. Physical examination was unremarkable.
EGD was performed and revealed well-demarcated, congested, erythematous, mosaic
mucosa in one sector of the gastric fundus. No other source of bleeding was seen.

Figure 1 EGD revealed a 4x5 cm well-

demarcated, congested, erythematous, mosaic
mucosal pattern in one sector of the gastric
fundus.

37
 Diagnosis:
Prolapse gastropathy

Discussion:
Prolapse gastropathy can be found in two percent of patients presenting
with upper GI bleeding.1 About half of patients with prolapse gastropathy present
with hematemesis and abdominal pain after multiple episodes of vomiting.2 Typical
endoscopic finding is well-demarcated, localized area of congested or hemorrhagic
mucosa in the upper stomach with several centrimeters distal to the EGJ. Transient gastric
mucosal prolapsed may be observed in some patients during the time of endoscopy.
Conservative treatment with antiemetic, prokinetic or tranquilizer medications is more
than appropriate.1,2

References
1. Byfield F, Ligresti R, Green PH, et al. Hematemesis due to prolapse gastropathy:
an emetogenic injury. Gastrointest Endosc 1998;48:527-9.
2. Shepherd HA, Harvey J, Jackson A, et al. Recurrent retching with gastric
mucosal prolapse. A proposed prolapse gastropathy syndrome. Dig Dis Sci
1984;29:121-8.

38
 Piyapan Prueksapanich, M.D.
Rapat Pittayanon, M.D., M.Sc.
Case 18 Satimai Aniwan, M.D., M.Sc.
Naruemon Wisedopas, M.D.
Rungsun Rerknimitr, M.D.
A 75-year-old male presented with iron deficiency anemia. He
denied a familial risk of colonic cancer. EGD and colonoscopy were
performed. The EGD revealed numerous carpet-liked sessile gastric polyps
occupying almost the entire of stomach, mostly at the body and fundus
(Figures 1 and 2). There were some duodenal adenomas without ampullary adenoma
(Figure 3). The colonoscopy showed numerous colonic sessile and pedunculated polyps
(Figure 4). NBI showed that the colonic polyps had a browner color relatively to the
background. There were also brown vessels surrounded with tubular white structures
compatible with NICE classification type 2 or adenomatous-type polyps type (Figure
5). Polypectomy was done and pathology confirmed the diagnosis of adenomatous
polyps. According to the age of the patient, atenuated familial adenomatous polyposis
was the mostly likely diagnosis.

39
 Figures 1 and 2 The EGD under white light and NBI revealed numerous
carpet-liked sessile gastric polyps occupying almost the entire of stomach,
mostly at the body and fundus.

Figure 3 There were some Figure 4 Colonoscopy showed

duodenal adenomas without numerous colonic polyps both sessile
ampullary adenoma. and pedunculated types.

40
 Figure 5 Under NBI examination,
colonic polyps had browner color
relatively to the background. There
were brown vessels surrounded
with tubular white structures which
compatible with NICE classification
type 2 or adenomatous-type polyps.

Diagnosis:
Attenuated familial adenomatous polyposis (AFAP)

Discussion:
Familial adenomatous polyposis (FAP) is an inherited adenomatous polyposis
syndrome related to APC gene mutation. Attenuated FAP (AFAP) is one of the subtypes
of FAP characterized with less than 100 colonic adenomas which are more predominant
in the proximal colon and more delayed in onset as compare to the classic FAP. The
duodenal, periampullary adenomas, gastric fundic gland polyps are also its features.
The median age of diagnosis in AFAP was reported to be in the fourth decade which
range from 12–77 years.1 The risk of the colorectal cancer is up to 80% by the age of
80 years in AFAP. The course of the disease is variable hence the therapeutic decisions
should be based on the colonoscopic findings in each individual.2

References
1. Knudsen AL, Bulow S, Tomlinson I, et al. Attenuated familial adenomatous
polyposis: results from an international collaborative study. Colorectal Dis
2010;12:e243-9.
2. Poovorawan K, Suksawatamnuay S, Sahakitrungruang C, et al. Colon cancer
prevention by detection of APC gene mutation in a family with attenuated
familial adenomatous polyposis. Asian Pac J Cancer Prev 2012;13:5101-4.

41
 Piyapan Prueksapanich, M.D.
Case 19 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 45-year-old female presented with early satiety, anorexia and significant

weight loss for 3 months. She had an unremarkable medical history and no family
history of cancer. EGD was done and revealed diffuse swelling gastric mucosa with poor
distension upon the air insufflations. The mucosa was friable with contact bleeding
(Figure 1). Under magnifying NBI, the microvascular pattern of gastric mucosa was
irregular, tortuous with asymmetrical distribution of microvessels. In certain area, the
microvascular pattern was absent. The microsurface pattern was also irregular (Figures
2 and 3). The pathology of the gastric biopsy was compatible with poorly-differentiated
adenocarcinoma. The computerized tomography was done for staging and showed
omental thickening with peritoneal nodules, multiple bony metastasis, and multiple
intraabdominal lymphadenopathy with moderate ascites.

Figure 1 Gastric mucosa was

friable with diffusely swelling and
it had poor distension upon air
insufflation.

42
 Figures 2 and 3 Under magnifying NBI, the microvascular pattern of gastric mucosa
was irregular, tortuous with asymmetrical distribution of microvessels. In certain
area that the microvascular pattern was absent. The microsurface pattern was also
irregular.

Diagnosis:
Diffuse type poorly-differentiated adenocarcinoma of the stomach (Linitis
plastica).

Discussion:
NBI can help to diagnose gastric cancer by demonstrating abnormal
microvessels and surface patterns. The findings are a well-demarcated lesion with
abnormal or absence of microvascular (MV) and microsurface (MS) patterns. The
accuracy, sensitivity and specificity were 90.4%, 60% and 94.3% respectively.1,2

References
1. Yao K, Nagahama T, Matsui T, et al. Detection and characterization of early
gastric cancer for curative endoscopic submucosal dissection. Dig Endosc
2013;25 Suppl 1:44-54.
2. Ezoe Y, Muto M, Uedo N, et al. Magnifying narrowband imaging is more
accurate than conventional white-light imaging in diagnosis of gastric mucosal
cancer. Gastroenterology 2011;141:2017-25.

43
 Kessarin Thanapirom, M.D.

Case 20
Rapat Pittayanon, M.D., M.Sc.
Nareumon Wisedopas, M.D.
Rungsun Rerknimitr, M.D.
A 42-year-old female with known case of peripheral T-cell lymphoma stage
IV (bone marrow and liver involvement) with secondary hemophagocytic
lymphohistiocytosis came for a disease staging with computerized tomography (CT)
of the abdomen. CT scan incidentally showed a contrast-enhanced gastric mass at
the gastric cardia (Figure 1). She denied gastrointestinal symptoms. EGD revealed a
submucosal mass, 3 cm in diameter at the fundus of stomach (Figure 2). Endoscopic
ultrasound (EUS) and fine needle aspiration was performed and found atypical
abnormal cell by histology. Subtotal gastrectomy was done. Pathology demonstrated
round cell tumor expressing diffuse immunoreactive for chromogranin, CD56 and
AE1/AE3 (Figure 3). Ultimately, a neuroendocrine tumor (NET) was diagnosed. The
percentage Ki-67 index is less than 2 compatible with well differentiated, grade 1, NET.

Figure 1 CT scan of Figure 2 EGD showed a

a b d o m e n s h ow e d submucosal mass, 3 cm in
contrast-enhanced diameter at the fundus of
gastric mass at the stomach.
gastric cardia (arrow).
44
 Figure 3 Pathology showed round cell tumor (A) expressing diffuse immunoreactive
for chromogranin (B), CD56 (C) and AE1/AE3 (D).

Diagnosis:
Well differentiated gastric neuroendocrine tumor (NET)

Discussion:
Gastric NETs are often incidentally found during upper GI endoscopy. The
prevalence of gastric well differentiated NETs (gastrointestinal carcinoids) has been
calculated at 35/100000.1 Gastric NET may present in a wide variety of endoscopic
morphological aspects of submucosal mass including sessile, papule and rarely
polypoid. Surgery is indicated for gastric NET larger than 10mm in diameter. Five-
year-survival of gastric NETs is high (71%) on average.2

45
 References
1. Yao JC, Hassan M, Phan A, et al. One hundred years after “carcinoid”:
epidemiology of and prognostic factors for neuroendocrine tumors in 35,825
cases in the United States. J Clin Oncol 2008;26:3063-72.
2. Landry CS, Brock G, Scoggins CR, et al. A proposed staging system for gastric
carcinoid tumors based on an analysis of 1,543 patients. Ann Surg Oncol
2009;16:51-60.

46
 Sittikorn Linlawan, M.D.

Case 21
Piyapan Prueksapanich, M.D.
Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 59-year-old female with a history of familial adenomatous polyposis (FAP)

underwent a surveillance EGD. There were multiple, small, velvety sessile polyps in
the gastric body and antrum (Figure 1) and a 1.5-cm pedunculated polyp at gastric
body (Figure 2) was also observed. Under NBI, the pedunculated polyp had clear
marginal crypt epithelium (MCE) with unclear microvessel pattern (MVP). These were
compatible with gastric adenoma (Figure 3). As shown in the figure 3, the fundic
gland polyp (left; short arrow) was seen next to the gastric adenoma (right; long arrow).
Biopsy and polypectomy were performed and pathology confirmed all
endoscopic readings.

Figure 1 Multiple gastric polyps in Figure 2 Large pedunculated

the gastric body and antrum. adenomatous polyp in the gastric
body.

47
 Figure 3 NBI with magnification
of the fundic gastric polyp (short
arrow) and the adnomatous polyp
(long arrow).

Diagnosis:
Gastric adenoma arising among multiple fundic gland polyps (FGPs) in a patient
with familial adenomatous polyposis (FAP)

Discussion:
Familial adenomatous polyposis (FAP) is an inherited autosomal dominant
disease caused by a mutation in the APC gene on chromosome 5. Apart of hundreds
of adenomatous colonic polyps, multiple adenomas can also be observed throughout
the upper gastrointestinal tract.1,2 Fundic gland polyps (FGPs) are the most common
gastric lesion in FAP and have higher rate of foveolar dysplasia in contrast to the
sporadic FGPs. The adenomas of stomach which usually arise in the gastric antrum
also have the mutation in APC gene and have been reported to occur in up to 6-60% of
patients with FAP.3 All gastric adenomas and FGPs larger than 1 cm should be removed
for histopathological assessment and need to be scheduled in a surveillance program
for recurrence and early cancer detection. H. pylori eradication followed by biopsy
examination or urea breath test is necessary for those patients with gastric adenoma.4

48
References
1. Mochizuki Y, Saito Y, Kobori A, et al. Magnifying endoscopy with narrow-band
imaging in the differential diagnosis of gastric adenoma and carcinoma and
identification of a simple indicator. J Gastrointestin Liver Dis 2012;21:383-90.
2. Lopez-Ceron M, van den Broek FJ, Mathus-Vliegen EM, et al. The role of high-
resolution endoscopy and narrow-band imaging in the evaluation of upper GI
neoplasia in familial adenomatous polyposis. Gastrointest Endosc 2013;77:542-
50.
3. Abraham SC, Nobukawa B, Giardiello FM, et al. Fundic gland polyps in familial
adenomatous polyposis: neoplasms with frequent somatic adenomatous
polyposis coli gene alterations. Am J Pathol 2000;157:747-54.
4. Shaib YH, Rugge M, Graham DY, et al. Management of gastric polyps: an
endoscopy-based approach. Clin Gastroenterol Hepatol 2013;11:1374-84.

49
 Puth Muangpaisarn, M.D.
Case 22 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 77-year-old male with underling disease of essential hypertension and
chronic kidney disease admitted to the hospital with aortic dissection type B followed
by a cardiac arrest. He was stable after aortic graft operation. On admission day 20,
moderate amount of hematemesis was observed in his nasogastric tube. EGD was
performed and showed submucosal gangrene with mucosal bleeding from the fundus
and upper part of gastric body (Figure 1). There was only erythematous and edematous
mucosa at the lower part of gastric body (Figure 2).

Figure 1 Submucosal gangrene Figure 2 Erythematous and

(arrow) with clot blood at the edematous mucosa of the gastric
fundus. body.

50
Diagnosis:
Gastric infarction

Discussion:
Gastric infarction is one of the extremely rare conditions because of the high
collaterally vascular supply of the stomach.1 There are various causes of gastric
infraction including mechanical cause (eg. acute gastric dilatation and gastric
vulvolus)2, thrombosis of the artery and vein, and poor perfusion from shock.3 Smoking,
hypertension and atherosclerosis are risk factors of gastric ischemia.4 Symptom and sign
of gastric infarction are non-specific such as abdominal pain, vomiting, hematemesis,
fever and tachycardia. Abdominal signs are epigatric pain and absence of bowel
sound.3 In this patient, the aortic dissection and circulatory failure may be the causes
of his gastric infarction.

References
1. Lin JI, Park YS, Gopalsway N. Gastric infarction. South Med J 1991;84:406-7.
2. Aydin I, Pergel A, Yucel AF, et al. Gastric Necrosis due to Acute Massive Gastric
Dilatation. Case Rep Med 2013;2013:847238.
3. Thomas M. Gastric infarction associated with septic shock and high-dose
vasopressor use. Anaesth Intensive Care 2003;31:470-4.
4. Kim SY, Han SH, Kim KH, et al. Gastric ischemia after epinephrine injection in
a patient with liver cirrhosis. World J Gastroenterol 2013;19:411-4.

51
 Sittikorn Linlawan, M.D.
Case 23 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

An 82-year-old female with a history of old ischemic stroke, hypertension, and

old myocardial infarction underwent percutaneous endoscopic gastrostomy (PEG)
without complication. During the routine schedule of PEG replacement at 6 months,
only the tube was removed but the inner PEG button was still left in the patient body.
EGD was performed and showed the bumper was embedded into the gastric wall at
the PEG site (Figures 1 and 2).

Figure 1 The bumper embedded in Figure 2 The PEG tub e after

the gastric wall. removal without the bumper.

52
Diagnosis:
Buried bumper syndrome (BBS)

Discussion:
Buried bumper syndrome (BBS) is a major complication in a patient after a
percutaneous endoscopic gastrostomy (PEG), it occurs as a result of excessive tension
between the internal and external bumpers. The bumper of PEG tube can lodged
anywhere between the skin and the gastric wall along the PEG tract. Most common
symptoms of BBS are the inability to infuse feeding content through the tube, leakage
around the tube, abdominal pain, and gastric ulceration at the bumper site.1 A buried
bumper should be removed even if the patient is asymptomatic, because of the risks
of tube impaction in the abdominal wall and/or gastric perforation.2, 3 However, there
is no report of buried bumper syndrome that left without treatment as shown in this
case. In our opinion, this patient was not fit enough to have a therapeutic endoscopy
and the tube was completely removed from the PEG tract; therefore, the endoscopic
therapy was not required at that time.
Endoscopic therapies for releasing the bumper are external traction, endoscopic
traction, external pressure and dissection of the overgrowing tissue using a needle-
knife, argon plasma coagulation, or a balloon dilatation.3, 4

References
1. Rino Y, Tokunaga M, Morinaga S, et al. The buried bumper syndrome: an early
complication of percutaneous endoscopic gastrostomy. Hepatogastroenterology
2002;49:1183-4.
2. Tanaka Y, Akahoshi K, Motomura Y, et al. Pretherapeutic evaluation of buried
bumper syndrome by endoscopic ultrasonography. Endoscopy 2012;44 Suppl
2 UCTN:E162.
3. Schrag SP, Sharma R, Jaik NP, et al. Complications related to percutaneous
endoscopic gastrostomy (PEG) tubes. A comprehensive clinical review. J
Gastrointestin Liver Dis 2007;16:407-18.
4. Cyrany J, Repak R, Douda T, et al. Cannulotome introduced via a percutaneous
endoscopic gastrostomy (PEG) tube--new technique for release of a buried
bumper. Endoscopy 2012;44 Suppl 2 UCTN:E422-3.

53
 Narisorn Lakananurak, M.D.

Case 24
Rapat Pittayanon, M.D., M.Sc.
Nauremon Wisedopas, M.D.
Rungsun Rerknimitr, M.D.

A 61-year-old healthy male presented with melena for 2 days. His physical
examination showed mild pale conjunctiva. EGD revealed three gastric submucosal
masses with clean based ulcer on top of the cardia and body of stomach (Figures 1 and
2). Pathology from gastric masses showed acute ulcer with patchy malignant round cell
infiltration compatible with malignant lymphoma (Figure 3). Immunohistochemistry
stain was positive for CD20 but negative for CD3. This confirmed the diagnosis of
diffuse large B-cell lymphoma (DLBCL). His bone marrow study was normal.

Figure 1 Gastric submucosal mass size 3 Figure 2 Gastric submucosal mass

cm at the cardia with clean based ulcer size 2 cm at the body with pigmented
on top (short arrow). Another submucosal spot on top of the ulcer.
mass size 1.5 cm was also discovered at
the gastric body (long arrow).

54
 Figure 3 Malignant round cell (left) with positive immunohistochemistry for CD20
(right).

Diagnosis:
Primary gastric diffuse large B-cell lymphoma (DLBCL)

Discussion:
The most common extranodal site involved by lymphoma is the gastrointestinal
tract that accounting for 5%-20% of all lymphoma cases.1 It occurs most commonly
in the stomach (60-75% of the cases), followed by the small intestines, ileum, cecum,
colon, and rectum.2 Mucosa-associated lymphoid tissue (MALT) and diffuse large
B cell lymphomas (DLBCL) are the two most common histologic subtypes.3 The
symptoms include dyspepsia, nausea, vomiting, weight loss, anemia, a lesser extent
ulceration, and perforation. Interestingly, a few patients were reportedly asymptomatic
in GI symptom while the disease was discovered from other organs.2
Endoscopic findings of gastric lymphoma may show multiple nodular lesions
similar to reactive lymph nodes or lymphoma can manifest as mucosal ulceration,
hyperplasia, polyp, or as an infiltrative lesion. Biopsy is essentially needed to
differentiate between neoplastic lymphoid nodules and benign reactive lymphoid
follicles.4

55
 References
1. Freeman C, Berg JW, Cutler SJ. Occurrence and prognosis of extranodal
lymphomas. Cancer 1972;29:252-60.
2. Bautista-Quach MA, Ake CD, Chen M, et al. Gastrointestinal lymphomas:
Morphology, immunophenotype and molecular features. J Gastrointest Oncol
2012;3:209-25.
3. Psyrri A, Papageorgiou S, Economopoulos T. Primary extranodal lymphomas of
stomach: clinical presentation, diagnostic pitfalls and management. Ann Oncol
2008;19:1992-9.
4. Ghimire P, Wu GY, Zhu L. Primary gastrointestinal lymphoma. World J
Gastroenterol 2011;17:697-707.

56
 Suppakorn Malikhao, M.D.

Case 25
Rapat Pittayanon, M.D., M.Sc.
Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 9-year-old boy came with anemic symptom without obvious GI bleeding.
He had a previous episode of iron deficiency anemia requiring blood transfusion for
several times. Since infancy, the patient had repeatedly suffered from multiple soft,
bluish nodules at the skin and all extremities. On examination, he had severe anemia.
There were multiple, bluish-black rubbery blebs (nevi), measuring 5 mm to 1 cm on
both palms and soles (Figures 1 and 2). The similar lesions were also noted at his
tongue (Figure 3). The lesions were non-tender, compressible with wrinkled surface
and had never bled. EGD showed multiple purplish polyp-like mass lesions with
abundant vasculature in the stomach and duodenum (Figures 4-6).

Figures 1-3 Demonstrated multiple violaceous, nonpulsatile, soft, compressible

papules and nodules, 0.5-1 cm in diameter at both palms and soles and undersurface
of the tongue.

57
 Figure 4-6 Multiple purplish, polyp-like lesions, 0.5-1 cm in diameter, located in
stomach and duodenum (arrows).

Diagnosis:
Blue Rubber Bleb Nevus Syndrome

Discussion:
Blue Rubber Bleb Nevus Syndrome (BRBNS) is a vascular malformation of the
skin and multiple visceral organs. Cutaneous lesions are often first noticed at birth
or in the neonatal period, but sometimes can present during adulthood.1 Although,
autosomal dominant (AD) pattern of inheritance has been documented, most cases
are sporadic. The lesions typically increase in size and number with age and progress
throughout patient’s life. However, spontaneous resolution has been reported.
Fortunately, no malignant transformation of the lesions has been demonstrated.2
The gastrointestinal tract is the most common affected visceral organ, which
predominantly located in small intestine and distal large bowel. Therefore, occult
blood loss and iron deficiency anemia commonly result. Abdominal pain, infarction,
intussusception and volvulus are possible complications.3 Endoscopic treatments for
GI bleeding in BRBNS include electrocoagulation, laser photocoagulation, injection
of sclerotic, band ligation, and polypectomy with saline lift. Enterotomy with excision
of lesions have been shown to be effective in case of refractory and life-threatening
hemorrhage.1

58
References
1. Dwivedi M, Misra SP. Blue rubber bleb nevus syndrome causing upper GI
hemorrhage: a novel management approach and review. Gastrointest Endosc
2002;55:943-6.
2. Nahm WK, Moise S, Eichenfield LF, et al. Venous malformations in blue rubber
bleb nevus syndrome: variable onset of presentation. J Am Acad Dermatol
2004;50:S101-6.
3. Dobru D, Seuchea N, Dorin M, et al. Blue rubber bleb nevus syndrome: case
report and literature review. Rom J Gastroenterol 2004;13:237-40.

59
 Piyapan Prueksapanich, M.D.
Case 26 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 50-year-old male with a history of NSAIDs abuse, presented with melena.

EGD was done and showed antral gastritis with duodenitits. There were two connecting
channels between gastric antrum and the duodenal bulb. As shown in figures 1 and 2,
the upper pseudopylorus led to a clean based ulcer in the duodenal bulb whereas the
lower channel was a native pylorus. Multiple small clean based duodenal ulcers were
also noted. The rapid urease test for H.pylori was positive. The patient was treated with
standard triple therapy.

Figures 1 and 2 EGD showed two connecting channels between gastric

antrum and the duodenal bulb. The upper pseudopylorus led to a clean
based ulcer in the duodenal bulb (arrow) whereas the lower channel was
a native pylorus.

60
Diagnosis:
Acquired double pylorus

Discussion:
The double pylorus can be congenital or acquired. The acquired double pylorus
is a rare finding with a reported incidence of 0.02-0.4%. It occurs as a complication
of peptic ulcer disease. The common location is at the lessor curvature of the gastric
antrum near the native pylorus and it usually connects to the superior part of the
duodenal bulb. Hypothetically, gastric ulcer could induce adhesions between the
adjacent walls of the duodenum and the stomach. If the further ulceration occurs, the
fistulous tract is generated. The association between the double pylorus and H.pylori
has also been reported. Most patients with double pylorus are asymptomatic and do
not require treatment.1,2 In a small group of patients, a spontaneous fusion of both
channels may occur.3

References
1. Linea C, Sinagra E, La Seta F, et al. Acquired double pylorus, due to penetrating
gastric ulcer, presenting with melena. World J Gastrointest Endosc 2012;4:94-
5.
2. Lee TH, Park SH. Double pylorus secondary to recurrent ulcer: serial endoscopy
follow-up. Endoscopy 2008;40 Suppl 2:E226.
3. Arhan M, Oztas E, Ibis M, et al. A rare endoscopic finding: acquired double
pylorus. Surg Endosc 2010;24:244-5.

61
 Narisorn Lakananurak, M.D.
Case 27 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 43-year-old Thai male diagnosed as advanced stage hilar cholangiocarcinoma

and liver metastasis had undergone metallic stent placement 10 months ago. He
presented with hematemesis for 1 day with stable vital signs. His physical examination
was unremarkable except mild RUQ pain. EGD showed choledochoduodenal fistula
at the first part of duodenum (Figure 1). A previously placed metallic stent was found
in the fistula (Figure 2).

Figure 1 Choledochoduodenal fistula

at the first part of duodenum with
clean based ulcer at the fistula opening
(arrow). A previously placed metallic
stent was found inside the fistula.

62
 Figure 2 Distal end of the metallic stent
located at the second part duodenum.

Diagnosis:
Choledochoduodenal fistula caused by radial expansile force of metallic stent.

