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Berger: I encourage everybody, whether they’ve had diverticulitis or not, over the
age of 30 to 35 to be taking two scoops of Metamucil every morning for the rest of
their lives.
That will reduce their chance of getting diverticulosis. It will also help reduce
their cholesterol and their chance of developing colon cancer or colitis. Yes, I’m a
big fan of ber. Is it going to turn things back after you have somebody who already
has a signicant diverticular disease? Not really, but it may minimize symptoms and
complications.
I think everybody ought to be on ber anyway because of our diet. Do you
remember the story about Denis Burkitt of Burkitt’s lymphoma? He went to Uganda
and not only discovered Burkitt’s lymphoma, but he also noted that colon cancer,
diverticular disease, and colitis were rarely seen in Uganda, and he attributed all of
that to ber. In Uganda, they eat huge amounts of very brous food, and he found
that they would have four to ve soft bowel movements every day. In contrast, the
average Irish stool was round and hard and was produced once a day or even once
every other day, and he concluded that it was the ber that made the difference in
their colonic health.
What do you think about NSAIDs increasing the risk of diverticulitis?
Berger: When I see NSAIDs causing an issue, it’s usually something in the ter-
minal ileum or proximal colon. I don’t usually see them causing a problem down-
stream, in the sigmoid. So, from my experience I’m not big on that one.
Sobin: In my experience, it has not been a signicant contributing factor. In spite
of that, I recommend NSAID avoidance in patients with a history of diverticulitis.
Case 4 A 47-year-old man has had one episode of sigmoid diverticulitis. He is
treated, and all inammatory markers resolve. However, months later, he has ongo-
ing pain in the same region. His WBC and CRP are normal. A repeat CT scan shows
no active inammation.
Is this SUDD (symptomatic uncomplicated diverticular disease)? Is this a
real, distinct entity? If so, how would you treat it?
Browning: If abdominal pain is present in patients with diverticulosis, in the
absence of diverticulitis or clinical bleeding, they may have SUDD.Some think of
this as a continuum of irritable bowel syndrome (IBS), with benign physical exami-
nation and colonoscopy (other than diverticula), normal inammatory laboratories,
presence of abdominal fullness symptoms, and symptoms that improve with defeca-
tion [1].
Several medications have been used for prevention of recurrent diverticulitis or
management of SUDD.Proposed regimens include mesalamine 800mg twice daily
for 3 months to help prevent SUDD relapse, rifaximin 400 mg twice daily for
7 days, or combination therapy with mesalamine and rifaximin. Most studies
resulted in symptomatic improvement, but these studies were open-label. A
Cochrane meta-analysis in 2017 reviewed the use of mesalamine for prevention of
diverticulitis. They did not nd evidence that mesalamine prevented recurrent diver-
ticulitis, although the trials were heterogeneous [6].
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Sobin: My bias is to manage these patients as if they have IBS, with visceral
hypersensitivity. In fact, some have suggested that diverticulitis may predispose to
IBS. There may be an entity of post-diverticulitis IBS, along the lines of post-
infectious IBS. I would not be inclined to try mesalamine unless they were not
responding to IBS therapy (which could include rifaximin).
Case 5 A 47-year-old woman presents to the ER with severe LLQ pain, a fever of
101, and marked tenderness on examination. Her WBC is 21,000, and a CT scan
shows phlegmonous sigmoid diverticulitis with an adjacent abscess, 4cm in size.
She has no past history of diverticulitis.
Are patients with diverticulitis more likely to have perforations, and other
complications, after their rst episode or subsequent ones?
Browning: Complicated diverticulitis is dened by abscess, stula, obstruction,
or free perforation. Complicated diverticulitis should be suspected when there is
persistent pain, fever, and leukocytosis despite IV antibiotics. Complications are
more likely to occur with the rst episode than subsequent episodes [2]. The
Hinchey classication was developed to stratify patient management [1]. Stage I is
conned pericolic abscess, stage II is distant abscess, stage III is generalized perito-
nitis due to rupture of pericolic/pelvic abscess, and stage IV is fecal peritonitis due
to free perforation of diverticulum.
