This document provides an overview of pancreatitis including: - Defining pancreatitis and describing the types as acute or chronic. - Stating the common causes as biliary disease, alcohol, ERCP, trauma, and drugs. - Explaining the pathophysiology as premature activation of digestive enzymes in the pancreas causing autodigestion. - Identifying clinical manifestations such as abdominal pain, nausea, fever, and diagnostic tests including blood tests and imaging. - Describing the management of fluid resuscitation, pain control, nutritional support, and antibiotics as well as surgical interventions for complications.

1. Pancreatitis
Neelima Shakya
M. Sc. Nursing
2013 Batch
10/4/2023
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2. Outline of seminar
At the end of the session the students will be able to
• Define pancreatitis
• State the types of pancreatitis
• List the causes
• Explain the pathophysiology
• Identify the clinical manifestations
• List the diagnostic investigations
• Describe the management
• Discuss the nursing management
• List the complications
• State the prognosis
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3. Anatomy of pancreas
• Structure-12-15 – cm long J-
shaped, soft, lobulated,
retroperitoneal organ.
• Location-lies transversely behind
the stomach, at (L1-2) spine.
• The head of the pancreas lies in
the duodenal C loop in front of
the inferior vena cava constitutes
about 50% of the total pancreas
• The body and tail of the pancreas
run obliquely upward to the left
in front of the aorta and left
kidney
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4. Functions of pancreas
Exocrine
• 1.5–3 L of alkaline (pH >
8.0) fluid/day containing
about 20 enzymes under
stimulation of secretin and
cholecystokinin
• joins the common bile duct
to form the
hepatopancreatic ampulla
controlled by the
hepatopancreatic sphincter
(of Oddi).
• Constitute 80% of
pancreatic parenchyma
Endocrine
• Scattered throughout the
gland containing beta cells
(secrete insulin), alpha cells
(secrete glucagon), delta
cells (secrete somatostatin)
• constitute only about 2% of
the pancreatic
parenchyma.
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6. AUTOPROTECTIONOFTHE PANCREAS
• Autodigestion of the pancreas is prevented by packaging
of proteases in precursor form and by the synthesis of
protease inhibitors, i.e., pancreatic secretory trypsin
inhibitor (PSTI) and serine protease inhibitor found in
the acinar cell.
• low calcium concentrations within the pancreas also
decrease trypsin activity.
• After reaching to duodenum trypsinogen converts to
trypsin by enterokinase which facilitates conversion of
other proenzymes.
• Loss of any of these protective mechanisms leads to
zymogen activation, autodigestion, and acute
pancreatitis.
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7. Pancreatitis
• Inflammation of the pancreas
• Can be acute or chronic
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8. Acute pancreatitis
• Acute nonbacterial inflammatory condition of
the pancreas, derived from the early activation
of digestive enzymes with variable compromise
of the gland itself, nearby tissues and other
organs and generally resolves over time.
• Range from mild discomfort to a severe, life-
threatening illness.
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9. Epidemiology
• Worldwide, the incidence ranges between 5 and
80 per 100,000 population
• In Finland and USA the main cause of AP is alcohol,
whereas studies from Hong Kong, England, Italy,
and Greece showed biliary AP to be more
common.
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10. Common causes of pancreatitis
• Biliary disease- 40%
• Alcohol intake more than 5-15 years or
binge drinking- 35%
• ERCP- 4%
• Trauma
• Drugs- azathioprine, valproic acid,
methyldopa, estrogen
• Hyperlipidemia- triglyceride >1000 mg/dl
• Scorpion bite
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11. Uncommon Causes
• Bacterial, viral, fungal and parasitic infection
• Vascular causes and vasculitis
• Cancer of the pancreas
• Hypercalcemia
• Cystic fibrosis
• Renal failure
• Postoperative (abdominal and nonabdominal operations)
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12. Etiology
GET SMASHED
G - Gall stones, most common
E – Ethanol, second most common
T – Trauma
S – Steroids
M – Mumps
A –Autoimmune Pancreatitis
S – Scorpion sting
H–hyperlipidaemia triglyceride >11.3 mmol/L(>1000
mg/dL).Hypothermia, Hyperparathyroidism
E - Endoscopic retrograde cholangiopancreatography
D - Drugs - azathioprine, valproic acid, methyldopa, estrogen.
