Gastrointestinal and Abdominal: Pancreas Flashcards
Pancreas
The pancreas is a key regulator of digestion and
metabolism through both endocrine and exocrine
functions. Disorders of surgical importance include
acute pancreatitis, chronic pancreatitis, and pancre-
atic cancer
Pancreas: Embryology
Formation of the pancreas begins during the first few
weeks of gestation, with the development of the ventral
and dorsal pancreatic buds. Clockwise migration of the
ventral bud allows fusion with the larger dorsal bud,
creating the duct of Wirsung, which is the main pan-
creatic duct. Failure of this process results in pancreas
divisum, wherein the duct of Santorini drains a portion
of the exocrine pancreas through a separate minor duo-
denal papilla (Fig. 9-1). This anatomic variant is associ-
ated with pancreatitis. Annular pancreas occurs when
the ventral bud fails to rotate, resulting in pancreatic tis-
sue completely or partially encircling the second por-
tion of the duodenum. This situation may result in duo-
denal obstruction, requiring duodenojejunostomy or
gastrojejunostomy in some cases.
Pancreas: Anatomy & Physiology
The pancreas is a retroperitoneal structure located
posterior to the stomach and anterior to the inferior
vena cava and aorta. This yellowish, multilobed gland
is divided into four portions: head, which includes
the uncinate process; neck; body; and tail (Fig. 9-2). It
lies in a transverse orientation, with the pancreatic
head in intimate association with the C loop of the
duodenum, the body draped over the spine, and the
tail nestled in the splenic hilum.
The arterial blood supply to the pancreatic head is
derived from the anterior and posterior pancreatico-
duodenal arteries (Fig. 9-3). These arteries arise from
the superior pancreaticoduodenal artery, which is a
continuation of the gastroduodenal artery, and from
the inferior pancreaticoduodenal artery, which arises
from the superior mesenteric artery. The body and
tail are supplied from branches of the splenic and left
gastroepiploic arteries. Venous drainage follows arte-
rial anatomy and enters the portal circulation.
Sympathetic innervation is responsible for trans-
mitting pain of pancreatic origin, whereas efferent
postganglionic parasympathetic fibers innervate islet,
acini, and ductal systems. In patients with intractable
pain from chronic pancreatitis who have failed oper-
ative drainage or resection, splanchnicectomy (sym-
pathectomy) can be performed to interrupt sympa-
thetic nerve fibers.
The functional units of the endocrine pancreas
are the islets of Langerhans, which are multiple small
endocrine glands scattered throughout the pancreas
that make up only 1% to 2% of the total pancreatic
cell mass. The bulk of the pancreatic parenchyma is
exocrine tissue. Four islet cell types have been identi-
fied: A cells (alpha), B cells (beta), D cells (delta), and
F cells (pancreatic polypeptide [PP] cells).
Alpha cells produce glucagon, which is secreted
in response to stimulation by amino acids, cholecys-
tokinin, gastrin, catecholamines, and sympathetic and
parasympathetic nerves. The role of alpha cells is to
ensure an ample supply of circulating nutritional fuel
during periods of fasting. It promotes hepatic gluco-
neogenesis and glycogenolysis and inhibits gastroin-
testinal motility and gastric acid secretion.
Pancreas: Anatomy & Physiology: Part 2
The largest percentage of islet volume is occupied by
the insulin-producing beta cells. The main function of
insulin is to promote the storage of ingested nutrients.
Insulin is released into the portal circulation in response
to glucose, amino acids, and vagal stimulation. Insulin
has both local and distant anabolic and anticatabolic
activity. Local paracrine function is the inhibition of
glucagon secretion by alpha cells. In the liver, insulin
inhibits gluconeogenesis, promotes the synthesis and
storage of glycogen, and prevents glycogen breakdown.
In adipose tissue, insulin increases glucose uptake by
adipocytes, promotes triglyceride storage, and inhibits
lipolysis. In muscle, it promotes the synthesis of glyco-
gen and protein.
Somatostatin is secreted by islet delta cells in
response to the same stimuli that promote insulin
release. Pancreatic somatostatin slows the movement
of nutrients from the intestine into the circulation by
decreasing pancreatic exocrine function, reducing
splanchnic blood flow, decreasing gastrin and gastric
acid production, and reducing gastric emptying time.
Somatostatin also has paracrine-inhibitory effects on
insulin, glucagon, and PP secretion.
F cells secrete PP after ingestion of a mixed meal.
The function of PP is unknown; however, it may be
important in priming hepatocytes for gluconeogene-
sis. Patients with pancreatic endocrine tumors have
been noted to have elevated levels of circulating PP.
