Pancreas

Dr. Gerardo R. Wencelao, MD, FPCS

Exocrine Gland Anatomy

Pancreas
Exocrine pancreas
Comprises 85% of pancreatic mass
Secretes 500-800 ml/day of colorless, alkaline,
isosmotic juice
Secretion is inhibited by:
Somatostatin
PP
Glucagon
Centroacinar and Intercalated Duct Cells
Secretes water and electrolytes
They contain carbonic anhydrase
Responsible for the formation of
bicarbonate
Bicarbonate (HCO3)
Amount is directly proportional to the rate
of secretion
Chloride
Amount is inversely proportional to the rate
of secretion
Sodium and Potassium- amount is constant
Secretin
Major stimulant for bicarbonate secretion
Released from duodenal mucosa in
response to acidic chyme from the stomach
CCk, gastrin, accetylcholine
Weak stimulants of HCO3
Acinar Cells-Secretes digestive enzymes
CCK-primary stimulant
Carbohydrates
Amylase
Secreted in its active form
Completes the digestive process started by
the salivary amylase
Hydrolyzes starch and glycogen to simple
sugars (glucose, maltose, dextrins)
Acinar Cells
Protein
Proteolytic enzymes-secreted as proenzymes
Endopeptidase
Proelastase Elastase
Chymotrypsinogen chymotrypsin
Trypsinogen trypsin

Exopeptidase
Procarboxypepetidase
Carboxypeptidase

Fat

Lipase-active
Phospholipase A2
Secreted as pro-enzyme
Requires bile for its action
Trypsinogen
Converted to trypsin in the dueodenum by
enterokinease
Also activated by acidic enviroment ( pH <7)
Activates the proenzyme to active form
Mutation of trypsinogen results to premature
intrapancreatic activation---familial pancreatitis
Pancreatic secretory trypsin inhibitor (PSTI) or SPINKI
Inhibits action of trypsin by blocking active site
Ensures activation of digestive enzymes occurs
only within the duodenum
Failed expression of PSTI results familial
pancreatitis

Endocrine Pancreas
They are composed of various cells located in the Islet
of Langerhans
(1 2%)
The primary function is to regulate glucose homeostasis
Beta Cells
70% of Islet cell mass
Located in the central portion if the islet
Hormones produced
Insulin
Inhibit endogenous glucose production
Facilitates glucose transport into the cells
Inhibits
glycogenolysis,
fatty
acid
breakdown and ketone formation
Stimulates protein synthesis
Amylin counterregulates insulin secretion and
function
Pancreastatin
Decrease insulin and somatostatin release
Decrease pancreatic exocrine secretion
Increase glucagon release
Stimulates insulin secretion
Amino acids (arginine, lysine,leucine)
Glucagon

Glucose dependent insulinotropic polypeptide (

GIP)
Glucagon like peptide 1(GLP1)
Fatty acids
CCK
Inhibits insulin release
Somatostatin
Amylin
pancreastatin
Alpha cells
15 20 % secretes glucagon
Glucagon counter balance insulin by stimulating
hepatic glycogenolysis, ketogenesis and lipolysis
Glucagon also inhibits intestinal motility and gastric
acid secretion
The release of glucagon is stimulated by hypoglycemia,
stress, CCK, arginine,alanine
PP cell
15% of the total islet mass
Highest concentration in the head and uncinate process
Secretes Pancreatic polypeptide
Functions
Facilitates the effect of insulin on the liver
by increasing the sensitivity of hepatic
insulin receptors
Inhibits pancreatic exocrine secretion/bile
secretion
Delta cells
Makes up 5% of the total islet cell mass
Secretes Somatostatin
Release of somatostatin occurs during meal
Stimulants for the release of Somatostatin
Intraluminal fat- major stimulant
Acidification of gastric and duodenal mucosa
Functions of Somatostatin
Inhibits GI secretion/ exocrine
secretion
Inhibits secteion and action of all GI
endocrine pepides
Epsilon cell
Secretes hormone Ghrelin
Functions of Ghrelin
An appetite stimulating hormone
Blocks insulin effects on the liver
Inhibits insulin release

Acute Pancreatitis
Pathogenesis of Pancreatitis
Involves activation of inactive enzymes within the pancreatic
parenchyma
The primary defect-extrusion of zymogen granules are
blocked
Fusion of zymogen granules w/ Lysosomes
Lysosomal enzymes (Cathepsin B) actvitates
trypsinogen to trypsin

Gallstone Obstruction

Alcohol-Induced Acute Pancreatitis

Pancreatic duct obstruction

Increased ampullary resistance
Protein deposition and precipitation [ w/ Calcium]
Pancreatic exocrine hypersecretion
Ethanol stimulates gastric acid secretion
Activation of secretinexocrine hypersecretion
Impaired trypsin inhibition
Acetydehyde-by product of ethanolol causes increase duct
permeability
Hypertriglyceridemia-causes endothelial injury
Ethanol decreases pancreatic blood flow causing ischemic
injury
2 years or more of alcohol consumption
Usual daily intake of 100 -150 g of ethanol
7-10 drinks
Nature of alcohol (beer, wine, hard liquor)-not significant