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13. Pathophysiology
• Pancreatic enzymes are present in acinar cells in the proenzyme
form and have to be activated to fulfill their enzymatic potential.
• Trypsin has a major role in the autodigestion
• Once trypsin is generated, it activate other proenzymes such as
prophospholipase and proelastase, which then take part in the
process of autodigestion.
• The activated enzymes cause disintegration of fat cells and
damage the elastic fibers of blood vessels.
• Trypsin also converts prekallikrein to kinin system cause
inflammation and small-vessel thromboses.
• Macrophase activation- local inflammatory response
• Increased vascular permability
• Excreted into circulation causing systemic complications
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15. Clinical features
• Abdominal pain- Constant, midepigastric
or periumbilical, radiating to the back or
flank. Patient assumes a fetal position or
leans forward while sitting to relieve
pressure of the inflamed pancreas on
celiac plexus nerves.
• Nausea and vomiting.
• Fever.
• Involuntary abdominal guarding,
epigastric tenderness to deep palpation
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16. Contd..
• Dry mucous membranes; hypotension; cold,
clammy skin; cyanosis; and tachycardia
• Korte's sign: pain in the zone where the head
of pancreas is located (in epigastrium, 6–7 cm
above the umbilicus)
• Jaundice due to compression of common bile
duct.
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17. • Erythematous skin nodules due to subcutaneous
fat necrosis.
• Pulmonary findings -rales, atelectasis, and pleural
effusion most frequently left-sided.
• Bowel sounds are usually diminished or absent.
• An enlarged pancreas with organized necrosis or a
pseudocyst may be palpable in the upper
abdomen.
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18. Contd…
• Turner's sign -Purplish discoloration
of the flanks indicate
retroperitoneal hemorrhage
• Cullen's sign - Purplish discoloration
of periumbilical area
• occurs in extensive hemorrhagic
necrosis of the pancreas as the
result of hemoperitoneum
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19. Diagnostic investigations
• History- History should be taken regarding
alcohol , Gall stone , abdominal pain, vomiting
etc.
• Physical examination- Cullen’s sign, Turner’s
sign, hypotension, cold, clammy skin, cyanosis,
dehydration and tachycardia.
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20. Blood test
Blood amylase or lipase- lipase a better indicator
Amylase
• More than four times normal (normal 25-100 IU/L)
• Rises within 2 - 3 hr, peaks at 12 - 24 hr and returns to normal after
3 - 5 days
Lipase
• Increase within 4 - 8 hr, peak at 24 hr to > 2 times the upper limit
of normaland may remain elevated for 10 - 14 days.
Plasma C-reactive protein -‘gold-standard’ in predicting the
severity of acute pancreatitis, as a peak level of > 210 mg/L (on
the second, third or fourth day), or a level > 120 mg/L at the
end of the first week
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21. Contd…
• The plasma procalcitonin level- predictor of a
pancreatic infection.
• ABG-hypoxia, and lactic acidosis in severe
• Hyperglycemia
• Hypocalcemia
• LFT-Hyperbilirubinemia, return to normal in 4–7 days.
• serum lactic dehydrogenase (LDH) levels - >500 U/L
(normal <200)
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22. Contd…
• Abdominal ultrasound- to detect gallstones, alcoholic fatty liver
• ECG-ST segment and T-wave abnormalities
• CT Scan/MRI of abdomen- CECT -to identify inflammation of the
pancreas, fluid collection and any changes in the density of the
gland.
• ERCP to determine the exact location of a gallstone.
• Abdominal X-ray- To detect an ileus or isolated loop of small bowel
overlying pancreas.
• Chest X-ray- collapsed lung tissue, pleural effusion.
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23. Classification of acute pancreatitis
This classification defines three degrees of severity:
mild acute pancreatitis, moderately severe acute
pancreatitis, and severe acute pancreatitis.
