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Pancreas
ANATOMY
Pancreas is an
elongated
retroperitoneal organ;
15-20 cm in length; lies
against L1L2 vertebra.
It lies posterior to
stomach, separated by
lesser sac.
Parts
It is divided into head, neck,
body, tail.
The head lies in the
concavity of duodenum
and tail reaches the hilum
of the spleen.
The posterior surface of
the neck of pancreas is
related to terminal part of
superior mesenteric vein
and beginning of portal
vein.
Ducts of Pancreas
1. Main duct of pancreas
(Duct of Wirsung): It
begins in the tail of pancreas and
runs on the posterior surface of
the body and head of pancreas,
receives numerous tributaries at
right angle along its length
(Herring bone pattern).
 It joins the bile duct in the wall of the second part of
duodenum to form hepatopancreatic ampulla (of Vater)
and opens on the summit of major duodenal papilla (8-10
cm from pylorus).

2. Accessory pancreatic duct (Duct of Santorini): It

begins in the lower part of the head and opens into the
duodenum at minor duodenal papilla (6-8 cm from the
pylorus).
Blood Supply of Pancreas
1. Pancreatic branches of
splenic artery.
2. Superior
pancreaticoduodenal
artery.
3. Inferior
pancreaticoduodenal
artery.
 Venous drainage is into portal vein.
Nerve Supply