Discussion:
A choledochoduodenal fistula is an abnormal passage between the common
bile duct (CBD) and the duodenum. It is an uncommon finding during EGD with
the reported incident rate of 3-5%.1 Common etiologies include instrumentation
(Iatrogenic), choledocholithiasis, duodenal ulcer, and can cancer associated fistula
(ampullary cancer, duodenal cancer, gallbladder cancer, pancreatic cancer, and
cholangiocarcinoma).2 The clinical manifestations vary from asymptomatic, nonspecific
abdominal pain to gastrointestinal bleeding. CT abdomen often shows pneumobilia.
EGD or endoscopic retrograde cholangiopancreatography (ERCP) is employed to
diagnose choledochoduodenal fistulas.3 A biliary stent-related choledochoduodenal
fistula is very rare complication with incident rate below 1%. It is usually caused by
the sharp end of a metallic stent, stent migration and rarely caused by direct the radial
expansile force of the metallic stent.4
Management of choledochoduodenal fistula depends on the type and etiology.
In fistula with complicating duodenal ulcer, medical management or surgery can be
used. Endoscopic management and the extraction of a bile duct stone (if present), may
be needed.5

63
 References
1. Lin CT, Hsu KF, Yu JC, et al. Choledochoduodenal fistula caused by
cholangiocarcinoma of the distal common bile duct. Endoscopy 2009;41 Suppl
2:E319-20.
2. Kuroki T, Fukuda K, Tajima Y, et al. Parapapillary choledochoduodenal
fistula associated with cholangiocarcinoma. J Hepatobiliary Pancreat Surg
2005;12:143-6.
3. Ji JS, Kim HK, Kim SS, et al. Periampullary choledochoduodenal fistula
associated with ampulla of Vater carcinoma. Dig Dis Sci 2007;52:1592-3.
4. Lee TH, Park SH, Kim SP, et al. Spontaneous choledochoduodenal fistula after
metallic biliary stent placement in a patient with ampulla of vater carcinoma.
Gut Liver 2009;3:360-3.
5. Yamashita H, Chijiiwa K, Ogawa Y, et al. The internal biliary fistula--reappraisal
of incidence, type, diagnosis and management of 33 consecutive cases. HPB
surgery : J Hepatobiliary Pancreat Surg 1997;10:143-7.

64
 Suppakorn Malikhao, M.D.

Case 28
Rapat Pittayanon, M.D., M.Sc.
Yuthana Sattawatthamrong, M.D.
Rungsun Rerknimitr, M.D.

A 22-year-old female presented with longstanding dyspepsia and flatulence.

She has visited various health centers. She was diagnosed as having IBS and managed
accordingly with negative response. EGD found atrophic and subtle scalloping along
mucosa at the first part of the duodenum (Figures 1 and 2). Duodenal biopsy was
obtained and histopathology revealed total villous atrophy (flat and shortened) with
moderate inflammation in lamina propia. The anti-gliadin antibody IgG and antitissue-
transglutaminase IgA were positive. The patient was managed as celiac disease and
dramatically responded to gluten-free diet.

Figures 1 and 2 EGD found atrophic and subtle scalloping folds along the
first part of duodenum.

65
 Diagnosis:
Celiac disease

Discussion:
Celiac disease is a chronic immune-mediated disorder that occurs in genetically
predisposed populations.1 Patients affected by the disease may be asymptomatic or
manifest with classic malabsorption symptoms of bloating, abdominal pain, weight
loss, diarrhea, and steatorrhea after gluten ingestion (and related derivatives found
in other grains).1 The clinician must be aware of a more subtle GI picture as well as
non-GI signs and symptoms. Diagnosis and screening begin with the use of serologic
tests: IgA anti-tissue transglutaminase (tTG), IgA antiendomysial antibodies (EMAs),
and serum IgA level.1, 2 The endoscopic appearance of celiac disease can vary widely,
ranging from normal to atrophic mucosal folds. Endoscopic markers of celiac disease
include the following: a reduction or absence of duodenal folds, scalloping, mosaic
pattern and mucosal fissures or grooves. The overall sensitivity and specificity of
endoscopic markers of celiac disease vary from 6% to 94% and from 83% to 100%,
respectively.3 Duodenal biopsy, still considered by many as the standard criterion
necessary for the correct diagnosis. Histology demonstrates small intestinal villous
atrophy, intraepithelial lymphocytosis, and crypt hyperplasia that occur on exposure to
dietary gluten.4 These changes exhibit improvement after withdrawal of gluten from the
diet. Resolution of clinical symptoms after initiation of gluten-free diet is considered to
be part of the diagnostic picture.2,5 Genetic tests revealing permissive haplotypes may
be helpful in confirming the diagnosis as well as identifying susceptible individuals.2

References
1. Evans KE, Sanders DS. Celiac disease. Gastroenterol Clin North Am 2012;41:639-50.
2. Rubio-Tapia A, Hill ID, Kelly CP, et al. ACG clinical guidelines: diagnosis and
management of celiac disease. Am J Gastroenterol 2013;108:656-76; quiz 677.
3. Cammarota G, Fedeli P, Gasbarrini A. Emerging technologies in upper
gastrointestinal endoscopy and celiac disease. Nat Clin Pract Gastroenterol
Hepatol 2009;6:47-56.
4. Bao F, Green PH, Bhagat G. An update on celiac disease histopathology and
the road ahead. Arch Pathol Lab Med 2012;136:735-45.
5. Rashtak S, Murray JA. Review article: coeliac disease, new approaches to
therapy. Aliment Pharmacol Ther 2012;35:768-81.

66
 Pradermchai Kongkam, M.D., M.Sc.

Case 29
Piyapan Prueksapanich, M.D.
Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 56-year-old female presented with painless jaundice and significant weight

loss. Computed tomography showed a delayed contrast enhancing 8 cm liver mass
at right hepatic lobe invading posterior aspect of liver capsule with multiple intra-
abdominal lymphadenopathy causing distal common bile duct obstruction. Liver
biopsy was done and showed moderately differentiated adenocarcinoma. Endoscopic
retrograde cholangiography (ERC) was done and failed to cannulate into the biliary
ampulla. Then EUS-guided choledochoduodenostomy was performed. Unfortunately,
an iatrogenic duodenal perforation sized 1 cm in diameter occurred during the
procedure (Figure 1). Ovesco Twin Grasper and Over-The-Scope Clip (OTSC) (Ovesco
Endoscopy AG, Tubingen, Germany) were used for full thickness duodenal wall closure
(Figures 2 and 3). Post-procedural contrast injection confirmed the successful closure of
the wall defect with no extraluminal contrast leakage. Large amount of intraperitoneal
air was also noted (Figure 4). The patient had a clinical of mild peritonitis which
resolved without surgical treatment and oral intake was resumed at one week later.

Figure 1 A 1-centimetered iatrogenic

duodenal perforation was seen in the first
part of duodenum (arrow).

67
 Figure 2 The twin grasper was used Figure 3 The Ovesco OTSC clip
to grasp the two opposing ends of was applied successfully.
the wall defect.

Figure 4 Post-procedural contrast

injection confirmed the successful
closure of the wall defect with
no extraluminal contrast leakage
(long arrow). Large amount of
intraperitoneal air was also noted
(short arrow).

68
Diagnosis:
Successful duodenal perforation closure with the Ovesco OTSC Clip

Discussion:
The OTSC system, also known as “bear claw”, has been used to close mucosal
or luminal gastrointestinal defects larger than 5 millimeters which the traditional clips
may not have enough tensile force. For perforation closure, the defect can be as large
as 10-20 millimeter in size. The OTSC clip is made of nitinol. The other uses are
anastomotic leak or fistular closure, gastrointestinal bleeding, stent anchoring and
resection of submucosal lesions. The overall success rate has been reported as 75-
82.6%.1, 2

References
1. Monkemuller K, Peter S, Toshniwal J, et al. Multipurpose use of the ‘bear claw’
(over-the-scope-clip system) to treat endoluminal gastrointestinal disorders. Dig
Endosc 2013. doi: 10.1111/den.12145. [Epub ahead of print]
2. Nishiyama N, Mori H, Kobara H, et al. Efficacy and safety of over-the-scope
clip: including complications after endoscopic submucosal dissection. World J
Gastroenterol 2013;19:2752-60.

69
 Narisorn Lakananurak, MD.
Case 30 Rapat Pittayanon, MD., M.Sc.
Rungsun Rerknimitr, MD.
A 59-year-old Thai female with advanced stage pancreatic head cancer
having tumor invasion to celiac axis and superior mesenteric artery/vein came for
a palliative management of his obstructive jaundice. An endoscopic retrograde
cholangiopancreatography (ERCP) found dilated, tortuous vessel at the second part of
duodenum, just above the ampulla of Vater (Figure 1).

Figure 1 Dilated, tortuous vessel (arrow) at

the second part duodenum.

70
Diagnosis:
Duodenal varices

Discussion:
The term “ectopic varices ” has been used to describe varices other than
those found in the esophagus and stomach.1,2 The “duodenal varices” is one of the
rare ectopic varices and has the afferent vessel originates either from the superior
mesenteric vein (SMV) or from the portal vein trunk via either the superior or inferior
pancreaticoduodenal vein, whereas the efferent vein drains into the inferior vena cava.3
A single-center retrospective review of 5,664 endoscopic procedures performed over4
years found the prevalence of duodenal varices to be 1 in every 435 endoscopic
procedures.4 They are located in the duodenal bulb in 3.5%, the descending part in
82.5%, and the transverse part in 14.0%.5
Most underlying cause of duodenal varices is alcoholic liver diseases. Pancreatic
cancer, as in this case, is a very rare cause of ectopic varices and account for only
0.6% of all ectopic varices. Duodenal varices is the second most common site of
bleeding of ectopic varices follow by rectal varices (34% and 38% respectively). The
management of duodenal varices is mainly endoscopic and interventional approach
(31.6% and 21% respectively).5

References
1. Lebrec D. Ectopic varices in patients with portal hypertension. Arch Surg
1980;115:890.
2. Almadi MA, Almessabi A, Wong P. Ectopic varices. Gastrointest Endosc
2011;74:380-8.
3. Hashizume M, Tanoue K, Ohta M, et al. Vascular anatomy of duodenal
varices: angiographic and histopathological assessments. Am J Gastroenterol
1993;88:1942-5.
4. Al-Mofarreh M, Al-Moagel-Alfarag M. Duodenal varices. Report of 13 cases. Z
Gastroenterol 1986;24:673-80.
5. Watanabe N, Toyonaga A, Kojima S, et al. Current status of ectopic varices in
Japan: Results of a survey by the Japan Society for Portal Hypertension. Hepatol
Res 2010;40:763-76.

71
 Puth Muangpaisarn, M.D.
Case 31 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
An 85-year-old male presented with near-syncope for 5 hour prior to this
admission. Physical examination showed stable vital signs but moderately pale icteric
conjunctiva. Rectal examination revealed maroon stool. His hemoglobin level was 7
g/dL. After fluid resuscitation and blood transfusion, EGD was performed.
EGD revealed a large blood clot at the medial wall of D1-D2 junction (Figure 1).
Diluted adrenaline 1:20,000 was injected 11 ml at this lesion. Subsequently, CT scan of
the abdomen was done and revealed a distended gallbladder containing heterogenous
hyperdensity content, measured about 9.2x6.2 cm. There was asymmetrical thickening
with focal discontinuity of gallbladder. It also presented air in the gallbladder together
with fistula tract connecting the gallbladder to the 2nd part of duodenum. Pericholecystic
fat stranding was observed (Figure 2). Moreover, small area of gallbladder wall was
found to invade into the duodenum (Figure 3). Due to the poor general health of the
patient, he and his family decided not to pursue with any further treatment.

Figure 1 A large blood clot found at

the medial wall of D1-D2 junction.

72
 Figure 2 Distended gallbladder Figure 3 Gallbladder wall invading into
containing heterogenous hyperdensity the second part of duodenum (arrow).
content with air bubble (arrow).

Diagnosis:
Hemocholecyst with cystoduodenal fistula

Discussion:
Hemocholecyst (HC) is defined as a clot-filled gallbladder caused by bleeding
into its lumen, which does not result in rupture of the gallbladder wall.1 HC is
rarely reported with a variety of etiology including trauma, iatrogenic manipulation,
gallbladder tumor, cholecystitis, gall stones and ruptured cystic artery aneurysm.2
Additionally, hematological disorders such as hemophilia was reported as the cause of
HC.3 It could be presented as several manifestations, including, cholecystitis from cystic
obstruction1, obstructive jaundice by hilar compression, and upper gastrointestinal
(GI) bleeding from hemobilia or cholecystoenteric fistula.2
Based on the clinical presentations of this patient, HC with upper GI bleeding in
this case presumably developed from a gallbladder tumor invading into the duodenal
wall and resulting to a cholecystoenteric fistula with GI bleeding.

73
 References
1. Ku J, DeLaRosa J, Kang J, et al. Acute cholecystitis with a hemocholecyst as
an unusual presentation of gallbladder cancer: report of a case. Surg Today
2004;34:973-6.
2. FanY, Wu SD, Kong J. Obstructive jaundice and melena caused by hemocholecyst:
a case report. World J Gastroenterol 2013;19:2126-8.
3. Suaud O, Savoye-Collet C, Suaud L, et al. [Answer to February e-quid.
Spontaneous hemocholecyst in a hemophiliac patient]. J Radiol 2010;91:314-
6.

74
 Sasipim Sallapant, M.D.
Case 32 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 63-year-old female with underlying of ischemic heart disease and diabetes was
admitted in the intensive care unit due to acute pyelonephritis with septic shock. She
was treated with intravenous ceftriaxone and vasopressor. Two days later, she had small
amount coffee ground content via her NG tube. Hematocrit dropped inappropriately
and then hypotension developed. Her abdomen was distended with hypoactive bowel
sound but no point of tenderness. EGD showed multiple small ulcers in the gastric
body (Figure 1), with areas of sharply demarcated necrotic mucosa at the third part of
duodenum (Figures 2 and 3).
She then underwent an emergency exploratory laparotomy. The operative
finding was suggestive of non-occlusive mesenteric ischemia (NOMI). Part of the
gangrenous bowel was resected. The patient could not recover from infection and
finally passed away from multiple organ failure.

Figure 1 The multiple ulcers at the gastric

body of stomach.

75
 Figures 2 and 3 EGD showed well demarcated area of necrotic tissue at
the 3rd part of duodenum (arrow).

Diagnosis:
Acute mesenteric ischemia (AMI)

Discussion:
Acute arterial mesenteric ischemiai includes SMA embolus, SMA thrombosis,
non-occlusive mesenteric ischemia (NOMI). NOMI is responsible for 20% to 30%
of AMI.1 A spectrum of bowel injury ranges from transient bowel function alteration
to transmural gangrene and multiple organ failure. If intestinal infarction developed,
the mortality rate is as high as 70%.2 Identification of AMI requires a high index of
suspicion.
Unexplained abdominal distention or gastrointestinal bleeding may be the only
symptom and sign of AMI when pain is absent, especially when AMI is due to NOMI.3
Currently, CT angiography is the mainstay of diagnosis.4 Endoscopy is not indicated.5
But in some difficult cases, this etiology is not suspected before performing EGD.
The endoscopic spectrum of intestinal ischemia includes edema, pale mucosa,
erosion, ulcer, hemorrhage, and dark bluish necrotic tissue with segmental or
circumferential involvement. The presence of pseudomembrane overlying the intestinal
mucosa can develop. The well demarcated margin of lesion is the characteristic of
mesenteric ischemia.3

76
References
1. Acosta S. Epidemiology of mesenteric vascular disease: clinical implications.
Semin Vasc Surg 2010;23:4–8.
2. Oldenburg WA, Lau LL, Rodenberg TJ, et al. Acute mesenteric ischemia: a
clinical review. Arch Intern Med 2004;164:1054–62.
3. Alhan E, Usta A, Çekiç A, et al. A study on 107 patients with acute mesenteric
ischemia over 30 years. Int J Surg 2012;10:510-3.
4. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia:
systematic review and meta-analysis. Radiology 2010;256:93–101.
5. Early DS, Ben-Menachem T, Decker GA, et al. Appropriate use of GI endoscopy.
Gastrointest Endosc 2012;75:1127-31.

77
 Sittikorn Linlawan, M.D.
Case 33 Nopporn Anukulkarnkusol, M.D.
Rungsun Rerknimitr, M.D.

A 60-year-old woman presented with chronic dyspepsia for 3 months. She

had no other alarm features except the complete blood count showed microcytic
anemia. EGD revealed a 5.5-cm pedunculated polyp with a wide-based in the
lesser curvature of gastric body. NBI confirmed as inflammatory mucosa. There was
a central umbilication of the polyp (Figures 1-3). After placement of a detachable
nylon snare loop (Endoloop, MAJ-254; Olympus, Aomori, Japan) at the base of mass
for 5 days (Figures 4 and 5), a repeated EGD was performed for electrosurgical snare
polypectomy. There was no complication (Figure 6). Histopathology demonstrated
mucosal ulceration with multinodular submucosal mass, composed of bundles of
spindle cells with elongated nuclei and epitheloid tumor cells.

Figures 1-3 Large gastric polypoid mass at lesser curvature of stomach (White
light and Narrow band imaging).

78
 Figure 4 Figure 5

Figure 4 After Endoloop

placement on day 0.

Figure 5 Showed necrotic

tissue above endoloop.

Figure 6 Post snare poly-

pectomy.

Figure 6

Diagnosis:
Gastric gastrointestinal stromal tumor (GIST) removed by a snare polypectomy
after an endoloop strangulation

Discussion:
Management of patients with gastrointestinal stromal tumor (GIST) need
multidisciplinary approach involving of endoscopic, surgical, pathologic, and
pharmacologic interventions. Diagnosis of GIST should be considered whenever
a submucosal lesion is detected endoscopically.1 NBI usually shows only non-
neoplastic changes of the polyp mucosa. The use of snare polypectomy with endoloop
is the technique described for removal of giant polyps and minimize postprocedural
bleeding.2, 3
79
 References
1. Mullady DK, Tan BR. A multidisciplinary approach to the diagnosis and
treatment of gastrointestinal stromal tumor. J Clin Gastroenterol 2013;47:578-
85.
2. Kouklakis G, Mpoumponaris A, Gatopoulou A, et al. Endoscopic resection of
large pedunculated colonic polyps and risk of postpolypectomy bleeding with
adrenaline injection versus endoloop and hemoclip: a prospective, randomized
study. Surg Endosc 2009;23:2732-7.
3. Lee BI, Kim BW, Kim HK, et al. Routine mucosal closure with a detachable
snare and clips after endoscopic submucosal dissection for gastric epithelial
neoplasms: a randomized controlled trial. Gut Liver 2011;5:454-9.

80
 2 Lower

Sasipim Sallapant, M.D.

Case 1 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 36-year-old female with a 2-year history of ulcerative colitis. She had

been in remission with mesalamine until she developed lower abdominal pain and
hematochezia for 2 weeks. Physical examination was unremarkable except mild
tenderness at left lower abdomen. Colonoscopy revealed diffuse inflammatory
ulcerations with friable and spontaneous bleeding mucosa at the sigmoid colon. NBI
showed an inflamed mucosa as a dark green area. There were multiple pseudopolyps
in the transverse colon.

Figures 1 and 2 White light imaging showed severe inflammatory ulcerations with
friable mucosa. NBI demonstrated inflamed area in dark green color.

81
 Figures 3 and 4 White light imaging showed multiple pseudopolyps at transverse
colon. NBI demonstrated the polyps as non-inflamed mucosa by showing only light
green area.

Diagnosis:
Active ulcerative colitis with non-inflamed pseudopolyps

Discussion:
Ulcerative colitis (UC) is a chronic idiopathic inflammatory disease of
the gastrointestinal tract that affects the large bowel. Approximately, 40-65% of
patients have an intermittent flare episode following the initial flare.1 In the active
UC, NBI colonoscopy reveals mucosal edema and granularity in inflamed mucosa
with obscuration of intra-mucosal capillary network.2 Area of bleeding or marked
erythematous mucosa are recognized as dark green mucosa. Ulcers or mucous
exudates are found as distinctive whitish areas.3

Inflammatory pseudopolyps result from a regenerative and healing process

that leaves inflamed colonic mucosa in a polypoid configuration.1 On endoscopic
findings, pseudopolyps have varied widely in size and shape and may be flat, sessile
or pedunculate. Because they are not true adenomas, therefore in a non-inflamed
polyp, NBI image reveals a normal pit and mucosal vascular pattern.4

82
References
1. Edwards FC, Truelove SC. The Course and Prognosis of Ulcerative Colitis. Gut
1963;4:299-315.
2. Esaki M, Kubokura N, Kudo T, et al. Endoscopic findings under narrow band
imaging colonoscopy in ulcerative colitis. Dig Endosc 2011;23 Suppl 1:140-2.
3. Kudo T, Matsumoto T, Esaki M, et al. Mucosal vascular pattern in ulcerative
colitis: observations using narrow band imaging colonoscopy with special
reference to histologic inflammation. Int J Colorectal Dis 2009;24:495-501.
4. Choi YS, Suh JP, Lee IT, et al. Regression of giant pseudopolyps in inflammatory
bowel disease. J Crohns Colitis 2012;6:240-3.

83
 Narisorn Lakananurak, M.D.
Case 2 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 67-year-old Thai male known as end-stage renal disease and coronary heart
disease. He was admitted due to severe pneumonia with septic shock. One week after
hospitalization, he developed bright red blood per rectum. Sigmoidoscopy showed
an irregular border rectal ulcer size 3 cm in diameter just above the dentate line. The
ulcer involved 75% of rectal circumference and it contained a non-bleeding visible
vessel (NBVV) (Figures 1 and 2). A hemoclip was applied at NBVV and hemostasis was
achieved (Figure 3).

Figures 1 and 2 A hemicircumferential irregular border rectal ulcer located just

above the dentate line with a visible vessel (yellow arrow).

84
 Figures 3 Post hemoclipping

Diagnosis:
Acute hemorrhagic rectal ulcer syndrome (AHRUS) with non-bleeding visible
vessel.

Discussion:
Acute hemorrhagic rectal ulcer syndrome (AHRUS) is characterized by profuse
and painless rectal ulcer bleeding in elderly patients who were hospitalized with serious
illness and comorbidities.1 The common underlying diseases are cerebrovascular
disease, chronic renal disease, and cardiovascular disease.1 The typical location is
around the dentate line. Endoscopic findings were classified in 4 types ; type A = Partial
or whole circumferential, type B = Linear or nearly round small ulcer(s), type C =
Mixture of types A and B, and type D = Dieulafoy’s type.1 Many hemostatic treatments
of AHRUS were reported such as transanal suture ligation, APC, and clipping but
endoscopic treatment was the most preferred.2

References
1. Motomura Y, Akahoshi K, Matsui N, et al. Clinical and endoscopic characteristics
of acute haemorrhagic rectal ulcer, and endoscopic haemostatic treatment: a
retrospective study of 95 patients. Colorectal Dis 2010; 12: e320-5.
2. Oku T, Maeda M, Ihara H, et al. Clinical and endoscopic features of acute
hemorrhagic rectal ulcer. J Gastroenterol 2006; 41: 962-70.

85
 Narisorn Lakananurak, M.D.

Case 3
Satimai Aniwan, M.D., M.Sc.
Pradermchai Kongkam, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 52-year-old Thai female underwent a colorectal cancer screening program.

A colonoscopy showed a yellowish smooth soft subepithelial lesion measured as 7
mm in diameter in the descending colon. A surface indentation was observed upon
pushing the lesion with closed biopsy forceps (Pillow sign) (Figure 1).

Figure 1 a yellowish smooth soft subepithelial

lesion in the descending colon.

86
Diagnosis:
Colonic lipoma

Discussion:
Lipoma of the colon is a rare entity and its exact incidence is difficult to
estimate because most of them are asymptomatic.1 It has been reported in 0.15% of
all colonoscopies and 0.32-4.4% of autopsies.2 The common location are ileocecal
valve, cecum, rectum, sigmoid, and descending colon, respectively.1
Colonoscopy showed directly visualize mass with tenting of the mucosa, which
indent with a closed biopsy forceps. When the forceps is withdrawn, the tumor will
spring back to resume the previous shape (pillow or cushion sign). A pressure put
on the lesion compresses superficial vessels and a distinctive yellow color of fat will
disclose. When biopsy is taken, adipose tissue will protrude through the biopsy site
(naked fat sign) which is the fatty characteristic of tumor.3

References
1. Goyal V, Ungsunan P. Lipoma of the colon: should asymptomatic tumors be
treated? The American Surgeon 2013;79:E45-6.
2. Chung YF, Ho YH, Nyam DC, et al. Management of colonic lipomas. The
Australian and New Zealand Journal of Surgery 1998;68:133-5.
3. Notaro JR, Masser PA. Annular colon lipoma: a case report and review of the
literature. Surgery 1991;110:570-2.

87
 Piyapan Prueksapanich, M.D.
Case 4 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
An 89-year-old female with chronic atrial fibrillation has been taken a life-long
warfarin presented with hematochezia. One week earlier, she underwent colonoscopy
with polypectomy of the polyp at the rectosigmoid colon. She required three hemoclips
placement to control the bleeding after polypectomy. Warfarin was stopped before
colonoscopy and resumed right after the procedure. One day before admission, she
developed a new onset of hematochezia. Colonoscopy revealed a bleeding visible
vessel at the post-polypectomy stump where three hemoclips were still in-placed
(Figure 1). A band ligation was performed with no recurrence bleeding (Figures 2, 3
and 4).

