pancreatitis
DESCRIPTION
internal medicine gastroTRANSCRIPT
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
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
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; 1-
2% 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 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
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
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
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
Total pancreatectomy
• produces no better pain relief for their patients than
pancreaticoduodenectomy
• brittle form of diabetes
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.