SURGERY BLOCK 4

 Due to the increase pancreatic work  increase

I L OI L O D O CT O RS ’ C O L L E GE O F M E DI C I NE
Molo, Iloilo City
enzyme secretion  digestion of food and
S.Y. 2018-2019 autodigestion of the pancreas itself initial insult
 Iatrogenic
BATCH 2021
DISCIMUS SAPIENCIA UT VIRTUS
 Pancreatic Duct Obstruction
o Gall stone tends to impede the opening
of the pancreatic enzymes  auto
SURGERY digestion
o Inflammatory reaction  inflammatory
BLOCK 4
cascade
L E CT U RE R: DR. T RES PE CE S  Hypercalcemic State
MAIN TOPIC: PANCREAS  Hyperlipidemia
 Hereditary
 Protein Deficiency
ANATOMY  Trauma
 Drugs
 Located Retroperitoneal
 Sometimes adheres with the spinal column PATHOPHYDIOLOGY
 The head is located in the C-Loop of the
duodenum
 Closely related to the 2nd portion of the
duodenum; where the opening of the
ampulla of vater and CBD is located
 At the superior border of the pancreas isthe
SMV (+ splenic vein = PV)
 The portal vein opens to the neck of the

FUNCTION
Exocrine
 Cholecystokinin + vagal cholinergic stimulation
à
 Digestive enzymes (proteases,lipases, amylase)
Endocrine
 Insulin, glucagon, somatostatin, pancreatic
polypeptide

DISEASES OF PANCREAS
Pancreatitis
- Most common medical problem of the Pancreas
SIGNS AND SYMPTOMS

ACUTE PANCREATITIS Types of pain in pancreatitis

 Boring / STEADY PAIN / localized pain - pancreas
Biliary Tract Disease  Colicky - On/Off pain and felt in - the gallbladder
 Gall stone – most common cause and ureters
Alcoholic Binge  Cramping – colon and small intestine
 Epigastric Pain
 Back Pain

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 SURGERY BLOCK 4

 Cullen’s Sign d. Arterial PO2 <60 mmHg

- Found in hemorrhagic pancreatitis e. Base Deficit >4 mEq/L
- Bruising in the umbilicus f. Estimated fluid sequestration 6000 Ml
 Grey Turner’s Sign
- Found in hemorrhagic pancreatitis *it estimates mortality of the pt with pancreatitis based on
- Bruising in the flanks initial and 48 – hour lab values
NO – 0 YES +1 = solve
PANCREATIC DUCT OBSTRUCTION • 0-2 = 2% mortality; 3-4 = 15% mortality
• 5-6 = 40% mortality; 7-8 = 100% mortality
DIAGNOSTIC STUDIES
 Serum amylase – most common
GALLSTONE PANCREATITIS
 Urinary amylase – most common
 Serum lipase
 C-reactive protein  Most common cause of acute pancreatitis
 Scout film of the abdomen  Transient obstruction of the pancreatic duct by a
 Ultrasound - most common gallstone in the common bile duct at the ampulla
 CT scan – severity of vater
*most common diagnostic na na gamit dri sa PH  Request an ERCP (Endoscopic Retrograde
Cholangiopancreatography)
DIAGNOSIS REQUIRES T WO OF THE FOLLOWING  Do not operate because of the elevated amylase;
manipulation may increase pancreatic work-up
1. Abdominal pain consistent with acute pancreatitis  Only operate on gall bladder stone removal
(acute onset of persistent, severe, epigastric pain (Cholecystectomy) after the serum amylase had
normalize within a Week
often radiating to the back
2. Serum lipase activity (or amylase activity) at least  Antibiotics is only given when necessary
three times greater than the upper limit of
normal; and CRITERIA FOR ACUTE GALLSTONE PANCREATITIS
3. Characteristic acute findings of acute pancreatitis At admission
on contrast enhanced computed tomography a. Age >70 years
(CECT) and less commonly magnetic resonance b. WBC > 18,000
imaging (MRI) or transabdominal Ultrasonography c. Blood Glucose > 220 mg/dL
*classification of acute pancreatitis – 2012 revision of d. Serum LDH >400 IU/L
Atlanta classification and definitions by international e. Serum AST >250 U/dL
consensus During the initial 48 Hours
a. Hematocrit fall >10 points
RANSON’S PROGNOSTIC CRITERIA FOR ACUTE b. BUN elevation >2 mg/dL
PANCREATITIS c. Serum Ca <8 mg/dL
d. Base deficit >5 mEq/L
e. Estimated fluid sequestration 4000 mL
Present on admission
*it estimates mortality of the pt with pancreatitis based on
a. Age >55 years old
initial and 48 – hour lab values
b. WBC > 16,000
NO – 0 YES +1 = solve
c. Blood Glucose > 200 mg/dL
• 0-2 = 2% mortality; 3-4 = 15% mortality
d. Serum LDH (Lactate Dehydrogenase) 350 I.U/L
• 5-6 = 40% mortality; 7-8 = 100% mortality
e. Serum AST (Aspartate Transferase) >250 I.U/dL