The nerves of the pancreas

are derived from the vagus
and abdominopelvic
splanchnic nerves passing
through the diaphragm
The parasympathetic and
sympathetic fi bers reach
the pancreas by passing
along the arteries from the
celiac plexus and superior
mesenteric plexus
Functions
Exocrine part secretes pancreatic juice which helps in digestion of
proteins, carbohydrates and fats.
Endocrine part constitutes islets of pancreas which is distributed
more numerous in tail of pancreas.
cells of islets secrete insulin.
cells secrete glucagon
INVESTIGATIONS
Estimation of pancreatic enzymes in body fluids
When the pancreas is damaged, enzymes such as amylase, lipase,
trypsin, elastase and chymotrypsin are released into the serum.
Measurement of serum amylase is the most widely used test of
pancreatic damage (serum lipase is more sensitive and specific, but
is not widely available). The serum amylase rises within a few
hours of pancreatic damage and declines over the next 48 days.
A markedly elevated serum level is highly suspicious but not
diagnostic of acute pancreatitis
 If confirmation of the diagnosis is required, computed tomography
(CT) of the pancreas is of greater value
Pancreatic function tests
Secretin stimulation test:
o secretin stimulates the pancreas to release bicarbonate-rich fluid.
o secretin stimulation test measures the ability of the exocrine
pancreas to respond to secretin.
Lundh Test:
o it involves administration of a liquid test meal, containing protein, fat, and
sugar.
o The TRYPSIN concentration in duodenal aspirates is the measured.
NBTPABA Test:
o It involves oral administration of nitrobluetetrazoliumpara-aminobenzoic
acid (NBTPABA)
oThis is degraded in the gut by the pancreatic enzyme, and the
breakdown product(PABA) is excreted in urine and its urine level
is measured.
Fecal elastase test:
o it involves measurement of the enzyme elastase in stool.
oIt is simple and specific test for pancreatic exocrine insufficiency.
 These tests are cheap and easy to perform, but are non-specific,
especially following gastrectomy and in conditions that may alter
gastrointestinal transit and intestinal absorptive capacity.
Measurement of the enzyme elastase in stool is simple, specific
and now used widely.
Imaging investigations
Ultrasonography
oUltrasonography is the initial investigation of choice in patients
with jaundice to determine whether or not the bile duct is dilated,
the coexistence of gallstones or gross disease within the liver, such
as metastases.
oIt may also define the presence or absence of a mass in the
pancreas
Computed tomography:
o CT scan is the best test for most significant pathologies within the
pancreas.
oUnenhanced CT scan is essential to determine the presence of
calcification within the pancreas and gallbladder.
oEnhenced CT scan is essential for:
site and size of pancreatic cancer .
pancreatic endocrine tumors.
necrotic areas in pancreatitis.
PANCREATITIS
Pancreatitis is inflammation of the gland parenchyma of the
pancreas
oFor clinical purposes, it is useful to divide pancreatitis into
acute, which presents as an emergency, and
chronic, which is a prolonged and frequently lifelong disorder
resulting from the development of fibrosis within the pancreas.
Acute pancreatitis
Acute pancreatitis
Acute pancreatitis is defined as an acute condition presenting
with abdominal pain and is usually associated with raised
pancreatic enzyme levels in the blood or urine as a result of
pancreatic inflammation.
oAcute pancreatitis may recur.
The underlying mechanism of injury in pancreatitis is thought to
be premature activation of pancreatic enzymes within the
pancreas, leading to a process of autodigestion. Anything that
injures the acinar cell and impairs the secretion of zymogen
granules, or damages the duct epithelium and thus delays
enzymatic secretion, can trigger acute pancreatitis.
 Once cellular injury has been initiated, the inflammatory process
can lead to pancreatic oedema, haemorrhage and, eventually,
necrosis.
As inflammatory mediators are released into the circulation,
systemic complications can arise, such as haemodynamic
instability, bacteremia (due to translocation of gut flora), acute
respiratory distress syndrome and pleural effusions, gastrointestinal
haemorrhage, renal failure and disseminated intravascular
coagulation (DIC).
Acute pancreatitis may be categorized as mild or severe
 Mild acute pancreatitis is characterized by interstitial oedema of
the gland and minimal organ dysfunction. Eighty per cent of
patients will have a mild attack of pancreatitis, the mortality from
which is around 1 per cent.
Severe acute pancreatitis is characterized by pancreatic necrosis, a
severe systemic inflammatory response and often multi-organ
failure. In those who have a severe attack of pancreatitis, the
mortality varies from 20 to 50 per cent.
Chronic pancreatitis
Chronic pancreatitis is defined as a continuing inflammatory
disease of the pancreas characterised by irreversible morphological
change typically causing pain and/or permanent loss of function.
Many patients with chronic pancreatitis have painful
exacerbations, but the condition may be completely painless.
Acute pancreatitis
Etiology
Biliary tract disease 50%stonescommon cause
Alcoholism 25%
Gallstone pancreatitis is thought to be triggered by the passage of
gallstones down the common bile duct. If the biliary and
pancreatic ducts join to share a common channel before ending at
the ampulla, then obstruction of this passage may lead to reflux of
bile or activated pancreatic enzymes into the pancreatic duct.
Patients who have small gallstones and a wide cystic duct may be
at a higher risk of passing stones.
The proposed mechanisms for alcoholic pancreatitis include the
effects of diet, malnutrition, direct toxicity of alcohol, concomitant
tobacco smoking, hypersecretion, duct obstruction or reflux, and
hyperlipidaemia. The remaining cases may be due to rare causes or
be idiopathic
Clinical presentation
Sudden onset of upper abdominal pain which is referred to back.
Pain is severe, agonizing and refractory. Pain may be relieved or
reduced by leaning forward
Vomiting and high fever, tachypnoea with cya nosis
Tenderness, rebound tenderness, guarding, rigidity and abdominal
distension, severe illness.
Often mild jaundice (due to cholangitis). Jaundice may also be due
to bile duct disease / obstruction or cholestasis.
Features of shock and dehydration.
Oliguria, hypoxia and acidosis.
Haematemesis/malaena due to duodenal necrosis, gastric
erosions, decreased coagulability/DIC.
Hiccough when present is refractory.
Ascites may be present. Paralytic ileus is common.
Pleural effusion (20%), pulmonary oedema, consolidation,
features of rapid onset ARDS is often observed.
Neurological derangements due to toxaemia, fat embolism,
hypoxia, respiratory distress can occur. It may be mild psychosis to
coma.
Occasionally haematemesis or melaena can occur.
Grey-Turners sign, Cullens sign, Fox sign.

