PANCREATITIS

Anatomy with Arterial Supply

Anatomy with Venous Drainage

Lymphatic Drainage

Nerve Supply

HISTOLOGY
Exocrine pancreas
accounts for about 85% of the pancreatic mass
Pancreatic juice
Acinar cells secrete amylase, proteases, and lipases

Endocrine pancreas 2%
Islet cell types:

alpha cells that secrete glucagon

beta-cells that secrete insulin
delta cells that secrete somatostatin
epsilon cells that secrete ghrelin
PP cells that secrete PP

Acinar cells
Amylase
hydrolyzes starch and glycogen to glucose, maltose,
maltotriose, and dextrins

Proteolytic enzymes
Trypsin, chymotrypsin and elastase
Cleaves bonds between amino acids

Lipases
hydrolyzes triglycerides to 2-monoglyceride and fatty acid

Pancreatic Enzymes
Enzyme

Substrate

Product

Starch; glycogen

Glucose, maltose, maltotriose,

dextrins

Cleave bonds between amino acids

Amino acids, dipeptides

Carbohydrate
Amylase (active)
Protein

Endopeptidases
Trypsinogen (inactive)Trypsin
(active)
Chymotrypsinosin (inactive)
Chymotrypsin (active)
Proelastase (inactive) Elastase
(active)
Exopeptidases

Cleave amino acids from end of

peptide chains

Procarboxy peptidase A&B (inactive)

Carboxypeptidase A&B (active)
Fat
Pancreatic lipase (active)

Triglycerides

Phospholipase A2 (inactive)
Phospholipase A2 (active)

Phospholipase

Cholesterol esterase

Neutral lipids

2-Monoglycerides fatty acids

Pancreatic Islet Peptide Products

Hormones

Islet Cells

Function

Insulin

Beta cells

Decreased gluconeogenesis, glycogenolysis, fatty

acid breakdown, and ketogenesis
Increased glycogenesis, protein synthesis

Glucagon

Alpha cells

Opposite effects of insulin; increased hepatic

glycogenolysis and gluconeogenesis

Somatostatin

Delta cells

Inhibits GI secretion
Inhibits secretion and action of all GI endocrine
peptides
Inhibits cell growth

Pancreatic
polypeptide

PP cells

Inhibits pancreatic exocrine secretion and section

of insulin
Facilitates hepatic effect of insulin

Amylin (IAPP)

Beta cells

Counterregulates insulin secretion and function

Pancreastatin

Beta cells

Decreases insulin and somatostatin release

Increases glucagon release
Decreases pancreatic exocrine secretion

Ghrelin

Epsilon cells

Decreases insulin release and insulin action

ACUTE PANCREATITIS
an inflammatory disease of the pancreas that is
associated with little or no fibrosis of the gland
Initiated by gallstones, alcohol, trauma, and
infections, and, in some cases, it is hereditary

Biliary tract stones and alcoholism account for 8090% of cases

ACUTE PANCREATITIS
1. GALLSTONE PANCREATITIS
Common channel hypothesis by Opie
Incompetent Sphincter of Oddi
Colocalization theory by Steer and Saluja

ACUTE PANCREATITIS
2. ALCOHOL INDUCED
Consumed 100-150g of Ethanol in at least 2 years up
to 10 years
Secretion with blockage spasm of the Spinhcter of
Oddi
Metabolic Toxin to pancreatic acinar cells
Calcium cause multiple obstruction
Increase ductal permeability
Ischemic injury

PATHOPHYSIOLOGY
Inciting event (GB stone passage, alcohol, drug induced)
Changes in acinar cells (Inhibition of digestive enzyme secretion)

Colocalization of lysosomal hydrolase

Enzyme activation and acinar cell injury
Elaboration of proinflammatory factors (nuclear factor Kappa B)
Activator protein I
Stress activated kinase
Mitogen activated protein and kinase
Extracellular signal regulated kinase
Interleukin 2,IL-6, IL-8
Pancreatic injury systemic inflammatory syndrome (SIRS)