Developed during the first 48 hours

a. Hematocrit falls >10 points
b. BUN increase > 5 mg/dL
c. Serum Ca <8 mg/dL

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TYPES OF ACUTE PANCREATITIS SURGICAL MANAGEMENT (FOR COMPLICATED

PANCREATITIS ONLY)
INTERSTITAL EDEMATOUS
 diffuse (or occasionally localized) enlargement of
the pancreas due to inflammatory edema. Clinical
symptoms may resolve within the first week

NECROTIZING PANCREATITIS
 5-10% of patients develop necrosis of the
pancreatic parenchyma, the peripancreatic tissue
or both natural history of pancreatic and
peripancreatic necrosis is variable because it may
remain solid or liquefy, remain sterile or become
infected, persist, or disappear over time.

INFECTED PANCREATIC NECROSIS

 Presence of infection can be presumed when

there I extraluminal gas in the pancreatic and/or
peripancreatic tissues of CECT or when
percutaneous, image-guided, fine-needle
aspiration (FNA) is positive for bacteria and/or
fungi on Gram stain and culture. There may be a
varying amount of suppuration (pus) associated
with infected pancreatic necrosis, and this
suppuration tends to increase with liquefaction.
 Diagnosis of the infected pancreatic necrosis is
important because of the need for antibiotic
treatment and likely active intervention.
- Pancreatitis is sterile. The patient may be having SIRS.
- Prolonged pancreatitis may be infected by necrosis
MANAGEMENT
MEDICAL TREATMENT
*confirmation- Fine needle aspiration
LOCAL COMPLICATIONS ARE SUSPECTED WHEN
 There is persistence or recurrence of abdominal
pain
 Secondary increases in serum pancreatic enzyme
activity
 Increasing organ dysfunction, and/or the
development of clinical signs of sepsis, such as
fever and leukocytosis
 Acute pancreatic accumulation (Pancreatic
Ascites); Unencapsulated

 Fluid replacement APFC (ACUTE PERIPANCREATIC FLUID

 Pain management COLLECTION)
 Nutritional support (PARENTERAL)
 ERCP
 Interventional Radiology (PTBD  Peripancreatic fluid associated with interstitial
PROCEDURE/ PERCUTANEOUS oedematous pancreatitis with no associated
TRANSHEPATIC BILIARY DRAINAGE) peripancreatic necrosis.
 Antibiotic Lecturer
 This term applies only to areas of peripancreatic
fluid see within the first 4 weeks after onset of
interstitial oedematous pancreatitis and without
the featues of a pseudocyst