Complicated diverticulitis is treated with hospitalization, IV antibiotics, surgical
consultation, and co-management. When patients develop worsening sepsis or have
recurrent abscess, it means that they have failed antibiotic treatment and should be
considered for drainage [7]. In general, if an abscess is greater than 3cm in size,
percutaneous drainage is recommended in addition to IV antibiotics [7].
Berger: My bias is that I tend to see complicated diverticulitis in elderly patients
who have had problems before. In my experience, the rst episode may not be
the worst.
On a per-episode basis, rst may be most likely to be complicated, but on a per-
patient basis, I worry most about the elderly patients with multiple prior episodes.
Tick, tick, tick.
Sobin: I believe the literature that says perforation is most likely with the rst
episode. I tell patients who have had multiple admissions for diverticulitis that I am
less worried about them needing emergency surgery for perforated diverticulitis.
Case 6 A 46-year-old man with a history of prior diverticulitis comes in for screen-
ing colonoscopy. He is found to have moderate inammatory change limited to an
8-cm length of sigmoid with moderate diverticulosis, where the inammation
seemed to spare the diverticula themselves. Biopsies did not suggest chronic colitis.
Do you think this may be SCAD—segmental colitis associated with
diverticulosis?
Browning: Segmental colitis associated with diverticulosis (SCAD) is an inam-
matory process affecting regions of colon that have diverticula [8]; SCAD can
mimic the presentation of inammatory bowel disease (IBD), with clinical features
including rectal bleeding, chronic diarrhea, cramping abdominal pain, and fever.
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Systemic symptoms like fever, weight loss, or leukocytosis are rare. It is present in
1.5% of colonoscopies, with the majority of patients being male, with a mean age
of 63 [1].
Pathogenesis of this condition is thought to be the effect of excessive mucosa
from bowel shortening in the setting of diverticulosis, leading to mucosal prolapse
and inammation associated with this [6]. However, when examined microscopi-
cally, there can be chronic crypt changes such as crypt distortion, that mimic
changes seen in ulcerative colitis. It has also been suggested that there may be bac-
terial stasis in diverticula leading to increased bacterial mucinase activity and
mucosal injury.
Lastly, given the overall older age of presentation in SCAD, there is also a
hypothesis of relative colon ischemia, leading to segmental mucosal inammation.
Interestingly, despite chronic inammation, there is not a higher risk of diverticulitis
or colon cancer [1].
There are four subtypes of SCAD: crescentic fold (A), mild-moderate UC-like
(B), Crohn’s disease-like (C), and severe UC-like (D). These are delineated at time
of endoscopy, but importantly all have sparing of the diverticula and regions of
colon without diverticula, which separates this disease from other conditions such
as IBD [6]. Type A is most likely to present with chronic diarrhea, has no crypt
distortion on histologic appearance, and appears as red round lesions 0.5–1.5cm at
top of mucosal folds. Types B and D have loss of vascular pattern with severe ulcer-
ation in type D and have crypt distortion on biopsy with goblet cell depletion. Type
C mucosa has isolated aphthous ulcers and evidence of transmucosal inammation
on biopsy. Types C and D are more likely to have rectal bleeding. Types B and D
tend to have a high risk of relapse [6].
Berger: Segmental colitis associated with diverticulosis? I have seen cases where
a patient has a single diverticulum exuding pus, and even though some of these folks
were asymptomatic, but others were mildly symptomatic, in these cases, there’s that
one tic and it’s red and there’s pus coming out of it, and I usually treat them with
antibiotics if they have symptoms to see if they get better.
