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Etymologically, the term "pancreas", a modern Latin adaptation of Greek πάγκρεας, [πᾶν ("all", "whole"), and κρέας ("flesh")],originally means sweetbread, although literally meaning all-flesh, presumably because of its fleshy consistency
The most common cause of AP is gallstones (40– 7 0% ) and alcohol. Clinically evident AP occurs in < 5 % of heavy drinkers. Rare Causes Infections (mumps, coxsackievirus, cytomegalovirus, echovirus, parasites) Autoimmune (e.g., Sjögren’s syndrome)
Other symptoms: Nausea, vomiting, and abdominal distention Fever.
The Name Game
Herophilus (335–280 BC) Rufus of Ephesus
I found it! Dude, I named it!!
He defeated the world but Pancreatitis defeated him
Alexander The Great June 10, 323 BC
Incidence in US
Incidence in India-
1.9 per 1,000 patient years
…. And still increasing
Alcohol (acute &chronic both)
ERCP, especially after biliary manometry
Blunt abdominal trauma
Postoperative (abdominal and nonabdominal
Drugs (azathioprine, 6-mercaptopurine,
tetracycline, valproic acid, anti-HIV
Sphincter of Oddi dysfunction
Vascular causes and vasculitis
Connective tissue disorders and thrombotic
thrombocytopenic purpura (TTP)
Phase I: Intra-pancreatic digestive enzymes activation &
acinar cell injury
Phase II: Activation, Chemoattraction, & sequestration of
leucocytes & macrophages
Phase III: Effects of activated proteolytic enzymes and
cytokines, released by the inflammed pancreas, on distant
•Steady and boring
•Epigastric and periumbilical
often radiates to the back
•More intense on supine position,
•May be relieved by sitting with the
trunk flexed and knees drawn up.
Low-grade fever, tachycardia, and hypotension
are fairly common. Shock is not unusual.
Jaundice (due to edema of the head of the pancreas with
compression of the intrapancreatic portion of the common
Erythematous skin nodules due to subcutaneous fat necrosis
Basilar rales, atelectasis, and pleural effusion,
the latter most frequently left sided.
Abdominal tenderness and muscle rigidity.
Bowel sounds are usually diminished or absent.
An enlarged pancreas with walled off necrosis
or a pseudocyst.
Ultra Sound (US)
Little part in the diagnosis of the
Role in biliary pancreatitis
Stones in gallbladder
Common Bile Duct dilation
of the whole pancreas
Abnormal -Non-visualization of a part
of the pancreas
Sensitivity of 90-95%
Specificity – 100%
A dynamic CT scan should be performed in
all (predicted) severe cases between 3 and
10 days after admission
Severity of Acute Pancreatitis
Risk Factors for Severity:
• Age >55 years
• Obesity, BMI >30
• Co-morbid disease
• Altered mental status
Markers of Severity within 24 Hours
SIRS [temperature >38° or <36°C (>100.4° or 96.8°F), Pulse >90,
Tachypnea >24, ↑ WBC >12,000]
• Hemoconcentration (Hct >44%)
• (B) Blood urea nitrogen (BUN) >22 mg%
• (I) Impaired mental status
• (S) SIRS: 2/4 present
• (A) Age >60 years
• (P) Pleural effusion
• Organ Failure
• Cardiovascular: systolic BP <90 mmHg, heart rate >130
• Pulmonary: PaO2 <60 mmHg
• Renal serum creatinine >2.0 mg%
Markers of Severity during Hospitalization
Persistent organ failure
• Pancreatic necrosis
• Hospital-acquired infection
Bedside Index of Severity in Acute Pancreatitis(BISAP)
CT Findings and Grading of Acute Pancreatitis
[CT Severity Index (CTSI)]:
CT severity Index= unenhanced CT score + necrosis score: (maximum = 10; ≥6 = severe disease.)
Grade Findings Score
A Normal pancreas: normal size, sharply defined,
smooth contour, homogeneous enhancement,
retroperitoneal peripancreatic fat without
B Focal or diffuse enlargement of the pancreas,
contour may show irregularity, enhancement
may be inhomogeneous but there is no
C Peripancreatic inflammation with intrinsic pancreatic
D Intrapancreatic or extrapancreatic fluid collections 3
E Two or more large collections or gas in the pancreas
Grading of the disease:
Atlanta criteria (1993) Atlanta Revision (2013)
Mild acute pancreatitis Mild acute pancreatitis
Absence of organ failure Absence of organ failure
Absence of local complications Absence of local complications
Severe acute pancreatitis Moderately severe acute pancreatitis
1. Local complications AND / OR 1. Local complications AND / OR
2. Organ failure 2. Transient organ failure ( < 48hrs)
GI bleeding ( > 500 cc/24hr) Severe acute pancreatitis
Shock – SBP 90 mm Hg Persistent organ failure > 48hrs
PaO 2 60 %
Creatinine 2 mg/dl
80% of cases
<5% of mortality
Recommended (All Pts.)
