Introduction

Howtotreat
Acute pancreatitis
Chronic
pancreatitis
Pancreatic cancer
Case studies
inside
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DR JONATHAN BROMLEY,
advanced trainee in
gastroenterology, The Canberra
Hospital, ACT.
The authors
ASSOCIATE PROFESSOR
PAUL PAVLI,
senior specialist, The Canberra
Hospital; and Associate Professor,
Australian National University
Medical School, ACT.
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THE main diseases of the pancreas
that present wi th gastroi ntesti nal
mani f estati ons ar e acute and
chronic pancreatitis and pancreatic
cancer. Cysti c fi brosi s, as i t affects
pancreatic function, is also covered
bri efl y i n thi s arti cl e.
Acute pancreatitis is an important
cause of abdominal pain. GPs need
to have a good understanding of the
presentati on, prognosti c markers
and aeti ol ogy of thi s r el ati vel y
uncommon but potenti al l y l i fe-
threatening condition. Management
generally involves admission to hos-
pital for intravenous fluids, analge-
sia and the management of compli-
cations.
Chroni c pancreati ti s has si gni fi -
cant effects on a patients quality of
l i fe and provi des major treatment
challenges, such as meeting the anal-
gesi c requi rements of the pati ent,
particularly in the long-term.
An often underesti mated aspect
of management is the correction of
nutri ti onal defi ci enci es resul ti ng
from pancreati c enzyme i nsuffi -
ci ency. Absti nence from al cohol
i s al so an i mpor tant par t of
management.
Pancreati c cancer i s a condi ti on
that generally presents late in its clin-
ical course and carries a poor prog-
nosi s. Common pr esentati ons
include painless jaundice, weight loss
or anorexi a associ ated wi th new-
onset abdominal pain, or the devel-
opment of di abetes i n an el derl y
patient without risk factors.
Disorders of the
pancreas
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AD_HTT_029_036___OCT06_06 29/9/06 11:38 AM Page 29
MOST pati ents wi th acute
pancreatitis do not present
to their GP, but the diagno-
sis should be considered in
all patients presenting with
upper abdominal pain.
Acute pancreatitis usually
causes severe epigastric pain
that requires hospitalisation
for pain relief or for man-
agement of complications. In
a recent survey of the gas-
troenterology ward of The
Canberra Hospital, patients
wi th pancreati c condi ti ons
accounted for about 10% of
the total bed days.
1
The major di ffi cul ti es i n
management r el ate to
maki ng the di agnosi s i n
pati ents who have onl y
mi l dl y el evated amyl ase
and/or lipase levels, and in
correctl y i denti fyi ng those
with severe pancreatitis.
The pathogenesi s of thi s
disease is unclear but, what-
ever the triggers, the end result
i s an acute i nfl ammatory
response due to inappropri-
ately enhanced secretion of
pancreatic enzymes.
Aetiology
Gallstones and excessive alco-
hol consumption account for
most cases of acute pancreati-
tis in Australia.
Gallstones
Gallstones are responsible for
30-50% of cases, and women
are affected more often than
men. Smaller stones, which
can travel into the common
bile duct, are more likely to
cause pancreatitis than larger
ones. Increased levels of serum
aminotransferases or bilirubin,
or both, early in the course of
the illness suggests gallstones
as the cause.
Because gal l stones are a
common precipitating factor,
one approach to establishing
the cause i s to arrange an
ul tr asound wi thi n 24-48
hours of presentation in all
pati ents wi th di agnosed
acute pancreatitis.
I f gal l stones are present
and there is additional sup-
porti ng evi dence such as
duct di l ati on, abnor mal
LFTs and fevers, manage-
ment usually includes endo-
scopi c retrograde chol an-
giopancreatography (ERCP)
and sphi ncter otomy (see
Authors case studies Epi-
gastric pain and weight loss
i n a pati ent wi th normal
pancreati c enzyme l evel s,
page 34).
In the few centres where
i t i s avai l abl e, endoscopi c
ul trasound can be used to
help determine if there are
stones in the common bile
duct (which are rarely seen
on transabdomi nal ul tra-
sound) and to hel p deci de
whi ch pati ents shoul d
undergo ERCP. When gall-
stones are found, cholecys-
tectomy i s i ndi cated (usu-
al l y by l apar oscopy),
preferably during the same
admission.
Alcohol and prescription drugs
Excessive alcohol consump-
tion accounts for up to 40%
of cases of acute pancreatitis
and also causes the bulk of
cases of chronic pancreatitis.
It is more common in men
because al cohol abuse i s
more common in males. The
blood levels of alcohol asso-
ci ated wi th an i ncrease i n
risk have not been defined.
Acute pancreatitis related to
use of prescription drugs is an
unusual but well-recognised
entity. Drugs that have been
clearly associated with pan-
creatitis include:
Di ureti cs (thi azi des and
frusemide [Frusemide, Fruse-
hexal, Frusid, Lasix]).
Antimicrobials (metronida-
zol e [Fl agyl , Metrogyl ,
Metronidazole, Metronide]
and tetracycline).
Immunosuppressive agents
(azathi opri ne [Azahexal ,
Azamun, Azapin, Azathio-
prine, Imuran, Thioprine]).
Anti convul sants (sodi um
valproate [Epilim, Valpro]).
All medications in patients
with suspected or proven pan-
creatitis should be reviewed
for their potential to cause
pancreatitis.
Trauma
Trauma accounts for 5% of
cases of acute pancreatitis and
i s usual l y postoperati ve or
post-ERCP. Blunt trauma to
the abdomen (eg, seat bel t
i njuri es) can occasi onal l y
cause the condition.
Hypertriglyceridaemia
Serum tri gl yceri de l evel s
>11mmol/L can precipitate
attacks of acute pancreatitis
(although the pathogenesis is
uncl ear) and accounts for
about 2% of cases. Pancreati-
ti s may be the presenti ng
symptom of hypertriglyceri-
daemia or the condition may
have already been diagnosed.
Hypercalcaemia
Although uncommon, hyper-
calcaemia of any cause can
trigger acute pancreatitis.
