desene diverticule

140 Indian Journal of Surgery 2004 Volume 66 Issue 3 (June)

Duodenal diverticulum: Review of literature

Sanjay K.Mahajan, Rajesh Kashyap, Upender K. Chandel*, Jatinder Mokta, Satinder S. Minhas*Department of Medicine and *Surgery, Indira Gandhi Medical College, Shimla - 171001, India.

ABSTRACTDuodenal Diverticulum was first reported by Chomell in 1710 and was regarded an anatomic curiosity until 1913when first radiological demonstration was done by JT Case. With modern radiological techniques and widespreaduse of endoscope it has been found that these diverticula occur more frequently than was formely supposed. Mostof these are asymptomatic, situated in second part of duodenam and are rarely associated with complication whichare usually cause of presentation.

KEY WORDSDuodenal Diverticulum, Extra luminal Duodenal Diverticulum, Periampullary Duodenal Diverticulum, Juxta papillaryDuodenal Diverticulum. Intra luminal Duodenal Diverticulum

How to cite this article: Mahajan SK, Kashyap R, Chandel UK, Mokta J, Minhas SS. Department of Medicine and Surgery, Indira GandhiMedical College, Shimla-171001, India. Duodenal Diverticulum: Review of literature. Indian J Surg 2004;66:140-5.

Review Article

Address for correspondence: Dr. Sanjay Mahajan, 31/3, US Club, Shimla-171001, India. E-mail: [email protected] Received: July 2003. Paper Accepted: October 2003. Source of Support: Nil.

INTRODUCTION

Duodenal diverticula was first reported by Chomall in

1710 and first well documented report was made by

Morgagni in 1762 and it was regarded an anatomic

curiosity until 1913 when radiological demonstration

was done by JT Case, who displayed roentgenograms

of 4 cases in the Scientific Exhibit of the American

Medical Association. With lengthening of life span,

diverticulosis has come to occupy a more important

position in the sphere of clinical gastroenterology.

Duodenum is second most common site of diverticula

in alimentary tract after colon followed by jejunum,

ileum and stomach.2,3 Duodenal diverticula are found

in up to 25% of patients, but rarely cause symptoms

when complications occur, early diagnosis is essential

if treatment is to be successful.3 Diverticula of

duodenum are classified as primary and secondary.

Majority of secondary or false diverticula are result of

chronic duodenal ulceration, so called prestenotic

diverticulum where as primary are true diverticula.4

These occur mainly in later decades of life with peak

incidence between 50 and 60 years of age and it

increases with age.1,2,4-6 There is no gender

predisposition but female preponderance has also been

reported.1-5 Incidences varies with diagnostic method

used.3 In UGI barium series it is 0.016 to 6%,2,4-8 in

autopsy series 22 to 23%,2,4,5,7 where as on ERCP studies

incidence is 9 to 23%.6,7 Over 95% of duodenal

diverticula project from inner or pancreatic border of

duodenal curve in second, third and fourth parts.

Second part is most common site with 85 to 90% of

total DD.1,2,4,9 Third and fourth parts of duodenum have

20 and 10% of diverticula respectively,2 but up to 30

to 40% of these may arise from third and fourth part of

duodenum.10 Diverticulum may be single or multiple

and as many as 6 or more has been reported. Incidence

of multiplicity at x-ray series is 1.4 to 23.5% and in

autopsy series it is 3.5 to 30%. These are usually

spherical or hemispherical and when filled with barium

usually oval in shape often resembling Erlenmeyer flask

showing narrow neck.2 These are classified into EDD

and IDD. EDD are more common3 and can be further

classified into PAD and JPDD. PADS are extra luminal

mucosal out pouching of duodenum arising adjacent

to or containing the ampulla of Vater or intraluminal

portion of CBD (common bile duct). JPDD are defined

as EDD located with in radius of 2 cm of major papilla

but not containing it. Some has referred to above

definition as ampullary and periampullary while others

refer both type of EDD collectively as JPDD. However,

consistent and precise terminology needs to establish.

