Chronic pancreatitis (Treatment)
INTRODUCTION
1.
2.
Chronic pancreatitis typically presents as chronic unrelenting pain with episodic flares.
Although it is sometimes stated that chronic pancreatitis "burns out" over time, the duration
of time over which this may occur is highly variable, if it occurs at all. In addition, pancreatic
endocrine and exocrine dysfunction may develop as the disease progresses, and a variety of
complications can occur, including pseudocysts, bile duct or duodenal obstruction, pancreatic
ascites, splenic vein thrombosis, and pseudoaneurysms.
Thus, the natural history of chronic pancreatitis is relatively bleak. Most therapies are aimed
at "resting" the pancreas by minimizing exocrine pancreatic secretion; unfortunately, this is
relatively ineffective. The goals of treatment include pain management, correction of
pancreatic insufficiency, and management of complications. Therapy is similar in patients
with acquired and hereditary pancreatitis.
3. The treatment of chronic pancreatitis (principally pain and pancreatic exocrine insufficiency)
will be reviewed here. Other complications and their management, the etiology, clinical
manifestations, and diagnosis of chronic pancreatitis are discussed separately.
ESTABLISH A SECURE DIAGNOSIS
1. When there is a significant change in pain pattern or sudden onset of persistent symptoms,
other potential etiologies (PUD, biliary obstruction, pseudocysts, pancreatic carcinoma, and
pancreatic duct stricture or stones) should be ruled out. It is difficult to be secure in the
diagnosis of chronic pancreatitis, particularly in the first two to three years of disease when
most diagnostic studies can be normal.
PAIN MANAGEMENT
1. The principal symptom of chronic pancreatitis is abdominal pain. The pain may range from
occasional postprandial discomfort to debilitating persistent pain associated with nausea,
vomiting, and weight loss. Pain control can be difficult in some cases. However, when
considering the appropriate strategy to relieve pain, it should be recognized that placebo
alone is effective in up to 30% of patients in most studies.
2. The first step in alleviating pain is to recognize the underlying cause of chronic pancreatitis
and to treat the underlying etiology to reduce progressive pancreatic damage.
3. Pain is associated with pancreatic hyperstimulation, ischemia and acidosis, obstruction of
4.
larger or small ducts, inflammation or neuropathic mechanisms. Patients with chronic
pancreatitis are at increased risk of pancreatic cancer which may cause change in pain
pattern, and often have extra-pancreatic sources of pain associated with maldigestion.
As a general rule, pain management should proceed in a stepwise approach beginning with
general recommendations followed by pancreatic enzyme supplementation and then
judicious use of analgesics. Patients with continued symptoms may be candidates for more
invasive options.
5.
General recommendations
A. Cessation of alcohol intake
i.
Cessation of alcohol intake is imperative, particularly if this is the underlying
etiology of pancreatitis. Abstinence can but does not always lead to symptomatic
improvement; however, patients with alcohol-induced chronic pancreatitis who
continue to drink have increased mortality.
B. Small meals and hydration
i.
Small meals that are low in fat may also help to varying degrees. Although evidence
is anecdotal, keeping patients well hydrated may help prevent flares of pancreatitis.
ii.
Supplementation with medium chain triglycerides (MCTs) may be of benefit. In a
pilot study of eight patients, oral administration of the enteral formula Peptamen,
6.
which is enriched in MCTs and hydrolyzed peptides, for 10 weeks resulted in
improvement in pain, which in some patients was sustained after stopping this oral
supplement. The mechanism of action may relate to the fact that administration of
this enteral formulation resulted in a minimal increase in plasma CCK levels or
alternatively may be due to its antioxidant effects. MCTs may also be administered
to prevent weight loss in individuals who develop steatorrhea.
C. Cessation of smoking
i.
Smoking may accelerate the progress of chronic pancreatitis and may increase the
risk of pancreatic cancer.
Pancreatic enzyme supplements
A.
B.
C.
D.