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24. Contd…
Mild acute pancreatitis
• No organ failure
• No local or systemic complications
Moderately severe acute pancreatitis
• Organ failure that resolves within 48 h (transient organ failure)
• Local or systemic complications
Severe acute pancreatitis
• Persistent organ failure (>48 h)
• Single or multiple organ failure
• one or more local complications.
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25. Differential diagnosis
• Cholangitis
• Cholecystitis
• Gastritis
• Intestinal perforation
• Myocardial infarction
• Pancreatic cancer
• Peptic ulcer disease
• Pneumonia
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26. DIAGNOSTIC CRITERIA
Several scoring systems are used to predict the severity of an attack of
pancreatitis.
According to Ranson’s criteria
1. Age >55 years
2. WBC >16,000 mm3
3. Serum glucose >200 mg/dL (>11.1 mmol/L)
4. Serum LDH >350 IU/L (>350 U/L)
5. AST >250 U/mL (120 U/L)
6. Fall in hematocrit >10% (>0.10)
7. BUN increase >5 mg/dL (>1.7 mmol/L)
8. Serum calcium <8 mg/dL (<2.0 mmo/L)
9. Base deficit >4 mEq/L (>4 mmol/L)
10. Fluid retention or sequestration >6 L
11. PO2<60 mm Hg
• Total Score= 11
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27. Ransoncriteriaforpredictingtheseverityof
acutepancreatitis
At admission
1. Age in years > 55 years
2. white blood cell count >
16000 cells/mm3
3. Blood glucose >
10 mmol/L (> 200 mg/dL)
4. serum AST > 250 IU/L
5. serum LDH > 350 IU/L
The presence of 3 or more
criteria indicates severe
pancreatitis
At 48 hours
1. Calcium (serum calcium <
2.0 mmol/L (< 8.0 mg/dL)
2. Hematocrit fall >10 %
3. Oxygen (hypoxemia PO2 <
60 mmHg)
4. BUN >5 mg/dL after IV fluid
hydration
5. -Base deficit (negative base
excess) > 4 mEq/L
6. Sequestration of fluids > 6 L
The presence of 3 or more
criteria indicates severe
pancreatitis
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28. Other criteria used
• BISAP score
• Glasgow score
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29. Management
• self-limited in 85–90% and subsides spontaneously,
usually within 3–7 days after treatment is
instituted.
• No definite treatment
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30. General approach
Fluid resuscitation
• NPO
• intravenous fluid-250-500 ml/hour (RL preferred)
Pain management
• Morphine avoided as it cause spasm of the sphincter of oddi;
paracetamol, tramadol, pethidine used.
• If gallstones- cholecystectomy during the same hospital
admission.
• Antiemetic.
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31. Nutritional support
• Feeding enterally- NG, FJ
• low-fat and low protein diet initially.
• In mild uncomplicated pancreatitis oral feedings once the
patient’s pain and anorexia resolve.
• Total parenteral nutrition when calorie requirement not
met by enteral nutrition
Antibiotics
• Routine prophylactic antibiotics not recommended
• Infected necrosis who fail to improve after 7 – 10 days
antibiotics E.g.- carbapenems, quinolones, and
metronidazole
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32. • Patients with severe acute pancreatitis
require intensive care.
• discharged when their pain is well controlled
with oral analgesia, able to tolerate an oral
diet and all complications have been
addressed adequately
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33. Surgical Intervention if complications
occur
• In patients with gallstones- cholecystectomy
• If necrotizing biliary AP, cholecystectomy deferred until
active inflammation subsides
• In stable patients with infected necrosis, surgical,
radiologic, and endoscopic drainage should be delayed
preferably for more than 4 weeks to allow liquefication
of the contents and the development of a fibrous wall
around the necrosis.
•
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34. Surgical intervention
Distal Pancreatectomy
• resection of variable amounts of the body and tail of the
pancreas.
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35. Endoscopic Pancreatic Sphincterotomy
• to reduce pancreatic duct pressure and to
facilitate other procedures such as pancreatic
stent placement, tissue sampling, dilation of
strictures, or stone removal.
