SURGICAL DISEASES

PARTS OF PANCREAS
PARTS OF PANCREAS
 UNCINATE PROCESS- The part of the gland that bends backwards and
underneath the body of the pancreas. Two very important blood
vessels, the superior mesenteric artery and vein cross in front of the
uncinate process.

 HEAD-The widest part of the gland. It is found in the right part of

abdomen, nestled in the curve of the duodenum which forms an
impression in the side of the gland.

 NECK-The thin section between the head and the body of the gland.

 BODY- The middle part of gland between the neck and the tail. The
superior mesenteric blood vessels run behind this part of the gland.

 TAIL- The thin tip of gland in the left part of abdomen in close
proximity with the spleen.
 ANATOMY
 The pancreas is an elongated,
tapered organ located across
the back of the abdomen,
behind the stomach.
 The right side of the organ
(called the head) is the widest
part of the organ and lies in the
curve of the duodenum.
 The tapered left side extends
slightly upward (called the body
of the pancreas) and ends near
the spleen (called the tail).
 ANATOMY
It functions to produce digestive
enzymes which are delivered to the
duodenum and various hormones,
which are delivered to the bloodstream.
One of the most important hormones
produced by the pancreas is insulin.
 Insulin is produced by specialized cells
of the pancreas called islets of
Langerhans.
 Insulin regulates blood sugar levels.
 Anatomy
The pancreas
secretes the
enzymes into the
pancreatic duct.
It joins the common
bile duct from the
liver and drains into
the duodenum
The pancreas is made up of
two types of tissue

exocrine tissue
The exocrine tissue secretes digestive enzymes.
These enzymes are secreted into a network of
ducts that join the main pancreatic duct, which
runs the length of the pancreas.

endocrine tissue
The endocrine tissue, which consists of the islets
of Langerhans, secretes hormones into the
bloodstream.
 Functions of the
pancreas
The enzymes secreted by the exocrine tissue in the
pancreas help break down carbohydrates, fats, proteins,
and acids in the duodenum.
These enzymes travel down the pancreatic duct into the
bile duct in an inactive form.
When they enter the duodenum, they are activated.
The exocrine tissue also secretes a bicarbonate to
neutralize stomach acid in the duodenum.

The hormones secreted by the endocrine tissue in the

pancreas are insulin and glucagon (which regulate the
level of glucose in the blood), and somatostatin (which
prevents the release of the other two hormones).
Blood supply to the
pancreas
Anatomy
Procedures which outline the gland to
delineate enlargement, irregularities
and calcification
Standard radiological studies to visualize the effect of the
enlarged pancreas on adjacent organs: stomach,
duodenum, small bowel, transverse colon and bile duct:
plain abdominal x-ray, contrast studies of the
gastrointestinal tract, cholangiography.
Direct imaging techniques to visualize the pancreatic
parenchyma: ultrasonography, CT, scintigraphy

Direct imaging technique to visualize the pancreatic duct

system: ERCP
Direct imaging technique to visualize the pancreatic and
peripancreatic
vessels: angiography
Procedures to define pancreatic
exocrine and endocrine function
Fecal fat excretion
Pancreatic function tests
Measurement of fasting blood levels of glucose and
hormons which are secreted by the pancreas: insulin,
glucagon, somatostatin.
Provocative tests to measure the serum level of the above
substances if the fasting levels are not conclusive:
- calcium infusion test (insulinoma, gastrinoma)
- tolbutamide tolerance test (insulinoma)
- secretin test (gastrinoma)
Analysis of serum for
markers of pancreatic
disease
 enzymes such as amylase, lipase,
trypsin, ribonuclease

 tumour- associated antigens such as

carcino-embryonic antigen and
pancreatic oncofetal antigen
Pancreatic biopsy and
cytology
 percutaneous fine needle aspiration
cytology using USS or CT for guidance.

 endoscopic transgastric or
transduodenal needle aspiration
cytology or brush cytology
Surgical exploration
Laparoscopic visualization and direct
vision biopsy or aspiration
cytology of the pancreas.

Operative visualization, palpation

and biopsy of the pancreas.
CASE 1, History
The 34 year-old patient appears in severe distress.
He explains that his sudden and intense, mid-epigastric
pain is worse when lying down and that it radiates to
the lower thoracic area of his back.
He reports some GI symptoms including anorexia,
nausea and vomiting.
The patient is a chronic alcoholic and recently went on
a binge where he consumed several bottles of whiskey
at one sitting.
Physical examination
Vitals: HR 120, BP 90/55, RR 22
His skin looks pale and feels diaphoretic.
His abdomen is distended and there are markedly
decreased bowel sounds.
He has significant epigastric tenderness with
diffuse rebound tenderness, but minimal rigidity.
His abdomen does not reveal Cullen's sign
(periumbilical ecchymoses) or Grey Turner's sign
(flank ecchymoses).
Cullen’s and Gray-
Turner’s signs
Lab and Test Results

CBC: Hgb 11.0 mg/dl, Hct 32%

WBC: 18,500 /ml
ABG: 7.35 / 32 / 70 / 92%
elevated serum amylase and elevated serum
lipase??
Elevated glucose
Elevated LDH
Hypocalcemia
Elevated SGOT
 Pathophysiology

Acute pancreatitis - acute inflammation.