Then, on occasion, it’s 5years later and we’re scoping them again. They have the
same darn thing with the same pus coming out of the same tic, and they’ve never had
any symptoms, and in cases like that it’s hard to justify treating that, unless of
course you had somebody who was about to undergo chemotherapy.
And sometimes, I’ll be working with the fellows, and we’ll be coming through a
really tight sigmoid with a lot of tics and very thick muscular haustra, and there will
be these red splotches. Then, the fellow will say “Oh, that’s colitis,” and sometimes,
I even say, “Okay, go ahead and take a biopsy of it,” and it comes back with nothing,
and that’s because it’s prolapsed, and you usually see the prolapse in the setting of
a sigmoid that’s also full of tics, and presumably there’s a high-pressure zone that’s
causing the tics and the hypertrophy and the prolapse. Just because it’s red doesn’t
mean it’s inamed. Mucosa isn’t skin.
Sobin: I’ve primarily seen these mucosal changes on routine surveillance colo-
noscopy, and I believe that it’s a residual change from prior diverticulitis. In a few
cases, I have seen this pattern that looks like IBD, but there’s sparing of the
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diverticula themselves, and the inammation is limited to a short segment of sig-
moid diverticula. Generally, these patients were asymptomatic, and before the des-
ignation of SCAD came about, I thought this was mild ischemia or mild Crohn’s
with just an unusual sparing of the diverticula themselves.
Browning: For patients who have more severe SCAD, with signicant symp-
toms, treatment regimens have been based on case series and extrapolation of expe-
rience from IBD.
One rst-line regimen starts with ciprooxacin 500mg BID and metronidazole
400mg TID for 7days, followed by mesalamine 2.4–3.2g/day for 4weeks and then
long-term maintenance dosing of 1.6g/day of mesalamine. For patients not respond-
ing, second-line therapy that uses beclomethasone dipropionate (BDP) with VSL
for 4 weeks with tapering dose for another 4 weeks has been tried, followed by
maintenance mesalamine. Third-line therapy with high-dose prednisolone has been
offered, with surgery for refractory cases [4].
However, in those cases where second- or third-line therapies have been neces-
sary, one must consider a misdiagnosis, and the patient has IBD instead. In fact,
some patients later develop IBD at the site of anastomosis when resection was
needed for SCAD [4].
Case 7 A 70-year-old man presents with his fth episode of sigmoid diverticulitis.
He has tried everything and has failed all conservative measures and is ready to
have elective surgery. On colonoscopy and CT scan, it is clear that he has diffuse
diverticulosis involving all portions of the colon (except the rectum). However, the
documented episodes of diverticulitis have only involved the sigmoid.
With this history do you think it is sufcient to recommend a sigmoid colec-
tomy, or do you think the patient should have a subtotal colectomy?
Berger: I would recommend just removing the sigmoid colon. I look at the colon
as two different organs, three if you include the rectum. The proximal and distal
colons have different motility, different pressures, different blood supply, and nerve
supply. The proximal colon is supplied by the superior mesenteric artery and is
innervated by the vagus. It is more-thin walled, and its contractions are segmental
contractions designed to mix and churn, to increase exposure of the bolus to the wall
to help extract salt and water. The distal colon is designed to store and expel, and its
motility is propulsive with much higher pressure, and it’s innervated by the sacral
outow and the vascular system is the inferior mesenteric artery, and so, they’re
actually two different organs and I don’t really see diverticulitis in the proximal
colon. I will see more bleeding from proximal colon diverticula, probably because
the superior mesenteric artery has more perfusion pressure than the inferior mesen-
teric artery.
Really, they are two distinct organs and if you have pandiverticulosis, the more
likely to bleed is the proximal, but the more likely to get diverticulitis is far and
away the distal, either the descending or the sigmoid, but the lower down you go, the
more likely it is to occur. So, I’m comfortable having him remove the sigmoid, or
the sigmoid and descending colon, leaving the rest intact.
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References
1. Feldman M, etal. Sleisenger and Fordtran's gastrointestinal and liver disease. 11th ed. Elsevier-
OHCE; 2020.