CLINICAL DIAGNOSIS
Severe epigastric pain knifing or boring through
Vomiting does not relieve pain
PE: tachycardia, tachypnea, hypotension,
hyperthermia, voluntary and involuntary guarding,
decreased or absent bowel sounds, no palpable
masses
Cullen sign bluish discoloration around the
umbilicus
Grey Turner sign bluish discoloration in the flanks
Hx GB stone or choledocholithiasis

SERUM MARKERS
Amylase rises within 2 hours of disease
peaks within 48 hours ( >1000 IU/L)
remains elevated for 3-5 days
Lipase 3x the upper limit
serum indicator of highest probability of
the disease
ALT
an increase of 3x the upper limit
CRP
can differentiate between mild to
severe pancreatitis; 150mg/L at 48 hours after
onset

IMAGING MODALITY
Ultrasound best way to confirm gallstones,
extrapancreatic ductal dilations, pancreatic edema
and fluid collections
70-80% accuracy; 95% sensitivity
EUS 95% accuracy; 98% sensitivity
CT with contrast can diagnose and exclude other
causes; gold standard for detecting and assessing
the severity
MRI/MRCP does not need ionizing radiation or
nephrotoxic IV contrast agents

Assessment of Severity
Early prognostic signs
Serum markers
CT scan

RANSONS CRITERIA:

5 clinical data first 24 hours

Admission

Age
WBC (mm3)
Serum glucose
(mg/dl)
Serum LDH (u/L)
Serum AST (u/L)

Biliary
Pancreatitis
>70
>18,000
>220

Non-biliary
Pancreatitis
>55
>16,000
>200

>400
>250

>350
>250

RANSONS CRITERIA:
6 clinical data 2nd 24 hours
Within 48 hours

Hematocrit Fall (%)

BUN rise (mg/dl)
Serum Ca + (mg/dl)
PaO2 (mmHg)
Base deficit (mEq/L)
Fluid sequestration
(L)

Biliary
Pancreatitis
>10
>2
<8
<60
>5
>4

Non-biliary
Pancreatitis
>10
>5
<8
<60
>4
>6

RANSONS CRITERIA
Score >3 is consistent with severe pancreatitis
Mortality
0-2 points <1%
3-4 points 15%
More than 6 points 100%

Limitation of the Ranson Scoring It evolves over a

48 hour period of time and is applicable only during
the initial causes of the disease

APACHE
(Acute Physiology, Age, and Chronic Health
Evaluation)
The first attempt to characterize acute severity of
illness in the ICU by predicting the risk of
nonsurvival using data available at the time of ICU
admission was the APACHE system developed by
Knaus and colleagues at George Washington
University.
Measured within the first 24 hours

12 physiological variables; > 8 is severe

APACHE II SCORE
The APACHE II SCORE SHEET:
Physiological Variable

Use the worst physiological values within first 24 hours of ICU Care
low abnormal range
high abnormal range

Temperature in Celcius
Mean Arterial Pressure
Heart Rate
Respiratory Rate (px + ventilator)
Oxygenation
a. FIO2 > 0.5 record A-aDO2
b. FIO2< 0.5 record only PO2
Arterial pH
Serum Sodium (mmol/L)
Serum Potassium (mmol/L)
Serum Creatinine (mmol/L)
Hemoglobin (g/L)
White Blood Count (total/mm3)
Glasgow Coma Score (GCS)
Acute Physiology Score (APS)

<30
<50
<40
<6

30-31.9

36-38.4 38.5-38.9
39-40.9
70-109
110-129 130-159
70-109
110-139 140-179
12.0-24 25-34
35-49