It is caused by the activation of pancreatic
enzymes that lead to autodigestion of the
pancreas.
There is no permanent morphological or
functional damage after recovery.
Possible Causes and Risk
Factors

Gallstones (transient obstruction of the ampulla of Vater,

which leads to increased pancreatic duct pressure)
Alcohol abuse
Infections (ex: Mumps)
Trauma or shock
Hypercalcemia
Hypertriglyceridemia
Drugs (ex: thiazides, sulfonamides, steriods)
Scorpion stings
Post-ERCP procedure
Possible
Complications

DIC
Shock
ARDS
Hypocalcemia
Acute renal failure
Pancreatic pseudocyst (a collection of
pancreatic fluid encased by granulation
tissue)
Key Radiology, Histology and
Pathology Findings
CXR and Abdominal XR: no free air under the diaphragm,
distended loop of bowel in the proximal jejunum (sentinel
loop)
Abdominal CT: diffuse enlargement and poor homogeneity
of the pancreas, streaky peripancreatic inflammation, fat
stranding
Histology: connective tissue edema, polymorphonuclear
infiltration, hemorrhage and necrosis of pancreatic acini,
fat necrosis (pale blue amorphous foci where the
adipocyte membranes have dissolved)
Gross Pathology: pancreas reveals fat necrosis (pasty white
foci), hemorrhage and cystic cavitation
TREATMENT
Supportive
Analgesics
Close observation for possible complications
No oral intake of food or fluids, use a nasogastric tube
IV fluid replacement
- In patients with mild pancreatitis, fluid replacement may
be sufficient if rapid recovery is expected
- May need to consider jejunal feedings if a prolonged
course is expected
Antibiotics if the CT scan reveals areas of necrosis
Prognosis in acute pancreatitis is aided by certain
signs, which are associated with a higher mortality
rate and are, therefore, useful prognosis indicators
(Ranson’s criteria).

 Signs at admission  Signs 48 hours after

 1- patient’s age over 55
years
 2- white blood cell count
over 16000/mm3 of blood.
 3- fasting blood sugar level
over 200 mg/dl
 4- lactic dehydrogenase
(LDH) over 350 units/ml
 5- glutamic oxalacetic
transaminase(GOT) over
250 units/ml.
admission
 1- a 10% drop in hematocrit
 2- an increase of 5 mg/dl in
blood urea nitrogen
 3- serum calcium levels under 8
mg/dl
 4- arterial oxygen partial
pressure (PaO2) below 60 mm
Hg.
 5- anion base deficit greater
than 4 mEq/l
 6- third space fluid loss greater
than 6 l.
Prognosis after Ranson’s
criteria
If 0-2 of the above signs are present, the
mortality rate is 0,9%
If 7-8 signs are present it is 100%.
The poor prognostic signs at 48 hours are
generally related to the severe local effects of
pancreatitis, which result in massive third-
space fluid loss and hemorrhage.
Systemic effects such as shock and hypoxia
may also be a consequence of circulating
toxins released by the pancreas.
 Indications for surgery
1- to confirm the diagnosis in severe cases
that do not respond to medical management.
The symptoms of severe acute pancreatitis
can be mimicked by visceral perforation,
mesenteric arterial occlusion and other intra-
abdominal catastrophes.

Surgery may be needed to establish the

diagnosis before the situation is ireversible.
 Indications for surgery
2- to relieve biliary and pancreatic duct obstruction.
Early biliary tract surgery should be delayed until the
pancreatitis has subsided.
The offending stone will have passed by the time of
exploration in more than 90% of cases.
If the patient’s status continues to deteriorate, surgical
exploration may become necessary: cholecystectomy and T-
tube drainage of the common bile duct.
Indications for surgery
3- to drain the lesser sac.
Pancreatic or lesser sac drainage increases
morbidity if it is done before septic
complications have occurred.
It is not effective as a prophylactic measure.
Drainage has been shown to improve the
prognosis when sepsis has occurred and the
lesser sac collections are present.
CASE 2, History
The 45 year-old man explains that sometimes
the pain radiates to his back.
It is also sometimes is associated with nausea
and vomiting.
He also complains of bulky, greasy, foul-
smelling stool (steatorrhea).
He has lost weight. The patient's breath
smells of alcohol.
Physical Exam