Acute Pancreatitis
Etiology
Tumors
Should be considered in non-alcoholic
1-2% have pancreatic Ca
Drugs
Thiazide diuretics furosemide, tetracycline.. Etc..
Infections
Mumps,
coxsackie
virus,
Mycoplasma
pneumonia
Hyperlipidemia
Fatty acids
Endothelial injury, sludging of blood cells
Ishemic states
Iatrogenic
Pancreatic biopsy, gastrectomy
Splenectomy
ERCP

Mild pancreatitis
No systemic complications
Low Ransons
Sustained clinical improvement
Severe pancreatitis
High Ransons
Encephalopathy, ARDS
Hct >50% , urine output-< 50 mL/h
Hypotension, fever, peritonitis

Clinical Presentations
Acute pancreatitis may vary from mild abdominal discomfort
to profound shock, hypotension and hypoxemia
May present with epigastric pain radiating to the back with
nausea and vomiting
Discomfort may be relieved by sitting and aggravated by
lying
Findings may vary with severity of inflammatory process
May have mild to moderate abdominal tenderness
In severe cases may have rigid abdomen, epigastric guarding
and rebound tenderness
Severe pancreatic inflammation and necrosis may cause
retroperitoneal hemorrhage which leads to:
Large 3rd space fluid loss
Hemococentration- elevated HCT
Hypovolemia
Pre-renal azotemia
Hypotension
Tachycardia
Blood dissection along different planes
Grey Turners sign
Blood extends to the flank tissues resulting to
flank ecchymosis

Cullens sign
Blood dissects up to the falciform ligament and
create peri-umbilical ecchymosis

Note the hemorrhage and foci of chalky fat necrosis in

pancreas and fats

Mesentery and omentum extensive fat necrosis due to Acute

Panreatitis

Surgical Specimen

A. Stomach
B. Spleen
C. Fat
D. Pancreas
Diagnosis
Serum Markers
1. Serum amylase

Increased in 95 % of cases; 5 % false negative

75 % of patients with abdominal pain and increase

amylase have pancreatitis

Other causes of marked elevations of serum amylase:

Acute cholecystitis
CBD stones with or without pancreatitits
Perforated peptic ulcer
Strangulated small bowel
Acute alcoholism
Cancer of the pancreas
Mumps

> 1,000 Somogyi-Nelson Units o indicates biliary tract

disease with pancreatitis

200 500 units indicate alcoholic pancreatitis

Remains elevated for 3-5 days
Urine amylase remains elevated for several days after serum
levels have returned to normal
P-amylase -more specific (88-93%)
LIPASE-remains elevated longer than total or P-amylase.
The serum indicator of highest probability

Mumps

Abdominal X-ray of Alcoholic Pancreatitis

Other Causes of Elevated Serum Amylase

Acute Cholecystitis

Colon Cut-off Sign

CBD Stones

Sentinel Loop Sign

Perforated Peptic Ulcer

Ultrasound
The best way to confirm biliary pancreatitis
Changes from normal anatomy and vascular landmarks;
presence of swelling and loss of tissue plane

CT Scan w/ Bolus IV Contrast

More commonly used to diagnose pancreatitis
Gold standard in assessing severity
Used to distinguish mild (non-necrotic) to severe necrotizing
or infected pancreatitis
Pancreatitis
RANSONS prognostic signs (non-gallstone pancreatitis)
At admission
>55 y/o
WBC > 16,000/mm3
Blood glucose >200mg/dL
LDH >350iu/L
AST >250u/dL
Initial 48 hours
Fall in Hct of >10pts
BUN elevation of >5mg/dL
Serum Ca <8mg/dL
Arterial pO2 <60mmHg
Base deficit >4mEq/L
Est. fluid seq. >6L
RANSONS for Gallstone pancreatitis
At admission
>70 yrs old
WBC >18,000/mm3
Bld glucose>220 mg/dL
LDH >400 IU/L
AST > 250 U/dL
Initial 48 hours
Fall in Hct of >10pts
BUN elevation of >2mg/dL
Serum Ca <8mg/dL
Base deficit >5mEq/L
Est. fluid seq. > L
Acute Pancreatitis
Prognosis
CT scan with bolus IV contrast
Gold standard in assessing severity of pancreatitis
Biochemical marker
C-reactive protein
Ransons criteria
<2 mortality is : 0
3-5 mortality is: 10-20%
>7 mortality is >50%
Treatment
Mild pancreatitis
Resting the pancreas through restriction of oral
foods and fluids
Maintenance of fluid balance
Pain management
Important in preventing cholinergic discharge
Procaine gcl
Meperidine

