Pancreas: One of The Largest Surgical Chapters !!

Pancreas
One of the largest surgical chapters !!
Dr. Mahmoud W. Qandeel

Pancreas basics
Anatomy, Embryology, Histology and
Physiology

• The pancreas is perhaps the most unforgiving organ in the
human body, leading most surgeons to avoid even palpating it
unless necessary.

Anatomy
• 15-20 cm long
• 2.5 – 3.8cm broad
• 1.2 – 1.8 cm thick
• Weighs 80g
• Situated in retroperitoneum

Parts
• Divided: Head 30%, Body and Tail 70%
• Head corresponds with the curve of duodenum overlying the body of

the 2nd lumbar vertebra and the vena cava.
• Aorta and superior mesenteric vessels lie behind the neck.

• Near upper border of neck superior mesenteric vein joins splenic
vein to form portal vein.

• Coming of side of pancreatic head and passing to the left and behind
superior mesenteric vein is uncinate process.
• Tip of pancreatic tail extends up to the splenic hilum.

Relations

Blood supply
• Arterial:
• Pancreatic Branches of splenic artery
• Superior pancreaticoduodenal artery
• Inferior pancreaticoduodenal artery
• Venous:
• Drain into splenic, superior mesenteric and portal veins

The arterial supply to the pancreas includes the:
• Gastroduodenal artery from the common hepatic artery (a branch of the celiac trunk) ,
• anterior superior pancreaticoduodenal artery from the gastroduodenal artery,
• posterior superior pancreaticoduodenal artery from the gastroduodenal artery,
• Splenic artery (a branch of the celiac trunk)

– dorsal pancreatic artery from the inferior pancreatic artery (a branch of the splenic
artery),
– great pancreatic artery from the inferior pancreatic artery (a branch of the splenic artery),
• Inferior pancreaticoduodenal (a branch of the superior mesenteric artery),

– anterior inferior pancreaticoduodenal artery from the inferior pancreaticoduodenal
artery (a branch of the superior mesenteric artery), and
– posterior inferior pancreaticoduodenal artery from the inferior pancreaticoduodenal
artery (a branch of the superior mesenteric artery) .
Lymphatics
• Head & Neck – Pancreaticoduodenal

• Body & Tail - Pancreaticosplenic

Nerve Supply
• Parasympathetic: Vagus
• Sympathetic: plexuses around its arteries

Pancreatic duct

Embryology

Pancreas Divisum

• Because most pancreatic exocrine secretions exit through the dorsal duct,
pancreas divisum can lead to a condition of partial obstruction caused by a
small minor papilla, leading to chronic backpressure in the duct.
• This relative outflow obstruction has been implicated in the development

of relapsing acute or chronic pancreatitis.
• Although 10% of the population is affected by pancreas divisum, only

rarely do affected individuals develop pancreatitis.

Annular pancreas
• Annular pancreas results from aberrant migration of the ventral
pancreas bud, which leads to circumferential or near-circumferential
pancreas tissue surrounding the second portion of the duodenum.
• This abnormality may be associated with other congenital defects,

including Down syndrome, malrotation, intestinal atresia, and cardiac
malformations.
• If symptoms of obstruction occur, surgical bypass through

duodenojejunostomy is performed
Ectopic Pancreas
• Ectopic pancreas may arise anywhere along the primitive foregut but is most
common in the stomach, duodenum, and Meckel’s diverticulum.
• Clinically, ectopic nodules may result in bowel obstruction caused by

intussusception, bleeding, or ulceration.
• They can sometimes be found incidentally as firm yellow nodules that arise from the
submucosa.
• Although there have been rare case reports of adenocarcinoma arising in ectopic
pancreas tissue, resection is not necessary unless symptoms occur.

Histology
• 80-90% of pancreatic tissue – Exocrine acinar tissue organized as lobules
• Pancreatic duct-- Interlobular & Intralobular ducts--- ductules --- acini
• Main duct – Columnar cells
• Ductules – Cuboidal cells
• Acinar cells clumped around central lumen which communicates with
duct system.

Histology
• Clusters of endocrine cells distributed throughout called Islets of
Langerhans
• Islet:
– 75% - B Cells – Insulin
– 20% - A Cells – Glucagon
– 5% - D Cells – Somatostatin
• Small number of pancreatic polypeptide cells
• B cells form inner core surrounded by other cells.
• Capillaries draining islet cells drain into portal vein

Physiology
• Exocrine and endocrine functions

Exocrine function
• In response to food – secretes digestive enzymes in an alkaline

bicarbonate rich fluid.
• Secretion enhanced by:

– Secretin
– Cholecystokinin
– Vagal Stimulation
• Within cells enzymes are in inactive form.

Pancreatic secretions
• Electrolytes:
• Cations: Na+, K+, Ca2+, Mg2+, Zn2+
• Anions: HCO3-, Cl- and traces of SO42-, HPO42
• Enzymes:
• Pancreatic alpha-amylase
• Pancreatic lipase
• Pancreatic esterase
• Pancreatic pro-phospholipase A2

• Pancreatic proteolytic enzymes:
– Trypsinogen
– Chymotrypsin
– Pro – carboxypeptidase A and B
– Ribonuclease
– Deoxy-ribonuclease
– Pro-elatase
– Trypsin inhibitor

Endocrine function

Total removal of pancreas
• Diabetes mellitus due to pancreatic endocrine deficiency of insulin
• Development of digestive disturbances:

• Increase of fecal fats – bulky, foul smelling, pale and greasy stools
• Increased fecal nitrogen due to incomplete proteolysis
• No abnormality of carbohydrate digestion
• Pancreatic insufficiency – loss of 30% of calorific value of ingested food.

Acute Pancreatitis
Causes, pathophysiology, presentation and
Management

Definition
• Acute pancreatitis is a common and challenging disease that can
develop both local and systemic complications.
• Its hallmark is acute pancreatic inflammation associated with little or no

fibrosis.
• It ranges from a mild self-limiting inflammation of the pancreas to

critical disease characterized by infected pancreatic necrosis, multiple
organ failure and a high risk of mortality.

• Worldwide the incidence of acute pancreatitis ranges from 5 to
80/100,000 population with the highest incidence recorded in Finland
and United States
• 10% to 20% of patients have a rapidly progressive inflammatory

response associated with prolonged length of hospital stay and
significant morbidity and mortality

• The median age of the onset varies with etiology;
– Alcohol and drug induced pancreatitis typically present in the 3rd ,
4th decade compared with gallstone induced disease in the 6th
decade.
• The gender difference is probably more related to etiology.

– In males alcohol is more often the cause while in females it is
gallstones.

Causes
• The most common causes are gallstones and alcohol, accounting for up
to 80% of cases.
• In pediatric patients, abdominal blunt trauma and systemic diseases are

the two most common conditions that lead to pancreatitis.
• Autoimmune and drug-induced pancreatitis should be a differential

diagnosis in patients with rheumatologic conditions such as systemic
lupus erythematosus and Sjögren syndrome.

Gallstones
• The mechanism by which small gallstones migrating down the common

bile duct, past the pancreatic duct junction and into the duodenum,
cause acute pancreatitis is not clear.
“Common channel” hypothesis.

• It was proposed that a gallstone transiently lodged in the distal
common channel of the ampulla of Vater allowed bile to reflux into the
pancreatic duct.

• Transient incompetence caused by the passage of a stone through the
sphincter might allow duodenal fluid and bile to reflux into the
pancreatic duct, but this is refuted by the usual absence of acute
pancreatitis after endoscopic sphincterotomy or surgical
sphinteroplasty.

