PANCREAS AND SPLEEN

Chronic pancreatitis require repeated hospital admissions due to high analgesia

requirements, various investigations and for medical, interven-
tional radiological or surgical intervention for complications
Magnus Johnston as required. CP resultant pancreatic functional loss and
Ravi (Rajan) Ravindran disease complications have been shown to significantly reduce
patients’ quality of life. There is an overall increased mortality
rate of 30% and 55% at 10 and 20 years, respectively, from the
time of diagnosis in patients with CP which is significantly
Abstract
more than the general population. Given the rising incidence
Chronic pancreatitis (CP) is a complex progressive fibro-
and prevalence of CP, the potential complications and high
inflammatory disease of the pancreas with a variable clinical course
mortality rate, it is important that the pathophysiology, risk
often progressing to a permanent loss of exocrine and endocrine
function. Over the last 20 years the incidence has continued to in-
factors, disease process and management of this disease is
understood.
crease. CP has multifactorial aetiological risk factors with chronic
alcoholism being the most common. The updated TIGAR-O_V2 clas-
sification identifies the pertinent risk factors and aetiology. The most Pathophysiology
susceptible patients to develop CP have a sentinel acute pancreatitis
The majority of patients with CP have a protracted course of
event which initiates the chronic progressive inflammation, scarring
illness with varying degrees of symptoms over the years. The
and fibrosis of the pancreas. Symptomatically CP presents as intrac-
natural course is very variable and there is no tool available to
table abdominal pain, with weight loss and functional loss (steator-
accurately predict disease progression for an individual patient.
rhoea and type 3c diabetes mellitus) being late manifestations of
In the majority of patients, the onset is an acute episode of
the disease. Diagnosis is made by a combination of clinical history,
abdominal pain followed by recurrent episodes, although in
examination and cross sectional imaging, combined with pancreatic
some patients there may be an insidious onset. At a cellular level,
function tests (only in equivocal cases). Complications include
the secretory parenchyma is destroyed by necrosis/apoptosis,
gastric and biliary obstruction, pseudocyst formation, pancreatic as-
inflammation or duct obstruction leading to pancreatic stellate
cites, pseudoaneurysms, venous thrombosis and an increased risk of
cells (PSC) meditating the creation of an extracellular matrix in
developing pancreatic adenocarcinoma. Management includes:
the interstitial spaces and cellular areas. This ongoing process
diagnosis and identifying the aetiology, instituting life-style changes
results in progressive loss of normal pancreatic lobular
to abstain from alcohol and smoking, and involving the specialist
morphology and irreversible structural and functional impair-
multidisciplinary team (including pain team, dietician, clinical psy-
ment. The exact mechanism of development of CP is unknown
chologist, endoscopist, GI physician and pancreatic surgeon) in pa-
but there are various theories regarding the underlying
tients with on-going symptoms or when there is doubt in the
pathophysiology.
diagnosis.
Keywords Chronic pain; chronic pancreatitis; exocrine insufficiency; Oxidative stress
pancreas It has been proposed that the root cause of pancreatic inflam-
matory disease is the overactivity of hepatic mixed-function ox-
idases. These enzymes are useful in the detoxification of harmful
Background blood-borne substances in the liver. The reactive molecules,
which are the by-products of their activity, can cause oxidative
Chronic pancreatitis (CP) is a progressive irreversible inflam- damage to the tissues. The pancreas is exposed to this ‘oxidative
matory disease where pancreatic parenchyma is gradually stress’ either through the systemic circulation or through the
replaced by fibrotic tissue. CP is typically characterized by reflux of bile into the pancreatic duct, leading to inflammation
abdominal pain associated with varying degrees of loss of and tissue damage. There are critics to this theory who feel that
exocrine and endocrine function depending on the extent of oxidative stress may have a role in the pathogenesis of CP but
the parenchymal fibrosis over time. The incidence and preva- does not initiate it.
lence are increasing with a recent paper reporting an adjusted
prevalence rate of 50 cases/100,000 population and an inci- Toxic metabolites
dence of 5e12/100,000 person years. The primary reason for Encompasses agents that cause injury or malfunction of the
the incidence rate increasing is due to increased alcohol con- pancreatic cells. Alcohol is the most common of these agents
sumption, increased awareness of the disease and improved with smoking, hypercalcaemia, hypertriglyceridemia and some
access to diagnostic facilities. Symptomatic patients often medications contributing. Alcohol is directly toxic to the
pancreatic acinar cell and also increases lithogenicity of pancre-
atic juice leading to the formation of protein plugs and stones.
Alcohol consumption can lead to accumulation of lipids within
Magnus Johnston MBChB is a Clinical Fellow in General Surgery at the acinar cells and can lead to fatty degeneration, cellular ne-
Ninewells Hospital, Dundee, UK. Conflicts of interest: none declared. crosis and fibrosis. However, as only 5e10% of people who
Ravi (Rajan) Ravindran MS FRCSEd is a Consultant HPB Surgeon at consume alcohol develop clinically apparent chronic pancrea-
the Royal Infirmary of Edinburgh, UK. Conflicts of interest: none titis, this alone does not explain alcohol as a single aetiological
declared. factor.