Pancreatic enzyme supplements to suppress pancreatic exocrine secretion relieve pain
in some patients.
Rationale for this therapy is based upon suppression of feedback loops in duodenum
that regulate release of CCK, the hormone that stimulates digestive enzyme secretion
from exocrine pancreas. CCK-release from the duodenum is regulated by CCK-releasing
factors, and these factors are destroyed by pancreatic digestive enzymes. Reduction of
intraduodenal free enzyme activity by increasing undigested proteins, protease
inhibitors, or inadequate pancreatic enzyme secretion in pancreatic diseases allows the
CCK releasing factors to survive protease digestion, stimulate CCK release, and stimulate
the pancreas. As a result, increasing intraduodenal enzyme activity may reduce
stimulation-associated pancreatic pain.
However, results from controlled clinical trials showed mixed results, which may have
been due to differences in the enzyme preparations used, the endpoints measured, and
the high placebo response (approximately 30%).
Which subsets of patients may benefit most is unclear from the available data. However,
the two positive controlled trials suggested that patients with less advanced disease
(without involvement of large ducts and without steatorrhea), women, and those with
idiopathic chronic pancreatitis may benefit the most. Treatment was unlikely to be
successful in patients with large duct disease (mainly those with alcoholic pancreatitis).
E.
F.
7.
reflect a placebo effect. Enzyme supplementation is safe and thus is a reasonable initial
strategy in patients with severe pain who have not responded to other conservative
measures.
High doses of the non-enteric coated enzymes were used in the clinical trials. The two
clinical trials that demonstrated improvement of pain with pancreatic enzyme
supplements used non-enteric coated preparations with each meal, although the newer
enteric-coated preparations have not been adequately tested. Patients taking
non-enteric coated pancreatic enzyme supplements should also be treated with acid
suppression (either with H2 blocker or PPI) to reduce inactivation of enzymes from
gastric acid. Non-enteric coated preparations are given in the same manner as the
enteric-coated preparations that are used for the treatment of malabsorption. Currently,
Viokace is the only non-enteric coated preparation currently approved by the US Food
and Drug Administration.
Analgesics
A. Analgesia can be considered if pancreatic enzyme therapy fails to control pain.
Amitriptyline and nortriptyline have been shown to reduce daily pain from neuropathic
conditions. In many patients, a short course of opiates coupled with low dose
amitriptyline (10 mg nightly for 3 weeks to determine efficacy) and NSAID will break the
pain cycle. Simultaneous short-term hospitalization, with patient kept NPO to minimize
B.
C.
8.
Despite the mixed results, clinical experience plus some evidence from controlled clinical
trials suggests a benefit from enzyme supplementation, albeit some of the benefit may
pancreatic stimulation, may also be of benefit in breaking pain cycle.
Chronic opioid analgesia may be required in patients with persistent significant pain.
Long-acting agents such as morphine sulfate continuous release or fentanyl patches are
generally more effective than short acting medications, which last only 3 or 4 hours. In
RCT, adjuvant therapy with pregabalin (75 mg BID with incremental increases to 300 mg
BID) caused effective pain relief in more patients after 3 weeks compared to placebo in
patients with chronic pancreatitis (36 vs. 24%).
The extent to which patients should be maintained on analgesics before pursuing more
aggressive options is matter of clinical judgment. As general rule, additional options
should be considered in patients in whom pain significantly reduces their quality of life
or their ability to carry on normal social and work functions, especially those who
require long-term opiates.
Antioxidant therapy
A. There is insufficient evidence to support the use of antioxidants in patients with chronic
pancreatitis. Studies evaluating the efficacy of antioxidant therapy in reducing pain in
patients with chronic pancreatitis have had conflicting results.
B.