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o CECT criteria
 Occurs in the setting of interstitial oedematous
pancretitis
 Homogenous collection with fluid density
 Confined by normal peripancreatic fascial planes
 Undefinable wall encapsulating the collection
Adjacent to pancreas (no intrapancreatic
extension)
PANCREATIC PSEUDOCYST
 Refers to a specifically to a fluid collection in the
peripancreatic tissues (occasionally it may be
partly or wholly intrapancreatic). Surrounded by a
well defined walland contains essentially no solid
material
 Arise from disruption of the main pancreatic duct
or its intra-pancreatic branches without any
recognizable pancretaic parenchymal necrorsis;
this theoury suggests that consequent leakage of
pancreatic juice results in persistent, localised
fluid collection, usually after more than 4 weeks.
 An encapsulated collection of fluid with a well
defined inflammatory wall usually outside the
pancreas with minmal or no necrosis. This entity
usually occurs more than 4 weeks after onset of
interstitial oedematous pancreatitis to mature.
CECT criteria
 Well circumscribed, usually round or oval
 Homogenous fluid density
 No non-liquid component
 Well-defined wall; that is completely
encapsulated
 Maturation usually requires > 4 weeks after onset
of acute pancreatitis; occurs after interstitial
oedematous pancreatitis
PROCEDURE
1. Internal drainage
2. External drainage
INTERNAL DRAINAGE
- Cystogastrostomy – 1 cm thick; to open the stomach
down to the pancreatic pseudocyst wall and suture the
stomach to the pancreas
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SURGERY BLOCK 4
- Cystojejunustomy – when pancreas does not abate to
the stomach; join the pancreas with the jejunum
EXTERNAL DRAINAGE
Thin wall pseudocyst located at posterior wall of stomach
*
ANC (ACUTE NECROTIC COLLECTI ON)
 A collection contatining variable amounts of both
fluid and necrosis associated with necrotising
pancreatitis; the necrosis can involve the
pancreatic parenchyma and/or the peripancretic
tissues
CECT criteria
 Occurs only in the setting of acute necrotizing
pancreatitis
 Heterogenous and nonliquid density of varying
degrees in different locations (some appear
homogenous early in their course)
 No definable wall encapsulating the collection
 Location – intrapancreatic and/or extrapancreatic
*Principles of surgical management of infected pancreatic
necrosis include debridement of all infected necrotic
material and drainage of the remaining pancreatic bed.
Debridement is done bluntly and gently, with hyrdosonic
irrigation frequently used to avoid vascular injury.
WON (WALLED – OFF NECROSIS)
 A mature, encapsulated collection of pancreatic
and/or peripancreatic necrosis that has developed
a well defined inflammatory wall. Usually occurs
>4 weeks after onset of necrotising pancreatitis
CECT criteria
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 SURGERY BLOCK 4

 Heterogenous with liquid and non liquid densisty
with varying degrees of loculations (some may
appear homogenous)
 Well defined wall, that is, completely
encapsulated
 Location – intrapancreati and/or extrapancreatic
 Maturation usually requires 4 weeks after onset
of acute necrotizing pancreatitis
and mortality are greater than those of mild acute
pancreatitis. The even usually does not last more than 2-3
weeks
• Severe – characterized by persistent organ failure >48
hours and locoregional as well as systemic complications.
Patients with severe acute pancreatitis that develops
within the early phase have a higher mortality (36-50%).
Development of infected nerosis carries a grave prognosis.

COMPLICATIONS OF ACU TE PANCREATITIS CHRONIC PANCREATITIS

I. Local  A progressive inflammatory disease of the
II. Systemic / Organ Failure pancreas, characterized by irreversible
a. Pulmonary morphological changes and gradual fibrotic
b. Cardiovascular replacement of the gland
c. Renal  Loss of exocrine and endocrine function results
III. GI hemmorhage from parenchymal fibrosis
IV. Hematologic  The primary symptoms of CP are abdominal pain
V. Metabolic and maldigestion
VI. Central Nervous System  Essential pathologic features include irregular
VII. Fat Necrosis and patchy loss of acinar tissue, chronic
inflammation, ductal changes and fibrosis
MODIFIED MARSHALL SCORING SSYSTEM FOR
ORGAN DYSFUNCTION ETIOLOGY
o Alcohol
o Cigarrete Smoking
o Hyperparathyroidism
o Hyperlipidemia
o Drugs
o Gallstone
o Stricture
o Idiopathic

SYMPTOMATOLOGY

 Abdominal pain
 Weight loss
 Diabetes
 Malabasorption

CLASSIFICATION

• Mild – lacks organ failure; locorgeional as well as  Chronic Calcific (Lithogenic)

 Chronic Obstructive
systemic complications. The episode resolves itself within
 Chronic Inflammatory
a week, mortality is rare and pancreatic imaging is often
 Chronic Autoimmune
not required  Asymptomatic Pancreatic
 Fibrosis
• Moderately Severe – distinguished by the presence of

transient organ failure. Locoregional as well as systemic
complications and/or transient organ failure. Morbidity

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DIAGNOSTIC  It may sometime not drain the head of the

pancreas
o Ultrasound
o Endoscopic Ultrasound 2. Frey Procedure
o ERCP*
o CT Scan

TREATMENT
o Decompressive Procedures
o Neural Ablative Procedures
o Resectional Procedures
o Drainage Procedures

1. Puestow Procedure

 pour out the head of the pancreas

 With a loop of the jejunum that is mobilized and
attached over the exposed pancreatic duct to
allow better drainage

3. Beger Procedure

 Most common
 Incise the pancreas to have a clear view of the
pancreatic ducts; get the tip of the jejunum and
suture it to the ducts to relieve the obstruction