Figure 1 A bleeding visible vessel

at the post-polypectomy stump
where the three hemoclips were
still in-placed.

88
 Figure 2 Figure 3

Figures 2, 3 and 4 Endoscopic band

ligation was performed successfully
over the stumps and the three hemoclips
were still intact.

Figure 4

Diagnosis:
Endoscopic band ligation for treatment of post-polypectomy bleeding

Discussion:
Post-polypectomy bleeding rate has been reported to be 0.3-6.1%. The post-
polypectomy bleeding can occur immediately or can be delayed up to 30 days. Risk
factors are the large sessile polyp, polyp in the right side colon, cold snaring, elderly
patient, patient with underlying of chronic renal insufficiency and the coagulation
status of the patient. The delayed bleeding occurs in up to 2% of patients which
develops mostly within 5-7 days after polypectomy.1 Endoscopic treatment including
endoscopic band ligation (EBL) is the mainstay for post-polypectomy bleeding with

89
 various techniques. EBL is known as the standard treatment for esophageal variceal
bleeding. Recently, EBL has been widely used for the treatment of many non-variceal
gastrointestinal bleeding such as angiodysplasia, Dieulafoy’s lesion, Mallory-Weiss
tears, polypectomy bleeding, and colonic diverticular bleeding.2 EBL has also been
reported to have a role as the treatment of gastric, duodenal and colonic perforations.3

References
1. Hong SP. How do I manage post-polypectomy bleeding? Clin Endosc
2012;45:282-4.
2. Ji JS, Cho YS. Endoscopic band ligation: beyond prevention and management
of gastroesophageal varices. World J Gastroenterol 2013;19:4271-6.
3. Han JH, Lee TH, Jung Y, et al. Rescue endoscopic band ligation of iatrogenic
gastric perforations following failed endoclip closure. World J Gastroenterol
2013;19:955-9.

90
 Piyapan Prueksapanich, M.D.
Case 5 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

An 88-year-old male with type 2 diabetes mellitus and hypertension presented

with iron deficiency anemia. A colonoscopy revealed a hemi-circumferential mass
measured as 5 cm in size at the rectosigmoid colon (Figure 1). A colonoscope was
able to pass through the location and showed no synchronous lesion. Under NBI
exam, it showed irregular, elongated, tortuous vessels with some disrupted and absent
vessels area which was compatible with NBI international colorectal endoscopic
(NICE) classification type III (Figures 2 and 3). Pathology confirmed as an invasive
adenocarcinoma of the colon. A computerized tomography was done for staging and
showed focal thicken wall of the upper sigmoid colon without pericoloic fat stranding
or sentinel node.

Figure 1 A hemi-circumferential
mass measured as 5 cm in size. at
the rectosigmoid colon.

91
 Figures 2 and 3 NBI showed dark brown mucosa with irregular, elongated, tortuous
vessels and some area of the mucosa contained disrupted with absent vessels pattern.

Diagnosis:
Invasive adenocarcinoma of the colon.

Discussion:
Colonoscopy is one of investigations for patients with iron deficiency anemia.
Although, previous studies showed NBI did not increase adenoma or polyp detection
rates as compare to the new high definition white light colonoscopy1, 2, However NBI
could enhance lesion characterization. According to NBI International Colorectal
Endoscopic (NICE) Classification, the lesion color, the surface pit pattern and the
microvascular architecture were evaluated. NICE type III provides a high accuracy to
diagnose deeply SM-invasive carcinoma.3

References
1. Dinesen L, Chua TJ, Kaffes AJ. Meta-analysis of narrow-band imaging versus
conventional colonoscopy for adenoma detection. Gastrointest Endosc
2012;75:604-11.
2. Nagorni A, Bjelakovic G, Petrovic B. Narrow band imaging versus conventional
white light colonoscopy for the detection of colorectal polyps. Cochrane
Database Syst Rev 2012;1:CD008361.
3. Iwatate M, Ikumoto T, Hattori S, et al. NBI and NBI Combined with Magnifying
Colonoscopy. Diagn Ther Endosc 2012;2012:173269.

92
 Sasipim Sallapant, M.D.
Case 6 Rapat Pittayanon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 63-year-old female with underlying of ischemic heart disease and diabetes
admitted to the intensive care unit with a diagnosis of acute pyelonephritis and septic
shock. She had been treated with intravenous ceftriaxone and vasopressor. Two days
later, she presented with a small amount of coffee ground content via the NG tube. She
became hypotensive. Her abdomen was distended with hypoactive bowel sound but
no tenderness. The upper endoscopy was performed and showed multiple small ulcers
in the gastric body (Figure 1). A deeper push with a gastroscope demonstrated an area
of sharply demarcated necrotic mucosa in the third part of duodenum (Figures 2 and 3).
She then underwent an emergency exploratory laparotomy. The operative
finding was suggestive of long segment small bowel gangrene. The patient failed to
recover from the infection and finally succumbed.

Figure 1 Multiple ulcers in gastric body

93
 Figures 2 and 3 EGD showed well demarcated area of necrotic tissue at
the 3rd part of duodenum (arrow).

Diagnosis:
Acute mesenteric ischemia (AMI) causing infarction of the entire small bowel.

Discussion:
Ethiopathogeneses of acute arterial mesenteric ischemia include SMA embolus,
SMA thrombosis, nonocclusive mesenteric ischemia (NOMI). NOMI is responsible for
20% to 30% of AMI.1 A spectrum of bowel injury ranges from transient bowel function
alteration to transmural gangrene with multiple organ failure. If intestinal infarction
developed, the mortality rate can be as high as 70%.2 Identification of AMI requires a
high index of suspicion.
Unexplained abdominal distention or gastrointestinal bleeding may be the
only symptom and sign of AMI when pain is absent, especially when AMI is due to
NOMI.3 Currently, CT angiography is the mainstay for diagnosis.4 Endoscopy is not
routinely indicated.5 In certain difficult cases, this etiology cannot be predicted before
performing EGD.
The endoscopic spectrum of intestinal ischemia includes edema, pale mucosa,
erosion, ulcer, hemorrhage, and dark bluish necrotic tissue with segmental or
circumferential involvement. The presence of pseudomembrane overlying the intestinal
mucosa can develop. The well demarcated margin of lesion is the characteristic of
mesenteric ischemia.3

94
References
1. Acosta S. Epidemiology of mesenteric vascular disease: clinical implications.
Semin Vasc Surg 2010;23:4–8.
2. Oldenburg WA, Lau LL, Rodenberg TJ, et al. Acute mesenteric ischemia: a
clinical review. Arch Intern Med 2004;164:1054–62.
3. Alhan E, Usta A, Çekiç A, et al. A study on 107 patients with acute mesenteric
ischemia over 30 years. Int J Surg 2012;10:510-3.
4. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia:
systematic review and meta-analysis. Radiology 2010;256:93–101.
5. Early DS, Ben-Menachem T, Decker GA, et al. Appropriate use of GI endoscopy.
Gastrointest Endosc 2012;75:1127-31.

95
 Satimai Aniwan, M.D., M.Sc.
Case 7 Yudthana Sattawatthamrong, M.D.
Rungsun Rerknimitr, M.D.

An 80-year-old female presented with abdominal pain and abdominal

distension. Physical examination demonstrated that he had sinus tachycardia.
Her abdomen was markedly distended with normal bowel sound. There were no
tenderness and no ascites. Laboratory results showed a leukocytosis. Plain abdomen
x-ray revealed markedly dilated small bowel and colon (Figure 1). A colonoscopy
was performed. The scope was able to pass to 20 cm from the anus. Then the lumen
was narrow with inflamed mucosa with thick exudate (Figures 2-5). Tatoo was done.
Biopsy was performed. The diagnosis was gangrenous ischemic colitis. She underwent
an emergency surgical exploration. Operative findings showed colonic necrosis with
reduction in vascular supply started from sigmoid colon to proximal colon. Left
hemicolectomy was performed (Figures 6 and 7). Histology was compatible with
ischemic colitis with no evidence of vasculitis or thrombosis.

Figure 1 Generalize dilatation

of small bowel and colon.

96
Figures 2-5 Diffuse thick exudate on an inflamed colonic mucosa starting from
the sigmoid colon to the transverse colon.

Figures 6 and 7 Surgical specimen showed discoloration of colonic wall with

transitional zone.

97
 Diagnosis:
Gangrenous ischemic colitis

Discussion:
Clinical presentations of ischemic colitis may be classified into non-gangrenous
and gangrenous from.1 A gangrenous ischemic colitis is an uncommon form occurring
in 15% of colonic ischemia.2 Gangrenous ischemic colitis is quite different from
usual non-gangrenous ischemic colitis because it develops in a rapid progression and
leads to a fatal outcome.1 Patients with gangrenous colitis commonly present with
nausea/vomiting and hyperleukocytosis whereas hematochezia and diarrhea are less
frequently found than that of in patients with non-gangrenous from.3 Most patients
required an emergency operative treatment. Many medical comorbidities have been
reported as risk factors for infarction including hypertension, chronic renal disease,
diabetes mellitus, and history of cancer.3

References
1. Theodoropoulou A, Koutroubakis IE. Ischemic colitis: clinical practice in
diagnosis and treatment. World J Gastroenterol 2008;14:7302-8.
2. Baixauli J, Kiran RP, Delaney CP. Investigation and management of ischemic
colitis. Cleve Clin J Med 2003;70:920-1, 925-6, 928-30 passim.
3. Barouk J, Gournay J, Bernard P, et al. [Ischemic colitic in the elderly: predictive
factors of gangrenous outcome]. Gastroenterol Clin Biol 1999;23:470-4.

98
 Kessarin Thanapirom, M.D.
Case 8 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 72-year-old female was brought to an emergency room for a history of
hematochezia. She had a history of chronic kidney disease, coronary artery disease,
and diabetes mellitus. Three days before admission, she passed maroon stool without
abdominal pain. On physical examination, she was hypostensive and appeared anemic.
After intravenous fluid resuscitation and rapid bowel preparation, a colonoscopy was
performed. Colonoscopy showed segmental erythema with longitudinal ulcers, and
subepithelial hemorrhage at the rectosigmoid colon (Figures 1-3). A well-demarcated
line between normal and abnormal area was demonstrated. Biopsy was performed.
The diagnosis was ischemic colitis (non-gangrenous type).

Figures 1-3 Colonoscopy revealed segmental colonic erythema with ulcerations

and subepithelial hemorrhage at the rectosigmoid colon.

99
 Diagnosis:
Ischemic colitis (non-gangrenous type)

Discussion:
Non-gangrenous ischemic colitis occurred in 80-85% of ischemic colitis cases.1
Usual clinical manifestation is a sudden onset of left lower quadrant abdominal pain,
followed by a passage of bright red blood per rectum. Most common location of ischemic
colitis is left-sided colon (80%).2 Colonoscopy and biopsy play an important role for the
early diagnosis. Typical endoscopic findings of transient ischemic colitis are petechial
hemorrhages, edematous with fragile mucosa, segmental erythema, scattered erosion,
longitudinal single linear ulcerations, and sharply defined segment of involvement.2
Later, blue–black mucosal nodules with a darker, dusky background can be seen. If no
clinical signs of complete gangrene or perforation, the managements include usually
bowel rest, parenteral fluid administration, and broad-spectrum antibiotic. The natural
course of disease is usually transient and the complete reversibility can be expected in
50% of patients.3

References
1. Theodoropoulou A, Koutroubakis IE. Ischemic colitis: clinical practice in
diagnosis and treatment. World J Gastroenterol 2008;14:7302-8.
2. Zou X, Cao J,YaoY, et al. Endoscopic findings and clinicopathologic characteristics
of ischemic colitis: a report of 85 cases. Dig Dis Sci 2009;54:2009-15.
3. Montoro MA, Brandt LJ, Santolaria S, et al. Clinical patterns and outcomes
of ischaemic colitis: results of the Working Group for the Study of Ischaemic
Colitis in Spain (CIE study). Scand J Gastroenterol 2011;46:236-46.

100
 Narisorn Lakananurak, M.D.

Case 9
Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
Sombat Treeprasertsuk, M.D., Ph.D.
A 65-year-old Thai male underwent a colonoscopy for colorectal cancer
screening. He had a history of essential thrombocytosis for 30 years. He had been
treated with hydroxyurea. Recently, he was asymptomatic with normal platelets
count. Physical examination showed splenomegaly. A routine colonoscopy for colon
cancer screening was performed. White light endoscopy and NBI exam revealed blue-
colored, dilated, tortuous veins starting from the rectum (Figure 1), to the sigmoid
colon (Figure 2), and the descending colon (Figure 3).

Figure 1 Blue-colored, dilated, tortuous veins in the rectum (left) and under narrow
band imaging exam (right).

101
 Figure 2 Blue-colored, dilated, tortuous veins in the sigmoid colon (left) and under
narrow band imaging exam (right).

Figure 3 Blue-colored, dilated, tortuous veins in the descending colon (left) and
under narrow band imaging exam (right).

Diagnosis:
Colonic varices

Discussion:
Colonic varices are one pattern of ectopic varices. The site of colonic varices
depends on venous systems that draining venous blood from the colon i.e. superior
mesenteric vein (cecum to transverse colon), inferior mesenteric vein (descending
colon to rectum).1 The prevalence of colonic varices is about 34-46% in patients with

102
cirrhosis.2 About five percent of patients with myeloproloferative disorders such as
essential thrombocytosis may develop asymptomatic colonic varices.3 Endoscopic
findings are serpiginous, dilated, blue-colored veins which is similar to varices in the
esophagus and stomach.1

References
1. Almadi MA, Almessabi A, Wong P, et al. Ectopic varices. Gastrointest Endosc
2011;74:380-8.
2. Dhiman RK, Saraswat VA, Choudhuri G, et al. Endosonographic, endoscopic,
and histologic evaluation of alterations in the rectal venous system in patients
with portal hypertension. Gastrointest Endosc 1999;49:218-27.
3. Jain P, Nijhawan S. Portal vein thrombosis: etiology and clinical outcome of
cirrhosis and malignancy-related non-cirrhotic, non-tumoral extrahepatic
portal venous obstruction. World J Gastroenterol 2007;13:5288-9.

103
 Sayamon Kimtrakool, M.D.
Case 10 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 20-year-old male presented with chronic right lower abdominal pain with
significant weight loss for 3 months. He had a history of bilateral episcleritis. On
physical examination, he had anemia and pretibial edema of both legs. Colonoscopy
showed multiple ileal ulcers with inflamed mucosa at the terminal ileum, however
colonic mucosa appeared normal. Histology revealed chronic and mild acute ileitis.
AFB stain and PCR-TB study were negative.

Figures 1 and 2 Multiple ulcers with inflamed mucosa at the terminal ileum.

104
 Figures 3 and 4 White light imaging showed edematous mucosa with ulcerative
inflammation and NBI imaging exam showed dark color area of inflammation.

Diagnosis:
Isolated Crohn’s disease (CD) in the terminal ilum.

Discussion:
Isolated ileal CD can be found in about 30% of CD patients.1 Typically, clinical
presentations of CD are abdominal pain, diarrhea, fever, weight loss and extraintestinal
features. The common GI involved segments are terminal ileum and colon. Immune
response is one of the importance roles for developing CD. As a result, CD usually
occurs in terminal ileum which is rich in gut-associated lymphoid tissues.2 However,
the isolated lesion is considered as rare.

References
1. Gasche C, Scholmerich J, Brynskov J, et al. A simple classification of Crohn’s
disease: report of the Working Party for the World Congresses of Gastroenterology,
Vienna 1998. Inflamm Bowel Dis 2000;6:8-15.
2. Caprilli R. Why does Crohn’s disease usually occur in terminal ileum? J Crohns
Colitis 2008;2:352-6.

105
 Sayamon Kimtrakool, M.D.
Case 11 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 54-year-old woman underwent a colorectal cancer screening. Her fecal

immunochemical test was positive. Colonoscopy was performed and revealed a 0.7-
cm sessile polyp withish exudate covered on the hyperemic smooth surface mucosa
at the descending colon (Figures 1 and 2). Narrow band imaging (NBI) showed a dark
color surface polyp with round pit pattern surrounded by normal capillary vessels
(Figures 3 and 4).
Polypectomy was performed. Histological diagnosis was an inflammatory
polyp.

Figures 1 and 2 White light colonoscopy showed a sessile polyp with hyperemia
smooth surface covered by whitish exudate.

106
 Figures 3 and 4 Narrow band imaging (NBI) with magnification revealed a uniform
dark color surface polyp with normal capillary pattern and some area of the polyp
contained whitish exudate.

Diagnosis:
Colonic inflammatory polyp

Discussion:
Inflammatory polyp of the colon is a result of mucosal inflammation and
regeneration with healing process after inflammation or ulceration. The etiology of
inflammatory polyps may be classified into two group; pseudopolyps and prolapse-
induced inflammatory polyp.1 Pseudopolyps are the most common cause of
inflammatory polyps and associated with inflammatory bowel disease (IBD) which
can be found about 10-20% of the patients.2 Inflammatory polyps may also develop
after severe colitis from any causes.3
Endoscopic appearances are vary; a sessile or pedunculated, single or multiple,
smooth with hyperemic mucosa with/without exudation, or erosion on the surface of
polyps.
Inflammatory polyps do not significantly increase the risk for dysplasia or
carcinoma.4

107
 References
1. Chetty R, Bhathal PS, Slavin JL. Prolapse-induced inflammatory polyps of the
colorectum and anal transitional zone. Histopathology 1993;23:63-7.
2. Hizawa K, Nakamori M, Taniguchi M, et al. Gastrointestinal: inflammatory
granulation polyp of the colon. J Gastroenterol Hepatol 2008;23:1307.
3. Iofel E, Kahn E, Lee TK, et al. Inflammatory polyps after necrotizing enterocolitis.
J Pediatr Surg 2000;35:1246-7.
4. Odze R. Diagnostic problems and advances in inflammatory bowel disease.
Mod Pathol 2003;16:347-58.

108
 Sittikorn Linlawan, M.D.
Case 12 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 48-year-old man with a family history of colorectal cancer underwent
a colonoscopy screening. White light image (Figure 1) showed a 1.2 cm semi-
pedunculated polyp (Paris classification Isp) at the sigmoid colon. Under magnifying
NBI (dual focus) the pits were confirmed as villous pattern and surrounded by the
thick, high density with tortous brown vessels (Sano’s classification type IIIa). It was
compatible with NICE classification type 2 (Figure 2). Polyp removal was done (Figure
3). Pathology confirmed as a villous adenoma.

Figure 1 White light image of a semi- Figure 2 Narrow band image of villous
pedunculated polyp (Isp). adenoma.

109
 Figure 3 Snare polypectomy

Diagnosis:
Villous adenoma

Discussion:
Colorectal cancer (CRC) is a major cause of death worldwide. Magnified
colonoscopy is a useful diagnostic tool for a real-time evaluation of many polypoid
lesions. Under magnifying NBI, microvascular architecture and surface pits pattern
are clearly demonstrated. Its role is also for the assessment of the depth of invasion
in early CRC without the need for dye spraying.1, 2 Villous adenoma can be showed
as type IIIa in Sano’s classification and type 2 in NICE classification. According the
ESGE guideline, patients with villous adenoma was classified as a high risk group.3 The
surveillance colonoscopy at 3 years after polypectomy is recommended.3

References
1. Hewett DG, Kaltenbach T, Sano Y,et al. Validation of a simple classification
system for endoscopic diagnosis of small colorectal polyps using narrow-band
imaging. Gastroenterology 2012;143:599-607.
2. Tanaka S, Sano Y. Aim to unify the narrow band imaging (NBI) magnifying
classification for colorectal tumors: current status in Japan from a summary
of the consensus symposium in the 79th Annual Meeting of the Japan
Gastroenterological Endoscopy Society. Dig Endosc 2011;23 Suppl 1:131-9.
3. Hassan C, Quintero E, Dumonceau JM, et al. Post-polypectomy colonoscopy
surveillance: European Society of Gastrointestinal Endoscopy (ESGE) Guideline.
Endoscopy 2013;45:842-64.

110
 Sittikorn Linlawan, M.D.
Case 13 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 51-year-old female underwent colonoscopy for a colorectal cancer screening.
She also complained of vague abdominal pain for a month. Colonoscopy showed a
linear white movable parasite in the terminal ileum (Figures 1 and 2). She was treated
with praziquantel 600 mg single dose, then she passed a tapeworm (95 cm-in-length)
(Figure 3). After an ink injection for identification, the diagnosis was confirmed as
Taenia sagitnata infestation (Figure 4).

Figures 1 and 2 Taenia saginata in the terminal ileum

111
 Figures 3 and 4 Taenia saginata and a proglottis of Taenia saginata after an ink injection.

Diagnosis:
Taenia saginata infestation

Discussion:
Ingestion of imperfectly or raw cooked beef may result to T. saginata infestation.
In the host’s stomach, proteolytic enzymes digest the capsule of cysticerci and later
a scolex attaches to the intestine. Subsequently, it develops to an adult tapeworm.1
T. saginata is a large tapeworm with an average size of 2-5 meter and its size may be up
to 6-8 meter in length.1 The adult worm may contain more than hundreds to thousands
of proglottids. Taenia species bud off distal segments from the rest of the body that
are passed through the feces.1 Most patients carrying an adult T. saginata tapeworm
are asymptomatic. Rarely, non-specific symptoms, such as abdominal discomfort,
epigastric pain, nausea, vomiting, diarrhea, weight loss, and perianal symptoms
associated with the discharge of proglottids, can be observed.2 The treatment of
human intestinal Taeniasis (T. saginata and T. solium) is usually effective (85–98%)
with anthelmintics such as praziquantel (5 mg/kg, single oral dose) or niclosamide ( 2
g, single oral dose).3

112
References
1. Ito A, Nakao M, Wandra T. Human Taeniasis and cysticercosis in Asia. Lancet
2003;362:1918-20.
2. Craig P, Ito A. Intestinal cestodes. Curr Opin Infect Dis 2007;20:524-32.
3. Howell J, Brown G. Education and imaging. Gastrointestinal: beef tapeworm
(Taenia saginata). J Gastroenterol Hepatol 2008;23:1769.

113
 Sittikorn Linlawan, M.D.
Case 14 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 44-year-old man presented with chronic diarrhea and abdominal pain. Stool
examination and stool culture were unremarkable. Colonoscopy was performed. A
giant long roundworm was detected at the ascending colon (Figures 1 and 2). The
diagnosis was Ascaris lumbricoides infestation. His clinical symptoms improved after
a single dose of albendazole.

Figures 1 and 2 A giant long roundworm was detected at the ascending colon.

114
Diagnosis:
Ascaris lumbricoides infestation

Discussion:
Ascaris infection in human occurs after accidentally after an ingestion of
contaminated food with the parasite’s eggs. The eggs become larvae that penetrate the
duodenal wall and enter blood circulation to heart and lungs.1 The larvae pass from
the respiratory system and return to the small intestine after swallowing.1 Male and
female adult worms size are 15-25 cm and 20-35 cm respectively. Symptoms of adult
worm infestation or chronic ascariasis are abdominal pain, distension, nausea, and
diarrhea. Entangled adult worms have also been reported as leading to mechanical
intestinal obstruction in 0.005-2 per 1,000 infestations per year.2 Treatments of choice
are a single-dose oral mebendazole (500 mg), albendazole (400 mg), with response
rates in 88-95% of patients.3 Colonoscopy and EGD may be useful in removing the
obstructive masses formed by the worms.3

References
1. Dold C, Holland CV. Ascaris and ascariasis. Microbes Infect 2011;13:632-7.
2. Crompton DW. Ascaris and ascariasis. Adv Parasitol 2001;48:285-375.
3. Keiser J, Utzinger J. Efficacy of current drugs against soil-transmitted helminth
infections: systematic review and meta-analysis. JAMA 2008;299:1937-48.

115
 Sittikorn Linlawan, M.D.
Case 15 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 53-year-old man presented with painless rectal bleeding. He had a history

of chronic constipation. Colonoscopy was done. In retroflexed view, colonoscopy
showed cherry-red spots of prominent internal hemorrhoids (Figures 1 and 2).

Figures 1 and 2 White light imaging showed prominent internal hemorrhoids with
cherry-red spots and dark color of the spots was also demonstrated under NBI.