• A 3rd possibility is that acute pancreatitis is due to a gallstone
obstructing the pancreatic duct, leading to ductal hypertension, leading
to minor ductal disruption, extravasation of pancreatic juice into the less
alkaline interstitium of the pancreas, and promotion of enzyme
activation.

• When gallstones and other etiological factors cannot be identified, there
is still the possibility of finding microlithiasis, seen as birefringent
crystals, on bile microscopy.
• This occult microlithiasis is probably responsible for up to half of those

with idiopathic acute pancreatitis.

Alcohol
• The type of alcohol consumed is less important than the amount
consumed (typically 100 to 150 grams per day).
• It triggers proinflammatory pathways such as nuclear factor κB which

increase the production of TNF-α and IL-1.
• Alcohol decreases pancreatic perfusion.
• Ethanol is a metabolic toxin to pancreatic acinar cells and causes a brief

secretory increase followed by inhibition.
• The secretory burst coupled with ethanol induced spasm of the
sphincter of Oddi is thought to incite acute pancreatitis.
• Ethanol also induces ductal permeability.

• Ethanol also increases the protein content of pancreatic juice,
decreases bicarbonate levels, and trypsin inhibitor concentration.
• The formation of protein plugs may also contribute by causing an

obstructive element to pancreatic outflow.

Iatrogenic
• Most commonly, acute pancreatitis occurs as a complication of ERCP in
5% to 10% of procedures, and in many series it is the third most
common identified etiological factor.
• The risk is increased if the contrast agent is infused under high pressure
and in patients with sphincter of Oddi dysfunction.
• Recent evidence demonstrates that the risk can be decreased with

prophylactic, rectally administered, nonsteroidal drugs.

Drug-Induced Pancreatitis
• Up to 2% of AP cases are caused by medications.
• The most common agents include sulfonamides, metronidazole,

erythromycin, tetracyclines, didanosine, thiazides, furosemide, 3-
hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors
(statins), azathioprine, 6-mercaptopurine, 5-aminosalicylic acid,
sulfasalazine, valproic acid, and acetaminophen.
• More recently, antiretroviral agents used for the treatment of AIDS have
been implicated in AP.
FAT SHEEP
F- Furosemide (lasix)
A- Asa, AZT, Asaparaginase, acetaminophen, AB (metronidazole, erythromycin)
T- Tetracyclines
S- Statins, (sulfonamides), Steroids
H- HCTZ
E- Estrogens (OCP)
E- EtOH
P- Pentamidine

Metabolic Factors
• Hypertriglyceridemia and hypercalcemia can also lead to pancreatic damage.
• Direct pancreatic injury can be induced by triglyceride metabolites.
• It is more common in patients with type I, II, or V hyperlipidemia.
• It should be suspected in patients with a triglyceride level higher than
1000 mg/dL.
• A triglyceride level higher than 2000 mg/dL confirms the diagnosis.
• Amylase ?
• Hypertriglyceridemia secondary to hypothyroidism, diabetes mellitus, and
alcohol does not typically induce AP.

• Hypercalcemia is postulated to induce pancreatic injury through the
activation of trypsinogen to trypsin and intraductal precipitation of
calcium, leading to ductal obstruction and subsequent attacks of
pancreatitis.
• Approximately 1.5% to 13% of patients with primary hyperparathyroidism

develop AP.

Hereditary Pancreatitis
• Hereditary pancreatitis is an autosomal dominant disorder usually
related to mutations of the cationic trypsinogen gene (PRSS1).
• Mutations in this gene cause premature activation of trypsinogen to

trypsin and cause abnormalities of ductal secretion, both of which
promote acute pancreatitis

I GET SMASHED

Pathogenesis
• Several protective mechanisms have evolved to prevent autodigestion under normal
conditions.
• Enzymes are synthesized as inactive precursors called proenzymes or zymogens,
which are then transported and secreted outside the gland.
– Their activation occurs safely in the duodenum, where the brush-border enzyme enteropeptidase
(or enterokinase) activates the trypsinogen, and the resulting trypsin then activates the other
zymogens in a cascade reaction.
• Another layer of protection is provided by the synthesis of trypsin inhibitors, which

are transported and stored along with the digestive enzyme zymogens.
• These are available to inhibit small amounts of prematurely- activated trypsinogen
within the pancreatic acinar cells.
• In the presence of injurious stimuli, the zymogens responsible for
initiating the disease are not secreted outside, but are observed to co-
localize with cytoplasmic vacuoles that contain lysosomal enzymes such
as cathepsin B.

• Cathepsin B activates trypsinogen to trypsin within the co-localization
vacuoles.
• Trypsin then permeabilizes these co-localization vacuoles causing the

release of cathepsin B into the cytosol.
• Once in the cytosol, cathepsin B initiates apoptotic cell death by

permeabilizing mitochondrial membranes, which allows cytochrome C
to be released into the cytosol.

• These inflammatory mediators cause an increased pancreatic vascular
permeability, leading to edema, hemorrhage, and microthrombi.
• Fluid may collect in and around the pancreas.
• The failure of the pancreatic microcirculation, a feature of more severe

acute pancreatitis, results in pancreatic hypoperfusion and necrosis.

• Although intra-acinar events initiate acute pancreatitis, events occurring
subsequent to acinar cell injury determine the severity of pancreatitis.
• Once recruited to the pancreas, various inflammatory cells lead to

further acinar cell injury and cause an elevation of various pro-
inflammatory mediators such as TNF-α; IL-1, IL-2, IL-6, and other factors.

Clinical presentation
• Epigastric or periumbilical pain that radiates to the back.
• The nature of the pain is constant; therefore, if the pain disappears or
decreases, another diagnosis should be considered.
• Up to 90% of patients have nausea or vomiting that typically does not
relieve the pain.
• Dehydration, poor skin turgor, tachycardia, hypotension, and dry

mucous membranes are commonly seen in patients with AP.

• With mild pancreatitis, the PE findings of the abdomen may be normal
or reveal only mild epigastric tenderness.
• Significant abdominal distention, associated with generalized rebound

and abdominal rigidity, is present in severe pancreatitis.
• Nature of the pain described by the patient may not correlate with the
physical examination findings or the degree of pancreatic inflammation.

• Rare findings include flank and periumbilical ecchymosis: (Grey Turner
and Cullen signs, respectively).
• Patients with concomitant choledocholithiasis or significant edema in

the head of the pancreas that compresses the intrapancreatic portion of
the common bile duct can present with jaundice.
• Dullness to percussion and decreased breath sounds in the left or the

right hemithorax suggest pleural effusion

Diagnosis
• Clinical findings plus an elevation of pancreatic enzyme levels in the plasma.
• A 3 fold or higher elevation of amylase and lipase levels confirms the diagnosis.
• The serum half-life of amylase is shorter than that of lipase.
• In patients who do not present to the emergency department within the first 24 to
48 hours after the onset of symptoms, lipase levels is a more sensitive indicator.

• Lipase is also a more specific marker of AP because serum amylase
levels can be elevated in a number of conditions, such as:
– Peptic ulcer disease
– Mesenteric ischemia
– Acute cholecystitis
– Salpingitis
– Macroamylasemia.

• Patients with AP are typically hyperglycemic, they can also have
leukocytosis and abnormal elevation of liver enzyme levels.
• The elevation of ALT levels in the serum in the context of AP confirmed

by high pancreatic enzyme levels has a PPV of 95% in the diagnosis of
acute biliary pancreatitis.

• Contrast enhanced CT scanning is only required for the diagnosis of
acute pancreatitis when these diagnostic criteria are not met.