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36. Roux-en-Y Choledochojejunostomy
• The choledochojejunostomy is indicated in patients who
have recurrent stones, intrahepatic stones, or distal
biliary strictures.
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37. The Puestow Procedure
• An 8–10-cm segment of the pancreatic duct is unroofed and
intraductal concretions removed . The jejunum is divided and
the opened pancreatic duct is anastomosed to the jejunum.
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38. Prevention
• Avoiding heavy alcohol use will help to prevent
pancreatitis.
• Prevent gallstones may help to prevent gallstone-
related acute pancreatitis.
• If the cause is gallstones, gallbladder surgery will
usually be recommended to prevent future attacks.
• When a medication is the likely cause, it will be
stopped if possible.
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39. Prognosis
• Overall mortality in patients with acute pancreatitis
is 10-15%. Patients with biliary pancreatitis tend to
have a higher mortality than patients with alcoholic
pancreatitis.
• In patients with severe disease (organ failure), who
account for about 20% of presentations, mortality is
approximately 30%.
• In patients with necrosis without organ failure,
mortality approaches zero.
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40. Complication
local
• Necrosis
• Pseudocyst
• Intraperitoneal
hemorrhage
• Thrombosis of blood
vessels
• Bowel infarction
• Obstructive jaundice
systemic
• Pulmonary- pleural effusion,
atelectesis, pneumonitis, ARDS,
• Renal- Oliguria, Azotemia
• Metabolic-Hyperglycemia,
Hypertriglyceridemia, Hypovolemia
• Cardiovascular Hypotension,
Nonspecific ST-T changes
• Hematologic - (erythematous
nodules)
• Gastrointestinal hemorrhage , Peptic
ulcer disease ,Erosive gastritis
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41. Chronic pancreatitis
• Continuing, chronic, inflammatory process of the
pancreas, characterized by irreversible
morphologic changes
• Presence of histologic abnormalities, including
chronic inflammation, fibrosis, and progressive
destruction of both exocrine and eventually
endocrine tissue.
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42. Epidemiology
• The worldwide prevalence 4-5%
• The incidence of CP ranges from 1.6 to 23 cases per
100,000 per year worldwide.
• It affects 10-15 per 100,000 population in Western
countries but is much higher in Japan - 45 per 100,000.
• male:female ratio 4:1 and a median patient age of 51
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43. Etiology
Toxic-metabolic- Alcoholic, smoking,Hypercalcemia,
hyperlipidemia, Chronic renal failure, Medications
Genetic- Hereditary pancreatitis, gene mutation
Obstructive causes- Sphincter of Oddi disorders, Duct
obstruction (e.g., tumor, scars)
Autoimmune- Sjögren’s syndrome, Inflammatory bowel
disease, Primary biliary cirrhosis
Recurrent and severe acute pancreatitis
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44. Clinical features
• The abdominal pain radiating to the back,
both upper and lower quadrants.
• Eating may exacerbate the pain
• Epigastric tenderness
• Sitting up and leaning forward relieve.
• Maldigestion - chronic diarrhea (>6/ day),
steatorrhea, weight loss, and fatigue.
• Diabetes mellitus.
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45. Diagnostic evaluation
• Serum amylase and lipase may be normal to low because
of decreased pancreatic exocrine function.
• Fecal fat analysis
• Bilirubin and alkaline phosphatase may be elevated
• Secretin and cholecystokinin stimulatory test results
abnormal
• Plain abdominal X-ray to determine diffuse calcification of
the pancreas.
• CT scan for calcifications, masses, ductal irregularities,
enlargement, and pseudocysts.
• ERCP defines ductal anatomy and localizes complications,
such as pancreatic pseudocysts and ductal disruptions.
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46. Management
• Avoidance of alcohol
• Enzyme therapy to control diarrhoea and restores absorption
of fat.
• Tricyclic antidepressants to decrease pain and potentiate the
effects of opiates. Eg: Amitriptyline hydrochloride
• Octreotide subcutaneous injection 3 times daily at 200mcg
• high-protein, high-calorie diets.
