Inflammation I - Pancreatitis PDF

Critical Care Nursing Program Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Introduction Inflammation will be further explored as it relates to the pa...

Critical Care Nursing Program Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Introduction Inflammation will be further explored as it relates to the patient experiencing acute pancreatitis. Acute pancreatitis is a painful inflammatory process in which the pancreas is auto digested by its own enzymes. The severity of acute pancreatitis may range from mild, acute edema, to severe, acute pancreatitis with extensive necrosis and hemorrhage. Mild, acute, edematous pancreatitis responds well to conservative management and is associated with a good prognosis. Severe, acute, hemorrhagic, necrotic pancreatitis which comprises approximately 20-30% of patients suffering from this disease, often requires intensive, aggressive therapy. Severe pancreatitis can be life-threatening with hospital mortality rates of about 15% making the management of these patients crucial in the Critical Care setting (Leppaniemi et al., 2019). Learning Outcomes On completion of this unit, the learner will be able to: 1. Describe inflammatory processes associated with acute pancreatitis. 2. Relate the pathophysiology to the associated assessment findings and diagnostic evaluation. 3. Explain the treatment strategies used for acute pancreatitis. Required Reading Please refer to your reading list for Inflammation I Acute Pancreatitis The leading causes of pancreatitis are gallstones, accounting for approximately 30-60% of cases and alcohol abuse in 15-30% of cases. Pancreatitis can be also be caused by endoscopic retrograde cholangiopancreatography (ERCP), hypertriglyceridemia, infection, trauma, and complications from certain medications (Derrick et al., 2019). Normally the pancreas secretes enzymes that are activated in the duodenum to help digest proteins. With pancreatitis, the activation of pancreatic enzymes occurs inside the pancreas, before they are released into the duodenum. This activation leads to the Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 1 of 5  Critical Care Nursing Program inflammatory process that can lead to edema, necrosis, and hemorrhage of the pancreas and other organs. If the pancreatitis is really severe, pancreatic enzymes, vasoactive and other toxic substances leak out into the peritoneal space and can cause third spacing. They may also enter the lymphatic and venous systems directly affecting other organs such as the lungs and the kidneys. Case Study: Roger Parker Roger Parker is a white, 58-year-old, able-bodied, self-identified male with a history of chronic alcoholism, malnutrition, and hypertension. He was admitted to ICU with a GCS of 13 (E-4, M-5, V -4), Temp 38.5, BP 80/32, HR 135 (SR), and RR 28. He is confused, drowsy, and difficult to assess. As you are assessing him he starts to vomit and complain of abdominal pain. You note that his abdomen is large, distended and tender to light palpation. He is being worked up for pancreatitis. Common Assessment Findings in Pancreatitis Please refer to your reading list for Inflammation I Although it is unclear how exactly the pancreatic enzymes become activated, initiating auto digestion, the following theories have been proposed: 1. Alcohol causes the protein of pancreatic enzymes to precipitate and block small pancreatic ducts leading to auto digestion by trapped enzymes. 2. An obstruction of the pancreatic duct (e.g., by a stone) prevents the outflow of pancreatic enzyme-rich fluid leading to increased ductal pressures that trigger auto digestion. Although most pancreatic enzymes are secreted in inactive forms, lipase is produced in an active form leading to the necrosis of fat (Derrick et al., 2019). 3. Reflux of duodenal contents containing digestive juices into the pancreatic duct (e.g., by an incompetent sphincter of Oddi or blockage of the distal end of the common bile duct) triggers activation of pancreatic enzymes resulting in auto digestion. 4. Oxidative stress, caused by smoking, alcohol abuse, or high fat diets, causes injury to pancreatic acinar cells which leads to the release of digestive enzymes and the auto digestion of pancreatic tissues (Derrick et al., 2019). Severe acute pancreatitis may affect all of the body’s systems as the pancreatic enzymes are released into the circulatory system and the inflammatory process affecting the pancreas can spread to other organs. Pancreatic enzymes can also travel to other organs via the lymph. Common assessment findings in acute pancreatitis are listed in your readings. Other responses and their pathophysiology which may or may not occur include: Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 2 of 5  Critical Care Nursing Program 1. Toxic psychosis - Occurs due to lipolytic demyelination of the CNS by pancreatic enzymes. 2. Hypocalcemia – ionized calcium levels drop due to calcium binding to areas of fat necrosis. 3. DIC – Disseminated intravascular coagulation is precipitated by the release of pancreatic enzymes into the circulation. 