About 75% of EDD occur with in 2 cm of ampulla of

Vater.2-6,10-12

© 2004 Indian Journal of Surgery www.indianjsurg.com

141


Indian Journal of Surgery 2004 Volume 66 Issue 3 (June)

AETIOLOGY AND PATHOLOGYThese are true pouches or sacs protruding from

duodenal lumen not caused by any recognizable

intrinsic or extrinsic disease. EDD are acquired and

consist of a sac of mucosal or sub mucosal layers

herniated through a muscular defect in bowel wall but

precise manner of the development is not known.2,6,10

However, there exists a locus minoris resistentiae which

may be created by (i) passage of the biliary, pancreatic

duct and blood vessels through the wall of duodenum.

(ii) Congenital absence of an adequate muscle coat (iii)

heterotrophic pancreatic tissue. Once diverticulum is

formed it may increase in size through the years.2,6,10

The position of fundus and body of EDD is variable and

mostly lie in retro peritoneum with large portion lying

close to concave medial surface close to CBD and

pancreatic duct. Rarely, the diverticula may be localized

on the convex side of the second part of duodenum.

The sac lie along side, extend behind or even penetrate

into the pancreas and occasionally CBD and duct of

Wirsung may open into the diverticulum3,4,6 IDD or

windsock diverticula are not true diverticula and occur

as single saccular structure which are connected to the

entire circumference or only part of the wall of the

duodenum. Only less than 100 cases have been

reported in the literature. During early foetal life

duodenal lumen is initially occluded by proliferating

epithelial cells and recanalises later on. Abnormal

recanalising may lead to a duodenal diaphragm or web

which may not produce symptoms in child hood

however over the period of time peristaltic stretching

may transform it into an IDD. IDD may project as distally

as fourth part of duodenum and often a second opening

is located eccentrically in the sac and both sides of the

diverticulum are lined by mucosa.3,6,10

Pathologically the larger pouches usually lack a

muscular coat although often the smaller one do contain

some fibers. Attempts have been made to divide

duodenum diverticulum in to true or congenital

pouches and false or acquired pouches. If all muscle

coats are presents it was termed true or congenital

and if muscle layer was not present it was thought to

be acquired or false, such a division seems untenable

as there is nothing to prove that certain pouches are

basically congenital and others entirely acquired. The

amount of muscle fibers in the pouch depends more

upon its age and size. Histologically in majority, the

circular and longitudinal muscle coats of duodenum

are missing and the mucosa and muscularis mucosae

make up the wall of the diverticulum.2

CLINICAL FEATURESGreat majority of duodenal diverticula are

asymptomatic.2,4,6,7,9,10 Clinical presentation may be

characterized by non-specific abdominal symptoms4

and less than 5% of patients have abdominal

symptoms.2 Abdominal discomfort is usually located

in epigastrium, right upper abdomen or umbilical area

which is made worse or brought on by eating and

relieved by vomiting, belching or assuming certain

posture.2,4,6 There are no characteristic symptom

complex from which one may make a positive

diagnosis of DD. Many believe that there are three main

factors in production of symptoms.

