Pancreatitis: Nursing process (ADPIE)

Tanya 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 out of 10, along with nausea and vomiting.

An abdominal CT scan confirms pancreatic enlargement and edema, and Tanya 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 these 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 asinar 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 asinar 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 asinar cells to be released and activated within the pancreas before they reach the digestive tract.

All of these potential causes may allow the digestive enzymes produced by the asinar 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 digest and destroy the peripancreatic fat. Sometimes, blood vessels may even rupture, causing hemorrhage.

All of the tissue digestion and hemorrhage can ultimately liquefy the pancreatic tissue, a process called liquefacttive 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 the 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 these body areas, there might also be a bluish discoloration around the belly button or the perambilical region called Cullen sign, as well as along the flank of the body between the hip bone and the ribs, called gray Turner's sign.

In addition, when there's extensive peripancreatic 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 distention and reduce pancreatic secretion.

However, oral or enteral nutrition should resume as tolerated, to help maintain the integrity of the gut mucosa. Now, asymptomatic pseudocysts are treated with watchful waiting and monitoring, while pseudocysts that present with symptoms, infection, or hemorrhage, require drainage, either endoscopically or surgically.

Finally, it's very important to treat the underlying cause, like gallstones, and the complications by administering antibiotics as needed.

As you enter the room, you begin your assessment. Tanya appears restless, and is gritting her teeth and occasionally holding her breath.

She tells you, nothing is helping my pain. She describes it as a 9 out of 10 sharp pain all over her abdomen, which radiates around her back.

Tanya's vital signs are temporal temperature, 101 °F or 38.3 °C, heart rate, 116 BPM, respiratory rate, 22 breaths per minute, with shallow depth, and diminished lung sounds, BP, 100/60 millimeters of mercury, and SPO2, 91% on room air.

You administer 2 L per minute of supplemental oxygen via nasal cannula, and her SPO2 improves to 95%. Tanya's abdomen is distended and tender with hypoactive bowel sounds.

Her lab results from this morning include WBC 18,000 millimeters cubed, amylase 440 units per liter, lipase, 526 units per liter, LDH 420 units per liter, BUN 24.8 mg per deciliter, hematocrit 44%.

Serum glucose, 200 mg per deciliter, creatinine 1.8 mg per deciliter, and CRP 128 mg per deciliter. As you document your assessment findings and interventions, you update the hospitalist overseeing Tanya's care.

The nursing diagnoses that you identify for Tanya are deficient fluid volume related to fluid shifts, vomiting, and fever, acute pain related to inflammation and abdominal distention, and ineffective breathing pattern related to abdominal distention and pain.

Next, you collaborate with Tanya's healthcare team and plan goals for her care. By the end of your shift, her fluid balance will begin to stabilize, her body temperature will normalize, tachycardia will improve, and BP will remain stable.

Throughout her hospitalization, Tanya will have adequate depth of respirations with clear lung sounds, and she'll maintain SPO2 over 95%.

And her abdominal pain will be managed at her stated level of tolerance of 5 out of 10. You also plan a long-term goal for Tanya, that she will seek support to manage her alcohol use.

Now it's time to implement Tanya's plan of care. First, you administer the ordered IV fluids and the medications, hydromorphone for pain, ondansetron for nausea, and omeprazole to decrease stomach acid secretion.

Next, you let Tanya know she will be NPO and you place a nasogastric tube or NG tube, confirm its placement via X-ray, and connect it to low, intermittent wall suction.

Then, you insert a urinary catheter, and you let Tanya know you'll be closely monitoring her fluid balance. Next, you coach her through deep breathing and coughing exercises, teaching her how to use an incentive spirometer to help fully expand her lungs.

Then, you assist Tanya into a side-lying position of comfort, knees flexed, and her head elevated 45 degrees. Finally, you increase the frequency of your assessments of Tanya, monitoring for signs of clinical deterioration.

You will contact the medical team if you observe problems such as worsening tachycardia, hypotension, respiratory distress, or altered mental status.

You return to reassess Tanya and evaluate her progress on the plan of care. Tanya's vital signs are temporal temperature, 100.5 °F or 38.3 °C, heart rate 120 BPM, respiratory rate, 18 breaths per minute with adequate depth and crackles in bilateral bases, BP, 90/60 millimeters of mercury, and SPO 2 90% on 2 L per minute of oxygen via nasal cannula.

You increase her supplemental oxygen to 4 L per minute and update the medical team while remaining at the bedside. You note her NG tube is draining bilious fluid, and her urine output has decreased.

Tanya is restless, and her pain is now 7 out of 10. Her abdomen remains distended and tender to palpation with absent bowel sounds.

The hospitalist arrives at Tanya's bedside to examine her, and together, you review the results of her labs. Her WBC count is 29,000 millimeters cubed, amylase, 520 units per liter, and lipase, 680 units per liter.

You update the healthcare team regarding Tanya's vital signs, increasing oxygen requirements, and adventitious lung sounds.

The hospitalist orders a transfer to the intensive care unit for further treatment and monitoring. Your client, Tanya Abbott, was being cared for on the progressive care unit for acute alcohol-induced pancreatitis, in which the pancreas experiences inflammation and cellular destruction.

Your assessment revealed fever and tachycardia, along with abdominal pain and altered respirations. You identified nursing diagnoses to address Tanya's deficient fluid volume, acute pain, and ineffective breathing pattern.

You collaborated with the healthcare team to plan goals for Tanya, and then implemented strategies to meet them. Your evaluation of the change in Tanya's status prompted a need for a higher level of care.