The basic functional unit of the exocrine pancreas is
the acinus. Acinar cells contain zymogen granules in the
apical region of the cytoplasm. Acini are drained by a
converging ductal system that terminates in the main
pancreatic excretory duct. The centroacinar cells of
individual acini form the origins of the ducts, with
intercalated duct cells lining the remainder.
Pancreas: Anatomy & Physiology: Part 3
Exocrine pancreatic secretions are products of
both ductal and acinar cells. Ductal cells contribute a
clear, basic-pH, isotonic solution of water and elec-
trolytes, rich in bicarbonate ions. Secretion of pancre-
atic fluid is principally controlled by secretin, a hor-
mone produced in the mucosal S cells of the crypts of
Lieberkühn in the proximal small bowel. The pres-
ence of intraluminal acid and bile stimulates secretin
release, which binds pancreatic ductal cell receptors,
causing fluid secretion.
Pancreatic digestive enzymes are synthesized by
and excreted from acinar cells after stimulation by sec-
retagogues (cholecystokinin, acetylcholine). Excreted
enzymes include endopeptidases (trypsinogen, chy-
motrypsinogen, and proelastase) and exopeptidases
(procarboxypeptidase A and B). Other enzymes pro-
duced are amylase, lipase, and colipase. All peptidases
are excreted into the ductal system as inactive precur-
sors. Once in the duodenum, trypsinogen is converted
to the active form, trypsin, by interaction with duode-
nal mucosal enterokinase. Trypsin, in turn, serves to
activate the other excreted peptidases. In contrast to
the peptidases, the enzymes amylase and lipase are
excreted into the ductal system in their active forms.
Acute Pancreatitis: Pathogenesis
Acute pancreatitis is a disease of glandular enzymatic
autodigestion that has varying presentations, ranging
from mild parenchymal edema to life-threatening hem-
orrhagic pancreatitis. Multiple causes have been identi-
fied, with alcoholism and gallstone disease accounting
for 80% to 90% of cases among Western populations.
The remaining cases are attributed to hyperlipidemia,
hypercalcemia, trauma, infection, ischemia, trauma
from endoscopic retrograde cholangiopancreatography
(ERCP), and cardiopulmonary bypass (Table 9-1). The
exact pathogenesis of acute pancreatitis remains unclear.
One possibility is that obstruction of the ampulla of
Vater by gallstones, spasm, or edema causes elevated
intraductal pressure and bile reflux into the pancreatic
duct. Activation and extravasation of intraparenchymal
enzymes results in tissue destruction and ischemic
necrosis of the pancreas and retroperitoneal tissues.
Acute Pancreatitis: History
Because of the different degrees of pancreatic tissue
destruction seen in cases of pancreatitis, the presentation
of acute disease is varied, and diagnosis may be difficult.
Important past medical history includes information
regarding prior episodes of pancreatitis, alcoholism, and
biliary colic. Patients present with upper abdominal pain
(often radiating to the back), nausea, vomiting, and a
low-grade fever. A severe attack of pancreatitis is mani-
fested by hypotension, sepsis, and multiorgan failure.
Patients with an alcoholic cause usually experience pain
12 to 48 hours after alcohol ingestion.
Acute Pancreatitis: Physical Examination
Patients have upper abdominal tenderness, usually
without peritoneal signs. The abdomen may be
slightly distended secondary to a paralytic ileus. Low-
grade fever and tachycardia are common
Acute Pancreatitis: Differential Diagnosis
Acute pancreatitis is often difficult to differentiate
from other causes of upper abdominal pain. The clin-
ical presentation may mimic that of a perforated pep-
tic ulcer or acute biliary tract disease. Other condi-
tions that may have similar presentations are acute
intestinal obstruction, acute mesenteric thrombosis,
and a leaking abdominal aortic aneurysm.
Acute Pancreatitis: Diagnostic Evaluation
More than 90% of patients who present with acute
pancreatitis have an elevated serum amylase. However
amylase levels are relatively nonspecific, because many
other intra-abdominal conditions, including intestinal
obstruction and perforated peptic ulcer, may cause
amylase elevation. If the diagnosis is unclear, a lipase
level should also be measured, because it is solely of
pancreatic origin.
Leukocytosis
greater than
10,000/mL is common, and hemo-
concentration with azotemia may also be present
because of intravascular depletion secondary to signif-
icant third-space fluid sequestration. Hyperglycemia
frequently occurs as a result of hypoinsulinemia, and
hypocalcemia occurs from calcium deposition in areas
of fat necrosis.
Routine chest x-ray may reveal a left pleural effu-
sion, known as a sympathetic effusion, secondary to
peripancreatic inflammation. Air under the
diaphragm
indicates perforation of a hollow viscus, such as a
perforated peptic ulcer.