116
Diagnosis:
Internal hemorrhoids with cherry-red spots

Discussion:
Internal hemorrhoids (originate above the dentate line) classified into 4
grades: Grade 1, hemorrhoids with bleeding; Grade 2, hemorrhoids with bleeding
and protrusion, with spontaneous reduction; Grade 3, hemorrhoids with bleeding
and protrusion that require manual reduction; and Grade 4, prolapsed hemorrhoids
that cannot be replaced.1 With the recent advancement in video endoscopy including
NBI, hemorrhoids can be clearly demonstrated the stigmata with the determination
for the site of potentially bleeding such as the Cherry-red spots. A proposed theory
is that of the displacement of anal lining mucosa of the anal cushions.2 Conservative
treatment is effective for an early stage. High dietary fiber, oral fluids, non-steroidal
anti-inflammatory drugs (NSAIDs), sitz baths, and rest are recommended. Several
new minimally invasive surgical procedures including stapled mucopexy and
doppler-guided hemorrhoid artery ligation, are now offered to patients with grade 3
hemorrhoids. Endoscopic infrared coagulation therapy (IRC) improved visibility and
efficiency. In addition, simultaneous treatment of symptomatic internal hemorrhoids at
the time of endoscopy was allowed.3

References
1. Lorenzo-Rivero S. Hemorrhoids: diagnosis and current management. Am Surg
2009;75:635-42.
2. Altomare DF, Giuratrabocchetta S. Conservative and surgical treatment of
haemorrhoids. Nat Rev Gastroenterol Hepatol 2013;10:513-21.
3. McLemore EC, Rai R, Siddiqui J, et al. Novel endoscopic delivery modality
of infrared coagulation therapy for internal hemorrhoids. Surg Endosc
2012;26:3082-7.

117
 Sayamon Kimtrakool, M.D.
Case 16 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 62-year-old female underwent a colonoscopy for a colorectal cancer

screening. She had end-stage renal disease and has been on a regular hemodialysis.
She has no symptom. Colonoscopy showed multiple small shallow clean base discrete
ulcers with acute inflammation edge (detected under NBI) along the descending
colon (Figure 1). Biopsy was taken. Pathology showed only mild ischemic change of
ulcerative tissue lesion.

Figure 1 Colonoscopy showed multiple small shallow clean base ulcers along the
descending colon .The inflamed edge was enhanced by NBI.

118
Diagnosis:
End-stage renal disease related ischemic colitis

Discussion:
Chronic hemodialysis patients usually have higher risks to develop intestinal
ischemia such as atherosclerosis, hemodialysis induced hypotension, and others
comorbid conditions including arrhythmia, myocardial infarction, and congestive heart
failure.1 All of these factors can contribute to the poor perfusion to colonic wall and
eventually can develop ischemic colitis. Important factors for prediction the severity in
chronic hemodialysis related ischemic colitis are the short duration between symptoms
occurrence until the diagnosis and patient’s co-morbid conditions.2, 3
To prevent the disease, physicians should avoid or minimize the hypotensive
period between dialysis sessions. Intravenous fluid replacement and bowel rest should
be managed in almost cases and empirical antibiotics should be designed in only
moderate to severe cases.1

References
1. Saeed F, Agrawal N, Greenberg E, et al. Lower gastrointestinal bleeding in
chronic hemodialysis patients. Int J Nephrol;2011:272535.
2. Flobert C, Cellier C, Berger A, et al. Right colonic involvement is associated
with severe forms of ischemic colitis and occurs frequently in patients with
chronic renal failure requiring hemodialysis. Am J Gastroenterol 2000;95:195-8.
3. Norden MA, Rabb H. Two haemodialysis patients with unclear abdominal
symptoms of similar origin. Nephrol Dial Transplant 2001;16:2426-8.

119
 Kessarin Thanapirom, M.D.
Case 17 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
Asymptomatic 64-year-old man underwent a colonoscopy for colorectal cancer
screening. Colonoscopy revealed a large sessile polyp with cerebreform pit pattern
and avascular capillary network (Sano’s classification type IIIb) (Figure 1). Under
NBI exam, the endoscopic finding was compatible with NICE classification type 3.
Endoscopic mucosal resection was performed. Pathology showed an intramucosal
well-differentiated adenocarcinoma.

Figure 1 A large sessile polyp with cerebreform pit pattern and avascular capillary
network (Sano’s classification type IIIb) that compatible with NICE classification
type 3.

120
Diagnosis:
Intramucosal colon cancer

Discussion:
Half of patients with early colorectal cancer have intramucosal cancer or
noninvasive cancer.1 Endoscopic characteristic findings of intramucosal cancer are
varied, 80% of the lesions have a size less than 2 cm, 56% of lesions have sessile
morphology.2 Most patients with intramucosal cancer have cancer arising on the
adenoma background and have no angiolymphatic invasion.1 Intramucosal cancer
usually have a good prognosis, with a low recurrent rate after a complete tumor
removal either by surgery or endoscopy.1 A previous study reported that no patient
developed recurrence during 20 months follow-up period after an endoscopic mucosal
resection.1

References
1. Kim MN, Kang JM, Yang JI, et al. Clinical features and prognosis of early
colorectal cancer treated by endoscopic mucosal resection. J Gastroenterol
Hepatol 2011;26:1619-25.
2. Mainprize KS, Mortensen NJ, Warren BF. Early colorectal cancer: recognition,
classification and treatment. Br J Surg 1998;85:469-76.

121
 Sayamon Kimtrakool, M.D.
Case 18 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 65-year-old-female underwent colonoscopy for a colorectal cancer screening.

She has no GI symptoms. Colonoscopy revealed one polyp, Isp (Paris classification) size
1.2 cm with central depression and ulceration in the ascending colon (Figure 1). NBI
showed a high density of capillary network with lack of uniformity (Sano’s classification
typeIIIa ). The polyp also showed the absence of surface pattern compatible with NBI
international Colorectal Endoscopic (NICE) type 3 (Figure 2). The sessile polyp was
removed by an endoscopic mucosal resection (EMR) by using a snare polypectomy
and then one hemoclip was applied to cover the mucosal defect (Figures 3 and 4).
Histology demonstrated well-differentiated adenocarcinoma with abnormal gland
infiltration through muscularis mucosa into submucosa. The diagnosis was submucosal
invasive colonic cancer (well-differentiated adenocarcinoma).

Figures 1 and 2 White light imaging showed a 1.2 cm colonic polyp Isp
with central ulceration and depression. Narrow band imaging showed
darker color of polyp surface relative to the background. This was
read as Sano’s classification type IIIa, and NICE classification type 3.

122
 Figures 3 and 4 En-
doscopic mucosal
resection

Diagnosis:
Submucosal invasive colonic cancer (Well-differentiated adenocarcinoma)

Discussion:
NBI exam during colonoscopy provides a high accurate test for the differentiation
of neoplastic from non-neoplastic polyps. Comparing with pathology, NBI provided
91% sensitivity and 82.6% specificity.1 Additionally, NBI technique can provide a
high confidence in diagnosis of flat and diminutive (< 5 mm) polyps.1 The evaluation is
based on microvascular architecture change reading for the angiogenesis in carcinoma
development.2 Vessels and surface patterns read by magnifying NBI are essential for
Sano’s classification and NBI International Colorectal Endoscopic (NICE) classification.
A recent study demonstrated that NICE classification type 3 could predict a deep
submucosal (SM-d) invasive colonic cancer with high accuracy.3

References
1. McGill SK, Evangelou E, Ioannidis JP, et al. Narrow band imaging to differentiate
neoplastic and non-neoplastic colorectal polyps in real time: a meta-analysis of
diagnostic operating characteristics. Gut 2013.
2. Iwatate M, Ikumoto T, Hattori S, et al. NBI and NBI Combined with Magnifying
Colonoscopy. Diagn Ther Endosc 2012;2012:1-10.
3. Hayashi N, Tanaka S, Hewett DG, et al. Endoscopic prediction of deep
submucosal invasive carcinoma: validation of the Narrow-Band Imaging
International Colorectal Endoscopic (NICE) classification. Gastrointest Endosc
2013;78:625-32.

123
 Puth Muangpaisarn, M.D.
Case 19 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 62-year-old Thai female underwent colonoscopy for a colorectal cancer

screening. Colonoscopy showed a sessile polyp sized 0.5 cm at the descending colon.
NBI showed vascular pattern with high density of capillary vessels (Sano’s classification
type IIIa). Pit pattern showed branch-like pit (Kudo’s classification type IV). Based
on the NICE classification, its color was browner relative to the background and its
vessels were thick brown. Surface pattern showed branch white structure surrounded
by brown vessels. Therefore it was compatible with NICE classification type II (Figure
1). Polypectomy was performed. Histopathology revealed a tubular adenoma with high
grade dysplasia.

Figure 1 White light imaging (a) showed a sessile polyp with branch-liked pit pattern
and high density vascular pattern under NBI (b).

124
Diagnosis:
Tubular adenoma with high grade dysplasia

Discussion:
Technically, NBI can enhance the visualization of mucosal surface structure and
vascular pattern and help for identifying colonic neoplasia.1 Several studies supported
the effectiveness in differential diagnoses of colorectal polyps.1 NBI international
colorectal endoscopic (NICE) classification system is a simple categorical classification
(types 1–3) based on 3 parameters: (i) lesion color; (ii) microvascular architecture; and
(iii) surface pattern.2 Most likely pathology in NICE type II is adenoma.2 In this case,
based on the NICE classification, NBI read as type II that compatible with adenoma
that later confirmed by pathology.

References
1. Uraoka T, Saito Y, Ikematsu H, et al. Sano’s capillary pattern classification for
narrow-band imaging of early colorectal lesions. Dig Endosc 2011;23 Suppl
1:112-5.
2. Iwatate M, Ikumoto T, Hattori S, et al. NBI and NBI Combined with Magnifying
Colonoscopy. Diagn Ther Endosc 2012;2012:173269.

125
 Sittikorn Linlawan, M.D.
Case 20 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 46-year-old male presented with intermittent cramping abdominal pain,

along with postprandial vomiting, and melena. He had undergone a Roux-en-Y
hepaticojejunostomy due to common bile duct injury from the previous laparoscopic
cholecystectomy 3 years ago. One day before admission, he developed an
acute intermittent abdominal pain followed by a severe vomiting. He also passed
melena. Push enteroscopy revealed anastomotic ulcer with granulation tissue at the
jejunojejunostomy site (Figure 1). During enteroscopy there was a small bowel loop
protruding through the anastomotic site representing the intussusceptum (Figure 2).
However, there was no sign of gangrene. Later his clinical symptoms improved by a
conservative management.

Figure 1 Anastomotic ulcer with Figure 2 Antergrade jejunojejunal

granulation tissue at the jejunoje- intussusception without evidence of
junostomy site. gangrene.

126
Diagnosis:
Intermittent jejunojejunal intussusception with anastomotic ulcer

Discussion:
Jejunojejunal intussusception is an uncommon complication of hepatico-
jejunostomy.1 Jejunojejunal intussusception can cause acute or chronic bowel
obstruction, haemorrhage, and perforation.2 A computed tomography scan of the
abdomen with oral and intravenous contrast is the most accurate diagnostic tool for
diagnosis. It typically showed a target lesion, reniform pattern (bi-lobed mass with
peripheral high attenuation due to thickened bowel wall) and sausage pattern.3 It
may resolve with conservative management because of intermittent intussusception.
However, endoscopic diagnosis is sometimes possible such as in this patient. Surgical
treatment is usually not indicated if there is no gangrenous change, perforation or
stenosis.4

References
1. Tapia J, Murguia R, Garcia G, et al. Jejunostomy: techniques, indications, and
complications. World J Surg 1999;23:596-602.
2. Akter F, Harilingam M. Jejunal intussusception: a cause of upper gastrointestinal
bleeding? BMJ Case Rep 2012;2012.
3. Byrne AT, Geoghegan T, Govender P, et al. The imaging of intussusception. Clin
Radiol 2005;60:39-46.
4. Napora TE, Henry KE, Lovett TJ, et al. Transient adult jejunal intussusception.
J Emerg Med 2003;24:395-400.

127
 Sayamon Kimtrakool, M.D.
Case 21 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 75 year-old-male presented with chronic left lower abdominal quadrant pain.
Five months earlier, he had developed left lower abdominal pain and mucous diarrhea
for one week. He was diagnosed as acute diverticulitis and treated with antibiotic. His
diarrhea resolved however his abdominal pain still persisted. He had no fever and
no weight loss. On abdominal examination, he had abdominal tenderness at the left
lower quadrant. A compute tomography (CT) scan of abdomen revealed a segmental
circumferential bowel wall thickening involving the mid portion of sigmoid colon
and distal descending colon. There were also multiple diverticula (Figures 1 and 2).
A colonoscopy revealed pus emanating from one of the diverticular orifices (Figures
3 and 4)

Figures 1 and 2 A CT scan of the abdomen showed a segmental circumferential

bowel wall thickening of the sigmoid colon with multiple diverticula (arrow).

128
 Figures 3 and 4 Colonoscopy revealed pus emanating from a diverticular orifice
(arrow).

Diagnosis:
Smoldering diverticulitis

Discussion:
Diverticular disease has a wide clinical spectrum ranging from asymptomatic
disease to symptomatic or complicated diverticular disease.1 Patients with chronic
diverticular disease usually present with chronic abdominal pain which can be
misunderstood as irritable bowel syndrome (IBS). Chronic left lower abdominal pain
without the document of fever or leukocytosis in patients with a history of diverticulosis
defined the term “smoldering diverticulitis”.2 The diagnosis includes radiologic or
endoscopic finding of inflammed diverticula with no evidence of complications such
as abscess, obstruction or stricture.2 Surgical treatment should be preserved only for
patients who failed medical therapy.2, 3

References
1. Sheth AA, Longo W, Floch MH. Diverticular disease and diverticulitis. Am J
Gastroenterol 2008;103:1550-6.
2. Horgan AF, McConnell EJ, Wolff BG, et al. Atypical diverticular disease: surgical
results. Dis Colon Rectum 2001;44:1315-8.
3. Stocchi L. Current indications and role of surgery in the management of sigmoid
diverticulitis. World J Gastroenterol 2010;16:804-17.

129
 Piyapan Prueksapanich, M.D.
Case 22 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 70-year-old male presented with iron deficiency anemia. He had chronic

constipation with no significant weight loss. A colonoscopy was performed. In a
rectal retroflexion view, a 3-centimeter diverticuli was observed at 5 cm from the anal
verge (Figures 1 and 2). Under NBI exam, there was a diverticulum with a normal
vascular pattern. There was no stigmata of bleeding (Figure 3). The diagnosis was rectal
diverticulum.

Figures 1 and 2 In a rectal retroflexion view, NBI showed a 3-centimetered

diverticulum at rectum.

130
 Figure 3 NBI imaging
showed a normal vascular
pattern with no stigmata
of bleeding.

Diagnosis:
Rectal diverticulum

Discussion:
Diverticulum is not a common finding in the rectum because the rectum is
encased in firm musculature tissues and internal pressure is also constant with less
peristaltic activity than colon.1 Unlike colonic diverticulosis, the rectal diverticula are
usually solitary and considered to be true diverticula which generally larger than the
usual diverticula. They occurred at the point of weakness in the rectal wall. The etiologies
include congenital diverticulum and iatrogenic diverticulm developed postsurgical
trauma.1 Most of the rectal diverticula reported in the literature are asymptomatic.2

References
1. Lim CH, Wong M, Chew MH. Unusual cases of rectal mass. Rectal pocket
syndrome or iatrogenic rectal diverticulum. Gastroenterology 2013;145:e5-6.
2. Halpert RD, Crnkovich FM, Schreiber MH. Rectal diverticulosis: a case report
and review of the literature. Gastrointest Radiol 1989;14:274-6.

131
 Kessarin Thanapirom, M.D.
Case 23 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 68-year-old female known case of diabetes mellitus, hypertension, chronic
kidney disease presented with hematochezia for 1 day. Colonoscopy showed an active
diverticular bleeding from the ascending colon. Endoscopic therapy with adrenalin
injection followed by hemoclipping was performed. An immediate hemostasis was
achieved.

Figure1 Colonoscopic finding of a Figure2 Adrenaline injection and

bleeding diverticulum. hemoclipping was done with
successful endoscopic hemostasis.

132
Diagnosis:
Colonic diverticular bleeding

Discussion:
Diverticular bleeding is a common cause of lower gastrointestinal bleeding.
Patient with diverticular bleeding typically presents with an abrupt onset painless rectal
bleding The bleeding usually stop spontaneously.1 In active bleeding, colonoscopy is
an important tool for the diagnosis and treatment. Non-surgical treatment modalities
include endoscopic treatment and embolization. Results of the endoscopic therapy
including hemoclipping, electrocoagulation, endoscopic band ligation with or
without adrenaline injection are usually acceptable. The immediate hemostasis can
be obtained in 62% -100% of patients with a low rebleeding rate within 30 days.2-6

References
1. McGuire HH, Jr. Bleeding colonic diverticula. A reappraisal of natural history
and management. Ann Surg 1994;220:653-6.
2. Green BT, Rockey DC, Portwood G, Tarnasky PR, Guarisco S, Branch MS, Leung
J, Jowell P. Urgent colonoscopy for evaluation and management of acute lower
gastrointestinal hemorrhage: a randomized controlled trial. Am J Gastroenterol
2005;100:2395-402.
3. Bloomfeld RS, Rockey DC, Shetzline MA. Endoscopic therapy of acute
diverticular hemorrhage. Am J Gastroenterol 2001;96:2367-72.
4. Yen EF, Ladabaum U, Muthusamy VR, Cello JP, McQuaid KR, Shah JN.
Colonoscopic treatment of acute diverticular hemorrhage using endoclips. Dig
Dis Sci 2008;53:2480-5.
5. Kaltenbach T, Watson R, Shah J, Friedland S, Sato T, Shergill A, McQuaid K,
Soetikno R. Colonoscopy with clipping is useful in the diagnosis and treatment
of diverticular bleeding. Clin Gastroenterol Hepatol 2012;10:131-7.
6. Jensen DM, Machicado GA, Jutabha R, Kovacs TO. Urgent colonoscopy for
the diagnosis and treatment of severe diverticular hemorrhage. N Engl J Med
2000;342:78-82.

133
 Suppakorn Malikhao, M.D.
Case 24 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 78-year-old female known for malignant histiocytoma of the abdominal

wall with lung metastasis was admitted due to severe pneumonia. After receiving an
intravenous Meropenem for 2 weeks, she developed fever, abdominal pain, and watery
diarrhea. A stool test for clostridium difficile toxins was negative. A sigmoidoscopy
found multiple raised whitish plaques from the rectum to sigmoid colon. These
plaques ranged in size from small distinct nodules (5–15 mm) to a confluent layer of
pseudomembrane overlying the inflamed colonic mucosa. The colonic mucosa also
showed erythema, friability and edema (Figures 1 and 2). Biopsy was obtained. Her
symptoms improved after a treatment with oral vancomycin.

Figures 1 and 2 Multiple whitish raised, 5-10-mm plaques overlying an

erythematous, edematous mucosa.

134
Diagnosis:
Pseudomembranous colitis (PMC)

Discussion:
Clostridium difficile is the most common pathogen for nosocomial diarrhea. The
main risk factors are exposure to antibiotics and exposure to the organism.1, 2 Clinical
presentations of Clostridium difficile infection include diarrhea, usually nonbloody, and
colitis associated with severe abdominal pain with fever.1 Although stool studies are
now widely available, an endoscopic evaluation remains very useful in many aspects
such as; for excluding other pathology, for making the diagnosis, and for assessing
severity. Colonoscopy has generally been preferred over sigmoidoscopy because
the characteristic findings of pseudomembranes may be limited to the right colon in
approximately one-third of cases.1, 3 Endoscopic findings usually show characteristic
raised yellow-tan or white plaques with contact bleeding. These plaques coaleased
to form a layer of pseudomembrane overlying the inflammed mucosa. The colonic
mucosa may show erythema, friability, and edema.4 Other causes of diarrhea which
may mimic PMC, are medications/toxin (alcohol, NSAID, gold, etc.), other chronic
conditions (inflammatory bowel disease, ischemic colitis) and other infectious colitis
(Campylobacter, Salmonella, Shigella, Escherichia coli 0157:H7).3

References
1. Stanley JD, Bartlett JG, Dart BWt, et al. Clostridium difficile infection. Curr Probl
Surg 2013;50:302-37.
2. Stanley JD, Burns RP. Clostridium difficile and the surgeon. Am Surg 2010;76:235-
44.
3. Surawicz CM, McFarland LV. Pseudomembranous colitis: causes and cures.
Digestion 1999;60:91-100.
4. Kawamoto S, Horton KM, Fishman EK. Pseudomembranous colitis: spectrum
of imaging findings with clinical and pathologic correlation. Radiographics
1999;19:887-97.

135
 Phonthep Angsuwatcharakon, M.D., M.Sc.
Case 25 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 45-year-old homosexual, non-HIV infected man presented with bright red

blood per rectum after defecation. Rectal examination revealed a polypoid nodule in
the anal canal with contact bleeding. A colonoscopy was done and revealed a 1-cm.
papilliform nodule at the dentate line (Figures 1 and 2). A magnified NBI revealed
dilated and elongated microvessels in the papillae (Figures 3 and 4). The other parts of
colon were normal.

Figures 1 and 2 A 1 cm papilliform nodule at the dentate line.

136
 Figures 3 and 4 Magnifying NBI revealed dilated and elongated microvessels
in the papillae.

Diagnosis:
Condyloma acuminatum

Discussion:
Condyloma acuminatum is caused by human papilloma virus (HPV) infection1
and associated with the increased risk of anal, penile, cervical, vulva, vaginal, and
head and neck cancers.2 Condyloma acuminata can be diagnosed by inspection of a
typical verrucous or villiform appearance. NBI enhanced the vascular structures and
demonstrated dilated and elongated microvessels in the papillae, and the papillae of
the lamina propria were increased in length.3 Magnifying NBI is reported to be useful
for making a diagnosis of early-stage squamous cell carcinoma associated with HPV
infection. The finding of early cancer is irregular intraepithelial papillay capillary loop
which is similar to superficial squamous cell carcinoma of the esophagus.3, 4 In this
case, there is no evidence of squamous cell carcinoma by endoscopy or histology.

137
 References
1. Duggan MA, Boras VF, Inoue M, et al. Human papillomavirus DNA determination
of anal condylomata, dysplasias, and squamous carcinomas with in situ
hybridization. Am J Clin Pathol 1989;92:16-21.
2. Blomberg M, Friis S, Munk C, et al. Genital warts and risk of cancer: a Danish
study of nearly 50 000 patients with genital warts. J Infect Dis 2012;205:1544-
53.
3. Horimatsu T, Miyamoto S, Ezoe Y, et al. Education and gastrointestinal imaging:
case of early-stage squamous cell carcinoma of the anal canal diagnosed using
narrow-band imaging system with magnification. J Gastroenterol Hepatol
2012;27:1406.
4. Chou YP, Saito Y, Matsuda T, et al. Novel diagnostic methods for early-stage
squamous cell carcinoma of the anal canal successfully resected by endoscopic
submucosal dissection. Endoscopy 2009;41 Suppl 2:E283-5.

138
 Sasipim Sallapant, M.D.
Case 26 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

An asymptomatic 62-year-old male underwent a colonoscopy for colorectal

cancer screening. A colonoscopy showed a 0.5 cm sessile polyp at the appendiceal
orifice. Under NBI exam, it showed uniform round pit central with central dark dots
(type I Sano’s classification) which was compatible with type 1 NICE classification.
Snare polypectomy was successfully done without complication. Pathology confirmed
as a hyperplastic polyp.

Figure 1 White light image (A, B) of a 0.5 cm sessile colonic polyp at the
appendiceal orifice.

139
 Figure 2 NBI image of type 1 NICE classification.

Diagnosis:
Hyperplastic polyp at the appendiceal orifice

Discussion:
Hyperplastic polyps are found more common than adenomas. They are usually
small and located in the left sided colon without potential for malignancy.1 NBI
international colorectal endoscopic (NICE) classification can be used as a diagnostic
tool to predict histology.2- 4 The evaluation of both the vascular pattern and surface
pattern are important. However a polypoid inverted appendiceal orifice can mimic
a true polyp5, but it can easily differentiate from a polyp by using NBI which usually
show normal appearing mucosa. Although there was no risk for malignancy in this
case, the polyp was removed due to the worry of potential risk for polyp occluding the
appendiceal orifice.

140
References
1. Lane N. The precursor tissue of ordinary large bowel cancer. Cancer Res
1976;36:2669-72.
2. Kutsukawa M, Kudo SE, Ikehara N, et al. Efficiency of endocytoscopy in
differentiating types of serrated polyps. Gastrointest Endosc 2013.
3. Oka S, Tanaka S, Takata S, et al. Clinical usefulness of narrow band imaging
magnifying classification for colorectal tumors based on both surface pattern
and microvessel features. Dig Endosc 2011;23 Suppl 1:101-5.
4. Tanaka S, Sano Y. Aim to unify the narrow band imaging (NBI) magnifying
classification for colorectal tumors: current status in Japan from a summary
of the consensus symposium in the 79th Annual Meeting of the Japan
Gastroenterological Endoscopy Society. Dig Endosc 2011;23 Suppl 1:131-9.
5. Koff JM, Choi JR, Hwang I. Inverted appendiceal orifice masquerading as a cecal
polyp on virtual colonoscopy. Gastrointest Endosc 2005;62:308; discussion
308.

