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Focus on Pancreatitis (Relates to Chapter 44, “Nursing Management: Liver, Pancreas, and Biliary Tract Problems” in the textbook)
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Acute Pancreatitis An acute inflammatory process of the pancreas
Degree of inflammation varies from mild edema to severe necrosis
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Acute Pancreatitis Etiology and Pathophysiology
Most common in middle-aged men and women Severity of the disease varies according to the extent of pancreatic destruction Can be life-threatening African American rate three times higher than for whites
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Acute Pancreatitis Etiology and Pathophysiology (Cont’d)
Primary etiologic factors are Biliary tract disease Most common: Gallbladder disease Alcoholism
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Acute Pancreatitis Etiology and Pathophysiology (Cont’d)
Less common causes Trauma (postsurgical, abdominal) Viral infections (mumps, coxsackievirus HIV) Penetrating duodenal ulcer Cysts Idiopathic
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Acute Pancreatitis Etiology and Pathophysiology
Less common causes (cont’d) Abscesses Cystic fibrosis Kaposi’s sarcoma Metabolic disorders Vascular diseases Postop GI surgery
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Acute Pancreatitis Etiology and Pathophysiology
Less common causes (cont’d) Drugs Corticosteroids Thiazide diuretics Oral contraceptives Sulfonamides NSAIDs
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Acute Pancreatitis Etiology and Pathophysiology
Caused by autodigestion of pancreas Etiologic factors Injury to pancreatic cells Activate pancreatic enzymes
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Acute Pancreatitis Fig
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Acute Pancreatitis Etiology and Pathophysiology
Trypsinogen Activated to trypsin by enterokinase Inhibitors usually inactivate trypsin Enzyme can digest the pancreas and can activate other proteolytic enzymes
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Pancreatitis Etiology and Pathophysiology
Elastase Activated by trypsin Plays a major role in autodigestion Causes hemorrhage by producing dissolution of the elastic fibers of blood vessels
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Acute Pancreatitis Etiology and Pathophysiology
Phospholipase A Plays a major role in autodigestion Activated by trypsin and bile acids Causes fat necrosis
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Acute Pancreatitis Etiology and Pathophysiology (Cont’d)
Trypsin Edema, necrosis, hemorrhage Elastase Hemorrhage Phospholipase A Fat necrosis Kallikrein Edema, vascular permeability, smooth muscle contraction, shock Lipase
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Acute Pancreatitis Etiology and Pathophysiology (Cont’d)
Alcohol May stimulate production of digestive enzymes Increases sensitivity to hormone cholecystokinin Stimulates production of pancreatic enzymes
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Acute Pancreatitis Etiology and Pathophysiology (Cont’d)
Edematous pancreatitis Mild and self-limiting Necrotizing pancreatitis Degree of necrosis correlates with severity of manifestations
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Acute Pancreatitis Clinical Manifestations
Abdominal pain is predominant symptom Pain located in the left upper quadrant Pain may be in the midepigastrium Commonly radiates to the back
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Acute Pancreatitis Clinical Manifestations
Abdominal pain (cont’d) Sudden onset Severe, deep, piercing, steady Aggravated by eating Not relieved by vomiting
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Acute Pancreatitis Clinical Manifestations
Flushing Cyanosis Dyspnea Edema Nausea/vomiting Bowel sounds decreased or absent
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Acute Pancreatitis Clinical Manifestations (Cont’d)
Low-grade fever Leukocytosis Hypotension Tachycardia Jaundice Abdominal tenderness
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Acute Pancreatitis Clinical Manifestations (Cont’d)
Abdominal distention Abnormal lung sounds Crackles Discoloration of abdominal wall
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Acute Pancreatitis Complications
Two significant local complications Pseudocyst Abscess
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Acute Pancreatitis Complications (Cont’d)
Pseudocyst Cavity surrounding outside of pancreas filled with necrotic products and liquid secretions Abdominal pain Palpable epigastric mass
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Acute Pancreatitis Complications
Pseudocyst (cont’d) Nausea, vomiting, and anorexia Elevated serum amylase May resolve spontaneously within a few weeks or may perforate, causing peritonitis Treatment: Internal drainage procedure
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Acute Pancreatitis Complications
Pancreatic abscess A large fluid-containing cavity within pancreas Results from extensive necrosis in the pancreas Upper abdominal pain Abdominal mass
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Acute Pancreatitis Complications
Pancreatic abscess (cont’d) High fever Leukocytosis Requires surgical drainage
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Acute Pancreatitis Complications
Main systemic complications Pulmonary Pleural effusion Atelectasis Pneumonia
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Acute Pancreatitis Complications
Systemic complications (cont’d) Cardiovascular Hypotension Tetany (caused by hypocalcemia)
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Acute Pancreatitis Diagnostic Studies
History and physical examination Laboratory tests Serum amylase Serum lipase 2-hour urinary amylase and renal amylase clearance
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Acute Pancreatitis Diagnostic Studies