2. Peery AF, Strate SA, LL.AGA clinical practice update on medical Management of Colonic
Diverticulitis: expert review. Gastroenterology. 2021;160:906–11.
3. Santos A, Mentula P, Pinta T, Ismail S, Rautio T, Juusela R, Lähdesmäki A, Scheinin T, Sallinen
V.Quality-of-life and recurrence outcomes following laparoscopic elective sigmoid resection
vs conservative treatment following diverticulitis: Prespecied 2-year analysis of the LASER
randomized clinical trial. JAMA Surg. 2023;158(6):593–601.
4. Sheth AA, Longo A, Floch MH. Diverticular disease and diverticulitis. Am J Gastroenterol.
2008;103:1550–6.
5. Strate LL, Modi R, Cohen E, Spiegel BMR.Diverticular disease as a chronic illness: evolving
epidemiologic and clinical insights. Am J Gastroenterol. 2012;107:1486–93.
6. Carter F, Alsayb M, Marshall JK, Yuan Y.Mesalamine (5-ASA) for the prevention of recurrent
diverticulitis. Cochrane Database Syst Rev. 2017;10:CD009839.
7. Hall J, Hardiman K, Lee S, Lightner A, Stocchi L, Paquette IM, Steele SR, Feingold DL.The
American Society of Colon and Rectal Surgeons clinical practice guidelines for the treatment
of left-sided colonic diverticulitis. Dis Colon Rectum. 2020;63:728–47.
8. Schembri J, Bonello J, Chrisodoulou DK, Katsanos KH, Ellul P.Segmental colitis associated
with diverticulosis: is it the coexistence of colon diverticulosis and inammatory bowel dis-
ease? Ann Gastroenterol. 2017;30:257–61.
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139© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_20
Chapter 20
Pancreatic Cysts andRecurrent
Pancreatitis
PhillipChisholm
Case 1 A 49-year-old man has a CT scan for LLQ pain. The CT reveals mild sig-
moid diverticulitis and an incidental 3-cm cyst in the tail of the pancreas. The pan-
creas otherwise appears normal. He has no history of pancreatic disease, does not
smoke, and reports only occasional alcohol use. Once he completes antibiotic treat-
ment for his diverticulitis, he sees you about the pancreatic cyst. His CBC, LFTs,
and lipase were all normal..
Is a 3-cm cyst large enough to warrant a workup, and if so, how would you
proceed?
When a patient like this is referred to us, we always review the history trying to
tease out any symptoms that may have been missed and any signicant social or
medication history. We want to know, was there an episode of pain earlier that might
signal unrecognized pancreatitis? In a young patient like this, we want to make sure
there wasn’t more signicant alcohol intake. Is there a medication that might have
caused pancreatitis, or a family history of pancreatic disease? We try to identify any
old imaging of the pancreas to compare with the latest study. The differential for a
cyst like this includes non-communicating pancreatic cysts that might be mucinous
or serous, pancreatic pseudocysts, and branch-chain IPMNs.
After reviewing the history, physical and any laboratories previously performed
we will generally order a dedicated pancreatic radiologic examination, either a dedi-
cated pancreatic CT (which includes ne cuts, non-contrast, and timed contrast
administration) or an MRCP.In our institution, we generally prefer the CT because
a number of our patients have claustrophobia or can’t hold still long enough to get
a high-quality MRI.Another advantage of CT is that it can pick up ne pancreatic
calcications. Pancreatic calcications won’t be seen on MRI.On the other hand, an
MRCP has the advantage of lack of radiation, which is important in patients who
may have serial surveillance examinations. In addition, the MRCP is better at pick-
ing up IPMNs and is better at picking up subtle mural nodularity.