Enzymes seep across the

retroperitoneum causing
haemorrhagic spots and
ecchymosis in the flanks (Grey
Turners sign), or
Through falciform ligament
causing discoloration around
the umbilicus (Cullens sign),
umbilical black eye or
Below the inguinal ligament
(Fox sign).
Fluid, Metabolic, Haematologic and
Biochemical Changes
Hypovolemia due to diffuse capillary leak and vomiting causing
raised haematocrit, blood urea, serum creatinine levels.
Hypoalbuminemia which is more revealed after fluid correction.
Hypocalcaemia is either due to decreased albumin level or specific
loss of ionized calcium.
Hypochloraemic metabolic alkalosis is common due to repeated
vomiting.
Reduced insulin secretion, increased glucagon and catecholamine
secretion causes hyperglycemia, more so in diabetic patients.
 Hyperbilirubinemia may be due to biliary stone/obstruction or
cholangitis or non-obstructive cholectasis.
Hypertriglyceridaemia is common especially in hyperlipidemia
patients.
Methemalbuminemia, when it occurs in acute pancreatitis indicates
poor prognosis.
Investigations
Typically, the diagnosis is made on the basis of the clinical
presentation and an elevated serum amylase level. Serum amylase
level three to four times above normal is indicative of the disease.
A normal serum amylase level does not exclude acute pancreatitis,
particularly if the patient has presented a few days later.
If there is doubt, and other causes of acute abdomen have to be
excluded, contrast-enhanced CT is probably the best single imaging
investigation
Assessment of severity
Management
Regardless of the cause or the severity of the disease, the
cornerstone of the treatment of chronic pancreatitis is aggressive
fluid resuscitation using isotonic crystalloid solution.
The rate of administration should be individualized and adjusted
based on age, comorbidities, vital signs, mental status, skin turgor,
and urine output.
Patients who do not respond to initial fluid resuscitation or have
significant renal, cardiac or respiratory comorbidities often require
invasive monitoring with central venous access and a Foley catheter.
 patients with AP require continuous pulse oximetry because one of
the most common systemic complications of AP is hypoxemia
caused by the acute lung injury associated with this disease.
Patients should receive supplementary oxygen to maintain arterial
saturation above 95%.
It is also essential to provide effective analgesia. Narcotics are
usually preferred, especially morphine. One of the physiologic
effects described after systemic administration of morphine is an
increase in tone in the sphincter of Oddi; however, there is no
evidence that narcotics exert a negative impact in the outcome of
patients with AP.
 It is also essential to provide effective analgesia. Narcotics are
usually preferred, especially morphine. One of the physiologic
effects described after systemic administration of morphine is an
increase in tone in the sphincter of Oddi; however, there is no
evidence that narcotics exert a negative impact in the outcome of
patients with AP.
There is no proven benefit in treating AP with antiproteases (e.g.,
gabexate mesilate, aprotinin), platelet-activating factor inhibitors
(e.g., lexipafant), or pancreatic secretion inhibitors
 Special Considerations:
Endoscopic Retrograde Cholangiopancreatography: Early ERCP,
with or without sphincterotomy, was initially advocated to reduce
the severity of pancreatitis because the obstructive theory of AP
states that pancreatic injury is the result of pancreatic duct
obstruction.
However, three randomized trials have demonstrated that ERCP is
only beneficial for patients with severe acute biliary pancreatitis
 Laparoscopic Cholecystectomy:
With the exception of older patients and those with poor
performance status, laparoscopic cholecystectomy is indicated for
all patients with mild acute biliary pancreatitis.
Choledocolithiasis can be excluded via intraoperative
cholangiography, ERCP, or laparoscopic common bile duct
exploration.
 For patients with severe pancreatitis, early surgery may increase the
morbidity and length of stay. Current recommendations suggest
conservative treatment for at least 6 weeks before laparoscopic
cholecystectomy is attempted in this setting. This approach has
significantly decreased morbidity.
Complications
Acute fl uid collection : It is collection of fl uid in or near the
pancreas during an attack of acute pancreatitis with an ill-defi ned
or lackingfi brin wall or granulation tissue.
Acute pseudocyst : It is collection of fl uid with pancreatic juice in
or near the pancreas localised by thin fi brin wall or granulation
tissue.
Pancreatic pseudocyst : It is collection of fl uid in a false cavity
which commonly contains brownish pancreatic enzyme rich fl uid,
lined by granulation tissue but not true epithelium with an organised
thick fi brous covering.
 Pancreatic necrosis It is focal/diffuse area of non-viable
pancreatic parenchyma with peripancreatic fat necrosis. It is
initially sterile but eventually gets infected.
Pancreatic abscess
Pancreatic fistula: It can occur due to ductal wall disruption and
necrosis or after surgical intervention for acute pancreatitis
(necrosectomy).
Chronic pancreatitis

