Acute pancreatitis is caused by the activation of pancreatic enzymes within the pancreas, leading to its auto-digestion. The most common causes are gallstones and alcohol. Clinically, it presents with severe mid-epigastric pain radiating to the back along with nausea and vomiting. Investigations show elevated serum amylase and lipase along with imaging findings of pancreatic swelling. Treatment is supportive with bowel rest, IV fluids, pain control and monitoring for complications like necrosis, abscess, pseudocyst and respiratory failure. Severe necrotizing pancreatitis may require endoscopic or surgical drainage and debridement.

1. ACUTE
PANCREATITIS
acute pancreatitis

2. INTRODUCTION
• Acute pancreatitis is a condition in which
activated pancreatic enzymes leak into the
substance of the pancreas and initiate the
auto-digestion of the gland.
introduction

3. ETIOLOGY
Common (90%)
• Gall stones
• Alcohol
• Idopathic
Rare
• Metabolic: hypercalcemia, hypertrigyceridemia
• Drugs: thiazide, azathioprine, sodium valporate,
pentamidine
• Infection: mumps, coxsackie virus
• Post ERCP (due to back pressure of contrast into ductal
system)
• Trauma
• Organ transplantation
• Post surgical
etiology

5. etiology

6. PATHOPHYSIOLOGY
pathophysiology
• The pancreas secretes the digestive enzymes as
proenzymes which are activated in the intestinal lumen.
• Acute pancreatitis may result when activation occurs in
pancreatic duct system or acinar cells. May include edema
or obstruction of the ampulla of Vater resulting in reflux of
bile into pancreatic ducts or direct injury to the acinar cells.
• The pancreas show edema and necrosis. The release of
enzymes lead to fat necrosis both in the pancreas and in
the peritoneal cavity.
• Premature activation of trypsinogen into trypsin while it is
still in pancreas. Resulting in auto digestion of the pancreas.

7. Proenzymes
Activated
proteolytic
enzymes
DEFECTIVE
INTRACELLULAR
TRANSPORT AND
SECRETION OF
PANCREATIC
ZYMOGENS
Pancreatic duct
obstruction (common
bile duct stones,
tumors)
Acute pancreatitis
Hyperstimulation of
pancreas (alcohol,
triglycerides)
Reflux of infected bile
or duodenal contents
into pancreatic duct
(sphincter of Oddi
dysfunction)
Pancreatic
secretory
trypsin
inhibitors
+
+
+ +
-
pathophysiology

8. pathophysiology

9. CLINICAL PRESENTATION
clinical presentation
• Midepigastric pain with tenderness. Sudden severe pain
occurring often within 12-24 hours of a large meal or
alcohol. The pain is persistent and radiates frequently
through to the back to either shoulder or to one iliac fossa
before spreading to involve the whole abdomen.
Exacerbated on walking and lying supine. Relieved on
sitting and leaning forward.
• Nausea and vomiting has always been the presentation of
acute pancreatitis in the majority of cases.
• When pancreatitis is extremely severe, it mimics septic
shock; fever, hypotension, respiratory distress from ARDS,
elevation of the WBC and a rigid abdomen.

10. clinical presentation

11. ABDOMINAL EXAMINATION
abdominal examination
• Tenderness in epigastrium
• Although severe pain, there may be little or no
guarding of abdominal muscles at first. Later the upper
abdomen becomes tender and rigid as peritoneal
irritation increases.
• Mild abdominal distention if paralytic ileus develops.
• Severe advanced cases may develop bruising and
discoloration in the left flank (Grey Turner’s sign due to
tissue catabolism of Hb) and around the umbilicus
(Cullen’s sign due to hemoperitoneum). These are the
rare and late signs of extensive pancreatic destruction.

12. CULLEN’S
SIGN
abdominal examination
Grey Turner’s sign

13. complications
Complications of acute pancreatitis
Complications Causes and features
Shock and renal failure Pancreatic failure is associated with leakage of fluid
in the pancreatic bed also ileus with fluid filled loops
of bowel leading to pre-renal azotemia and then
acute tubular necrosis.
Hypoxia ARDS due to micro thrombi in pulmonary vessels.
Hyperglycemia Due to disruption of pancreatic islets.
Hypocalcemia Sequestration of calcium in fat necrosis.
Hypoalbuminemia Increased capillary permeability.

