Pancreatitis is a painful inflammatory condition in which the pancreatic enzymes are prematurely activated resulting in autodigestion of the pancreas. The most common cause of pancreatitis are biliary tract disease and alcoholism, but can also result from such things as abnormal organ structure, blunt trauma, penetrating peptic ulcers, and drugs such as sulfonamides and glucocorticoids. Pancreatitis may be acute or chronic, with symptoms mild to severe.
CARE SETTING
Inpatient acute medical unit for initial incident or exacerbations with serious complications; otherwise condition is managed at the community level.
RELATED CONCERNS
Alcoholism (acute); intoxication/overdose
Substance dependence/abuse rehabilitation
Diabetes mellitus/diabetic ketoacidosis
Peritonitis
Psychosocial aspects of care
Renal failure: acute
Sepsis/septicemia
Total nutritional support; parenteral/enteral feeding
Patient Assessment Database
CIRCULATION
May exhibit: Hypertension (acute pain); hypotension and tachycardia (hypovolemic shock or toxemia)
Edema, ascites
Skin pale, cold, mottled with diaphoresis (vasoconstriction/fluid shifts); jaundiced (inflammation/ obstruction of common duct); blue-green-brown discoloration around umbilicus (Cullen’s sign) from accumulation of blood (hemorrhagic pancreatitis)
EGO INTEGRITY
May exhibit: Agitation, restlessness, distress, apprehension
ELIMINATION
May report: Diarrhea
May exhibit: Bowel sounds decreased/absent (reduced peristalsis/ileus)
Dark amber or brown, foamy urine (bile)
Frothy, foul-smelling, grayish, greasy, nonformed stool (steatorrhea)
Polyuria (developing DM)
FOOD/FLUID
May report: Food intolerance, anorexia; frequent/persistent vomiting, retching, dry heaves
Weight loss
May exhibit: Diffuse epigastric/abdominal tenderness to palpation, abdominal rigidity, distension
Hypoactive bowel sounds
Urine positive for glucose
NEUROSENSORY
May exhibit: Confusion, agitation
Coarse tremors of extremities (hypocalcemia)
PAIN/DISCOMFORT
May report: Unrelenting severe deep abdominal pain, usually located in the epigastrium and periumbilical regions but may radiate to the back; onset may be sudden and often associated with heavy drinking or a large meal
Radiation to chest and back, may increase in supine position
May exhibit: Abdominal guarding, may curl up on left side with both arms over abdomen and knees/hips flexed
Abdominal rigidity
RESPIRATION
May exhibit: Tachypnea, with/without dyspnea
Decreased depth of respiration with splinting/guarding actions
Bibasilar crackles (pleural effusion)
SAFETY
May exhibit: Fever
SEXUALITY
May exhibit: Current pregnancy (third trimester) with shifting of abdominal contents and compression of biliary tract
TEACHING/LEARNING
May report: Family history of pancreatitis
Diabetic ketoacidosis
History of cholelithiasis with partial or complete common bile duct obstruction; gastritis, duodenal ulcer, duodenitis; diverticulitis; Crohn’s disease; recent abdominal surgery (e.g., procedures on the pancreas, biliary tract, stomach, or duodenum); external abdominal trauma
Excessive alcohol intake (90% of cases)
Uses of medications, e.g., salicylates, pentamidine, antihypertensives, opiates, thiazides, steroids, some antibiotics, estrogens
Infectious diseases, e.g., mumps, hepatitis B, Coxsackie viral infection
Discharge plan
DRG projected mean length of inpatient stay: 5.7 days
May require assistance with dietary program, homemaker/maintenance tasks
Refer to section at end of plan for postdischarge considerations
DIAGNOSTIC STUDIES
CT scan: Shows an enlarged pancreas, pancreatic cysts and determines extent of edema and necrosis.
Ultrasound of abdomen: May be used to identify pancreatic inflammation, abscess, pseudocysts, carcinoma, or obstruction of biliary tract
Endoscopic retrograde cholangiopancreatography: Useful to diagnose fistulas, obstructive biliary disease, and pancreatic duct strictures/anomalies (procedure is contraindicated in acute phase).
CT–guided needle aspiration: Done to determine whether infection is present.
Abdominal x-rays: May demonstrate dilated loop of small bowel adjacent to pancreas or other intra-abdominal precipitator of pancreatitis, presence of free intraperitoneal air caused by perforation or abscess formation, pancreatic calcification.