Morphine Causes spasm of sphincter of

Oddi
Nutritional support
Oral feeding
Gradually resumed once the clinical
condition improves ( normal amylase,
resolution of abdominal pain) which
generally occurs after 3-7 days in mild
pancreatitis
Low fat , low protein
Total parenteral nutrition
Enteral nutrition
Severe pancreatitis
Encephalopathy
Hct- >50%
Urine output- <50ml/hr
Hypotension
Fever
peritonitis
Broad spectrum antibiotics
Assisted ventilation
Pts with ARDS Phospolipase A-damage alveolar tissue and
capillaries
Peritoneal lavage
Deteriorating resp function
In shock
Infections
May occur few hours or few days after the attack
Manifest as retroperitoneal air in CT scan
Infected necrosis- Most common cause of death
Caused by translocation of enteric bacteria
Gram stain and culture of fluid or tissue (CT
scan or US guided FNA)
Surgical debridement
Empiric tx with Flucanazole (candida)-severe
acute pancreatitis
Sterile necrosis
Treatment
No systemic complication
Supportive care
With systemic complication w/o infection
Very ill,with high Ransons criteria
Aggressive dedridement
Pancreatic abcess
Usually occurs 2-6 weeks after the attack
Treatment
External drainage
Biliary Pancreatitis
Open cholecystectomy and CBD exploration
Best treatment for healthy patient with
gallstone pancreatitis
Urgent- within 48-72 hours of admission
Delayed- after 72 hours
ERCP- (sphincterotomy)

For patients
intervention

with

risk

for

surgical

Chronic Pancreatitis

o Increased calcium formation

Hyperlipidemia
o >300 mg/dL
o Effect is potentiated with estrogen

Gross

Histopathology

Organ becomes small, indurated and nodular and edges

becomes rounded
Alternating areas of stricture and dilatation of the main
pancreatic duct (late)
Calcifications
Loss of exocrine acinar cells & increase interstitial fibrous
tissue
Isles of langerhans are relatively preserved

Etiology
Alcohol
Most common cause worldwide -70%
Risk is dose related (150g/d)
Risk is still present even at low exposure ( 1-20 g/d)
Related also to the duration
Typically after 16-20 years of alcohol
consumption
Directly alters the integrity of the pancreatic ducts acini
Acetydehyde Interferes with the intracellular
transport of digestive enzymes & colocalization with
lyzosomes
o Leads to autodigestion
High protein, low carbohydrate, low volume secretory
output
o Precipitation of protein
Decreased Lithostathine
Other causes
Hyperparathyroidism

Classification of Chronic Pancreatitis

Chonic
Calcificlargest
grp.alcohol,
hereditary,
hypercalcemia, hyperlipidemia, drug induced
Chronic Obstructive-pancreatic tumors,gallstones, ductal
strictures, trauma, pancreatic divisum
Chronic autuimmune-primary billiary cirrhosis
Asymptomatic Pancreatic Fibrosis-chronic alc, endemic for
residents in tropical climates
Chronic Inflammatory Pancreatitis-unknown
Tropical pancreatitis
Prevalent among adolescents and young adults in
Indonesia, southern India, Tropical Africa
Associated with:
Protein caloric malnutrition
Deficiency in trace elements
Indigenous food
Cassava root contains toxic glycosides
Hereditary pancreatitis
Presents in childhood or adolescence
Progressive pancreatic dysfunction
Increased incidence of carcinoma
Due to mutation of SPINKI gene
Chronic autoimmune
Non-obstructive, diffusely infiltrative (lympocytes,
plasma cells)
Associated with other autoimmune disorder (Sjogrens
syndrome, rheumatoid arthritis, type 1 DM)
There is compressive stenosis of intrapancreatic portion
of CBD, obstructive jaundice
There is an increased level of B-globulin or
immunuglobulin G4
Treatment
Steroid therapy
Clinical Manifestations
Pain most common symptom, midepigastric, steady not
cloicky, temporarily relieved by alcohol followed by
recurrence after.
Pain can be short (<10days) and absent for long periods or
relentless or frequent lasting for months
Exocrine and endocrine deficiency-burned out pancreatitis
2/3 will have abnormal glucose tolerance and subclinical fat
malabsorption
30-50% - overt diabetes mellitus
10-15% - frank steatorrhea
Manifestations:
o Malabsorption and Weight loss
o Steatorrrhea-exocrine capacity fall below 10% of the
normal.bulky foul smelling, loose and pale in color
o Diminished secretion of bicarbonate to the duodenum
Impairs absorption of nutrients

o Decreased food intake due to anorexia and vomiting

Steatorrhea
Fat droplets in stool specimen

Atrophic lobules of acinar cells are surrounded by dense

fibrous scar tissue infiltrated by lymphocytes

ERCP

Treatment
o Restriction of fat to 75 g/day
o Exogenous pancreatic enzyme

Enteric coated pancreatic enzyme

Non-enteric
coated
pancreatic
enzyme + prton pump inhibitor
Manifestations:
o Apancreatic Diabetes (typeIII):

Islets are smaller but are relatively

preserved. They are isolated by
fibrosis to the surrounding vascular
network

Deficient in all glucoregulatory

hormones

Enhanced peripheral sensitivity to

insulin

Decreased hepatic sensitivity to

insulin
Radiologic imaging-principal method of diagnosis
o ERCP-most sensitive
o CT-scan sensitive only when calcification,
ductal dilatation is present
o EUS-safer than ERCP, more widely used

Capable in detecting small ( <1cm)

abnormalities in the pancreas

Most frequently used as preliminary

step in evaluation of pancreatic dse..
Chronic calcifying pancreatitis. Numerous calculi are
noted in the pancreatic duct