In one randomized controlled trial, a total of 147 patients with chronic pancreatitis
(either alcoholic or idiopathic) were randomly assigned to antioxidant supplement or
placebo for 6 months. At the end of the study, the intervention group experienced a
significant reduction in the number of painful days per month and the number of
analgesic tablets consumed. In addition, a significantly higher proportion of patients
became pain free (32 vs. 13%). In contrast, in another RCT in which 70 patients with
chronic pancreatitis (predominantly alcoholic) received antioxidant supplement or
placebo for 6 months, there was no difference in pain scores, QoL, number of hospital
admissions, or outpatient visits between groups. It is unclear if the conflicting results are
due differences in study population (mean age and nutritional status), prevalence of
smoking, etiology of pancreatitis (idiopathic vs. alcoholic), or composition of the
9.
antioxidant supplement.
Specialized approaches
A. Celiac nerve block
i.
Percutaneous or endoscopic celiac nerve blocks with either alcohol or steroids have
had only limited success in chronic pancreatitis and should be considered to be
unproven therapy. Even among responders, symptoms frequently recur within 2 to
6 months, although nerve block can be repeated as needed. Furthermore, serious
complications have been described.
B. Endoscopic therapy
i.
Although RCT are lacking, several reports have suggested that endoscopic therapy
ii.
iii.
aimed at decompressing obstructed pancreatic duct can be associated with pain
relief in some patients. The rationale for this approach is based upon the hypothesis
that ductal hypertension due to sphincter of Oddi dysfunction or strictures of the
main pancreatic duct lead to pain.
The largest report with long-term follow-up included 1018 patients treated at eight
different centers who were followed for average of 5 years. Obstruction of
pancreatic duct was due to strictures (47%), stones (18%), or strictures plus stones
(32%). Patients were treated using a variety of endoscopic techniques. At the end of
follow-up, 60% had completed endoscopic therapy, while 16% were still undergoing
some form of endoscopic therapy and 24% had undergone surgery. Pain relief
(based upon a structured questionnaire) was achieved in 86% of the entire group
and in 65% of patients on intention-to-treat analysis. Pancreatic function did not
improve.
Few studies have compared endoscopic approaches to surgery. A small RCT
comparing endoscopic therapy to surgical drainage found that surgical drainage
was more effective in relieving obstruction and achieving pain relief. Surgery may
also be more cost-effective as compared with endoscopic therapy. However, most
centers would attempt endoscopic therapy prior to surgery unless there is suspicion
for pancreatic cancer.
C.
Extracorporeal shock wave lithotripsy
i.
Pancreatic duct stones are found in approximately 22 to 60% of patients with
ii.
chronic pancreatitis. The stones can lead to obstruction of outflow of pancreatic
secretions, causing increased intraductal pressure. Because pancreas is relatively
noncompliant, the rise in intraductal pressure can induce tissue HTN and ischemia,
which may be major factor causing pain in patients with chronic pancreatitis. ESWL
creates millimetric fragmentation of pancreatic stones, which has improved the
results of endoscopic therapy and may have additional indications in treatment of
patients with chronic pancreatitis.
ESWL is used mostly in Europe, although it is also available in few specialized
centers in the US. Complete or partial pain relief was observed in 62 to 86% of
carefully selected patients in the largest series during a mean follow-up ranging
from 7 to 44 months.
iii.
The role of ESWL remains unclear, since there have been no definitive RCT that
have proven its benefit. Furthermore, the relationship between pancreatic stones
and symptoms is not straightforward since many patients with stones (even with
ductal dilation) are asymptomatic, while those with symptoms generally have pain
due to small duct obstruction and other factors such as parenchymal inflammation
and ischemia.
D. Radiation
i.
A pilot study involving single-dose external beam radiotherapy in 15 patients with
chronic pancreatitis suggested benefit in improving pain. The mechanism of benefit
is unclear but may be related to anti-inflammatory properties of radiotherapy.
Additional studies are needed.
10. Surgery
A. Surgery has generally been considered for patients who fail medical therapy, or as first
line therapy if there is suspicion of pancreatic cancer. Notably, up to 15% of patients in
surgical series had unrecognized pancreatic cancer at the time of the procedure,
underscoring the need for firm diagnosis prior to surgery. Although role for surgery in
chronic pancreatitis is generally accepted, there have been very few controlled clinical
trials to demonstrate its benefit.
