2. ā¢ Inflammation of pancreatic parenchyma.
ā¢ Broadly of 2 types:
1. Acute: Presents as an emergency
2. Chronic: Prolonged and frequently lifelong disorder resulting from
development of fibrosis within the pancreas.
ā¢ Acute pancreatitis is defined as an acute condition presenting with:
ā¢ Abdominal pain
ā¢ Threefold or greater rise in serum levels of pancreatic enzymes
amylase or lipase.
ā¢ And/or characteristic findings of pancreatic inflammation on CECT.
ā¢ Acute pancreatitis may be categorized as mild (interstitial edematous
pancreatitis) or severe (necrotizing pancreatitis).
3. ā¢ Acute pancreatitis has an early phase that usually lasts a week and is
characterized by a Systemic Inflammatory Response Syndrome(SIRS)
ā¢ The late phase is characterized by persistent systemic signs of
inflammation and/or local complications, particularly fluid collection and
peripancreatic sepsis.
4. RISK FACTORS
ā¢ Biliary or Gallstone Pancreatitis
ā¢ Most common cause
ā¢ Seen more frequently in women between 50& 70 years of age
ā¢ Triggered by passage of gall stone down the CBD and getting
impacted at Ampulla of Vater which allows reflux of bile or activated
pancreatic enzyme into pancreas
ā¢ Alcohol induced injury
ā¢ 2nd most common cause
ā¢ More prominent in young male than women
5. ā¢ Anatomic Obstruction
ā¢ Abnormal flow of pancreatic juice into duodenum can result in
pancreatic injury.
ā¢ May be due to pancreatic tumours, parasites (Ascaris lumbricoides)
and congenital defects.
ā¢ ERCP induced pancreatitis
ā¢ Acute pancreatitis is the most common complication after ERCP
probably as a consequence of duct disruption and enzyme
extravasation.
ā¢ Patient with Sphincter of Oddi dysfunction or a history of recurrent
pancreatitis and those who undergo sphincterotomy or balloon
dilatation of sphincter carry higher risk.
6. ā¢ Drug induced Pancreatitis
ā¢ Most common agents include Sulfonamides, Furosemide,
Metronidazole, erythromycin, Thiazides
ā¢ Metabolic Factors
ā¢ Hypertriglyceridemia
ā¢ Hypercalcemia (Through activation of trypsinogen to trypsin and
intraductal precipitation of calcium leading to ductal obstruction )
10. CLINICAL FEATURES
ā¢ The cardinal symptom is epigastric or periumbilical pain that radiates to
back.
ā¢ Dehydration
ā¢ Poor skin turgor
ā¢ Tachycardia
ā¢ Hypotension
ā¢ Tachypnoea
ā¢ Bleeding into fascial planes can produce bluish discolouration of flanks
(Grey Turner sign) or Umbilicus (Cullen sign)
ā¢ Muscle guarding in upper abdomen although marked rigidity is unusual
12. DIAGNOSIS
ā¢ Requires two of the following 3 features:
1. Abdominal Pain
2. Threefold or higher elevation of serum amylase or lipase levels
above normal.
3. Characteristic finding of pancreatitis by imaging
13. ASSESSMENT OF SEVERITY
ā¢ Atlanta Classification of acute pancreatitis (revised in 2013)
1. Mild pancreatitis
ļ No organ failure
ļ No local or systemic complications
2. Moderate Pancreatitis
ļ Organ failure that resolves within 48hrs
ļ Local or systemic complication without persistent organ failure
3. Severe Acute Pancreatitis
ļ Persistent organ failure
ļ Single organ failure
ļ Multiple organ failure
14.
15.
16.
17. Severity of
pancreatitis
Ransonās criteria APACHE II CT SEVERITY INDEX
MILD PANCREATITIS ā¤ 3 < 8 < 7
SEVERE
PANCREATITIS
> 3 ā„ 8 > 7
ā¢ Other scoring systems used are SAPS, SOFA, Modified Marshal
scoring System
18. IMAGING STUDIES
ā¢ These are not required for diagnosis but may be helpful in determining
need for intervention in severe cases or to rule out other diseases.
ā¢ Non specific findings in pancreatitis includes a generalized or local ileus,
Colon cut off sign and Renal halo sign
ā¢ Occasionally calcified gallstone or pancreatic calcification may be seen.
ā¢ Chest radiograph may show pleural effusion.
19. ā¢ COLON CUTOFF SIGN
ļ¶Abrupt cutoff of colonic gas at the
splenic flexure.
ļ¶Infiltration of the phrenicocolic
ligament results in functional spasm
and/or mechanical narrowing of the
splenic flexure at the level colon
returns to the retroperitoneum.
20. ā¢ B/L RENAL HALO SIGN
ļ¶The halo appears as ground glass
attenuation on imaging, due to
enhancement of the peri-renal fat from
the retroperitoneal collection of
pancreatic exudates.
21. ā¢ USG doesnāt establish a diagnosis but it should be performed within
24hrs in all patients:
ļ To detect gallstones as a potential cause
ļ Rule out acute cholecystitis as a differential diagnosis
ļDetermine whether the CBD is dilated
ā¢ Indication for CT:
ļDiagnostic uncertainty
ļConfirmation of severity based on clinical predictors
ļFailure to respond to conservative treatment or clinical deterioration.
22. ā¢ Abdominal MRI is also useful to
evaluate the extent of necrosis,
inflammation and presence of
free fluid.
