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bsc pancreatitis 8.pptx
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.
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bsc pancreatitis 8.pptx
- 1. Pancreatitis Neelima Shakya M. Sc.Nursing 2013 Batch 10/4/2023 Neelima Shakya 1
- 2. Outline of seminar Atthe 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 10/4/2023 Neelima Shakya 2
- 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 10/4/2023 Neelima Shakya 3
- 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. 10/4/2023 Neelima Shakya 4
- 5.
- 6. AUTOPROTECTIONOFTHE PANCREAS • Autodigestionof 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. 10/4/2023 Neelima Shakya 6
- 7. Pancreatitis • Inflammation ofthe pancreas • Can be acute or chronic 10/4/2023 Neelima Shakya 7
- 8. Acute pancreatitis • Acutenonbacterial 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. 10/4/2023 Neelima Shakya 8
- 9. Epidemiology • Worldwide, theincidence 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. 10/4/2023 Neelima Shakya 9
- 10. Common causes ofpancreatitis • 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 10/4/2023 Neelima Shakya 10
- 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) 10/4/2023 Neelima Shakya 11
- 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. 10/4/2023 Neelima Shakya 12
- 13. Pathophysiology • Pancreatic enzymesare 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 10/4/2023 Neelima Shakya 13
- 14.
- 15. Clinical features • Abdominalpain- 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 10/4/2023 Neelima Shakya 15
- 16. Contd.. • Dry mucousmembranes; 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. 10/4/2023 Neelima Shakya 16
- 17. • Erythematous skinnodules 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. 10/4/2023 Neelima Shakya 17
- 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 10/4/2023 Neelima Shakya 18
- 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. 10/4/2023 Neelima Shakya 19
- 20. Blood test Blood amylaseor 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 10/4/2023 Neelima Shakya 20
- 21. Contd… • The plasmaprocalcitonin 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) 10/4/2023 Neelima Shakya 21
- 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. 10/4/2023 Neelima Shakya 22
- 23. Classification of acutepancreatitis This classification defines three degrees of severity: mild acute pancreatitis, moderately severe acute pancreatitis, and severe acute pancreatitis. 10/4/2023 Neelima Shakya 23
- 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. 10/4/2023 Neelima Shakya 24
- 25. Differential diagnosis • Cholangitis •Cholecystitis • Gastritis • Intestinal perforation • Myocardial infarction • Pancreatic cancer • Peptic ulcer disease • Pneumonia 10/4/2023 Neelima Shakya 25
- 26. DIAGNOSTIC CRITERIA Several scoringsystems 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 10/4/2023 Neelima Shakya 26
- 27. Ransoncriteriaforpredictingtheseverityof acutepancreatitis At admission 1. Agein 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 10/4/2023 Neelima Shakya 27
- 28. Other criteria used •BISAP score • Glasgow score 10/4/2023 Neelima Shakya 28
- 29. Management • self-limited in85–90% and subsides spontaneously, usually within 3–7 days after treatment is instituted. • No definite treatment 10/4/2023 Neelima Shakya 29
- 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. 10/4/2023 Neelima Shakya 30
- 31. Nutritional support • Feedingenterally- 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 10/4/2023 Neelima Shakya 31
- 32. • Patients withsevere 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 10/4/2023 Neelima Shakya 32
- 33. Surgical Intervention ifcomplications 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. • 10/4/2023 Neelima Shakya 33
- 34. Surgical intervention Distal Pancreatectomy •resection of variable amounts of the body and tail of the pancreas. 10/4/2023 Neelima Shakya 34
- 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. 10/4/2023 Neelima Shakya 35
- 36. Roux-en-Y Choledochojejunostomy • Thecholedochojejunostomy is indicated in patients who have recurrent stones, intrahepatic stones, or distal biliary strictures. 10/4/2023 Neelima Shakya 36
- 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. 10/4/2023 Neelima Shakya 37
- 38. Prevention • Avoiding heavyalcohol 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. 10/4/2023 Neelima Shakya 38
- 39. Prognosis • Overall mortalityin 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. 10/4/2023 Neelima Shakya 39
- 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 10/4/2023 Neelima Shakya 40
- 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. 10/4/2023 Neelima Shakya 41
- 42. Epidemiology • The worldwideprevalence 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 10/4/2023 Neelima Shakya 42
- 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 10/4/2023 Neelima Shakya 43
- 44. Clinical features • Theabdominal 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. 10/4/2023 Neelima Shakya 44
- 45. Diagnostic evaluation • Serumamylase 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. 10/4/2023 Neelima Shakya 45
- 46. Management • Avoidance ofalcohol • 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. 10/4/2023 Neelima Shakya 46
- 47. • In severelymalnourished 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 10/4/2023 Neelima Shakya 47
- 48. Surgical management • Thepuostow 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. 10/4/2023 Neelima Shakya 48
- 49. Nursing Assessment • abdominalpain • 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. 10/4/2023 Neelima Shakya 49
- 50. Nursing Diagnoses • Acuteand 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 10/4/2023 Neelima Shakya 50
- 51. Controlling pain • Assesscharacter, 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. 10/4/2023 Neelima Shakya 51
- 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 • 10/4/2023 Neelima Shakya 52
- 53. Improving nutrition • Assessnutritional 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. 10/4/2023 Neelima Shakya 53
- 54. Maintaining adequate fluidvolume • 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. 10/4/2023 Neelima Shakya 54
- 55. Improving skin integrity •Turnthe patient every 2 hours. •Apply moisturizers •Provide skin care •Bedmaking as necessary 10/4/2023 Neelima Shakya 55
- 56. Relieving anxiety • Describepatient 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. 10/4/2023 Neelima Shakya 56
- 57. Patient education • graduallyresume 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 10/4/2023 Neelima Shakya 57
- 58.