3. He defeated the world but Pancreatitis defeated him
Alexander The Great June 10, 323 BC
4. Incidence in US
70 hospitalizations/100,000
persons annually.
Incidence in India-
1.9 per 1,000 patient years
…. And still increasing
Acute Pancreatitis
5. Etiology:
Common Causes
Gallstones disease
Alcohol (acute &chronic both)
Hypertriglyceridemia
ERCP, especially after biliary manometry
Blunt abdominal trauma
Postoperative (abdominal and nonabdominal
operations)
Drugs (azathioprine, 6-mercaptopurine,
sulfonamides, estrogens,
tetracycline, valproic acid, anti-HIV
medications)
Sphincter of Oddi dysfunction
Uncommon Causes
Vascular causes and vasculitis
Connective tissue disorders and thrombotic
thrombocytopenic purpura (TTP)
Ca. pancreas
Hypercalcemia
Periampullary diverticulum
Pancreas divisum
Hereditary pancreatitis
Cystic fibrosis
Renal failure
6. Pathogenesis:
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
organs.
7. Symptoms:
Abdominal Pain:
•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.
8. Physical examination:
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
bile duct.)
Erythematous skin nodules due to subcutaneous fat necrosis
may occur.
9. 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.
13. Ultra Sound (US)
Little part in the diagnosis of the
acute pancreatitis
Role in biliary pancreatitis
Stones in gallbladder
Common Bile Duct dilation
14. CT Scan
Normal-Homogeneous enhancement
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
16. Severity of Acute Pancreatitis
Risk Factors for Severity:
• Age >55 years
• Obesity, BMI >30
• Co-morbid disease
• Altered mental status
17. 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%)
• BISAP
• (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)
18. 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
enhancement
0
B Focal or diffuse enlargement of the pancreas,
contour may show irregularity, enhancement
may be inhomogeneous but there is no
peripancreatic Inflammation
1
C Peripancreatic inflammation with intrinsic pancreatic
abnormalities
2
D Intrapancreatic or extrapancreatic fluid collections 3
E Two or more large collections or gas in the pancreas
or retroperitoneum
4
Necrosis,% Score
0 0
<33% 2
33-50% 4
≥50% 6
19. 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
20. Management:
Acute Pancreatitis
Mild AP
80% of cases
<5% of mortality
Recommended (All Pts.)
Admit to general wards
Re-feed when pain
subsides
Not Recommended
Antibiotics
CT scan
Severe AP
20% of cases
>95% of mortality
Recommended
Admit to ICU
Antibiotics
CT scan on Day 3rd
Necrosis
Sterile-Observe
Infection suspected-FNA
Infected necrosis-
Necrosectomy
21. 1. Aggressive hydration, 250 – 500 ml
per hour of isotonic crystalloid. Early
aggressive intravenous hydration is
most beneficial during the first 12 – 24
hrs.
•Lactated Ringer’s preferred isotonic
crystalloid replacement fluid.
3. Reassessment at frequent intervals
within 6hrs of admission and for the
next 24–48 hrs.
Management:
22. Hypertriglyceridemia-associated Pancreatitis:
(1) weight loss to ideal weight,
(2) a lipid restricted diet,
(3) exercise
(4) avoidance of alcohol and of drugs that can elevate serum triglycerides (i.e.,
estrogens, vitamin A, thiazides, & propranolol),
(5) control of diabetes.
23. 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
infected necrosis
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.
24.
25. 1. ERCP should be done within 24 h of admission in AP with concurrent acute
cholangitis.
2. No early need in gallstone pancreatitis lacking
laboratory or clinical evidence of ongoing biliary
obstruction.
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:
26. 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.
27. 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
requirements.
4. Nasogastric and nasojejunal delivery of enteral feeding appear
comparable in efficacy and safety.
Feeding:
28. Complications of Acute Pancreatitis:
Local complications
Necrosis
Sterile
Infected
Walled-off necrosis
Pancreatic fluid collections
Pancreatic abscess
Pancreatic pseudocyst
Pain
Rupture
Hemorrhage
Infection
GI Obstruction
Pancreatic ascites
Main pancreatic duct
disruption
Leaking pseudocyst
Involvement of contiguous
organs by necrotizing
pancreatitis
Massive intraperitoneal
hemorrhage
Thrombosis of blood vessels
(splenic vein, portal vein)
Bowel infarction
Obstructive jaundice
30. 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
hours.
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.
Summary:
32. • “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
insufficiency.