ā¢ ERCP allows the identification
and removal of stones in the
CBD in gallstone pancreatitis.
23. MANAGEMENT
ļCornerstones of treating acute pancreatitis:
1. Aggressive fluid resuscitation
2. Pain control
3. Early nutrition
ļFrequent measurement of vital signs, urine output, central venous
pressure.
ļSupplemental oxygen should be administered and serial ABG analysis
performed.
ļThe Haematocrit, Clotting profile, Blood glucose and serum levels of
Calcium & Magnesium should be closely monitored.
ļAdequate analgesia should be administered. Narcotics are usually
preferred, especially morphine.
24. ļNutritional support is vital in treatment of acute pancreatitis. The main
options to provide this are enteral feeding and total parenteral nutrition.
ļAs per current recommendations, antibiotics are to be administered if a
pre-existing infection is present or radiographic imaging suggests infected
peripancreatic fluid collection.
ļERCP can be done in case of gallstone pancreatitis.
26. 1. Acute Peripancreatic Fluid collection
ļOccurs early in the course of mild pancreatitis without necrosis and is
located adjacent to the pancreas.
ļHas no encapsulating walls and is confined within normal fascial
planes.
ļFluid is sterile and no intervention is necessary unless a large
collection causes symptoms or pressure effects.
ļPercutaneous aspiration under USG or CT guidance.
ļTransgastric drainage under Endoscopic USG guidance is another
option.
27. 2. Sterile and infected pancreatic necrosis
ļPancreatic necrosis refers to a diffuse or local area of non- viable
parenchyma.
ļTypically associated with lysis of peripancreatic fat.
ļ< 4weeks: Acute Necrotic Collection
ļ>4 weeks: Walled off necrosis (due to development of well defined
inflammatory capsule)
ļCollections are sterile to begin with but often become infected due to
translocation of gut bacteria.
ļInternal drainage into the stomach under endoscopic USG guidance should
be considered first.
ļIf not possible then percutaneous drainage should be considered. The tube
drain inserted should have widest bore possible.
ļPancreatic Necrosectomy should be considered if sepsis worsens despite
conservative measures.
28.
29. ļPancreatic Necrosectomy
ā¢ Midline laparotomy approach.
ā¢ Duodenocolic and Gastrocolic ligaments
divided and lesser sac opened
ā¢ Thorough debridement of dead tissue
ā¢ Retroperitoneal approach through left flank
incision if body and tail are involved.
ā¢ Blunt dissection preferred over sharp
dissection
ā¢ Feeding Jejunostomy may be a useful
adjunct.
ā¢ Cholecystectomy if gallstones are
precipitating factors
30. ļMethods to deal with further necrotic tissue formation:
a. Closed continuous lavarge using tube drains.
b. Closed drainage using gauge filled penrose drains (removed after 7 days)
c. Open packing
d. Closed and relaparotomy every 48-72 hrs until raw area granulates
31. 3. Psuedocyst
ļIt is a collection of amylase-rich fluid enclosed in a well defined wall of
fibrous or granulation tissue.
ļPseudocysts are often single but are occasionally multiple.
ļMore than half have communication with main pancreatic duct.
ļPseudocysts that are thick walled or large, have lasted for a long time
or have arisen in context of chronic pancreatitis are less likely to
resolve spontaneously.
ļ3 approaches to drain a pseudocyst:
a. Percutaneous
b. Endoscopic
c. Surgical
32. ļPercutaneous approach:
ļ§ Should be avoided
ļ§ Carries high risk of recurrence
ļ§ Not advisable until it is confirmed that cyst is not neoplastic and it has no
communication with pancreatic duct.
ļEndoscopic approach:
ļ§ Usually involves puncture of cyst through the stomach or duodenal wall under
endoscopic guidance and placement of a tube drain with one end in cyst cavity and
the other end in gastric lumen.
ļ§ ERCP and placement of a pancreatic stent across the ampulla to drain a pseudocyst
having communication with duct.
33. ļSurgical approach:
ļ§ Involves internally draining cyst into gastric or jejunal lumen.
ļ§ The approach is conventionally through open incision but laparoscopic
cystgastrostomy is also feasible.
ļ§ Pseudocyst that have developed complications are best managed surgically.
34. 4. Pancreatic abscess
ļCircumscribed intra-abdominal collection of pus usually in proximity of
pancreas.
ļEndoscopic internal drainage or percutaneous drainage with widest
possible drains is the treatment along with appropriate antibiotics and
supportive care.
ļRepeated scans may be required depending on the progress of
patient and drains may need to be flushed, repositioned or reinserted.
5. Pancreatic ascites
ļChronic, generalized, peritoneal, enzyme rich effusion usually
associated with pancreatic duct disruption.
ļAdequate drainage with wide bore drains placed under imaging
guidance is essential.
35. 6. Pancreatic effusion
ļEncapsulated collection of fluid in peritoneal cavity, arising as a
consequence of acute pancreatitis.
ļConcomitant pancreatic ascites may be present or there may be a
communication with an intra abdominal collection.
37. TAKE HOME MESSAGE
ā¢ Pancreatitis is a multi system pro-inflammatory disease
associated with many complications.
ā¢ The majority of presentations with pancreas are self-limiting.
ā¢ Gallstone & alcohol are the leading causes of acute
pancreatitis.
ā¢ Severe acute pancreatitis mortality is approximately 40%
ā¢ Early enteral feeding is preferred.
ā¢ Routine antibiotics are not required unless there is evidence of
an infective complication.