P. Chisholm (*)
Department of Medicine, GI/Hep Division, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: pchisholm@mcw.edu
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Another laboratory we occasionally order is a serum CA 19–9. A high CA 19–9
may be found in high-grade dysplasia or cancer of the pancreas. However, we are
selective with which patients we order the test, since an elevated CA 19–9 is not
specic for pancreatic malignancy (elevated CA19–9 may be seen in cases of biliary
obstruction, pancreatitis, liver cysts, and hepatitis). Also, some pancreatic cancers
don’t produce CA 19–9 so a normal result doesn’t rule it out.
In most patients, we generally do an EUS and FNA on all cystic lesions larger
than 2–3cm in size. With the FNA, we want to see if the uid is mucinous, and we
order a CEA and glucose. A mucinous lesion is much more likely to be neoplastic,
while a serous lesion or pseudocyst is very unlikely to be neoplastic. An elevated
cyst uid amylase suggests that the cyst is in communication with the pancreas—
either a pseudocyst or a branch-chain IPMN.An elevated CEA suggests that the
lesion is mucinous, either a dysplastic lesion or neoplasm. The cutoff for abnormal
CEA is >192 although the specicity of elevated CEA is much higher when we use
a cutoff of 1000. We also send off cytology, although the utility of cytology on these
aspirates is low, there are many false-negative results.
When we aspirate these lesions, we draw off as much uid as possible—until the
cyst collapses. We make sure we have enough uid for the CEA, glucose, amylase,
and mucin stain and then send off whatever is left for the cytology. Hopefully, a
larger volume of uid may increase the sensitivity of the cytology examination. We
hope to draw off at least 3–5cc, and part of the reason we don’t investigate smaller
cysts is that it is difcult to draw off sufcient uid.
With a mucinous cyst greater than 3 cm, we generally call in a multidisciplinary
pancreatic team. Assuming the patient is a surgical candidate, most of these patients
should have surgical resection since the risk of cancer in a mucinous cyst is rela-
tively high. If the uid is serous or suggestive of a pancreatitis related pseudocyst,
we assume this is a benign cyst that does not require any follow-up, and repeat
radiologic examinations are not indicated.
Case 2 A 42-year-old woman presents to her primary care physician complaining
of gradually increasing pain and fullness over the past 10days. Her physician
orders an ultrasound followed by a CT scan that shows cholelithiasis and a 7-cm
cyst off the body of the pancreas. The pancreas otherwise appears normal. The com-
mon bile duct is not dilated. Her liver enzymes and lipase are normal. Five weeks
earlier, she had an episode of severe pain that woke her in the middle of the night
but resolved by morning.
She has no history of alcohol use, prior pancreatitis, or family history of pancre-
atic disease. The distinct possibility of an episode of gallstone pancreatitis 5weeks
earlier is raised.
Is it necessary to do an EUS to evaluate this cyst?
In this case, we suspect the cyst could be a pancreatic pseudocyst. In considering
other etiologies, we want to make sure there wasn’t a prior history of weight loss,
abdominal pain, or any new-onset diabetes, all of which could suggest neoplasm or
chronic pancreatitis. If the symptoms continue to improve and the cyst gets smaller,
we would simply observe the patient and repeat imaging studies in 1–2months.
P. Chisholm
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Assuming any pancreatitis has resolved, you would want to order a cholecystec-
tomy to prevent any repeated gallstone pancreatitis.
If the cyst does not get smaller, and symptoms don’t abate, it would be reason-
able to do an EUS and FNA.A cyst aspirate uid with an amylase greater than 1000
and CEA<192 would be compatible with a pancreatic pseudocyst.
If the cyst did not decrease in size, draining the cyst, perhaps with an Axios stent,
would be called for.
Case 3 A 48-year-old man is seen for abdominal pain. He has a history of cigarette
smoking of 28-year duration and has 2–3 drinks a day, 4–5 on weekends. A CT scan
reveals a dilated pancreatic duct. MRCP is performed, showing cystic dilation of
the pancreatic duct without proximal stricture, suggesting a main duct IPMN in the
body of the pancreas.