Pancreas divisum
This is an anatomical variant
caused by embryological fail-
ure of the fusion of the dorsal
and ventral pancreas, result-
ing in two separate pancreatic
ductal systems. It is seen in
7% of people at post-mortem
but onl y 5% of affected
patients suffer from pancre-
atitis, which calls its signifi-
cance into question.
Infection
A range of infections can be
associated with episodes of
acute pancreati ti s but the
exact i nci dence i s uncl ear.
Whether treatment of the
infection has significant bear-
ing on the natural history of
the di sease process i s al so
unknown. Causation has been
demonstrated by culture of
the infective organism from
the pancreas. Proven infective
agents include:
Viruses (CMV, hepatitis B,
vari cel l a zoster, HI V
although this may be due to
drug treatment such as
didanosine [Videx]).
Bacteri a (sal monel l a,
legionella).
Fungi (aspergillus).
Cancer
Cancer of the pancreas is a
rare cause (<2-3% of acute
pancreatitis) but it should be
considered.
No cause found
In about 15-20% of cases no
obvi ous cause i s found.
Al though bi l i ary sl udge i s
often seen on ultrasound in
this group, no clear link has
been firmly established.
Making the diagnosis
The enzymes el evated i n
patients with acute pancreati-
tis are serum amylase (normal
range [NR] 30-110U/L) and
lipase (NR <80U/L).
Maki ng a di agnosi s of
acute pancreatitis is straight-
forward when there is a typi-
cal clinical presentation and
pancreatic enzyme levels are
markedly elevated (eg, >10
ti mes the upper l i mi t of
normal). However, lower ele-
vations of serum amylase or
lipase levels (ie, >3-4 times
the upper l i mi t of normal )
can sti l l occur i n pati ents
with acute pancreatitis.
If the amylase and/or lipase
levels are only slightly elevated
in the presence of significant
pain, other conditions should
be considered. For example,
elevated serum amylase level
can occur wi th pancreati c
cancer, cholecystitis, appen-
di ci ti s, bowel perforati on,
ectopic pregnancy, drugs and
salivary gland diseases.
Conditions associated with
an elevated lipase level include
cholecystitis, duodenal ulcera-
tion, pancreatic tumours and
as a side effect of some drugs.
Sometimes no obvious cause
of an el evated amyl ase or
lipase level can be found.
It is important to correlate
biochemical results with the
clinical findings and, if the
di agnosi s i s i n doubt, to
exclude other life-threatening
conditions that may mimic
acute pancreati ti s, such as
mesenteric ischaemia, visceral
perforati on and l eaki ng
abdominal aortic aneurysm.
Reference ranges for pan-
creatic enzymes vary between
laboratories so they should be
speci fi ed, especi al l y when
transferring patients between
hospitals.
When to refer
All patients with suspected or
proven acute pancreatitis are
best referred to hospital for
assessment, pain relief and
management of fluid replace-
ment and compl i cati ons.
Although most patients have
severe pain, some may have
milder pain and appear rea-
sonabl y wel l cl i ni cal l y, yet
have prognostic markers of
severe pancreatitis; they may
need to be managed in a high-
dependency unit (see below).
After the diagnosis has been
made, determining the severity
of the epi sode i s the most
important issue. Overall about
20% of cases are classified as
severe; these have a mortality
rate of about 20-30% a
rate that has changed little
over the past 30 years despite
intensive care advances.
By contrast, the mortality
rate for mild pancreatitis is
low. About 75% have mild
disease and the mortality in
this group is <3%.
I n the earl y phases of a
severe attack, mortality is gen-
erally from multiple organ fail-
ure, and patients require inten-
sive supportive care during
this period. Most deaths that
occur l ater (after the fi rst
week) are due to i nfecti ve
compl i cati ons, especi al l y
infected pancreatic necrosis.
Patients with severe pancre-
atitis are best managed in a
high-dependency or intensive
care unit, where they can be
monitored closely. Immediate
management includes:
Assessing the severity of the
attack.
Aggressive fluid resuscitation
and cl ose moni tori ng of
haemodynamic status.
Provi di ng adequate pai n
relief.
Determining the cause.
Providing adequate nutrition
when prolonged hospitalisa-
tion is expected.
Severity
Severe acute pancreati ti s
occurs when there is organ
failure and/or local complica-
tions (table 1). There are sev-
eral ways of gauging the sever-
i ty of an attack and the
prognosi s for the pati ent.
Measurements of either the
haematocrit and/or the serum
C-reactive protein (CRP) have
useful prognostic significance,
independent of other findings.
Haemoconcentration indi-
cates si gni fi cant fl ui d l oss
i nto the thi rd space and
reflects severe acute pancre-
atitis. An admission haemat-
ocrit >45% or a failure to
reduce the haematocrit in 24
hours are ri sk factors for
both pancreatic necrosis and
distant organ failure.
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Acute pancreatitis
contd next page
Table 1: Complications
of pancreatitis
Local
Pseudocyst formation
Ascites
Pancreatic necrosis
GI haemorrhage
Pancreatic fistula
Abscess
Systemic
Acute respiratory distress
syndrome
Acute renal failure
Sepsis
Cardiac failure
Acidaemia (pH <7.25)
Disseminated
intravascular coagulation
After the
diagnosis has
been made,
determining the
severity of the
episode is the
most important
issue.
Gallbladder
Pancreas
Pseudocysts
Acute pancreatitis showing pseudocysts, sludge or stones in the gall bladder and ascites.
AD_HTT_029_036___OCT06_06 29/9/06 11:38 AM Page 31
How to treat disorders of the pancreas
32 | Australian D octor | 6 O ctober 2006 w w w .australiandoctor.com .au
An admission haematocrit
>45% has a sensi ti vi ty of
34% and a specificity of 91%
for identifying patients with
severe pancreatitis, but when
the same reading is present
after 24 hours the sensitivity
and specificity are 81% and
88-91%, respectively.
Conversely a haematocrit
<40% on admi ssi on has a
100% negati ve predi cti ve
value for pancreatic necrosis,
and is a reassuring result.
CRP is an acute-phase reac-
tant that, in severe episodes,
is markedly elevated on the
second day. The normal range
in our laboratory is 0-10mg/L.
It is as reliable as the Ranson
criteria (see below) for pre-
dicting severe acute pancreati-
tis. It has high sensitivity (70-
86%) and specificity (71%)
for predi cti ng pancreati c
necrosis, but only after the
third day.