Imaging
• US:
• Should always be ordered in patients with AP because of its high
sensitivity (95%) in diagnosing gallstones.
• Combined elevations of liver transaminase and pancreatic enzyme levels

and the presence of gallstones on ultrasound have an even higher
sensitivity (97%) and specificity (100%) for diagnosing acute biliary
pancreatitis

Abdomen X- RAY
• Simple abdominal radiographs are not useful for diagnosis of

pancreatitis, they can help rule out other conditions, such as
perforated ulcer disease.
• Nonspecific findings in patients with AP include ileus, cutoff colon sign

as a result of colonic spasm at the splenic flexure, and widening of the
duodenal C loop caused by severe pancreatic head edema (sentinel
loop).

Cutoff colon sign Sentinel loop
Abdomen CT
• Contrast-enhanced (CT) is currently the best modality for evaluation of the

pancreas, especially if the study is performed with a multidetector CT scanner.
• The most valuable contrast phase in which to evaluate the pancreatic parenchyma is
the portal venous phase which allows evaluation of the viability of the pancreatic
parenchyma, amount of peripancreatic inflammation, and presence of intra-
abdominal free air or fluid collections.

Indications for CT
• For significant clinical deterioration and elevated CRP

• For suspicion of local pancreatic complications
• For suspected bowel ischemia
• For acute bleeding (if stable enough & consider embolization)
• For abdominal compartment syndrome

Assesing Severity
• RANSON Criteria
• APACHE score
• CT Severity index
• Sequential Organ Failure Index ( SOFA)
• Revised Atlanta Criteria
• CRP level

CRP
• C-reactive protein (CRP) is an inflammatory marker that peaks 48 to 72
hours after the onset of pancreatitis and correlates with the severity of
the disease.
• A CRP level of 150 mg/mL or higher defines severe pancreatitis.

• The major limitation is that it cannot be used on admission; the
sensitivity of the assay decreases if CRP levels are measured within 48
hours after the onset of symptoms.

CTSI 0-3, mortality 3%, morbidity 8%; CTSI 4-6, mortality 6%, morbidity 35%; CTSI 7-10, mortality
17%, morbidity 92%.

Severe pancreatitis
• Ranson ≥ 3
• Glasgow ≥ 3
• APCHE II ≥ 8
• CRP > 150 after 48 hr
• Positive Atlanta
• BISAP > 3

• Mild acute pancreatitis, the most common form, has no organ failure, local or systemic
complications and usually resolves in the first week.
• Moderately severe acute pancreatitis is defined by the presence of transient organ failure,
local complications or exacerbation of co-morbid disease.
• Severe acute pancreatitis is defined by persistent organ failure, that is, organ failure >48 h.

Management
• Fluid resuscitation
• Pain control
• Nutritional support
• ERCP
• Lap cholecystectomy
• Antibiotics
• Imaging
• Management of complications

Fluid resuscitation
• The cornerstone of AP management is hydration with isotonic
crystalloid solution.
• The rate of administration should be individualized and adjusted on the

basis of:
– 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
– Foley catheter.

Oxygen monitoring
• 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%

Pain control
• 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 on the
outcome of patients with AP.

Nutritional support
• It is no longer acceptable to “rest the pancreas” by avoiding enteral
nutrition, and parenteral nutrition should only be offered if the
patient’s calculated nutritional requirements can’t be achieved by the
enteral route.

• The main options are enteral feeding and total parenteral nutrition
(TPN).
• Although there is no difference in the mortality rate between both types

of nutrition.

• Enteral nutrition is associated with fewer infectious complications and
reduces the need for pancreatic surgery.
• Although TPN provides most nutritional requirements, it is associated

with mucosal atrophy, decreased intestinal blood flow, increased risk of
bacterial overgrowth in the small bowel, antegrade colonization with
colonic bacteria, and increased bacterial translocation.

• Enteral nutrition should be commenced after initial fluid resuscitation
and within the first 24 hours of admission.
• It can be introduced through a nasogastric tube and increased in step-

wise fashion over 2 to 3 days.
• The tube can be advanced to the jejunum, by endoscopy or fluoroscopy.

Antibiotics
• Prophylactic antibiotics do not decrease the frequency of surgical

intervention, infected necrosis, or mortality in patients with severe
pancreatitis.
• In addition, they are associated with gram-positive cocci infection, such

as by Staphylococcus aureus, and Candida infection, which is seen in 5%
to 15% of patients.
• Not recommended in absence of infection

ERCP
• Routine use of ERCP is not indicated for patients with mild pancreatitis
because the bile duct obstruction is usually transient and resolves
within 48 hours after the onset of symptoms.
• ERCP is indicated for patients

– Who develop cholangitis and
– Those with persistent bile duct obstruction
– Others ?

Laparoscopic cholecystectomy.
• In the absence of definitive treatment, 30% of patients with acute biliary

pancreatitis will have recurrent disease.
• With the exception of older patients and those with poor performance
status, laparoscopic cholecystectomy is indicated for all patients with
mild acute biliary pancreatitis.
• When ?

• 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.

Local Complications post
Acute Pancreatitis
Principles, Management and Updates

Revised Atlanta Classification

Revised Atlanta

Sterile and Infected Peripancreatic Fluid Collections
• The presence of acute abdominal fluid during an episode of AP has been

described in 30% to 57% of patients.
• In contrast to pseudocysts and cystic neoplasias of the pancreas, fluid

collections are not surrounded or encased by epithelium or fibrotic capsule.
• Treatment is supportive because most fluid collections will be

spontaneously reabsorbed by the peritoneum.

• Fever, elevated white blood cell count, and abdominal pain
suggest infection of this fluid, and percutaneous aspiration is
confirmatory.
• Percutaneous drainage and IV administration of antibiotics

should be instituted if infection is present.

• A 63-year-old man with acute
interstitial edematous
pancreatitis.
• There is peripancreatic fat

stranding (arrows) without an
acute peripancreatic fluid
collection; the pancreas
enhances completely but has a
heterogeneous appearance due
to edema.

• A 38-year-old woman with acute
interstitial edematous pancreatitis and
acute peripancreatic fluid collection
(APFC) in the left anterior pararenal
space (white arrows showing the
borders of the APFC).
• The pancreas enhances completely, is

thickened, and has a heterogeneous
appearance due to edema.
• APFC has fluid density without an
encapsulating wall.

B) A few weeks later, a follow
up CT shows complete
resolution of the APFC with
minimal residual
peripancreatic fat stranding.

Pancreatic Necrosis and Infected Necrosis
• Pancreatic necrosis is the presence of nonviable pancreatic parenchyma
or peripancreatic fat; it can be manifested as a focal area or diffuse
involvement of the gland.
• Contrast-enhanced CT is the most reliable technique to diagnose

pancreatic necrosis.
• It is typically seen as areas of low attenuation (<40 to 50 HU) after the
IV injection of contrast material.
• Normal parenchyma usually has a density of 100 to 150 HU.

• Up to 20% of patients with AP develop pancreatic necrosis.
• It is important to identify and to provide proper treatment of this

complication
– Most patients who develop multiorgan failure have necrotizing pancreatitis;
– Pancreatic necrosis has been documented in up to 80% of the autopsies of
patients who died after an episode of AP.

Acute necrotic collection (ANC)
• During the first 4 weeks, a collection containing variable amounts of fluid and necrotic
tissue is termed an ANC to distinguish it from an APFC.
• The necrosis can involve the pancreatic parenchyma and/or the peripancreatic tissues.
• On CECT, acute pancreatic or peripancreatic necrotic collections contain varying

amounts of solid necrotic material and fluid, may be multiple, and may appear
loculated.
• An ANC may be associated with disruption of the main pancreatic duct within the zone
of parenchymal necrosis and can become infected.