B.
C.
D.
The timing of surgery is controversial. While some studies suggest that early surgery may
prevent development of progressive disease, and reduce need for long-term opioid use,
others have noted progressive loss of endocrine and exocrine pancreatic function
despite lateral pancreaticojejunostomy.
When choosing among surgical options, one must consider the areas of the pancreas
that are involved in chronic pancreatitis and whether the pancreatic duct is dilated.
Three surgical approaches have been described: decompression/drainage operations;
pancreatic resections; and denervation procedures. Some surgical procedures employ
combination of these approaches.
E.
Decompression
i.
Decompression procedures have generally been recommended for patients with
ii.
refractory pain who have dilated main pancreatic duct. The normal pancreatic duct
ranges from 2 to 4 mm in diameter (most narrow in the tail, enlarging as it passes
toward ampulla). A dilated duct (from surgical standpoint) is one that would permit
anastomosis to loop of jejunum. Consensus has not been achieved at the threshold
at which this can be achieved; some surgeons will perform such procedure in those
with ducts that are only 5 to 6 mm in diameter, while others require dilation to
around 10 mm.
Multiple series have described the outcome of this procedure and its variants. A
review of these data in consensus statement from AGA focused on five reports that
were selected because of their relatively large numbers of patients, longer
follow-up, and methodologic quality. The data suggest that short-term pain relief is
achieved in approximately 80% of patients. Morbidity and mortality related to the
operation are generally low when procedure has been performed by experienced
surgeons (0 to 5%).
iii.
iv.
v.
However, pain relief persists for > 2 years in only about 60% of patients. Patients
with recurrent pain may require additional surgery. The cause of pain recurrence is
unclear. It may be related to progressive pancreatic injury or inadequate drainage
of secondary ducts.
How these outcomes compare with resection procedures has not been extensively
studied in randomized studies, but tend to favor drainage approaches.
Surgery may be superior to endoscopic approaches for pain control in patients with
obstructive chronic pancreatitis and dilated pancreatic duct. In a study of 140
patients, surgery was superior to endotherapy in reduction of pain at 5-year
follow-up, although initial success rates were similar. However, in this study,
surgery included both resection and drainage procedures and endoscopic
lithotripsy was not performed.
vi.
A subsequent RCT compared operative pancreaticojejunostomy to endoscopic
treatment in 39 patients with chronic pancreatitis and distal obstruction of
pancreatic duct without inflammatory mass. Endoscopic treatment included
transampullary drainage with or without lithotripsy. Pain scores were significantly
lower in the surgery group after 24 months of follow-up. Complete or partial pain
relief was achieved in a great proportion of patients who underwent surgery
compared with endoscopic therapy (75 vs. 32%). Complications rates were similar.
In a follow-up study of the same cohort, patients who underwent surgery as the
initial treatment as compared to endoscopic therapy required significantly fewer
additional drainage procedures (68 vs. 5%) and had more pain relief (80 vs. 38%)
during 79 months of follow-up. Furthermore, 47% of patients who underwent
endoscopic therapy eventually underwent surgery.
F. Resection
i.
This surgical approach involves resection usually of portion of pancreas (typically
tail or head) and less commonly entire pancreas. Several specific procedures have
been described including Whipple, pylorus-preserving pancreaticoduodenectomy,
distal pancreatectomy, total pancreatectomy, and duodenal-preserving resection
of pancreatic head. Resection is considered in patients who have failed other forms
of therapy and in those who are not candidates for drainage procedure (usually
patients with predominantly small duct disease).
ii.
Patients who have undergone pancreatectomy may develop exocrine and
endocrine dysfunction. In otherwise healthy people, only about 20% of the
pancreatic parenchyma is required to maintain clinically adequate function.