How do you manage a patient with pancreatic IPMNs?
IPMNs are mucous-producing tumors of the pancreatic duct that result in cystic
dilation of either the main pancreatic duct, a side branch, or both. There is an impor-
tant distinction between main duct IPMNs, which have a much higher malignant
potential than branch-chain IPMNs. Diagnosis of IPMNs can be challenging, and
radiologic examinations may confuse main duct IPMNs and chronic pancreatitis,
both of which can cause cystic dilation of the pancreatic duct. MRCP is better than
CT at picking up IPMNs but can miss the calcications seen in chronic pancreatitis,
which are well seen on CT.An EUS is best at identifying any solid component to
the cysts or mural nodules in the IPMNs, and you can often see mucous extruding
from the ampulla, the so-called sh-eye appearance. However, calcications can
interfere with EUS evaluation. Therefore, we frequently employ multiple imaging
modalities if thee is clinical uncertainty. If the diagnosis of main duct IPMN is con-
rmed, we generally refer the patient to a multidisciplinary pancreatic team for
evaluation for surgery because of the high malignant potential.
Branch-chain IPMNs, on the other hand, have a much lower malignant potential.
These lesions are being identied more frequently in our senior population. In stud-
ies of patients who had an MRI for non-pancreatic problems, the frequency of pan-
creatic cystic lesions in patients over age 70 is 40%. In general, we don’t investigate
these lesions unless they are at least 2cm in size, in which case we do our standard
EUS with FNA with mucous stain, CEA, glucose, and amylase. Surgery and amy-
lase. Surgery would only be recommended if there were high-risk ndings on
EUS or FNA.
“Idiopathic” Recurrent Pancreatitis
Case 4 A 53-year-old man is admitted for his second episode of pancreatitis. His
rst episode was 3months earlier. Prior to the rst episode, he was a social drinker
on weekends only. Since that episode, he has had no alcohol. During each episode,
his liver enzymes were normal. His lipase was 1100 on admission with the rst epi-
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sode and 700 for the second. His triglycerides were 350 during the rst episode with
normal calcium. An US shows a normal gallbladder. There is no family h/o pancre-
atic disease, and he is on no meds that would cause pancreatitis.
How do you evaluate a patient with recurrent idiopathic pancreatitis?
Remember, the vast majority of cases of pancreatitis, 70%, are due to gallstones
(40%) or alcohol (30%). So, it’s important to investigate whether there actually is
signicant alcohol use in the history, and if not, gallstones are going to be the most
common etiology. Of course, in a 53years old presenting with idiopathic pancreati-
tis we always want to consider, and rule out, a pancreatic neoplasm, particularly if
the patient has a history of weight loss or new-onset diabetes.
Ultrasound is our rst test looking for cholelithiasis. After that, we do our dedi-
cated pancreatic imaging. In this instance, MRCP might be more sensitive for evalu-
ating occult cholelithiasis and pancreatic ductal abnormalities. If these studies are
unrevealing, we would do an EUS to rule out an occult neoplasm and look for evi-
dence of microlithiasis, and sludge in the gallbladder (with the proviso that if the
patient has been NPO for a number of days’ sludge might form as a result of fasting
and be a red herring).
If, after these investigations, an etiology is not discovered, we would generally
recommend a cholecystectomy anyway, because many of these cases of recurrent
“idiopathic” pancreatitis are due to occult microlithiasis.
What about a genetic etiology for recurrent pancreatitis?
This is a 53-year-old patient, and genetic pancreatitis usually presents earlier in
life. If the patient was a 25years old with recurrent pancreatitis, we would order
genetic tests early on. After discussing the risks and benets of genetic testing, we
would order a genetic panel that includes CFTR, SPINK1, PRSS1, and CTRC.Most
patients with genetic pancreatitis don’t have a family history. If there is a family
history of pancreatitis, the more common genetic abnormality is PRSS, which is
autosomal dominant, while the other genetic diseases are autosomal recessive.