• Sequential imaging may be useful to characterise acute collections.
• Within the first week of the disease, it may be difficult to differentiate an APFC from
an ANC.
– At this stage, both types of collections may appear as areas with fluid density.
• After the first week, the distinction between these two important types of
collections becomes clear, such that at this stage of necrosis, a peripancreatic
collection associated with pancreatic parenchymal necrosis can be properly termed
an ANC and not an APFC.
• MRI, transcutaneous ultrasonography or endoscopic ultrasonography may be helpful

to confirm the presence of solid content in the collection.

(A) Acute necrotic collections (ANC) in a
44-year-old man with acute necrotising
pancreatitis involving only the
peripancreatic tissues.
Note enhancement of the entire

pancreatic parenchyma (white stars)
and the heterogeneous, non-liquid
peripancreatic components in the
retroperitoneum (white arrows pointing
at the borders of the ANC).

• Acute necrotic collection (ANC)
in a 47-year-old woman with
acute necrotising pancreatitis
involving the pancreatic
parenchyma alone.
• Thin white arrows denote a

newly developed, slightly
heterogeneous collection in the
region of the neck and body of
the pancreas, without extension
in the peripancreatic tissues.

Walled-off necrosis (WON)
• WON consists of necrotic tissue contained within an enhancing wall of reactive tissue.
• It is a mature, encapsulated collection of pancreatic and/or peripancreatic necrosis
and has a well defined inflammatory wall; usually this maturation occurs ≥4 weeks
after onset of necrotising pancreatitis.
• Previous suggested nomenclature had designated this entity as

– Organised pancreatic necrosis,
– Necroma,
– Pancreatic sequestration,
– Pseudocyst associated with necrosis, and
– Subacute pancreatic necrosis.
• WON derives from necrotic pancreatic parenchyma and/or necrotic
peripancreatic tissues and may be infected, may be multiple, and may be
present at sites distant from the pancreas.
• CECT may not readily distinguish solid from liquid content, and, for this
reason, pancreatic and peripancreatic necrosis may be misdiagnosed as a
pancreatic pseudocyst.
– For this purpose, MRI, transabdominal ultrasonography or endoscopic
ultrasonography may be required for this distinction.

Three different patients with walled-off necrosis (WON) after an acute attack of necrotising
pancreatitis. In all three patients, a heterogeneous, fully encapsulated collection is noted in the
pancreatic and peripancreatic area. (A) Non-liquid components of high attenuation (black
arrowheads) in the collection are noted. The collection has a thin, well defined, and enhancing wall
(thick white arrows). (B, C) A largely liquefied collection in the bed of the pancreas is observed with
non-liquid components representing areas of trapped fat (black arrowheads).

(D) represents the corresponding T2-weighted MRI to (C), showing the true
heterogeneity of the collection. Black arrowheads denote areas of necrotic debris
surrounded by fluid (white on T2-weighted image).

• Infected pancreatic necrosis should be suspected in patients
with
– Prolonged fever,
– Elevated white blood cell count, or
– Progressive clinical deterioration.
• Evidence of air within the pancreatic necrosis seen on a CT scan

confirms the diagnosis but is a rare finding.

• If infected necrosis is suspected, fine-needle aspiration (FNA) may be
performed if the diagnosis is equivocal; from the aspirate, a positive
Gram stain or culture establishes the diagnosis. ?? (Sabiston)
– Although positive cultures are confirmatory, a review has demonstrated that

despite negative preoperative cultures, 42% of patients with so-called persistent
unwellness will have infected necrosis.
• Fine needle aspiration is now rarely used to confirm infection. (Schwartz)

• A 47-year-old man with acute
necrotising pancreatitis
complicated by infected pancreatic
necrosis.
• There is a heterogeneous, acute

necrotic collection (ANC) in the
pancreatic and peripancreatic area
(white arrows pointing at the
borders of the ANC) with presence
of gas bubbles (white
arrowheads), usually a
pathognomonic sign of infection of
the necrosis (infected necrosis).

• Once infection has been demonstrated, IV antibiotics should be given.
• Because of their penetration into the pancreas and spectrum coverage,
carbapenems are the first option of treatment.
• Alternative therapy includes quinolones, metronidazole, third

generation cephalosporins, and piperacillin

Management
• Historically, the definitive treatment of infected pancreatic necrosis is
surgical débridement with necrosectomy, closed continuous irrigation,
or open packaging
• The overall mortality rate after open necrosectomy has been as high
as 25% to 30%.
• Outcomes are time dependent; patients who undergo surgery in
– The 1st 14 days have a mortality rate of 75%,
– 15 and 29 days mortality rate of 45%
– after 30 days have mortality rate 8%
• As a result of the elevated morbidity and mortality rates with open
débridement, endoscopic and laparoscopic techniques are being used
more often.
• In general, the longer a patient can be medically optimized and

managed with enteral nutrition and antibiotics (if indicated), the more
mature a fluid collection (with or without necrosis), and therefore the
extent of an endoscopic or operative débridement (if needed) will be
better delineated and tolerated.

Endoscopic step up approach
Step 1
ETD: the collection is

punctured through the
gastric wall, followed by
balloon dilatation of the
tract.
Two double-pigtail
stents and a nasocystic
catheter for continuous
postoperative irrigation
are placed.

Step 2
ETN: the cystostomy tract

is dilated, the collection is
entered with a endoscope,
and necrosectomy is
performed.

Surgical step up approach
Surgical step-up approach consisting of percutaneous catheter drainage (PCD) and video-assisted
retroperitoneal débridement (VARD).
(A) Cross-sectional image and torso depicting a peripancreatic collection. The preferred route is through the
left retroperitoneal space between the kidney, spleen and descending colon. A percutaneous catheter drain is
inserted in the collection to mitigate sepsis and postpone or even obviate necrosectomy.

The area of detail is shown in (B).
(C) A 5 cm subcostal incision is made and the percutaneous drain is followed into the
collection.
The first necrosis is removed under direct vision with a long grasping forceps, followed
by further debridement under videoscopic assistance (D)

Pathogenesis
• Pancreatic pseudocysts occur in 5% to 15% of patients who have
peripancreatic fluid collections after AP.
• It requires disruption of the pancreatic ductal system and an

inflammatory reaction of surrounding tissues resulting in formation of a
fibrous capsule composed of collagen and granulation tissue, and it is
not lined by epithelium.
• The fibrotic reaction typically requires at least 4 to 8 weeks to develop.

• When there is evident solid necrotic material within a largely fluid-filled
cavity, the term pseudocyst should not be used.
• A pseudocyst may also arise in the setting of acute necrotising pancreatitis

as a result of a ‘disconnected duct syndrome’, whereby pancreatic
parenchymal necrosis of the neck or body of the gland isolates a still viable
distal pancreatic remnant.
• A pseudocyst may be evident many weeks after operative necrosectomy due

to localised leakage of the disconnected duct into the necrosectomy cavity.

• On the other hand, pathogenesis of pseudocysts formation following
chronic pancreatitis is not well understood.
• It seems that apart from the acute fluid exacerbation, blockage of the
main pancreatic duct from a protein plug or calculus can lead to the
pseudocyst formation

• The prevalence of PPs is ranging from 5% to 15% in acute pancreatitis and
20–40% in chronic pancreatitis.
• Patients with chronic pancreatitis present with a pseudocyst more often

after alcohol induced chronic pancreatitis (70–78%), followed by idiopathic
chronic pancreatitis (6–16%) and biliary chronic pancreatitis (6–8%).