Upper GI series: Frequently exhibits evidence of pancreatic enlargement/inflammation.
Serum amylase: Increased because of obstruction of normal outflow of pancreatic enzymes (normal level does not rule out disease). May be five or more times normal level in acute pancreatitis.
Serum lipase: usually elevates along with amylase, but stays elevated longer.
Serum bilirubin: Elevation is common (may be caused by alcoholic liver disease or compression of common bile duct).
Alkaline phosphatase: Usually elevated if pancreatitis is accompanied by biliary disease.
Serum albumin and protein: May be decreased (increased capillary permeability and transudation of fluid into extracellular space).
Serum calcium: Hypocalcemia may appear 2–3 days after onset of illness (usually indicates fat necrosis and may accompany pancreatic necrosis).
Potassium: Hypokalemia may occur because of gastric losses; hyperkalemia may develop secondary to tissue necrosis, acidosis, renal insufficiency.
Triglycerides: Levels may exceed 1700 mg/dL and may be causative agent in acute pancreatitis.
LDH/AST: May be elevated up to 15 times normal because of biliary and liver involvement.
CBC: WBC count of 10,000–25,000 is present in 80% of patients. Hb may be lowered because of bleeding. Hct is usually elevated (hemoconcentration associated with vomiting or from effusion of fluid into pancreas or retroperitoneal area).
Serum glucose: Transient elevations of more than 200 mg/dL are common, especially during initial/acute attacks.
Sustained hyperglycemia reflects widespread cell damage and pancreatic necrosis and is a poor prognostic sign.
Partial thromboplastin time (PTT): Prolonged if coagulopathy develops because of liver involvement and fat necrosis.
Urinalysis: Glucose, myoglobin, blood, and protein may be present.
Urine amylase: Can increase dramatically within 2–3 days after onset of attack.
Stool: Increased fat content (steatorrhea) indicative of insufficient digestion of fats and protein.
NURSING PRIORITIES
1. Control pain and promote comfort.
2. Prevent/threat fluid and electrolyte imbalance.
3. Reduce pancreatic stimulation while maintaining adequate nutrition.
4. Prevent complications.
5. Provide information about disease process/prognosis and treatment needs.
DISCHARGE GOALS
1. Pain relieved/controlled.
2. Hemodynamically stable.
3. Complications prevented/minimized.
4. Disease process/prognosis, potential complications, and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.
CARE SETTING
Inpatient acute medical unit for initial incident or exacerbations with serious complications; otherwise condition is managed at the community level.
RELATED CONCERNS
Alcoholism (acute); intoxication/overdose
Substance dependence/abuse rehabilitation
Diabetes mellitus/diabetic ketoacidosis
Peritonitis
Psychosocial aspects of care
Renal failure: acute
Sepsis/septicemia
Total nutritional support; parenteral/enteral feeding
Patient Assessment Database
CIRCULATION
May exhibit: Hypertension (acute pain); hypotension and tachycardia (hypovolemic shock or toxemia)
Edema, ascites
Skin pale, cold, mottled with diaphoresis (vasoconstriction/fluid shifts); jaundiced (inflammation/ obstruction of common duct); blue-green-brown discoloration around umbilicus (Cullen’s sign) from accumulation of blood (hemorrhagic pancreatitis)
EGO INTEGRITY
May exhibit: Agitation, restlessness, distress, apprehension
ELIMINATION
May report: Diarrhea
May exhibit: Bowel sounds decreased/absent (reduced peristalsis/ileus)
Dark amber or brown, foamy urine (bile)
Frothy, foul-smelling, grayish, greasy, nonformed stool (steatorrhea)
Polyuria (developing DM)
FOOD/FLUID
May report: Food intolerance, anorexia; frequent/persistent vomiting, retching, dry heaves
Weight loss
May exhibit: Diffuse epigastric/abdominal tenderness to palpation, abdominal rigidity, distension
Hypoactive bowel sounds
Urine positive for glucose
NEUROSENSORY
May exhibit: Confusion, agitation
Coarse tremors of extremities (hypocalcemia)
PAIN/DISCOMFORT
May report: Unrelenting severe deep abdominal pain, usually located in the epigastrium and periumbilical regions but may radiate to the back; onset may be sudden and often associated with heavy drinking or a large meal
Radiation to chest and back, may increase in supine position
May exhibit: Abdominal guarding, may curl up on left side with both arms over abdomen and knees/hips flexed
Abdominal rigidity
RESPIRATION