>40.9
>159
>179
>49

AaDO2 = (710 x FIO2)-(PCO2 x 1.25) - PO2 <200

200-349 350-499
<55
55-60
61-70
>70
7.15 7.15-7.24 7.25-7.32
7.33-7.49 7.5-7.59
7.6-7.69
<111
111-119 120-129
130-149 150-154 155-159 160-179
<2.5
2.5-2.9 3.0-3.4 3.5-5.4 5.5-5.9
6.0-6.9
Acute Renal Failure: score 2x
<53
53-129
130-169 170-304
<67
67-99
100-153 154-166 167-200
<1
1-2.9
3-14.9 15-19.9 20-39.9
Actual Points = 15 - GCS = (use best GCS for post-op/sedated patients)
Total points from 12 variables above =

>500

40-54

32-33.9 34-35.9
50-69
55-69
6.0-9.0 10.0-11.0

>7.69
>179
>6.9
>305
>200
>39.9

APACHE II SCORE
Chronic Health Score =
Score:
0
2
5

No organ insufficiency
Organ insufficiency + elective post-op
Organ insufficiency + emergency post-op
Non-operative organ treatment
Definition of organ insufficiency

As defined below AND occurred prior to ICU admission

RESPIRATORY
1. severe COPD or restrictive lung disease i.e. unable to climb stairs/perform household duties
2. Documented chronic hypoxia, hypercapnia, or systolic pulmonary pressure >40
CVS
Shortness of breath or angina on minimal activities
LIVER
1. Cirrhosis
2. Past hepatic encephalopathy or variceal bleeding
RENAL
Dialysis/ESRD
IMMUNOCOMPROMISED 1. Due to treatment: recent chemotherapy, radiation, high dose steroids
2. Due to disease: e.g. leukemia, lymphoma, AIDS

APACHE II SCORE
AGE SCORE =
<45
45-54
55-64
65-74
>75

0
2
3
5
6

APACHE II SCORE =
APS SCORE + CHRONIC HEALTH SCORE + AGE SCORE

CT GRADING OF ACUTE PANCREATITIS

Grading System and Total Point Calculations for the Computed Tomography Severity Index (CTSI)
CT Grade
Points Necrosis Points CTSI
Morbidity Mortality
A
Normal Pancreas
0
B Pancreatic enlargement 1
None
0
1
0-2
4%
0%
inflammation of
pancreas &/or
C
peripancreatic fat
2
<30%
2
4
3-6
35%
6%
single peripancreatic
D
fluid collection
3 30% - 50% 4
7
7-10
92%
17%

>2 fluid collections &/or

retroperitoneal air

>50%

10

Atlanta classification of pancreatitis

1. Necrotizing pancreatitis pancreatitis with
devitalized tissues
A. Infected pancreatic necrosis
B. Non-infected pancreatic necrosis

2. Pancreatic Abscess presence of collection of

infected fluid in the absence of significant necrosis
3. Infected pancreatic pseudocyst

TREATMENT: Mild pancreatitis

Definition: Ransons score <3; APACHE II <8; CTSI
<2; no systemic complications
Treatment is mostly supportive and has the
important aim of resting the pancreas through
restriction of oral food and fluids
Nasogastric suction and H2-blockers
Pain control (buprenorphine, pentazocine, procaine
hydrochloride, meperidine)
Morphine is avoided (cause spasm to Sphnincter of
Oddi)

TREATMENT: Mild pancreatitis

For Gallstone Pancreatitis:
Elective laparoscopic cholecystectomy with intraoperative biliary imaging (cholangiography or
laparoscopic ultrasonography)

97% effective in preventing recurrent episodes

Interval cholecystectomy: approximately 50%
early recurrence rate of acute cholecystitis
Poor candidates: endoscopic sphincterotomy
(94% success rate at 2 years ff-up

TREATMENT: Severe Pancreatitis

Definition: Ransons score >3; APACHE II >8; CTSI
>2; fail to improve in 24 hours
ICU admission
Intravenous antibiotics (metronidazole, imipenem,
and third-generation cephalosporins; Fluconazole )
when there is high evidence of pancreatic necrosis,
preferably following percutaneous aspiration of
peritoneal fluid for culture
Feed with enteral nutrition via nasogastric tube
placed beyond the ligament of Trietz (if no ileus)