Chronic pancreatitis is a progressive inflammatory disease in which

there is irreversible destruction of pancreatic tissue. Its clinical course
is characterized by severe pain and, in the later stages, exocrine and
endocrine pancreatic insufficiency. In the early stages of its evolution,
it is frequently complicated by attacks of acute pancreatitis, which are
responsible for the recurrent pain that may be the only clinical
symptom.
Aetiology and pathology
High alcohol consumption is the most frequent cause of chronic
pancreatitis, accounting for 6070% of cases, but only 510% of
people with alcoholism develop chronic pancreatitis.
The exact mechanism of how alcohol causes chronic inflammation in
these patients is unclear; genetic and metabolic factors may be at
play.
 Other causes include pancreatic duct obstruction resulting from
stricture formation after trauma, after acute pancreatitis or even
occlusion of the duct by pancreatic cancer.
Congenital abnormalities, such as pancreas divisum and annular
pancreas, if associated with papillary stenosis, are rare causes of
chronic pancreatitis.
 Hereditary pancreatitis, CF, infantile malnutrition and a large
unexplained idiopathic group make up the remainder. Normally, if
trypsinogen does become prematurely activated within the
pancreas, it is inhibited by SPINK1 and then gets destroyed.
Hereditary pancreatitis is an autosomal dominant disorder with an
80 per cent penetrance, associated with a gainof- function mutation
in the cationic trypsinogen gene (PRSS1) on chromosome 7, which
leads to production of a degradationresistant form of trypsin
 Tropical pancreatitis is a form of idiopathic pancreatitis that begins
at a young age and is associated with a high incidence of diabetes
mellitus and stone formation. This has been described in Kerala, in
southern India, as well as in other developing countries in Asia,
Africa and central America.
Malnutrition, ingestion of cyanogenic glycosides in cassava, and
exposure to hydrocarbons released by kerosene or paraffin lamps
have been proposed as possible mechanisms for tropical
pancreatitis.
 Autoimmune pancreatitis has been described relatively recently.
Features include diffuse enlargement of the pancreas, diffuse and
irregular narrowing of the main pancreatic duct. It may occur in
association with other autoimmune diseases, as a multi-system
disorder, or may affect the pancreas alone. The changes may be
confused with neoplasia. Autoantibodies may be present and levels
of the immunoglobulin subtype IgG4 are elevated
 At the onset of the disease when symptoms have developed, the
pancreas may appear normal. Later, the pancreas enlarges and
becomes hard as a result of fibrosis. The ducts become distorted
and dilated with areas of both stricture formation and ectasia.
Calcified stones weighing from a few milligrams to 200 mg may
form within the ducts.
The ducts may become occluded with a gelatinous proteinaceous
fluid and debris, and inflammatory cysts may form.
Clinical features
Pain is the outstanding symptom in the majority of patients. The
site of pain depends to some extent on the main focus of the
disease. If the disease is mainly in the head of the pancreas, then
epigastric and right subcostal pain is common, whereas if it is
limited to the left side of the pancreas, left subcostal and back pain
are the presenting symptoms.
In some patients, the pain is more diffuse. Radiation to the
shoulder, usually the left shoulder occurs. Nausea is common
during attacks and vomiting may occur.
 Weight loss is common, because the patient does not feel like
eating.
Loss of exocrine function leads to steatorrhoea in more than 30%
of patients with chronic pancreatitis.
Investigations
Only in the early stages of the disease will there be a rise in serum
amylase. Tests of pancreatic function merely confirm the presence
of pancreatic insufficiency.
Pancreatic calcifications may be seen on abdominal x-ray
CT or MRI scan will show the outline of the gland, the main area
of damage and the possibilities for surgical correction
Calcification is seen very well on CT, but not on MRI.
An MRCP will identify the presence of biliary obstruction and the