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 PANCREAS AND SPLEEN

Duct obstruction and stone formation major risk factors associated with development of CP are cate-
The presence of stones in the pancreatic duct after a variable gorized according to the TIGAR-O classification (Figure 1).
amount of time results in irritation, inflammation, ulceration,
stricture formation and pancreatic duct obstruction. Toxic and metabolic
Alcohol remains the most common risk factor associated with
Necrosis-fibrosis CP, with 5e10% of alcoholic patients developing clinically
This hypothesis proposes that the development of CP occurs as a apparent CP, though at autopsy 10e20% of alcoholics are found
consequence of recurrent episodes of acute pancreatitis. Inflam- to have evidence of CP. The quantity and duration of alcohol
mation and necrosis from acute pancreatitis produces fibrosis or consumption is very variable among patients with CP, but evi-
scarring in the peri-ductular areas. This scarring and fibrosis may dence shows that it is linked in a dose-dependent manner and to
cause obstruction of the ducts, stasis and stone formation ‘binge’ drinking. In most patients, a large quantity of alcohol
resulting in atrophy of the gland. (>60 g/day) over several years is needed to develop CP but, in
some patients, a smaller amount may be sufficient to produce
Primary duct theory pancreatic damage suggesting a genetic susceptibility.
This proposes that CP represents a primary autoimmune or in- Smoking is considered an independent risk factor for CP.
flammatory condition beginning in the pancreatic duct, similar to Smoking may be an isolated factor in some patients but could be
primary sclerosing cholangitis. This theory assumes that the a cofactor potentiating the toxic effects of alcohol. Evidence
primary pathogenic factor leading to duct destruction is an shows that the risk increases with the number of cigarettes
immunogenic attack of the duct epithelium, destroying the duct, smoked per day.
leading to inflammation and scarring of the ductal architecture. Hypercalcaemia is a well-known risk factor and causes pre-
mature trypsinogen activation, direct damage to acinar cells and
Sentinel acute pancreatitis event (SAPE) theory modifies pancreatic secretion leading to protein plug formation
This hypothesis combines the knowledge about molecular and and chronic pancreatitis. Causes of hypercalcaemia should be
cellular mechanisms of CP pathogenesis in an effort to bring investigated with 90% being attributed to primary hyperpara-
previous hypotheses together. This SAPE hypothesis attempts to thyroidism or malignancy.
explain the ‘final pathway’ for various aetiologies of CP. A Hypertriglyceridaemia was initially controversial in CP but
‘sentinel’ attack of acute pancreatitis is essential in a susceptible was recently shown in the NAPS2-Continuation and Validation
person (due to genetic or other mechanisms) with risk factors study to be an important risk factor in 13% of patients.
(like toxins, alcohol, infections) to trigger the process of fibrosis, Medications such as azathioprine, methylprednisolone, feno-
calcification and atrophy. fibrate, angiotensin-converting enzyme inhibitors, statins, oes-
trogens and valproic acid are known to cause CP. The exact
mechanistic relationship is unknown but they should be
Aetiology and risk factors
considered. Metabolic conditions such as CKD, diabetes, obesity
The aetiology of chronic pancreatitis is multifactorial with no one and metabolic syndromes are likely to contribute. Diabetes is
clear cause but a better understanding of the pathophysiology defined as a high-risk factor due to its ability to cause pancreatic
has led to a realization that the presence of multiple risk factors atrophy and insufficiency; however, it is often difficult to ascer-
in a susceptible person makes them prone to develop CP. The tain its chronicity.