Antibiotic of choice:

1st Imipenem gram (-) and anaerobic coverage

2nd Fluoroquinolone (+) metronidazole
Vancomycin for gram (+) coverage
Fluconazole for yeast coverage

TREATMENT: Severe Pancreatitis

For Gallstone Pancreatitis
- Elevated bilirubin, severe and continuous
epigastric pain, spiking fevers, or a bile free
gastric aspirate imply persistent ampullary
obstruction
- Urgent ERC/ES to assess ampullary obstruction

- Absoulte risk reduction of 13% in complication

and 4% in mortality rate; 5-10% failure rate; 12% major morbidity rate
- Cholangitis occurs in 3-14% of patients

TREATMENT: Severe Pancreatitis

The main indication for surgery is sepsis resulting
from infected pancreatic necrosis documented by
image guided FNAB for GS/CS
Operation of choice: Pancreatic debridement with
external drainage + cholecystectomy with IOC
If (+) CBD stones: open CBDE with T-tube placement
In sterile pancreatitis: cholecystectomy delayed at
least 3 weeks, then lap chole is feasible
Large Peripancreatic fluid: wait 6 weeks to allow
maturation, then chole with internal drainage

TREATMENT: Severe Pancreatitis

ERCP with sphincterotomy
Surgery where there is infection and necrosis.
Establish feeding jejunostomy.
HBOT
administration of 100% oxygen at a pressure of 2.5
atmospheres for 90 min twice daily for 5 days has been
shown to improve APACHE II and CTSI grading scores*
*Christophi C. Millar I, Nikfarjam M. Et.al; Hyperbaric oxygen therapy for severe acute pancreatitis.
J Gastroenterol Hepatol. 2007 Nov;22(11):2042-6.

Complications of Acute Pancreatitis

I. Local
A. Pancreatic phlegmon
B. Pancreatic abscess
C. Pancreatic pseudocyst

D. Pancreatic ascites
E. Involvement of adjacent organs, with hemorrhage,
thrombosis, bowel infarction, obstructive jaundice, fistula
formation, or mechanical obstruction

Complications of Acute Pancreatitis

II. Systemic
A. Pulmonary
1. Pneumonia, atelectasis
2. Acute respiratory distress syndrome
3. Pleural effusion

B. Cardiovascular

1. Hypotension
2. Hypovolemia
3. Sudden death
4. Nonspecific ST-T wave changes
5. Pericardial effusion

Complications of Acute Pancreatitis

C. Hematologic
1. Hemoconcentration
2. Disseminated intravascular coagulopathy

D. GI hemorrhage
1. Peptic ulcer
2. Erosive gastritis
3. Portal vein or splenic vein thrombosis with varices

Complications of Acute Pancreatitis

E. Renal
1. Oliguria
2. Azotemia
3. Renal artery/vein thrombosis

F. Metabolic

1. Hyperglycemia
2. Hypocalcemia
3. Hypertriglyceridemia
4. Encephalopathy
5. Sudden blindness (Purtscher's retinopathy)

Complications of Acute Pancreatitis

G. Central nervous system
1. Psychosis
2. Fat emboli
3. Alcohol withdrawal syndrome

H. Fat necrosis
1. Intra-abdominal saponification
2. Subcutaneous tissue necrosis

Complications
Pancreatic necrosis
Rising CRP suggests necrosis confirmed by dynamic CT
Infection occurs in 30%-70% cases of necrosis

Infected Necrosis
aggressive surgical pancreatic debridement
(necrosectomy) involving drain placement and reoperation as required
Open or semi-open management uses repeat laparotomy
or open packing with wound exposed
Closed management uses large bore drainage tubes for
high volume, continuous irrigation after closure

Complications
Acute Fluid Collections
majority will resolve spontaneously and in an otherwise
stable patient they do not require treatment

