Acute Pancreatitis

In the United States, about 185,000 cases of pancreatitis are reported each year. Pancreatitis affects people of all ages, however, the mortality rate that is associated with pancreatitis tends to be higher for people in older age. The mortality rate of patients with pancreatitis ranges from about 2% to 10%. It is unsure if the 5000 new cases that are reported each year are new patients or patients that have reoccurring pancreatitis (Belleza 2016). In some cases, pancreatitis can lead to the complications of pancreatic cancer, the fifth leading cause of cancer death in the United States (Feldman, 2006).
Pancreatitis is the inflammation in the pancreas. The pancreas is a gland that rests just behind the stomach in the upper abdomen. The pancreas produces enzymes and hormones. There are two types of glandular cells that the pancreas has: exocrine and endocrine cells. Pancreatitis affects the functions of the exocrine and endocrine of the pancreas. The pancreas has two main functions 1) where it produces enzymes that help digestion and neutralize gastric acid and 2) that it helps regulate the glucose levels in the blood from the release of insulin.
Pancreatitis is a severe illness that has several forms of it. The two main forms of pancreatitis are acute and chronic. Acute pancreatitis is the most common reason for hospitalization for a gastrointestinal-related disease in the United States (Aghani, Elham 2014). Acute pancreatitis is a reversible process that doesn’t lead to chronic pancreatitis unless complications start to develop. Acute pancreatitis has no long-term effects on the pancreatic parenchyma or the function of it. Chronic pancreatitis is the inflammation of the pancreas that doesn’t heal or improve. It is an irreversible process that starts to get worse over the course of time which leads to severe complications and permanent damage.

Most patients have acute pancreatitis, and 10% or fewer have chronic pancreatitis (Lowe, M 2011). The most common type of pancreatitis is mild acute pancreatitis, also called interstitial or edematous pancreatitis. Areas of fat necrosis and interstitial edema develop in and around the pancreas (the peripancreatic tissues). Mild acute pancreatitis is usually self-limiting without organ failure or local or systemic complications. Severe acute pancreatitis, also known as necrotizing pancreatitis, is a life-threatening disorder associated with local and systemic complications including intra-abdominal infections, pancreatic necrosis, and organ failure.4 An additional type, moderately severe acute pancreatitis, is described as transient organ failure or local or systemic complications. (See Severity of pancreatitis for a breakdown of levels.) (Krenzer 2016).
Pancreatitis has become more recognized in children and adolescents. It sometimes is misdiagnosed or mistaken for as a stomach virus. Symptoms for acute pancreatitis come on pretty quickly. The pancreas gets inflamed and usually stays in this state for a few days. While in that state, there is no permanent damage however, there are certain complications the patient endures. Symptoms of acute pancreatitis include: fever, nausea, vomiting and abdominal pain that is behind the ribs and starts to feel like it is spreading throughout the back. Chronic pancreatitis, in contrast, happens at a slower case than acute pancreatitis. Symptoms of chronic pancreatitis include: weight loss, back pain, jaundice, and a recurring severe pain that is behind the ribs and spreads throughout the back. Pancreatitis can occur to anyone, and is most common in people with certain risk factors.
The general risk factors for pancreatitis display the causes with most commonly being associated with alcohol abuse, infection, medications, and genetic or developmental disorders. Risk factors could fall into the category of being non-modifiable or modifiable. Modifiable risk factors are risk factors that you are able to take measure to change them. For instance, alcohol consumption, smoking, diabetes and a non-vegetarian diet. Non-modifiable risk factors are risk factors that you do not have the ability to change. For example, inherited mutations and genetic or developmental disorders. 80% of the patients with pancreatitis have biliary tract disease or history of long-term alcohol abuse (Belleza 2011).