A. Normal biliary and pancreatic ducts during an ERCP

B. ERCP image

A, B, ERCP demonstrating mild chronic pancreatitis

A, B, ERCP demonstrating moderate chronic pancreatitis

Direct measurement after ingesting

known quantity of fat
Triolein breath-indirect measurement of
fat by measuring exhaled CO2 after
ingestion of triolein
High false negative rate
Medical treatment
Analgesia
Complete abstinence from alcoholprovides relief in 60-75% of patients
Analgesics
Opioids
Gabapentin
Enzyme therapy
Initial medication used to treat pain
Non-enteric coated enzyme-binds to
CCK-releasing
peptide-inhibits
endogenous pancreatic enzyme secretionreduced pressure on the obstructed duct.
Given for at least 1 month
Anti-secretory tx
Somatostatin (Octreotide acetate)
Inhibits exocrine sectation and CCK
release
Endoscopic therapy:
Pancreatric duct stenting
Can induce inflammatory reaction
Neurolytic therapy;
EUS guided celiac plexus blockade
Uses short acting analgesics
Effective in 55% but of short
duration only

A, B. ERCP demonstrating severe chronic pancreatitis

Plain Abdominal Film

Abdominal x-ray showing diffuse calcification

Chronic Pancreatitis
Diagnostics:
Measurement of pancreatic product in bld.
Endocrine
Pancreatic polypeptide
The most sensitive indicator
Blunted or negative response to test meal
Normal PP response to test meal doesnt rule out
chronic pancreatitis
Measurement of exocrine secretion:
Direct measurement
Endoscopic aspiration of exocrine secretion in the
duodenum
Lundh test meal-nutrient is given to the
patient
CCK or Secretin stimulation test
Indirect measurement
Bentiromide test
Urinary excretion of PABA is measured
after ingesting nitroblue tetrazoliumparaaminobenzoic acid (NBT-PABA)
degraded by chymotrypsin
100% sensitivity rate
Low specificity rate-seen also in hepatic
and kidney dse.
Used to determine the extent of pancreatic
insufficiency of pt. with known chronic
pancreatitis
Indirect measurement of exocrine secretion
Schilling test-recovery of urinary cobalamin
after ingestion of vitamin B12
Fecal fat,chymotrypsin or elastase

Surgical celiac plexus nerve block

Surgical therapy
Can delay progression of chronic pancreatitis
Drainage procedures
Transduodenal sphincteroplasty
Duval procedure
Puestow procedure
Side to side pancreaticojejenostomy
Duct must be 6mm
Pain relief in 75-85%
20% recurrence

Resectional procedures
Distal pancreatectomy Focal inflammation localized to the body
and tail
No ductal dilatation
Resection of 40-80%
With significant risk of recurrence

Duval Procedure Caudal PancreaticoJ

The Puestow Procedure

Complications:
Pseudocyst:
Most common complication of chronic
pancreatitis
Acute pseudocyst-collection of pancreatic juice 34 weeks after acute pancreatitis. Persistence of
the pseudocyst for >6weeks-Chronic pseudocyst
Resolve spontaneously in 50% of cases
over acourse of 6 weeks or longer
>6cm resolves less frequently but may
regress over period of months
May form an abcess if w/ secondary
bacterial infection

Diagnosis
Continued elevation of serum amylase
CT scan is the most helpful examination
Ultrasound
UGIS
ERCP

Distal Pancreatectomy

Resectional procedurtes:
Total pancreatectomy
95% distal pancreatectomy:
Intented for sclerotic (small duct) dse.
Pain relief in 77% nof patients
High risk for brittle diabetes,hypoglycemic
comma and malnutrition

Pseudocyst
Treatment:
Observation:
50-60% resolution rate for asymtomatic patients
Surgery:
Persistence of sypmtoms(pain, inability to
eat,GIT and biliary obstruction
Enlargement
Complications
Infection
Hemorrhage
Rupture
External Drainage-for infected pseudocyst
Internal drainage (best treatment)
Small piece of cyst wall should be excised for
histopathology to rule out malignancy
Cystogastrostomy - most commonly used
Cystojejenostomy - most verastlie; can be used
for those that penetrate the transverse mesocolon,
paracoloic gutter or lesser sac
Cystoduodenostomy

Cystgastrostomy Completes

Endoscopic stenting of the pancreatic duct

Preferred treatment for persistent pseudocyst
Complications:
Pancreatic ascites Pancreatic fluid extravasation that does not
sequestered as pseudocyst but drains freely into
the peritoneal cavity.
Internal pancreatic fistula pancreatic
fluid tracks to the thorax resulting to
pleural effusion
DX
Progressive
abdominal
enlargement
despite wt. loss
CT scan
ERCP
Markedly elevated serum amylase
Paracentesis or thoracentesis Non-infected fluid
Elevated amylase
protein > 25grams
Treatment:
Antisecretory tx w/ octreotide acetate w/
bowel rest and parenteral nutritionsuccesful in >50% of cases
Complete paracentesis reapposition of
serosal surface
Chest tube drainage-closure of internal
fistula
ERCP-pancreatic duct stenting
Surgery:
Roux-en Y pancreaticojejenostomy leak
from the central region of the pancreas
Distal pancreatectomy-leak on the tail
Internal drainage
Head of pancreas mass
Severe pain
Stenosis of distal CBD
Duodenal stenosis
Stenosis of the proximal pancreatic duct
Compression of portal vein
Lower incidence of exocrine and endocine
deficiency
Higher expression of epidermal growth factor
There is an accelerated transformation of
hyperplasia to dysplasia

