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Pancreatitis
Pancreatitis is an inflammation of the pancreas that can be acute or chronic. In acute pancreatitis, digestive enzymes are abnormally activated within the pancreas, causing the pancreas to digest itself. Symptoms include severe abdominal pain. Complications can include organ failure. Treatment focuses on pain control, intravenous fluids, and treating any complications. Chronic pancreatitis results from long-term or repeated damage to the pancreas over many years, often due to alcohol abuse. This destroys pancreatic tissue and can lead to diabetes and malnutrition.
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Pancreatitis
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- 2. pancreatitis • pancreatitis, acuteor 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. logman Mohammed 2
- 3. Acute pancreatits • Isacondition 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) logman Mohammed 3
- 4. causes • Biliary tractdiease • Alcohol • Hyperlipidemia • Viral infection • Hypothermia • trauma • Post operative • Familal • Scorpion sting • Idiopathic • Autoimmune • Post ERCP • cancer logman Mohammed 4
- 5. Pathophysiology • Acute pancreatitisresults 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. logman Mohammed 5
- 6. • The destructionof 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 logman Mohammed 6
- 7. Acute Severe PancreatitisPathophysiology Injury or disruption of pancreatic ducts leakage of active pancreatic enzymes autodigestion 7logman Mohammed
- 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 • Severeepigastric 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 logman Mohammed 9
- 10. • Grey Turnersign • Cullen’s sign logman Mohammed 10
- 11. investigations • Hb,WBC,U/E,LFT,BG, • Amylaseraised <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. logman Mohammed 11
- 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. logman Mohammed 12
- 13. • 3. AbdominalX-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) logman Mohammed 13
- 14. complications • ARF,ARDS, gastricerrosion,DIC, DM,necrosis,abscesformation ,relapes, chronic pancreatitis logman Mohammed 14
- 15. Management • Mild case: •N/G Suction • IV fluid • NPO • Antibiotics • Intake and out put chart • Monitor WCC,LFT,BG,U&E logman Mohammed 15
- 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 logman Mohammed 16
- 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 forsurgery: • 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 logman Mohammed 18
- 19. Chronic pancreatitis • etiology: • chronic alcohol abuse (90%) • Gallstones • Hyperparathyroidism • Congenital malformation • Idiopathic • MRCP of pancreas logman Mohammed 19
- 20. Pathophysiology • In chronicpancreatitis, 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. logman Mohammed 20
- 21. cont • These pseudocystscan 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. logman Mohammed 21
- 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 logman Mohammed 22
- 23. investigations • ornormal amylase and lipase • Plain AXR / CT may show calcified pancreas • Blood glucose may be raised • Lipd profile • CT ,MRCP/ERCP • Calcium may be raised logman Mohammed 23
- 24. CT - chronicpancreatitis logman Mohammed 24
- 25. Management • Medical: • stopalcohol • Low fat diet • Pancreatic extracts given orally(pancrex or creon) • Treat DM, • Pain control logman Mohammed 25
- 26. cont • Surgical: • Decompressionof 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 logman Mohammed 26
- 27. cont • If totalpancreatectomy is required consider isolating the islets cells from the pancreas and carrying out autotransplantation. logman Mohammed 27
- 28. Complications • Exocrine insufficiencytypically 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 logman Mohammed 28
- 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. logman Mohammed 29
- 30. • 6. Assessfor any changes in mental status in an older person with pancreatitis as an indicator of an underlying complication. logman Mohammed 30
- 31. Nursing Diagnoses • AcutePain 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 logman Mohammed 31
- 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. logman Mohammed 32
- 33. Restoring Adequate FluidBalance 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. logman Mohammed 33
- 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. logman Mohammed 34
- 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 logman Mohammed 35
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