A CRP level >210mg/L on
days 2-4, or >120mg/L at the
end of the first week, discrim-
inates well between mild and
severe pancreatitis.
The degree of elevation of
amylase and lipase assays does
not correl ate wi th di sease
severity or recovery. In most
cases serum amylase level nor-
malises before serum lipase
during recovery, but enzyme
levels remain elevated if there
is ongoing pancreatic inflam-
mation or a complicating pan-
creatic pseudocyst.
Several scori ng systems
have been devised to assess
severi ty and prognosi s i n
patients with acute pancreati-
tis. These include:
Atlanta criteria based on
the presence of l ocal (eg,
abscess, pseudocyst) and sys-
temic (eg, sepsis, acute renal
failure) complications. Mor-
tal i ty i n the severe group
approaches 45%.
Ransons criteria based
on haematological (eg, white
cell count, haematocrit), bio-
chemical (eg, blood sugar
level, blood urea nitrogen)
and patient (eg, age) para-
meters on admission and in
the first 24 hours. Patients
with more than five positive
parameters have a mortality
rate of 50%.
Apache II scoring system
calculated using parameters
such as heart rate and serum
sodi um at admi ssi on and
after 24 hours and allows
i ncorporati on of age and
chronic health points into
the scoring system. Higher
scores correlate well with
disease activity and the need
for ICU admission. It has
high sensitivity and speci-
ficity for diagnosis of acute
severe pancreatitis (75% and
92%, respectively).
Investigations
Contrast-enhanced CT is the
gold standard for evaluating
the presence and extent of
pancreatic necrosis, peri-pan-
creati c i nfl ammati on and
other l ocal compl i cati ons
(pleural effusions and ascites).
CT shoul d be performed
between days 3 and 7 for any
patient with severe disease.
I f pancreati c necrosi s
(defined as the absence of con-
trast enhancement) is found
on CT, the pati ent i s best
managed i n a hi gh-depen-
dency setting with a combined
medi cal and surgi cal
approach.
Morbidity and mortality
i ncreases wi th i ncreasi ng
extent of glandular necrosis.
If there is clinical deteriora-
tion, percutaneous aspiration
of the necrotic tissue should
be considered either under
ultrasound or CT guidance.
If there is evidence of infec-
tion, treatment with antibi-
otics and debridement of the
infected necrotic tissue (by
radiological, surgical or endo-
scopic means depending on
expertise) is appropriate.
Management
Fluid resuscitation
Patients can have high fluid
requirements because of loss
of fluid into the abdominal
cavity (third space) and from
vomiting.
Pati ents need aggressi ve
fluid resuscitation. They often
require 5-10L or more in the
first 24 hours, and fluid bal-
ance must be moni tored
closely. Normal saline is often
used but, i f the pati ent i s
hypotensive, replacement with
a colloid should be considered
initially. Potassium replace-
ment may be necessary, espe-
cially if there is ongoing vom-
iting.
Most patients require uri-
nary catheterisation and main-
tenance of an hourly fluid bal-
ance chart. In more complex
cases, such as patients with
coexisting cardiac failure, a
central venous line and more
intensive monitoring in a high-
dependency or intensive care
unit may be needed.
Antibiotics are not given
routinely because there is no
evidence that their use in mild
cases affects outcome or
reduces the incidence of septic
complications. There is some
evidence for the use of pro-
phylactic antibiotics (such as
IV ceftriaxone [Ceftriaxone,
Rocephi n] or meropenem
[Merrem IV]) in patients with
severe pancreatitis associated
with necrosis, to prevent septic
complications.
Pain management
Acute pancreatitis is associ-
ated with severe pain usually
requi ri ng opi oi d anal gesi a.
Patient-controlled analgesia
supervised by an acute pain
team may be appropriate if
repeated doses of parenteral
opioid are needed. There is no
evidence that morphine wors-
ens pancreatitis or that pethi-
dine should be used in prefer-
ence to morphine.
Anal gesi c requi rements
differ enormously depending
on many factors such as age,
sex, body mass and previous
exposure to opioids.
Nutrition
Duri ng the acute phase,
patients are kept nil by mouth
to rest the GI tract and to
minimise secretion of pancre-
ati c enzymes and further
inflammation: passing a naso-
gastri c tube i s no l onger
common practice.
The optimal timing for re-
introducing oral fluids and
foods i s not known. Some
experts advocate being guided
by the patient: they will not
want to eat when unwell and
the return of appeti te nor-
mal l y mi rrors an i mprove-
ment in pancreatitis.
Others monitor pancreatic
enzymes and rei ntroduce
fluids, then food, only when
the lipase level drops to less
than twice the normal level.
Pain can recur and enzyme
levels rise when oral intake is
re-established, and the patient
should be warned of this pos-
sibility.
Nutri ti onal support for
more complex patients such
as those wi th pancreati c
pseudocyts or necrosis, and in
whom prolonged fasting is
necessary, can be difficult and
i s controversi al . Choi ces
i ncl ude naso-jejunal tube
insertion for enteral feeding,
or parenteral nutrition.
With a naso-jejunal tube the
food is released distal to the
pancreas to avoid stimulating
pancreatic enzyme produc-
tion. Placement of the tube
can be di ffi cul t and may
involve multiple trips to the
radi ol ogy department. The
tube is best sited under image
intensification or fluoroscopic
guidance by an experienced
radiologist.
An alternative is surgical
i nserti on of a jejunostomy
tube, whi ch al so provi des
mucosal protecti on. I f the
patient requires repeat endo-
scopic aspirations of pancre-
atic pseudocysts, tubes often
become displaced or have to
be removed, and bl ockage
requiring a tube change is not
uncommon.
Parenteral nutrition does
not provide mucosal protec-
tion and there is significant
ri sk of l i ne-rel ated sepsi s.
However, the supply of nutri-
tion is more constant, as tube
blockages are not an issue.
A recent meta-anal ysi s
showed superiority of enteral
feedi ng wi th respect to
decreased infection and surgi-
cal intervention rates, reduced
hospital stay and reduced cost,
compared wi th parenteral
feeding.
2
It should be consid-
ered in patients who are likely
to need frequent tube chang-
ing or when placement is tech-
nically difficult.