A. Mechanical causes producing

1. Delayed empting of diverticula

2. Pressure on the common bile or pancreatic duct

3. Obstruction of the duodenum

B. Inflammatory causes producing

1. Symptoms simulating peptic ulcer, gall bladder

or pancreatic disease

2. Pyloro-spasm

3. Perforation

C. Neoplasia

Patients may complain of pain radiating to the back

between the scapulae and between costo-vertebral

angles. The pain caused by the diverticula in the third

part of the duodenum is situated near the mid line

where as that caused by the pressure upon the pancreas

may be situated to the left. The peptic ulcer like

syndrome has been noted in several patients, however

in the absence of ulcers, the symptoms may be due to

inflammation and stasis in the sac. The simulation of

peptic ulcer disease by DD may be close. Intermittent

diarrhea and constipation, weight loss because of the

fear of eating and steatorrhea may also occur in some

patients.2,3,10,11

The symptoms simulating primary biliary tract disease

may occur in DD located near ampulla of Vater and

some time CBD may terminate in the diverticulum. The

“perivaterian diverticulitis” may give rise to obstructive

jaundice. The greater propensity for the pigment stones

in the presence of EDD is not fully understood and

excess release of calcium bilirubinate by ascending

Beta-Lucuronidase colonization into CBD has been the

possible cause.2,3,5 Several authors have shown that

compression of CBD, dysfunctions of ampulla or a

poorly emptying diverticulum with a narrow neck can

lead to pancreatico-biliary disease and acute

Mahajan SK, et al


pancreatitis. Some even suggested that PAD be

included in the aetiology of acute pancreatitis especially

in the elderly.13 JPDD are important causative factors in

the bile duct stone formation.14,15 Since

choledocholithasis leading to biliary obstruction is a

well known etiology of acute pancreatitis there is

debate whether the increased incidence of pancreatitis

with EDD is due primarily to the mechanical

complications or associated biliary stones. As most DD

occur on the concave border of second part of

duodenum in close contact with or embedded in to

the head of pancreas, perforation of diverticulum can

also cause pancreatitis.2,5,6 The majority of IDD, in

contrast to EDD, will become symptomatic and can

present at any age from the first through the eighth

decade of life. The most common symptoms are those

of incomplete duodenal obstruction by retention of

vegetable or foreign bodies. Pancreatitis and

hemorrhage has also been reported in IDD. In

childhood cases 20% can have symptoms and it is to

be dif ferentiated from duodenal intrinsic defect,

extrinsic defects, and anal rotation with congenital

bands.3,6,10,16

COMPLICATIONSAs diverticula are usually asymptomatic, complications

are responsible for presentation most of the times.11

The complications may be divided into two groups.

Those related to pressure on the adjacent structures

and those caused by inflammation. Jaundice,

cholangitis, acute and chronic pancreatitis and

duodenal obstruction are caused as a result of

mechanical compression by diverticula, whereas

diverticulitis and ulceration are caused by

inflammation.2-4,6,10,11

Diverticulitis and PerforationWhen drainage of sac is inadequate or neck is narrow

or ostium is buried, these conditions favour

inflammation and may lead to perforation which in turn

may lead to localized abscess formation, generalised

peritonitis. Ulceration, enteroliths and foreign body can

be other reasons for per foration. The on set of

perforation is acute in majority but can be gradual also.

The perforated diverticulum should be considered in

the presence of bile stained phlegmon in the para-

duodenal area, retroperitoneal edema or emphysema,

retroperitoneal yellow flaky exudates or pus or a right

sub-hepatic abscess.

Ulceration can occur because of presence of ectopic

gastric mucosa or inflammation. Diverticular ulceration

may give rise to massive bleeding or perforation into

aorta or a mesenteric vessel. The intake of NSAIDs has

also been attributed to ulcerations or

hemorrhage.2,3,10,11,17 Although it is extremely

uncommon nevertheless massive GI hemorrhage

leading to shock can be due to diverticula.2,9,11,12 Some

believe that bleeding from diverticula is more common

than thought, and index of suspicion should be raised

in UGI hemorrhage where causes have been excluded

by endoscopy.2,7 Duodeno-colic, gastro-jejuno colic

fistula formation may occur secondary to inflammation

in diverticula. Pancreatic and / or biliary fistula as a

complication during surgery has also been reported.

Intestinal obstruction as a result of blockage of the distal

part of the bowel by a large calculus (enteroliths) which

has been extruded from a DD has been reported.

Neoplastic changes including adenocarcinoma,

sarcoma, leiomyosarcoma or fibroma is also known.