• Up to 50% of patients with pancreatic pseudocysts will develop symptoms.
• Persistent pain, early satiety, nausea, weight loss, and elevated pancreatic
enzyme levels in plasma suggest this diagnosis.
• The diagnosis is corroborated by CT or MRI.

CT Findings
Atlanta
A 40-year-old man with two pseudocysts in
the lesser sac 6 weeks after an episode of
acute interstitial pancreatitis on CT (A, B).
Note the round to oval, low-attenuated,

homogeneous fluid collections with a well
defined enhancing rim (white arrows
pointing at the borders of the pseudocysts),
but absence of areas of greater attenuation
indicative of non-liquid components.
White stars denote normal enhancing

pancreas.

• EUS with FNA is indicated for patients in whom the diagnosis
of pancreatic pseudocyst is not clear.
• Characteristic features of pancreatic pseudocysts include

– High amylase levels
– Absence of mucin and
– Low CEA levels.
✓ Low amylase in cyst fluid could suggest either mucinous or serous

cystadenoma

Complications of pancreatic pseudocysts include
• Bleeding and
• Pancreaticopleural fistula
• Bile duct and duodenal obstruction;
• Rupture into the abdominal cavity; and
• Infection.

• Observation
• Drainage
– Surgical
• Cystogastrostomy
• Cystoduodenostomy
• Roux-en-Y cystojejunostomy
– Endoscopic Options
• Transgastric
• Transduodenal
• Transpapillary
– Percutaneous
• ERCP and stent
• Pancreatic resection
Observation
• Observation is indicated for asymptomatic patients because
spontaneous regression has been documented in up to 70% of cases;
this is particularly true for patients with
– < 4 cm in diameter,
– In the tail, and
– No evidence of pancreatic duct obstruction or communication with
the main pancreatic duct.

• Invasive therapies are indicated for symptomatic patients or when the
differentiation between a cystic neoplasm and pseudocyst is not
possible.
• Because most patients are treated with decompressive procedures and

not with resection, it is imperative to have a pathologic diagnosis.

Endoscopic transmural drainage
• Transgastric endoscopic drainage :

– Pseudocysts in close contact (defined as <1 cm) with the stomach
• Transduodenal endoscopic drainage:

– Pseudocysts in close contact (defined as <1 cm) with the duodenum
• Transpapillary endoscopic drainage:

– Pseudocysts communicating with the main pancreatic duct.

ERCP and Stent
• For patients in whom a pancreatic duct stricture is associated
with a pancreatic pseudocyst, endoscopic dilation and stent
placement are indicated.

• ERCP should be performed for pseudocysts resulting from
blunt abdominal trauma since there is a high incidence of
pancreatic duct disruption in these cases.

Surgical Interventions
• Surgical drainage is indicated for patients with pancreatic pseudocysts
that cannot be treated with endoscopic techniques and for patients who
fail to respond to endoscopic treatment.

• Indications for open surgery for patients with:
– Recurrent pseudocysts,
– Pseudocysts with concomitant duodenal and/or biliary stenosis,
– symptomatic pseudocysts with associated main duct dilation, and
– those cysts that have been either nonamenable or refractory to
minimally invasive drainage techniques.
– Can not rule out malignancy

Internal drainage via cyst-enterostomy
• The choice of surgical technique for internal drainage is merely based on

cyst geometry and location.
Cystenteric communication via

• Cyst-gastrostomy : in contact with stomach
• Cyst–duodenostomy : in contact with duodenum
• Roux-en-Y cyst-jejunostomy : not in contact with the stomach or
duodenum.

Percutaneous drainage
• Percutaneous drainage is indicated only for septic patients secondary to
pseudocyst infection because it has a high incidence of external fistula.
• This technique can be complicated by formation of an external

pancreatic fistula, secondary infection of the pseudocyst, as well as a
high recurrence rate
• Contraindications include intracystic hemorrhage and pancreatic ascites.

Pancreatocutaneous Fistula
• The frequency of pancreatic fistulas is low.
• Only 0.4% of patients have this complication after an acute episode.
• However, the incidence of this complication increases in patients with

other complications after AP:
– 4.5% in patients with pancreatic pseudocysts
– 40% in patients with infected necrosis after surgical débridement.
• Treatment is conservative for most patients.

Vascular Complications
• AP is rarely associated with arterial vascular complications.

• The most common vessel affected is the splenic artery, but the SMA,
cystic artery, and GDA have also been found to be affected.
• It has been proposed that pancreatic elastase damages the vessels,

leading to pseudoaneurysm formation.
• Spontaneous rupture results in massive bleeding.

• Clinical manifestations include sudden onset of abdominal pain,
tachycardia, and hypotension.
Management:
• If possible, arterial embolization should be attempted to control the
bleeding.
• Refractory cases require ligation of the vessel affected.
• The mortality ranges from 28% to 56%.

• Pancreatic inflammation can also produce vascular thrombosis;
the vessel usually affected is the splenic vein, but in severe
cases, it can extend into the portal venous system.
• Imaging demonstrates
– Splenomegaly,
– Gastric varices, and
– Splenic vein occlusion.

• Thrombolytics have been described in the acute early phase; however,
most patients can be managed with conservative treatment.
• Recurrent episodes of upper gastrointestinal bleeding caused by venous

hypertension should be treated with splenectomy.

Pancreatic Ascites
• Although very rare, complete disruption of the pancreatic duct can lead
to significant accumulation of fluid.
• When a disrupted pancreatic duct leads to pancreatic fluid extravasation

that does not become sequestered as a pseudocyst, but drains freely
into the peritoneal cavity, pancreatic ascites occurs.
• If into pleural cavity > pleural effusion.

• More in chronic pancreatitis
• Pancreatic ascites and pleural effusion occur together in 14%

of patients, and 18% have a pancreatic pleural effusion alone
• This condition should be suspected in patients who have an
episode of AP, develop significant abdominal distention, and
have free intraabdominal fluid.
• Diagnostic paracentesis typically demonstrates elevated

amylase and lipase levels.

• Treatment consists of percutaneous abdominal drainage combined
with endoscopic placement of a pancreatic stent across the disruption.
• Other option: Peritoneal lavage
• Failure of this therapy requires surgical treatment; it consists of distal

resection and closure of the proximal stump.

Pancreaticopleural Fistulas
• Posterior pancreatic duct disruption into the pleural space has been described
rarely.
• Symptoms that suggest this condition include dyspnea, abdominal pain, cough, and
chest pain.
• The diagnosis is confirmed with chest radiography, thoracentesis, and CT scan.

• Amylase levels above 50,000 IU in the pleural fluid confirm the diagnosis.
• It is more common after alcoholic pancreatitis and in 70% of patients is associated

with pancreatic pseudocysts.

• Initial treatment requires chest drainage, parenteral nutritional support, and
administration of octreotide.
• Up to 60% of patients respond to this therapy.
• Persistent drainage should also be treated with endoscopic sphincterotomy and

stent placement.
• Patients who do not respond to these measures require surgical treatment, similar
to that described for pancreatic ascites.