Pancreatitis with Pseudocyst and Calcification

Surgical Cystogastrostomy For Pancreatic Pseudocyst

Anterior Gastrotomy

Creation of the Cystgastrostomy

Complex Fluid-Containing Necrotic Debris is Aspirated

10

Treatment
Duodenum preserving
resection (DPPHR)
Splenic and portal vein thrombosis
Pancreatic-enteric fistula

7.

pancreatic

head

PANCREATIC TUMORS
Adenocarcinoma of the Pancreas
Most are>60 years old
Mutation of K-ras oncogene
Slightly more common in men
2/3-head or uncinate process
Diagnosed earlier because of obstructive jaundice
15%-body
10%-tail
85-90%-unresectable at the time of dx
Risk factors
Family hx
Cigarette smoking
Dietary high in fat low in fiber, fruits and vegetable
Diabetes mellitus
Chronic pancreatitis
Pancreatic CA may arise anywhere in the pancreas, with the
most frequent focus in the head

Pancreatic Carcinoma
A typical Pancreatic Carcinoma patient
Note marked weight loss and jaundice

A tissue section of AdenoCA of pancreas reveals markedly

atypical neoplastic glands that infiltrate the connective tissue
of the pancreas

Clinical Manifestations:
1. Weight loss (most common)
2. Pain (dull and aching epigastric and radiates to the back,
aggravated by eating and lying down) due to obstruction
to the pancreatic duct and perineuralinvasion
3. Progressive jaundice 75 % (cancer of the head of the
pancreas)
4. Anorexia and weakness (50 %)
5. Pruritus
6. Hepatomegaly

Enlarged palpable gallbladder not tender and without

fever is a reliable diagnostic criteria for malignant
choledochal obstruction

Diagnostic examinations
1. Ultrasound
2. CT-scan
o Multidetector ,dynamic,contrast enhanced CT scan
90-95% accuracy in predicting unresectablity
Criteria of unresectability
o Invasion of superior mesenteric
artery
o Invasion of the hepatic artery
o Enlarged
LN
outside
the
boundaries of resection
o Ascites and distant metastasis
3. EUS
o Used when there is high suspicion of pancreatic CA
but no mass seen on CT scan
o Sensitive test for portal and superior mesenteric
vein invasion
o Transluminal biopsy of pancreatic mass
o 80%-accuracy in predicting resectabilty
4. Diagnostic laparoscopy :
o Advocated in patients felt resectable by CT
scan.Improves the accuracy in predicting
resectability by 98%
o Best applied in pt. with large tumors (>4cm)
located on the body and tail
o Pts. with eqiuvocal findings of metastasis or ascites
o Advanced dse. e.g. marked wt loss Ca19-9
(>1000U/mL)
Treatment
o Prior to surgery
Improve nutrition, correct anemia
Preoperative renal function
Adequate hydration
o Whipples Surgery
The only definitive and potentially curative
treatment of periampullary carcinoma. It is
performed for localized cancer of the ampulla,

11

duodenum and CBD in good risk patient and

done to pancreatic cancer if no evidence of spread
to the liver

Distal Pancreatectomy

Kills malignant cells before they can spread

intraoperatively
Decrease the incidence of pancreatic fistula
Postoperative surveillance
Recurrence usually manifest as liver metastasis
CA19-9
CT scan
Palliative treatment:
Pain
Oral narcotics
Celiac pexus nerve block
Jaundice:
Pruritus-most troublesome aspect of jaundice
Cholangitis,coagulopathy, hepatocellular failure
Endoscopic stents;
Biliary enteric by-pass
Choledochojejunostomy preferred
procedure
Duodenal obstruction:
A late event
Occurs only in 20%
Gastrojejenostomy
Not done unless with signs of obstruction or
the tumor is seen enroaching on the
duodenum

Surgical Celiac Plexus Nerve Block

Pancreatic tumor in the body of the pancreas
Adenocarcinoma of the Pancreas
Value of Pancreaticoduodenectomy
Few are cured indefinitely
Tumor tend to recur locally and hematogenously with
liver metastasis
Median survival-22 months
Provides better palliation
Complications of Pancreaticoduodenectomy
Post operative complications
Delayed gastric emptying
Pancreatic fistula
hemorrhage
Most common cause of death
Sepsis
Hemorrhage
Cardiovascular events
Adjuvant chemotherapy and radiotherapy
Gemcitabine
Standard chemotherapeutic agent
Toxic when given with radiotherapy
Given weekly for 6 months after 5fu and
radiotherapy
Neoadjuvant Treatment
Decrease the tumor size before surgery
Increase rate of resectabilty

ERCP
Pancreatic CA has a fairly characteristic appearance on
ERCP, with pancreatic ductal obstruction, often combined
with bile duct obstruction

12

Pancreatic Carcinoma

Metal wall stent in CBD of patient with Pancreatic CA

Choledochojejunostomy

ZOLLINGER ELLISON SYNDROME

Gastrin producing tumor of the pancreas
Male > females (6:4); 3rd 4th decades
70-90%- are in the Passaro triangle
80%-are malignant
Slow growing tumors and compatible w/ long survival even
if malignant
Zollinger Ellison Triad
Atypically located peptic ulcers
Extreme gastric hypersecretion
Non-beta pancreatic islet cell tumor
25% are associated w/ MEN-1- they are multiple and benign
Sporadic gastrinomas- they are single and malignant; not
associated w/ MEN-1
Critera of malignancy
Blood vessel invasion
+ for metastatic disease