May exhibit: Tachypnea, with/without dyspnea
Decreased depth of respiration with splinting/guarding actions
Bibasilar crackles (pleural effusion)
SAFETY
May exhibit: Fever
SEXUALITY
May exhibit: Current pregnancy (third trimester) with shifting of abdominal contents and compression of biliary tract
TEACHING/LEARNING
May report: Family history of pancreatitis
Diabetic ketoacidosis
History of cholelithiasis with partial or complete common bile duct obstruction; gastritis, duodenal ulcer, duodenitis; diverticulitis; Crohn’s disease; recent abdominal surgery (e.g., procedures on the pancreas, biliary tract, stomach, or duodenum); external abdominal trauma
Excessive alcohol intake (90% of cases)
Uses of medications, e.g., salicylates, pentamidine, antihypertensives, opiates, thiazides, steroids, some antibiotics, estrogens
Infectious diseases, e.g., mumps, hepatitis B, Coxsackie viral infection
Discharge plan
DRG projected mean length of inpatient stay: 5.7 days
May require assistance with dietary program, homemaker/maintenance tasks
Refer to section at end of plan for postdischarge considerations
DIAGNOSTIC STUDIES
CT scan: Shows an enlarged pancreas, pancreatic cysts and determines extent of edema and necrosis.
Ultrasound of abdomen: May be used to identify pancreatic inflammation, abscess, pseudocysts, carcinoma, or obstruction of biliary tract
Endoscopic retrograde cholangiopancreatography: Useful to diagnose fistulas, obstructive biliary disease, and pancreatic duct strictures/anomalies (procedure is contraindicated in acute phase).
CT–guided needle aspiration: Done to determine whether infection is present.
Abdominal x-rays: May demonstrate dilated loop of small bowel adjacent to pancreas or other intra-abdominal precipitator of pancreatitis, presence of free intraperitoneal air caused by perforation or abscess formation, pancreatic calcification.
Upper GI series: Frequently exhibits evidence of pancreatic enlargement/inflammation.
Serum amylase: Increased because of obstruction of normal outflow of pancreatic enzymes (normal level does not rule out disease). May be five or more times normal level in acute pancreatitis.
Serum lipase: usually elevates along with amylase, but stays elevated longer.
Serum bilirubin: Elevation is common (may be caused by alcoholic liver disease or compression of common bile duct).
Alkaline phosphatase: Usually elevated if pancreatitis is accompanied by biliary disease.
Serum albumin and protein: May be decreased (increased capillary permeability and transudation of fluid into extracellular space).
Serum calcium: Hypocalcemia may appear 2–3 days after onset of illness (usually indicates fat necrosis and may accompany pancreatic necrosis).
Potassium: Hypokalemia may occur because of gastric losses; hyperkalemia may develop secondary to tissue necrosis, acidosis, renal insufficiency.
Triglycerides: Levels may exceed 1700 mg/dL and may be causative agent in acute pancreatitis.
LDH/AST: May be elevated up to 15 times normal because of biliary and liver involvement.
CBC: WBC count of 10,000–25,000 is present in 80% of patients. Hb may be lowered because of bleeding. Hct is usually elevated (hemoconcentration associated with vomiting or from effusion of fluid into pancreas or retroperitoneal area).
Serum glucose: Transient elevations of more than 200 mg/dL are common, especially during initial/acute attacks.
Sustained hyperglycemia reflects widespread cell damage and pancreatic necrosis and is a poor prognostic sign.
Partial thromboplastin time (PTT): Prolonged if coagulopathy develops because of liver involvement and fat necrosis.
Urinalysis: Glucose, myoglobin, blood, and protein may be present.
Urine amylase: Can increase dramatically within 2–3 days after onset of attack.
Stool: Increased fat content (steatorrhea) indicative of insufficient digestion of fats and protein.
NURSING PRIORITIES
1. Control pain and promote comfort.
2. Prevent/threat fluid and electrolyte imbalance.
3. Reduce pancreatic stimulation while maintaining adequate nutrition.
4. Prevent complications.
5. Provide information about disease process/prognosis and treatment needs.
DISCHARGE GOALS
1. Pain relieved/controlled.
2. Hemodynamically stable.
3. Complications prevented/minimized.
4. Disease process/prognosis, potential complications, and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.
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