His epigastric pain is reproducible with deep

palpation
Lab and Test Results

Serum Amylase and Serum

lipase are mildly elevated

Stool exam: reveals high lipid

content and steatorrhea
Pathophysiology
Chronic pancreatitis is a persistent inflammatory
disease characterized by progressive parenchymal
fibrosis of the pancreas.
It can have a waxing and waning course but the
functional and morphological damage is irreversible.
It cause pain and permanent impairment of exocrine
function.
Endocrine dysfunction, such as diabetes mellitus, is a
late sequeale.
Possible Causes and Risk
Factors

Alcohol abuse (in adults)

Cystic fibrosis (in children)
Obstruction of the pancreatic duct by
stones
Neoplasm
Idiopathic
Complications
Fat malabsorption can lead to a deficiency of
fat-soluble vitamins. This can lead to night
blindness (vitamin A deficiency) and
osteomalacia (vitamin D deficiency).
Diabetes mellitus
Ruptured pseudocyst can lead to pancreatic
ascites or pancreatic pleural effusion
Obstructive jaundice or cirrhosis - due to
chronic obstruction of bile duct that is encased
in a scar or compressed by an enlarged
pancreas (due to edema or a pseudocyst)
 Key Radiology, Histology and
Pathology Findings
Abdominal Xray: pancreatic calcifications
Abdominal CT and Ultrasound: pancreatic atrophy, pseudocyst
and calcifications
ERCP (endoscopic retrograde cholangiopancreatography): might
reveal a small stricture of the pancreatic duct in the head of the
pancreas, the distal duct shows sacculations with intervening
short strictures (called a "chain of lakes")
* ERCP is usually reserved for when a diagnosis is in question

Histology: Patchy disease with dilated ducts, fibrotic stroma,

atrophy of the exocrine glands and islets due to enzymatic fat
necrosis

Gross Pathology: Fibrotic and scarred pancreas with cystic

cavitation and white areas of fat necrosis
Treatment and
Prognosis

Supportive: management of symptoms

- Analgesics
- Exocrine pancreatic enzyme supplements
- Surgical drainage of pseudocyst (often
laparoscopically) may be necessary
 Treatment
Small pseudocysts may resolve with medical treatment.
Mature pseudocysts are treated surgically by:
- internal drainage: pseudocysto-gastrostomy, pseudocysto-
jejunostomy
- or external drainage which is used if the pseudocyst is not
found to be mature and if suturing of the pseudocyst wall is
not safe.

The external drainage results in a pancreatic fistula which

usually will heal with continued parenteral nutrition.
 
 CASE 3
History and Physical Exam
A 55 year-old man complains of abdominal pain
radiating to his back.
Over the last few months he has noticed some
weight loss and increased fatigue.
PE: The patient appears thin and the eye exam
reveal scleral icterus
Lab and Test Results
Total bilirubin: 4.7 mg/dl
Alkaline phosphase: 285 U/L
Pathophysiology

Almost all pancreatic ductal carcinomas

are adenocarcinomas, arising in ductal
epithelium.
The tumor may secrete mucin and have
a fibrous stroma.
 Acinar cell carcinoma is rare
Pathophysiology
Pancreatic carcinoma is very
aggressive and has usually already
metastasized at presentation.
Tumors can arise in the head (70%),
body (20%) and tail (10%).
Often pancreatic carcinoma can
obstruct bile outflow and cause
progressive obstructive jaundice.
Tumors that occur in the body and tail
of the pancreas may remain silent for
a longer period of time.
Pathophysiology

The malignancy can move locally

through retroperitoneal spaces and
impinge on pain fibers.
Other possible metastatic sites are the
spleen, adrenal glands, vertebral
column, transverse colon, stomach and
adjacent local nodes.
Prognosis is usually 6 months or less.
 Complications

Migratory thrombophlebitis
(appearing and disappearing
thromboses)

Pancreatic ductal obstruction

(malabsorption with palpable gall
bladder)
Key Radiology, Histology and
Pathology Findings

Abdominal Ultrasound and CT: dilated bile ducts

and mass in head of pancreas
Histology: moderately to poorly differentiated
adenocarcinoma, with cell clusters and tubular
structure, very infiltrative, inflammatory cells are
present. There is dense stromal fibrosis.
Gross Pathology: Pancreatic adenocarcinoma can
often be cystic or solid composed of gray-white
desmoplastic tissue
Histopathology: adenocarcinoma
Treatment and Prognosis

Pancreatico-duodenectomy (if the mass is

limited to the head of the pancreas at biopsy)
* This patient's tumor was 2 cm. There was no
tumor at the resected margins and it was
limited to the head of the pancreas.
All lymph nodes were negative.
Despite these optimistic findings, 5-year
survival is only 20%.