Signs and Symptoms

1. Acid peptic disease perforation, hemorrhage, obstruction,
internal fistulization, and intractability
2. Distressing watery diarrhea of 2 8 liters of liquid stool daily
3. Steatorrhea
Inactivation of pancreatic, and intestinal lipase by
abnormal acid environment of the upper intestine
Precipitation of bile salts
Irritative and inflammatory action of the acid upon
mucosa of the small bowel
Gastrojejunostomy

Gastrinoma
Diagnosis:
Serum gastrin > 200pg/ml
Basal acid output> 15mmol/hr
Secretin provocative test-if gastrin is not markedly
elevated.+ if >200pg/ml than the basal level
Octreotide scintigraphy-test of choice for localizing
gastrinoma.
EUS + Octreotide scintigraphy-90% success rate in
localizing gastrinomas
Treatment
Surgical
Pancreatic resection-solitary gastrinoma w/o mets
If w/ MEN 1 syndrome
Total parathyroidectomy
If located in the duodenum
Full thickness excision
On the pancreas w/o involvement of the ducts
enucleation
For inoperable malignant gastrinoma
Chemotherapy
Streptozocin
Doxouribicin
5 FU
Unresectable or Gastrinoma cannot be localized
Proton pump inhibitor
Highly Selective Vagotomy

13

HYPERINSULINISM
Insulinomas
Arise from Beta cells
Most common islet cell neoplasm
90% are solitary and benign
10%-malignant
<5% are associated with MEN 1
Mmultiple-they have high recurrence rate
Symptoms
Related to cerebral glucose deprivation
Bizarre behavior
Tremors
Syncope
Seizures
Whipples triad
Fasting hypoglycemia(bld glucose <50mg/dl
Hyperinsulinemia (>20uU/ml)
Relief of symptoms by intravenous glucose
Diagnosis
Fasting hypoglycemia
Hyperinsulinemia (> 20uU/ml)
Insulin/glucose ratio ->0.3
Imaging
EUS- 90% success rate in localizing the tumor
CT scan
Treatment
Most are treated by enucleation
Distal pancreatectomy or whipples
Large tumors ( >2cm)
Close to the main pancreatic duct
Tumor cannot be localized
Medical tx
Diazoxde-inhibits insulin release
Frequent feedings w/ slowly absorbed CHO
Serous Cystadenoma
Benign tumor w/o malignant potential
Commonly seen in elderly female
Spongy w/ multiple small cyst

can be observed safely if patient is asymptomatic

(-) stain for mucin
Low CEA (<200ng/mL

Mucinous Cystadenoma
Benign but w/ malignant potential
Common in elderly female
Most are located in the body and tail
Ovarian stroma-key path feature
+ stain for mucin
Almost all will evolve into CA if untreated

SPLEEN
Anatomy
Adult spleen weighs between 100 to 250 grams. 7-11cmlength
It is located in the left upper quadrant and protected by the
lower portion of the rib cage
Its position is maintained by several ligaments:
Splenophrenic
Splenorenal
Splenocolic
Gastrosplenic (contains the short gastric vessels)
It is supplied by the Splenic Artery (branch of the celiac
artery); venous drainage course through the splenic vein
Accessory spleens have been reported in 14 to 30 % of
patients usually seen at the hilum of the spleen, gastrosplenic,
splenocolic, gastrocolic, splenorenal ligaments and greater
omentum
Splenosis
Autotransplantation of splenenic fragments after trauma
Capable of performing some reticuloendothelial
function
The pulp is consist of three (3) zones:
Red pulp: 75% of total volume. Comprised of venous
sinuses.Separated
by
reticulum.Contains
macrophages.Serves as filter, removes microrganisms,
cellular debris,antigen-antibody complexes and old
erythrocytes
White pulp-consists of lymphoid follicles
Periarticular lymphatic sheath-T-lymphocytes
B-lymphocytes-lymphoid follicles
Serves the immunologic function of the spleen

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Marginal zone It contains sequestered foreign

materials and plasma as well as abnormal cellular
elements

Accessory Spleen
The accessory spleens seen here at the hilum of the normalsized spleen are not uncommon and by themselves have no
significance

Spleen
Open circulation - (90%)
Blood goes first to reticular space and cords
Comes in contact with macrophages
Closed circulation-(10%)
Goes directly to the arteriovenous anastomosis

Physiologic Functions of the Spleen

Filtering Functions
Splenic blood flow is approximately 350 L/day
Removal of abnormal red blood cells-Howell-jolly
bodies,Heinz
bodies,
Pappenheimer
bodies.
Approximately 20 ml of aged RBC are removed during
the course of the day
Removal of abnormal white cells, normal and abnormal
platelets and cellular debris
It can clear organisms contained w/in the erythrocytes(
malaria & Bartonella)
Can clear unopsonized bacteria and microrganisms for
w/c the body has no anti-bodies