Admit to general wards
Re-feed when pain
20% of cases
>95% of mortality
Admit to ICU
CT scan on Day 3rd
1. Aggressive hydration, 250 – 500 ml
per hour of isotonic crystalloid. Early
aggressive intravenous hydration is
most beneficial during the first 12 – 24
•Lactated Ringer’s preferred isotonic
crystalloid replacement fluid.
3. Reassessment at frequent intervals
within 6hrs of admission and for the
next 24–48 hrs.
(1) weight loss to ideal weight,
(2) a lipid restricted diet,
(4) avoidance of alcohol and of drugs that can elevate serum triglycerides (i.e.,
estrogens, vitamin A, thiazides, & propranolol),
(5) control of diabetes.
THE ROLE OF ANTIBIOTICS:
1. Extra-pancreatic infection, i.e. cholangitis,
catheter-acquired infections, bacteremia,UTI, RTI, etc.
1. Not recommended for Routine prophylaxis
2. Not recommended in sterile necrosis to prevent
1. Infected necrosis
(i) CT-guided fine-needle aspiration (FNA) Gram stain and culture
(ii) empiric use of antibiotics after obtaining necessary
cultures for infectious agents, without CT FNA.
(iii)antibiotics known to penetrate pancreatic necrosis, such as carbapenems,
quinolones, and metronidazole.
5. Routine administration of antifungal agents along with prophylactic or therapeutic
antibiotics is not recommended.
1. ERCP should be done within 24 h of admission in AP with concurrent acute
2. No early need in gallstone pancreatitis lacking
laboratory or clinical evidence of ongoing biliary
3. In the absence of cholangitis and / or jaundice, MRCP or
EUS rather than diagnostic ERCP should be used to screen
for choledocholithiasis if highly suspected.
4. Pancreatic duct stents and / or post-procedure rectal nonsteroidal
anti-infl ammatory drug (NSAID) suppositories should be utilized to lower the risk
of severe post-ERCP pancreatitis in high-risk patients.
Roll of ERCP:
THE ROLE OF SURGERY:
1. Gallstone pancreatitis -cholecystectomy before discharge to prevent
recurrence of AP.
2. In necrotizing biliary AP, cholecystectomy is to be deferred until active
inflammation subsides and fluid collections resolve or stabilize.
3. No active interventions are required in Asymptomatic pseudocysts and
pancreatic and/or extra-pancreatic necrosis.
4. In stable patients with infected necrosis, drainage should be delayed
preferably for >4 weeks to allow liquefication &walled-off necrosis.
5. Minimally invasive methods of necrosectomy are preferred to open
necrosectomy in symptomatic infected necrosis.
1. In mild AP
Oral feedings can be started immediately if there is no
nausea/vomiting & abdominal pain has resolved.
Initiate feeding with a low-fat solid diet.
3. In severe AP,
Enteral nutrition is recommended
Parenteral nutrition should be avoided, unless the enteral route
is not available, not tolerated, or not meeting caloric
4. Nasogastric and nasojejunal delivery of enteral feeding appear
comparable in efficacy and safety.
Complications of Acute Pancreatitis:
Pancreatic fluid collections
Main pancreatic duct
Involvement of contiguous
organs by necrotizing
Thrombosis of blood vessels
(splenic vein, portal vein)
o Early and accurate diagnosis of acute pancreatitis is crucial.
o Early treatment of acute pancreatitis with aggressive IV fluid
hydration saves lives and is most beneficial in the first 12-24
o Routine prophylactic antibiotic use is not recommended for
acute pancreatitis unless presence of infected necrosis is
established clinically or by FNA.
o Mild acute pancreatitis due to gallstones warrants
cholecystectomy before discharge.
• “Irreversible” damage
• Histological evidence of inflammation,
fibrosis, and destruction of exocrine (acinar)
& endocrine (islet) tissue.
• Can be inferred by clinical evidence of
Exocrine (secretory) and endocrine
• Obvious structural disease on radiography
– Calcifications, multiple beads and strictures
• Pain or steatorrhea not necessary.
Etiology of CP:
Consequences of Chronic Panc:
Chronic Pancreatitis: the Spectrum
Pain may dec
30% 60% 80-90%
Make the Correct Diagnosis
• Chronically elevated amylase/lipase do not
• In early CP, imaging and labs may be
negative or equivocal
• Avoid labelling as CP
• Avoid sick role, pyschosocial-economic
• Much acute relapsing pancreatitis is
actually early chronic pancreatitis
Atrophic pancreas, multiple
calcifications, stones dilated
Markedly dilated pancreatic
duct seen in through the body
MRI/MRCP- dilated pancreatic
duct with multiple filling defects
s/o pancreatic duct calculi.