Chronic pancreatitis
Etiology ,Prognosis and Management

Definition
• Chronic pancreatitis is an incurable, chronic inflammatory condition that
is multifactorial in its etiology, highly variable in its presentation, and a
challenge to treat successfully

Etiology
• Genetic mutations
• Alcohol exposure
• Duct obstruction due to trauma
• Gallstones, and tumors
• Metabolic diseases such as hyperlipidemia and hyperparathyroidism
• Auto-immune disease
• Nutritional causes include so-called tropical pancreatitis which has been
thought to result from ingestion of certain starches
• Idiopathic

Genetics

Alcohol
• There is a linear relationship between exposure to alcohol and the development of

chronic pancreatitis.
• The risk of disease is present in patients with even a low or occasional exposure to
alcohol
• Although the risk of disease is dose related and highest in heavy (>150 g/d) drinkers,
the prevalence of chronic pancreatitis among confirmed alcohol abusers is only 5%
to 15%

Hyperparathyroidism
• Chronic hypercalcemia caused by untreated hyperparathyroidism is

associated with chronic calcific pancreatitis.
• It’s also a stimulant for pancreatic calcium secretion, which contributes
to calculus formation and obstructive pancreatopathy

Hyperlipidemia
• Hyperlipidemia and hypertriglyceridemia predispose women to chronic

pancreatitis when they receive estrogen replacement therapy.

Autoimmune pancreatitis
• A variant of chronic pancreatitis, nonobstructive, diffusely infiltrative

disease associated with fibrosis, a mononuclear cell (lymphocyte,
plasma cell, or eosinophil) and an increased titer of one or more
autoantibodies.
• Associated with a variety of illnesses with suspected or proven

autoimmune etiology, such as Sjögren’s syndrome, rheumatoid arthritis,
and type 1 diabetes mellitus.

• AIP has been characterized as either type I, with accompanying systemic
or multiorgan dysfunction, or type II, which is restricted to the pancreas
• Increased levels of serum β-globulin or immunoglobulin G4 are also

present

Tropical (Nutritional) Pancreatitis
• Highly prevalent among adolescents and young adults in Indonesia,

southern India, and tropical Africa.
• Abdominal pain develops in adolescence, followed by the development
of a brittle form of pancreatogenic diabetes.
• Parenchymal and intraductal calcifications are seen, and the pancreatic
duct stones may be quite large.

• Many of the patients appear malnourished, some present with extreme
emaciation, and a characteristic cyanotic coloration of the lips may be
seen.

Pathology
• Fibrosis : pancreatic stellate cells.
• Stone formation: calcium carbonate crystals trapped in a matrix of
fibrillar and other materia
• Duct distortion

Clinical presentation
• Pain is the most common symptom of chronic pancreatitis.
• It is usually midepigastric in location but may localize or involve either
the lt or Rt upper quadrant of the abdomen.
• Described as penetrating through to the back
• The pain is typically steady and boring, but not colicky.

• It persists for hours or days and may be chronic with exacerbations
caused by eating or drinking alcohol.
• Chronic alcoholics also describe a steady, constant pain that is

temporarily relieved by alcohol, followed by a more severe recurrence
hours later.
• Typically, these Pts flex their hips.

Etiology of pain
• Ductal hypertension, due to strictures or stones
• Parenchymal disease or retroperitoneal inflammation with persistent
neural involvement.
• Acute exacerbations of pain in the setting of chronic pain may be due to
acute increases in duct pressure or recurrent episodes of acute
inflammation in the setting of chronic parenchymal disease.

• Nausea or vomiting may accompany the pain, but anorexia is the most
common associated symptom.

• The pain may disappear completely over a period of years, as symptoms
of exocrine and endocrine deficiency become apparent.
• This is referred to as burned out pancreatitis and correlates with the

progression of disease from a mild to severe destruction of the
pancreas.
• Noninterventional approaches to the treatment of chronic pancreatitis

are inevitably accompanied by the development of narcotic addiction,
inability to work, and the sequelae of chronic illness
• Malabsorption and Weight Loss:
• When pancreatic exocrine capacity falls below 10% of normal, diarrhea
and steatorrhea develop.
• Patients describe a bulky, foul-smelling, loose (but not watery) stool that
may be pale in color and float on the surface of toilet water.

• Lipase deficiency tends to manifest itself before trypsin deficiency, so
the presence of steatorrhea may be the first functional sign of
pancreatic insufficiency.

Pancreatogenic Diabetes:
• The islets comprise only 2% of the mass of the pancreas, but they are
preferentially conserved when pancreatic inflammation occurs.
• Frank diabetes is seen initially in about 20% of patients with chronic
pancreatitis, and impaired glucose metabolism can be detected in up to
70% of patients
• It’s called brittle diabetes.

Laboratory workup
• (lipase and amylase) is highly sensitive and specific in acute
pancreatitis but is seldom helpful in the diagnosis of chronic
pancreatitis.
• The pancreatic endocrine product that correlates most strongly with

chronic pancreatitis is the PP response to a test meal

• Measurement of pancreatic exocrine secretion aspiration of pancreatic
juice from the duodenum after nutrient or hormonal (CCK or secretin).
• Indirect tests are based on the measurement of metabolites of

compounds that are altered (“digested”) by pancreatic exocrine
products and can be quantified by serum or urine measurements.

• Bentiromide test, in which N-benzoyl-Ltyrosyl-p-aminobenzoic acid is
ingested by the subject, and the urinary excretion of the proteolytic
metabolite p-aminobenzoic acid (PABA) is measured
• Quantification of stool fat has also been used as a measure of

pancreatic lipase secretion
• Triolein breath test

– Measurement of exhaled 14CO2 after ingestion of [14C]-triolein or [14C]-olein.

Radiology
• Radiologic imaging of chronic pancreatitis assists in four areas:
– Diagnosis
– The evaluation of severity of disease
– Detection of complications
– Assistance in determining treatment options

Ultrasonography
• Frequently used as an initial imaging method in patients with abdominal
symptoms, changes consistent with chronic pancreatitis are :
– Pancreatic duct dilatation
– Intraductal filling defects
– Cystic changes
– Heterogeneous texture

EUS
• EUS provides not only imaging capability but also adds the capacity to
obtain cytologic and chemical samples of tissue and fluid aspirated.

Abdomen CT
• CT scanning is sensitive for the diagnosis of chronic pancreatitis when:

calcification, duct dilatation, or cystic disease is present
• It is not accurate in the absence of these findings

• CT scanning has a false-negative rate of 10%
• Early or mild chronic disease may go undetected by CT imaging.

MRCP
• The advantages of MRCP include its noninvasive methodology and its
ability to image obstructed ducts that are not opacified by ERCP
injection.
• It is a useful screening study to detect duct abnormalities and to confirm

the need for interventional procedures

ERCP
• Considered to be the gold standard for the diagnosis and staging of
chronic pancreatitis.
• Serves as a vehicle that enables other diagnostic and therapeutic

maneuvers, such as biopsy or brushing for cytology, or the use of stents
to relieve obstruction or drain a pseudocyst.

Prognosis and natural history
• The incidence of carcinoma in patients with chronic pancreatitis ranges
from 1.5% to 6%, which is at least 10-fold greater.
• In patients with chronic pancreatitis accompanied by diabetes, the risk

of carcinoma has been found to be increased 12- to 33-fold.

