Acute (Banks, et al., 2013). Mild AP

Acute Pancreatitis Alex WielingaLoyalist College What is Acute Pancreatitis?    Despite being such a small organ in the body, the pancreas has a huge role in several body systems including secretion of digestive enzymes, and the production of insulin.  Acute pancreatitis (AP) can effectively change a person’s life forever.  AP was overhauled in its definition and classification during the 2012 Atlanta revision.  Every source since this revision now uses this definition as the gold standard.  The revision defines AP as an acute inflammatory process of the pancreas caused by damage to the pancreas (Banks, Bollen, Dervenis, Gooszen, Johnson, Sarr, 2013).  The degree of inflammation varies from severe hemorrhagic necrosis to mild edema (Banks, et al., 2013).  AP is identified with two stages of the disease: early, which is found within one week of acute onset, or late, which is when it is developed beyond one week of acute onset.  It can be classified as mild, moderate and severe (Banks, et al., 2013).  Mild AP involves generalized mild edema of the pancreas (Banks, et al., 2013).The shift from mild to moderate occurs when complications occur at the pancreas, or when organ failure begins (Mifkovic, Pindak, Daniel, Pechan, 2006).  Severe pancreatitis is generally defined with the existence of persistent organ failure (Zhu, Shi, Sun, 2003).  Pathophysiology of AP    AP primarily involves the biliary tract.  This is the system involved in digestion of ingested foods including the pancreas, liver, gallbladder and the small intestine.  During severe acute cases, multiple organ failures may occur (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).  When there is an acute exacerbation of pancreatitis, the pancreas, which is involved with creating digestive enzymes, begins to digest the organ (HealthLink, 2017).  As the organ is attacked, and functions of the organ diminish, it can cause many pathological changes in the way the body functions.  Pathological Changes     In mild cases of AP, only injury directly to the pancreatic cells occur.  This can lead to edema and inflammation of the pancreas or tissues around the pancreas (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).  In moderate to severe cases, where there is an activation of pancreatic enzymes, several issues that may occur as a result of damage to the pancreas (Lewis, et al., 2014).  This damage is directly related to which type of enzyme is activated.  The pancreas is involved in creating the following enzymes: Trypsin, Elastase, Lipase, Phospholipase A, and Kallikrein.  These enzymes can cause varying effects to the pancreatic tissues.  Trypsin breaks down pancreatic cells by digesting the proteins in the pancreas (Hirota, Ohmuraya, Baba, 2006).  This can lead to tissue edema, necrosis, and hemorrhage (Lewis, et al., 2014).  Elastase is another enzyme used in the dissolution of protein and elastic fibres.  Over-activation can lead to hemorrhage.  This is due to the elastase’s ability to dissolve elastic fibres holding the pancreas together (Lewis, et al., 2014).  Lipase and Phospholipase A are enzymes used to break down fats (Lewis, et al., 2014).  If these enzymes are overproduced, they break down the fatty tissue energy stores that the pancreas uses to power the cells, causing fatty tissue necrosis (Lewis, et al., 2014).  If the energy stores are insufficient to provide fuel for the pancreas and biliary organs, tissue necrosis occurs leading to organ failure (Griesbacher, Rainer, Tiran, Evans.  2002).  Next, we will talk about the how these enzymes become overproduced.  Predisposing and Contributing Factors    In Canada, the most common cause of acute and chronic pancreatitis is alcoholism (Greenberg, et al., 2016).  Environmental factors, including smoking and high-fat diets, or genetic factors may be partial to blame (Greenberg, et al., 2016).  The second highest cause of pancreatitis is gallbladder disease (Greenberg, et al., 2016).  This is because gallstones may create blockages in the biliary tract, leading to the backup of enzymes that result in pancreatitis (Greenberg, et al., 2016).  Less common causes include abdominal trauma, viral infections, penetrating duodenal ulcer, cysts, abscesses, cystic fibrosis, drugs, metabolic disorders, and vascular disease (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).  While there are many causes of pancreatitis, there are also many classical signs and symptoms, which will be discussed next.  Signs and Symptoms    Generally speaking, an individual with AP will present with sudden and severe epigastric pain in the upper left quadrant.  Pain is described as being constant with radiation to the back, chest or flanks (Tenner, Baillie, DeWitt, Vege, 2013).  It may also be described as deep, piercing and continuous or steady.  