Recurrent acute
pancreatitis
Up to one-third of patients
experience a repeat attack.
Recurrences are more com-
mon in alcohol-associated dis-
ease and in gallstone disease
if cholecystectomy has been
delayed. Recurrences can be
di sti ngui shed from chroni c
pancreatitis by the absence of
exocri ne or endocri ne dys-
function in the former.
Discharge planning
It is important to identify the
underlying aetiology of the
pancreatitis before discharge.
If gallstones are present and
thought to be the likely cause,
the patient should have a firm
surgical plan on discharge if
the cholecystectomy cannot be
performed for some reason
during the admission.
It is also important to iden-
tify alcohol as a cause because
of the potenti al for future
attacks and the development
of chronic pancreatitis. Any
potentially offending drugs
should be identified and with-
drawn.
from previous page
Patients can
have high fluid
requirements
because of loss
of fluid into the
abdominal cavity
(third space) and
from vomiting.
Acute pancreatitis
management summary
Diagnosis confirmed pain
and elevated lipase or
amylase levels (at least >3
times the upper limit of
normal).
First 24 hours
Assess severity.
Estimate BMI, record vital
observations.
Blood tests: FBC for
haematocrit, WCC and
platelet count, CRP, BSL,
calcium, electrolytes,
creatinine and urea,
lactate dehydrogenase,
aspartate aminotrans-
ferase, estimate base
deficit in PaO2
Give aggressive fluid
resuscitation and keep nil
by mouth.
Provide appropriate pain
relief.
Determine cause
arrange abdominal
ultrasound to look for
evidence of gallstones
and consider ERCP if
present; check history of
alcohol intake.
Check medications if
appropriate. Consider
other causes (rare).
First 3-7 days
Continue fluid
resuscitation and pain
relief.
Monitor closely for
evidence of organ failure,
especially if there is
evidence of severe
pancreatitis on initial
assessment.
Arrange CT scan of
abdomen if pancreatitis is
severe or if pancreatic
cancer is suspected (rare).
Consider antibiotics if
pancreatic necrosis is
present on CT scan.
Consider enteral or
parenteral nutrition if
course is prolonged.
First 1-2 weeks
Continue management as
above.
If there is evidence of
sepsis, consider
percutaneous aspiration
of necrotic pancreatic
tissue and start
appropriate antibiotics if
an organism is identified.
Arrange surgical,
radiological or endoscopic
review for drainage if
infected necrosis is
present.
When pancreatic enzyme
levels fall to below twice
the upper limit of normal
and/or the patient is
pain-free: re-introduce
fluids and food (but pain
may recur).
If pancreatic enzyme
levels remain persistently
elevated: repeat
abdominal ultrasound to
exclude a pancreatic
pseudocyst.
Manage underlying cause
Contrast- enhanced CT is the gold standard for evaluating the presence and extent of pancreatic
necrosis.
AD_HTT_029_036___OCT06_06 29/9/06 11:38 AM Page 32
CHRONIC pancreatitis dif-
fers from acute pancreatitis by
the demonstration of a reduc-
ti on i n ex ocri ne and or
endocrine function of the pan-
creas. It is more common in
men and usually occurs after
one or several epi sodes of
acute pancreatitis, although
sometimes a patient presents
with no history of any previ-
ous attacks.
Clinical presentation
The two main manifestations
of chroni c pancreati ti s are
pain and pancreatic exocrine
and endocrine insufficiency.
Pain is typically epigastric,
often radiates to the back, is
commonly accompanied by
vomiting and may be exacer-
bated by food or al cohol .
Pai nful epi sodes gradual l y
improve as inflammation of
the pancreas is replaced by
fibrosis, but this process can
take years.
Although pain is the most
common presentation, not all
patients with chronic pancre-
atitis present with pain. About
20% present with exocrine or
endocrine pancreatic insuffi-
ciency. One study found that
45% of alcoholics had evi-
dence of chronic pancreatitis
in the absence of any symp-
toms.
3
The hallmark of exocrine
insufficiency is steatorrhoea
caused by defective secretion
of l i pase and bi carbonate,
causing fat malabsorption. A
90% loss of exocrine function
is needed before steatorrhoea
develops.
If the patient reduces fat
intake either intentionally or
as a result of anorexia and
general ill-health, the pre-
sentation may be masked.
Weight loss is exacerbated
by pr otei n catabol i sm
because deficient pancreatic
proteases also cause protein
malabsorption.
Although glucose intoler-
ance is a common feature of
patients with chronic pancre-
atitis, frank diabetes usually
occurs l ate and i s usual l y
i nsul i n dependent. Unl i ke
patients with type 1 diabetes,
al pha cel l s (whi ch secrete
glucagon to counter the effects
of insulin) are affected as well
as beta cells, making patients
more predisposed to hypogly-
caemic attacks.
Diabetic ketoacidosis and
end-or gan damage (nep-
hropathy or retinopathy) are
uncommon, so if these occur
the possibility of concomi-
tant diabetes mellitus should
be explored. The main risk
factor for devel opment of
diabetes is the presence and
extent of calcification of the
pancr eas, whi ch i s most
extensive in alcohol-related
pancreatitis.
Causes
Alcohol
More than 90% of chronic
pancreatitis is caused by exces-
sive alcohol consumption.
Genetic
Several genetic variants have
been associated with develop-
ment of chronic pancreatitis.
The most common i s an
abnormal i ty i n the cysti c
fibrosis transmembrane con-
ductance regulator (CFTR)
gene, which can cause chronic
pancreatitis as part of cystic
fibrosis or in the absence of
demonstrabl e pul monary
i nvol vement. Several other
rare genetic variants may also
cause chronic pancreatitis.
Ductal obstruction
Obstruction of the pancreas
from any cause, such as
benign or malignant biliary
strictures or stones, can result
in chronic pancreatitis.
Gallstones
Although a common cause of
acute pancreatitis, gallstones
rarely cause chronic disease.
Complications
Symptomatic obstruction of
the bile duct or duodenum
occurs in 5-10% of patients.
Symptoms include abdominal
pai n, abnormal LFTs and
postprandial pain.