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47. • In severely malnourished chronic pancreatitis
patients, total parenteral nutrition
• Diabetes mellitus treated with diet, insulin, or
oral antidiabetic agents.
• Endoscopic treatment -sphincterotomy, stenting,
stone extraction, and drainage of a pancreatic
pseudocyst.
• Surgery and autologous islet cell transplantation
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48. Surgical management
• The puostow procedure
• Whipple procedure-Standard
pancreaticoduodenectomy involves
resection of the head of the
pancreas, duodenum, gallbladder,
distal common bile duct and antrum.
• Distal pancreatectomy
• Celiac nerve block- The celiac plexus
is located on the anterolateral
surface of the aorta at the T12–L2
spinal level.
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49. Nursing Assessment
• abdominal pain
• nutritional status
• steatorrhea and malabsorption
• signs and symptoms of diabetes mellitus
• current alcohol intake and motivation and
resources available to abstain from
drinking
• Obtain history of gallbladder disease
• respiratory rate and pattern and breath
sounds.
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50. Nursing Diagnoses
• Acute and chronic pain related to acute/ chronic and
unrelenting insult to pancreas
• Imbalanced nutrition: less than body requirements related
to fear of eating, malabsorption, and glucose intolerance
• Deficient Fluid Volume related to vomiting, self-restricted
intake, fever, and fluid shifts
• Ineffective Breathing Pattern related to severe pain and
pulmonary complications
• Impaired skin integrity related to poor nutritional status,
bed rest, and multiple drains and surgical wound
• Anxiety related to surgical intervention
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51. Controlling pain
• Assess character, location, frequency, duration, precipitating
and alleviating factors of pain.
• Nonpharmacologic methods- distraction, imagery, and
progressive muscle relaxation.
• Administer opioid analgesics.
• Assist patient to a comfortable position.
• Maintain NPO status to decrease pancreatic enzyme
secretion.
• Maintain patency of NG suction.
• frequent oral hygiene and care.
• Administer antacids or H2-receptor antagonists.
• Report increase in severity of pain, which may indicate
hemorrhage, rupture of a pseudocyst, or inadequate dosage
of the analgesic.
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52. Improving respiratory function
• Assess respiratory rate and rhythm, effort,
oxygen saturation, and breath sounds
frequently.
• upright or semi-Fowler's position
• oxygen supplementation
• Report signs of respiratory distress
immediately.
• coughing and deep breathing
•
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53. Improving nutrition
• Assess nutritional status, weight loss,
dietary habits, alcohol intake.
• Administer pancreatic enzyme
replacement with meals.
• Administer antacids or h2-receptor
antagonists
• Monitor intake and output and daily
weight.
• Low-fat diet.
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54. Maintaining adequate fluid volume
• Monitor and record vital signs, skin color, and
temperature, intake/output, weight daily.
• Evaluate laboratory data for hemoglobin,
hematocrit, albumin, calcium, potassium, sodium,
and magnesium levels and administer replacements
as prescribed.
• Observe and measure abdominal girth if pancreatic
ascites is suspected.
• Report trends in falling blood pressure or urine
output or rising pulse, which indicate hypovolemia
and shock or renal failure.
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55. Improving skin integrity
•Turn the patient every 2 hours.
•Apply moisturizers
•Provide skin care
•Bedmaking as necessary
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56. Relieving anxiety
• Describe patient for surgery as well as adverse
effects and complications of surgery.
• Total pancreatectomy - permanent diabetes
mellitus, dependence on insulin, severe
malabsorption, and the need for lifelong
pancreatic enzyme replacement.
• encouraging abstinence of alcohol and intake of
nutritional and vitamin supplements.
• After surgery, provide meticulous care to prevent
infection, promote wound healing, and prevent
routine complications of surgery.
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57. Patient education
• gradually resume a low-fat diet.
• Instruct patient to increase activity gradually
• Reinforce information about disease process and
precipitating factors.
• eliminate all alcohol
• Instruct in proper administration of pancreatic enzyme
replacement.
• Take just before or during meals.
• Take with antacid or take H2-receptor antagonist as
directed to prevent pancreatic enzyme from being
destroyed by gastric acid secretions
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