Pancreatitis: Nursing process (ADPIE)

Tonya Abbott is a 58-year-old woman with a history of alcohol use disorder who presents to the emergency department with severe epigastric pain rated 9/10 along with nausea and vomiting. An abdominal CT scan confirms pancreatic enlargement and edema, and Tonya is admitted to the Progressive Care Unit to be treated for acute alcohol-induced pancreatitis.

Acute pancreatitis refers to the sudden inflammation and destruction of the pancreas. The pancreas is a long, skinny gland located in the upper abdomen, or the epigastric region, behind the stomach. It plays an endocrine role, since it has scattered islets of Langerhans that produce and secrete hormones like insulin and glucagon into the bloodstream. However, the vast majority of the pancreas also plays an exocrine role, since it has acinar cells that produce and secrete pancreatic juice, which contains digestive enzymes like trypsin, amylase, and lipase, into the duodenum to help digest food. In acute pancreatitis, the pancreas is destroyed by its own digestive enzymes, a process called autodigestion.

Now, acute pancreatitis can result from pancreatic duct obstruction, which can be caused by gallstones, tumors, or parasites. Other causes include genetic diseases like cystic fibrosis; or acinar cell injury caused by toxic substances like alcohol; certain medications, like some antibiotics: as well as viral infections like paramyxovirus; abdominal trauma; or even medical procedures like endoscopic retrograde cholangiopancreatography or ERCP.

All of these potential causes may allow the digestive enzymes produced by the acinar cells to be released and activated within the pancreas before they reach the digestive tract. As a result, there’s pancreatic tissue destruction, which ultimately triggers an inflammatory response. This can cause blood vessels to become leaky, causing fluid to collect around the pancreas, which leads to parenchymal edema. Ultimately, the edema causes the capsule of the pancreas to swell, and digestive enzymes digest and destroy the peripancreatic fat. Sometimes, blood vessels may even rupture, causing hemorrhage. All of the tissue digestion and hemorrhage can ultimately liquify the pancreatic tissue, a process called liquefactive hemorrhagic necrosis.

Most of the time, acute pancreatitis is relatively mild, but it can become severe and cause serious complications, so it requires prompt diagnosis and treatment. An important complication is the formation of a pancreatic pseudocyst, which is when fibrous tissue develops around the liquefactive necrotic tissue of the pancreas, forming a cavity that fills up with pancreatic juice. Pancreatic pseudocysts have the potential to rupture, causing severe hemorrhage and the release of pancreatic juice full of digestive enzymes into the abdominal cavity, which can lead to a massive inflammatory reaction that may develop into peritonitis. A pseudocyst can also get infected, most often by bacteria like Escherichia coli, and turn into a very dangerous pancreatic abscess.

Other complications of acute pancreatitis include serious internal hemorrhage from damaged blood vessels, which can quickly develop into hypovolemic shock; the systemic activation of blood coagulation factors or disseminated intravascular coagulation, or DIC for short. Ultimately, clients may develop multi-organ failure, involving the heart, kidneys, as well as lungs, which can lead to acute respiratory distress syndrome, or ARDS, which is the leading cause of death among clients with acute pancreatitis.

Now, the main symptom of acute pancreatitis is abdominal pain in the left upper quadrant or epigastric region, which radiates to the back like a belt, and tends to worsen after eating. Other frequent symptoms include nausea and vomiting. As necrosis induced hemorrhage spreads to the soft tissues of those body areas, there might also be bluish discoloration around the belly button, or the periumbilical region, called Cullen’s sign, as well as along the flank of the body, between the hip bone and the ribs, called Grey Turner’s sign. In addition, when there is extensive peri-pancreatic fat necrosis, the released fatty acids bind and deplete calcium to form soap, which is called saponification. As a result, another distinctive sign of acute pancreatitis is hypocalcemia, which can lead to tetany, meaning involuntary muscle contractions.

Diagnosis of acute pancreatitis is typically based on clinical findings, lab tests, and imaging. Lab tests generally show an increase in blood levels of amylase and lipase. In addition, a complete blood count may show increased white blood cells or an elevated hematocrit due to dehydration or acute hemorrhaging. The C-reactive protein or CRP and lactate dehydrogenase or LDH are usually elevated due to inflammation, and also glucose levels are often high, while calcium levels can be low. Finally, upon imaging studies like abdominal ultrasound, the pancreas will be enlarged. If the diagnosis of acute pancreatitis is still unclear, an abdominal CT scan can be done, usually showing evidence of pancreatitis, such as inflammation, necrosis, and the formation of pseudocysts.

Treatment of acute pancreatitis is focused on pain management and making sure that the client gets adequate IV fluids and electrolytes. In addition, clients are often initially NPO, or “nothing by mouth”; and gastric suction via a nasogastric tube can be used to decrease gastric distension and reduce pancreatic secretion; however, oral or enteral nutrition should resume as tolerated, to help maintain the integrity of the gut mucosa.