Patients with chronic pancreatitis, however, may not have normal remaining
pancreas, increasing the likelihood that pancreatic insufficiency will develop with
extensive resection. The resulting diabetes can be severe and associated with
considerable morbidity.
iii.
iv.
Autologous islet cell transplantation may hold promise for treatment of such
patients. The islets are crudely separated from pancreas and then infused into
portal vein. Many of these patients have had normoglycemia and normal serum
insulin responses to oral and IV glucose and IV arginine for up to 7 years after
transplantation. In one series, 10 of 14 patients receiving more than 300,000 islets
were insulin-independent two years after transplantation.
Several conclusions can be drawn from heterogeneous data.
1. Distal pancreatectomy alone is insufficient unless disease is confined to body
and tail of pancreas.
2. Resection of pancreatic head (by a conventional or pylorus-preserving
procedure) may provide pain relief in up to 85% of patients, including those
3.
with disease extending to the tail. However, it remains controversial whether
this type of surgery is effective in most patients vs. those whose disease is
primarily confined to this region. A meta-analysis of four trials concluded that
duodenum-preserving pancreatic head resection was as effective as
pancreatoduodenectomy for relief of pain, overall morbidity and
postoperative endocrine insufficiency and was superior in some postoperative
outcomes and quality of life.
Total pancreatectomy is treatment option in carefully selected patients with
chronic pancreatitis in whom substance abuse is not confounding factor. A
systematic review included 5 observational studies in which 296 patients with
chronic pancreatitis underwent total pancreatectomy followed by islet cell
autotransplant. In 2 studies that reported postoperative morphine
requirements, there was a significant reduction in the frequency and severity
of pain following surgery.
G. Denervation procedures
i.
Most afferent nerves emanating from pancreas pass through celiac ganglion and
splanchnic nerves. Thus, interruption of these nerve fibers has the potential to
alleviate pain originating from the pancreas. Interruption of these pathways also
occurs with pancreaticoduodenectomy and with resection of pancreatic head,
which may in part explain the pain relief achieved with these procedures.
ii.
iii.
Denervation has been accomplished using open surgical approach and using
thoracoscopic surgery. However, in most series, pain relief with thoracoscopic
splanchnicectomy was incomplete and of short duration with only about 50% of
patients noting benefit after two years.
The overall benefit from denervation surgery is uncertain. While response rate as
high as 90% has been reported, patients in this series also underwent additional
procedures. Which patients may benefit the most from this option is incompletely
understood. One study suggested a higher response rate in patients who had not
undergone prior operative or endoscopic procedures.
STEATORRHEA
1. Patients with severe pancreatic exocrine dysfunction cannot properly digest complex foods or
2.
3.
4.
5.
6.
absorb digestive breakdown products. Nevertheless, clinically significant protein and fat
deficiencies do not occur until over 90% of pancreatic function is lost. Steatorrhea (fat
malabsorption) usually occurs prior to protein deficiencies since lipolytic activity decreases
faster than proteolysis.
The clinical manifestations of fat malabsorption include loose, greasy, foul smelling stools that
are difficult to flush. Malabsorption of the fat soluble vitamins (A, D, E, K) and vitamin B12
may also occur, although clinically symptomatic vitamin deficiency is rare.
A variety of tests can be used to detect fat malabsorption. Currently, gold standard for
diagnosis of steatorrhea is quantitative estimation of stool fat. Fecal elastase testing is the test
of choice due to its high sensitivity and specificity and because only random stool sample is
required.
Treatment of pancreatic exocrine insufficiency with pancreatic enzyme supplementation in
chronic pancreatitis is dependent on size and nature of meal (fat content), the residual
function of pancreas (which may be progressively lost), and goals of therapy (elimination of
steatorrhea, reduction in the abdominal symptoms of maldigestion (bloating, diarrhea), or
improvement in nutrition, depending on the size and condition of the patient).
Treatment depends upon the severity of disease. It may involve dietary modifications alone or
with the addition of pancreatic digestive enzyme supplementation.