Pseudocysts (single or mul-
ti pl e) devel op i n 10% of
patients secondary to pancre-
atic duct obstruction. Most
pseudocysts are asymptomatic
but, depending on their size
and location, they can cause
problems such as abdominal
pai n, duodenal or bi l i ary
obstruction and spontaneous
abscess formation.
Smal l , asymptomati c
pseudocysts tend ei ther to
improve or enlarge. They can
be safely monitored for up to
12 months and to a size of
12cm. I ndi cati ons for
drainage include pain
or visceral obstruc-
tion.
Asci tes and
pleural effusions
may develop and
can be managed
non-surgically using
diuretics and percuta-
neous drainage. Alter-
natively, stenting of a
disrupted duct can be
attempted endoscopically
and has variable success.
Investigations
Blood tests
Chroni c pancreati ti s i s a
patchy focal di sease, so
increases in pancreatic enzyme
l evel s are usual l y mi ni mal .
Possible changes to pancreatic
function include:
Rel ati ve defi ci ency of
enzymes in the pancreas and
blood, caused by fibrosis.
Liver function (demonstra-
ble as changes in levels of
serum al bumi n and cl ot-
ti ng factor s) may be
deranged if there is under-
lying cirrhosis of the liver
from alcohol abuse.
Decreased vitamin B12 and
serum calcium levels because
of mal absorpti on. To
demonstrate fat malabsorp-
tion and/or steatorrhoea the
most accurate test involves
three-day faecal fat collec-
ti on on a di et wi th con-
trolled fat intake (100g/day):
a value >7g/day is suggestive
of fat malabsorption. Fat
staining of a faecal specimen
is often used as a screening
test in hospital.
Fasting blood sugar levels or
a glucose tolerance test may
be abnormal when there is
endocrine involvement.
Imaging studies
In 30% of patients calcifica-
tion of the pancreas can be
seen on a pl ai n abdomi nal
X-ray. Calcium deposition is
more common when alcohol
is the underlying cause.
Ul trasound i s useful for
detecting dilated biliary ducts
and col l ecti ons around the
pancreas.
ERCP has been considered
the gol d standard test for
diagnosis and, when positive,
demonstrates characteristic
beading of the main pancre-
atic duct or clubbing of the
side branches. The distribu-
tion and extent of beading
correlates with the degree of
pancreatic dysfunction.
In the future, magnetic res-
onance cholangiopancreatog-
raphy (MRCP) i s l i kel y to
replace ERCP.
Functional assessment
A variety of functional assays
i s avai l abl e for di agnosi ng
pancreatic insufficiency but
these are not necessary i n
everyday clinical practice.
Management
Pain control
Pain is the most debilitating
component of chronic pancre-
atitis, and providing adequate
analgesic control is often diffi-
cul t. Obvi ous measures
include avoiding alcohol and
reducing dietary fat.
Opioid analgesia is often
required and, because of the
chronicity and severity of the
pain, large amounts may be
needed, leading to problems
wi th dependence. For thi s
reason, referral to a chronic
pain service is advisable and
the i nput of psychol ogi cal
services can be very helpful.
Coeliac axis nerve blocks
using alcohol or steroids and
l ocal anaestheti c are com-
monly tried, but long-lasting
benefits are infrequent. The
injection can be performed
under X-ray gui dance or
endoscopic ultrasound and
repeated as often as needed:
hypotension is fairly common
after blockade.
Relief is often temporary,
l asti ng weeks to months.
Sur gi cal ex ci si on of the
coeliac plexus is an option
for pati ents requi ri ng re-
peated blocks.
I f pai n i ncreases, repeat
ultrasound scans should be
considered, given the possi-
bility of strictures and resul-
tant obstruction.
Exocrine replacement therapy
A l ow-fat di et i s par t of
management and i s often
best gui ded by a di eti ti an.
Fat i ntake i s typi cal l y
restricted to <30g/day, so the
intake of fat-soluble vitamins
may be inadequate.
Pancreatic enzyme replace-
ment can be given in tablet
for mul ati on wi th meal s.
Timing of ingestion is vital:
capsules are best taken with
meals rather than before or
after.
Persistence or recurrence of
steatorrhoea is a sign of one
or more of the following:
I nadequate dose repl ace-
ment.
Poor patient compliance (the
tablets may be unpalatable).
Incorrect timing of ingestion.
Medium-chain fatty acids
are sometimes of benefit in
patients who are losing weight
despite enzyme replacement
and a low-fat diet because,
unlike long-chain fatty acids,
they do not require bile salts
for digestion.
I f symptoms persi st, the
possibility of another cause for
malabsorption (such as coeliac
disease) should be considered.
Endocrine replacement
therapy
Oral hypogl ycaemi cs are
sel dom useful and i nsul i n
repl acement i s normal l y
required. Treatment follows
the same principles as that for
patients with diabetes unre-
lated to chronic pancreatitis.
Surgical and other options
Surgery may have a beneficial
effect on pain when there is a
single isolated ductal stricture
demonstrated by ERCP. More
often the di sease i s di ffuse
(especi al l y when al cohol
related) and surgical interven-
tion is not possible.
When there i s ductal
obstruction and dilation due
to stones or a stricture, ductal
decompression may provide
effective pain relief. Extracor-
poreal shock wave lithotripsy
may also be used if there are
stones in the pancreatic duct;
complete clearance of stones
has been described in up to
50% of cases and improve-
ment in up to 70%.
Prognosis
If they abstain from alcohol,
80% of patients with alco-
hol-related chronic pancre-
atitis are alive 10 years after
di agnosi s. Death usual l y
occurs from the compl i ca-
tions of diabetes or attacks
of acute-on-chronic pancre-
atitis, cirrhosis or suicide.
When to refer?
When the diagnosis of chronic
pancreatitis has been made,
referral may be necessary if
there is poor pain control (a
chronic pain service can be
very hel pful for managi ng
ongoi ng pai n and l i festyl e
modification) or if abdominal
pain worsens rapidly (the pos-
sibility of a ductal obstruction
or other pathology needs con-
sideration, and urgent review
is warranted).
w w w .australiandoctor.com .au 6 O ctober 2006 | Australian D octor | 33
Chronic pancreatitis
More than 90% of chronic pancreatitis is caused by excessive alcohol consumption.
