m

1. pancreatitis
Logman Mohammed Alshaikh
logman Mohammed 1

2. pancreatitis
• pancreatitis, acute or chronic, is an inflammation
and potential necrosis of the pancreas.
• Tissue damage from pancreatitis occurs because of
activation of proteolytic and lipolytic pancreatic
enzymes that are normally activated in the
duodenum.
• Proteolytic enzymes, such as trypsin, elastase, and
phospholipase, break down protein;
• lipolytic enzymes break down fats.
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3. Acute pancreatits
• Is acondition presenting with acute onset of
abdomial painassisciatedwith raisedlevels of
pancreatic enzymese in the blood and urine.
• The gland normaly returns functional and
anatomical normality after the cause is
treated
• Recurrent attacks may occur(relapsing acute
pancreatitis)
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4. causes
• Biliary tract diease
• Alcohol
• Hyperlipidemia
• Viral infection
• Hypothermia
• trauma
• Post operative
• Familal
• Scorpion sting
• Idiopathic
• Autoimmune
• Post ERCP
• cancer
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5. Pathophysiology
• Acute pancreatitis results when an initiating
event causes the extrusion of zymogen
granules from pancreatic acinar cells, into
the interstitium of the pancreas.
• Zymogen particles cause the activation of
trypsinogen into trypsin.
• Trypsin causes auto-digestion of pancreatic
tissues.
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6. • The destruction of the acinar cells and islet cell
tissue) lead to auto digestion of pancreas with
leakage of the enzymes and fluid into
surrounding tissues.
• 2 types of pancreatitis
• Interstitial (80%) (edematous) mild, self limiting
(3-5 days), fluid accumulation with swelling and edema
• Necrotizing (20%) (death of tissue) hemorrhagic with
cellular death and systemic complications
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7. Acute Severe Pancreatitis Pathophysiology
Injury or disruption of pancreatic ducts leakage
of active pancreatic enzymes  autodigestion
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8. • STAGE 1: Pancreatic Injury
- Edema
- Inflammation
• STAGE 2: Local Effects
- Retroperitoneal edema
- Ileus
• STAGE 3: Systemic Complications
- Hypotension/shock
- Metabolic disturbances
- Sepsis/organ failure
SEVERITY
Mild
Severe
Acute Pancreatitis
Pathogenesis

9. Clinical presentation
• Severe epigastric pain radiating to the
back,nausea,vomiting,shock,tender in
epigastrium initialy spreading to whole
abdomen,abdominal distention,absent bowel
sound ,bluish discoloration in flanks(Turner’s
sign)or periumblical grey area (Cullen’s sign)
• Due to haemorrhagic pancreatits with spread
of blood retroperitoneally to these areas
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10. • Grey Turner sign • Cullen’s sign
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11. investigations
• Hb,WBC,U/E,LFT,BG,
• Amylase raised <1000u/l
• Be aware that pt with haemorrhagic
pancreatitis who present late and in whom
the amylase is normalB/C of extensve
destruction of the pancreas.
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12. cont
• 1. bilirubin, alkaline phosphatase, lactate
dehydrogenase, AST, ALT,and cholesterol
may be elevated.
• 2. Serum albumin, calcium, sodium,
magnesium and, potassium may be low
due to dehydration.
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13. • 3. Abdominal X-ray.
• 4. CT scan is the most definitive study for
determining pancreatic changes.
• 5. Chest X-ray for detection of pulmonary
complications.
• Endoscopic Retrograde Cholangiopancreatography
(ERCP)
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14. complications
• ARF,ARDS, gastric errosion,DIC,
DM,necrosis,abscesformation ,relapes, chronic
pancreatitis
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15. Management
• Mild case:
• N/G Suction
• IV fluid
• NPO
• Antibiotics
• Intake and out put chart
• Monitor WCC,LFT,BG,U&E
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16. cont
• Severe case: sevirity is
indcated by ranson
criteria):
• N/G Suction
• IV fluid
• NPO
• Antibiotics
• Intake and out put
chart/hour
• Analgesia
• H2 receptor antagonis
• Treat ARDS,ARF
• ERCP if common bile
duct stone
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17. Ranson Criteria
alcoholic Pancreatitis
• On admission
– Age > 55
– WBC > 16,000
– Glucose > 200
– LDH > 350
– AST > 250
• During first 48 hours
– Hematocrit drop > 10%
– Serum calcium < 8
– Base deficit > 4.0
– Increase in BUN > 5
– Fluid sequestration > 6L
– Arterial PO2 < 60
5% mortality risk with <2 signs
15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signslogman Mohammed 17

