Pancreatitis.

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Presentation transcript:

Pancreatitis

Acute Pancreatitis An acute inflammatory process of the pancreas Degree of inflammation varies from mild edema to severe necrosis

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

Acute Pancreatitis Etiology and Pathophysiology (Cont’d) Primary etiologic factors are Biliary tract disease Most common: Gallbladder disease Alcoholism

Acute Pancreatitis Etiology and Pathophysiology (Cont’d) Less common causes Trauma (postsurgical, abdominal) Viral infections (mumps, coxsackievirus HIV) Penetrating duodenal ulcer Cysts Idiopathic

Acute Pancreatitis Etiology and Pathophysiology Less common causes (cont’d) Abscesses Metabolic disorders Vascular diseases Postop GI surgery

Acute Pancreatitis Etiology and Pathophysiology Less common causes (cont’d) Drugs Corticosteroids Thiazide diuretics Oral contraceptives NSAIDs

Acute Pancreatitis Etiology and Pathophysiology Caused by autodigestion of pancreas Etiologic factors Injury to pancreatic cells Activate pancreatic enzymes

Acute Pancreatitis

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

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

Acute Pancreatitis Etiology and Pathophysiology Phospholipase A Plays a major role in autodigestion Activated by trypsin and bile acids Causes fat necrosis

Acute Pancreatitis Etiology and Pathophysiology (Cont’d) Alcohol May stimulate production of digestive enzymes Increases sensitivity to hormone cholecystokinin Stimulates production of pancreatic enzymes

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

Acute Pancreatitis Clinical Manifestations Abdominal pain (cont’d) Sudden onset Severe, deep Aggravated by eating Not relieved by vomiting

Acute Pancreatitis Clinical Manifestations Flushing Cyanosis Dyspnea Edema Nausea/vomiting Bowel sounds decreased or absent

Acute Pancreatitis Clinical Manifestations (Cont’d) Low-grade fever Leukocytosis Hypotension Tachycardia Jaundice Abdominal tenderness

Acute Pancreatitis Clinical Manifestations (Cont’d) Abdominal distention Abnormal lung sounds Crackles Discoloration of abdominal wall

Acute Pancreatitis Complications Pancreatic abscess A large fluid-containing cavity within pancreas Results from extensive necrosis in the pancreas Upper abdominal pain Abdominal mass

Acute Pancreatitis Complications Pancreatic abscess (cont’d) High fever Leukocytosis Requires surgical drainage

Acute Pancreatitis Diagnostic Studies History and physical examination Laboratory tests Serum amylase Serum lipase 2-hour urinary amylase

Acute Pancreatitis Diagnostic Studies Laboratory tests (cont’d) Blood glucose Serum calcium Triglycerides

Acute Pancreatitis Diagnostic Studies Flat plate of abdomen Abdominal/endoscopic ultrasound Endoscopic retrograde cholangiopancreatography (ERCP) Chest x-ray

Acute Pancreatitis Diagnostic Studies (Cont’d) CT of pancreas Magnetic resonance cholangiopancreatography (MRCP)

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

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

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

Acute Pancreatitis Collaborative Care Conservative therapy (cont’d) Suppression of pancreatic enzymes NPO NG suction Prevent infections Peritoneal lavage or dialysis

Acute Pancreatitis Collaborative Care Surgical therapy indicated if Presence of gallstones Uncertain diagnosis Unresponsive to conservative therapy Abscess or severe peritonitis

Acute Pancreatitis Collaborative Care Surgical therapy (cont’d) ERCP Endoscopic sphincterotomy Laparoscopic cholecystectomy

Acute Pancreatitis Collaborative Care (Cont’d) Drug therapy IV morphine Nitroglycerin Antispasmodics Antacids Histamine (H2) receptor

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

Acute Pancreatitis Collaborative Care Nutritional therapy (cont’d) Supplemental fat-soluble vitamins Supplemental commercial liquid preparations Parenteral nutrition No caffeine or alcohol

Acute Pancreatitis Nursing Assessment Health history Biliary tract disease Alcohol use Abdominal trauma Duodenal ulcers Infection Metabolic disorders

Acute Pancreatitis Nursing Assessment (Cont’d) Medication usage Thiazides, estrogens, corticosteroids, NSAIDs Surgical procedures Nausea/vomiting Dyspnea Severe pain