Peridiverticulitis and bezoar formation are other

complication described with this condition.2,3,6,10

ASSOCIATED DISEASESDuodenal ulcerIt has been noted in large number of patients with DD.

A suspicion of duodenal ulcer has been principal reason

for subjecting many patients to investigation. Although

relationship of duodenal ulcer with DD is important

one, there does not seem to be any cause and effect

relationship.2,3,10

Hiatus HerniaThe relative prevalence of hiatus hernia and DD steadily

increases after the fifth decade so their frequent

association in later life is to be anticipated.

Diverticula elsewhereThe reported range of associated jejunal and ileal

diverticula is 4% to 13% of all patients with DD. The

incidence of colonic diverticula in patients with DD is

much higher (20-50%) than in general population over

age of 50 years (10%). A 40% prevalence of coexisting

congenital anomalies has been reported in IDD and its

predecessor, congenital DD. These anomalies include

annular pancreas, choledochocele, omphalocele,

hypoplastic kidney, situs inversus, malrotation, Ladd-

band, portal vein anomalies and Down syndrome.2,16

DIAGNOSISUpper GI barium studiesDuodenal diverticulum is an incidental finding of UGI

barium examination after ingestion of barium, study is

made in erect, recumbent and oblique positions. One

Duodenal Diverticulum

143



of most important feature is abnormal retention of

barium in the sac. Barium retention for 6 or more hours

is diagnostic. The use of a small amount of barium may

help to avoid the overlapping of duodenum by jejunal

loops and by the completely filled stomach. At times

sac is better visualized from 1-2 hours following the

opaque meals.2,4,6,10,18

Differential diagnosis barium upper GI seriesIn first part of duodenum, pseudodiverticula occur

proximally to stenosing duodenal ulcer. These have

either no neck or a very wide neck and are much longer,

narrower than true diverticula, these are invariably

associated with duodenal deformity distally. In second

part a small diverticulum may resemble the niche of a

post bulbar ulcer. The presence of a small neck

differentiate ulcer niche. In the third part diverticulum

from upper jejunal loops may be confused with DD.

Antero-posterior film exposed in patients with

diverticula of 4th part of duodenum may be confused

with ulcer or cancer of lesser curvature of the stomach.

But films taken with patient in lateral position will

demonstrate normal out line of the stomach.2,18

In upper GI series in patients with IDD, the “duodenal

Wind Sock sign” may be seen. It consists of barium

filled sac that lies entirely within duodenum and is

surrounded by a narrow radio-luscent line which is well

demonstrated as the barium in the duodenum passes

distal to the diverticulum.16

Upper G.I. Endoscopy is an important investigation for

diagnosis of DD. It is successful in diagnosing DD in

more than 75% of patients.19 Side viewing endoscopy

may further increase the success rate. The rate of failure

of endoscopy to diagnose DD may increase if DD is

situated in third or fourth part of the duodenum. At

endoscopy IDD appears as a sac like structure with

eccentric aperture lying with normal mucosa or as a

soft polypoidal mass.6,16 JPDD make endoscopic

examination as well as possible subsequent

intervention more difficult. Guide wires should be used

for complicated procedures. Diverticula may even be

the cause of failure or complications such as

hemorrhage or perforations. It can also diagnose

associated lesions which may be responsible for

symptoms. But it has also failed to identify bleeding

diverticula in up to 70%7 few other studies have also

highlighted the failure of endoscopy to diagnose

bleeding diverticulum and more so when it was situated

in third or fourth part of duodenum.7,9-11 ERCP

(Endoscopic Retrograde Cholangiopancreatography)