Risk factors associated with chronic pancreatitis (TIGAR-O classification)

Idiopathic Genetic Autoimmune Recurrent Obstructive

Toxic-metabolic

Early onset PRSS1 Isolated Post necrotic Obstructing tumours

Alcohol
autoimmune of pancreatic duct
Late onset SPINK1 Recurrent acute
Tobacco
Syndromic Pancreatitis IPMN
Hypercalcaemia Tropical CFTR autoimmune
(associated with Ischaemic/vascular Pancreas divisum
Hypertriglyceridaemia other autoimmune
diseases)
Chronic renal failure

Figure 1

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 PANCREAS AND SPLEEN

Idiopathic abdominal pain consistent with recurrent acute pancreatitis.

Up to one-third of patients with CP have no known risk factors, Over a period of years, this leads to morphological and functional
i.e. idiopathic. There are two groups of patients e early onset changes in the pancreas. With time, patients develop the classical
and late onset. Patients with early onset CP tend to present with triad of abdominal pain, exocrine pancreatic insufficiency (with
abdominal pain before the age of 35 years. Patients with late weight loss) and diabetes.
onset CP usually present in their fifth decade of life without pain Pain in CP usually occurs after a meal, mainly in the
but with associated poor pancreatic function related symptoms. epigastric area with radiation to the back, often associated with
nausea and vomiting. Pancreatic ductal hypertension, pancreatic
Genetic parenchymal hypertension (like ‘compartment syndrome’),
Hereditary pancreatitis is associated with CP and typically cate- activation of intrapancreatic nociceptors, hypertrophy and
gorized into ‘suspected’, autosomal dominant and autosomal inflammation of intrapancreatic nerves, abnormal pain process-
recessive. Genetic patients are usually suspected with early onset ing in the central nervous system, and onset of local or remote
and absence of an obvious cause. There are a few gene mutations complications of CP are all reasons that may cause severe
described e gain of function mutation (e.g. PRSS-1 mutation persistent pain in patients with CP. There is often little correla-
associated with premature activation of trypsinogen to trypsin) tion between the severity of pain and demonstrable abnormal
or loss of function mutation (e.g. SPINK1 or CTRC mutation vital signs or morphological changes of the pancreas on cross-
associated with lack of inhibition of trypsin, or CFTR mutation sectional imaging. This often results in undertreatment of pain
causing impairment of secretary function of duct cells and inhi- in patients with CP.
bition of pancreatic enzyme flow). Hereditary pancreatitis in- Pancreatic enzymes, bile salts and an intact intestinal mucosa
cludes autosomal dominant PRSS-1 mutation with variable are essential for the complex process involved in fat digestion
expression and autosomal recessive SPINK1/CTRC and CFTR and absorption. Pancreatic exocrine enzyme insufficiency due to
mutations. There is also growing evidence that many patients CP is one of the causes of steatorrhoea, i.e. excess mal-digested
with toxic, metabolic or idiopathic CP have a strong pathogenic and mal-absorbed fat in the stool. The pancreas has a large
genetic element with active modifier genes making the disease functional reserve and it requires up to 90% of the gland to be
more insidious. These patients tend to have higher risk of destroyed before a patient develops symptoms of pancreatic
developing pancreatic ductal adenocarcinoma due to onset of enzyme deficiency.
chronic inflammation at a young age and duration of illness. Progressive fibrosis with loss of endocrine cells in the
pancreas leads to development of type 3C (or pancreatogenic)
Autoimmune diabetes mellitus. These patients lose not only beta cells (as a
Autoimmune pancreatitis (AIP) is a rare form of pancreatitis result of scarring/fibrosis) resulting in hyperglycaemia, but are at
which is immune mediated by abnormal B cells and responds a higher risk of developing hypoglycaemia due to loss of alpha
well to steroid treatment. It is classified as type 1 or type 2. Type and delta cells resulting in lack of counter hormones such as
1 autoimmune lymphoplasmacytic sclerosing pancreatitis is part glucagon and vasoactive intestinal polypeptide.
of a multi-organ fibro-inflammatory syndrome characterized by Some patients develop complications from CP. Pancreatic
increased serum IgG4 concentrations and may have multi-organ duct rupture with recurrent inflammation may lead to forma-
involvement, typical histological findings with lymphocytic tion of pseudocysts, pancreatic ascites or pancreato-pleural
infiltration and a rapid response to steroids. AIP type 2 is fistula; scarring and fibrosis may lead to duodenal or biliary
distinctly different in that it is pathologically defined by gran- duct obstruction; portal and splenic vein thrombosis may lead
ulocyte epithelial lesions, mainly duct centric, presents with to left-sided (‘sinistral’) portal hypertension and formation of
acute recurrent episodes and has neutrophilic infiltration without gastric varices; erosion of the peripancreatic arteries may lead
response to steroids. to pseudoaneurysm and bleeding from splenic, gastroduodenal,
superior and inferior pancreatico-duodenal arteries (Figure 2).
Recurrent severe
The strongest risk factor for the development of CP is an episode
of acute severe necrotic pancreatitis. Recurrent acute pancreatitis Diagnosis
and severe acute pancreatitis (SAP) due to any cause may result The diagnosis of CP is based on thorough clinical history,
in a post-necrotic morphology of scarring, fibrosis and perma- physical examination, appropriate cross-sectional imaging with
nent dysfunction of the pancreas and chronic pancreatitis. or without additional pancreatic function tests. Diagnosis can be
obvious in patients with advanced disease but may be chal-
Obstructive
lenging in the early stages and suspicion of CP in the correct
Ductal obstruction secondary to pancreatic malignancy, trauma,
clinical context is key to making the diagnosis.
inflammatory strictures and calcification (ductal and calculi) can
In addition to the main clinical symptoms of abdominal pain,
cause chronic obstructive pancreatitis. There is ongoing debate
weight loss, steatorrhoea and diabetes mellitus, patients may
as to whether pancreas divisum and ampullary stenosis
present with symptoms related to local complications (Figure 2).
(sphincter of Oddi dysfunction) can cause CP.
These symptoms may present in various combinations with
different severity during evolution of the disease. Abdominal
Clinical features
pain is the most common symptom, but may be absent in 15% of
Patients rarely present with classical symptoms of CP initially. patients with alcohol-related CP (and in up to 23% of patients
Typically, they present with repeated episodes of upper with non-alcoholic pancreatitis). Patients can have a bloating

