Pancreatitis

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 EnzymesEnzyme Substrate ProductCarbohydrate

Amylase (active) Starch; glycogen Glucose, maltose, maltotriose,

dextrins

Protein

Endopeptidases Cleave bonds between amino acids Amino acids, dipeptides

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 2-Monoglycerides fatty acids

Phospholipase A2 (inactive)

Phospholipase A2 (active)

Phospholipase

Cholesterol esterase Neutral lipids

Pancreatic Islet Peptide ProductsHormones 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 80-

90% 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

RANSON’S CRITERIA:

5 clinical data first 24 hours

Admission Biliary

Pancreatitis

Non-biliary

Pancreatitis

Age >70 >55

WBC (mm3) >18,000 >16,000

Serum glucose

(mg/dl)

>220 >200

Serum LDH (u/L) >400 >350

Serum AST (u/L) >250 >250

RANSON’S CRITERIA:

6 clinical data 2nd 24 hours

Within 48 hours Biliary

Pancreatitis

Non-biliary

Pancreatitis

Hematocrit Fall (%) >10 >10

BUN rise (mg/dl) >2 >5

Serum Ca + (mg/dl) <8 <8

PaO2 (mmHg) <60 <60

Base deficit (mEq/L) >5 >4

Fluid sequestration

(L)

>4 >6

RANSON’S 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

4 3 2 1 0 1 2 3 4Temperature in Celcius <30 30-31.9 32-33.9 34-35.9 36-38.4 38.5-38.9 39-40.9 >40.9

Mean Arterial Pressure <50 50-69 70-109 110-129 130-159 >159

Heart Rate <40 40-54 55-69 70-109 110-139 140-179 >179

Respiratory Rate (px + ventilator) <6 6.0-9.0 10.0-11.0 12.0-24 25-34 35-49 >49

a. FIO2 > 0.5 record A-aDO2 <200 200-349 350-499 >500

b. FIO2< 0.5 record only PO2 <55 55-60 61-70 >70

Arterial pH 7.15 7.15-7.24 7.25-7.32 7.33-7.49 7.5-7.59 7.6-7.69 >7.69

Serum Sodium (mmol/L) <111 111-119 120-129 130-149 150-154 155-159 160-179 >179

Serum Potassium (mmol/L) <2.5 2.5-2.9 3.0-3.4 3.5-5.4 5.5-5.9 6.0-6.9 >6.9

Serum Creatinine (mmol/L) <53 53-129 130-169 170-304 >305

Hemoglobin (g/L) <67 67-99 100-153 154-166 167-200 >200

White Blood Count (total/mm3) <1 1-2.9 3-14.9 15-19.9 20-39.9 >39.9

Glasgow Coma Score (GCS)

Acute Physiology Score (APS)

Actual Points = 15 - GCS = (use best GCS for post-op/sedated patients)

Total points from 12 variables above =

Physiological Variable

Use the worst physiological values within first 24 hours of ICU Care

The APACHE II SCORE SHEET:

low abnormal range high abnormal range

Oxygenation

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

Acute Renal Failure: score 2x

APACHE II SCORE

Chronic Health Score = Score:

0 No organ insufficiency

2 Organ insufficiency + elective post-op

5 Organ insufficiency + emergency post-op

Non-operative organ treatment

CVS

RENAL

IMMUNOCOMPROMISED

Shortness of breath or angina on minimal activities

1. Cirrhosis

2. Past hepatic encephalopathy or variceal bleeding

Dialysis/ESRD

1. Due to treatment: recent chemotherapy, radiation, high dose steroids

2. Due to disease: e.g. leukemia, lymphoma, AIDS

Definition of organ insufficiencyAs defined below AND occurred prior to ICU admission

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

RESPIRATORY

LIVER

APACHE II SCORE

AGE SCORE =<45 0

45-54 2

55-64 3

65-74 5

>75 6

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

CT GRADING OF ACUTE PANCREATITIS

CT Grade Points Necrosis Points CTSI Morbidity Mortality

A Normal Pancreas 0

B Pancreatic enlargement 1 None 0 1 0-2 4% 0%

C

inflammation of

pancreas &/or

peripancreatic fat 2 <30% 2 4 3-6 35% 6%

D

single peripancreatic

fluid collection 3 30% - 50% 4 7 7-10 92% 17%

E

>2 fluid collections &/or

retroperitoneal air 4 >50% 6 10

Grading System and Total Point Calculations for the Computed Tomography Severity Index (CTSI)

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: Ranson’s 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 intra-

operative 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: Ranson’s 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


• 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; 1-

2% major morbidity rate

- Cholangitis occurs in 3-14% of patients


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


• 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


• 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


• 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


• 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)


• 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 re-

operation 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 Sjögren'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


• B. Indirect measurement

– 1. Bentiromide test

– 2. Schilling test

– 3. Fecal fat, chymotrypsin, or elastase concentration

– 4. [14C]-olein absorption


• 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

Chronic

Pancreatitis Diagnostic work-up:

CT

ERCP

MRCP/EUS

Upper endoscopy

Exocrine and endocrine function

Low-fat diet, no alcohol,

pancreatic enzymes, pain

medication regimen

Good response No response

Continue

medical therapyMain pancreatic

duct stricture and

dilatation

No obstruction

Interventional therapeutic

endoscopy

pancreatic sphincterotomy

stone extraction

Pancreatic duct stenting

Continue over 12 months

No responseSurgical

resection

Treatment

algorithm for

chronic

pancreatitis

No pain Recurrent pain Head involvement Tail

No further

treatment

Lateral

pancreaticojejunostomyPancreaticoduode-

nectomy

Frey procedure

Beger procedure

Distal pancreatectomy

Subtotal

pancreatectomy

Treatment failure

Thoracoscopic splanchnicectomy

Total pancreatectomy islet cell autotransplantation

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)

Procedure Pain relief Morbidity Early Mortality

Pancreatic duct stenting 65-94 13-19 0-1

Lateral pancreaticojejunostomy 65-86 6-21 0-1

Pancreaticoduodenectomy 40-100 20-53 0-2

Frey Procedure 75-90 8-22 0-3

Beger Procedure 75-95 8-29 0-1

Distal Pancreatectomy 57-84 32-46 0-1

Thoracoscopic splanchnicectomy 20-85 0-11 0

Treatment Results for Chronic Pancreatitis (%)

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 Puestow-

Gillesby 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 CancerLowenfels 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 1–4 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 6–12 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.

Pancreatitis

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