Pancreatitis, acute or chronic, is an inflammation and potential necrosis of the pancreas. Tissue damage from pancreatitis occurs because of activation of proteolytic and lipolytic pancreatic enzymes that are normally activated in the duodenum. Proteolytic enzymes, such as trypsin, elastase, and phospholipase, break down protein; lipolytic enzymes break down fats. The enzymes cause autodigestion (destruction of the acinar cells and islet cell tissue), with leakage of the enzymes and fluid into surrounding tissues. The pancreas can return to normal after an attack of acute pancreatitis with successful treatment, or it may progress to a state of chronic inflammation and disease.
The mortality rate of people with acute pancreatitis is as high as 15%, but in patients with severe disease, it can reach 30%, particularly when people develop multiple organ dysfunction syndrome (MODS). In chronic pancreatitis, there is permanent destruction. Precipitation of proteins causes pancreatic duct obstruction. Edema and distension cause damage and loss of the acinar cells, which normally produce digestive enzymes. The normal cells are replaced with fibrosis and necrosis. As the autodigestion process of the pancreas progresses, the cells form walls around the fluid that contains enzymes and the necrotic debris. These pseudocysts can rupture into the peritoneum and surrounding tissues, resulting in complications of infection, abscesses, and fistulae. The islet cells within the pancreas may also be damaged and destroyed, leading to diabetes mellitus. Other complications include massive pancreatic hemorrhage and shock, acute respiratory distress syndrome, atelectasis, pleural effusion, pneumonia, paralytic ileus, and rarely, cancer.
Three factors cause premature enzyme activation. Mechanical causes—such as pancreatic duct damage and obstruction—may result from gallstones migrating into the duct, bile reflux from the duodenum into the duct, tumors, radiation therapy, ulcer disease, or inflammation. Metabolic causes result from changes in the secretory processes of the acinar cells in conditions such as alcoholism (90% of the cases), diabetic ketoacidosis, hyperlipidemia, hypercalcemia, and drugs (acetaminophen, estrogen). Miscellaneous causes include infectious diseases (mumps, hepatitis B, coxsackie viral infections) and ischemic injury as a result of lupus erythematosus, cardiopulmonary bypass surgery, post-transplantation complications, or shock.
Nursing care plan assessment and physical examination
Obtain a detailed history of alcohol use and ingestion patterns. Assess for a family history of pancreatitis or a history of external abdominal trauma, surgery, cancer, recent bacterial infections, and biliary or gastrointestinal disease. Obtain a complete medication profile of prescribed and over-the-counter drugs. Determine the onset and severity of symptoms. Patients often seek medical attention for severe upper abdominal pain they describe as knifelike, twisting, and deep in the midepigastrium or umbilical region. The pain may radiate to the dorsal area of the back or around the costal margins. Pain begins 12 to 48 hours after excessive alcohol intake or, with gallstone-related pancreatitis, can occur after a large fatty meal. Nausea and vomiting are present in up to 90% of the cases.
The patient appears acutely ill with restless, apprehensive, and agitated behavior. Some become confused and, if shock or hypoxemia is impending, unresponsive. Respirations are often rapid and shallow. The patient may assume a fetal position with legs drawn upward to relieve abdominal pain. You may note mottled or jaundiced skin. You may see a bluish discoloration in the flanks (Grey-Turner’s sign) and around the umbilicus (Cullen’s sign), which indicates blood accumulation in these areas. Skin may be cold and diaphoretic. You may also note coarse tremors of the extremities as a sign of low calcium. Other findings include tea-colored or foamy urine (indicating the presence of bile) and gray, foul-spelling, foamy stools that indicate the presence of undigested fat. Ascultate the abdomen before palpation and percussion to check for decreased bowel sounds, which is a common finding in patients with pancreatitis. On palpation, note extreme abdominal tenderness, distension, guarding, and rigidity. Ascites and rebound tenderness are present in severe disease. When you percuss the abdomen, you may find abdominal tympany. The patient often has labile vital signs. During periods of pain, the patient may be hypertensive, but as hypovolemic shock progresses to late stages, blood pressure may fall. Patients usually have rapid heart rates; rapid, thready pulses; and decreased breath sounds in the lower lobes because of shallow respirations, pain, and increased abdominal size.
Assess the patient’s anxieties and coping abilities related to the demands of an acute care environment and a sudden illness. The patient with chronic pancreatitis needs assistance with feelings of hopelessness and apathy that may result from chronic pain and general debilitation. Assess the family’s coping with role changes and responsibilities. Alcohol abuse counseling may be necessary.
Nursing care plan primary nursing diagnosis: Pain (acute or chronic) related to inflammation, edema, peritoneal irritation.