This description may be non-specific.  Pain is aggravated by eating but is not relieved by vomiting.  While the level of pain is variable, most often it is severe and requires hospitalization.  Pain may be accompanied by cyanosis, flushing, and dyspnea (Lewis, et al., 2014).  During an AP attack, the pain is caused by distension of the pancreas, peritoneal irritation, and biliary tract obstruction (Lewis, et al., 2014).  The radiation of pain into the back, chest, and flanks is a result of the retroperitoneal location of the pancreas (Lewis, et al., 2014).    Jaundice is another side effect often seen (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).  It is the yellowing of external tissues as a result of increased bilirubin in the bloodstream.  Bilirubin, or bile, is produced by the liver.  During digestion, it passes through the biliary tract.  If there is an obstruction, caused by inflammation of the pancreas, the bilirubin backs up in the pancreas.  As there is a vascular response to inflammation, the bile will often shift into the bloodstream, causing a yellowing appearance (Lewis, et al., 2014).  As a result of this, there can be intravascular damage.      Intravascular damage is caused by the self-digestion of the pancreas seen in pancreatitis.  During inflammation, vascular systems have a system response to the trauma (Lewis, et al., 2014).  When the harsh digestive enzymes back up, they can cause damage to the vascular system in the surrounding organs leading to intravascular damage.  This damage leads to infection, and if left untreated, the infection can enter the bloodstream (Lewis, et al., 2014).      Once the infection reaches the bloodstream, the patient may be at a high risk of septic shock.  This is a severe form of shock that is fatal in patients with AP (Greenburg, Hsu, Bawazeer, Marshall, Friedrich, Nathens, et al., 2016).  Sepsis develops in 40-70% of patients and has an 80% mortality rate (Greenburg et al., 2016).  That is why it is very important to have proper diagnostics in AP cases.  Diagnostic Testing of AP    Several diagnostic tests are used to determine if the above signs and symptoms are related to AP, or if they are part of a different disease process.  When it comes to testing in lab settings, two lab values are of the most importance: serum lipase and serum amylase.  These are collected through blood tests (Tenner, Baillie, DeWitt, Vege, 2013).  While a normal value for serum amylase is around 23-85 units per litre, some ranges for normal may be as high as 140U/L (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).  A normal lipase level can range from 0-160U/L.  (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).  In a patient with AP, a diagnosis of AP is confirmed with serum amylase of >200U/L, and or a serum lipase of >200U/L (Marcin,2017).  Elevated levels of amylase and lipase, which are both digestive enzymes secreted by the pancreas, show an increase in hepatic inflammatory response as a response to pancreas damage, which allows more of a serum shift into the bloodstream (Marcin,2017).    Second to lab value testing for the serum lipase and amylase, is diagnostic imaging testing.  Abdominal imaging is perhaps the most useful tool at diagnosis AP, and Contrast Enhanced Computed Tomography (CECT) allows for over 90% sensitivity and specificity for the diagnosis of AP (Tenner, et al., 2013).  Magnetic Resonance Imaging (MRI) is also used in the diagnosis of AP.  CECT allows for the identification of blockages to the bile ducts in the pancreas and can be helpful for the detection of necrotic tissues.  It is also useful at looking for inflammation and edema of the pancreas.  Where pancreatic necrosis is concerned, MRI is the most useful tool for identifying underlying necrosis that may not be visible from CECT (Tenner, et al., 2013).  By identifying the severity of edema, bile duct blocks, inflammation and necrosis, a healthcare team member, such as a doctor or gastroenterologist specialist, is able to identify the stage as either early or late, the severity, and gain a better understanding of the plan of care based on priority concerns.  Priority Health Concerns    Due to the differences between the severity of AP, there are two primary concerns with any form of pancreatitis.  These concerns involve management of acute pain related to the inflammation and bile buildup in the pancreas and dealing with the risk of infection and sepsis as a result of the inflammatory process and tissue necrosis.  When dealing with pancreatitis, the most notable sign or symptom is the acute onset of sudden severe pain.  This pain can be debilitating, and reduce a patient’s ability to perform ADL’s, maintain proper hydration, and maintain proper nutrition.  With these factors diminished by the pain, the patient will lose body density, have decreased energy, be unable to sleep, and will likely end up increasing the severity of AP.  