Based on current evidence and guidelines, enforced bed rest is no longer recommended for acute pancreatitis. The goals of treatment are to provide pain management and fluid resuscitation, prevent/treat complications, and maintain adequate nutrition while minimizing pancreatic stimulation. Resting the gut by withholding oral intake until symptoms resolve is still recommended, but complete bed rest does not provide additional benefits and may even be harmful by risking complications from immobility. Nurses should focus on supportive care, monitoring for complications, and early mobilization as tolerated.

1. Acute
Pancreatitis

2. 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

3. 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

4. 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

6. 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)

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

10. 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

11. CAUSES
 The Big Three:
 Biliary disease (40%)
 Alcohol (35%)
 Others (20%)

12. Other 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

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
 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. 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

18. 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

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

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. 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

26. NURSING PRIORITIES

1. Control pain and promote comfort.
2. Prevent / treat fluid and electrolyte
imbalance.
3. Reduce pancreatic stimulation while
maintaining adequate nutrition.
4. Prevent complications.
5. Provide information about disease
process/prognosis and treatment needs.

27. 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

28. 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

29. 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

30. 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.

31. Pancreatitis Low Fat Diet
The presence of large amount of fats in the blood of
humans is a major cause of pancreatitis. The aim of a
pancreatitis low fat diet is to keep the daily fat intake
strictly under control and ensure that it is not more than
thirty percent of the total calorie intake of the body. A
pancreatitis diet plan with low fat is very useful in
preventing steatorrhea, which is due to the pancreatic
insufficiency. Following a proper chronic pancreatitis diet
will result in less than one-fourth as much steatorrhea,
as compared to the fat intake by following a normal diet.
Now let us discuss a typical pancreatitis diet plan.

32. Rest
 What about enforced bed rest,
a traditional strategy intended
to help the pancreas "rest"?
Although still sometimes
suggested in nursing texts, the
value of bed rest has never
been proved by research.

34.  Pancreatitis Low Carb Diet
A pancreatitis diet plan with low carbs
focuses on the utilization of fats as the
chief sources of energy and reducing
the insulin production capacity of the
body. The Atkin's diet, Zone diet and
Hollywood diet are known to be the
best low carb diets.