Pancreatic abscess
collection of pus adjacent to pancreas presenting 2-6
weeks after attack; requires surgery

Acute pseudocyst
Arises 4 weeks after attack
Can rupture or haemorrhage
Requires surgery

Complications
Pancreatic Ascites
when a pseudo-cyst collapses into peritoneal cavity or
major pancreatic duct breaks down and releases
pancreatic juices into peritoneal cavity
Treat with IV feeding plus synthetic somatostatin or
surgical excision of segment of pancreas drained by
broken duct

Prognosis
5% mortality in mild cases, <30% mortality in
severe cases.
Severe cases may be deficient in pancreatic
enzymes for up to 2 years, but only those with
steatorrhoea and weight loss need treatment

CHRONIC PANCREATITIS
incurable, chronic inflammatory condition that is
multifactorial in its etiology, highly variable in its
presentation, and a challenge to treat successfully
Etiology: Alcohol 70%
Idiopathic (including tropical), 20%
Other, 10%
Hereditary
Hyperparathyroidism
Hypertriglyceridemia
Autoimmune pancreatitis
Obstruction
Trauma
Pancreas divisum

Alcohol
risk of disease is present in patients with even a
low or occasional exposure to alcohol (1 to 20 g/d)
heavy drinkers (150 g/d)
Onset: 35 to 40, after 16 to 20 years of heavy
alcohol consumption
Recurrent episodes of acute pancreatitis are
typically followed by chronic symptoms after 4 or 5
years

Alcohol
Multiple hit theory
Multiple episodes of acute pancreatitis cause
progressively more organized inflammatory changes that
ultimately result in chronic inflammation and scarring

acetaldehyde, combined with oxidant injury, result

in local parenchymal injury
Repeated or severe episodes of toxin-induced
injury activate a cascade of cytokines, inducing
pancreatic stellate cells (PSCs) to produce collagen
and cause fibrosis

Alcohol
interfere with the intracellular transport and
discharge of digestive enzymes, and may
contribute to the colocalization of digestive
enzymes and lysosomal hydrolase within acinar
cells, leading to autodigestion
Decrease in Lithostantine a protein found in
pancreatic juice inhibits the formation of calcium
carbonate crystals.

Cigarette smoking
strongly associated with chronic pancreatitis and
with the development of calcific pancreatitis
In hereditary pancreatitis, smoking has been found
to lower the age of onset of carcinoma by about 20
years
definite risk factor for the late complications of
alcoholic pancreatitis, if not an early cofactor

Hyperparathyroidism
Hypercalcemia is a known cause of pancreatic
hypersecretion
stimulant for pancreatic calcium secretion, which
contributes to calculus formation and obstructive
pancreatopathy

Hyperlipidemia
predispose women to chronic pancreatitis when
they receive estrogen replacement therapy
Fasting triglyceride levels less than 300 mg/dl

Classification of Chronic Pancreatitis

Chronic
Calcific
Pancreatitis

Chronic
Obstructive
Pancreatitis

Chronic
Inflammatory
Pancreatitis

Chronic
Autoimmune
Pancreatitis

Asymptomatic
Pancreatic
Fibrosis

Alcohol

Pancreatic
tumors

Unknown

Primary
sclerosing
cholangitis

Chronic alcoholic

Hereditary

Ductal stricture

Sjgren's
syndrome

Endemic in
asymptomatic
residents in
tropical climates

Tropical

Gallstone or
trauma-induced
pancreas divisum

Primary biliary
cirrhosis

Hyperlipidemia
Hypercalcemia
Drug-induced
Idiopathic

Radiologic Imaging

Assists in four areas:

Diagnosis
Evaluation of severity of disease
Detection of Complications
Assistance in determining treatment options

Ultrasonography
Transabdominal
48 -96 % sensitive, operator dependent
Reliable method for periodid re-examination to determine
the efficacy of treatment