• Obvious structural disease on radiography
– Calcifications, multiple beads and strictures
• Pain or steatorrhea not necessary.
Definations:
35. Consequences of Chronic Panc:
Pain
Steatorrhea
Diabetes
Biliary obs.
B12 def.
Cancer
36. Chronic Pancreatitis: the Spectrum
Damage
Starts
PAIN
“Minimal ∆”
“Small Duct”
(pos secretin)
Structural damage
(Pos CT/EUS/ERCP)
Steatorrhea
“BIG DUCT”
CANCER RISK
Diabetes
Pain may dec
30% 60% 80-90%
% Damage
37. Make the Correct Diagnosis
• Chronically elevated amylase/lipase do not
make CP.
• In early CP, imaging and labs may be
negative or equivocal
• Avoid labelling as CP
• Avoid sick role, pyschosocial-economic
consequences.
• Much acute relapsing pancreatitis is
actually early chronic pancreatitis
39. Atrophic pancreas, multiple
calcifications, stones dilated
pancreatic duct
Markedly dilated pancreatic
duct seen in through the body
and tail
Gadolinium-enhanced
MRI/MRCP- dilated pancreatic
duct with multiple filling defects
s/o pancreatic duct calculi.
40. Pancreatic Function Tests (PFTs):
Indirect (often tubeless)
Fecal fat
Trypsin
Glucose/GGT
Pancreatic
polypeptide
Dual Label Schilling test
Direct
S-MRCP
S-EUS
e-SST
SST (Gold standard
functional test)
CCK/SST
Bentiromide test
(historical)
Lundh test (Europe)
41. Quick and “dirty” PFTs:
Trypsin
Fecal fat
Fecal elastase
Fecal chymotrypsin
Only stage disease, don’t usually pick up early
disease.
42. Trypsin:
• 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
43. Fecal fat:
• Spot
– 6 or more droplets
– Only picks up extensive steatorrhea
• 72hr
– Must be on 100g fat diet several days before
– >7grams/24hrs is steatorrhea
– Very nonspecific
– Noncompliance high
44. Fecal Elastase:
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
100-200 borderline
>200 normal
“Not affected” by porcine enzymes
Must use monoclonal ELISA
45. E-SST:
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.
46. S-EUS:
Combined EUS plus SST
`
Better coding for SST
EUS may add something to SST
See pancreatic duct directly and after secretin
47. EUS
Findings:
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)
Major criteria:
(1) hyperechoic foci with shadowing & main pancreatic duct (PD)
calculi &
(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
noncontiguous lobules
48. EUS: problems:
Give subtle changes in absence of clinical
chronic pancreatitis
Lots of inter and intraobserver variability
Change in “gain” can have big impact
Lack of gold standard
50. New Horizons:
Diffusion weighted MRI with secretin
EUS elastography
MR elastography
C14 bicarbonate breath test
Secretin-PET
51. Diffusion weighted (DWI) MRI with
secretin:
DWI measures sum of random motions of
protons
Lower values or delayed peak in chronic
pancreatitis, especially with secretin
Can also better distinguish AP from CANCER
Small insulinomas being detected.
52. EUS elastography:
Measure of tissue stiffness also uses sound
waves to detect reverberations.
Good sensitivity
But analysis occurs after procedure.
Magnetic Resonance Elastography:
Better known for liver, but also works for
pancreas/spleen.
53. Treatment:
What are we treating?
Pain
–Attacks of acute pancreatitis
–Disease flares w/o acute pancreatitis
–Chronic pain
–Other reasons – Pseudocyst, biliary obstruction, etc.
•Exocrine and endocrine insufficiency
•Other complications
–Gastric outlet obstruction
–Pancreatic ascites
–Uncommon complications
57. • 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)
•Biliary stricture
•Symptomatic pseudocysts (not amenable or after failed
endoscopic therapy)
Pain in Chronic Pancreatitis: Surgery
59. Exocrine and Endocrine Insufficiency:
•Exocrine Insufficiency
–Often undertreated
–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
61. •Clinical presentation mimics Pancreas cancer
•Less common
•Pancreatitis, persistent pancreatic mass, scarred or shrunken pancreas,
malabsorption
•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
62. 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
63. Prednisone :
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.
Tratment:
64. 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
content
Pancreatic cancer
65. •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
management
•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
Hinweis der Redaktion
Etymologically, the term "pancreas", a modern Latin adaptation of Greek πάγκρεας,[24] [πᾶν ("all", "whole"), and κρέας ("flesh")],[25]originally means sweetbread,[26] 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.