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 PANCREAS AND SPLEEN

Figure 2

sensation, abdominal pain, or a change in bowel habit due to

impaired pancreatic exocrine secretion, and steatorrhoea usually
develops late.
Physical examination may reveal signs of malnutrition, ery-
thema ab igne, jaundice, ascites, splenomegaly, signs of liver
failure or it may be normal.
The most accurate method for diagnosing CP is histologic
examination of the pancreatic gland. It is not always practical to
obtain pancreatic tissue due to the difficulty in accessing the
pancreas and the risks associated with biopsy of the pancreas.
Although endoscopic and percutaneous biopsy options are
available, sample error (resulting in false negative diagnosis) and
adverse effects (from complications like acute pancreatitis) are Figure 3 Plain X-ray of the abdomen showing diffuse calcification of
the pancreas with advanced chronic pancreatitis.
the main limitations in obtaining pancreatic tissue for diagnosis.
Other causes for patient’s symptoms should be considered
such as: peptic ulcer disease, gallstone disease, chronic mesen- Ultrasound
teric ischaemia and irritable bowel syndrome. It is important to Abdominal ultrasound is usually done as a first step in investi-
consider pancreatic cancer as a main differential diagnosis, gation of abdominal pain. However, it has limited application in
particularly when there is a mass lesion in the pancreas or if the pancreatic pathology due to its retroperitoneal location and the
patient presents with obstructive jaundice. presence of gas containing viscera anterior to the pancreas
Blood tests including full blood count (assess anaemia), interfering with ultrasound images.
serum albumin (to assess nutritional status) and liver function
tests (to assess cholestasis) are helpful. Often serum amylase Computed tomography of abdomen with IV contrast
level is normal in patients with chronic pancreatitis. (CT)
Based on the patient’s presentation (acute or chronic), CT is sensitive in demonstrating both pancreatic parenchymal
severity of symptoms, availability and access for investigations, and pancreatic duct changes in CP and is widely available
the following imaging should be considered: (Figure 4). CT is very sensitive to identify (ductal and paren-
chymal) calcification, pancreatic mass, pancreatic parenchymal
Plain abdominal X-ray atrophy and CP-associated complications such as: pseudocysts,
Focal or diffuse calcification in the distribution of the pancreas ascites, pseudoaneurysms, venous thrombosis and biliary
gland area is a definite indication of advanced chronic pancrea- obstruction. Limitation of CT is its lack of sensitivity and speci-
titis (Figure 3). Absence of this does not rule out the diagnosis. ficity in picking up early mild forms of CP, its inherent risk of