Endoscopic
Able to evaluate subtle changes in 2-3mm structures
within the pancreas
Small intraductal lesions, intraductal mucus, cystic
lesions, and subtle ductular abnormalities are
recognizable
More sensitive than ERCP in detecting mild disease

CT scan
Duct dilatation, calculous disease, cystic changes,
inflammatory events, and anomalies are detectable
with a resolution of 3-4 mm
Limitations: lower sensitivity for detecting small
neoplasms and a false-negative rate of <10% for
chronic pancreatitis

ERCP
gold standard for the diagnosis and staging of
chronic pancreatitis
biopsy or brushing for cytology, or the use of stents
to relieve obstruction or drain a pseudocyst
procedure-induced pancreatitis that occurs in
approximately 5% of patients

MRCP
effective screening technique for disclosing ductal
abnormalities that correlates closely with the
contrast-filled ducts imaged by ERCP
Advantages: noninvasive; ability to image
obstructed ducts that are not opacified by ERCP
injection; safest method to image the ductal system
in high-risk patients

Signs and Symptoms

Etiologies of Pain from Chronic Pancreatitis

1. Ductal hypertension, due to strictures or stones
2. Parenchymal disease or retroperitoneal
inflammation with persistent neural involvement
3. Acute increases in duct pressure or recurrent
episodes of acute inflammation in the setting of
chronic parenchymal disease

Tests for Chronic Pancreatitis

I. Measurement of pancreatic products in blood
A. Enzymes
B. Pancreatic polypeptide

II. Measurement of pancreatic exocrine secretion

A. Direct measurements
1. Enzymes
2. Bicarbonate

Tests for Chronic Pancreatitis

B. Indirect measurement

1. Bentiromide test
2. Schilling test
3. Fecal fat, chymotrypsin, or elastase concentration
4. [14C]-olein absorption

Tests for Chronic Pancreatitis

III. Imaging techniques

A. Plain film radiography of abdomen

B. Ultrasonography
C. Computed tomography
D. Endoscopic retrograde cholangiopancreatography
E. Magnetic resonance cholangiopancreatography
F. Endoscopic ultrasonography

Complications of Chronic Pancreatitis

Intrapancreatic complications

Pseudocysts
Duodenal or gastric obstruction
Thrombosis of splenic vein
Abscess
Perforation
Erosion into visceral artery

 Inflammatory mass in head of pancreas

Bile duct stenosis
Portal vein thrombosis
Duodenal obstruction
Duct strictures and/or stones
Ductal hypertension and dilatation
Pancreatic carcinoma
Extrapancreatic complications
Pancreatic duct leak with ascites or fistula
Pseudocyst extension beyond lesser sac into
mediastinum, retroperitoneum, lateral pericolic
spaces, pelvis, or adjacent viscera

Treatment
algorithm for
chronic
pancreatitis

Chronic
Pancreatitis
Low-fat diet, no alcohol,
pancreatic enzymes, pain
medication regimen

Good response

Continue
medical therapy

Diagnostic work-up:
CT
ERCP
MRCP/EUS
Upper endoscopy
Exocrine and endocrine function
No response

Main pancreatic
duct stricture and
dilatation

Interventional therapeutic
endoscopy
pancreatic sphincterotomy
stone extraction
Pancreatic duct stenting
Continue over 12 months

No obstruction

No response

Surgical
resection

No pain

No further
treatment

Recurrent pain

Lateral
pancreaticojejunostomy

Head involvement

Pancreaticoduodenectomy
Frey procedure
Beger procedure

Treatment failure

Thoracoscopic splanchnicectomy
Total pancreatectomy islet cell autotransplantation

Tail

Distal pancreatectomy
Subtotal
pancreatectomy

Treatment
Medical
Analgesics, such as Gabapentin
cessation of alcohol use results in 60-70% pain
reduction
oral enzyme therapy (Viokase, Ku-Zyme HP,
Ccreon, Pancrease)
selective use of antisecretory therapy
Octreotide acetate 200 microgram
subcutaneously TID (65% pxs were relieved)

