Pancreatitis Nursing Care and Management: Study Guide

Pancreatitis is the pancreas digesting itself. It runs the full range from a mild, self-limited illness to a fulminant, rapidly fatal one that resists every treatment, so treat every case as a potential emergency. The patient hurts, third-spaces fluid, and can crash into shock fast. Control the pain, restore volume, rest the gland, protect the lungs, and watch hard for necrosis and sepsis.

What is Pancreatitis?

Pancreatitis is inflammation of the pancreas, acute or chronic, driven by edema, necrosis, or hemorrhage. In men it commonly tracks with alcoholism, peptic ulcer, or trauma; in women, with biliary tract disease. Prognosis is generally good when it follows biliary disease and poor when alcohol is the cause. When necrosis and hemorrhage are involved, the mortality rate climbs as high as 60%. The defining process is autodigestion.

Classification

Acute pancreatitis does not usually progress to chronic disease unless complications develop. Chronic pancreatitis is an inflammatory disorder marked by progressive destruction of the gland.

Pathophysiology

Acute pancreatitis is self-digestion by the pancreas's own proteolytic enzymes, trypsin above all. Gallstones enter the common bile duct and lodge at the ampulla of Vater, obstructing pancreatic juice or forcing bile to reflux from the common bile duct into the pancreatic duct. Normally these powerful enzymes stay inactive until they reach the duodenal lumen. When they activate prematurely, they cause vasodilation, increased vascular permeability, necrosis, erosion, and hemorrhage. Enzymes that back up into the bile duct become activated and, together with bile, reflux into the pancreatic duct to ignite the inflammation.

Statistics and Epidemiology

About 185,000 cases of pancreatitis occur in the United States each year, and 150,000 of those stem from cholelithiasis or sustained alcohol abuse. Overall mortality runs 2% to 10%. Roughly 5000 new cases appear annually with a mortality of about 10%, though the true number of patients with recurrent acute or chronic pancreatitis is unknown. Incidence varies by country and cause (alcohol, gallstones, metabolic factors, drugs). In the United States, acute pancreatitis is tied to alcohol more often than to gallstones, the second most common cause; in England the order is reversed.

Causes

Eighty percent of patients have biliary tract disease or a history of long-term alcohol abuse. Pancreatitis can also follow a bacterial or viral infection (mumps virus is a classic trigger), duodenitis with spasm and edema of the ampulla of Vater, and the use of corticosteroids, thiazide diuretics, oral contraceptives, and other medications.

Clinical Manifestations

Severe abdominal pain is the major symptom that brings the patient in, from irritation and edema of the inflamed gland. A rigid, boardlike abdomen with guarding may develop. Ecchymosis in the flank or around the umbilicus signals severe disease. Nausea and vomiting are common, with emesis usually gastric but sometimes bile-stained. Hypotension is typical, reflecting hypovolemia and shock as large volumes of protein-rich fluid shift into the tissues and peritoneal cavity.

Complications

Fluid and electrolyte disturbances are common, driven by vomiting, fluid shifting from the vascular compartment into the peritoneal cavity, diaphoresis, fever, and gastric suction. Pancreatic necrosis is a major cause of morbidity and mortality through hemorrhage, septic shock, and multiple organ failure. Septic shock can follow bacterial infection of the pancreas.

Assessment and Diagnostic Findings

Diagnosis rests on a history of abdominal pain, known risk factors, exam findings, and labs. Serum amylase rises with obstruction of pancreatic enzyme outflow and may run five or more times normal in acute pancreatitis, though a normal level does not rule out disease; serum lipase rises alongside it and stays elevated longer. Serum bilirubin is commonly elevated (from alcoholic liver disease or compression of the common bile duct), and alkaline phosphatase is usually elevated when biliary disease accompanies the attack. Serum albumin and protein may fall as capillary permeability lets fluid transude into the extracellular space. Hypocalcemia may appear 2 to 3 days after onset and usually indicates fat necrosis with possible pancreatic necrosis. Potassium swings either way: hypokalemia from gastric losses, or hyperkalemia from tissue necrosis, acidosis, and renal insufficiency. Triglycerides may exceed 1700 mg/dL and can themselves cause the attack. LDH and AST may rise up to 15 times normal from biliary and liver involvement. On CBC, a WBC count of 10,000 to 25,000 is present in 80% of patients; hemoglobin may drop from bleeding while hematocrit is usually elevated from hemoconcentration. Transient serum glucose elevations above 200 mg/dL are common in acute attacks, and sustained hyperglycemia signals widespread cell damage and necrosis, a poor prognostic sign. PTT prolongs if coagulopathy develops. Urinalysis may show glucose, myoglobin, blood, and protein, and urine amylase can climb sharply within 2 to 3 days of onset. Stool shows increased fat (steatorrhea) from poor digestion of fats and protein.