This patient has a negative MRCP and EUS, and cholecystectomy is performed.
He presents 2months later with a third episode of pancreatitis.
How would you proceed now?
In the patient with negative imaging who has had a cholecystectomy, we would
order a secretin-stimulated MRCP to look for subtle ductal abnormalities. Following
that, we consider an ERCP for the possibility of sphincter of Oddi stenosis or pan-
creas divisum, which we discuss further in the next two cases.
Case 5 A 57-year-old woman has gone to the ER four times for acute pancreatitis
over the past 8months. There is no signicant alcohol use. She had gallstones, and
a cholecystectomy was performed after the rst episode. In spite of that, she pres-
ents with two more episodes of pancreatitis.
After the third episode, she had an MRCP that suggested a pancreas divisum.
There are no medications that should produce pancreatitis, and there is no sug-
gestion of autoimmune pancreatitis.
P. Chisholm
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How would you manage this patient?
MRCP is fairly accurate at picking up pancreas divisum, but the nding of pan-
creas divisum does not necessarily make it the culprit, the cause of the recurrent
pancreatitis. However, in this case, other etiologies appear unlikely—the patient had
a cholecystectomy, and there is no suggestion of autoimmune pancreatitis nor med-
ication-induced pancreatitis. Because of her age, we would rst offer her an EUS to
rule out any subtle suggestions of malignancy. Assuming that is negative, we would
recommend proceeding to ERCP.The marked frequency of the episodes—four epi-
sodes in 8months, dictates the more aggressive management. We would suggest an
ERCP with minor ampulla sphincterotomy. This would likely end the cycle of
recurrent pancreatitis.
Case 6 A 38-year-old woman presents with recurrent pancreatitis. One year ear-
lier, she had suspected biliary pancreatitis treated with cholecystectomy. She has
occasional alcohol and does not smoke. She presents in the ER with acute abdomi-
nal pain. Examination revealed marked abdominal tenderness, decreased bowel
sounds, and increased tympany. She had a lipase of 600, white cell count of 10,000,
AST of 220, ALT of 350, alkaline phosphatase of 240, and bilirubin of 1.4. Ultrasound
revealed a dilated CBD of 11mm.
How would you manage this patient?
If available, you’d like to know the post-cholecystectomy ductal diameter as a
baseline. In this case, you’re questioning a possible sphincter of Oddi dysfunction
(SOD), most likely type 1, vs a retained stone. We would order a secretin-stimulated
MRCP.Secretin increases pancreatic secretions and relaxes the pancreatic sphinc-
ter. If there is a problem with the pancreatic sphincter or sphincter of Oddi, the
pancreatic duct dilates. Secretin-stimulated MRCP could help rule out choledocho-
lithiasis and provide evidence for any sphincter dysfunction. We no longer do bili-
ary manometry to evaluate for SOD because of the high risk of post-ERCP
pancreatitis, without much benet. While in the past we did more isolated pancre-
atic duct sphincterotomies, it has been found that a routine biliary sphincterotomy
will benet most patients whether the defect is in the pancreatic sphincter or biliary
sphincter.
Case 7 A 47-year-old man is referred with a history of intermittent abdominal pain
accompanied by episodes of elevated lipase. There is no signicant history of alco-
hol use, smoking, or family history of pancreatitis. A CT scan reveals enlargement
of the head of the pancreas, a sausage-shaped pancreas, with atrophy of the pancre-
atic tail, and some surrounding lymph nodes that are mildly enlarged. The diagnosis
of autoimmune pancreatitis is questioned. You send off an IgG4, and it comes back
negative.
Do you think this is autoimmune pancreatitis?
If the IgG4 had returned positive, the treatment would be clear-cut. This would
almost certainly be type 1 autoimmune pancreatitis, and high-dose steroids would
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