Acute Pancreatitis
An acute inflammatory process of the pancreas
Degree of inflammation varies from mild to edema to severe necrosis
Etiology
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
Primary etiologic factors are
Biliary tract disease
Most common: Gallbladder disease
Alcoholism
Less common causes
Trauma (postsurgical, abdominal)
Viral infections (mumps, coxsackievirus HIV)
Penetrating duodenal ulcer
Cysts
Idiopathic
Abscesses
Cystic fibrosis
Kaposi's sarcoma
Metabolic disorders
Vascular diseases
Postop GI surgery
Less common causes (cont'd)
Drugs:
Caused by
Autodigestion of pancreas
Etiologic factors:
Injury to pancreatic cells
Activate pancreatic enzymes
Trypsinogen
Activated to trypsin by enterokinase
Inhibitors usually inactivate trypsin
Enzyme can digest the pancreas and can activate other proteolytic enzymes
Elastase
Activated by trypsin
Plays a major role in autodigestion
Causes hemorrhage by producing dissolution of the elastic fibers of blood vessels
Phospholipase A
Plays a major role in autodigestion
Activated by trypsin and bile acids
Causes fat necrosis
Enzymes
Trypsin: Edema, necrosis, hemorrhage
Elastase: Hemorrhage
Phospholipase A: Fat necrosis
Kallikrein: Edema, vascular permeablility, smooth muscle contraction, shock
Lipase: Fat necrosis
Alcohol
May stimulate production of digestive enzymes
Increases sensitivity to hormone cholecystokinin
Stimulates production of pancreatic enzymes
Abdominal pain is predominant symptom
Pain located in the left upper quadrant
Pain may be in the midepigastrium
Commonly radiates to the back
Sudden onset
Severe, deep, piercing, steady
Aggravated by eating
Not relieved by vomiting
Clinical Manifestations
Flushing
Cyanosis
Dyspnea
Edema
Nausea/vomiting
Bowel sounds decreased or absent
Low-grade fever
Leukocytosis
Hypotension
Tachycardia
Jaundice
Abdominal tenderness
Abdominal distention
Abnormal lung sounds: Crackles
Discoloration of abdominal wall
Two significant local complications
Pseudocyst
Abscess
Pseudocyst
Cavity surrounding outside of pancreas filled with necrotic products and liquid secretions
Abdominal pain
Palpable epigastric mass
Nausea, vomiting, and anorexia
Elevated serum amylase
May resolve spontaneously within a few weeks or may perforate, causing
Pancreatic abscess
A large fluid-containing cavity within pancreas
Results from extensive necrosis in the pancreas
Upper abdominal pain
Abdominal mass
High fever
Leukocytosis
Requires surgical drainage
Main systemic complications
*Pulmonary
Pleural effusion
Atelectasis
Pneumonia
CV: Hypotension
Tetany (caused by hypocalcemia)
S/S Hypocalcemia
Trousseas and Chovesteks
Diagnostics
History and physical examination
LABS:
Serum amylase (most often, cheaper)
Serum lipase (most specific)
2hr urinary amylase and renal amylase clearance
Blood glucose
Serum calcium
Triglycerides
Flat plate of abdomen
Abdominal/endoscopic ultrasound
Endosco
Objectives include
Relief of pain
Prevention or alleviation of shock
? of pancreatic secretions
Fluid/electrolyte balance
Removal of the precipitating cause
Conservative therapy
Supportive care
Aggressive hydration
Pain management: IV morphine, Combined with antispasmodic agent
Management of metabolic complications
Minimizing stimulation
Shock (hypovolemic): Plasma or plasma volume expanders (dextran or albumin)
Fluid/electrolyt
Conservative therapy (cont'd)
Suppression of pancreatic enzymes
NPO
NG suction
Prevent infections
Peritoneal lavage or dialysis
Remove kinin and phospholipase A exudate
Why NG tube?
Prevent gastric acid frm enetering duodenum, and prevent/decrease stimulation of pancreas- allow it to rest
Surgical therapy indicated if
Presence of gallstones
Uncertain diagnosis
Unresponsive to conservative therapy
Abscess, pseudocyst, or severe peritonitis
Surgical therapy
ERCP
Endoscopic sphincterotomy
Laparoscopic cholecystectomy
Drug therapy
IV morphine
Nitroglycerin or papaverine
Antispasmodics
Carbonic anhydrase inhibitor
Antacids
Histamine (H2) receptor
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
Supplemental fat-soluble vitamins
Supplemental commercial liquid preparations
Parenteral
Diet
High-carbohydrate, low-fat, high-protein diet
Bland diet
Nursing Assessment
Health history
Biliary tract disease
Alcohol use
Abdominal trauma
Duodenal ulcers
Infection
Metabolic disorders
Medication usage:
Thiazides, estrogens, corticosteroids, NSAIDs
Surgical procedures
Nausea/vomiting
Dyspnea
Severe pain
Physical examination findings
Fever
Jaundice
Discoloration of abdomen/flank
Tachycardia
Hypotension
Abdominal distention/tenderness
Abnormal laboratory findings
? Serum amylase/lipase
Leukocytosis
Hyperglycemia
Hyperlipidemia
Hypocalcemia
Abnormal ultrasound/ CT/ ERCP
Health promotion
Assessment of predisposing factors
Early diagnosis/treatment of cholelithiasis
Eliminate alcohol intake
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
NG tube care
Frequent oral/nasal care
Ob
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
Chvostek Sign
...
Trousseau Sign
...
Ambulatory and home care
Physical therapy
Counseling regarding abstinence from alcohol, caffeine, and smoking
Assessment of narcotic addiction
Dietary teaching
High-carbohydrate, low-fat diet
Patient/family teaching
Signs of infection, high blood glucose, steatorrhea
Medications/
CHRONIC Pancreatitis
Continuous, prolonged inflammatory, and fibrosing process of the pancreas
Pancreas destroyed as it is replaced by fibrotic tissue
Strictures and calcifications can also occur
Chronic Pancreatitis Patho
May follow acute pancreatitis
May occur in absence of any history of acute condition
Two major types
Chronic obstructive pancreatitis
Chronic calcifying pancreatitis
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
Chronic calcifying pancreatitis
Inflammation
Sclerosis: Mainly in the head of the pancreas and around the pancreatic duct
Most common form of chronic pancreatitis
May be referred to as alcohol-induced pancreatitis
Ducts are obstructed with protein precipitates
Precipitates block pancrea
Alcohol-induced pancreatitis
Chronic calcifying pancreatitis
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
Constipation
Mild jaundice with dark urine
Steatorrhea
Frothy urine/stool
Diabetes mell
Complications include
Pseudocyst formation
Bile duct or duodenal obstruction
Pancreatic ascites
Pleural effusion
Splenic vein thrombosis
Pseudoaneurysms
Pancreatic cancer
Chronic Pancreatitis LABS
Serum amylase/lipase: May be ? slightly or not at all
? Serum bilirubin
? Alkaline phosphatase
Mild leukocytosis
Elevated sedimentation rate
ERCP: Visualize pancreatic/common bile duct
Secretin stimulation test
Assess degree of pancreatic function
Not useful in diagnosis
Chronic Pancreatitis Care
Prevention of attacks: During acute attack follow acute therapy
Relief of pain
Control of pancreatic exocrine and endocrine insufficiency
Bland low-fat, high-carbohydrate diet
Bile salts : Help absorption of fat-soluble vitamins, Prevent further fat loss
Surgery
Indicated when biliary disease is present or if obstruction or pseudocyst develops
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