141
 Sasipim Sallapant, M.D.
Case 27 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A healthy 56-year-old male underwent a screening colonoscopy. A colonoscopy
revealed a small slender shape white parasite attached to the descending colon. Its
head was embedded in the colonic wall and the tail was coiled liked a whip with
wider handles. Under NBI exam, human blood in its body cavity was demonstrated
(Figures 1 and 2). The surrounding mucosa was normal. The parasite was removed by
a forceps (Figure 3). A microscopic examination demonstrated Trichuria trichiura. The
patient was treated with an oral albendazole.

Figures 1 and 2 a movable small whitish worm with coiled tail (arrow)
embedded in the descending colon. Under NBI exam, the internal blood was
clearly detected.

142
 Figure 3 The parasite was removed
by a biopsy forceps.

Diagnosis:
Trichuris trichiura infestation

Discussion:
Trichuris trichiura or whipworm is known as a soil-transmitted helminth.
T.trichiura lives in the large intestine and the eggs are passed in the feces of infected
person. This infestation is caused by an ingestion of parasite’s eggs.1 The adult worm
is 3-4 cm in length and has a thin tapered anterior region. The adult worm invades
mucosa and produces localized mild inflammation.1 Most people with light infestation
usually have no symptoms. Only patients with heavy infestation develop nausea,
vomiting, abdominal pain, watery or mucus bloody diarrhea. The treatment is either
oral mebendazole or oral albendazole.2

References
1. Ok KS, Kim YS, Song JH, et al. Trichuris trichiura infection diagnosed by
colonoscopy: case reports and review of literature. The Korean journal of
parasitology 2009;47:275-80.
2. Keiser J, Utzinger J. Efficacy of current drugs against soil-transmitted helminth
infections: systematic review and meta-analysis. JAMA : the journal of the
American Medical Association 2008;299:1937-48.

143
 Piyapan Prueksapanich, M.D.
Case 28 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

An 80-year-old female presented with iron deficiency anemia. She had no

experiences of melena and no family history of colon cancer. She underwent a
colonoscopy. Colonoscopy showed a smooth shiny round-shaped submucosal mass at
the appendiceal orifice (Figure 1). Under NBI exam, there was no mucosal abnormality
(Figure 2). The lesion showed a dimple during poking by a biopsy forceps as shown in
Figures 3 and 4. The endoscopic diagnosis was appendicocele.

Figure 1 A smooth shiny round- Figure 2 NBI exam showed no

shaped submucosal mass at the mucosal abnormality.
appendiceal orifice.

144
 Figures 3 and 4 A dimple was made by a biopsy forceps.

Diagnosis:
Appendicocele

Discussion:
Appendicocele can be an incidental finding or can cause symptoms such as
right lower quadrant abdominal pain, intussusceptions, and gastrointestinal bleeding.1
Appendicocele was found more frequently in middle-aged women1. The etiologies of
appendicocele are appendiceal obstruction and distension, hyperplastic mucoceles,
and mucinous cystadenoma.2 Endoscopic biopsy is usually not informative because
an overlying mucosa is not involved, a miniprobe endoscopic ultrasound (EUS) may
be useful to characterize the cystic lesion and to exclude other look-alike solid lesions
such as carcinoid, lipoma, or lymphangioma.2, 3 Surgical treatment is the mainstay
of therapy especially in a patient with possible malignancy since there is a potential
rupture causing pseudomyxoma peritonei.4

145
 References
1. Zanati SA, Martin JA, Baker JP, et al. Colonoscopic diagnosis of mucocele of the
appendix. Gastrointest Endosc 2005;62:452-6.
2. Karakaya K, Barut F, Emre AU, et al. Appendiceal mucocele: case reports and
review of current literature. World J Gastroenterol 2008;14:2280-3.
3. Honnef I, Moschopulos M, Roeren T. Appendiceal mucinous cystadenoma.
Radiographics 2008;28:1524-7.
4. Stocchi L, Wolff BG, Larson DR, et al. Surgical treatment of appendiceal
mucocele. Arch Surg 2003;138:585-9; discussion 589-90.

146
 Sittikorn Linlawan, M.D.
Case 29 Satimai Aniwan, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 77-year-old female presented with chronic constipation. She used many

kinds of laxatives including sennosides to relief the symptoms. Colonoscopic finding
revealed diffuse, dark brown pigmentation from the rectosigmoid junction through the
ascending colon and multiple sessile polyps (0.3-0.8 cm in diameter) were found in
the sigmoid, descending, and ascending colon (Figures 1 - 4). Notably, all polyps were
not stained with the pigment. Polypectomy was done. Histology was compatible with
tubular adenoma.

Figures 1 and 2 diffuse brown pigmentation of mucosa at sigmoid colon

with sessile polyps under white light and Narrow band imaging (NBI).

147
 Figures 3 and 4 NBI imaging showed a pale, unpigmented lesion on the
pigmented background of colonic mucosa.

Diagnosis:
Melanosis coli with tubular adenoma

Discussion:
Melanosis coli is probably the most common pigmentation seen in the intestinal
mucosa during endoscopic evaluation especially with history of chronic constipation
or long-term use of anthraquinone cathartics (including cascara, senna, aloes and
rhubarb).1 Antraquinones damage the colonic epithelial cells causing irreversible
injury to the organelles. The apoptotic cells are ingested by macrophages and are
converted into brownish pigment in the lamina propria. Previous studies found this
substance primarily from lipofuscin, rather than melanin, so it has been suggested
to define as “pseudomelanosis coli” or colonic “lipofuscinosis”.2 Contrast to the
adenomatous epithelium, the apoptotic bodies remain in the epithelium because the
macrophages can not reach the lamina propria in the adenomatous epithelium. Due to
sparing of pigment deposition, it helps to identify the neoplastic colonic lesions such
as adenomas or carcinomas.3-5

148
References
1. Freeman HJ. “Melanosis” in the small and large intestine. World J Gastroenterol
2008;14:4296-9.
2. Ghadially FN, Walley VM. Melanoses of the gastrointestinal tract. Histopathology
1994;25:197-207.
3. Puppa G, Colombari R. Brown colon (melanosis coli) harbouring pale tumors
(adenocarcinoma and an adenomatous polyp). J Gastrointestin Liver Dis
2009;18:509-11.
4. Van Weyenberg SJ, Hoentjen F, Thunnissen F, et al. Pseudomelanosis coli and
adenomatous polyps. J Gastrointestin Liver Dis 2011;20:233.
5. Regitnig P, Denk H. Lack of Pseudomelanosis coli in colonic adenomas suggests
different pathways of apoptotic bodies in normal and neoplastic colonic
mucosa. Virchows Arch 2000;436:588-94.

149
 3 ERCP

Puth Muangpaisarn, M.D.

Case 1 Phonthep Angsuwatcharakon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 61-year-old Thai man presented with progressive painless jaundice and weight
loss for 2 months. The CT scan of abdomen revealed a soft tissue mass measuring 1.6
cm at peri-ampullary region with dilated biliary tree, markedly distended gallbladder,
and ascites (Figure 1). ERCP was performed for preoperative drainage. Endoscopic
findings showed an ulcerative tumor, 2 cm in size, at the ampulla of Vater (Figure 2).
The cholangiogram revealed a 1.5 cm distal CBD stricture with marked dilatation of
upstream bile duct (Figure 3). A fully-covered self-expandable metal stent (FCSEMS)
was inserted across the stricture (Figure 4). Histopathology of the biopsy specimen
confirmed as adenocarcinoma of the bile duct.

Figure 1 CT scan showed a soft

tissue mass at peri-ampullary region
(black arrow) causing bile duct
dilatation.

150
 Figure 2 Figure 3

Figure 2 An ulcerative mass at the

ampulla of Vater.

Figure 3 Cholangiogram showed

a 1.5 cm distal CBD stricture with
marked dilatation of upstream bile
duct.

Figure 4 A fully-covered self-

expandable metal stent (FCSEMS)
was inserted across the stricture.

Figure 4

Diagnosis:
Ampullary adenocarcinoma underwent preoperative biliary drainage with
FCSEMS

Discussion:
Ampullary adenocarcinoma is one of the differential diagnoses of periampullary
malignancies which can cause obstructive jaundice, or nonspecific upper abdominal
pain.1 Ampullary cancer has a better prognosis among all periampullary cancers with
five-year survival of 45%. The favorable prognosis of ampullary cancer is associated
with early diagnosis, and tumor biology.2 Pancreaticoduodenectomy is considered to
be the standard treatment.2

151
 Preoperative biliary drainage in the ampullary cancer reduces the incidence of
post-operative wound infection when compare with non-drainage group. However, the
median survival and 30-day mortality are not significantly different.3 In unresectable
groups, endoscopic biliary drainage is used for a palliation of obstructive jaundice.
When using uncovered metal stent the stent patency and stent malfunction (stent
occlusion and stent migration) are not different from using two plastic stents. The
median period of stent patency is 132.7 days and 128.5 days in metal stent and plastic
stents, respectively.4
Fully-covered self-expandable metal stent (FCSEMS) has recently emerged
for drainage of malignant distal biliary stricture. The FCSEMS can be used in both
operable and inoperable patients, because it can be successfully removed just before
the surgery. In palliative purpose, FCSEMS provides the 97% patency rate at 12 months.
The common complications of FCSEMS are pancreatitis (10%) and stent migration
(7%).5

References
1. El H, II, Cote GA. Endoscopic diagnosis and management of ampullary lesions.
Gastrointest Endosc Clin N Am 2013;23:95-109.
2. Ito K, Fujita N, Noda Y. Endoscopic diagnosis and treatment of ampullary
neoplasm (with video). Dig Endosc 2011;23:113-7.
3. Abdullah SA, Gupta T, Jaafar KA, et al. Ampullary carcinoma: effect of
preoperative biliary drainage on surgical outcome. World J Gastroenterol
2009;15:2908-12.
4. Park SB, Kim HW, Kang DH, et al. Metallic or plastic stent for bile duct
obstruction in ampullary cancer? Dig Dis Sci 2012;57:786-90.
5. Siddiqui AA, Mehendiratta V, Loren D, et al. Fully covered self-expandable
metal stents are effective and safe to treat distal malignant biliary strictures,
irrespective of surgical resectability status. J Clin Gastroenterol 2011;45:824-7.

152
 Puth Muangpaisarn, M.D.
Case 2 Phonthep Angsuwatcharakon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 77-year-old Thai woman presented with progressive painless jaundice and
weight loss for 2 months. The CT scan showed dilated bile duct and pancreatic duct
without an obvious cause of obstruction, there were numerous subcentimeter, intra-
abdominal lymph nodes (Figure 1). Endoscopy revealed a bulging ampulla with a
2 cm mass at the major duodenal papilla (Figure 2). Biliary cannulation via major
papilla was unsuccessful. The endoscopic ultrasound (EUS) revealed no peri-lesion
vascularity and cholangiogram was performed with 20G needle. The cholangiogram
demonstrated dilated CBD with distal CBD stricture, 1.5 cm in length (Figure 3). Then
the scope was switched to a side-viewing duodenoscope to perform supra-papillary
drainage by using needle knife followed by 7 Fr. Soehendra dilator, and non-covered
SEMS was inserted though the choledochoduodenostomy. The double pigtail plastic
stent was inserted in the metallic stent to prevent stent migration (Figure 4).
Å

Figure 1 CT scan revealed double

duct sign without demonstrable
cause of obstruction.

153
 Figure 2 Figure 3

Figure 2 Side-viewing duodenoscopy

revealed an ampullary mass with
bulging ampulla.

Figure 3 EUS-guided cholangiogram

revealed dilated CBD with 1.5 cm
stricture at distal CBD.

Figure 4 SEMS and pigtail stent

was inser ted acr oss the choledo-
choduodenostomy.

Figure 4

Diagnosis:
EUS guided suprapapillary drainage after failed conventional ERC in Ampullary
tumor

Discussion:
Endoscopic retrograde cholangiography (ERC) is the major procedure for
biliary drainage. But some patients could not achieve drainage by ERC because of
altered anatomy (e.g. Roux-en-Y, gastric outlet obstruction) or technical reasons
(e.g. failed cannulation, failed guide-wire access beyond the stricture, or failed stent
insertion).1 Endoscopic ultrasound (EUS) has been used as the salvage therapy. EUS
guided choledochoduodenostomy (EUD-CDS) is one of three types of EUS-guided

154
biliary drainage. Prospective study showed that insertion of plastic stent in EUS-CD
had technical and functional success rates of 94% and 100%, respectively. Median
duration of stent patency is 272 days.2 The recent study in EUS-CDS with FCSEMS
showed the technical success rate of 86.7% and the functional success rate of 100%.
Additionally, the mean duration of stent patency was 264 days. Therefore EUS-CD is
feasible and effective for biliary tract obstruction.3

References
1. Perez-Miranda M, de la Serna C, Diez-Redondo P, et al. Endosonography-guided
cholangiopancreatography as a salvage drainage procedure for obstructed
biliary and pancreatic ducts. World J Gastrointest Endosc 2010;2:212-22.
2. Hara K, Yamao K, Niwa Y, et al. Prospective clinical study of EUS-guided
choledochoduodenostomy for malignant lower biliary tract obstruction. Am J
Gastroenterol 2011;106:1239-45.
3. Song TJ, Hyun YS, Lee SS, et al. Endoscopic ultrasound-guided
choledochoduodenostomies with fully covered self-expandable metallic stents.
World J Gastroenterol 2012;18:4435-40.

155
 Puth Muangpaisarn, M.D.
Case 3 Phonthep Angsuwatcharakon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 65-year-old Thai male presented with non-specific epigastrium pain,

progressive painless jaundice, and weight loss for 3 months. The CT scan of abdomen
revealed an ill-defined hypodensity mass, 5.8x5.3 cm in size, at the head of pancreas
with common bile duct and pancreatic duct dilatation (Figure 1). The mass encased
SMV, and partially compressed duodenal bulb. The endoscopy showed normal major
duodenal papilla (Figure 2), and prominent minor duodenal papilla (Figure 3). The
cholangiogram revealed a malignant stricture at distal CBD, 4 cm in length, with
proximal dilatation of the bile duct (Figure 4). A SEMS was inserted across the stricture
and good bile flow was achieved (Figure 5). EUS-guided FNA was done later and the
histopathology confirmed as pancreatic adenocarcinoma.
Å

Figure 1 The CT scan of abdomen revealed

an ill-defined hypodensity mass at the head of
pancreas.

156
Figure 2 Endoscopy showed normal size Figure 3 Endoscopy showed prominent
but congested major duodenal papilla. minor duodenal papilla (noted a
metallic stent was already inserted via
major papilla).

Figure 4 Cholangiogram showed a 5 cm Figure 5 After SEMS deployment, good

long malignant distal CBD stricture. bile flow was observed.

157
 Diagnosis:
Unresectable pancreatic cancer underwent endoscopic drainage with
prominent minor papilla

Discussion:
More than 80% of pancreatic cancer patients presented at advanced stage of
the disease.1 Approximately 70% of pancreatic adenocarcinomas were located at the
head of pancreas and caused any degree of biliary compression.2 Endoscopic biliary
drainage is one of the choices for palliative drainage with favorable short-term success
rates (80-90%). The minor duodenal papilla receives pancreatic fluid mainly from the
head of pancreas.3 In cases of obstruction or decreased flow of the main pancreatic
duct, eg. pancreas divisum, chronic pancreatitis, or pancreatic head cancer, the minor
papilla might be prominent.

References
1. Hidalgo M. Pancreatic cancer. N Engl J Med 2010;362:1605-17.
2. Lo SK. Endoscopic palliation of pancreatic cancer. Gastroenterol Clin North
Am 2012;41:237-53.
3. Frierson HF, Jr. The gross anatomy and histology of the gallbladder, extrahepatic
bile ducts, Vaterian system, and minor papilla. Am J Surg Pathol 1989;13:146-
62.

158
 Piyapan Prueksapanich, M.D.
Case 4 Phonthep Angsuwatcharakon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.
A 67-year-old female with diabetes mellitus, hypertension and dyslipidemia
presented with biliary pain for 3 days and high grade fever for a day. She had the
similar, episodic pain since 5 years ago. She had no history of alcohol abuse. Her
abdomen was mildly tender without guarding. The Murphy’s sign and Fist test were
negative. Abdominal ultrasonography showed a dilated common bile duct and
a 1.3 cm round hyperechoic lesion with acoustic shadow at the distal part of the
common duct (Figure 1). Gallbladder appeared normal without gallstone. ERCP was
performed and revealed a bulging ampulla with an impacted, white stone at the major
duodenal papilla (Figure 2). A free-handed precut sphincterotomy over the stone with
a needle knife exposed a large whitish stone clogging the ampulla. Via common bile
duct sweeping, stone removal was unsuccessful (Figure 3). A pancreatogram showed
few filling defects within the dilated pancreatic duct. The obstructing 2-cm stone
was removed via pancreatic duct sweeping. The remaining pancreatic duct stones
were successfully removed by repeat balloon extraction (Figures 4 and 5). The final
cholangiogram showed an upstream-dilated common bile duct without any filling
defect (Figure 6).

Figure 1: Abdominal ultrasonography

showed a 1.3 cm dilatation of the
common bile duct and a 1.3 cm
round hyperechoic lesion with
Å

acoustic shadow at the distal part of

the common duct.
Å

159
 Figure 2 Side-viewing duodeno- Figure 3 Free-handed precut sphinc-
scopy revealed a bulging ampulla. terotomy over a stone with a needle
knife exposed a large whitish stone
clogging the major duodenal papilla
tightly.

Figures 4 and 5 Stone clearance via pancreatic duct was able to remove a
2 cm oval stone.

160
 Figure 6 The following cholangiogram
showed an upstream-dilated common
bile duct without any filling defect.

Diagnosis:
Pancreatic duct stone causing biliary obstruction and acute cholangitis.

Discussion:
An impacted pancreatic duct stone is a rare cause of obstructive jaundice which
has been reported for only less than 10 cases to date.1, 2 Malunion of pancreatobiliary
ducts may be one of the possible causative mechanisms in these patients.2 Successful
endoscopic treatment with a pre-cut papillotomy using a needle knife had been
reported.3 In this case, the color of stone is a clue to differentiate between pancreatic
and biliary stones. A pancreatic duct stone is mainly composed of calcium carbonate
without bile pigment resulting in chalk-white color,4 whereas pigmented biliary stone
have concentric layered pigment resulting in brown or black color. A cholesterol biliary
stone has bile stain resulting in yellow color.5

161
 References
1. Hernandez JA, Zuckerman MJ, Moldes O. Pancreatic stone presenting with
biliary obstruction. Gastrointest Endosc 1994;40:521-3.
2. Kinoshita H, Imayama H, Sou H, et al. A case of obstructive icterus caused
by incarceration of a pancreatic stone in the common channel of the
pancreatobiliary ducts. Kurume Med J 1996;43:79-85.
3. Yoo KH, Kwon CI, Yoon SW, et al. An impacted pancreatic stone in the papilla
induced acute obstructive cholangitis in a patient with chronic pancreatitis.
Clin Endosc 2012;45:99-102.
4. Takahashi W, Matsushiro T, Suzuki N, et al. Histochemical studies of pancreatic
calculi. Tohoku J Exp Med 1975;116:1-8.
5. Sandstad O, Osnes T, Skar V, et al. Structure and composition of common bile
duct stones in relation to duodenal diverticula, gastric resection, cholecystectomy
and infection. Digestion 2000;61:181-8.

162
 Piyapan Prueksapanich, M.D.
Case 5 Phonthep Angsuwatcharakon, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

An 85-year-old male who had experienced an episode of acute cholecystitis was

admitted for an elective laparoscopic cholecystectomy. Due to severe adhesion, only
partial cholecystectomy could be performed and the patient was complicated with bile
leakage after surgery. Endoscopic retrograde cholangiogram (ERC) was performed and
showed a contrast extravasation from the remnant of gallbladder with no intraductal
filling defect in the biliary tree (Figures 1 and 2). Endoscopic sphincterotomy was done
and a fully covered self-expandable metal stent (FCSEMS) was inserted to seal the
leakage (Figure 3). The proximal tip of the FCSEMS was above the cystic duct insertion
which resulted in an immediate closure of the cystic duct leakage as shown in the final
cholangiogram. After the procedure, the patient had no further bile leakage and the
draining tube was removed.
Å

Figures 1 and 2 Endoscopic retrograde cholangiogram (ERC) was performed and

showed contrast extravasation from the remnant of gallbladder with no intraductal
filling defect in the biliary tree.

163
 Figure 3 FCSEMS was inserted into the
common bile duct after endoscopic
sphincterotomy.

Figures 4 and 5 The proximal tip of

the FCSEMS was above the cystic
duct insertion which resulted in an
immediate closure of the cystic duct
leakage.

Figure 3

Figure 4 Figure 5

Diagnosis:
FCSEMS for a large cystic duct leak

Discussion:
Biliary leakage is an early complication after cholecystectomy which its
incidence has been reported to be 0.1-0.5% after conventional open cholecystectomy
and up to 3% after laparoscopic cholecystectomy especially during the learning
curve1. The biliary leakages can be resulted from common bile duct injuries, cystic
duct stump leaks with or without bile duct stone(s), or leakage from ducts of Luschka.
The leakages are usually treated successfully with endoscopic measures such as

164
biliary sphincterotomy (in patients having normal common bile ducts), biliary stent
placement, and nasobiliary drainage which results to reduction of the transpapillary
pressure gradient and the leakage can be healed spontaneously. ERCP can be done
safely within 24 hours after LC with a high success rate.2 Internal stents are usually
left for 30 days.3 The use of nasobiliary drainage is decreasing because of its risk for
displacement, epistaxis, collapse of the tube and the patients’ discomfort. Traditionally,
surgery is reserved for major duct leakages due to bile duct transection, complete
obstruction by clips, and leakage that failed to improve after endoscopic treatment.1, 4
Recently, FCSEMS has been introduced as another salvage therapy before considering
surgery since it can provide a high success rate in a case with complex bile leak or
failed treatment with plastic stent.5

References
1. Weber A, Feussner H, Winkelmann F, et al. Long-term outcome of endoscopic
therapy in patients with bile duct injury after cholecystectomy. J Gastroenterol
Hepatol 2009;24:762-9.
2. Pencev D, Brady PG, Pinkas H, et al. The role of ERCP in patients after
laparoscopic cholecystectomy. Am J Gastroenterol 1994;89:1523-7.
3. Pinkas H, Brady PG. Biliary leaks after laparoscopic cholecystectomy: time to
stent or time to drain. Hepatobiliary Pancreat Dis Int 2008;7:628-32.
4. Eisenstein S, Greenstein AJ, Kim U, et al. Cystic duct stump leaks: after the
learning curve. Arch Surg 2008;143:1178-83.
5. Pausawasadi N, Soontornmanokul T, Rerknimitr R. Role of fully covered self-
expandable metal stent for treatment of benign biliary strictures and bile leaks.
Korean J Radiol 2012;13 Suppl 1:S67-73.

165
 Puth Muangpaisarn, M.D.

Case 6
Phonthep Angsuwatcharakon, M.D., M.Sc.
Pradermchai Kongkam, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 25-year-old Thai man had intermittent biliary pain for 2 months, later he
developed fever with chills one day before admission. Physical examination showed
icteric sclera, tenderness at right upper abdomen with positive Murphy’s sign. Upper
abdominal ultrasonography revealed a distended gallbladder with a 1.2 cm gallstone
(Figure 1). Common bile duct (CBD) measured 1.2 cm in diameter without dilation
of intrahepatic bile ducts. CT scan of the upper abdomen revealed focal disruption of
posterior gallbladder wall with small locolated pericholecystic collection (Figure 2).
ERCP was performed. Cholangiogram revealed a 1.5 cm external compression effect
at mid common duct causing upstream dilatation of bile ducts (Figure 3). The contrast
did not fill the cystic duct or gallbladder despite vigorous contrast injection. There was
no filling defect in biliary tree. A 10-Fr double pigtail plastic stent was placed across
the stricture (Figure 4). His symptoms improved after the procedure.

Figure 1 A hyperechoic
Å

material with posterior

acoustic shadow in the
gallbladder. This was
consistent with a gall
stone.

166
 Å
Å

Figure 2 Focal disruption of the posterior

gallbladder wall (white arrow) with small
locolated pericholecystic collection (red arrow).

Figure 3 Extrinsic compression of mid- Figure 4 Plastic stent was placed

bile duct with upstream dilatation of across the stricture.
biliary tree (white arrow).

167
 Diagnosis:
Mirizzi’s syndrome type I with concealed ruptured of gallbladder.

Discussion:
Mirizzi’s syndrome is an uncommon complication of cholelithiasis. The reported
incidence was 1.07% in the patients underwent ERCP.1 Mirizzi’s syndrome consists of
external compression of the bile duct from impacted stone in the cystic duct. It may lead
to cholecystobiliary and cholecystoenteric fistulas. The syndrome is caused by an acute
or chronic inflammatory condition secondary to gallstone impacted in the Hartmann’s
pouch or infundibulum or cystic duct. Predisposing factors are a long cystic duct;
parallel to the bile duct, and a low insertion of the cystic duct into the bile duct.2 The
most common clinical manifestation is obstructive jaundice (60%-100%), followed
by abdominal pain over the right upper abdominal quadrant (50%-100%), and fever.3
The diagnostic accuracy of Mirizzi syndrome by ERCP was 55% to 90%. Typically,
cholangiogram shows narrowing or curvilinear extrinsic compression involving the
lateral portion of the distal common hepatic duct with proximal ductal dilatation and
normal distal caliber.2 Specific treatments are biliary stenting for temporarily drainage
of the obstruction then followed by cholecystectomy.

