Acute pancreatitis is inflammation of the pancreas that commonly results from gallstones or alcohol abuse. It requires hospital admission for intravenous fluids and pain management. The condition ranges from mild edema to severe necrosis and affects over 200,000 patients annually in the US. Diagnosis is based on abdominal pain and elevated pancreatic enzymes. Treatment focuses on fluid resuscitation, nutritional support to rest the pancreas, and managing complications.

1. Acute
Pancreatitis

2. Acute Pancreatitis
 Sudden onset of unrelenting upper abdominal
pain resulting from inflammation of the
pancreas
 Patients commonly present to ED due to
severe abdominal pain
 Requires admission to the hospital for medical
management, accounting for between
166,000 to 224,000 admissions each year
with an estimated annual cost of $3.6 to $6
billion

3. Pancreas
 Complicated exocrine
and endocrine gland
located in the upper
abdominal region
 Non-capsulated lobular
organ about 12 to 20
cm long and lies
behind the peritoneum
of the posterior
abdominal wall
 Divided into head,
body, and tail

4. Pancreas
 Tail
 Adjacent to hilum of spleen
 Body
 Extends horizontally behind stomach
 Head
 Nestled in the duodenal sweep
 Sphincter of Oddi
 Circular smooth muscle that surrounds
both the common bile duct and the main
pancreatic duct
 Ampule of Vater
 Site where the common bile duct and
main pancreatic duct drain into
duodenum

6. Pancreas
 The lobes of the pancreas are divided into
subunits of acini cells and the Islets of
Langerhans
 Acini cells are involved in the production of 20
different digestive enzymes and include amylase
released to digest starch and lipase released to
digest fats
 The most abundant of the enzymes is trypsin,
which is released into the duodenum
 These enzymes are activated by enterokinase,
which is produced by the intestinal mucosa

7. Pathophysiology
 Triggering mechanism not exactly understood
 Pancreatic enzymes that escape into the
surrounding tissue due to compromised
pancreatic function seem to be the primary
cause
 When the pancreas becomes damaged or the
ducts become blocked, the trypsin inhibitor
accumulates and activates the pancreatic
secretions that escape into the surrounding
tissue, resulting in inflammation, thereby
causing acute pancreatitis

8. Pathophysiology
 Release of kallikrein and chymotrypsin results in
increased capillary membrane permeability,
leading to leakage of fluid into the interstitium and
development of edema and relative hypovolemia
 Elastase is the most harmful in terms of direct cell
damage, it causes dissolution of the elastic fibers
of blood vessels and cuts, leading to hemorrhage
 Phospholipase A in the presence of bile, destroys
phosholipids of cell membranes causing severe
pancreatic and adipose tissue necrosis
 Lipase flows into damaged tissue and is absorbed
into systemic circulation, resulting in fat necrosis
of the pancreas and surrounding tissues

9. Acute Pancreatitis
 Inflammation of the
pancreas that
produces exocrine
and endocrine
dysfunction
 Results from
premature activation
of pancreatic
exocrine enzymes
(trypsin,
phospholipase A,
and elastase)

10. Edematous (Interstitial)
Pancreatitis
 Usually mild
 Resolves in about 7
days
 Results in fluid
accumulation and
swelling

11. Severe or Necrotizing
Pancreatitis
 Associated with a high
degree of
complications and
mortality
 Caused by the release
of cytokines and other
proinflammatory
mediators that
produce a
hyperinflammatory
reaction, resulting in
cell death and tissue
damage

12. Causes of Acute Pancreatitis
 Ethanol abuse
 Biliary diseases
 Gallstones
 Choledocholithiasis
 Biliary sludge
 Microlithiasis
 Mechanical/structural injury
 Sphincter of Oddi dysfunction
 Pancreas divisum
 Trauma
 Postendoscopic retrograde
cholangiopancreatography
 Pancreatic malignancy
 PUD
 IBD
 Medications
 Azathiprine/6-mercaptopurine
 Dideoxyinosine
 Pentamidine
 Sulfonamides
 Thiazide diuretics
 ACEI
 Metabolic
 Hypertriglyceridemia
 Hypercalcemia
 Infectious
 Viral
 Bacterial
 Parasitic
 Vascular
 Vasculitis
 Genetic predisposition
 idiopathic

13. Acute Pancreatitis: Damage and
Destruction
 Inflammation is caused by
premature activation of
enzymes which leads to
tissue damage
 If pancreatitis damages the
islets of Langerhans,
diabetes mellitus may result
 Severe sudden pancreatitis
causes massive hemorrhage
and total destruction of the
pancreas, manifested as
diabetic acidosis, shock and
coma

14. Clinical Presentation
 Upper abdominal pain rapidly increasing in severity,
often within 60 minutes
 Epigastric pain
 Right-sided pain
 Diffuse abdominal pain with radiation to back
 Pain rarely only in left upper quadrant
 Restless
 Prefer to sit and lean
 N/V
 Fever
 Tachycardia

15. Abdominal Examination
 Decreased or absent bowel sounds
 Abdominal tenderness
 Guarding
 Palpable mass in epigastric area
 Biliary colic
 Jaundice if there’s obstruction of the bile duct
 Cullen’s sign
 Grey Turner’s Sign