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 PANCREAS AND SPLEEN

Figure 4 Axial and coronal reconstruction of a CT scan of a patient with chronic pancreatitis.

radiation and the risk of inducing contrast associated malignancy is suspected in patients with known CP. The ‘Rose-
nephropathy. mont’ classification was developed in an attempt to define criteria
for EUS diagnosis of CP; however, its sensitivity is uncertain and
Magnetic resonance imaging (MRI)/magnetic resonance there is inter-observer reporting variation. Sometimes, it is diffi-
cholangiopancreatography (MRCP) cult to differentiate normal age related findings, and non-
MRCP is a non-invasive procedure which does not use ionizing diagnostic asymptomatic fibrosis from early changes of CP.
radiation. It has high sensitivity for identifying strictures and
dilatation of the main pancreatic duct and side branches. Dy-
Tests of pancreatic function
namic MRCP or secretin MRCP may be used to capture a series of
There are several direct and indirect tests which measure
images in rapid sequence for up to 10-minutes after intravenous
exocrine and endocrine function of the pancreas.
administration of secretin hormone and provides excellent
Direct pancreatic function tests include duodenal intubation
spatial resolution and functional information regarding exocrine
using fluoroscopy or endoscopy to collect the pancreatic juice.
pancreatic function. Intravenous contrast agent is not used dur-
The pancreatic juice is collected after stimulation of the pancreas
ing MRCP examination which may limit the identification of
with secretin. The total volume and biochemical content of the
other pancreatic parenchymal abnormalities or vascular com-
juice for bicarbonate level are measured. The procedure is
plications. Secretin is expensive, not available widely and
invasive and cumbersome with poor patient compliance due to
restricted to specialist practice.
the requirement of duodenal intubation, but can be considered in
a symptomatic patient with suspected CP and equivocal CT/MRI
MRI examination with IV contrast
images.
MRI of the pancreas usually uses intravenous contrast and gives
Non-invasive indirect pancreatic function such as a 72-hour
better information of the pancreatic parenchyma compared to
quantitative faecal fat determination can be used to diagnose
MRCP. Advanced MRI for estimation of tissue stiffness, quanti-
fat mal-digestion resulting in steatorrhoea; however, the
fication of fibrosis and pancreatic fluid flow dynamics are under
pancreatic gland has to lose significant function before clinical
evaluation for routine clinical use.
symptoms of steatorrhoea occur. It is not specific for CP and
Endoscopic retrograde cholangiopancreatography can give false positive results in patients with biliary
(ERCP) obstruction, small bowel mucosal disease and bacterial over-
ERCP was the gold standard investigation to diagnose CP in the growth. Measurement of faecal elastase-1 enzyme, which is
past but due to wider availability of non-invasive MRCP and its produced by the pancreas and remains unchanged in the
capacity to obtain good quality images of the pancreatic ducts, gastrointestinal tract, is a commonly used test in clinical
ERCP is now restricted to therapeutic purposes only. practice. It is not sensitive or helpful in patients with mild or
moderate pancreatic exocrine insufficiency. However, faecal
Endoscopic ultrasound (EUS) elastase-1 has been shown to be more specific, with a sensi-
EUS can be used to diagnose CP and is a useful tool to obtain tivity approaching 100% and specificity reported as 93% in
biopsy of a pancreatic mass (identified on CT or MRI) when patients with severe insufficiency.