Laboratory tests (cont’d) Blood glucose Serum calcium Triglycerides
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Acute Pancreatitis Diagnostic Studies
Flat plate of abdomen Abdominal/endoscopic ultrasound Endoscopic retrograde cholangiopancreatography (ERCP) Chest x-ray
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Acute Pancreatitis Diagnostic Studies (Cont’d)
CT of pancreas Magnetic resonance cholangiopancreatography (MRCP)
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Acute Pancreatitis Collaborative Care
Objectives include Relief of pain Prevention or alleviation of shock ↓ of pancreatic secretions Fluid/electrolyte balance Removal of the precipitating cause
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Acute Pancreatitis Collaborative Care (Cont’d)
Conservative therapy Supportive care Aggressive hydration Pain management IV morphine Combined with antispasmodic agent Management of metabolic complications Minimizing stimulation
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Acute Pancreatitis Collaborative Care
Conservative therapy (cont’d) Shock Plasma or plasma volume expanders (dextran or albumin) Fluid/electrolyte imbalance Lactated Ringer’s solution Ongoing hypotension Vasoactive drugs: Dopamine (Intropin) ↑ Systemic vascular resistance
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Acute Pancreatitis Collaborative Care
Conservative therapy (cont’d) Suppression of pancreatic enzymes NPO NG suction Prevent infections Peritoneal lavage or dialysis Remove kinin and phospholipase A exudate
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Acute Pancreatitis Collaborative Care
Surgical therapy indicated if Presence of gallstones Uncertain diagnosis Unresponsive to conservative therapy Abscess, pseudocyst, or severe peritonitis
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Acute Pancreatitis Collaborative Care
Surgical therapy (cont’d) ERCP Endoscopic sphincterotomy Laparoscopic cholecystectomy
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Acute Pancreatitis Collaborative Care (Cont’d)
Drug therapy IV morphine Nitroglycerin or papaverine Antispasmodics Carbonic anhydrase inhibitor Antacids Histamine (H2) receptor
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Acute Pancreatitis Collaborative Care (Cont’d)
Nutritional therapy NPO status initially to reduce pancreatic secretion IV lipids Monitor triglycerides Small, frequent feedings High-carbohydrate, low-fat, high-protein diet Bland diet
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Acute Pancreatitis Collaborative Care
Nutritional therapy (cont’d) Supplemental fat-soluble vitamins Supplemental commercial liquid preparations Parenteral nutrition No caffeine or alcohol
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Acute Pancreatitis Nursing Assessment
Health history Biliary tract disease Alcohol use Abdominal trauma Duodenal ulcers Infection Metabolic disorders
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Acute Pancreatitis Nursing Assessment (Cont’d)
Medication usage Thiazides, estrogens, corticosteroids, NSAIDs Surgical procedures Nausea/vomiting Dyspnea Severe pain
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Acute Pancreatitis Nursing Assessment (Cont’d)
Physical examination findings Fever Jaundice Discoloration of abdomen/flank Tachycardia Hypotension Abdominal distention/tenderness
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Acute Pancreatitis Nursing Assessment (Cont’d)
Abnormal laboratory findings ↑ Serum amylase/lipase Leukocytosis Hyperglycemia Hyperlipidemia Hypocalcemia Abnormal ultrasound/ CT/ ERCP
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Acute Pancreatitis Nursing Diagnoses
Acute pain Deficient fluid volume Imbalanced nutrition: Less than body requirements Ineffective therapeutic regimen management
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Acute Pancreatitis Planning
Overall goals Relief of pain Normal fluid and electrolyte balance Minimal to no complications No recurrent attacks
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Acute Pancreatitis Nursing Implementation
Health Promotion Assessment of predisposing factors Early diagnosis/treatment of cholelithiasis Eliminate alcohol intake
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Acute Pancreatitis Nursing Implementation (Cont’d)
Acute Intervention Monitor vital signs IV fluids Observe for side effects of medications Assess respiratory function Pain assessment and management Frequent position changes Side-lying with HOB elevated 45 degrees Knees up to abdomen
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Acute Pancreatitis Nursing Implementation
Acute Intervention (cont’d) Fluid/electrolyte balance Blood glucose monitoring Monitor for signs of hypocalcemia Tetany (jerking, irritability, twitching) Numbness around lips/fingers Positive Chvostek or Trousseau sign Monitor for hypomagnesemia
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Acute Pancreatitis Nursing Implementation
Acute Intervention (cont’d) NG tube care Frequent oral/nasal care Observe for signs of infection Wound care Observe for paralytic ileus, renal failure, mental changes
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Acute Pancreatitis Nursing Implementation
Ambulatory and Home Care Physical therapy Counseling regarding abstinence from alcohol, caffeine, and smoking Assessment of narcotic addiction
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Acute Pancreatitis Nursing Implementation
Ambulatory and Home Care (cont’d) Dietary teaching High-carbohydrate, low-fat diet Patient/family teaching Signs of infection, high blood glucose, steatorrhea Medications/diet
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Acute Pancreatitis Nursing Implementation
Expected outcomes Maintains adequate fluid volume Maintains weight appropriate for height Food and fluid intake adequate to meet nutritional needs
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Acute Pancreatitis Nursing Implementation