16. Clinical
Manifestations
 Abdominal distention
 Abdominal guarding
 Abdominal tympany
 Hypoactive bowel sounds
 Severe disease:
peritoneal signs, ascites,
jaundice, palpable
abdominal mass, Grey
Turner’s sign, Cullen’s
sign, and signs of
hypovolemic shock

17. What testing will reveal……
 Serum amylase and lipase levels elevated 3-5
times normal
 Urine amylase increased for 1-2 weeks
 Elevated WBC
 H/H decreased
 Decreased serum calcium
 Elevated serum bilirubin, AST, ALT, LD, and
alkaline phosphatase
 Abdominal XRAYS and CT’s showing pleural
effusions and bowel dilation and ileus
 Serum triglycerides >150mg/dl

18. Diagnostic Evaluation
 Patient’s history
 Physical examination
 Diagnostic findings
 Serum amylase levels greater than three times the
upper limit
 Serum amylase levels may be normal in patients
with pancreatitis related to alcohol abuse or
hypertriglyceridemia
 Levels greater than five times the top normal
value should be expected in patients with renal
failure because amylase is cleared by the kidneys

19. Diagnostic Evaluation
 Serum lipase is more sensitive and specific to the
pancreas
 An elevation of greater than three times the top
normal value usually confirms acute pancreatitis
 A lipase-to-amylase ratio of greater than 2 is
usually evident with pancreatitis related to alcohol
abuse
 A rise in urine amylase and lipase can be expected
and are indicative of pancreatic damage
 Leukocytosis
 Hemoconcentration due to third space fluid loss
 Pancreatitis due to gallstones: elevated AST, ALT,
and lactate dehydrogenase

20. Imaging Modalities
 Plain abdominal x-rays for visualizing
gallstones or a gas-filled transverse colon
ending at the area of pancreatic inflammation
 colon cut-off sign
 Abdominal ultrasound
 Cholelithiasis, biliary sludge, bile duct dilation, and
pseudocysts
 CT of abdomen
 MRCP (magnetic resonance
cholangiopancreatography)

21. Ranson’s Criteria
 The severity of acute pancreatitis is
determined by the existence of certain
criteria, called Ranson’s criteria
 The more criteria met by the patient, the
more severe the episode of pancreatitis
 1% mortality: fewer than three
 16%: three or four criteria
 40% with five or six criteria
 100%: seven or eight criteria

22. Ranson’s Criteria
 On admission
 Patient older than 55
 WBC > 16,000
 Serum glucose >200
 Serum lactate dehydrogenase >350
 Aspartate aminotransferase > 250
 During initial 48 hours after admission
 10% decrease in Hct
 BUN increase > 5
 Serum calcium < 8
 Base deficit > 4
 PaO2 < 60
 Estimated fluid sequestration > 6 liters

23. Common Complications of Acute
Pancreatitis
 Pulmonary
 Atelactasis
 Pleural effusions
 ARDS
 Cardiovascular
 Cardiogenic shock
 Neurologic
 Pancreatic encephalopathy
 Metabolic
 Metabolic acidosis
 Hypocalcemia
 Altered glucose metabolism
 Hematologic
 DIC
 GI bleeding
 Renal
 Prerenal failure

24. Management
 Fluid Management
 Nutritional support
 Rest gut
 TPN
 Pain management
 Supporting other organ systems

25. Treatment
 IV replacement of fluids,
proteins, and electrolytes
 Fluid volume replacement and
blood transfusions
 Withholding food and fluids to
rest the pancreas
 NG tube suctioning
 Drugs
 Peritoneal lavage
 Surgical drainage
 Laparotomy to remove
obstruction

26. Fluid Resuscitation
 Patients with acute pancreatitis may have
fluid shifts of 4 to 12 L into retroperitoneal
space and peritoneal cavity due to
inflammation
 In severe acute pancreatitis, blood vessels
in and around the pancreas may also
become disrupted, resulting in hemorrhage.
 Replace fluids with colloids, crystalloids, or
blood products
 Monitor for S/S of hemorrhage

27. Rest the Pancreas
 NPO status
 Avoiding use of GI tract is recommended until
the patient no longer reports abdominal pain and
the serum amylase has returned to normal
 Provide nutrition enterally using a jejunal tube to
prevent pancreatic enzyme secretion.
 If parenteral therapy is used, the solution is
usually a mixture of hypertonic glucose and
amino acids.
 The use of lipid emulsion is contraindicated
during acute phase because it increases
pancreatic exocrine secretion.

28. Pharmacologic Agents
 Somatostatin
 Used to decrease pancreatic secretion in
acute pancreatitis
 Decreases intestinal motility and reduces
endocrine/exocrine pancreatic secretion
 Anticholinergic agents
 Glucagon
 Cimetidine
 calcitonin

29. Pharmaceutical Treatment
 Demerol for pain
 Morphine causes spasm of Sphincter of
Oddi
 However, use of demerol leads to
metabolite accumulation
 Pneumatic compressions
 TPN/early enteral feedings

30. Goals for Treatment
 Supportive care
 Pain control
 Antiemetics
 IVF
 NPO
 Lessening inflammation and necrosis
 Endoscopic retrograde cholangiopancretography
(ERCP) with stone extraction or stent placement
 Anticipating and treating complications
 Preventing recurrence