Fat intake is
typically
restricted to
<30g/day, so
the intake of
fat-soluble
vitamins may
be inadequate.
AD_HTT_029_036___OCT06_06 29/9/06 11:38 AM Page 33
PANCREATIC cancer occurs most
often in the 60-80-year age group,
and men are more commonl y
affected than women. In Australia
the incidence is 8.8 per 100,000 of
population. The outlook is poor,
with a five-year survival rate of only
3%. The i nci dence of pancreati c
cancer is increasing in Western soci-
ety for unexplained reasons.
Risk factors
Risk factors include:
Smoking heavy smokers have a
2-3-fold increased risk of pancre-
atic cancer compared with non-
smokers.
Chronic pancreatitis the 25-year
cumulative risk of pancreatic cancer
in a person with chronic pancreati-
tis is about 4%.
Several geneti c syndromes are
linked with an increased risk of
pancreatic cancer: hereditary non-
polyposis colon cancer, familial
adenomatous polyposis and famil-
ial breast cancer (BRCA2 gene).
A positive family history up to
10% of patients with pancreatic
cancer have a positive family his-
tory.
Nei ther al cohol nor gal l stones
increase the risk of pancreatic cancer,
except when associated with chronic
pancreatitis.
Clinical features
Cancer can devel op i n the head
(70%), body (20%) and tail (10%)
of the pancreas, and the site can
influence likely clinical features. Jaun-
dice is common (80%) when the
head is affected, and many patients
also have steatorrhoea.
Pain is a feature common to all
sites although it often predomi-
nates if the cancer is in the body or
the tail these tumours are often
quite large before they are detected.
New-onset diabetes is seen in 15-
20% of cases, so a pancreati c
tumour should be considered when
risk factors for development of dia-
betes (excess weight, positive family
history) are absent.
Other symptoms such as weight
loss may provide a clue to diagnosis.
However, a del ay i n di agnosi s i s
common, gi ven the non-speci fi c
nature of many of the symptoms and
the limitations of imaging modalities.
Investigations
While ultrasound should be the first
imaging modality for a patient with
jaundice, its use in diagnosing pan-
creatic cancer is inferior to that of
CT. The sensitivity and specificity of
CT in diagnosing pancreatic cancer
exceeds 80% and 90%, respectively.
In addition, CT may give additional
information regarding liver metas-
tases and lymph node involvement.
The detection rate of ERCP is sim-
ilar to that of CT but the former is
preferable when jaundice is a pre-
senti ng feature because i t al l ows
ti ssue sampl i ng and stenti ng of
obstructed bile or pancreatic ducts.
Endoscopi c ul trasound i s an
emerging technique with high diag-
nostic accuracy (but is very operator
dependent) and allows fine-needle
sampling. It can also give informa-
tion about resectability.
Al though the tumour marker
CA19-9 is often used as a diagnostic
tool its role has not been validated.
However, it has use both as a prog-
nosti c marker and as a gui de to
treatment response.
Management
Most patients have incurable dis-
ease at the time of diagnosis, and a
multidisciplinary team involving sur-
geons, therapeuti c endoscopi sts,
radiologists, oncologists, and pain
and/or palliative care specialists gen-
erally provides best management.
Patients with biliary duct obstruc-
tion and symptoms such as jaundice
or pruritus benefit from drainage
and stenting, either endoscopically
or percutaneousl y. Endoscopi c
stenti ng, wi th regul ar schedul ed
changes (in anticipation of stents
blocked by external compression or
accretion of biological material) pro-
vides excellent palliation in most
patients.
Fewer than 20% of patients have
potentially resectable disease. Some
of thi s group wi l l be unfi t for
surgery and some will be found to
have disease spread at the time of
staging laparoscopy or surgery.
Pancreatoduodenectomy carries a
mortality rate of about 5% in the
hands of an experienced surgeon.
The five-year survival rate after this
procedure is <20%, compared with
an overall five-year survival of 3%.
If duodenal obstruction develops,
bypass surgery (eg, gastroenteros-
tomy) may be necessary.
Chemotherapy
The median survival time for patients
whose cancer i s surgi cal l y unre-
sectabl e i s si x months. Systemi c
chemotherapy provides little survival
advantage but the combination of 5-
flurouracil (5-FU) and gemcitabine
has been shown to provide sympto-
matic benefit. Other chemothera-
peutic combinations can also be used
as second-line treatment.
Palliative care
Perhaps more than in any other GI
malignancy, palliative care plays a
vital role in patients with pancreatic
cancer. Pain is a major problem, and
administering long-acting opioid-
based pain relief is important. Vom-
iting can become a problem, espe-
cially late in the disease if cerebral
metastasis or intestinal obstruction
develops.
How to treat disorders of the pancreas
34 | Australian D octor | 6 O ctober 2006 w w w .australiandoctor.com .au
ERCP yields the diagnosis
in a patient with acute
pancreatitis with several
possible causes
AH, 47, presents to the local
emergency department with
12 hours of progressi vel y
worseni ng epi gastri c pai n
and vomiting. She scores her
pain severity as 8/10.
She has a past history of
essential hypertension, which
i s wel l contr ol l ed on
aml odi pi ne (Norvasc) and
hydrochlorothiazide (Dithi-
azide). She also has a long-
standi ng hi stor y of
mi gr ai nes, tr eated wi th
sumatr i ptan (I mi gr an,
Suval an). Past hi stor y
includes appendicectomy at
age 20.
AH i s marri ed wi th two
children. She has smoked a
packet of cigarettes a day for
20 year s and dr i nks 2-3
standar d gl asses of wi ne
daily and sometimes more at
weekends.
Her mother had a history
of gal l stones tr eated by
cholecystectomy. Her father
di ed of col orectal cancer at
71.
Examination showed:
BMI 31.
Temperature 37.2C.
Pulse 102bpm.
BP 105/65mmHg.
Normal heart sounds.
Clear lung fields.
Abdomi nal tenderness i n
the epigastrium and right
upper quadrant.
Bowel sounds present, and
rectal examination normal.
No peripheral oedema.
Laboratory results were:
Haemoglobin 140g/L.
Haematocrit 44%.
Whi te cel l count 11.5
10
9
/L.
Platelets 180 10
9
/L.