• Periodic measurement of tumor markers such as CA19-9, and periodic
imaging of the pancreas with CT scan and EUS seem logical in order to
detect the development of carcinoma in the patient with chronic
pancreatitis

Management
• Conservative:
– Analgesics
– Cessation of alcohol use
– Oral enzyme therapy
– Selective use of antisecretory therapy.
– Interventional procedures to block visceral afferent nerve conduction
or to treat obstructions of the main pancreatic duct

Endoscopic management
• Pancreatic duct stenting is used for:
– Treatment of proximal pancreatic duct stenosis
– Decompression of a pancreatic duct leak
– Drainage of pancreatic pseudocysts that can be catheterized through
the main pancreatic duct

Surgical therapy
• Drainage procedures
– Duval procedure
– Puestow procedure
• Resectional procedures
– Distal pancreatectomy
– Proximal pancreatectomy “ whipple “
– Total pancreatectomy
• Hybrid procedures
- Duodenum-preserving Pancreatic Head Resection “Beger procedure “
- local resection of the pancreatic head with longitudinal pancreaticojejunostomy “frey
procedure “
Pancreatic Tumors
Adenocarcinoma, Cystic Tumors and
Endocrine Tumors

Types of pancreatic tumors
• Neoplasms of exocrine pancreas
– Ductal adenocarcinoma 75-90% of pancreatic cancers
– Cystic neoplasms account for <1% of pancreatic cancers
• Neoplasms of endocrine pancreas

– Neuroendocrine tumors or islet-cell tumors, rare

Pancreatic adenocarcinoma
• Ninth most common cancer diagnosis
• Fourth in cancer deaths
• Men> women (1.3 : 1)
• African Americans have a slightly higher risk
• Mean age at diagnosis is 72 years
• 74% of patients die within the first year after diagnosis.

Risk Factors
Environmental
• Smoking ( definitive association)
• Obesity
• Diet ( Rich in carbohydrate and cholestrol, salt)
• Chronic Pancreatitis
• Diabetes

Pathogenesis
• Most cases are sporadic.
• Sequential pathway has been observed in the development from
pancreatic intraepithelial neoplasia (PanIN) to invasive cancer.
• Genes identified- PDX1, KRAS2, CDKN2A/p16, P53, and DPC4 (SMAD4).
• KRAS2 oncogene is activated (by point mutation ) 95% of pancreatic

cancers
– Earliest event in tumorigenesis.

Molecular Genetic Progression From PanIN To Invasive Ductal Adenocarcinoma.

Location of the tumor
• About two-thirds of pancreatic adenocarcinomas arise within the head
or uncinate process of the pancreas
• 15% are in the body
• 10% in the tail,
• Remaining tumors demonstrating diffuse involvement of the gland.

Periampullary Carcinoma
• Head of the pancreas

• Ampulla of Vater
• Distal bile duct (cholangiocarcinoma)
• Duodenum .
• Less commonly, acinar cell carcinomas or pancreatic endocrine
neoplasms occur in the periampullary region of the pancreas

Carcinoma Body And Tail
• Late presentation
• Pain and weight loss are more common
• Rare
• Poor prognosis

Clinical examination
• A palpable distended gallbladder (Courvoisier’s law)
• Left supraclavicular node (Virchow’s node & Troisier’s sign )
• Periumbilical lymphadenopathy may be palpable (Sister Mary Joseph’s node).
• Peritoneal dissemination and perirectal tumor involvement may be palpable
via digital rectal examination (Blumer’s shelf)
• Migratory superficial thrombophlebitis (Trousseau ‘s sign)

Laboratory Evaluation
• Hepatic function evaluation
• Coagulation profile
• Nutritional assessment.
• Tumor markers : CEA, CA19-9
CA19-9
– Most sensitive most reliable tumor marker for pretreatment evaluation and
posttreatment surveillance

Imaging

Staging Laproscopy
• Indications
– Large tumors (>3 cm)
– Significantly elevated CA19-9 level (>100 U/mL)
– Uncertain findings on CT
– Body or tail tumors

Staging
• TX: Primary tumor cannot be assessed
• T0: No evidence of primary tumor
• Tis: Carcinoma in situ
• T1: Limited to pancreas, ≤ 2 cm in greatest dimension
• T2: Limited to the pancreas, >2 cm in greatest dimension
• T3: Extends beyond the pancreas, without involving of the celiac axis or the superior
mesenteric artery
• T4: Involves the celiac axis or the superior mesenteric artery (unresectable).

Management
• Surgical resection offers the only chance of cure.
– Only 15 to 20 % of patients have resectable disease at diagnosis

– 40 % have metastatic disease
– 30 to 40 % have locally advanced unresectable tumors.

Criteria For Unrespectability
• If any of:
– Distant metastases
– Metastases to lymph nodes beyond the field of resection
– Greater than 180 degrees SMA encasement,
– Any celiac abutment
– Unreconstructable SMV/portal vein occlusion
– Aortic invasion or encasement

Role of Surgery and Management of Borderline
Resectable Disease
• Such patients are treated initially with chemotherapy,
chemoradiotherapy or both followed by restaging and surgical
reevaluation.

Management of Resectable tumors
• Tumors in the head/uncinate process:
– Either a conventional or a pylorus-preserving Whipple operation.
• Tumors of the tail/body:

– Distal subtotal pancreatectomy, usually combined with splenectomy.

Palliative Therapy
• Biliary Obstruction:
– ERCP with metal stent placement
– Surgical biliary-enteric bypass (Roux-en-Y hepaticojejunostomy)

• Gastric Outlet Obstruction
– Endoscopic luminal stenting
– Double bypass consisting of a Roux-en-Y
– hepaticojejunostomy and gastrojejunostomy
• Pain Relief
– NSAIDS or long acting opioids
– Celiac nerve block
– Neurolysis

Cystic Neoplasms of The Pancreas
• Second most common exocrine pancreatic neoplasm next to
adenocarcinoma.
• Types
– Mucinous
– Serous
– IPMN

Mucinous Cystic Neoplasm
• Most common cystic neoplasms of the pancreas.
• Young women, Men are rarely affected.
• Fifth decade.
• Typically found in the body and tail of the pancreas

• Contain mucin-producing epithelium
• Presence of mucin-rich cells and ovarian-like stroma
• CT scan
– Solitary , fine septations, surrounded by a rim of calcification
• Predictors of malignancy
– Eggshell calcification
– Larger tumor size
– Mural nodule on cross-sectional imaging

• EUS and cyst fluid analyses demonstrate
– Mucin-rich aspirate and
– High CEA levels (>192 ng/mL)
– Low levels of amylase
• Standard treatment
Pancreatic resection

Serous Cystic Neoplasm
• Predilection for the head of the pancreas
• Vague abdominal pain and less frequently with weight loss and
obstructive jaundice
• Large , well circumscribed masses.
• Microscopy - multiloculated, glycogen-rich small cysts.

• CT Scan:
• Central calcification, with radiating septa giving the sunburst
appearance (10-20%)
• Treatment :
• Large (>4 cm) or rapidly growing, symptomatic lesion: treatment is
Resection
• Small (<4 cm) , asymptomatic can be observed.