References
1. Yonetci N, Kutluana U, Yilmaz M, et al. The incidence of Mirizzi syndrome
in patients undergoing endoscopic retrograde cholangiopancreatography.
Hepatobiliary Pancreat Dis Int 2008;7:520-4.
2. Beltran MA. Mirizzi syndrome: history, current knowledge and proposal of a
simplified classification. World J Gastroenterol 2012;18:4639-50.
3. Kelly MD. Acute mirizzi syndrome. JSLS 2009;13:104-9.

168
 Sayamon Kimtrakool, M.D.
Case 7 Phonthep Augsuwatcharakorn, M.D., M.Sc.
Rungsun Rerknimitr, M.D.

A 73-year-old woman presented with fever, right upper abdominal pain, and
jaundice for 3 days. Physical examination revealed marked jaundice with high grade
fever, and tenderness at right upper quadrant. Ultrasonography of the upper abdomen
showed diffusely dilated intrahepatic ducts and common bile duct (CBD) was 1.0 cm.
in diameter. Endoscopic retrograde cholangiopancreatography (ERCP) was performed.

Cholangiogram (Figures 1, 2 and 3)

revealed cholecystocholedochal
fistula with 2 cm filling defect
in common bile duct, dilatation
of common hepatic duct, and
contracted gallbladder.

169
 Endoscopic view of ERCP (Figure
4) showed a 10-Fr double
pigtailed was inserted into left
intrahepatic duct and another
7-Fr double pigtail stent was
inserted into the cystic duct.

Diagnosis:
Mirizzi’s syndrome type IV

Discussion:
Mirizzi’s syndrome is a rare complications of symptomatic gallstone disease.1
Inflammatory process together with gallstones obstruction at neck plays an importance
role to develop this conditions.2 Mirizzi’s syndrome was classified into 4 types
according to Csendes’s classification by different degrees of cholecystocholedochal
fistula.3 Mirizzi’s syndrome type IV, fistula involves complete destruction of the
common biliary ducts wall, is an uncommon type with reported incidence about 4%.4
Diagnosis was made during ERCP by demonstration of fistula between gallbladder
and bile duct wall. Surgical intervention is a treatment of choice for definite treatment.
Partial cholecystectomy and T-tube placement in distal common duct should be done
in robust bile duct tissue.3 Roux-Y reconstruction was performed for patients with
unsatisfactory destruction of bile ducts tissue.3

References
1. Beltran MA. Mirizzi syndrome: history, current knowledge and proposal of a
simplified classification. World J Gastroenterol 2012;18:4639-50.
2. Chatzoulis G, Kaltsas A, Danilidis L, et al. Mirizzi syndrome type IV associated with
cholecystocolic fistula: a very rare condition--report of a case. BMC Surg 2007;7:6.
3. Zaliekas J, Munson JL. Complications of gallstones: the Mirizzi syndrome,
gallstone ileus, gallstone pancreatitis, complications of “lost” gallstones. Surg
Clin North Am 2008;88:1345-68.
4. Csendes A, Diaz JC, Burdiles P, et al. Mirizzi syndrome and cholecystobiliary
fistula: a unifying classification. Br J Surg 1989;76:1139-43.
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 4 EUS

Case 1
Piyapan Prueksapanich, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 72–year-old female patient presented with abdominal distention for 14 days.

No significant past medical history. Physical examination revealed mild abdominal
distention. Abdominal CT demonstrated thickening gastric wall and omental cake.
EGD showed thickening gastric fold with negative endoscopic mucosal biopsy. EUS
was scheduled for an evaluation of gastric lesions and tissue diagnosis. It revealed a
heterogeneous hypoechoic mass infiltrating the whole layer of gastric wall (Figure 1).
It also demonstrated ascites, lymph nodes and omental cake (Figure 2). EUS guided
trucut biopsy was performed with a 19G needle. Preliminary onsite cytopathological
diagnosis was suggestive for lymphoma.

Diagnosis: Gastric lymphoma

Discussion:
Thickening gastric fold can be from various causes including linitis plastica,
lymphoma, or metastatic cancer. In this patient, endoscopic mucosal biopsy was
performed to make a tissue diagnosis, unfortunately, the result was negative. Then
EUS guided trucut biopsy successfully provided the tissue diagnosis without any
complication. A recent retrospective study recruiting 10 and 21 patients with thickening
esophageal and gastric wall, respectively. The EUS guided trucut biopsy with 19G
needles reported sensitivity, specificity, PPV, and NPV as 85%, 100%, 100%, and 74 %
respectively.1 In another large series reported the complication rate of EUS guided
trucut biopsy to be less than 2%. Additionally, authors concluded that diagnostic rate
is higher when lesions are close to the stomach.2 Therefore, EUS guided trucut biopsy is
considered the investigation of choice for thickening gastric wall lesions with negative
endoscopic mucosal biopsies.3

171
 Omentum

Figure 1 Thickening gastric wall with Figure 2 Omental cake was demon-
disruption of whole layers. strated by EUS.

References
1. Thomas T, Kaye PV, Ragunath K, et al. Endoscopic-ultrasound-guided mural
trucut biopsy in the investigation of unexplained thickening of esophagogastric
wall. Endoscopy 2009;41:335-9.
2. Thomas T, Kaye PV, Ragunath K, et al. Efficacy, safety, and predictive factors
for a positive yield of EUS-guided Trucut biopsy: a large tertiary referral center
experience. Am J Gastroenterol 2009;104:584-91.
3. Larghi A, Verna EC, Ricci R, et al. EUS-guided fine-needle tissue acquisition by
using a 19-gauge needle in a selected patient population: a prospective study.
Gastrointest Endosc 2011;74:504-10.

172
 Sukprasert Jutaghokiat, M.D., M.Sc.
Case 2 Pradermchai Kongkam, M.D., M.Sc.
Naeuemon Wisedopas, M.D.,

A 32-year-old female patient presented with mild abdominal pain for 2

months. No significant medical history. Physical examination was unremarkable. An
abdominal ultrasound suspected a pancreatic mass. Abdominal CT scan demonstrated
a hypodensity solid mass in the head of pancreas (Figure 1). The mass measured about
3.1x3.9x4.1 cm in diameter. It was a heterogeneous enhancing mass. No vessel
invasion. No peri-lesional lymph node was seen. Serum Ig G4 was 120 mg/dl.
EUS examination demonstrated a well-defined, irregular boarder, heterogeneous
hypo-echoic mass measuring 34x30 mm in diameter (Figure 2). A few tiny calcified
spots were seen inside the mass. There was an area of hypo-echoic area measuring
about 20x17 mm in diameter inside of the mass. No vessels invasion was seen. No
lymph node was seen. The patient underwent Whipple surgery. Pathology showed
findings consistent with the solid pseudopapillary tumor of the pancreas (Figures 3 and 4).

Diagnosis:
Solid Pseudopapillary Tumor of the Pancreas (SPT)

Discussion:
Solid pseudopapillary tumor of the pancreas (SPT) can be either benign or
low malignant potential tumor of the pancreas.1 The tumor occurs predominantly in
women as shown in a study of 96 patients by Buetow and colleagues which recruited
56 patients with solid pseudopapillary tumor of the pancreas.2 The study reported that
more than 90% of patients were female. Mean age of patients is around 30 years.1, 3

173
 Typically, the tumor is larger than 30 mm in diameters at time of presentation.
Radiologically, the tumor is an encapsulated mass with heterogeneous enhancement
including some cystic space and solid component. In our case, the tumor is a well
encapsulated mass with heterogeneous enhancement. Endosonographically, it was a
well-defined boarder, encapsulated, hypo-echoic solid lesions with irregular margin.
Deep hypoechoic area was seen inside the mass. This is likely the beginning of cystic
degeneration of the mass. This area could not be noted in CT scan which reflects
superiority of EUS over CT scan. The lesion was located in the head of the pancreas
without obstruction of the main pancreatic duct, no side branches dilation. In a recent
cases series, EUS-FNA can provide preoperative diagnosis of SPT in all 3 cases.4 In our
case, we decided not to perform FNA as it was felt that the lesion anyway required
surgical removal.

Figure 1 A heterogeneous hypodensity

mass in the head of pancreas.

Figure 2 A heterogeneous hypoechoic

mass with a few calcified spots and deep
hypoechoic lesions are found inside.

174
 Figure 3 Gross surgical specimen of
the mass.

Figure 4 Histology reveals a circums-

cribed mass composed of solid sheets
of uniform bland looking cells admixed
delicate blood vessels that are surround-
ed by myxoid material.

References
1. Butte JM, Brennan MF, Gonen M, et al. Solid pseudopapillary tumors of the
pancreas. Clinical features, surgical outcomes, and long-term survival in 45
consecutive patients from a single center. J Gastrointest Surg 2011;15:350-7.
2. Martin RC, Klimstra DS, Brennan MF, et al. Solid-pseudopapillary tumor of the
pancreas: a surgical enigma? Ann Surg Oncol 2002;9:35-40.
3. Buetow PC, Buck JL, Pantongrag-Brown L, et al. Solid and papillary epithelial
neoplasm of the pancreas: imaging-pathologic correlation on 56 cases.
Radiology 1996;199:707-11.
4. Park HY, Lee YJ, Lee JH, et al. Endoscopic ultrasound-guided fine needle
aspiration of solid pseudopapillary tumors of the pancreas: a report of three
cases. Korean J Intern Med 2013;28:599-604.

175
 Puth Maungpaisarn, M.D.

Case 3 Phonthep Angsuwatcharakon, M.D., M.Sc.

Pradermchai Kongkam, M.D., M.Sc.

A 66–year-old male patient presented with jaundice. He denied significant

medical history. CA 19-9 level was 486 IU/mL. CT scan revealed a solid pancreatic
mass measuring about 3 cm in diameter at the head of pancreas causing distal bile
duct obstruction with upstream dilation of the bile duct (Figure 1). No main pancreatic
ductal dilation was seen. The mass was considered potentially resectable. EUS was
scheduled for an evaluation of the lesion and tissue diagnosis. It revealed a solid-cystic
mass measuring 54x44 mm in diameter at the head of pancreas with communication
with non-dilated main pancreatic duct (Figures 2 and 3). The mass located closed to
the main portal vein (Figure 4). Endosonographic diagnosis was intraductal papillary
mucinous neoplasm (IPMN) of the pancreas.

Impression: Intraductal papillary mucinous neoplasm (IPMN)

Discussion:
IPMNs are classified into 3 types; main duct type, branch duct type, and
mixed type.1 Surgical removal is recommended in majority of IPMNs. Resection
of IPMNs before the development of invasive carcinoma is a curative treatment.
However, according to an international consensus of group of experts in 2006 (the
Sendai Consensus Guidelines), branch duct type IPMN should be resected only one
of more of the following features present; symptomatic cyst, main pancreatic duct
dilation more than 10 mm, diameter of cyst larger than 30 mm, presence of mural
nodules and suspicious of positive cytology for malignancy from cystic fluid.2 Later
on, the guideline was revised in 2012. The recent one classified IPMN in to high-risk
lesions and equivocal ones. For lesions with high-risk features, surgical resection is

176
recommended. Those features include obstructive jaundice in a patient with a cyst
in the pancreatic head, enhancing solid component of the cyst, and main pancreatic
duct dilatation ≥10 mm In this patient, the lesion caused obstructive jaundice and
contained solid component. Thus, surgical resection is the recommended treatment of
choice for this patient.3

PD

Figure 1 A multiloculated pancreatic Figure 2 Communication of the

cyst at the head of pancreas. main pancreatic duct (PD) with
the mass (M).

HOP
PD

PV

Figure 3 Cystic component of the Figure 4 The solid-cystic mass

solid-cystic mass. (M) located closed to portal vein
(PV) and pancreatic duct (PD).

177
 References
1. Hruban RH, Takaori K, Klimstra DS, et al. An illustrated consensus on the
classification of pancreatic intraepithelial neoplasia and intraductal papillary
mucinous neoplasms. Am J Surg Pathol 2004;28:977-87.
2. Tanaka M, Chari S, Adsay V, et al. International consensus guidelines for
management of intraductal papillary mucinous neoplasms and mucinous cystic
neoplasms of the pancreas. Pancreatology 2006;6:17-32.
3. Tanaka M, Fernandez-del Castillo C, Adsay V, et al. International consensus
guidelines 2012 for the management of IPMN and MCN of the pancreas.
Pancreatology 2012;12:183-97.

178
 Case 4 Piyachai Orkoonsawat, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 49-year-old female patient presented with back pain. She has a past medical
history of cervical cancer stage IIB diagnosed 9 months ago and treated with concurent
chemo-radiation. CT showed a heterogeneous enhancing mass measuring 27x18
mm in diameter with minimal calcification abutting lesser curve of gastric body and
superior aspect of pancreatic tail. EUS revealed a well-defined border, heterogeneous
hypoechoic solid mass measuring 16x14 mm in diameter adjacent to tail of the pancreas
(Figure 1). The pancreas and the spleen appeared unremarkable (Figure 2). EUS-FNA
was performed with a 22G needle (Olympus) without suction. Bloody content was
shown. Final cytopathological diagnosis was accessory spleen.

Impression: Accessary Spleen

Discussion:
Accessory spleen is a congenital anomaly caused by failure of the splenic
remnant to fuse with the spleen during embryology. It can be found in 10–15% of
the general population, mainly without any symptom. Anatomically, it can be either
a lesion connecting to the main spleen or a separate nodule. In general, lesions are
usually smaller than 2 cm; however, they can be as large as the spleen.1 About 80%
and majority of the rest of accessory spleens located adjacent to the splenic hilum
and tail of the pancreas, respectively. However, occasionally, they can be along the
course of the splenic artery or anywhere in the abdominal cavity. Lesions can be either
solitary or multiple ones in about 80% and 10% of them, respectively.2
Intrapancreatic accessory spleens are solid, well-defined, hypervascular
lesions by CT scan. Such lesions should be differentiated with well-differentiated

179
 adenocarcinoma, mucinous cystic neoplasm, soild pseudopapillary neoplasm of the
pancreas, neutoendocrine tumor, and metastasis.3 Endosonographically, the accessory
spleens are usually round or oval shaped lesions with regular and sharp margin.
They are typically homogeneous echogenic lesions with similar echogenic pattern
to the major spleen. The lesions can be either hyperechoic or hypoechoic structure.
It is difficult to differentiate from a splenic lobule. In equivocal cases, EUS-FNA can
provide the definite diagnosis.4 Classic cytopathological features are heterogeneous
population of lymphocytes, traversing small vascular structures, and a background of
mixed inflammatory cells and blood.3

Accessory spleen
spleen

Pancreas

Figure 1 A well-defined heterogeneous Figure 2 Similar appearance of the

hypoechoic mass seen adjacent to spleen to the lesion.
the pancreas.

References
1. Curtis GM, Movitz D. The surgical significance of the accessory spleen. Ann
Surg 1946;123:276-98.
2. Halpert B, Gyorkey F. Lesions observed in accessory spleens of 311 patients.
Am J Clin Pathol 1959;32:165-8.
3. Rodriguez E, Netto G, Li QK. Intrapancreatic accessory spleen: a case report
and review of literature. Diagn Cytopathol 2013;41:466-9.
4. Barawi M, Bekal P, Gress F. Accessory spleen: a potential cause of misdiagnosis
at EUS. Gastrointest Endosc 2000;52:769-72.

180
 Piyachai Orkoonsawat, M.D.

Case 5 Pradermchai Kongkam, M.D., M.Sc.

Rungsun Rerknimitr, M.D.

A 32-year-old male patient presented with hemoptysis, progressive dysphagia

and hoarseness of voice for 2 months. Laryngoscopy revealed a right vocal cord paralysis.
CT chest showed posterior mediastinal mass measuring 6x5x4 cm in diameter at T1-
T4 level with tracheal and esophageal stenosis. Upper endoscopy showed narrowing
esophageal lumen from extrinsic compression. EUS showed a well-defined border,
heterogeneous hypoechoic mass measuring at least 7x4 cm in diameter. The lesion
was located at 18 cm from incisor. Video-assisted thoracoscopic surgery (VATs) was
done for get tissue diagnosis. It showed a hypervascular tumor in the upper posterior
mediastinum behind superior vena cava. Final pathology revealed poorly differentiated
neuroendocrine carcinoma.

Figure 1 A well-defined border heterogeneous

hypoechoic mas measuring 60x43 mm in diameter.

181
 Impression: Mediastinal neuroendocrine tumor

Discussion:
Evaluation of posterior mediastinal mass usually can be performed by CT chest
as it is a non-invasive imaging and widely available. Posterior mediastinal tumors can
be lung cancer, lymphoma, tuberculosis, mediastinal cysts, abscess, atrial myxoma,
etc.1 Primary high grade neuroendocrine tumor of the esophagus is rare. A large
study recently identified 42 neuroendocrine tumors (3.8%) from 1,105 patients with
esophageal tumors.2 In this series, dysphagia was present in 79% of patients.
EUS and EUS-FNA is a test of choice for an evaluation of posterior mediastinal
lesions as it can provide much closer images of lesions and more importantly tissue
diagnosis. It is usually used for an evaluation of the mediastinum in patients with
lung cancer. However, in a case with narrowing lumen tissue acquisition may not be
possible.

References
1. Savides TJ. EUS for mediastinal disease. Gastrointest Endosc 2009;69:S97-9.
2. Huang Q, Wu H, Nie L, Shi J, et al. Primary high-grade neuroendocrine
carcinoma of the esophagus: a clinicopathologic and immunohistochemical
study of 42 resection cases. Am J Surg Pathol 2013;37:467-83.

182
 Case 6 Sayamon Kimtrakool, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 43-year-old male patient presented with painless jaundice and epigastric

abdominal pain for 1 month. He has lost weight for 5 kg. Physical examination
revealed markedly icteric sclera. He has a significant history of alcoholic drinking and
smoking. CT scan of the upper abdomen showed a well-defined border, homogeneous
hypodense, round lesion measuring 10x6.5x5 cm in diameter in the left upper
quadrant abdomen with dilated common and intrahepatic bile duct. EUS showed a
pseudocyst measuring 53x53 mm in diameter with internal echogenic material (Figure
1). A 19G needle was used for puncturing into the pseudocyst. Pus was aspirated
and sent for culture (Figure 2). A double pigtail plastic stent was successfully placed
into the pseudocyst although a double anchor metal stent (Nagi Stent) incidentally
migrated into the pseudocyst (Figure 3). Consequently, two days later, the migrated
metal stent was successfully removed under endoscopic and fluoroscopic guidance.
No post-procedural complication was observed.

Figure 1 A well-defined border

pseudocyst with internal
echogenic material inside the
cyst.

183
 Figure 2 Pus was aspirated from the
infected pseudocyst.

stent

Figure 3 A double plastic stent was

successfully placed.

Diagnosis: Infected pancreatic pseudocyst

Disscussion:
EUS guided pseudocyst drainage can be performed either by the endoscope
under sonographic or fluoroscopic guidance. The endoscopists mostly use a 19G
needle to puncture into the pseudocyst via gastrointestinal tract wall. Pseudocyst and
lumen will then connect to each other. Subsequently, puncture hole will be dilated
to allow stents to be placed across the wall of pseudocyst. The procedure will then be
named as a cysto-gastrostomy or cysto-duodenostomy depending upon the connecting organ.1

184
 Ultrasound that is used to guide puncturing into pseudocyst provides color
doppler flow which is used to check the intervening vessel. This feature is used to
avoid unnecessary bleeding from those vessels.2
EUS -guided pseudocyst drainage has disadvantage of technical feasibility
as the echoendoscope sometimes cannot be placed into the appropriate position to
drain pseudocyst. This made the procedure not possible in all cases despite it has
lower procedural related complication rate than surgery and lesser infection rate
than percutaneous drainage. In fact, side-viewed duodenoscope used for endoscopy
guided trans-mural pseudocyst drainage has more appropriate design in order to drain
pseudocyst. Therefore, in some cases that pseudocyst cause bulging gastro-intestinal
wall and no intervening vessels are expected from CT, the duodenoscope is considered
the scope of choice for an endoscopic guided pseudocyst drainage.

References
1. Yusuf TE, Baron TH. Endoscopic transmural drainage of pancreatic pseudocysts:
results of a national and an international survey of ASGE members. Gastrointest
Endosc 2006;63:223-7.
2. Panamonta N, Ngamruengphong S, Kijsirichareanchai K, et al. Endoscopic
ultrasound-guided versus conventional transmural techniques have comparable
treatment outcomes in draining pancreatic pseudocysts. Eur J Gastroenterol
Hepatol 2012;24:1355-62.

185
 Case 7 Piyachai Orkoonsawat, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 60-year-old female patient presented with fever and right upper abdominal
pain for three days A clinical diagnosis of cholangitis was made. Abdominal
ultrasound revealed common bile duct (CBD) dilatation, measuring 9 mm in diameter
without any stone in the gallbladder. Magnetic resonance cholangiopancreatography
(MRCP) showed circumferential thickening distal common bile duct wall without any
explainable cause. EUS demonstrated a hyperechoic material with posterior acoustic
shadow in the common bile duct (Figure 1). A small gall stone was identified in the
gallbladder. Consequently, the patient was diagnosed the common bile duct stone
and underwent Endoscopic retrograde cholangiopancreatography (ERCP) for stone
removal. The procedure was successful and confirmed the presence of stones in the
common bile duct.

Figure 1 A hyperechoic material

measuring about 5 mm in diameter
was identified in the common bile
duct. This was consistent with a
common bile duct stone.

186
 Figure 2 A stone(GS) was identified in the
gallbladders despite negative upper
abdominal ultrasound.

Impression: Choledocholithiasis with cholelithiasis

Discussion:
Mildly dilatation of the common bile duct can be observed in patients with
advancing age.1 Nevertheless, any bile duct larger than 8 mm in diameter in patients
with an intact gallbladder is usually suggestive for possible bile duct obstruction.2
In order to demonstrate cause of bile duct dilatation, trans-abdominal ultrasound
has a relatively poor sensitivity (22%-55%) for detecting common bile duct stones.3
In fact, ERCP is the gold standard tool for diagnosis and treatment of common bile
duct stone. Unfortunately, ERCP is associated with a significant complication rate.
In patients with intermediate risk for the presence of common bile duct stone, EUS
or MRCP should be utilized first to avoid unnecessary risk of the ERCP procedure.3
EUS and MRCP has sensitivity and specificity rate at 90% and 99% respectively, for
the detection of choledocholithiasis.4 In this case, both common bile duct and gall
stone were missed by MRCP, fortunately, EUS successfully identified stones in both
places and this lead to the appropriate treatment for the patient. In fact, a recent study
supported that EUS is recommended in cases of inconclusive MRCP in any patients
suspected for pancreas and bile duct disease.5

187
 References
1. Bachar GN, Cohen M, Belenky A, et al. Effect of aging on the adult extrahepatic
bile duct: a sonographic study. J Ultrasound Med 2003;22:879-82.
2. Baron RL, Stanley RJ, Lee JK, et al. A prospective comparison of the evaluation
of biliary obstruction using computed tomography and ultrasonography.
Radiology 1982;145:91-8.
3. Maple JT, Ben-Menachem T, Anderson MA, et al. The role of endoscopy in the
evaluation of suspected choledocholithiasis. Gastrointest Endosc 2010;71:1-9.
4. McMahon CJ.The relative roles of magnetic resonance cholangiopancreatography
(MRCP) and endoscopic ultrasound in diagnosis of common bile duct calculi: a
critically appraised topic. Abdom Imaging 2008;33:6-9.
5. Sotoudehmanesh R, Khatibian M, Ghadir MR, et al. Diagnostic accuracy of
endoscopic ultrasonography in patients with inconclusive magnetic resonance
imaging diagnosis of biliopancreatic abnormalities. Indian J Gastroenterol
2011;30:156-60.

188
 Case 8 Piyachai Orkoonsawat, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 56-year-old male patient presented with epigastric pain radiating to upper

back. He also complained of weight loss for 18 kg over the last 3 months. He has a
longstanding history of significant alcoholic drinking and smoking. Abdominal CT
scan showed swollen pancreatic head with heterogeneous parenchymal enhancement.
The lesion abutted the first part of the duodenum. Serum CA 19-9 level was 8.35
U/L. Differential diagnoses of the mass included pancreatic cancer and mass-forming
chronic pancreatitis. EUS showed an ill-defined, heterogeneous hypoechoic mass
measuring 31x26 mm in diameter at the head of pancreas (Figure 1). The rest of
pancreas appeared unremarkable. Pancreatic duct measured 2 mm in diameter at the
body of pancreas. EUS-FNA was performed. Final cytopathology was consistent with
chronic pancreatitis.