when done for investigating pancreatico-biliary system

can diagnose large number of diverticula.6,7,12,20

Whenever endoscopy can not determine the cause of

bleeding, angiography may be performed.7,21 Diagnosis

can also be established with combination of

arteriography and scanning with Technetium-99

lebelled red cells.7,9

CT scan and MRIWhen associated with diverticulitis or perforation the

CT appearance of DD include a mass like structure that

is interposed between the duodenum and the

pancreatic head containing air, an air fluid level, fluid,

contrast material, or debris. On perforation, duodenal

wall thickening and surrounding free air, fluid and fat

stranding may be noted.3,6,10,22,23 When diverticulum is

entirely filled with fluid it may mimic a cystic neoplasm

arising from the head of the pancreas. Location and

presence of small amount of intradiverticular gas when

present may aid in establishing the diagnosis. On MRI,

T2 weighted True FISP (Fast Imaging with Steady state

Precession) and HASTE (half Fourier Single Shot Fast

Spin ECHO) images demonstrate air fluid levels within

diverticula. Hypo intense oral contrast on T1 weighted

spoiled gradient ECHO images aid detection of the

smaller diverticula. MRCP images in coronal plane best

demonstrate the relationship of the diverticula to the

papilla. MRI facilitates precise delineation of the

complicated DD while MRCP allows assessment of the

effects of DD on biliary and pancreatic duct. IDD has

been reported to be evaluated with computed

tomography endoscopic Ultrasonography, intravenous

cholangiography, percutaneous transhepatic

cholangiography and ERCP.16,24,25

TREATMENTElective surgical treatment of asymptomatic

diverticulum is not justified as these are innocent.

However small percentage can cause problem ranging

from mild and slightly annoying symptoms to

dangerous and even fatal complications.

Diverticulectomy done for vague pain and abdominal

discomfort is dangerous and unrewarding2,6 and only

about 50% of patients treated by diverticulectomy

electively were entirely relieved of their symptoms.2-

6,26 Only 1-5% of diagnosed DD will require surgery

when complication has arisen having incapacitating

symptoms. In patients with symptoms due to distention

of diverticula, relief may be obtained by patient

assuming a position that allows dependent drainage

of diverticulum which may be determined by

fluoroscopy. Acute obstruction of diverticulum may be

Mahajan SK, et al


relieved by endoscopic clearance. Operative procedure

for diverticula of second part of duodenum needs

mobilization of duodenum by Kochar maneuver.

Duodenum is turned medially and thin walled

diverticulum comes in view. Diverticulum is dissected

which is frequently near communication of the CBD

and main pancreatic duct. Dissected sac is split open

and position of papillae of Vater confirmed.