Intraductal Papillary Mucinous Neoplasm
• Sixth to seventh decade of life.
• Commonly in head region.
• Wide spectrum ranging from benign adenoma, borderline, carcinoma in
situ, and invasive adenocarcinoma.
• Types:
– Side branch or branch duct IPMN,
– Main duct IPMNs,
– Mixed -type IPMNs

Side Branch IPMN
• Involves dilation of the pancreatic duct side branches that communicate
with but do not involve the main pancreatic duct.
• Focal (involving a single side branch) or multifocal
• Risk of malignant transformation directly related to:
– The size of the cystic dilation
– Others - mural nodules or general thickening of the cyst wall symptoms like
jaundice, pain, and diabetes

Small (<1 cm) IPMNs:
• Surveillance with CT or MRI in 1 year
Asymptomatic cysts ,1 -3 cm:

• Imaging at 6 months followed by
• Annual evaluation if no change in size.
Cysts larger than 3 cm:

• Surgical resection (Partial pancreatectomy)
• Risk of invasive malignancy- 10% to 15%
Main Duct IPMN
• Abnormal cystic dilation of the main pancreatic duct with columnar
metaplasia
• 30% to 50% risk of harboring invasive pancreatic cancer at the time of
presentation.
• Endoscopy :
– Thick mucinous secretions oozing from patulous papilla

• Aspirated fluid is typically:
– Viscous and clear, contains mucin and columnar mucinous cells with
variable atypia
– Elevated CEA level (>192 ng/mL)
• CT scans :
• Dilated main pancreatic duct, cysts of varying sizes, and possibly mural nodules.
• MRCP localization of mural nodules and pretreatment classification of suspected
side branch or main duct types of IPMN
• Treatment: Surgical resection (Risk of malignant potential)

Mixed-type IPMN
• Side branch IPMN that has extended to involve the main pancreatic duct
• Risk of invasive malignancy at the time of presentation (30% to 50%)
• Surgical resection is indicated for the treatment

Neoplasms of Endocrine Pancreas
• Alpha (A) – Glucagon
• Beta (B) – Insulin and amylin
• Delta (D) – Somatostatin and vasoactive intestinal peptide (VIP)
• F cells – Pancreatic polypeptide (PP)
• Gastrin-producing cells are normally present in the fetal pancreas only.

Islet Cell Tumors
• Very rare
• Most are benign and nonfunctional.
• The incidence of malignancy varies from 10% in insulinomas to almost
100% in glucagonomas.
• Insulinomas, glucagonomas, and VIPomas arise from the pancreas,

whereas most gastrinomas occur in the duodenum.

Insulinoma
• Most common functioning tumor
• Equal distribution in the head, body, and tail.
• 97% are located in the pancreas, remaining 3% are located in the
duodenum, splenic hilum, or gastrocolic ligament
• Whipple’s triad:
1. Fasting-induced neuroglyopenic symptoms of hypoglycemia
2. Low blood glucose levels (40 to 50 mg/dL),
3. Relief of symptoms after the administration of glucose.

• Lab tests:
– 72 hour fast test: High level of serum insulin (>5 μU/mL)
– Insulin-to-glucose ratio higher than 0.3
– C peptide levels higher than 1.2 μg/mL
• CT or MRI:
– Hyper attenuating because of their rich vascular supply

Gastrinoma
• Second most common functional pancreatic endocrine tumor
• Cell of origin is not clear, because the normal adult pancreas has no
gastrin-producing cells.
• More common in men
• Produce Zollinger-Ellison syndrome (ZES)
– Hypergastrinemia , subsequent severe peptic ulceration, severe diarrhea.

• Abdominal pain (75%)
• Symptoms of GERD
• Gastrinoma triangle (90%)

• Labs:
– Presence of hypergastrinemia in the presence of increased secretion of gastric acid.
– An elevated serum gastrin level coupled with a pH lower than 2 in the gastric aspirate
– Fasting levels of gastrin. higher than 1000 pg/mL (upper limit of normal of 100 pg/mL)
– An increase of more than 200 pg/mL in the gastrin value after administration of
secretin

Vipomas
• Release high levels of VIP
• Verner-Morrison syndrome
• Also known as WDHA syndrome (watery diarrhea, hypokalemia,
achlorhydria )
• Solitory , larger than 3 cm ; 75% body and tail
• Hypokalemia, hypomagnesemia, hypo or achlorhydria, hypercalcemia.

Glucagonomas
• Very rare
• Tend to be larger, averaging 5 to 10 cm in size
• Most are malignant (50 %)
• Almost always arise in the pancreas and 65% to 75% are found in the
body or tail.
• A fasting glucagon level higher than 50 pmol/L is considered
diagnostic.
• The glucagonoma syndrome:
– 4Ds: diabetes, dermatitis, deep vein thrombosis, and depression

Somatostatinomas
• Usually solitary and 85% are larger than 2 cm.
• Mostly at head of pancreas
• 70- 90% are malignant
• Steatorrhea , diabetes mellitus, hypochlorhydria, and gallstones
• Fasting somatostatin level higher than 14 mol/liter.

Nonfunctional Neuroendocrine Tumors
• Defined as a pancreatic tumor of endocrine origin, with no definable
hormonal syndrome.
• Late in seeking help hence most tumors are malignant and metastasized
at the time of presentation
• Identified by positive immunostaining for chromogranin A or
synaptophysin

Localization
• Cross -sectional imaging with CT or MRI
– First step in localization.
– Sensitivity is 71% to 82% and is directly related to the size of the tumor.
– Vascular blush in the arterial phase is critical
– Lesions smaller than 1cm cannot be identified.
• Endoscopic ultrasound (EUS)
– Overall sensitivity of 93%
– Greater sensitivity when compared with CT and MRI for detecting tumors < 3 cm
– Allows for fine-needle aspiration (FNA) of tumors

Somatostatin receptor scintigraphy (SRS)
• Not useful for insulinoma
• The sensitivity for SRS is over 80% for all pancreatic endocrine tumors excluding
insulinomas
• It has an overall sensitivity of 80% to 100% and specificity higher than 90% for
gastrinomas.
• SRS may not show the exact location of a tumor indicates its vicinity within a few
centimeters
Angiographic techniques and portal venous sampling (sensitivity higher

than 90%)
Blind exploration with intraoperative ultrasound

Treatment
• The treatment of endocrine tumors is surgical.
• (pancreatic head resection, distal pancreatic resection, or enucleation.)

Pancreas: One of The Largest Surgical Chapters !!

Uploaded by

Copyright:

Available Formats

You might also like

Pancreas: One of The Largest Surgical Chapters !!

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Pancreas: One of The Largest Surgical Chapters !!

Uploaded by

Copyright:

Available Formats

Pancreas

One of the largest surgical chapters !!

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• Head corresponds with the curve of duodenum overlying the body of

• Aorta and superior mesenteric vessels lie behind the neck.

Dr. Mahmoud W. Qandeel

• Tip of pancreatic tail extends up to the splenic hilum.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• Splenic artery (a branch of the celiac trunk)

• Inferior pancreaticoduodenal (a branch of the superior mesenteric artery),

• Head & Neck – Pancreaticoduodenal

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• This relative outflow obstruction has been implicated in the development

• Although 10% of the population is affected by pancreas divisum, only

Dr. Mahmoud W. Qandeel

• This abnormality may be associated with other congenital defects,

• If symptoms of obstruction occur, surgical bypass through

• Clinically, ectopic nodules may result in bowel obstruction caused by

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• In response to food – secretes digestive enzymes in an alkaline

• Secretion enhanced by:

• Within cells enzymes are in inactive form.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• Development of digestive disturbances:

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• Its hallmark is acute pancreatic inflammation associated with little or no

• It ranges from a mild self-limiting inflammation of the pancreas to

Dr. Mahmoud W. Qandeel

• 10% to 20% of patients have a rapidly progressive inflammatory

Dr. Mahmoud W. Qandeel

• The gender difference is probably more related to etiology.

Dr. Mahmoud W. Qandeel

• In pediatric patients, abdominal blunt trauma and systemic diseases are

• Autoimmune and drug-induced pancreatitis should be a differential

Dr. Mahmoud W. Qandeel

• The mechanism by which small gallstones migrating down the common

“Common channel” hypothesis.

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

Dr. Mahmoud W. Qandeel

• This occult microlithiasis is probably responsible for up to half of those

Dr. Mahmoud W. Qandeel

• It triggers proinflammatory pathways such as nuclear factor κB which