Sodium 140mmol/L.
Potassium 3.1mmol/L.
Urea 8.9mmol/L.
Creatinine 120mol/L.
Bilirubin 12mol/L.
Alanine aminotransferase
200U/L.
Al kal i ne phosphatase
300U/L.
Gamma-glutamyltranspep-
tidase 200U/L.
Albumin 33g/L.
Amylase 800U/L (NR 30-
110U/L).
Lipase 2000U/L (NR 30-
300U/L).
Acute pancreati ti s was
diagnosed, based on the clin-
ical presentation and the pan-
creatic enzyme findings. The
cause coul d be gal l stones
(gi ven the fami l y hi story,
LFTs showi ng an al ani ne
aminotransferase more than
three times normal and her
body habitus), alcohol (she
has a si gni fi cant al cohol
intake) or medications (she
takes a thi azi de di ureti c
known to cause pancreatitis).
AH was placed on nil by
mouth, and pati ent-con-
trol l ed anal gesi a was pre-
scribed. An abdominal ultra-
sound scan on the day of
admission revealed multiple
stones in the gallbladder and
a dilated common bile duct
(1cm wide). An ERCP was
arranged and a large stone
was seen in the common bile
duct.
A generous sphincterotomy
was performed. A bal l oon
was i ntroduced i nto the
common bile duct, inflated
and gently withdrawn, pulling
the stone and associ ated
debris into the duodenum.
Over the next 48 hours
her pain settled and her pan-
cr eati c enzyme l evel s
returned to normal. Fluids
and food were then reintro-
duced. A surgical consulta-
tion was arranged and the
patient underwent a laparo-
scopi c chol ecystectomy
before discharge.
Epigastric pain and
weight loss in a patient
with normal pancreatic
enzyme levels
RB, 68 and a retired builder,
presented wi th epi gastri c
pai n radi ati ng to hi s back
that tended to be worse after
eating and relieved by sitting
forward. He had lost 12kg
in three months.
RB had a past history of
i schaemi c hear t di sease
treated by CABG in 2001.
He also had well-controlled
hypertension and depression.
Cur r ent medi cati ons
i ncl uded peri ndopri l 4mg
daily, aspirin 150mg daily,
metoprol ol 25mg bd and
citalopram 20mg daily. He
had smoked a packet of cig-
arettes a day for 40 years
and drank three standard
glasses of wine a day. There
was no significant family his-
tory.
Examination showed:
BMI 18.
Dual heart sounds.
Clear lung fields.
No lymphadenopathy.
Fullness in the epigastrium
and mi l d tenderness on
abdomi nal ex ami nati on
(rectal ex ami nati on was
normal).
Laboratory results were:
Haemoglobin 102g/L.
Whi te cel l count 9.1
10
9
/L.
Neutrophils 8.7 10
9
/L.
Platelets 235 10
9
/L.
Mean corpuscular volume
93fL.
Sodium 146mmol/L.
Potassium 3.9mmol/L.
Urea 11mmol/L.
Creatinine 119mol/L.
Bilirubin 42mol/L.
Alanine aminotransferase
80U/L
Al kal i ne phosphatase
190U/L.
Gamma-glutamyltranspep-
tidase 260U/L.
Albumin 30g/L.
Amyl ase and l i pase
normal.
Coagul ati on pr ofi l e
normal.
Comment
This man had unexplained
abdominal pain and signifi-
cant weight loss. His LFTs
suggested a cholestatic pic-
ture and he had mi l d nor-
mochromic anaemia.
Given the site of pain and
abnormal LFTs, an abdomi-
nal ultrasound scan was the
investigation of choice. This
showed an empty gallbladder
with no wall thickening. The
intra- and extra-hepatic ducts
were mi l dl y di l ated, the
common bile duct was poorly
visualised and the pancreas
was obscured by bowel gas.
Because of the high degree
of suspicion of an obstruc-
tive lesion, a CT scan of the
abdomen with oral and IV
contrast was arranged and
showed dilation of the intra-
and extra-hepatic biliary tree
and a bulky pancreas .
However, RBs pancreatic
enzyme levels were normal,
essenti al l y excl udi ng acute
pancreatitis as the cause for
the bulky pancreas, and an
obstructi ng l esi on of the
pancreas was more likely.
An ERCP revealed steno-
si s of both the pancreati c
and common bile ducts: the
double duct sign, which is
highly suggestive of pancre-
atic cancer.
Authors case studies
Pancreatic cancer
Heavy smokers have
a 2-3-fold increased
risk of pancreatic
cancer compared
with non-smokers.
AD_HTT_029_036___OCT06_06 29/9/06 11:38 AM Page 34
Case study
JACK, 25, had an epi sode
of acute pancreatitis at age
19 after a prolonged period
of heavy dr i nki ng. He
required 48 hours of hospi-
tal admi ssi on at the ti me
and has remained well ever
si nce. He was tol d to
abstai n from al cohol and
has, up to this point, largely
followed that advice, with a
few minor exceptions.
Questions for the author
What is thelikelihood that,
if Jack returns to drinking
in moderation, a second
attack would occur?
Jack has demonstrated a
susceptibility to developing
alcohol-induced pancreatitis
and is at high risk of further
attacks even if he drinks in
moderati on. Reduci ng hi s
intake of alcohol will clearly
have a benefi ci al effect on
his risk for future attacks of
pancr eati ti s but wi l l not
compl etel y al l evi ate i t.
Despite reducing or abstain-
ing from alcohol he will still
have a ri sk of devel opi ng
chronic pancreatitis.
If it is safe for him to do
so, what would generally be
theadvisabletimebetween
a first attack and resump-
tion of alcohol consump-
tion?
The potenti al sever i ty
fr om a fur ther attack of
pancr eati ti s shoul d be
relayed to the patient. It is
not possi bl e to say what
l evel of al cohol consump-
tion would be low enough
to avoid further attacks.
General questions for the
author
Traditionally it was taught
that pethidinewas thedrug
of choicein acutepancreati-
tis secondary to gallstones,
as it did not causespasm of
the common bile duct. Is
this no longer correct?
There is some experimen-
tal evidence that morphine
is associated with the devel-
opment of spasm of the
sphincter of Oddi, but there
is no clinical evidence that
it worsens pancreatitis.