state of the pancreatic duct.
Treatment
There is no single therapeutic agent that has been shown to relieve
symptoms
Endoscopic, radiological or surgical interventions are indicated
mainly to relieve obstruction of the pancreatic duct, bile duct or
the duodenum, or in dealing with complications (e.g. pseudocyst,
abscess, fistula, ascites or variceal haemorrhage).
Endoscopic pancreatic sphincterotomy might be beneficial in
patients with papillary stenosis and a high sphincter pressure and
pancreatic ductal pressure.
 Pancreatic duct stones may be extracted at ERCP, and this may
sometimes be combined with extracorporeal shock wave
lithotripsy.
Some patients have a mass in the head of the pancreas, for which
either a pancreatoduodenectomy or a Beger procedure (duodenum-
preserving resection of the pancreatic head) is appropriate.
If the duct is markedly dilated, then a longitudinal
pancreatojejunostomy or Frey procedure can be of value
CARCINOMA OF THE PANCREAS
Pancreatic cancer is the sixth leading cause of cancer death in the
UK, and the incidence is ten cases per 100 000 population per year.
Worldwide, it constitutes 23 per cent of all cancers and, in the
United States, is the fourth highest cause of cancer death.
The incidence has declined slightly over the last 25 years. There is
no simple screening test; however, patients with an increased
inherited risk of pancreatic cancer should be referred to specialist
units for screening and counselling.
Pathology
More than 85 per cent of pancreatic cancers are ductal
adenocarcinomas. The remaining tumours constitute a variety of
pathologies with individual characteristics.
Ductal adenocarcinomas arise most commonly in the head
of the gland. They are solid, scirrhous tumours, characterised by
neoplastic tubular glands within a markedly desmoplastic fibrous
stroma.
 Fibrosis is also a characteristic of chronic pancreatitis, and
histological differentiation between tumour and pancreatitis can
cause diagnostic difficulties.
Ductal adenocarcinomas infiltrate locally, typically along nerve
sheaths, along lymphatics and into blood vessels. Liver and
peritoneal metastases are common.
 Proliferative lesions in the pancreatic ducts can precede invasive
ductal adenocarcinoma. These are termed pancreatic
intraepithelial neoplasia or PanIN, and can demonstrate a range
of structural complexity and cellular atypia
 Cystic tumours of the pancreas may be serous or mucinous.
Serous cystadenomas are typically found in older women, and are
large aggregations of multiple small cysts, almost like bubble wrap.
They are benign. Mucinous tumours, on the other hand, have the
potential for malignant transformation.
They include:
Mucinous cystic neoplasms (MCNs) and
Intraductal papillary mucinous neoplasms (IPMNs).
 MCNs are seen in perimenopausal women, show up as
multilocular thick-walled cysts in the pancreatic body or tail and,
histologically, contain an ovariantype stroma.
IPMNs are more common in the pancreatic head and in older
men, but an IPMN arising from a branch duct can be difficult to
distinguish from an MCN.
IPMNs arising within the main duct are often multifocal and have
a greater tendency to prove malignant. Thick mucus seen extruding
from the ampulla at ERCP is diagnostic of a main duct IPMN.
 Mucinous tumours can be confused with pseudocysts.
Occasionally, lymphoepithelial cysts, lymphangiomas, dermoid
cysts and intestinal duplication cysts can show up in the pancreas.
Solid pseudopapillary tumour is a rare, slowly progressive but
malignant tumour, seen in women of childbearing age, and
manifests as a large, part-solid, part-cystic tumour.
 Tumours arising from the ampulla or from the distal common bile
duct can present as a mass in the head of the pancreas, and
constitute around a third of all tumours in that area.
Adenomas of the ampulla of Vater are diagnosed at endoscopy as
polypoid submucosal masses covered by a smooth epithelium.
Ampullary adenocarcinomas often present early with biliary
obstruction.
Ampullary carcinomas are relatively small when diagnosed, which
may account for their better prognosis.
Clinical features