Treatment
Neurolytic Therapy
Celiac plexus neurolysis with alcohol injection
EUS guided celiac plexus blockade revealed
successful relief in 55% of patients; lasted 6
months in 10%

Endoscopic Management
Pancreatic duct stenting

Treatment
Surgical therapy
should be considered only when the medical therapy of
symptoms has failed
Nealon and Thompson published a landmark study in
1993, however, that showed that the progression of
chronic obstructive pancreatitis could be delayed or
prevented by pancreatic duct decompression

Treatment
choice of operation and the timing of surgery are
based:
patient's pancreatic anatomy
Likelihood that further medical and endoscopic therapy
will halt the symptoms of the disease
chance that a good result will be obtained with the lowest
risk of morbidity and mortality

Sphincteroplasty

DRAINAGE PROCEDURE:
Duval procedure

DRAINAGE PROCEDURE:
Puestow procedure

DRAINAGE PROCEDURE:
Partington and Rochelle (Modified Peustow)

DRAINAGE PROCEDURE:
Frey procedure

RESECTION PROCEDURES:
Distal pancreatectomy

95% Distal pancreatectomy

(1965: Fry and Child)
intended for patients with sclerotic (small duct)
disease
Preserves the rim of pancreas in the
pancreaticoduodenal groove, along with its
associated blood vessels and distal common bile
duct
Pain relief: 60-77%
high risk of brittle diabetes, hypoglycemic coma,
and malnutrition

Whipple procedure

Total pancreatectomy
produces no better pain relief for their patients than
pancreaticoduodenectomy
brittle form of diabetes

Duodenum preserving Pancreatic Head

Resection (DPHR)

Hamburg Modification

Organ-preserving pancreatic head resection

(OPPHR)

Treatment Results for Chronic Pancreatitis (%)

Procedure
Pancreatic duct stenting
Lateral pancreaticojejunostomy
Pancreaticoduodenectomy
Frey Procedure
Beger Procedure
Distal Pancreatectomy
Thoracoscopic splanchnicectomy

Pain relief
65-94
65-86
40-100
75-90
75-95
57-84
20-85

Morbidity
13-19
6-21
20-53
8-22
8-29
32-46
0-11

Early Mortality
0-1
0-1
0-2
0-3
0-1
0-1
0

INDICATIONS FOR SURGERY IN CHRONIC

PANCREATITIS
1. Chronic abdominal pain unresponsive to
nonsurgical therapies
2. Suspicion of pancreatic cancer
3. Persistent common bile duct obstruction
unresponsive to endoscopic therapy
4. Duodenal obstruction
5. Splenic vein thrombosis with bleeding gastric
varices
6. Symptomatic or enlarging pancreatic pseudocyst
7. Persistent pancreatic ascites or fistula

SURGICAL PROCEDURES FOR TREATING

PAIN IN CHRONIC PANCREATITIS
1. Duct drainage procedures
2. Lateral Roux-en-Y pancreaticojejunostomy
(Partington-Rochelle modification of PuestowGillesby procedure)
3. Combined resection-drainage procedures
4. Pancreaticoduodenectomy (Classic Whipple or
pylorus preserving)
5. Local resection of the head of the pancreas
combined with longitudinal pancreaticojejunostomy
(Frey Procedure)

SURGICAL PROCEDURES FOR TREATING

PAIN IN CHRONIC PANCREATITIS
6. Duodenum-preserving pancreatic head resection
(Beger Procedure)
7. Resection procedures
8. Total pancreatectomy with or without islet cell
autotransplantation
9. Distal pancreatectomy
10. Subtotal pancreatectomy/ (Duodenum preserving
pancreatic surgery?)
11. Neuroablative procedures
12. Thoracoscopic splanchnicectomy

Pancreatitis and the Risk of

Pancreatic Cancer
Lowenfels AB, Maisonneuve P, Cavallini G, et al; The International
Pancreatitis Study Group; New England Journal of Medicine 20:1433,
1993

* A large retrospective cohort studies of patients with

Pancreatitis have revealed the cumulative risk of
pancreatic cancer in subjects who were followed up at
10 & 20 years after the diagnosis of pancreatitis, it
was 1.8

% (95 percent confidence interval, 1.0 to 2.6

percent) and 4.0% (95 percent confidence interval,
2.0 to 5.9 percent), respectively.