Host Defense
Opsonins makes organism attractive to phagocytes
Tuftsin enhances the phagocytic activity of
leukocytes
Properdin stimulates the alternative pathway of
complement fixation
Circulating monocytes are converted to fixed
macrophages at the red pulp
Produces immunoglobulin (IgM) and IgG
Release opsonic antibodies from the white pulp

Functions of the Spleen

Storage- 30% of platelets are stored in the spleen
Cytopoeisis
Contributes to the process of RBC maturation
Minor role in hematopoeisis in the 4th mo.
Can be reactivated in childhood if the bone marrow
fails to meet the hematologic need.
Myeloid metaplasia-abnormal RBC are produced
Diagnostic
1. Evaluation of size

Physical Examination
Normally not palpable
Felt in about 2 % of healthy adults
No significant dullness elicited by percussion over
spleen either anteriorly or laterally
As organ enlarges, dullness is detected at the level
of the 9th ICS in the left anterior axillary line

MRI depicts the spleen and define abnormalities in

size, shape and parenchymal pathology, e.g. cyst, abscess
or tumor

Ultrasound

CT scan

Plain Radiography

Angiography
Localization and treatment of hemorrhage in
trauma cases
Alternative or adjunct in the treatment of
hematologic disorders (SAE)
Deliver y of therapies in patients with cirrhosis

Nuclear imaging
Tc 99 sulfur colloid
Demonstrates the location and size
Helpful in localizing accessory spleen after
unsuccessful splenectomy for ITP

15

Splenic index
Express the volume of spleen in ml.
Determined by multiplying the spleens length,
width and height
Normal SI 120ml-480ml
2. Evaluation of Function

Functional abnormality of hypersplenism is manifested

by reduction in number of RBC, neutrophils, platelets in
the peripheral blood

Increase in the rate of red cell destruction will always

result in compensatory rise in the rate of production
unless disease in bone marrow coexists the hallmark of
reticulocytosis in the absence of blood loss

Splenectomy

Kehrs sign at the tip of the shoulder indicative of

diaphragmatic irritation
Balances sign (mass or fixed dullness at the left quadrant
secondary to subcapsular hematoma)

Diagnostic Studies
CBC serial Hct determination; WBC count frequently
greater than 15,000/ml3
X-ray of the abdomen fractured ribs should arouse
suspicion of injury to the spleen; more specific findings:
o Elevated immobile diaphragm
o Enlarged splenic shadow
o Medial displacement of gastric shadow
o Widening of space between splenic flexures and
preperitoneal fat
CT scan
Angiography
Delayed Rupture

A, preoperative; B, postoperative
RUPTURE OF SPLEEN

American Association for the Surgery of Trauma Organ

Injury: Scale for the Spleen

Etiology:
Splenic injuries in which there is disruption of the organs
parenchyma, capsule and blood supply
Tranasabdominal or transthoracic penetrating trauma
Non-penetrating trauma spleen is the most frequently
injured organ following blunt abdominal trauma or
lower thoracic cage trauma
Operative trauma 2 % of patients whose operation
involved the viscera in the left upper quadrant of the
abdomen
Spontaneous rupture most often caused by malaria
and infectious mononucleosis
Clinical Manifestations:
Signs and symptoms vary according severity and rapidity of
infra-abdominal hemorrhage and the interval between injury
and examinations
Hypovolemia and tachycardia
Slight reduction in blood pressure
Generalized abdominal pain while of patients complain of
localized left upper quadrant pain

Splenic Injuries
Indications for early laparotomy
Need for transfusion within 24 hrs
Hemodynamic instability
Surgical management of splenic injunry
Splenorraphy
Partial splenectomy
Splenectomy

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Indication for Splenectomy

Hilar injuries
Pulverized splenic parenchyma
Grade 2 injury or higher
Multiple injuries
Coagulopathy
Complication of splenectomy/splenorrhapy
Post operative hemorrhage
Loosening of tie
Improperly ligated or unrecognized short gastric
A
Subphrenic abcess/ sepsis
WBC ct > 15,000/mm
Platelet/WBC ratio of < 20

Usually arises in the middle to distal portion

Mortality is higher in pt w/ portal hpn
Indication for treatment
Presence of symptoms
Pregnancy
Intention to become pregnant
Psuedoaneurysm associated with inflammatory process
Treatment
Resection or ligation
Concomitant splenectomy
Splenic artery embolization

Hereditary Spherocytosis

Splenic Injury

Autologous Splenic Transplantation

Splenic Artery Aneurysm

Splenic Artery Aneurysm

Third most common after aorta and iliac arteries
Most common visceral artery aneurysms
More common in females

Red Blood Cell Disorders
Hereditary spherocytosis
Deficiency in one of the membrane proteins
(spectrin,ankyrin,band3 protein, protein 4.2)
Spherical less deformable shape, they sequestered and
destroyed in the spleen
The
most common of hemolytic anemia which
splenectomy is the primary treatment
In children-delayed until ages of 4-6 years
Congenital Hemolytic Anemia
Red Cell enzyme deficiency
Glucose 6 phosphate deficiency
Enzyme needed to maintain the ratio of reduced
to oxidized glutathione protecting it from
oxidative damage
Pyruvate Kinase deficiency
Most common congenital hemolytic anemia
Enzyme needed for glycolysis
Hemoglobinopthies
Thalassemia
Reduced or absent production of hemoglobin chains
Alpha chains-needed for the production of fetal and
adult Hgb
Beta chains-involved in adult Hgb synthesis
Hypochromia and microcytosis
Unbalanced alpha and b subunits
Cannot release oxygen