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 PANCREAS AND SPLEEN

Treatment Endoscopic stenting of the obstructed pancreatic duct is an option

for patients with poor functional reserve as early intervention may
The aim of treatment in patients with CP is mainly to control
preserve pancreatic parenchymal function in the long term.
pain, address exocrine and endocrine insufficiency, and deal
Symptomatic fully formed pancreatic pseudocysts can be
with the resulting complications.
drained by transmural drainage using EUS or by transpapillary
Non-operative management pancreatic duct stenting at ERCP. With the advent of fully
Life style changes including abstaining from alcohol and stopping covered self-expanding metal stents (FCSEMS), bile duct stric-
smoking reduces the risk of recurrent episodes of CP and preserves tures secondary to CP can be successfully treated. A prospective
existing pancreatic function. Improved exercise and diet should be multicentre case series showed endoscopic FCSEMS as a viable
advocated to improve general conditioning. Pain control is the treatment option for CP patients with benign lower common bile
main problem in this complex group of patients. It is often very duct strictures, with a stricture resolution rate of 79.4% at 1 year
difficult to evaluate the patient’s analgesia requirements as they do and a stricture recurrence rate of 10.5% after a mean follow-up of
not show all the objective signs of pain and therefore their anal- 20 months.
gesia is often underestimated. Pain control should follow the
principles of the WHO ‘pain relief ladder’. Antidepressants (e.g. Operative treatment
amitriptyline), anticonvulsants (e.g. gabapentin and pregabalin) Surgery should only be considered in selected symptomatic pa-
and selective serotonin reuptake inhibitors sometimes work along tients and can be associated with good results. Surgery is typi-
with conventional analgesics in a synergistic way. It is important to cally indicated in patients with duodenal, pancreatic or biliary
involve a specialist pain team and clinical psychologist in man- obstruction, those with a symptomatic large pseudocyst, if a
agement of complex pain associated with CP. During acute epi- pancreatic mass is present (on the background of CP) where
sodes, patients with CP may benefit from short duration malignancy cannot be excluded and in patients with intractable
intravenous morphine administered using a patient-controlled pain. Invasive surgical procedures may be justified as a treatment
analgesia (PCA) device. Pancreatic enzyme supplementation or for the complications of CP but the risks and benefits should
antioxidants for treatment of pain in CP are not recommended. always be carefully weighed especially in offering major surgery
Invasive procedures like coeliac plexus block and thoracoscopic for intractable pain. The surgical rationale behind operating in
splanchnicectomy may provide short term benefit for intractable patients with intractable pain being that it may be caused by
pain but invariably the pain returns and these techniques are pancreatic ductal obstruction or increased intrapancreatic pres-
therefore not advocated for treatment of pain in patients with CP. sure (equivocal to ‘compartment syndrome’) or by ongoing
Exocrine failure leads to fat malabsorption resulting in stea- inflammation associated with a mass lesion usually located in the
torrhoea, deficiency of fat-soluble vitamins and ultimately weight head of the pancreas. None of the described operations are sham
loss. Involvement of a dietician is very important in nutritional controlled in trials and it is not possible to assess the placebo
assessment and advice regarding adequate supplements. effect of surgery or the natural course of the disease. However, in
Pancreatic enzymes can be administered orally to be taken along most studies, operative intervention (with pain as an indication)
with snacks and meals. Adequacy of dosage is determined by in selected patients is associated with significant long-term pain
reduction in frequency of steatorrhoea and weight gain. The relief (in 70e90% of patients).
usual starting dose is 25,000 lipase units with snacks and 50,000 Surgical procedures for CP are mainly divided into three
lipase units with meals, with increased titration based on the categories:
response. Addition of a proton pump inhibitor may enhance the
drainage or decompression (e.g. Peustow’s longitudinal
efficacy of pancreatic enzyme supplementation. However, if the pancreaticojejunostomy)
response to the pancreatic enzymes is poor, once compliance is
resection (e.g. Whipple’s pancreaticoduodenectomy, distal
assured, alternate causes need to be explored. pancreatectomy)
Endocrine failure leads to type 3c diabetes mellitus which can
combination of both (e.g. Frey’s procedure, Beger’s
initially be treated with oral hypoglycaemic drugs but will usu- procedure).
ally require insulin supplementation in time. A commonly performed procedure for CP is longitudinal pan-
Lifestyle modification (smoking and alcohol abstinence, daily creaticojejunostomy (Peustow’s operation). This involves
exercise and healthy eating habits etc) is a key component of exposing the anterior part of the pancreas and opening the entire
non-operative management. length of the pancreatic duct longitudinally from the ampulla along
the head, body and tail of the pancreas. After removal of all the
Endoscopic treatment stones from the opened duct, a Roux loop of jejunum is anasto-
Endoscopic treatment is considered in symptomatic CP with: mosed to the opened pancreatic duct longitudinally to establish