Expected outcomes (cont’d) Describes therapeutic regimen Expresses commitment to lifestyle changes
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Chronic Pancreatitis Continuous, prolonged inflammatory, and fibrosing process of the pancreas Pancreas becomes destroyed as it is replaced by fibrotic tissue Strictures and calcifications can also occur
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Chronic Pancreatitis Etiology and Pathophysiology
May follow acute pancreatitis May occur in absence of any history of acute condition Two major types Chronic obstructive pancreatitis Chronic calcifying pancreatitis
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Chronic Pancreatitis Etiology and Pathophysiology (Cont’d)
Chronic obstructive pancreatitis Associated with biliary disease Most common cause Inflammation of the sphincter of Oddi associated with cholelithiasis Other causes include Cancer of ampulla of Vater, duodenum, or pancreas
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Chronic Pancreatitis Etiology and Pathophysiology (Cont’d)
Chronic calcifying pancreatitis Inflammation Sclerosis Mainly in the head of the pancreas and around the pancreatic duct
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Chronic Pancreatitis Etiology and Pathophysiology
Chronic calcifying pancreatitis (cont’d) Most common form of chronic pancreatitis May be referred to as alcohol-induced pancreatitis
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Chronic Pancreatitis Etiology and Pathophysiology
Chronic calcifying pancreatitis (cont’d) Ducts are obstructed with protein precipitates Precipitates block the pancreatic duct and eventually calcify
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Chronic Pancreatitis Etiology and Pathophysiology
Chronic calcifying pancreatitis (cont’d) Calcification is followed by fibrosis and glandular atrophy Pseudocysts and abscesses commonly develop
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Chronic Pancreatitis Clinical Manifestations
Abdominal pain Located in the same areas as in acute pancreatitis Heavy, gnawing feeling; burning and cramp-like Abdominal tenderness Malabsorption with weight loss
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Chronic Pancreatitis Clinical Manifestations (Cont’d)
Constipation Mild jaundice with dark urine Steatorrhea Frothy urine/stool Diabetes mellitus
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Chronic Pancreatitis Clinical Manifestations (Cont’d)
Complications Pseudocyst formation Bile duct or duodenal obstruction Pancreatic ascites Pleural effusion
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Chronic Pancreatitis Clinical Manifestations
Complications (cont’d) Splenic vein thrombosis Pseudoaneurysms Pancreatic cancer
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Chronic Pancreatitis Diagnostic Studies
Confirming diagnosis can be challenging Based on signs/symptoms, laboratory studies, and imaging
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Chronic Pancreatitis Diagnostic Studies (Cont’d)
Laboratory tests Serum amylase/lipase May be ↑ slightly or not at all ↑ Serum bilirubin ↑ Alkaline phosphatase
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Chronic Pancreatitis Diagnostic Studies
Laboratory tests (cont’d) Mild leukocytosis Elevated sedimentation rate ERCP Visualize pancreatic/common bile duct
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Chronic Pancreatitis Diagnostic Studies
CT MRI MRCP Transabdominal ultrasound
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Chronic Pancreatitis Diagnostic Studies (Cont’d)
Endoscopic ultrasound Secretin stimulation test Assess degree of pancreatic function Not useful in diagnosis
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Chronic Pancreatitis Collaborative Care
Prevention of attacks During acute attack, follow acute therapy Relief of pain Control of pancreatic exocrine and endocrine insufficiency
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Chronic Pancreatitis Collaborative Care (Cont’d)
Bland low-fat, high-carbohydrate diet Bile salts Help absorption of fat-soluble vitamins Prevent further fat loss Control of diabetes No alcohol
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Chronic Pancreatitis Collaborative Care (Cont’d)
Pancreatic enzyme replacement Acid-neutralizing and acid-inhibiting drugs
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Chronic Pancreatitis Collaborative Care (Cont’d)
Surgery Indicated when biliary disease is present or if obstruction or pseudocyst develops Divert bile flow or relieve ductal obstruction
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Chronic Pancreatitis Nursing Management
Focus is on chronic care and health promotion Dietary control No alcohol Control of diabetes Taking pancreatic enzymes Patient and family teaching
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Case Study
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Case Study 63-year-old female enters the emergency department with nausea, vomiting, epigastric pain, left upper quadrant pain She claims the pain is severe, sharp, and boring and radiates through to her mid-back
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Case Study (Cont’d) Pain began 24 hours ago
She is divorced, retired, and smokes a half-pack of cigarettes a day
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Case Study (Cont’d) Vital signs
Blood pressure 100/70 mm Hg Heart rate 97 beats/min Respiratory rate 30 breaths/min Temperature 100.2°F She is diagnosed with acute pancreatitis and admitted to the medical-surgical unit
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Discussion Questions What are the possible causes of pancreatitis?
What is her priority of care?
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Discussion Questions (Cont’d)
What labs are the most important to monitor in acute pancreatitis? What patient teaching should you do with her?
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