17

Precipitate with cell aging

Thalassemia major (homozygous)
Reduction of alpha chain-manifestation is in utero
Reduction of beta chain-symptomatic at 4-6 mo
Hypochromic and microcytic anemia
Nucleated RBC
Clinical manifestations
Pallor
Jaundice
Growth reatrdation
Abdominal enlargement
Leg ulceration
Thalassemia major
Most die in the second decade due to hemosiderosis
Treatment
Blood tranfusion
Maintain Hgb- >9 mg/dL
Iron chelation therapy (deferoxamine)
Splenectomy-high risk of pulmonary hpn
Excessive tranfusion
> 200ml/kg per year
Discomfort

Sickle Cell Anemia

Sickle cell anemia
Mutant B chains (adenine to thymine) of hemoglobinHbS
Reduced oxygen tension-HbS undergoes crystallization
and sickling of RBC
Increased viscosity
Microvascular stasis
Thrombosis
Ischemia
Tissue necrosis
Indications for splenectomy
Splenic abcess
Hypersplenism
Recurrent acute sequestration-most common
indication
Painful intermittent episodes

Platelet Disorder
Idiopathic thrombocytopenic purpura
Premature removal of platelets opsonized by
antiplatelet IgG autoantibodies produced by the spleen
Children-70-80%-spontaneous remission
30,000-50,000/cu.mm-easy bruising
10,000-30,000/cu.mm-spontaneous petechiae and
eccymosis
<10,000/cu.mm-internal bleeding
Medical Tx
Prednisone 1mg/kg
Effective in 75% of pt (1-3 weeks)
Goal: platelet ct of > 100,000 /cu mm
Initiated when fall to <20,000-30,000/cu
mm
Only 15%-25% achieve a lasting response
IV IgG
Given when platelet ct remains low after
steroid tx
Given for 2 days
Splenectomy
Provides prompt and permanent response
1week
Failure of medical tx
Platelet count below 10,000/ cu mm
after 8 weeks of therapy
Prolonged use of steroids w/ undesirable
effects (> 10-20mg/d for 3-6 months to
maintain platelet ct of >30,000/cu.mm
Provides permanent response (75-85%) in 1
week
Portal Hypertension
One of the most common findings with portal hypertension is
splenomegaly, as seen here. The spleen is enlarged from the
normal 300 grams or less to between 500 and 1000 gm.

Portal hypertension secondary to splenic vein thrombosis

Splenectomy is curable in patients with isolated
bleeding gastric varices and normal liver function test

Splenic Cyst
True cyst- lined by squamous epithelium
Primary true cyst
Small (<8cm) asymptomatic. Can be observed.
>8cm
w/
symptoms-partial
splenectomy,unroofing

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Parasitic cyst
Secondary to Echinococcus
Tx. by splenectomy after sterilization by NaCL or
silver nitrate
Pseudocyst
Secondary to trauma
Most are small (<4cm) and undergo spontaneous
resolution
Can be observed safely

Hodgkins Disease

Splenic Abcess
Hematogenous spread-most common cause
Most are solitary and unilocular
Treatment:
Solitary and unilocular--image guided percutaneaous
drainge+antibiotics
Multilocular---splenectomy+ antibiotics
Hodgkin's disease, liver involvement

Sarcoidosis
Non-caseating inflammatory granulomatous lesion
Second organ most commonly affected
Indications for splenectomy
Massive splenomegaly (>1kg)
Thrombocytopenia
Anemia
Compression of adjacent organ
pain

Splenic Tumor
Hemangiomas
Angiosarcoma
Associated with exposure to vinyl chloride or thorium
dioxide

5 cm lymph node (obviously from a patient with

lymphadenopathy).
The node should normally be soft & pink and less than1 cm in size.
This lymph node is involved with Hodgkin's disease
Non-hodgkins Lymphoma

Splenectomy Outcome
Appearance of Howell-Jolly bodies
Increased in platelet count
Increase in WBC count
Consider sepsis if
WBC ct > 15,000/cu.mm after 5 days
Platelet/WBC ratio of < 20
Pulmonary: left lobe atelectasis-the most common
complication

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Thromboembolic phenomena- esp those w / hemolytic

dsordrs, myeloprolifertive , splenomegaly-portal vein
thrombosis
Overwhelming postsplectomy infection:
More common if splenectomy is done for
hematologic problem
Strep. Pneumoniae-most common org.(50-90%)
Most occur 2 years after splenectomy
Children <5 years and adults >50years old

Preventive Measures Against OPSI

Elective splenectomy in children should postponed if
possible until child is 4-10 years old
Role of vaccination:
Must be vaccinated against Strep pneumonia
Type b H. Influenza, meningococcus
Elective splenectomy-2 -4weeks before surgery
Emergency splenectomy-should be given ASAP or
w/in 7-10 days after
Annual vaccination
Role of antibiotics
Daily dose of antibiotics until 5 years old
Or daily dose of antibiotics 5 years after splenectomy

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