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PANCREATIC CANCER
Head, Body or Tail in Location
Head -Most common
Clinical Manifestations
o Obstructive, painless jaundiceecturer
o Abdominal/ back pain
o Abdominal obstruction
o Weight loss
o Abdominal mass

RISK FACTORS
o >60 years old
o Cigarette smoking
o Diets high in fat and low in fiberfruits and vegetables
o Preexisting type II diabetes
o Genetic (10%)

DIAGNOSTIC PROCEDURE
o Ultrasound
o Endoscopic Ultrasound
o CT scan – tri-phasic contrast
o MRCP / MRI
o ERCP / PTC
o PET scan
o CA 19-9 (tumor marker)
o Pre-op biopsy (+/-)
*Pancreatic Cancer is the fourth leading cause of cancer
death in the United States. While surgical resection
remains the only curative option, more than 80% of
patients present with unresectable disease. Unfortunately,
even among those who undergo resection, the reported
• Removal of the head of the pancreas and attachment of median survival is 15-23 mos. With a 5-year survival of
a part of the jejunum into the removed head of the approximately 20%.
pancreas
4. Pancreatic Resection STAGING
Lecturer
Lecturer o TIS – confined to pancreas
o T1 - </= 2 CM
NEOPLASM OF THE PANCREAS o T2 - >2CM
o T3 beyond no celiac involvement
o T4 with involvement of celiac axis
ADENOCARCINOMA
- Periampullary tumor PROGNOSIS
o Pancreas
o Stage 1 T1-T2 no LN – 20.3% 5 years
o Ampulla of Vater
o Stage 2 T3 with LN – 8.0% 5 years
Best prognosis
o Stage 3 T4
o Duodenum
o Stage 4 any T + M1 – 1.7%
o Bile Duct
o Unstaged – 4.1%

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TREATMENT
o Stenting COMPLICATIONS
o Pancreatic Resection; Distal Pancreatotomy
o Whipple’s Procedure (Pancreaticodudodenectomy) - <5% in high volume centers
o Double by-pass surgery - Sepsis, hemorrhage and CV events most common cause
o Chemotherapy: Gemcitabine of death
 Folfirinox (oxaliplatin 8 mg/m2, irinotecan 180 - Delayed gastric emptying
mg/m2, leucovorin 400 mg/m2, 5-fluorouracil - Pancreatic leak
2400mg/m2) followed by external beam radiation
therapy (50.4 Gy) with capecitabine (825 mg/m2) OTHER TUMORS

CONTRAINDICATING RESECTION 1. Insulinoma

o Liver Metastasis a. most common pancreatic endocrine tumor
o Celiac Lymph Node involvement b. Whipple’s Triad
o Peritoneal implants i. Symptomatic fasting hypoglycemia
o Hepatic Hilar Lymph Node involvement ii. Documented serum glucose level <50 mg/dL
o Involvement of major vessels iii. Relief of symptoms with glucose administration
c. 90% are benign and solitary
FINDINGS NOT CONTRAINDICATING RESECTION d. Treatment
i. Enucleation
o Invasion at duodenum or distal stomach ii. Pancreatectomy
o Peripancreatic lymph nodes
o Lymph nodes along the porta hepatis that can be swept 2. Gastrinoma
down with the specimen a. endocrine tumor that secretes gastrin causing Zollinger-
Ellison syndrome
BORDERLINE RESECTABLE TUMORS b. 70% located in Passaro’s triangle
1. Venous involvement of the SMV/PV demonstrating i. Junction of cystic duct and common duct
tumor abutment, encasement or short segment venous ii. 2nd and 3rd portion of duodenum
occlusion but with suitable vessel proximal and distal to iii. Neck and body of pancreas
the area of vessel involvement allowing for safe resection c. Treatment: pancreatic resection
and reconstruction d. Glucagonoma, VIP secreting tumor, somatostinoma
2. Gastroduodenal artery encasement up to the hepatic
artery and short segment encasement/direct tumor CYSTIC NEOPLASM
abutment of the hepatic artery with no extension to the 1. Serous Cystadenoma
celiac axis a. Low malignant potential
3. Tumor-SMA involvement <180° b. Surgery only for symptomatic patients
2. Mucinous cystic neoplasms
WHIPPLE’SPROCEDURE/PANCREATICODUOODENEC a. Potentially aggressive malignant tumor
TOMY b. Pancreatic resection

“The Pancreas is the most unforgiving organ of the

Human Body. It should always be handled with care and
great expertise.”

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