Figure 1 An ill-defined heterogeneous

hypoechoic mass measuring 35x29
mm in diameter at the head of
pancreas.

189
 Impression: Mass-forming chronic pancreatitis

Discussion:
Preoperative evaluation of solid pancreatic mass is a challenging clinical
problem. The mass can be either pancreatic cancer or benign masses including mass-
forming chronic pancreatitis, autoimmune panctreatitis, etc. If the diagnosis was wrong,
Unfortunate results such as changing early pancreatic cancer to unresectable stage and
unnecessary invasive surgery for benign lesion may occur. Multiple technologies are
used to ensure that the most likely diagnosis of solid masses was made before surgical
decision. CT, MRI, MRCP, EUS and EUS-FNA are commonly used to serve the purpose.
EUS can identify smaller pancreatic lesions than CT scan. However, in the setting of
chronic pancreatitis, EUS may miss certain lesions.1 Varadarajulu et al demonstrated
the decreased sensitivity rate of EUS-FNA of pancreatic masses in the background of
chronic pancreatitis to be at 73%.2

Reference
1. Bhutani MS, Gress FG, Giovannini M, et al. The No Endosonographic Detection
of Tumor (NEST) Study: a case series of pancreatic cancers missed on endoscopic
ultrasonography. Endoscopy 2004;36:385-9.
2. Varadarajulu S, Tamhane A, Eloubeidi MA. Yield of EUS-guided FNA of
pancreatic masses in the presence or the absence of chronic pancreatitis.
Gastrointest Endosc 2005;62:728-36.

190
 Case 9 Piyachai Orkoonsawat, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 36-year-old male patient presented with a history recurrent abdominal

pain for five months. He has a significant history of chronic alcoholic drinking and
heavy smoking for more than 20 years. Abdominal CT scan Showed an ill-defined
heterogeneous hypodense area at the head of pancreas, causing diffuse dilatation
of intrahepatic and extrahepatic bile ducts. Peripancreatic fluid and fat stranding as
well as an enlarged pancreatic head with scattered multiple small calcifications in
the parenchyma plus dilated main pancreatic duct were found. EUS demonstrated a
calcified mass measuring 26x24 mm in diameter in head of the pancreas (Figure 1). In
addition, lobulation, calcification and hyperechoic ductal wall were identified in the
entire pancreas (Figure 2 and 3). Main pancreatic duct measured 4 mm in diameter
at the head and neck of pancreas. EUS-FNA was done from pancreatic head mass.
Cytology was compatible with chronic pancreatitis.

Figure 1 A calcified mass in the head of pancreas.

191
 Figure 2 Lobulation of pancreatic Figure 3 Calcification and hyperechoic
parenchyma suggesting chronic ductal wall in pancreatic parenchyma.
pancreatitis.

Impression: Chronic pancreatitis

Discussion:
Early chronic pancreatitis can produce several non-specific symptoms including
symptom-free, indigestion and chronic abdominal pain. Diagnosis of early CP can lead
to effective treatment of the disease. When attempting to detect the first signs of change
in the pancreas using imaging, the various methods used can be divided between
non-invasive tests (CT, MRI and plain X-ray) and invasive procedures (ERCP, EUS).
The former tests are generally less sensitive than the latter ones. While non-invasive
procedures are very effective at determining the later stage of chronic pancreatitis,
ERCP and EUS are significantly more sensitive when trying to detect the disease in its
infancy. The lower complication rate of EUS when compared to ERCP makes it a far
less daunting procedure for the patients.
EUS signs for chronic pancreatitis can be conventionally divided into
parenchymal and ductal criteria as followings.

Parenchymal signs

• Calcification with shadowing

• Echogenic foci without shadowing

• Echogenic strands

• Lobulation

• Cystic change
192
 Ductal signs

• Main pancreatic ductal stone

• Dilation or irregular contour of main pancreatic duct

• Increase echogenicity of the main pancreatic ductal wall

• Side branches dilation

Based on the results of 2 prospective studies, when more than 2 criteria were
found, chronic pancreatitis is likely and having more than 6 criteria is generally accepted
as suggestive evidences for the diagnosis of moderate to chronic pancreatitis.1, 2 This
system is currently recognized as the conventional criteria for the diagnosis of chronic
pancreatitis.
Later on, an international consensus has weighted each EUS criterion of chronic
pancreatitis to major or minor criteria in order to make a more solid diagnosis and
standardize terminology. Major criteria included 1) echogenic foci with shadowing
and main pancreatic duct calculi and 20 lobularity with honeycombing. Minor criteria
included cystic changes, dilated main pancreatic duct ≥ 3 mm, irregular pancreatic
duct contour, dilated side branches ≥ 1 mm, hyperechoic ductal wall, strands, non-
shadowing hyperechoic foci, and lobularity with noncontiguous lobules. This consensus
has been known as the Rosemont classification and used for diagnosis of chronic
pancreatitis in several institutions.3 This patient was diagnosed as chronic pancreatitis
based on EUS findings that full of almost all major and some minor criteria.

References
1. Wiersema MJ, Hawes RH, Lehman GA, et al. Prospective evaluation of endoscopic
ultrasonography and endoscopic retrograde cholangiopancreatography in
patients with chronic abdominal pain of suspected pancreatic origin. Endoscopy
1993;25:555-64.
2. Sahai AV, Zimmerman M, Aabakken L, et al. Prospective assessment of the
ability of endoscopic ultrasound to diagnose, exclude, or establish the severity of
chronic pancreatitis found by endoscopic retrograde cholangiopancreatography.
Gastrointest Endosc 1998;48:18-25.
3. Catalano MF, Sahai A, Levy M, et al. EUS-based criteria for the diagnosis
of chronic pancreatitis: the Rosemont classification. Gastrointest Endosc
2009;69:1251-61.

193
 Case 10 Sasipim Sallapant, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 31-year-old female patient with ovarian mass underwent a pre-operative

evaluation. CT abdomen incidentally demonstrated thickening esophageal wall.
CT chest and upper abdomen showed asymmetrical circumferential and lobulated
thickening of distal esophageal wall measuring about 62x27 mm in maximum
thickness (Figures 1 and 2). Upper endoscopy revealed bulging distal esophageal wall.
The endoscope was able to pass into the stomach without any difficulty. EUS revealed
a heterogeneous hypoechoic mass occupying approximately 80% of the esophageal
circumference. The tumor was located at 34-38 cm from the incisors. It originated
from the 4th layer of the esophageal wall (Figures 3 and 4).

Figure 1 Thickening distal esophageal wall noted by

cross-sectional imaging of CT scan.

194
 Figure 2 CT upper abdomen
showed asymmetrical circumferential
thickening of the distal esophagus
to EG-junction, up to 2.7 cm in
maximum thickness and 6.2 cm in
length.The stomach is unremarkable.
No lymphadenopathy, no ascites.

Figure 3 The EUS image revealed

a heterogeneous hypo-echoic
mass occupying about 80% of the
esophageal circumference.

Figure 4 The mass arising from the

4th layer of esophageal wall.

Impression: Esophageal Leiomyoma

Discussion:
Benign esophageal tumor is rare. Among them, leiomyoma is the most common
one. Majority of leiomyoma is located between mid to distal esophagus. Larger tumor
cause more symptoms. About 70% of the tumor originated from muscularis propria.2 A
large study using EUS for management of esophageal leiomyoma recruiting 229 patients
fulfilled with EUS criteria for diagnosis of esophageal leiomyoma. It demonstrated

195
 that only 2 patients complained of dysphagia, retrosternal burning or chest distress.
Majority of lesions located between mid to distal esophagus. Lesions originated from
the muscularis mucosa (78.6%), submucosa (7%) and muscularis propria (14.4%).5 In
our patients, although the lesion was relatively large, the patient did not complain of
dysphagia.
Esophageal leiomyoma is much more common than esophageal stromal
tumors. It is difficult to use endosonographic findings alone in order to differentiate
between these two tumors. Immunohistochemical analysis is the most important factor
to discriminate esophageal leiomyoma form esophageal stromal tumors.1 In lesions
larger than 2 cm in diameter, they mostly are heterogeneous masses. In our patient, the
lesion is also heterogeneous. Based on frequency of the esophageal tumors, our case
is most likely esophageal leiomyoma.6
Esophageal leiomyoma is mostly asymptomatic, however, in symptomatic
patients, the tumors should be removed. Leiomyoma originating from muscularis
propria should be removed by surgery whereas those originating from muscularis
mucosa can be removed by endoscopy. Nevertheless, recently, endoscopic removal
of tumors originating from muscularis propria is feasible in some series.3, 4

References
1 Fei BY, Yang JM, Zhao ZS. Differential Clinical and Pathological Characteristics
of Esophageal Stromal Tumors and Leiomyomata. Dis Esophagus 2013;5 [Epub
ahead of print]
2 Jiang W, Rice TW, Goldblum JR. Esophageal Leiomyoma: Experience from a
Single Institution. Dis Esophagus 2013;26:167-74.
3 Li QL, Yao LQ, Zhou PH, et al. Submucosal Tumors of the Esophagogastric
Junction Originating from the Muscularis Propria Layer: A Large Study of
Endoscopic Submucosal Dissection (with Video). Gastrointest Endosc 2012;
75:1153-8.
4 Shi Q, Zhong YS, Yao LQ, et al. Endoscopic Submucosal Dissection for Treatment
of Esophageal Submucosal Tumors Originating from the Muscularis Propria
Layer. Gastrointest Endosc 2011;74:1194-200.
5 Xu GQ, Qian JJ, Chen MH, et al. Endoscopic Ultrasonography for the Diagnosis
and Selecting Treatment of Esophageal Leiomyoma. J Gastroenterol Hepatol
2012;27: 521-5.
6 Zhu X, Zhang XQ, Li BM, et al. Esophageal Mesenchymal Tumors: Endoscopy,
Pathology and Immunohistochemistry. World J Gastroenterol 2007;13:768-73.

196
 Case 11 Khin San Aye, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 73-year-old male patient presented with chronic epigastric discomfort for

4 months. He had lost his weight for 5 kgs in the last there weeks. CT scan revealed
asymmetrical thickened gastric wall at gastric cardia and fundus. Multiple large
regional lymph nodes were identified. This was suggestive for adenocarcinoma of the
stomach. Endoscopic ultrasound was scheduled for an evaluation of gastric mass. The
procedure was performed by a linear EUS probe. It revealed a hypoechoic mass (60 x
17 mm in diameter) infiltrating the whole layer of gastric wall. It occupied about 75%
of circumference. Hyper-echoic masses were seen on surface of the mass. (33 x 10
mm in diameter) (Figure 1). It was consistent with necrotic debris. Multiple hypoechoic
round lymph nodes were seen around the mass and one of them measured 24 x 22
mm (Figure 2). Multiple round hypoechoic pancreatic masses likely metastasis, were
also noted (Figure 3).

Figure 1 A hypoechoic mass (60 x 17

mm in diameter) infiltrating whole
layer of gastric wall, occupying about
75% of circumference.

197
 Body of pancreas

Figure 2 Multiple dark round lymph Figure 3 Multiple round hypoechoic

nodes seen around the mass. masses in body of the pancreas (likely
metastasis).

Diagnosis:
Gastric cancer

Discussion:
Gastric cancer is the second leading cause of death from malignant disease
worldwide and most frequently discovered in an advanced stages. Because curative
surgery is regarded as the only option for cure, early detection of resectable gastric
cancer is extremely important for good patient outcomes.1
Endoscopic ultrasound has a sensitivity superior to that of CT for the initial
staging of gastric tumors. EUS is becoming increasingly useful as a staging tool when
the CT scan fails to find evidence of T3, T4, or metastatic disease. The correct prediction
values of T and N stage range between 78-88% and 64-82%, respectively.2
The distinction between early and advanced gastric carcinoma before resection
is clinically important. Patients with inoperable, locally advanced gastric cancer
should be treated with palliative chemotherapy and may be reassessed for surgery if a
favorable response is achieved. Institutions that favor neoadjuvant chemoradiotherapy
for patients with locally advanced disease rely on endoscopic ultrasound data to
improve patient stratification.3

198
References
1. Takahashi T, Saikawa Y, Kitagawa Y. Gastric cancer: current status of diagnosis
and treatment. Cancers (Basel) 2013;5:48-63.
2. Xi WD, Zhao C, Ren GS. Endoscopic ultrasonography in preoperative staging of
gastric cancer: determination of tumor invasion depth, nodal involvement and
surgical resectability. World J Gastroenterol 2003;9:254-7.
3. Ychou M, Boige V, Pignon JP, et al. Perioperative chemotherapy compared with
surgery alone for resectable gastroesophageal adenocarcinoma: an FNCLCC
and FFCD multicenter phase III trial. J Clin Oncol 2011;29:1715-21.

199
 Wiriyaporn Ridtitid, M.D., M.Sc.

Case 12 Kessarin Thanapirom, M.D.

Pradermchai Kongkam, M.D., M.Sc.

A 49-year-old male patient presented with progressive epigastric pain, radiating

to his back, for 3 weeks. He was diagnosed as advanced hilar cholangiocarcinoma with
lungs, liver and adrenal glands metastasis since 6 months ago. Physical examination
revealed icteric sclera with hepatomegaly. EUS was done for celiac plexus neurolysis.
Injections of 10 cc of normal saline, 10 cc of 2.5% marcaine and 10 cc of absolute
alcohol were performed around celiac branch area (Figure 1). No immediate
complication was noted. After the procedure, his blood pressure was dropping for a
few minures then it returned to normal range after resuscitation. .

Figure 1 Alcohol injection around right celiac

branch area, post injection.

Diagnosis: Celiac plexus neurolysis for abdominal cancer pain in patient with
metastatic hilar cholangiocarcinoma

200
Disscussion:
Currently, celiac plexus neurolysis (CPN) has been increasingly used for relieving
abdominal cancer pain.1 A recent systemic review of CPN for upper abdominal cancer
showed significant improvement in pain, with a decrease in opioid consumption and
side effects.1 This can be performed not only percutaneously under CT or fluoroscopic
guidance, but also endoscopically under EUS guidance. A recent randomized
controlled trial of 96 patients (EUS-CPN in 48 versus conventional pain management
in 48) showed greater pain relief in the EUS-CPN group at 1 month and significantly
greater at 3 months.2 Morphine consumption tended toward lower at 3 months in the
neurolysis group.2 However, the technique of alcohol injection during EUS-guided
CPN for cancer pain has not been clear regarding the number of injections.

References
1. Nagels W, Pease N, Bekkering G, et al. Celiac plexus neurolysis for abdominal
cancer pain: a systematic review. Pain Med 2013;14:1140-63.
2. Wyse JM, Carone M, Paquin SC, et al. Randomized, double-blind, controlled
trial of early endoscopic ultrasound-guided celiac plexus neurolysis to prevent
pain progression in patients with newly diagnosed, painful, inoperable
pancreatic cancer. J Clin Oncol 2011;29:3541-6.

201
 Wiriyaporn Ridtitid, M.D., M.Sc.

Case 13 Kessarin Thanapirom, M.D.

Pradermchai Kongkam, M.D., M.Sc.

A 47-year-old female patient presented with epigastric pain and fever for 2
weeks. She was admitted to an outside hospital. CT scan of the upper abdomen showed
a large pancreatic pseudocyst measuring 5 cm x 8 cm x 8 cm at pancreatic body and tail.
After receiving an empiric antibiotic, fever improved, however, her pain still persisted.
Then, she was referred for further management. She also has a history of chronic
alcohol use. Physical examination revealed mild tenderness at the upper quadrant
area. EUS demonstrated a large pseudocyst measuring 56 mm x 78 mm in diameter
with internal echogenic material (Figure 1A). A 19G needle was used for puncturing
into the pseudocyst. Serosanguinous fluid was aspirated (Figure 1B). A double anchored
metallic stent 14 mm x 30 mm (NAGI-Stent, Taewoong Company, Seoul, Korea) was
successfully placed into the pseudocyst (Figures 2A and 2B). However, due to difficult
location of the punctured site, the distal tip of the stent was left at the esophagogastric
junction after deploying. To prevent aspiration, a nasogastric tube was placed through
the stent into the cyst (Figures 2C and 2D). Three days later, a follow-up CT scan
showed a complete resolution of the pancreatic pseudocyst. Subsequently, the metal
stent was successfully removed under endoscopic and fluoroscopic guidance (Figures
3A-3B). No post-procedural complication was observed.

202
Figures 1 A) A large pseudocyst measuring 56 mm x 77 mm at the
pancreatic body and tail, with internal heterogenous content seen
under EUS. B) Serosanguinous fluid was aspirated from the pseudocyst.

A. B.

C. D.

Figures 2 A) and B) A double anchored metallic stent placement (NAGI-

Stent, Taewoong Company, Seoul, Korea) C) and D) A nasogastric
tube placement through the stent into the cyst preventing aspiration.

203
 A. B.

Figure 3 (A-B): Successful metallic stent removal.

Diagnosis:
Large pancreatic pseudocyst post with double anchored metallic stent placement
for drainage

Disscussion:
The placement of plastic stent is technically difficult for pseudocyst drainage
due to the need to access the cyst cavity for multiple times. So, a single fully covered
metallic stent insertion has been proposed.1 However, high rate of stent migration has
been reported.1, 2 A new fully covered metallic stent (NAGI-Stent, Taewoong Company,
Seoul, Korea) has been recently developed to prevent migration.3, 4 The design of the
“NAGI” stent, with acute angled flare ends, provides a decrease in the migration rates
due to better anchoring in the gastric and pseudocyst wall. In addition, a retrieval
string at the distal end of the stent allows easy stent removal. However, the data of
its feasibility and safety for pseudocyst drainage has been reported in a few cases.3, 4
Comparative studies among multiple plastic stents, a single fully covered metallic
stent and a double anchored metallic stent are required to confirm the appropriate
management for pseudocyst drainage.

204
References
1. Penn DE, Draganov PV, Wagh MS, et al. Prospective evaluation of the use of
fully covered self-expanding metal stents for EUS-guided transmural drainage
of pancreatic pseudocysts. Gastrointest Endosc 2012;76:679-84.
2. Varadarajulu S, Bang JY, Sutton BS, et al. Equal efficacy of endoscopic and
surgical cystogastrostomy for pancreatic pseudocyst drainage in a randomized
trial. Gastroenterology 2013;145:583-90 e1.
3. Tellez-Avila FI, Villalobos-Garita A, Ramirez-Luna MA. Use of a novel covered
self-expandable metal stent with an anti-migration system for endoscopic
ultrasound-guided drainage of a pseudocyst. World J Gastrointest Endosc
2013;5:297-9.
4. Itoi T, Nageshwar Reddy D, Yasuda I. New fully-covered self-expandable metal
stent for endoscopic ultrasonography-guided intervention in infectious walled-
off pancreatic necrosis (with video). J Hepatobiliary Pancreat Sci 2013;20:403-
6.

205
 Case 14 Tanyaporn Chantarojanasiri, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 72-year-old female patient presented with abdominal bloating and weight

gain for 2 weeks. CT scan of the abdomen found markedly thickened wall of the
stomach. The upper endoscopy showed partially distensible friable gastric mucosa
with esophageal varices. EUS showed circumferential thickening gastric wall with
lymphadenopathy, ascites and omental cake. There was also a heterogeneous
hypoechoic mass extending from gastric mucosa through serosa measuring about 5
cm in thickness. EUS-guided fine needle aspiration was performed with a 22G Procore
needle. The cytopathology revealed round-cell tumor with positive staining of CD20,
Ki67 (>90%) but negative staining of CD3, AE1/AE3. It was compatible with aggressive
B-cell non-Hodgkin lymphoma.

1A 1B

Figures 1A and 1B Markedly thickening of gastric wall with a huge mass

extending from gastric wall demonstrated by CT scan.

206
 Gastric mucosa
mass

Figure 2 The Endoscopic ultrasound Figure 3 Heterogeneous hypoechoic

showed thickening gastric mucosa mass extending from gastric mucosal
with ascites. layer through serosa.

Diagnosis: Gastric lymphoma

Discussion:
Gastric lymphoma is the most common manifestation of gastrointestinal
lymphoma, comprise about 70%. Endoscopic findings of gastric lymphomas range
from slight irregularities to large ulcerative or polypoid mass.1, 2 On endoscopic
ultrasound, gastric lymphoma typically shows a hypoechoic lesion localized to 2nd or
3rd layer but it can extended through the entire wall.2
EUS is one the most accurate method for local staging of gastric lymphoma.
However, the data was conflicting. In earlier studies the accuracy was 80-92% for
T stage and 77-90% for N stage based on TNM staging.1 On the contrary, in the
subsequent studies the accuracy was only 53% based on Ann Arbor staging.2, 3 The
role of EUS to follow-up after treatment is also controversial.1, 3-5 In most studies,
endosonographic remission is significantly delayed when compared with histology.4, 5
However, false negative remission on EUS were seen in some patients.6 When
compared between low-grade and high-grade lymphoma, there were correlation
between endosonographic and histologic remission in MALT lymphoma but not in
high grade lymphoma.5 The role of EUS-guided fine needle aspiration for the diagnosis
of relapsed gastric lymphoma is not yet validated.1, 5

207
 References
1. Janssen J. The impact of EUS in primary gastric lymphoma. Best Pract Res Clin
Gastroenterol 2009;23:671-8.
2. Hwang JH, Rulyak SD, Kimmey MB. American Gastroenterological Association
Institute technical review on the management of gastric subepithelial masses.
Gastroenterology 2006;130:2217-28.
3. Fischbach W, Goebeler-Kolve ME, Greiner A. Diagnostic accuracy of EUS
in the local staging of primary gastric lymphoma: results of a prospective,
multicenter study comparing EUS with histopathologic stage. Gastrointest
Endosc 2002;56:696-700.
4. Di Raimondo F, Caruso L, Bonanno G, et al. Is endoscopic ultrasound clinically
useful for follow-up of gastric lymphoma? Ann Oncol 2007;18:351-6.
5. Vetro C, Romano A, Chiarenza A, et al. Endoscopic ultrasonography in gastric
lymphomas: appraisal on reliability in long-term follow-up. Hematol Oncol
2012;30:180-5.
6. Puspok A, Raderer M, Chott A, et al. Endoscopic ultrasound in the follow
up and response assessment of patients with primary gastric lymphoma. Gut
2002;51:691-4.

208
Case 15 Tanyaporn Chantarojanasiri, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 66-year-old male patient presented with jaundice. Past medical history was
significant for polycystic kidney disease. CT scan demonstrated a cystic lesion at the
head of pancreas with upstream dilatation of the common bile duct and intrahepatic
bile ducts. Endoscopic ultrasound was performed with a linear echoendoscope. It
showed a multiloculated and septated pancreatic cyst measuring about 69 x 43 mm
in diameter at the head of pancreas. It demonstrated an intra-cystic mural nodule
measuring 15 mm in diameter. The lesion was macro-cystic with mixed solid-cystic
cyst. Main pancreatic duct measured 3 mm in diameter at the body and tail of pancreas.
The diagnosis of intraductal papillary mucinous neoplasm was made and the patient
was sent for surgical resection.

Figure 1 A multi-loculated cyst with Figure 2 Internal echogenic mural

macro-cystic appearance. nodule seen from cystic wall (arrow).

209
 Diagnosis: Intraductal papillary mucinous neoplasm (IPMN)

Discussion:
Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas develop
from epithelial cells in the main pancreatic duct (MPD), namely main duct IPMNs
(MD-IPMNs), or branch duct, specifically branch duct IPMNs (BD-IPMNs). The
imaging and endoscopic feature varied among different type of IPMN. In classic MD-
IPMN, the pancreatic duct is markedly dilated, often larger than 1 cm in diameter,
with tortuosity and sometimes appears cystic. Solid part and calcification can also be
demonstrated.1 Endoscopic ultrasound can provide morphological details of dilated
pancreatic ducts and solid component. In addition, it can provide fluid sampling or
fine needle aspiration or biopsy of the solid components.1, 2 Cyst fluid analysis is
recommended in cases with small BD-IPMNs without worrisome features.2 The
aspirated fluid is typically viscous. The analysis may show elevated CEA in two-third
of the cases but the level does not correlate well with the degree of dysplasia.1 In
comparison with other modalities, EUS is the most effective method to determine
malignant characteristics and detect concomitant pancreatic ductal adenocarcinoma
in patients with IPMNs.3

References
1. Fernandez-del Castillo C, Adsay NV. Intraductal papillary mucinous neoplasms
of the pancreas. Gastroenterology 2010;139:708-13, 713 e1-2.
2. Tanaka M, Fernandez-del Castillo C, Adsay V, et al. International consensus
guidelines 2012 for the management of IPMN and MCN of the pancreas.
Pancreatology 2012;12:183-97.
3. Kamata K, Kitano M, Kudo M, et al. Value of EUS in early detection of pancreatic
ductal adenocarcinomas in patients with intraductal papillary mucinous
neoplasms. Endoscopy. 2013 Nov. 11. [Epub ahead of print] PMID:24218310

210
 Wiriyaporn Ridtitid, M.D., M.Sc.

Case 16 Kessarin Thanapirom, M.D.