The classic radiographic finding on abdominal
x-ray is a sentinel loop of dilated mid- to distal duo-
denum or proximal jejunum located in the left upper
quadrant, adjacent to the inflamed pancreas. In cases
of gallstone pancreatitis, radiopaque densities (gall-
stones) may be seen in the right upper quadrant.
Ultrasonography is the preferred modality for
imaging the gallbladder and biliary ductal system,
because it is more sensitive as compared with com-
puted tomography (CT) scan. Ultrasound is the study
of choice for the detection of cholelithiasis during the
workup of gallstone pancreatitis.
Acute Pancreatitis: Diagnostic Evaluation: Part 2
CT is the most sensitive radiologic study for con-
firming the diagnosis of acute pancreatitis. Virtually
all patients show evidence of either parenchymal or
peripancreatic edema and inflammation. CT is also
valuable in defining parenchymal changes associated
with pancreatitis, such as pancreatic necrosis and
pseudocyst formation. For severe cases, CT scanning
with intravenous contrast is important for determin-
ing the percentage of pancreatic necrosis, which is
a predictor of infectious complications. CT-guided
interventional techniques can also be performed
to tap peripancreatic fluid collections to rule out
infection.
ERCP is useful for imaging the biliary ductal system
and can be a diagnostic, as well as a therapeutic, modality.
In the case of gallstone pancreatitis, the presence of
common bile duct stones (choledocholithiasis) can be
confirmed and the stones extracted endoscopically.
Magnetic resonance cholangiopancreatography is a newer
noninvasive technique that is a diagnostic, but not thera-
peutic, modality.
Acute Pancreatitis: Disease Severity Scores
Because the clinical course of pancreatitis can vary from
mild inflammation to fatal hemorrhagic disease, prompt
identification of patients at risk for development of
complications may improve final outcomes. The Ranson
criteria are well-known prognostic signs used for pre-
dicting the severity of disease on the basis of clinical and
laboratory results (Table 9-2). The ability to predict a
patient’s risk of infectious complications and mortality
at the time of admission and during the initial 48 hours
allows appropriate therapy to be instituted early in
hospitalization. Mortality is correlated with the number
of criteria present at admission and during the initial 48
hours after admission: 0 to two criteria, 1% mortality;
three to four criteria, 16%; five to six criteria, 40%; and
seven to eight criteria, 100%. Since the publication of
the Ranson criteria in 1974, newer severity scores have
been developed (Acute Physiology and Chronic Health
Evaluation II score) to estimate mortality risk in criti-
cally ill patients. This calculation uses 12 variables in
intensive care unit patients to predict mortality.
Acute Pancreatitis: Treatment
Medical treatment of pancreatitis involves supportive
care of the patient and treatment of complications as
they arise. No effective agent exists to reverse the
inflammatory response initiated by the activated
zymogens. With adequate care, however, most cases
are self-limited and resolve spontaneously.
Hydration is the most important early intervention
in treating acute pancreatitis, because significant third-
spacing occurs secondary to parenchymal and retroperi-
toneal inflammation. Hypovolemia must be avoided
because pancreatic ischemia may quickly develop sec-
ondary to inadequate splanchnic blood flow.
Traditional treatment calls for putting the pancreas
“to rest” by not feeding the patient (NPO). The goal is
to decrease pancreatic stimulation, thereby suppressing
pancreatic exocrine function. Nasogastric suction can
be instituted to treat symptoms of nausea and vomiting.
Antibiotics should be initiated if there is infected
pancreatic necrosis, as confirmed by biopsy. In the
absence of this, antibiotics are widely used for pan-
creatitis, but their efficacy is controversial.
If the severity of disease necessitates a prolonged
period of remaining NPO, an alternative method of
administering nutrition must be instituted. Intravenous
nutrition (total parenteral nutrition/hyperalimentation)
is commonly initiated. Once pancreatic inflammation
resolves, gradual advancement of oral intake proceeds,
beginning with low-fat, high-carbohydrate liquids to
avoid pancreatic stimulation.
Oxygen therapy may be necessary for treatment of
hypoxia, which often occurs secondary to pulmonary
changes thought to be due to circulating mediators.
Evidence of atelectasis, pleural effusion, pulmonary
edema, and adult respiratory distress syndrome may
be seen on chest radiograph.
Acute Pancreatitis: Treatment: Part 2
Surgical treatment of acute pancreatitis is directed at
complications that develop secondary to the underlying
disease process. During the early phase of pancreatitis,
areas of necrosis may form because of tissue ischemia
from enzyme activation, inflammation, and edema.