pancreatic duct stricture þ/ pancreatic duct stone and adequate drainage. This operation often does not address an
upstream dilatation enlarged, inflamed pancreatic head which can cause persistent

pancreatic pseudocyst symptoms after the procedure. However, a Frey’s procedure

pancreatic ascites (Figure 5), where the tissue in the head of pancreas anterior to the

bile duct stricture with deteriorating obstructive liver pancreatic duct is cored out, gives better symptom control in the
function tests. long term. Alternatively, the whole of the pancreatic head can be
Symptomatic pancreatic duct stones with associated strictures removed with preservation of the duodenum as in a Beger’s pro-
can be treated by pancreatic duct dilatation and removal of stones cedure (Figure 6). A formal resection of the head of the pancreas,
combined with extracorporeal shockwave lithotripsy (ESWL). i.e. a Whipple pancreaticoduodenectomy should be performed

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 PANCREAS AND SPLEEN

Frey procedure
a The whole duct is laid widely b A Roux loop of
open, and the tissue anterior jejunum is laid on the
to the duct is removed to exposed pancreas
‘saucerize’ the head
of the gland

Figure 5

Beger procedure

a The head of the pancreas b The reconstruction

is excised within the duodenal with pancreatic duct
loop, leaving sufficient and bile duct
pancreas to maintain the anastomoses
blood supply to the
duodenum; the bile
duct is drained

Figure 6

when malignancy associated with CP cannot be excluded. Distal FURTHER READING

pancreatectomy is occasionally undertaken in selected patients Conwell DL, Banks PA, Sandhu BS, et al. Validation of demographics,
where disease is confined to the distal pancreas. Total pancrea- etiology, and risk factors for chronic pancreatitis in the USA: a
tectomy is associated with postoperative brittle diabetes and 50% report of the North American Pancreas Study (NAPS) Group. Dig
of patients will have persistent pain. Total pancreatectomy with Dis Sci 2017 Aug; 62: 2133e40.
islet autotransplantation is a viable option (in specialized centres) Cornwell DL, Lee LS, Yadav D, et al. American pancreatic
for patients with hereditary chronic pancreatitis, due to an association practice guidelines in chronic pancreatitis: evidence-
increased risk of pancreatic cancer in this group. based report on diagnostic guidelines. Pancreas 2014; 43:
1143e62.
Summary Deviere J, Reddy ND, Pu €k A, et al. Successful management of
€spo
Chronic pancreatitis is a complex, progressive, disabling fibro- benign biliary strictures with fully covered self-expanding metal
inflammatory disease that can be difficult to diagnose with a stents. Gastroenterology 2014; 147: 385e95.
multifactorial aetiology. Management is often conservative Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, classifica-
focussing on lifestyle changes and control of complications, but a tion, and new genetic developments. Gastroenterology 2001; 120:
select cohort of patients with intractable pain or disease-specific 682e707.
complications should have the involvement of an experienced Kleeff J, Whitcomb DC, Shimosegawa T, et al. Chronic pancreatitis.
multidisciplinary team and specialist therapeutic interventions.A Nat Rev Dis Primers 2017; 3. 17060:1-18.

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 PANCREAS AND SPLEEN

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challenges for prevention and treatment. Dig Dis Sci 2017 July; 62: Practice points
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Stevens T, Conwell D, Zuccaro G. Pathogenesis of chronic pancrea- ercise and healthy eating habits)
titis: an evidence-based review of past theories and recent de- C Some CP patients with refractory symptoms will need referral to a
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