Pradermchai Kongkam, M.D., M.Sc.

A 58-year-old female patient presented with epigastric pain for 2 weeks.

Physical examination was unremarkable. She denied history of alcoholic drinking or
smoking. EGD showed mildly bulging gastric wall at the lesser curve of gastric body.
A subepithelial lesion without ulcerative lesion was suspected (Figure 1). CT scan of
the upper abdomen showed an enhancing solid mass measuring 46 mm x 45 mm
in diameter with central calcification at lesser curve of stomach. EUS revealed a
heterogenous hypoechoic mass measuring 36 mm x 31 mm in diameter at lesser curve
of gastric body (Figure 2). The mass originated from the forth layer of the gastric wall.
No perigastric lymph node was noted. core biopsy was performed by using a 19G
needle and the tissue was sent for histopathology. No post-procedural complication
was observed. Histopathology showed spindle cell neoplasm.

Figure 1 Subepithelial lesion

seen during EGD.

211
 Figure 2 A heterogenous hypoechoic
mass measuring 36 mm x 31 mm in
diameter at lesser curve of gastric
body, which originated from the
forth layer of the gastric wall.

Diagnosis: Gastrointestinal stromal tumor

Disscussion:
Currently, EUS has been accepted as a useful tool for diagnosing gastric
submucosal lesion. For differentiating between a submucosal and an extraluminal
compression, the sensitivity and specificity of endoscopy were 87% and 29%,
respectively, whereas those of EUS were 92% and 100%, respectively.1 It can identify
the originating layer of intramural lesions. Also, this allows tissue samples to be obtained
from the lesions in the GI tract. The sensitivity, specificity, and diagnostic accuracy
of EUS-FNA in diagnosing GI tract neoplastic lesions were 89%, 88% and 89%,
respectively.2 However, regarding small gastric subepithelial lesions, EUS alone had
an accuracy rate of 30.8% and 66.7%, respectively, for the diagnosis of neoplastic and
non-neoplastic lesions.3 Due to its low accuracy of EUS for these groups, endoscopic
submucosal resection is required to confirm the diagnosis.

References
1. Rosch T, Kapfer B, Will U, et al. Accuracy of endoscopic ultrasonography in
upper gastrointestinal submucosal lesions: a prospective multicenter study.
Scand J Gastroenterol 2002;37:856-62.
2. Vander Noot MR, 3rd, Eloubeidi MA, Chen VK, et al. Diagnosis of gastrointestinal
tract lesions by endoscopic ultrasound-guided fine-needle aspiration biopsy.
Cancer 2004;102:157-63.
3. Karaca C, Turner BG, Cizginer S, et al. Accuracy of EUS in the evaluation of
small gastric subepithelial lesions. Gastrointest Endosc 2010;71:722-7.

212
 Wiriyaporn Ridtitid, M.D., M.Sc.

Case 17 Kessarin Thanapirom, M.D.

Pradermchai Kongkam, M.D., M.Sc.

A 54-year-old female patient presented with episodic pain at epigastric area.

She also had a significant weight loss during the last 3 months. She has a history
of chronic alcohol use. Physical examination was unremarkable. MRI of the upper
abdomen showed a 5.4 cm x 6.2 cm cystic lesion at the anterior aspect of body/tail
of pancreas and a 1.0 cm x 0.4 cm cystic lesion in the tail of pancreas and a 1.0 cm x
0.4 cm cystic lesion in the tail of pancreas with evidence of chronic pancreatitis and
no demonstrable connection with pancreatic duct, these were suggestive of pancreatic
pseudocysts (Figures 1A and 1B). EUS demonstrated a pseudocyst measuring 51 mm
x 54 mm in diameter with internal echogenic material and two layers of content
(Figures 2A and 2B). A 19G needle was used for puncturing into the pseudocyst. Thin,
turbid fluid was aspirated. A double anchored metallic stent 14 mm x 30 mm (NAGI-
Stent, Taewoong Company, Seoul, Korea) was successfully placed into the pseudocyst
(Figures 3A and 3B). No post-procedural complication was observed. Three days later,
the stent was successfully removed following the resolution pancreatic pseudocyst
seen on a follow-up CT scan.
A. B.

Figures 1(A-B) A cystic lesion at the body and tail of pancreas with no pancreatic
duct communication seen on axial and coronal view of MRI (arrows).

213
 A. B.

Figures 2 (A-B) A pseudocyst measuring 51 mm x 54 mm in diameter with

internal echogenic material (thin arrow) and two layers of content (thick
arrow).

A. B.

stent

Figure 3 (A-B) Successful double anchored metallic stent (NAGI-Stent)

placement.

Diagnosis:
Pancreatic pseudocyst with double anchored metallic stent placement for
drainage

Disscussion:
Equal efficacy of endoscopic and surgical cystogastrostomy for pancreatic pseudocyst
drainage was shown in a recent randomized trial. However, endoscopic treatment was
associated with shorter hospital stays and lower costs.1 A meta-analysis demonstrated
that EUS-guided versus conventional transmural methods were comparable regarding

214
the treatment outcomes in draining pancreatic pseudocyst.2 Various techniques have
been described for EUS-guided drainage, including multiple plastic stents and fully
covered self-expanding metal stent placement. Although the insertion of metallic stent
provides faster drainage due to its larger diameter than do plastic stent and reduction
in the number of procedures, this may have higher migration rate.3 Recently, a new
fully covered metallic stent (NAGI-Stent, Taewoong Company, Seoul, Korea) has been
developed to prevent migration with promising outcomes.4, 5 The design of the “NAGI”
stent, with acute angled flare ends, provides a decrease in the migration rates due to
better anchoring in the gastric and pseudocyst wall.

References
1. Varadarajulu S, Bang JY, Sutton BS, et al. Equal efficacy of endoscopic and
surgical cystogastrostomy for pancreatic pseudocyst drainage in a randomized
trial. Gastroenterology 2013;145:583-90 e1.
2. Panamonta N, Ngamruengphong S, Kijsirichareanchai K, et al. Endoscopic
ultrasound-guided versus conventional transmural techniques have comparable
treatment outcomes in draining pancreatic pseudocysts. Eur J Gastroenterol
Hepatol 2012;24:1355-62.
3. Penn DE, Draganov PV, Wagh MS, et al. Prospective evaluation of the use of
fully covered self-expanding metal stents for EUS-guided transmural drainage
of pancreatic pseudocysts. Gastrointest Endosc 2012;76:679-84.
4. Tellez-Avila FI, Villalobos-Garita A, Ramirez-Luna MA. Use of a novel covered
self-expandable metal stent with an anti-migration system for endoscopic
ultrasound-guided drainage of a pseudocyst. World J Gastrointest Endosc
2013;5:297-9.
5. Itoi T, Nageshwar Reddy D, Yasuda I. New fully-covered self-expandable metal
stent for endoscopic ultrasonography-guided intervention in infectious walled-
off pancreatic necrosis (with video). J Hepatobiliary Pancreat Sci 2013;20:403-
6.

215
 Wiriyaporn Ridtitid, M.D., M.Sc.

Case 18 Kessarin Thanapirom, M.D.

Pradermchai Kongkam, M.D., M.Sc.

A 64-year-old male patient presented with painless jaundice and weight

loss for a month. Physical examination revealed moderately icteric sclera without
hepatomegaly. He denied a history of alcoholic drinking or smoking. CT scan of the
upper abdomen showed enhancing soft tissue gallbladder mass with irregular contour
abutting hepatic segment V and IVb without intervening fat plance. There is irregular
thickened enhancing soft tissue lesion involving gallbladder neck, common hepatic
duct, cystic duct and proximal common bile duct, causing diffuse intrahepatic ducts
dilatation (Figures 1A and 1B). Several matted necrotic peripancreatic, periportal and
hepatoduodenal nodes suggested nodal metastasis. ERCP revealed a long stricture at
common hepatic duct (Figure 2A). An uncovered metallic stent (Wallstent) was placed.
(Figure 2B) Subsequent EUS demonstrated a solid-cystic gallbladder mass measuring
37 mm x 26 mm with multiple dark, round perigallbladder lymph nodes (Figure 3). A
25G needle was used for aspiration from solid mass and lymph nodes, then it was sent
for cytopathology. Histopathology confirmed as adenocarcinoma of the gallbladder.

A. B.

Figures 1(A-B) Enhancing gallbladder mass (arrow) with suspected

invasion hepatic invasion, together with irregular thickened enhancing
soft tissue lesion involving gallbladder neck, cysticduct and proximal
common bile duct, causing bilateral intrahepatic ducts dilatation.
216
 A. B.

Figures 2 A) A long stricture at common hepatic duct seen on cholangiogram

(arrow) B) Successful uncovered metallic stent placement.

A. B.

Figures 3 A) A solid-cystic gallbladder mass measuring 37 mm x 26 mm seen

on EUS B) Multiple dark, round perigallbladder lymph nodes.

Diagnosis: Unresectable gallbladder adenocarcinoma

Disscussion:
Mostly, patients with gallbladder cancer present at the late stage. Obtaining
histopathology and tumor staging are essential to determine the appropriate treatment.
For pre-operative evaluation, ERC is initially performed particularly in patients with
biliary obstruction. However, due to its extraductal lesions, it is difficult to get tissue
for diagnosis during ERC. EUS-FNA is an alternative tool for the workup of gallbladder

217
 tumors. A few publications have been reported for EUS-FNA in gallbladder lesions.1-3
A recent study compared the diagnostic value and safety of EUS-FNA with ERC in
patients with suspected gall bladder carcinoma.2 Of 83 patients with gall bladder
cancer, the sensitivity of ERC with cytopathologic sampling was 47.4% whereas EUS-
FNA provided 94.8% in diagnostic sensitivity.2

References
1. Kim HJ, Lee SK, Jang JW, et al. Diagnostic role of endoscopic ultrasonography-
guided fine needle aspiration of gallbladder lesions. Hepatogastroenterology
2012;59:1691-5.
2. Hijioka S, Hara K, Mizuno N, et al. Diagnostic yield of endoscopic retrograde
cholangiography and of EUS-guided fine needle aspiration sampling in
gallbladder carcinomas. J Hepatobiliary Pancreat Sci 2012;19:650-5.
3. Wu LM, Jiang XX, Gu HY, et al. Endoscopic ultrasound-guided fine-needle
aspiration biopsy in the evaluation of bile duct strictures and gallbladder
masses: a systematic review and meta-analysis. Eur J Gastroenterol Hepatol
2011;23:113-20.

218
Case 19 Khin San Aye, M.D.
Pradermchai Kongkam, M.D., M.Sc.

A 44-year-old male patient presented with seizure due to profound hypoglycemia.

CT of the upper abdomen demonstrated submucosal arterial enhancing lesion at the
gastric body. No pancreatic mass was found. Endoscopic ultrasound was scheduled to
search for pancreatic neuroendocrine tumors. in particular insulinoma EUS revealed
a homogenous hypoechoic mass measuring 11 x 9 mm in diameter at the neck of
pancreas (Figure 1). EUS-FNA was performed with a 22G needle. Cytopathology
demonstrated round-cell tumor consistent with neuroendocrine tumor.

Figure 1 A heterogeneous hypoechoic mass at

the pancreatic genu.

219
 Diagnosis:
Insulinoma

Discussion:
Insulinomas, the most common functioning endocrine neoplasms of the
pancreas, are characterized clinically by hypoglycemic symptoms resulting from
neuroglycopenia and catecholamine response.1 Approximately 5% to 10% of patients
with insulinomas have multiple endocrine neoplasia type 1 (MEN 1), and these patients
frequently have multiple lesions.2
More than 90% of insulinomas are benign tumors, being treatable by surgical
operation. While in the past, preoperative localization of insulinoma could be
problematic and blind pancreatic resections were performed, high-resolution imaging
techniques and endoscopic ultrasound currently allow high preoperative detection
rates, which is essential in planning the most appropriate surgical strategy.3
Endoscopic ultrasound (EUS) is currently the test of choice in most Western
centers, with reported detection rates of 86.6%-92.3% because most functioning
tumors are small. EUS-guided FNA is becoming increasingly popular, and it seems
likely that it will eventually become the standard tool for the diagnosis and staging of
functioning pancreatic neuroendocrine tumors.4

References
1. Mathur A, Gorden P, Libutti SK. Insulinoma. Surg Clin North Am 2009;89:1105-
21.
2. Davi MV, Boninsegna L, Dalle Carbonare L, et al. Presentation and outcome of
pancreaticoduodenal endocrine tumors in multiple endocrine neoplasia type 1
syndrome. Neuroendocrinology 2011;94:58-65.
3. Crippa S, Zerbi A, Boninsegna L, et al. Surgical management of insulinomas:
short- and long-term outcomes after enucleations and pancreatic resections.
Arch Surg 2012;147:261-6.
4. Okabayashi T, Shima Y, Sumiyoshi T, et al. Diagnosis and management of
insulinoma. World J Gastroenterol 2013;19:829-37.

220
 Khin San Aye, M.D.

Case 20 Sutep Gonlachanvit, M.D.

Pradermchai Kongkam, M.D., M.Sc.

A 47-year-old male patient presented with melena. Upper endoscopy revealed

a polypoidal lesion with a small ulcer in the duodenum bulb (Figure 1). Endoscopically,
the lesion was diagnosed as duodenal polyp. EUS demonstrated a hyperechoic mass
measuring 21 x 13 mm in diameter and the lesion was originating from 1st and 2nd layer
of intestinal wall (Figure 2). This confirmed the safety of endoscopic removal.

Figure 1 A polypoid lesion in Figure 2 A duodenal polyp arising from

duodenal bulb. 1st and 2nd layer of mucosa.

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 Diagnosis;
Duodenal polyp

Discussion;
Duodenal polyps are a rare finding in patients presenting for gastroscopy, being
found in 0.3–4.6% of cases. Several types of polyps can occur in the duodenum and
most of them are non-neoplastic. Non-neoplastic duodenal polyps include Brunner’s
gland hyperplasia, ectopic gastric mucosa, and hyperplastic polyps.1
Brunner’s gland hyperplasia and hamartomas were often encountered in the
bulb of the duodenum. Although most duodenal polyps had a benign clinical course,
some of them can transform to tumors including adenomas or carcinoid tumors.
Therefore, early diagnosis and treatment are important for these cases.2
Role of EUS in the assessment of duodenal polyps has been determined for con­
firming the diagnosis and determining the layer of origin. Any polyp that not extend
beyond the 3th layer by EUS is consider resectable by endoscopy. Endoscopic treatment
of duodenal polyps pro­vides a challenge since the risk for perforation is very high.

References
1. Basford PJ, Bhandari P. Endoscopic management of nonampullary duodenal
polyps. Therap Adv Gastroenterol 2012;5:127-38.
2. Jung SH, Chung WC, Kim EJ, et al. Evaluation of non-ampullary duodenal polyps:
comparison of non-neoplastic and neoplastic lesions. World J Gastroenterol
2010;16:5474-80.

222
 5 Index

A B
Accessary Spleen, 179 Band ligation, 10, 133
Achalasia cardia, 25 Barrett’s esophagus, 8
Achalasia, 24 Bear claw, 69
Acquired double pylorus, 61 Blue Rubber Bleb Nevus Syndrome, 58
Acute cholangitis, 161 Blue–black mucosal nodules, 100
Acute gastric dilatation, 51 Blue-colored veins, 103
Acute mesenteric ischemia, 76, 94 Bluish-black rubbery blebs, 57
Adenomatous polyps, 39 Branch duct IPMNs, 210
Adrenaline injection, 10 Brunner’s gland hyperplasia, 222
Ampullary adenocarcinoma, 151 Buried bumper syndrome, 53
Anastomotic ulcer, 127
Angiodysplasia, 90
Anti-gliadin antibody IgG, 65
Antitissuetransglutaminase IgA, 65
APC gene, 48
C
APC, 31
Appendicocele, 145 CA 19-9, 189
Ascaris lumbricoides, 114 Carcinoid tumors, 222
Atenuated familial adenomatous polyposis, 39 Carcinoid, 145
Atrial myxoma, 182 Carpet-liked sessile gastric polyps, 39
Autoimmune panctreatitis, 190 Caustic injury, 24
CD20, Ki67, 206
CD3, 206

223
 CEA, 210 Diverticular bleeding, 133
Celiac disease, 6, 65 Ducts of Luschka, 164
Celiac plexus neurolysis, 200 Duodenal perforation, 69
Central umbilication, 35 Duodenal poly, 222
Chalk-white color, 161 Duodenal varices, 71
Cherry-red spots, 116
Cholecystoenteric fistulas, 168
Choledochoduodenal fistula, 62, 63
Choledochoduodenostomy, 153
Choledocholithiasis, 187
E
Cholelithiasis, 187
Chronic pancreatitis, 158, 189, 191 Ectopic varices, 71
Colonic lipoma, 87 Electrocoagulation, 10, 133
Colonic varices, 102 EMR, 19
Concealed ruptured of gallbladder, 168 Endoscopic band ligation, 89
Condyloma acuminatum, 137 Endoscopic mucosal resection, 18
Cowden’s syndrome, 6 Endoscopic submucosal dissection, 27
Crescent (Duck bill) snare, 18 Endoscopic variceal ligation, 16
Crohn’s disease, 105 Episcleritis, 104
Csendes’s classification, 170 Episodic dysphagia, 15
Cushion sign, 87 Erythematous stripes, 30
Cyanoacrylate, 17 ESCC, 24
Cyst fluid analysis, 210 Escherichia coli, 135
Cystic artery aneurysm, 72 ESD, 29
Cystic duct leak, 164 Esophageal cancer, 1
Cystic glands, 28 Esophageal candidiasis, 22
Cystoduodenal fistula, 72 Esophageal dilatation, 15
Cysto-duodenostomy, 184 Esophageal glycogenic acanthosis, 5
Cysto-gastrostomy, 184 Esophageal Leiomyoma, 195
Esophageal ring, 14
Esophageal squamous cell carcinoma, 24
Esophageal stenosis, 181

D Esophageal stromal tumors, 196

Esophageal ulcer, 3
Esophageal varices, 206
Dentate line, 117 Esophageal varix, 16
Dieulafoy’s type, 85 Essential thrombocytosis, 103

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EUS guided choledochoduodenostomy , 154 Gastrointestinal carcinoids, 45
EUS-CPN, 201 Gastrointestinal stromal tumor, 212
EUS-FNA, 190, 212, 217 GAVE, 31
GCP, 28
GERD, 8
Glue injection, 16

F
Familial adenomatous polyposis,41
FAP, 41
H
Fat stranding, 191
Field cancerization, 13 H.pylori, 60
Foveolar dysplasia, 48 Hartmann’s pouch, 168
Foveolar hyperplasia, 28 Hematemesis, 4, 7
Fully-covered self-expandable metal stent, 150 Hematochezia, 81
Hemocholecyst, 72
Hemoclipping, 10, 133
Hemophilia, 72

G Heterotopic pancreas, 36
High grade dysplasia, 19, 27, 125
Hilar cholangiocarcinoma, 62, 200
Gallbladder adenocarcinoma, 217 Histoacryl, 16
Gangrenous bowel, 75 Hoarseness, 181
Gangrenous ischemic colitis, 96 Hyperplastic mucoceles, 145
Gastric adenoma, 47, 48 Hyperplastic polyp, 140
Gastric antral vascular ectasia, 31
Gastric cancer, 198
Gastric carcinomas, 29
Gastric cardia, 25
Gastric infarction, 51
I
Gastric lymphoma, 171, 207
Gastric mass, 44 Ig G4, 173
Gastric NETs, 45 IgA antiendomysial antibodies, 66
Gastric submucosal lesion, 212 IgA anti-tissue transglutaminase, 66
Gastric vulvolus, 51 Ileal ulcers, 104
Gastritis cystica profunda, 27 Infected pancreatic pseudocyst, 184

225
 L
Inflammatory polyp, 107
Inflammatory pseudo, 82
Infrared coagulation therapy, 117
Inlet patch, 1
Inoue’s classification, 11 LA classification, 8
Insulinoma, 220 Laparoscopic Heller myotomy, 26
Internal hemorrhoids, 117 Laparoscopic myotomy, 26
Intraductal papillary mucinous neoplasm, 176 Leiomyoma, 195
Intramucosal colon cancer, 120 Linear echoendoscope, 209
Intrapapillary capillary loops, 11 Linear EUS probe, 197
Invasive adenocarcinoma, 92 Linitis plastic, 43, 171
Invasive colonic cancer, 122 Lipiodol, 16
IPMN, 176 Lipoma, 145
Iron deficiency anemia, 8, 30, 91 Long cystic duct, 168
Ischemic colitis, 99, 119 Lymphangioma, 145

J M
Jejunojejunal intussusceptions, 127 Magnetic resonance
cholangiopancreatography, 186
Malignant lymphoma, 54
Mallory-Weiss syndrome, 10

K Mallory-Weiss tears, 90
MALT lymphoma, 207
Malunion of pancreatobiliary ducts, 161
Kissing ulcer, 4 Marginal crypt epithelium, 47
Kudo’s classification, 124 Maroon stool, 72
Mediastinal cysts, 182
Mediastinal mass, 181
Mediastinal neuroendocrine tumor, 182
Melena, 23
Metachronous squamous cell carcinoma, 13

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 P
Microsurface pattern, 32
Microvascular pattern, 32
Minor duodenal papilla, 158
Mirizzi’s syndrome, 168
Mucinous cystadenoma, 145 Painless jaundice, 67, 150, 216
Mucosa-associated lymphoid tissue, 55 Pancreas divisum, 158
Multiple endocrine neoplasia type 1, 220 Pancreatic cancer, 190
Pancreatic cys, 209
Pancreatic duct stone, 161
Pancreatic ductal dilation, 176

N Pancreatic head cancer, 70

Pancreatic heterotopias, 36
Pancreatic pseudocyst, 202, 213
NAGI-Stent, 204 Pancreatic rest, 36
Naked fat sign, 87 Pancreaticoduodenectomy, 151
Neuroendocrine carcinoma, 181 Pancreatitis, 213
Neuroendocrine tumor, 44, 219 Paris classification Isp, 109
NICE classification, 92, 110 Paris classification, 122
Nitinol, 69 Percentage Ki-67 index, 44
NOMI, 76 Percutaneous endoscopic gastrostomy, 52
Non-bleeding visible vessel, 85 Pericholecystic collection, 166
Non-Hodgkin lymphoma, 206 Peripancreatic fluid, 190
Non-inflamed pseudopolyps, 82 Peroral endoscopic myotomy, 25
Non-occlusive mesenteric ischemia, 75, 94 PHG, 31
Non-sigmoid type, 25 Pill-induced esophagitis, 4
Pillow sign, 86
Pneumatic balloon dilatation, 26
POEM, 26

O Polycystic kidney disease, 209

Poorly-differentiated adenocarcinoma, 42
Portal hypertensive gastropathy, 31
Occult GI bleeding, 31 Post EVL scar, 16
Odynophagia, 4, 24 Post-polypectomy bleeding, 89
Omental cake, 171 Preoperative biliary dra, 151
Ovesco OTSC Clip, 69 Procore needle, 206

227
 Progressive dysphagia, 181 Small bowel gangrene, 93
Prolapse gastropathy, 38 Smoldering diverticulitis, 129
Pseudocyst, 183 Snake-skin mosaic pattern, 31
Pseudomembranous colitis, 135 Solid Pseudopapillary
Pseudopapillary tumor, 173 Tumor of the Pancreas, 173
Pseudopolyps, 81, 107 Spindle cell neoplasm, 211
SPT, 173
Squamous cell carcinoma, 11
Submucosal gangrene, 50

R Submucosal invasive colonic cancer, 123

Subtotal gastrectomy, 44
Superior mesenteric vein, 71
Rectal diverticulum, 131
Rectal ulcer syndrome, 85
Reflux esophagitis, 8
Retching, 37
Rosemont classification, 193
T
Round cell tumor, 44, 219
Roux-Y reconstruction, 170 Taenia saginata, 112
Tis staging, 11
TNM stag, 207
Tortuous ectatic vessels, 30

S Transmural gangrene, 76, 94

Trichuris trichiura, 143
Tubular adenoma, 125
Salmon-colored patch, 1
Sano’s classification, 110, 120
Scalloping, 66
Schatzki´s ring, 15
U
Serum IgA level, 66
Side branches dilation, 193
Sliding hiatal hernia, 14 Ulcerative colitis, 82
SMA embolus, 76 Ulcerative mass, 23
SMA thrombosis, 76 Unresectable pancreatic cancer, 158

228
 V
Vascular malformation, 58
Vascular pattern, 82
Video-assisted thoracoscopic
surgery, 181
Villous adenoma, 109

W
Wallstent, 216
Whipple surge, 173

229