4. Metabolic acidosis – Occurs secondary to a rapid, shallow respiratory rate that occurs as patients attempt to splint to avoid pain. 5. ARDS – Acute Respiratory Distress Syndrome can occur as pancreatic fluid leaks into the pleural space causing a left pleural effusion. Pancreatic enzymes further increase the permeability of the alveolar-capillary membrane and destroy surfactant. Coupled with atelectasis, alveolar edema and pneumonia, symptoms can progress to ARDS. 6. Hypovolemic shock and hypotension – Caused by massive exudation of plasma and haemorrhage into the retroperitoneal space and accumulation of fluid from leaky vasculature in combination with the massive vasodilation associated with shock (Derrick et al., 2019). Diagnostic Evaluation Elevated WBC count, serum amylase and lipase (generally lipase is more elevated in acute pancreatitis and is elevated for a longer period of time than amylase), elevated BUN, Hct, lactate, triglycerides and C-reactive protein (CRP) (Leppaniemi et al., 2019). Hypocalcemia may manifest as muscle spasms. Abdominal x-ray. Contrast-enhanced computed tomography (shows the degree of inflammation and necrosis). Ultrasound (to rule out biliary stones). Treatment Strategies Treatment for the most part, is supportive instead of surgical. Fluid management is crucial due to massive fluid shifts. Goal for fluid resuscitation is a decrease in Hct and BUN and to maintain normal levels of creatinine during the first 24 hours of hospitalization. Must be cautious in elderly and patients with history of cardiac/renal failure as this can lead to pulmonary edema and worsening compartment syndrome (Derrick et al., 2019). Nutritional support- Historically, pancreatitis patients were kept NPO. New concept of “gut rousing not gut resting” was introduced which recommends early initiation of enteral feeds via gastric or jejunal routes to maintain gut mucosal barrier and to prevent translocation of bacteria therefore reducing risk of infection and necrosis. TPN is no longer recommended (Derrick et al., 2019). Medications given to suppress gastric acid secretion include histamine - 2 antagonists such as Ranitidine/Zantac or proton pump inhibitors such as Pantoprazole/Pantoloc. Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 3 of 5  Critical Care Nursing Program All patients with acute pancreatitis must receive analgesics within first 24hrs of admission to keep patient comfortable. Hydromorphone Hydrochloride/Dilaudid is the preferred choice over Morphine Sulfate/Morphine and Fentanyl/Sublimaze in non-intubated patients (Leppaniemi et al., 2019). Antiemetics are also given. Monitor patients hemodynamic status and watch for signs of shock and acute kidney injury such as tachycardia; hypotension; cool, clammy skin; and urinary output less than 30 ml/hour. Closely monitor patients’ respiratory status. Case Study: Roger Parker Roger is admitted to ICU, placed on cardiac monitor, and an arterial and right subclavian central line placed. His blood work revealed the following: WBC, LDH, lipase, amylase, glucose, and LFT’s all elevated. Hemoglobin, haematocrit, calcium, potassium and magnesium all decreased. His chest x-ray revealed a pleural effusion and atelectasis. A diagnosis of acute pancreatitis is made. Critical care nurses need to be vigilant about monitoring patients with acute pancreatitis for signs of infection, as pancreatic infection is the leading cause of mortality. A pancreatic necrosectomy may be required to debride and/or remove infected areas. This may be done in one or several laparotomies depending on severity of disease. Laparoscopic and endoscopic necrosectomy approaches however are now the preferred methods in less severe cases. It is recommended that stable patients diagnosed with infected necrosis are treated with antibiotics for 30 days after hospital admission prior to receiving necrosectomy to allow the inflammatory reaction to settle. Although unstable patients with this diagnosis should undergo urgent debridement, postponing this procedure in stable patients decreases mortality rates. Procedures such as percutaneous drainage of fluid collections may also be necessary in these patients (Derrick et al., 2019). Case Study: Roger Parker Roger is aggressively fluid resuscitated with lactated ringers. Three days after admission, Roger’s abdominal distention and tenderness has worsened. Urinary output has been minimal. The physician requests the nurse measure the Roger’s abdominal pressure. Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 4 of 5  Critical Care Nursing Program Abdominal Compartment Syndrome The aggressive fluid resuscitation required by patients with severe acute pancreatitis can sometimes increase the abdominal pressures to the point where surgical decompression is necessary to improve renal perfusion. This condition is known as abdominal compartment syndrome. Please refer to your reading list for Inflammation I Patients with gallstone pancreatitis with cholangitis or bile duct obstruction may require an ERCP and/ or cholecystectomy). ERCP involves the use of an endoscope through which a cannula is passed to visualize the pancreas and common bile duct. A contrast dye is introduced into the ducts and x-rays are taken. Physicians use this technique to remove impacted gallstones and drain infected bile. Laparoscopic cholecystectomy is recommended during the same admission for mild acute pancreatitis to avoid reoccurrence and to reduce the risk of biliary complications (Leppaniemi et al., 2019). Conclusion Pancreatitis is a classic exemplar of inflammation. Critical care nurses need to identify those at risk for developing pancreatitis, recognize and respond appropriately to mitigate the complications that can ensue to improve patient outcomes using evidence informed practice guidelines. Module #7: Inflammation I Unit #2: Inflammatory Processes - Pancreatitis Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 5 of 5