Journal
Transluminal endoscopic necrosectomy after
acute pancreatitis: a multicentre study with
long-term follow-up (the GEPARD Study)
Seifert et al
Data for all patients undergoing transluminal endoscopic
removal of (peri)pancreatic necroses between 1999 and
2005 in six different centres were collected
retrospectively, and the patients were followed up
prospectively until 2008

METHODS
Creation of a transgastric or transduodenal access
to the retroperitoneal cavity using endoscopic or
endosonographic guidance, followed by insertion of
two or more stents and in some cases nasocystic
irrigation catheters

 balloon dilation (maximal diameter 15 or 20 mm)

was carried out to permit the introduction of a
conventional gastroscope to allow forceful irrigation
and suction, as well as active endoscopic removal
of debris using snares, forceps, and stone removal
baskets.
Repeated sessions at intervals of 14 days were
carried out until all debris and necrotic material had
been removed and the walls of the collections could
be seen as vital structures

 stent drainage of the emptied cavity was carried out

for 612 weeks and checked using external
imaging (ultrasound or CT).

RESULTS
Ninety-three patients (63 men, 30 women; mean
age 57 years) underwent a mean of six interventions
starting at a mean of 43 days after an attack of
severe acute pancreatitis
After establishment of transluminal access to the
necrotic cavity and subsequent endoscopic
necrosectomy, initial clinical success was obtained
in 80% of the patients, with a 26% complication and
a 7.5% mortality rate at 30 days. After a mean
follow-up period of 43 months, 84% of the initially
successfully treated patients had sustained clinical
improvement, with 10% receiving further endoscopic
and 4% receiving surgical treatment for recurrent
cavities; 16% suffered recurrent pancreatitis.

Journal
Severe acute pancreatitis: role for laparoscopic
surgery
Pavars M, Irmejs A, Maurins U, Gardovskis J.
Zentralbl Chir. 2003 Oct;128(10):858-61.

Methods
65 patients complied with Atlanta
recommendations for SAP
presented with intraabdominal or retroperitoneal
exudates and detected by ultrasound (US)
and/or contrast enhanced computer tomography
(CT) scan, and the presence of acute calculous
cholecystitis when 3 to 5 days of conservative
treatment did not show clinical improvement and
surgical treatment was considered

Results
39 patients were operated and 26 were treated
conservatively
Laparoscopic surgery was started in 31 patients
and completed in 26 patients.
The overall conversion rate was 16.1 %

 Laparoscopic drainage of the intraabdominal

exudate was done in 26 patients including drainage
of the lesser sac in five of them.
Laparoscopic cholecystectomy in 25 cases and
laparoscopically assisted jejunostomy in 6 cases
were performed as a part of the procedure.

 Conventional surgery was the primary procedure in

8 patients. Peripancreatic abscess formation was
observed in one case one month after laparoscopic
procedure and was cured with conventional
surgical drainage. Bile leakage from the cystic
stump was successfully treated with endoscopic
papillotomy in one case. All patients survived after
laparoscopic procedures. Overall complication rate
was 7.7 % and mortality reached 3.1 %

Conclusion
Laparoscopic drainage of the abdominal cavity,
drainage of the lesser sac and revision of the
retroperitoneal compartment can be safely carried
out as an alternative to the conventional surgical
approach. Laparoscopic cholecystectomy and/or
jejunostomy may be additionally performed if
indicated.

Thank you.