Dietary modification
A.
7.
One approach in patients with steatorrhea is to restrict fat intake. The degree of
restriction depends upon severity of fat malabsorption; generally intake of 20 grams per
day or less is sufficient. Patients who continue to suffer from steatorrhea following fat
restriction require medical therapy.
Lipase supplementation
A. Since all of the digestive enzymes are secreted in parallel, lipase can be used to titrate
pancreatic enzyme supplement doses. The contents of the stomach empty into the
intestine at a slow continuous rate, so the pancreas functions at a high rate for most of
the day. The pancreas normally responds with between 700,000 and 1,000,000 lipase
units (USP) per meal. With no pancreatic function, 10% of normal pancreatic lipase
replacement (70,000 to 100,000 USP) will control steatorrhea, but may not correct other
effects of pancreatic exocrine failure. Patients with chronic pancreatitis typically have
some residual pancreatic function, thus supplementation rather than complete
replacement is usually sufficient. The dosing of pancreatic enzyme supplements is based
on relief of the target symptoms or achievement of nutritional goals since residual
pancreatic function is difficult to measure and changes with progression of disease, the
size and content of meals vary, and multiple commercial products are available.
B.
In order to correct for malabsorption due to exocrine pancreatic insufficiency, it is
necessary to provide approximately 5 to 10% of the pancreatic enzymatic output.
Studies have shown that the quantity of enzymatic output needed to provide
approximately 5 to 10% of pancreatic enzyme output is approximately 30,000
international units (IU) or 90,000 United States Pharmacopeia units (USP) of lipase per
meal. The minimal amount of lipase needed will differ among individuals, but in most
persons 90,000 USP of lipase per meal is the amount that will be needed to abolish
steatorrhea. Dosing depends on an individual's weight, the degree of pancreatic
insufficiency, and the size and fat content of a meal. Protein malabsorption with
associated diarrhea (azotorrhea) can also be seen in chronic pancreatitis. In general,
protein malabsorption is easier to correct than fat malabsorption. This is due to the fact
C.
D.
E.
8.
that proteases are much more resilient to degradation than lipases, and proteases in the
stomach and small intestine can compensate for decreased amounts of pancreatic
proteases.
Once the appropriate dose of pancreatic enzymes is determined, patients should be
instructed on how to take the pancreatic enzymes. Enzymes should be taken with the
first bite of a meal. Depending on how rapidly a meal is consumed and the amount of
food consumed, the enzyme supplements may be given entirely at the beginning of a
meal or, alternatively, with one half of the total dose at the beginning of the meal and
the other half taken in the middle of the meal. This dosing regimen ensures that there
will be appropriate mixing of enzymes with food.
Pancreatic enzyme supplements come in various forms (including delayed release,
enteric coated, and non-enteric coated), which contain varying concentrations of lipase,
protease, and amylase (table 1). Viokace is currently the only non-enteric coated
formulation currently approved by the US Food and Drug Administration.
Treatment can be with either enteric coated formulations such as Creon-24,000 lipase,
one to two capsules with meals and one capsule with a snack, or a non-enteric coated
form such as Viokace Lipase 20,880, three tablets with meals and one to two tablets
with a snack. This dose is typically sufficient to improve symptoms. Non-enteric coated
enzyme supplements may be inactivated at an acidic pH. Thus, patients taking
non-enteric coated pancreatic enzyme supplements require addition of an H2 antagonist
or proton pump inhibitor. Non-enteric coated formulations may be more successful in
patients who are achlorhydric or who have dyssynchronous gastric emptying (Billroth II
anatomy), since there is no need to protect the enzymes from acid.
Vitamin supplementation
A. Patients with substantial steatorrhea may require fat-soluble vitamin analogues. The
25-hydroxylated form of vitamin D (calcifediol) is more polar than vitamin D2 or D3 and
is therefore more easily absorbed in patients with fat malabsorption. The serum calcium
should be monitored for first few weeks of therapy with this naturally analogue since it
is more potent than vitamin D2 or D3, and can more easily produce hypercalcemia.