Diverticulum is excised and opening of duodenum

closed transversely. When duodenum is near the

common bile duct closure of duodenum may press on

it. Supra-duodenal part of CBD is opened and T-Tube

passed well into duodenum before closure of duodenal

wall after diverticulum excision. Diverticulum arising

from second and third part may be approached through

mesocolon. If the ampulla of Vater enters the

diverticulum in presence of CBD obstruction,

Scudamore et al reported that they per formed

choledochoduodenostomy than directly attack the

diverticulum.27 Choledochoduodenostomy,

Choledochojejunostomy alone do not relieve problems

arising from pancreatic duct. Resection however may

be difficult in cases where diverticulum is buried in the

head of pancreas or the papilla lies deep in the

diverticulum. Therefore in cases in which a direct

approach to the diverticulum seems to be hazardous,

division of duodenum 2 cm distal to the pylorus with

drainage by a Roux-en-Y duodenojejunostomy may be

performed. “Diverticulisation” of duodenum is another

method of bypassing diverticulum (Antrectomy,

Vagotomy, Choledochostomy and Billroth II

anastomosis).3,6

Surgical excision is not without complications and

mortality rate of 30% in post operative period has been

reported. A delay in diagnosis can lead to perforation

in DD which carries a mortality rate of 90%.10 Injury to

adjacent ampulla of Vater leading to interference with

drainage of bile or pancreatic secretions may lead to

jaundice, pancreatitis, or development of duodenal

fistula. An overaggressive attempt to dissect the

duodenum from pancreas may lead to pancreatitis and

hemorrhage. Laparoscopic duodenal diverticulectomy

can be done by using intraoperative endoscopic

guidance.27-30 All IDD require treatment as recurrence

of symptoms is certain. Curative treatment consists of

removal of diverticulum by laparotomy and

duodenotomy or by endoscopy. If diverticulum is not

circumferentially attached, it can be resected

endoscopically with an electrocautery snare. If it is

attached circumferentially it can be inverted with the

endoscope, partially resected to create an opening in

the blind end. When papilla, CBD, or pancreatic duct

cannot be clearly identified duodenostomy should be

performed. If at the time of duodenotomy the papilla

cannot be identified, choledochotomy and placement

of a bile duct probe to localize the papilla should be

per formed prior to the resection of the

diverticulum.3,4,10

Duodenal diverticulum present in about 25% of

patients. DD can be commoner than EDD, which are

acquired or IDD which are congenital and rare. Majority

are asymptomatic, only a small percentage of patients

will develop symptoms ranging from mild abdominal

discomfort to serious complications like diverticulitis,

perforation, ulceration and haemorrhage. Majority of

diverticula can be diagnosed by endoscopy, especially

Figure 1: Barium follow through showing diverticulum insecond part of duodenum.

Figure 2: Schematic diagram showing surgical steps. (A & B):Exposure of the diverticulum of second part of duodenum. (C& D): Surgical removal of diverticulum of second part ofduodenum.

Duodenal Diverticulum

145



side viewing endoscopy and upper GI barium studies.

Asymptomatic diverticula do not require surgical

management. Surgical procedures in this area are

difficult to perform and are associated with high rate

of post-operative complications and mortality. Early

recognition is essential if treatment is to be successful.

REFERENCES

1. Lane JE, Ajjan M, Sedghi S. GI bleeding from duodenal diver-

ticula. Am J Gast; 2001:2799.

2. Pimparkar BD. Diverticulosis of the small intestine In: Bockus Henry

L, (Ed). Gastroenterology. 3rd (Ed). Philadelphia: WB Saunders

Co 1976:437-58.

3. Knoefel WT, Ratttner DW. Duodenal diverticula and duodenal tu-

mours In: Morris PJ, Malt RA, (Ed). Oxford Text Book of Surgery.

New York: Oxford University Press 1994;1:943-6.

4. Cheshire NJ, Glezer G. Diverticula, volvulus, superior mesenteric

artery syndrome and foreign bodies. In: Zinner MJ, Schwartz SI,

Ellis H, (Ed). Maingoats Abdominal operation 10th (Ed). London:

Prentice Hall International Ince (UK) Limited 916-21.

5. Lobo DN, Balfour TW, Iftikhar SY, Rowlands BJ. Periampullary di-

verticula and pancraeticobiliary disease. Br J Surg 1999;86:588-

97.

6. Harford WV. Diverticula of the hypopharynx and esophagus, the

stomach and small bowel. In: Feldman M, Scharschmidt BF,

Sleisenger MH, (Ed). Sleisenger and Fordtran’s Gastrointestinal

and Liver Diseases. 6th (Ed). Philadelphia: WB Saunders Co

1998;1:313-6.

7. Yin WY, Chen HT, Huang SM, Lin HH, Chang TM. Clinical analysis

and literature review of massive duodenal diverticular bleeding.

World J Surg 2001;25:848-55.

8. Balkissoon J, Balkissoon B, Leffall LD Jr, Posey DA Jr. Massive up-

per gastrointestinal bleeding in a patient with a duodenal diver-

ticulum: A case report and review of literature. J Natl Med Assoc

1992;84:365-7.

9. Rioux L, Des Groseilliers S, Fortin M, Mutch DO. Massive upper

gastrointestinal bleeding originating from a fourth stage duode-

nal diverticulum: A case report and review of the literature. Can J

Surg 1996;39:510-2.