Acute Pancreatitis Nursing Assessment (Cont’d) Physical examination findings Fever Jaundice Discoloration of abdomen/flank Tachycardia Hypotension Abdominal distention/tenderness

Acute Pancreatitis Nursing Assessment (Cont’d) Abnormal laboratory findings ↑ Serum amylase/lipase Leukocytosis Hyperglycemia Hyperlipidemia Hypocalcemia Abnormal ultrasound/ CT/ ERCP

Acute Pancreatitis Nursing Diagnoses Acute pain Deficient fluid volume Imbalanced nutrition: Less than body requirements Ineffective therapeutic regimen management

Acute Pancreatitis Planning Overall goals Relief of pain Normal fluid and electrolyte balance Minimal to no complications No recurrent attacks

Acute Pancreatitis Nursing Implementation Health Promotion Assessment of predisposing factors Early diagnosis/treatment Eliminate alcohol intake

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

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 Monitor for hypomagnesemia

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

Acute Pancreatitis Nursing Implementation Ambulatory and Home Care Physical therapy Counseling regarding abstinence from alcohol, caffeine, and smoking Assessment of narcotic addiction

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

Acute Pancreatitis Nursing Implementation Expected outcomes Maintains adequate fluid volume Maintains weight appropriate for height Food and fluid intake adequate to meet nutritional needsDescribes therapeutic regimen Expresses commitment to lifestyle changes

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

Chronic Pancreatitis Etiology and Pathophysiology May occur in absence of any history of acute condition Two major types Chronic obstructive pancreatitis Chronic calcifying pancreatitis

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 duodenum, or pancreas

Chronic Pancreatitis Etiology and Pathophysiology (Cont’d) Chronic calcifying pancreatitis Inflammation Sclerosis Mainly in the head of the pancreas and around the pancreatic duct

Chronic Pancreatitis Etiology and Pathophysiology Chronic calcifying pancreatitis (cont’d) Most common form of chronic pancreatitis May be referred to as alcohol-induced pancreatitis

Chronic Pancreatitis Etiology and Pathophysiology Chronic calcifying pancreatitis (cont’d) Ducts are obstructed with protein precipitates Precipitates block the pancreatic duct and eventually calcify

Chronic Pancreatitis Etiology and Pathophysiology Chronic calcifying pancreatitis (cont’d) Calcification is followed by fibrosis and glandular atrophy abscesses commonly develop

Chronic Pancreatitis Clinical Manifestations Abdominal pain Located in the same areas as in acute pancreatitis Abdominal tenderness Malabsorption with weight loss

Chronic Pancreatitis Clinical Manifestations (Cont’d) Constipation Mild jaundice with dark urine Steatorrhea Diabetes mellitus

Chronic Pancreatitis Clinical Manifestations (Cont’d) Complications Bile duct or duodenal obstruction Pancreatic ascites Pleural effusion Pancreatic cancer

Chronic Pancreatitis Diagnostic Studies Confirming diagnosis can be challenging Based on signs/symptoms, laboratory studies, and imaging

Chronic Pancreatitis Diagnostic Studies (Cont’d) Laboratory tests Serum amylase/lipase May be ↑ slightly or not at all ↑ Serum bilirubin ↑ Alkaline phosphatase

Chronic Pancreatitis Diagnostic Studies Laboratory tests (cont’d) Mild leukocytosis Elevated sedimentation rate ERCP Visualize pancreatic/common bile duct

Chronic Pancreatitis Diagnostic Studies CT MRI MRCP Transabdominal ultrasound Endoscopic ultrasound

Chronic Pancreatitis Collaborative Care Prevention of attacks During acute attack, follow acute therapy Relief of pain

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

Chronic Pancreatitis Collaborative Care (Cont’d) Pancreatic enzyme replacement Acid-neutralizing and acid-inhibiting drugs

Chronic Pancreatitis Collaborative Care (Cont’d) Surgery Indicated when biliary disease is present or if obstruction Divert bile flow or relieve ductal obstruction

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

Case Study

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

Case Study (Cont’d) Pain began 24 hours ago She is divorced, retired, and smokes a half-pack of cigarettes a day

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

Discussion Questions What are the possible causes of pancreatitis? What is her priority of care?

Discussion Questions (Cont’d) What labs are the most important to monitor in acute pancreatitis? What patient teaching should you do with her?