Nursing care plan intervention and treatment plan
The immediate goal of therapy is to control and decrease the inflammation of the pancreas. The fluid lost into the retroperitoneal space can be as much as 4 to 12 L with severe disease. Volume replacement with fluids such as lactated Ringer’s injection or normal human serum albumin is used to restore blood volume and prevent hypovolemic shock. Normal human serum albumin is often used if low albumin levels lead to a loss of osmotic pressure in the vascular system. Urinary output is monitored hourly to measure volume status: less than 1 mL/kg per hour is a sign of hypoperfusion. The physician may insert a pulmonary artery catheter for hemodynamic monitoring to assess the adequacy of the volume replacement and cardiac output. Patients who develop sepsis and shock may not respond to fluid volume replacement and remain hypovolemic. This complication requires vasoactive parenteral medications. Hypocalcemia is a common electrolyte imbalance that accompanies pancreatic necrosis and requires calcium replacement. It may cause tetany, seizures, respiratory complications, and myocardial changes. Magnesium deficits often accompany hypocalcemia and need replacement as well. Loss of potassium through vomiting, fluid loss in the third spaces, acidosis, and renal insufficiency can lead to ventricular dysrhythmia. The blood glucose is monitored as a part of the renal profile and by finger sticks every 6 hours to determine the need for exogenous insulin replacement. Respiratory support involves administering oxygen by a variety of routes, which may include mechanical ventilation. Because of inadequate breathing patterns and the risk of laryngospasm, the patient may require endotracheal intubation; also, position end-expiratory pressure, pressure control ventilation, and inverse inspiratory-to-expiratory ratio ventilation (increasing inspiratory time) may be used.
The goal of therapy is to reduce the secretion of pancreatic enzymes, which stops the inflammatory process. The inflammation leads to nerve irritation and pain. Obtain a baseline pain assessment, and reassess every 4 hours using a pain-rating scale; provide narcotic analgesia as needed. Bedrest is important to decrease the basal metabolic rate, which, in turn, decreases pancreatic secretions. Insertion of a nasogastric tube for intermittent suction also contributes to this goal by preventing the release of secretion in the duodenum. Nothing-by-mouth (NPO) status is strictly maintained, with no ice chips or sips of water during the acute phase. Nutritional support to restore the damaged pancreatic cells is provided by initiating total parenteral nutrition within 3 days of the onset of the acute phase.
Surgical interventions may be indicated for managing the complications that are associated with pancreatic necrosis. The procedures include pancreatic drainage, pancreatic resection or débridement, and removal of obstructions (biliary stones). The current therapy for removal of stones is early endoscopic retrograde cholangiopancreatography and endoscopic sphincterotomy. Peritoneal lavage is used for patients who do not respond to intensive treatment after 3 days; it has significantly decreased the incidence of complications and the mortality rate.
During the acute phase of pancreatitis, focus on continued monitoring and teaching. Monitor the patient’s pain to determine intensity, location, characteristics, and factors that aggravate or relieve the pain. Frequent doses of analgesics are required. Other measures to provide comfort include positioning the patient in a knee-chest posture, stress reduction, and relaxation exercises. Provide a restful environment, but also initiate diversional activities. Monitor the patient’s respiratory status continually. Place the patient in high Fowler position to improve lung expansion, and use other mechanisms to enhance gas exchange. If the patient is not intubated, keep emergencyintubation equipment close by in case tetany and laryngospasm occur. The risk of tetany is enhanced if the patient hyperventilates. Maintain a calm environment, a constant presence, and medications to assist the patient with quiet breathing.
After the removal of the nasogastric tube, the diet progresses slowly from liquids to a diet high in calories and low in fat. During the immediate recovery period, arrange for small, frequent meals. Explain the need to avoid food and drinks with caffeine, spicy foods, and heavy meals that stimulate pancreatic secretion. Develop a realistic weight gain goal. Assist with dietary teaching by planning a week’s menu, incorporating the patient’s specific dietary needs and restrictions.
Nursing care plan discharge and home health care guidelines
Prevention involves correcting the initiating events. If the disease is related to alcohol use, reinforce the importance of abstaining and provide appropriate referrals. Teach the patient to recognize early symptoms that may indicate recurrence and when to contact the physician. Emphasize the importance of follow-up care. Teach the rationale, action, dosage, and side effects of all prescribed medications. Instruct the patient to take prescribed pancreatic enzyme replacements with or immediately after meals and to swallow them whole and not with hot liquids that would disrupt the protective coating. If the patient is being discharged with the requirement for continued insulin injections, the patient and family should demonstrate the injection technique and the procedure for blood glucose self-monitoring. Provide a log and show them how to keep a record of glucose levels and insulin dosages. The patient with a loss of pancreatic endocrine function requires extensive ongoing diabetic teaching after discharge; refer for additional counseling if necessary. Encourage the patient to seek nutritional follow-up with clinic or physician visits, especially for hyperglycemic management.