A care plan for management of acute pain can be found in Appendix 1.  With late-stage AP, there is a severe risk of sepsis, especially if the pancreatitis was caused by a viral or bacterial infection that is left untreated for too long.  Sepsis can lead to fever, aches and tremors, and mass organ failure and death if not treated timely.  Sepsis in AP is the leading cause of mortality in AP (Tenner, et al., 2013).  A nursing care plan for infection risks and control can be found in Appendix 2.Primary Care Services for APEmergency Hospitalization and Collaborative Care    Those experiencing AP for the first time may be hit by a whirlwind of pain and out of control symptoms as discussed above.  During the initial onset of severe pain, patients will visit the emergency room, where a medical team will evaluate and diagnose the issues.  Included in the medical team are the primary physician or gastroenterology specialist, and critical care nurses.  The primary physician or GE specialist will perform an assessment of area of pain, level of pain, and order serum blood tests and imaging for the diagnosis of AP.  After a diagnosis is made, and severity of pancreatitis is assessed, the physician will begin orders to provide supportive care.  Supportive care includes fluid resuscitation with isotonic IV fluids, pain control, nutrition management, and, except in mild cases, a transfer of the patient to a monitored unit such as the ICU (Greenberg, et al., 2016).  With the severity of pain, a multimodal analgesic regimen is recommended, which includes the use of narcotics and anti-inflammatory medications to manage pain and inflammation (Greenberg, et al., 2016).  Fluid resuscitation helps to support pancreatic microcirculation (Greenberg, et al., 2016).  This aids in preventing necrosis.  For AP, Ringers Lactate is preferred over Normal Saline due to RL having an 84% reduction in systematic inflammatory response syndrome, which prevents further complications (Greenberg, et al., 2016).  If the pancreatitis is caused by gallstones, a cholecystectomy may be required, and this surgery will take place in the first 24-48 hours of care.  After the diagnostics are completed, and supportive care orders are given, a moderate or severe AP patient will move into a monitored unit.      Once moved to an intensive care unit, the patient is monitored for complications of AP.  The health team in the ICU is lead by the critical care nurse.  The critical care nurse provides complex and challenging nursing care to critically ill patients who are at high risk of life-threatening health problems, such as AP.  The critical care nurse will monitor and assess the patient regularly with their healthcare team.  A patient with AP will be NPO due to needing to prevent excess digestive enzyme production and to decrease the risk of increased pain levels (Greenberg, et al., 2016).  As a result, the critical care team will provide enteral nutrition to reverse anorexia within 48 hours of admission (Greenberg, et al., 2016).  In the ICU, the patient will be monitored for organ failure, sepsis, shock, and other related issues as discussed above.  Once the patient is treated successfully, there are many new lifestyle changes that will be needed once released from the hospital.Ongoing Community Based Care    For many who suffer from an AP attack, there is often irreversible tissue damage that will require constant treatment and care.  This is due to damage to the hepatic organs, which can become diminished due to necrosis.  A single acute attack can lead to chronic pancreatitis.  The pancreas is involved in several processes, including insulin production and digestive enzyme production.  If the damage is severe enough, a patient will need insulin therapy to manage blood glucose levels.  This may require regular monitoring of blood glucose levels and insulin therapy teaching.  Other lifestyle changes include the removal of alcohol from the diet, a decrease of fat in the diet, drug therapy to replace the loss of digestive enzyme production, and management of long-term pain.      Access to care.  Due to the lifestyle changes required to deal with chronic pancreatitis caused by an acute attack, there can be blocks with access to the proper care and management needed to prevent further complications.  This includes blocks to learning for insulin therapy, which may lead to Ketoacidosis, organ failure, increased pain, and malnutrition.  For those who are afraid this may affect their lifestyle, there are recent innovations that will make it easier to manage.      With the advance of Bluetooth technology and smartphones, there are devices, such as Tandem Diabetes Care’s t:slim X2 pump, which is not only a smaller device but also gives regular feedback via Bluetooth about blood glucose levels.  