Jaundice secondary to obstruction of the distal bile duct is the

most common symptom that draws attention to ampullary and
pancreatic head tumours. It is characteristically painless jaundice
but may be associated with nausea and epigastric.
discomfort. Pruritus, dark urine and pale stools with steatorrhoea
are common accompaniments of jaundice.
 In the absence of jaundice, symptoms are often non-specific,
namely vague discomfort, anorexia and weight loss, and are
frequently dismissed by both patient and doctor.
On examination, there may be evidence of jaundice, weight loss, a
palpable liver and a palpable gall bladder.
Other signs of intra-abdominal malignancy should be looked for
with care, such as a palpable mass, ascites, supraclavicular nodes
and tumour deposits in the pelvis; when present, they indicate a
grim prognosis
Investigation

In a jaundiced patient, the usual blood tests and ultrasound scan

should be performed.
Ultrasound will determine whether or not the bile duct is dilated.
If it is, and there is a genuine suspicion of a tumour in the head of
the pancreas, the preferred test is a contrast-enhanced CT scan.
In the majority of instances, this should establish if there is a
tumour in the pancreas and if it is resectable.
 ERCP and biliary stenting should be carried out if there is any
suggestion of cholangitis, if there is diagnostic doubt (small
ampullary lesions may not be seen on CT, and ERCP is the best
way to identify them), if the patient is deeply jaundiced (serum
bilirubin >250 mmol/L), or there are distressing symptoms (e.g.
pruritus) and there is likely to be a delay between diagnosis and
surgery.
 EUS is useful if CT fails to demonstrate a tumour, if tissue
diagnosis is required prior to surgery ,if vascular invasion needs to
be confirmed and in separating cystic tumours from pseudocysts
Histological confirmation of malignancy is desirable but not
essential, particularly if the imaging clearly demonstrates a
resectable tumour.
The tumour marker CA19-9 is not highly specific or sensitive, but a
baseline level should be established; if it is initially raised, it can be
useful later in identifying recurrence.
Management
Surgical resection:
The standard resection for a tumour of the pancreatic head or the
ampulla is a pylorus-preserving pancreatoduodenectomy (PPPD).
This involves removal of the duodenum and the pancreatic head,
including the distal part of the bile duct. The original
pancreatoduodenectomy as proposed by Whipple included
resection of the gastric antrum.
 Total pancreatectomy is warranted only in situations where one is
dealing with a multifocal tumour (e.g. a main duct IPMN), or the
body and tail of the gland are too inflamed or too friable to achieve
a safe anastomosis with the bowel.
The PPPD procedure includes a local lymphadenectomy.
If the tumour is adherent to the portal or superior mesenteric vein,
but can still be removed by including a patch or a short segment of
vein in the resection, with an appropriate reconstruction of the
vessel, then that should be done.
Pancreatoduodenectomy
The patients coagulation screen should be checked preoperatively
and adequate hydration ensured.
The operation has three distinct phases:
exploration and assessment
resection;
reconstruction.
 A cholecystectomy is performed. The bile duct and hepatic artery
are exposed, removing the lymphatic tissue in this area. Exposure
of the hepatic artery enables division of the gastroduodenal artery
and visualisation of the portal vein.
The distal part of the gastric antrum is mobilised. The duodenum
and right colon are mobilised from the retroperitoneal tissues.
 The superior mesenteric vein is exposed inferior to the pancreatic
neck.
Careful dissection into the plane between the vein and the
pancreatic substance (see Figure 68.2) will reveal whether the
tumour is adherent to the vein. At this juncture, a decision has to
be made whether to proceed to the next phase of resection or not.
If resection is to be performed, the fourth part of the duodenum is
dissected and freed from the ligament of Treitz so that the upper
jejunum can be brought into the supracolic compartment.
 The jejunum is divided 2030 cm downstream from the
duodenojejunal flexure, and the mesentery of the proximal
jejunum is detached. The first part of the duodenum is divided.
The neck of the pancreas is divided, and then the uncinate process
is separated from the superior mesenteric artery and vein working
up towards the upper bile duct, which is divided, releasing the
specimen.
Retroperitoneal lymph nodes within the operative field are
completely removed with the specimen. Reconstruction is carried
out.
Adjuvant therapy