Necrotic areas eventually liquefy and may become
infected if they are unable to reabsorb and heal. CT scan-
ning with intravenous contrast is the key test for defin-
ing the extent of pancreatic necrosis. Nonenhancement
of 50% or more of the pancreas on CT scan is a strong
predictor for the development of infectious complica-
tions. Infected collections require surgical debridement
and drainage to avoid fatal septic complications.
Initially, collections around the pancreas during
episodes of pancreatitis are termed acute pancreatic
fluid collections. Peripancreatic collections that per-
sist after the inflammatory phase has subsided may
develop a thickened wall, or “rind.” Such collections
are called pancreatic pseudocysts. To alleviate symp-
toms or prevent major complications, surgical drainage
is usually required for cysts
greater than
6 cm in diameter that
have persisted for more than 6 weeks. Standard therapy
is internal drainage into the stomach, duodenum, or
small intestine.
During the later stage of disease, abscess formation
may occur. The pathogenesis is a progression: an
ischemic parenchyma progresses to necrosis and is
seeded by bacteria, with eventual abscess formation.
Most bacteria are of enteric origin, and standard
antibiotic therapy is insufficient treatment. If surgical
drainage and debridement are not performed, the
mortality nears 100%. Percutaneous drainage is usu-
ally inadequate, because only the fluid component is
removed and the necrotic infected tissue remains.
These patients are often remarkably sick. Multiple
debridements may be required when the episode is
severe. It is not uncommon for anasarca to result from
massive volume resuscitation, and it may be difficult
to close the abdomen. In this case, a temporary clo-
sure should be used. Definitive closure is performed
as early as possible after the infection is controlled
and the edema has improved. Operations to remove
infected pancreatic tissue can be extremely bloody
and adequate access and blood should be available.
Hemorrhage secondary to erosion of blood vessels
by activated proteases can be a life-threatening com-
plication. Often it is the main hepatic, gastroduode-
nal, or splenic artery that bleeds. All efforts should be
made to control this with angiography, because it can
be exceedingly difficult to control this lesion in the
operating room
Chronic Pancreatitis
Of patients with acute pancreatitis, a small number
progress to chronic pancreatitis. The chronic form of
disease is characterized by persistent inflammation
that causes destructive fibrosis of the gland. The clin-
ical picture is of recurring or persistent upper abdom-
inal pain with evidence of malabsorption, steator-
rhea, and diabetes.
Chronic Pancreatitis: Treatment
Effective treatment of chronic abdominal pain is
often the focus of care for patients with chronic pan-
creatitis. Opiates are useful for controlling visceral
pain; however, many patients become opiate depen-
dent over the long term. Alcohol nerve blocks of the
celiac plexus have only moderate success.
Pancreatic exocrine insufficiency is treated with oral
pancreatic enzymes, and insulin is used to treat diabetes
mellitus. Ethanol intake by the patient must cease.
Surgical intervention is undertaken only if medical
therapy has proved unsuccessful in relieving chronic
intractable pain. Functional drainage of the pancreatic
duct and the resection of diseased tissue are the goals
of any procedure. Given ERCP and CT findings, the
correct operation can be planned.
For patients with a “chain of lakes”–appearing
pancreatic duct, caused by sequential ductal scarring
and dilatation, a longitudinal pancreaticojejunostomy
(Puestow procedure) is indicated to achieve adequate
drainage. A Roux-en-Y segment of proximal jejunum
is anastomosed side-to-side with the opened pancre-
atic duct, facilitating drainage (Fig. 9-4). Distal pan-
creatic duct obstruction causing localized distal
parenchymal disease is best treated by performing a
distal pancreatectomy.
Adenocarcinomas of the Pancreas: Diagnostic Evaluation
The most common laboratory abnormalities are ele-
vated alkaline phosphatase and direct bilirubin levels,
indicating obstructive jaundice. The average bilirubin
level in neoplastic obstruction is typically higher than
that seen in bile duct obstruction from gallstone
disease.
CT and ERCP are the modalities of choice for evalu-
ating pancreatic cancer. CT reveals the location of the
mass, the extent of tumor invasion or metastasis, and the
degree of ductal dilatation (Fig. 9-5). ERCP defines
the ductal anatomy and the extent of ductal obstruction
and provides biopsy specimens for tissue diagnosis.
Drainage stents can be placed into the common bile
duct during ERCP for biliary tree decompression.
Imaging information suggesting unresectability includes
local tumor extension, contiguous organ invasion, supe-
rior mesenteric vein or portal vein invasion, ascites, and
distant metastases.
Adenocarcinomas of the Pancreas: Treatment
The operation for resectable tumors in the head of
the pancreas is pancreaticoduodenectomy (Whipple
procedure; Fig. 9-6). This major operation entails the
en bloc resection of the antrum, duodenum, proximal
jejunum, head of pancreas, gallbladder, and distal
common bile duct.