Pethi di ne i s no l onger
used as a fi rst-l i ne opi oi d
agent in emergency depart-
ments for this indication. It
has a hi gher potenti al for
abuse than morphi ne and
the l atter i s now the pre-
ferred analgesic agent.
Patients with chronic pan-
creatitis arenotoriously dif-
ficult to managebecauseof
opioid dependence and a
severeshortageof pain clin-
ics. Is it likely that a patient
with this disorder can be
weaned off opioids over the
longer term?
Over time the inflamma-
ti on may be gr adual l y
replaced by fibrosis, which
may result in reduced anal-
gesi c requi rements. How-
ever, it is not often possible
to wean patients off opioids,
and realistic treatment goals
should be set.
There seems to have been
very little progress in the
treatment of pancreatic
cancer over theyears it
still has a median survival
measured only in months.
Why is this and are there
any new treatments on
the horizon that look
promising?
Most cases of pancreatic
cancer arent identified until
the disease is in an advanced
stage, by which point surgi-
cal resection is not possible.
There have been i mprove-
ments i n pal l i ati ve chemo-
therapy but the survival rate
i n thi s condi ti on remai ns
very poor.
How to treat disorders of the pancreas
36 | Australian D octor | 6 O ctober 2006 w w w .australiandoctor.com .au
HOW TO TREAT Editor: Dr Lynn Buglar
Co-ordinator: J ulian McAllan
Quiz: Dr Lynn Buglar
Disorders of the pancreas
6 October 2006
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1. Which THREE statements about acute
pancreatitis are correct?
a) Patients with acute pancreatitis always
have significantly elevated amylase and/or
lipase levels (>10 times the upper limit of
normal)
b) Most cases of acute pancreatitis in
Australia are caused by gallstones or alcohol
abuse
c) Infection with CMV, hepatitis B and
varicella-zoster can cause acute pancreatitis
d) Trauma-induced acute pancreatitis occurs
most often after ERCP or surgery
2. You are called to see Paloma, 45, on a
home visit because of upper abdominal pain
and vomiting. She describes similar
episodes in the past. History and
examination suggest gallstones or acute
pancreatitis. Palomas vital signs are normal
and she does not want to be admitted to
hospital. Which THREE tests are you most
likely to order?
a) Serum amylase and lipase levels
b) CT of the abdomen
c) Ultrasound scan of the gall bladder
d) Serum bilirubin and serum
aminotransferase levels
3. If Paloma has drug-induced acute
pancreatitis which TWO drugs are most
likely to be implicated?
a) Antihistamines
b) Paracetamol
c) Tetracyclines
d) Thiazide diuretics
4. Palomas tests are consistent with acute
pancreatitis secondary to gallstones. Her
pain worsens and she is admitted to
hospital. Which TWO test results would
suggest mild uncomplicated pancreatitis?
a) A haematocrit <40%
b) Mildly elevated amylase and lipase levels
c) WCC of 22 10
9
/L
d) A CRP level of <210mg/L on days 2-4
5. Palomas mild pancreatitis settles with
treatment. Which THREE investigations or
treatments would be part of optimal
management, depending on access to
equipment and expertise?
a) An ERCP
b) Endoscopic ultrasound
c) Cholecystectomy at least six months
after the last episode of acute pancreatitis
d) Sphincterotomy
6. Stephen, 43, presents with pain,
steatorrhoea and weight loss. Which TWO
symptoms or findings would support a
diagnosis of chronic pancreatitis?
a) Epigastric pain that radiates to the back
b) Diabetic nephropathy
c) Previous episodes of acute pancreatitis
d) Bilateral supraclavicular lymph-
adenopathy
7. Which TWO test results would be
consistent with a diagnosis of chronic
pancreatitis?
a) Abnormal glucose tolerance test
b) 4g/day faecal fat on a controlled high-fat
(100g/day) diet
c) Minimally raised levels of serum lipase
and amylase
d) Elevated TSH level
8. Stephen has a history of alcohol abuse
and his blood tests are consistent with
chronic pancreatitis. Which THREE
imaging findings would support your
diagnosis?
a) Calcification of the pancreas on plain
abdominal X-ray
b) Mass in the head of the pancreas on CT
c) Beading of the main pancreatic duct on
ERCP
d) Dilated biliary ducts on ultrasound
9. Stephens tests confirm chronic
pancreatitis. How would you be most likely
to manage him (choose TWO)?
a) Begin regular pethidine injections for
pain
b) Advise strict alcohol avoidance
c) Restrict his fat intake to no more than
60g/day
d) Start pancreatic enzyme replacement
with meals
10. Which TWO statements about
pancreatic cancer are correct?
a) The sensitivity and specificity for
diagnosis of pancreatic cancer using CT
scan are >80% and >90%, respectively
b) Pancreatic cancer has a five-year
survival rate of 13%
c) Alcohol abuse and gallstones are
independent risk factors for pancreatic
cancer
d) Fewer than 20% of patients with
pancreatic cancer have potentially
resectable disease
Photocopy form How to Treat quiz www.australiandoctor.com.au/cpd/
and fax to Reply Paid 60416 for immediate feedback
(02) 9422 2844 Chatswood DCNSW2067
CONTACT DETAILS
GPs contribution
DR MATILDA METLEDGE
Sydney, NSW
References
1. Malki SA, et al. Inflam-
matory bowel disease, acute
pancreatitis and cirrhosis: a
prospective comparison.
Gastroenterology 2000;
118 [Suppl 2, part 2 of 2].
2. Marik PE, Zagola GP.
Meta-analysis of parenteral
nutrition versus enteral
nutrition in patients with
acute pancreatitis. BMJ
2004; 328:1407.
3. Clark, E. Pancreatitis
in acute and chronic
alcoholism. American
J ournal of Digestive
Diseases1942; 9:428.
Online resources:
information for patients

National Digestive Dis-

eases Information Clear-
inghouse (NDDIC):
http://digestive.niddk.nih.
gov/ddiseases/pubs/
pancreatitis/index.htm

Pancreatitis explained.
Better Health Channel,
Victoria: www.better-
health.vic.gov.au/bhcv2/
bhcarticles.nsf/pages/
Pancreatitis_explained
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