Pancreatic Function Tests (PFTs):
Indirect (often tubeless)
Dual Label Schilling test
SST (Gold standard
Lundh test (Europe)
Quick and “dirty” PFTs:
Only stage disease, don’t usually pick up early
• Rarely done well
• RIA (I131) >>>> ELISA
• <20pg/dL, correlates well with pancreatic Steatorrhea
• 20-29 Equivocal, often small duct.
• >30 Normal
• In practice values >80 or so are suggestive of AP
• If >150, very specific for AP
– 6 or more droplets
– Only picks up extensive steatorrhea
– Must be on 100g fat diet several days before
– >7grams/24hrs is steatorrhea
– Very nonspecific
– Noncompliance high
Intermediate (100-200) values PROBLEMATIC!
21% of asymptomatic or non-pancreatic control pts.
>60yr had fecal elastase <200, 6% <100:
CCK and SST correl. better with 72 h FF than FE.
False positives if watery stool
<100 correlates well with steatorrhea
“Not affected” by porcine enzymes
Must use monoclonal ELISA
Probably about as good as SST
Recent study by Conwell showed CCK still may be
more sensitive (not true in past)
More cumbersome, takes at least one hour.
Combined EUS plus SST
Better coding for SST
EUS may add something to SST
See pancreatic duct directly and after secretin
Foci, Strands, Lobularity (w/w/o honeycombing)
Hyperechoic duct walls,
Visible side branches, Main PD dilated,Calcific, Cysts
Rosemont (GIE June 2009, Catalano, et al)
(1) hyperechoic foci with shadowing & main pancreatic duct (PD)
(2) lobularity with honeycombing.
Minor criteria: cysts, dilated ducts ≥3.5mm, irregular PD contour,
dilated side branches ≥1mm, hyperechoic duct wall, strands,
nonshadowing hyperechoic foci, and lobularity with
Give subtle changes in absence of clinical
Lots of inter and intraobserver variability
Change in “gain” can have big impact
Lack of gold standard
Diffusion weighted MRI with secretin
C14 bicarbonate breath test
Diffusion weighted (DWI) MRI with
DWI measures sum of random motions of
Lower values or delayed peak in chronic
pancreatitis, especially with secretin
Can also better distinguish AP from CANCER
Small insulinomas being detected.
Measure of tissue stiffness also uses sound
waves to detect reverberations.
But analysis occurs after procedure.
Magnetic Resonance Elastography:
Better known for liver, but also works for
What are we treating?
–Attacks of acute pancreatitis
–Disease flares w/o acute pancreatitis
–Other reasons – Pseudocyst, biliary obstruction, etc.
•Exocrine and endocrine insufficiency
–Gastric outlet obstruction
• Failed endoscopic therapy (usually)
–Use as first line in –
•Pancreatic ductal stones with heavy stone burden, especially in the
body/tail region, usually with pancreatic ductal dilatation and stricture(s)
•Inflammatory mass (typically in pancreatic head)
•Symptomatic pseudocysts (not amenable or after failed
Pain in Chronic Pancreatitis: Surgery
•Total Pancreatectomy with Islet Auto-Transplantation
Chronic Pancreatitis: Surgery
Exocrine and Endocrine Insufficiency:
–Timing with meals
–Clinical history of steatorrhea seen in severe insufficiency
–Fat soluble vitamin deficiencies
– 80,000-100,000Units of lipase per meal
•Endocrine insufficiency (Type 3c Diabetes)
–Often needs Insulin treatment
•Clinical presentation mimics Pancreas cancer
•Pancreatitis, persistent pancreatic mass, scarred or shrunken pancreas,
•Elevation of serum IgG4 levels
•Typical appearance on imaging tests and biopsy
•Patients often have involvement of other organs
•Absence of pancreatic calcification or cysts
•Two forms have been recognized - Type I and II
•Excellent response to steroids
Mayo Clinic criteria:
(1) Diagnostic histology;
(2) Characteristic findings on CT & pancreatography combined
with elevated IgG4 levels; &
(3) Response to glucocorticoid therapy, with improvement in
pancreatic & extrapancreatic manifestations
Initial dose of 40 mg/d for four weeks followed by a
taper of the daily dosage by 5 mg/week based on
monitoring of clinical parameters.
Complications of Chronic Pancreatitis:
Narcotic addiction Gastrointestinal bleeding
Impaired glucose tolerance Jaundice
Gastroparesis Cholangitis and/or biliary cirrhosis
Cobalamin malabsorption Subcutaneous fat necrosis
Nondiabetic retinopathy Bone pain
Effusions with high amylase
•The spectrum of risk factors for CP have broadened
•Treatment of pain in CP needs a multidisciplinary approach
•Cross sectional imaging helps to assess pancreatic morphology and guides
•An initial conservative approach is reasonable in all patients with painful CP
•When appropriate endoscopic therapy/surgery should be considered for pain relief
•Autoimmune Pancreatitis is a unique form of CP with excellent response to steroids
Take Home Points