10. Afridi SA, Fichenbaum CJ, Taubin H. Review of duodenal diver-

ticula. Am J Gastroenterology 1991;86:935-8.

11. Donald JW. Major complications of small bowel diverticula. Ann

Surg 1979;190:183-8.

12. Zoeof T, Zoepf DS, Arnold JC, Benz C, Riemann J. The relationship

between juxtapapillary and duodenal diverticula and disorders of

the biliopancreatic system. Analysis of 350 patients. Gastrointest

Endosc 2001;54:56-61.

13. Uomo G, Manes G, Ragozzino A, Cavallera A, Rabbiti PG.

Periampullary extra luminal duodenal diverticula and acute pan-

creatitis. An underestimated eitiological association. Am J Gas-

troenterology 1996;91:1186-8.

14. Christoforidis E, Goulimaris I, Kanellos I, Tsalis K, Dadoukis I. The

role of juxtapapillary duodenal diverticula in biliary stone disease.

Gastrointest. Endosc 2002;55:543-7.

15. Leivonen MK, Halthenen JA, Kivilaakso EO. Duodenal diverticu-

lum at endoscopic retrograde cholangiopancreaticography, analy-

sis of 123 patients. Hepatogastroenterology 1996;43:961-6.

16. Materne R. The duodenal windsock sign. Radiology

2001;218:749-50.

17. Mahajan SK, Vaidya P, Sood BR, Gupta D, Sharma A. Duodenal

diverticular hemorrhage in a patient taking NSAID. J Assoc Physi-

cians India 2003;51:416-8.

18. Eisenberg RL. Gastrointestinal Radiology. Philadelphia: Lippincott;

1990:529-34.

19. Zemlianoi AG, Gorbunov GM, Kerzikov AF. The role of duode-

noscopy in the diagnosis of duodenal diverticulosis. Khirurgiia

(Mosk) 1990;12:44-6.

20. Riebel O, Piskac P. Juxtapapillary diverticulum-the effect on en-

doscopic interventions and diagnosis. Rozhl Chir 1996;75:429-

32.

21. Mosimann F, Bronnimann B. The duodenal diverticulm: An ex-

ceptional site of massive bleeding. Hepatogastroentrology

1998;45:603-5.

22. Rao PM. Per forated duodenal diverticulitis. Radiology

1999;211:711-3.

23. Macari M, Lazarus D, Israel G, Megibow A. Duodenal diverticula

mimicking cystic neoplasms of the pancreas: CT and MRI imaging

findings in seven patients. AJR Am J Roentgenol 2003;180:195-

9.

24. Balci NC, Noone T, Akon E, Akinci A, Kler HV. Juxtapapillary di-

verticulum: findings on MRI. Journal of Magnetic Resonance

Imaging 2003;17:487-92.

25. Balci NC, Akinci A, Akon E, Kler HV. Juxtapapillary diverticulum:

Findings on CT and MRI. Clinical Imaging 2003;27:82-8.

26. Cattell RB, Mudge TJ. The surgical significance of duodenal diver-

ticula. N Engl J Med 1952;246:317-24.

27. Scudamore CH, Harrison RC. Management of duodenal diver-

ticula. Can J Surg 1982;25:311.

28. Solhang JH, Semb BK. Duodenal diverticulum with intermittent

biliary stasis. Acta Chir Scand 1974;140:670-3.

29. Fujii K, Fujioka S, Kato K, Machiki Y, Kutsuna Y, Ishikawa A, et al.

Recurrent bleeding from a duodenal diverticulum 8 years after

endoscopic treatment: Case report and review of the literature.

Hepatogastroenterology 2001;48:1058-60.

30. Callery MP, Aliperti G, Soper NJ. Laparoscopic duodenal diverti-

culectomy following heamorrhage. Surge Laparosc Endosc

1994;4:134-8.

Mahajan SK, et al

desene diverticule

Documents

Transcript of desene diverticule