14. complications
Complications of acute pancreatitis
Pancreatic complications Causes and features
Necrosis
Abscess Rising fever, leukocytosis, localized tenderness and
epigastric mass. It may be associated with left sided
pleural effusion and enlarged spleen due to splenic
vein thrombosis.
Pseudocyst Encapsulated fluid collection with high enzyme
content. Usually less than 6cm sized pseudocysts
resolve spontaneously. They may become secondarily
infected requiring drainage of abscess.
Ascites Gradual increase in abdominal girth and persistent
elevation of serum amylase in the absence of frank
abdominal pain. It results from rupture of pancreatic
duct or drainage of pseudocyst into the pancreatic
cavity.

15. complications

16. PSEUDOCYST ON CT
SCAN
complications

17. complications
Complications of acute pancreatitis
Gastrointestinal complications Causes and features
Upper GI bleeding Gastric or duodenal erosion
Duodenal obstruction Compression by pancreatic mass
Obstructive jaundice Compression of common bile duct

18. INVESTIGATIONS
investigations
Serum amylase
• Increased level of 3-fold or more the normal value
indicates acute pancreatitis, however other causes of
elevation should be excluded such as mumps and
perforation or infarction of the intestine.
• Levels turn normal after 48-72 hrs even with the
continuing of pancreatitis, serum lipase should also be
sent that remains high for 7-14 days.
• Persistent elevation suggests pseudocyst, pancreatic
abscess or non pancreatic causes (intestinal
obstruction, mumps, narcotics)

19. Serum lipase
• Remains elevated for 7-14 days. It is diagnostic.
Other laboratory findings
• WBC: 15000 – 30000
• Glucose : high
• BUN: may be elevated
• Serum calcium: low in 25% of cases
• AST, bilirubin, alkaline phosphatase are transiently
elevated. Serum albumin is low in 10% of patients and
indicates severe pancreatitis.
• Markedly elevated LDH (>500U/dl) suggests poor
prognosis
• Serial assessment of C-reactive is a good indicator of
progress
• ABGs show hypoxia
investigations

21. Plain x-ray abdomen
• It may show gall stones, sentinel loop, colon cut off
sign, features of paralytic ileus, left pleural effusion or
collapsing of lung
CT scan
• Useful in detecting large pancreas, pseudocyst,
abscess, hemorrhagic pancreas
• Presence of gas bubbles indicate abscess
Ultrasound
• To detect gallstone and biliary obstruction and serial
assessment of pseudocysts, although in the earlier
stages the gland may not be grossly swollen and may
be missed on US.
investigations

22. ACUTE EXUDATIVE PANCREATITIS
CT SCAN
investigations
Acute necrotizing pancreatitis CT scan

23. DIFFERENTIAL DIAGNOSIS
• Perforated peptic ulcer
• Acute cholecystitis and biliary colic
• Acute intestinal obstruction
• Renal colic
• Myocardial infarction
• Vasculitis
• Pneumonia
• Diabetic ketoacidosis
differentialdiagnosis

24. MANAGEMENT
management
• In most patients it is a mild disease that subsides
spontaneously within several days. Withhold food and
liquids by mouth, bed rest and in patients with severe pain
and ileus nasogastric suction.
Supportive treatment
• Bed rest NPO
• IV fluids; saline or whole blood
• Nasogastric suctioning; if severe nausea, vomiting or
development of paralytic ileus
• Pethidine 3-4 hourly to control pain, avoid morphine
• Oxygen for hypoxia, ventilator may be required for ARDS
• Dopamine may be required for shock nonresponsive to
fluid

25. • Calcium gluconate IV only if hypocalcemia is associated
with tetany
• Fresh frozen plasma for coagulopathy
• Serum albumin for hypoalbuminemia
• Insulin for hyperglycemia
• Total parenteral nutrition for severe cases
• Antibiotics; prophylactic broad spectrum antibiotic is
given even in sterile pancreatitis to prevent infection
• Imipenem 500mg IV 8 hourly or cefuroxime 1.5g IV 8
hourly
• ERCP; when severe pancreatitis results from stone in
biliary tract; particularly if there is jaundice or
cholangitis ERCP with endoscopic sphincterotomy and
stone extraction is indicated
management

26. management

27. Surgery
• Cholecystectomy should be undertaken within 2
weeks of resolution of pancreatitis.
• Patients with necrotizing pancreatitis or abscess
require urgent endoscopic or minimally invasive
retroperitoneal pancreatic (MIRP) necrosectomy
to debride all cavities of necrotic material.
• Pancreatic pseudocysts can be treated by
draining into stomach, duodenum or jejunum.
Performed after 6 weeks, once capsule matures,
by surgery or endoscopic cystogastrostomy.
management

29. management

30. REFERENCES
• Davidson’s principles and practice of medicine
22nd edition
• Short textbook of medical diagnosis and
management 11th international edition (Inam
Danish)
• Kaplan medical USMLE step 2 CK internal
medicine lecture notes
references

31. THANK YOU