This allows a user to input ranges, and a phone app will not only alert the wearer to their levels if exceeding the limits but also allows them to discreetly administer a bolus of insulin without ever having to do more than look at a phone screen and pushing a button.  This allows people much more freedom when managing insulin deficiencies as a result of pancreatic damage (Wynn, 2017).  Web Resources for Pancreatitis    In Canada, there are a variety of web-based resources available to people with mild acute and chronic pancreatitis.  Two such resources are the Canadian Digestive Health Foundation (CDHF), and HealthLink BC  The CDHF provides a brief overview of the signs and symptoms of pancreatitis and offers advice and resources on how to live with pancreatitis, manage the symptoms, provides treatments options, and has an area for FAQ regarding pancreatitis.  One flaw with this resource is it does not provide the resources to find community-based healthcare resources, such as home-care nurses and dietitians.  HealthLink BC provides a very in-depth resource for those with acute and chronic pancreatitis.  It does provide all the resources necessary, but only if you live in the province of BC.Conclusion    Pancreatitis is an illness with deadly complications if left untreated.  Learning to identify the signs and symptoms may prevent the illness from causing permanent damage to the pancreas and biliary tract.  Early detection and treatment allows for near full recovery.  Healthcare advances have greatly improved survivability with this acute illness.  Lifestyle changes and drug therapy are the most important factor when dealing with this illness chronically.  People who experience permanent pancreatic damage have many available options and resources to help them cope with their chronic illness, and live a near-normal lifestyle.  References Greenburg, J., Hsu, J., Bawazeer, M., Marshall, J., Friedrich, J., Nathens, A., Coburn, N., May,             G., Pearsall, E., McLeod, R.  (2016).  Clinical practice guideline: management of acute             pancreatitis.  Canadian Journal of Surgery.  59(2): 128-140.  doi:10.1503/cjs.015015Grisbacher, T., Rainer, I., Tiran, B., Evans, M.  (2002).  Involvement of tissue kallikrein but not             plasma kallikrein in the development of symptoms mediated by endogenous kinins in             acute pancreatitis in rats.  British Journal of Pharmacology.  137(5).  692-700.  doi:            10.1038/sj.bjp.0704910    Wynn, P.  (2017, March 22).  New diabetes products for 2017: insulin delivery devices.  Diabetes     Self Management.  Retrieved from            resources/tools-tech/new-diabetes-products-2017-insulin-delivery-devices/Hirota, M., Ohmuraya, M.  & Baba, H.  J.  (2006).  The role of trypsin, trypsin inhibitor, and             trypsin receptor in the onset and aggravation of pancreatitis.  Journal of Gastroenterology.      41(9).  832-836.  doi:, J., Markus, J.  (2017, February 13).  Acute pancreatitis treatment and management.              Medscape.  Retrieved from                reatment?pa=4f291eUgZdAXlQGORxzvpKrpvPKCTmQg%2Fk9y7KHPn                 gkF%2Bk9x2i3UTXfc0I1j7CSiSqDRvJALL7UehLkcSrV9zCchrzF%2F7vlnSF6AE             X%2F09M8%3DBanks, P., Bollen, T., Dervenis, C., Gooszen, H., Johnson, C., Sarr, M., Tsiotos, G., Vege, S.              (2013).  Classification of acute pancreatitis—2012: revision of the Atlanta classification             and definitions by international consensus.  BMJ Journals: Gut.  62(1).  102-111.Tenner, S., Baillie, J., DeWitt, J., Vege, S.  (2013).  American College of Gastroenterology             Guideline: Management of Acute Pancreatitis.  American Journal of Gastroenterology.              108.  1400-1415.  doi:10.1038/ajg.2013.218Zhu, A., Shi, J., Sun, X.  (2003).  Organ failure associated with severe acute pancreatitis.  World             Journal of Gastroenterology.  9(11).  2570-2573.  doi:10.3748/wjg.v9.i11.2570Mifkovic, A., Pindak, D., Daniel, I., Pechan, J.  (2006).  Septic complications of acute                 pancreatitis.  National Centre for Biotechnology Information.  107(8).  296-313.  Marcin, J.  (2017, September 25).  Amylase and lipase tests.  Healthline.  Retrived from https://   Staff.  (2017, May 5).  Pancreatitis.  HealthLink BC.  Retrieved from  https://        (2018).  Canadian Digestive Health Foundation.  Retrieved from, S.  L., Dirksen, S.  R., Heitkemper, M.  M., Bucher, L., & Camera, I.  M. (2014).                  Medical-surgical nursing in Canada: Assessment and management of clinical problems             (3rd Cdn.  ed.).  Toronto, ON: Elsevier Canada.Appendix 1care plan for Appendix 1 adapted from: (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).Appendix 2* Appendix 2 care plan adapted from (Lewis, Dirksen, Heitkemper, Bucher, Camera, 2014).