9.
Medium chain triglycerides
A. Medium chain triglycerides (MCTs) can provide extra calories in patients with weight loss
and poor response to diet and pancreatic enzyme therapy. Unlike long chain
triglycerides, which require bile salts and pancreatic lipase, MCTs are readily degraded
by gastric and pancreatic lipase, and do not require the presence of bile. In addition,
MCTs can be directly absorbed by the intestinal mucosa and are less of a stimulant to
pancreatic secretion.
GLUCOSE INTOLERANCE
1. Glucose intolerance occurs with some frequency in chronic pancreatitis, but overt diabetes
mellitus usually occurs late in the course of disease. Annual fasting glucose levels are
generally checked and, if elevated, would indicate development of diabetes. Diabetes that
develops in patients with chronic pancreatitis is usually insulin requiring. However, it is
different from typical T1DM in that the pancreatic alpha cells, which produce glucagon, are
also affected; as a result, there is increased risk of hypoglycemia, both treatment-related and
spontaneous. A trial of oral hypoglycemic agents followed by insulin therapy when the need
arises has been the line of management in these patients.
SUMMARY AND RECOMMENDATIONS
1. Chronic pancreatitis typically presents as chronic unrelenting pain with episodic flares. The
goals of treatment include pain management, correction of pancreatic insufficiency, and
management of complications.
2. It is important to establish a secure diagnosis. A significant change in the pain pattern or the
3.
sudden onset of persistent symptoms suggests the need to rule out other potential etiologies,
including peptic ulcer disease, biliary obstruction, pseudocysts, pancreatic carcinoma, and
pancreatic duct stricture or stones.
Pain management should proceed in a stepwise approach.
A. Initial treatment begins with recommendations to stop alcohol and tobacco and to eat
small meals that are low in fat.
B. We suggest the use of pancreatic enzyme supplements in patients with pain persisting
after the above interventions. These relieve pain in some patients and are generally safe.
C. Treatment with acid suppression (either with H2 blocker or PPI) should be given along
with pancreatic enzyme supplements to reduce inactivation from gastric acid.
D.
E.
F.
Analgesics with opiates and/or NSAID agents can be considered if pancreatic enzyme
therapy fails to control pain. Adjuvant therapy with pregabalin can be considered in
patients whose pain is not adequately controlled with opiates and/or NSAID.
Other specialized approaches for patients who continue to have pain include endoscopic
therapy, extracorporeal shock wave lithotripsy, celiac nerve block, and surgery.
Surgery has generally been considered for patients who fail medical therapy. Three
surgical approaches have been described: decompression/drainage operations,
pancreatic resections, and denervation procedures. The choice of procedure is made
based upon size of pancreatic ducts and the regions of pancreas that are involved.
4.
Steatorrhea (fat malabsorption) may develop in patients with severe pancreatic exocrine
dysfunction. Treatment depends upon the severity of disease.
A.
B.
5.
6.
Dietary modification should begin with restriction of fat intake (to < 20 g per day).
For patients who do not respond to dietary restriction, we suggest lipase
supplementation. As a general rule, 30,000 international units (IU) of pancreatic lipase
(90,000 United States Pharmacopeia units [USP]) swallowed during each meal should
suffice in reducing steatorrhea and preventing weight loss. Fat soluble vitamin
replacement may be required.
C. Medium chain triglycerides (MCTs) can provide extra calories in patients with weight loss
and a poor response to diet and pancreatic enzyme therapy.
Glucose intolerance occurs with some frequency in chronic pancreatitis, but overt DM usually
occurs late in the course of disease. A trial of oral hypoglycemic agents followed by insulin
therapy when the need arises has been the line of management in these patients.
Management of other complications (such as pseudocysts, bile duct or duodenal obstruction,
pancreatic ascites, splenic vein thrombosis, and pseudoaneurysms) is presented separately.