18. Cont
• Indications for surgery:
• Uncertainty of diagnosis
• Deterioration of patient condition.drainge of
abcsess or removal of necrotic pancreas may
be required
• Drainge of pseudocyst
• Early cholecystectomy if gallstones are the
cause
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19. Chronic pancreatitis
• etiology :
• chronic alcohol abuse (90%)
• Gallstones
• Hyperparathyroidism
• Congenital malformation
• Idiopathic
• MRCP of pancreas
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20. Pathophysiology
• In chronic pancreatitis, there is permanent
destruction.
• Edema and distension cause damage and loss of
the acinar cells.
• The normal cells are replaced with fibrosis and
necrosis.
• As the autodigestion process of the pancreas
progresses, the cells form walls around the fluid
that contains enzymes and the necrotic debris.
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21. cont
• These pseudocysts can rupture into the
peritoneum and surrounding tissues, resulting
in complications of infection, abscesses, and
fistulae.
• The islet cells within the pancreas may also be
damaged and destroyed, leading to diabetes
mellitus.
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22. Symptoms and signs
• Upper abdominal pain often raditing to the
back.
• Weight loss ,nausea,vomiting,steatorhea
• 30-4-% develops DM
• Jaundice if CBD obstructed
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23. investigations
•  or normal amylase and lipase
• Plain AXR / CT may show calcified
pancreas
• Blood glucose may be raised
• Lipd profile
• CT ,MRCP/ERCP
• Calcium may be raised
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24. CT - chronic pancreatitis
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25. Management
• Medical:
• stop alcohol
• Low fat diet
• Pancreatic extracts given orally(pancrex or
creon)
• Treat DM,
• Pain control
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26. cont
• Surgical:
• Decompression of duct by endoscopic
sphincterotomy and insertion of pancreatic
duct stent at ERCP.
• Longitudinal pancreaticojejunostomy
maybe carried out.
• Other options:
• Resection of head,body and tail or whole
gland
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27. cont
• If total pancreatectomy is required
consider isolating the islets cells from the
pancreas and carrying out
autotransplantation.
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28. Complications
• Exocrine insufficiency typically manifests
as weight loss and steatorrhea
 If steatorrhea present, a trypsinogen level < 10
is diagnostic for chronic pancreatitis
 Manage with low-fat diet and pancreatic
enzyme supplements
 Endocrine insufficiency may result from islet
cell destruction which leads to diabetes
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29. Nursing Assessment
• 1. Obtain history of gallbladder disease,
alcohol use, or precipitating factors.
• 2. Assess GI distress, including nausea and
vomiting, diarrhea, and passage of stools
containing fat.
• 3. Assess characteristics of abdominal pain.
• 4. Assess nutritional and fluid status.
• 5. Assess respiratory rate and pattern and
breath sounds.
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30. • 6. Assess for any changes in mental status
in an older person with pancreatitis as an
indicator of an underlying complication.
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31. Nursing Diagnoses
• Acute Pain related to disease process
• Deficient Fluid Volume related to vomiting,
self-restricted intake, fever, and fluid shifts
• Ineffective Breathing Pattern related to
severe pain and pulmonary complications
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32. Nursing Interventions
Controlling Pain
1. Administer analgesics to control pain.
2. Assist patient to a comfortable position.
3. Maintain NPO status to decrease pancreatic enzyme
secretion.
4. Maintain patency of NG suction to remove gastric
secretions and to relieve abdominal distention, if
indicated.
5. Provide frequent oral hygiene and care.
6. 6. Administer antacids or H2-receptor antagonists
7. Report increase in severity of pain, which may
indicate hemorrhage of the pancreas, rupture of a
pseudocyst, or inadequate dosage of the analgesic.
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33. Restoring Adequate Fluid Balance
1. Monitor and record vital signs, skin color, and
temperature.
2. Monitor intake and output and weigh daily.
3. Evaluate laboratory data for hemoglobin,
hematocrit, albumin, calcium, potassium, sodium,
and magnesium levels. and administer
replacements as prescribed.
4. Observe and measure abdominal girth if
pancreatic ascites is suspected.
5. Report any falling in BP or urine output or rising
pulse, because this may indicate hypovolemia
and shock or renal failure.
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34. Improving Respiratory Function
• 1. Assess respiratory rate and rhythm, effort,
oxygen saturation, and breath sounds
frequently.
• 2. Position in upright or semi-Fowler’s
position to enhance diaphragmatic excursion.
• 3. Administer oxygen to maintain adequate
oxygen levels.
• 4. Report signs of respiratory distress
immediately.
• 5. Instruct patient in coughing and deep
breathing to improve respiratory function.
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35. Patient Education
• 1. Instruct patient to gradually resume a
low-fat diet.
• 2. Instruct patient to increase activity
gradually, providing for daily rest periods.
• 3. Reinforce information about disease
process and precipitating factors.
• 4. If pancreatitis is a result of alcohol
abuse, patient needs to be reminded of
the importance of eliminating all alcohol
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