Imaging rounds out the workup. Abdominal and chest x-rays help separate pancreatitis from look-alike disorders; plain abdominal films may show a dilated loop of small bowel next to the pancreas, free intraperitoneal air from perforation or abscess, or pancreatic calcification. Ultrasound identifies an increased pancreatic diameter and can reveal inflammation, abscess, pseudocysts, carcinoma, or biliary obstruction. CT shows an enlarged pancreas and pancreatic cysts and gauges the extent of edema and necrosis, while CT-guided needle aspiration determines whether infection is present. ERCP diagnoses fistulas, obstructive biliary disease, and pancreatic duct strictures or anomalies, but is contraindicated in the acute phase. An upper GI series frequently shows pancreatic enlargement or inflammation.

Medical Management

Care aims to relieve symptoms and prevent or treat complications. Adequate analgesia (morphine, fentanyl, or hydromorphone) is essential, both for relief and to limit restlessness that further stimulates pancreatic secretion. Intensive care corrects fluid and blood loss and low albumin to maintain volume and prevent renal failure. Aggressive respiratory care is indicated given the high risk of an elevated diaphragm, pulmonary infiltrates, effusion, and atelectasis. Biliary drains for external drainage and stents placed endoscopically in the pancreatic duct can reestablish drainage of the gland.

Surgical Management

Several procedures are available. Side-to-side pancreaticojejunostomy (ductal drainage) is used when dilated pancreatic ducts are associated with septa and calculi, the most successful option with success rates of 60% to 90%. Caudal pancreaticojejunostomy (ductal drainage) addresses uncommon proximal pancreatic ductal stenosis not involving the ampulla. Pancreaticoduodenal (right-sided) resection, the pylorus-preserving Whipple procedure, is used when major changes are confined to the head of the pancreas, and preserving the pylorus avoids the usual sequelae of gastric resection. A patient who has pancreatic surgery may have multiple drains and a surgical incision left open for irrigation and repacking every 2 to 3 days to remove necrotic debris.

Nursing Management

Nursing Assessment

Assess current nutritional status and the patient's increased metabolic demands, respiratory status, and fluid and electrolyte status, including the sources of fluid and electrolyte loss. Examine the abdomen for ascites.

Diagnosis

Major diagnoses include acute pain related to edema, pancreatic distention, and peritoneal irritation; imbalanced nutrition, less than body requirements, related to inadequate intake, impaired pancreatic secretions, and increased needs; and ineffective breathing pattern related to splinting from severe pain, pulmonary infiltrates, pleural effusion, and atelectasis.

Planning and Goals

The goals are relief of pain and discomfort, improved nutritional status, improved respiratory function, and improved fluid and electrolyte balance.

Nursing Interventions

For pain, give parenteral opioids (morphine, hydromorphone, or fentanyl) by patient-controlled analgesia or bolus. Keep the patient in semi-Fowler's position and encourage frequent position changes to improve breathing. Between acute attacks, feed a diet high in carbohydrates and low in fats and proteins. Carry out wound care as prescribed and protect intact skin from contact with drainage.

Evaluation

The patient reports relieved pain, improves nutritional status, regains respiratory function, and restores fluid and electrolyte balance.

Discharge and Home Care Guidelines

Recovery is slow, and returning to a prior activity level takes time. Repeat and reinforce teaching, since the patient may struggle to recall instructions. Cover the factors that trigger pancreatitis and the need to avoid high-fat foods, heavy meals, and alcohol. Give verbal and written instructions on the signs and symptoms of pancreatitis and the complications that warrant prompt reporting to the physician. On home visits, assess physical and psychological status and adherence to the regimen.

Documentation

Document the patient's description of pain and acceptable level, prior medication use, caloric intake, and any cultural, religious, or personal dietary preferences. Record respiratory pattern, breath sounds, use of accessory muscles, and any respiratory aids. Capture laboratory values, the plan of care, the teaching plan, the response to interventions and teaching, progress toward outcomes, modifications to the plan, and long-term needs.