The risk of pancreatitis starts to increase with the amount of alcohol a person has consumed. Alcohol is a trigger factor to pancreatitis and does not necessary indicate that all heavy alcohol drinkers will clinically be diagnosed with pancreatitis. The effects of alcohol in the pancreas changes the pancreatic blood flow. The effects on alcohol on the pancreas result from the direct toxic effects from its metabolism. The risk factors for acute pancreatitis are, heavy consumption of alcohol and gallstones. Gallstones can be a first sign to acute and chronic pancreatitis. Gallstones are small stone-like formations that develop in the gallbladder. As a result of too much cholesterol present in the bile, gallstones start to block the pancreatic duct as they try to make their way out of the bile ducts and into the intestines. Gallstones blocking the bile ducts affect the pancreas in a way that prevents the pancreases from achieving its function of releasing enzymes into the intestines.
The risk factors for chronic pancreatitis include heavy consumption of alcohol for a long period of time, hereditary conditions like cystic fibrosis, gallstones, high triglycerides levels in the blood etc. The development of bacterial and virus infections can lead to pancreatitis. There were several clinical settings that described the cause of pancreatitis due to bacterial pathogens exposed to the individual. It is most seen in acute pancreatitis where the bacteria, for instance, Salmonellosis, which is a food poisoning that is from the cause of the bacteria Salmonella is exposed to the pancreas. Pancreatitis can usually occur when there is a complication with the mumps virus. There are medications can cause the occurrence of pancreatitis like Thiazide, Pentamidine etc.
However, drug-induced pancreatitis are relatively rare and not many incidences have been reported. Lastly, genetic and developmental disorders could be the case for some for acquiring pancreatitis. Hereditary pancreatitis refers to recurrent acute or chronic pancreatitis in an individual from a family in which the pancreatitis phenotype appears to be inherited through a disease-causing gene mutation expressed in an autosomal dominant pattern. Individuals with pancreatitis who carry a gene mutation that causes autosomal dominant pancreatitis have hereditary pancreatitis (Lowe 2015). Genetically developing pancreatitis is called abdominal trauma to the pancreas.
Severe mutations to important major genes can alter and lead to developmental and or genetic disorders that can result to pancreatitis. Inherited conditions like cystic fibrosis increases the risk for pancreatitis. The best-characterized gene mutation–associated pancreatic disorders follow classic Mendelian inheritance patterns, which are recognized as autosomal dominant (e.g., hereditary pancreatitis) or autosomal recessive (e.g., cystic fibrosis [CF]) genetic disorders. Complex trait genetics refers to inherited traits that do not follow Mendelian patterns of single-gene genetics (Lowe, 2015).
The pathophysiology of pancreatitis is characterized by the self-digestion of the pancreas that is from the cause of its own enzymes. The understanding of the pathophysiology of acute pancreatitis is not very well understood. It is suggested that the digestive enzymes play a significant role in the early stages of acute pancreatitis. Entrapment of gallstones, obstruction of gallstones, enzyme activities, activation of enzymes, reflux of enzymes etc. is the makeup of the process of pancreatitis. When gallstones enter the bile duct they often create a blockage. The gallstones then obstruct the flow of the pancreatic juices which then results in a reflux of bile from the bile duct into the pancreatic duct.
Since the pancreas’ functions involve the synthesis of enzymes which have the ability to cause tissue damage, it is the digestive enzymes that are capable of inducing tissue injury. When enzymes are activated they are located in the pancreatic parenchyma, pancreatic juice, and ascitic fluid. These enzymes when are in combination with bile and bile acid, lead to an induction of pancreatitis. This results in the activation of powerful enzymes to activate within the pancreas. These inactive enzymes are in the form of proenzymes or zymogens. These powerful enzymes stay inactive until the pancreatic secretions reach the lumen of the duodenum. It is in the duodenum where these enzymes are then activated where the proteolytic enzymes are then catalyzed usually to trypsin, which then the trypsin activates the zymogens. The enzyme activities lead to series of incidents like vasodilation, necrosis, hemorrhage etc. Bile is not the trigger of the activation of these enzymes, however, when these enzymes enter the bile duct, they are triggered by reflux bile which is later traveled into the pancreatic duct which results in pancreatitis.
The annual incidence of acute pancreatitis in the US ranges from 13 to 45/100,000 persons, and chronic pancreatitis from 5 to 12/100,000; the prevalence of chronic pancreatitis is about 50/100,000 persons (Yadav, 2013). The increase in the prevalence of acute and chronic pancreatitis could lead to a much greater availability to be able to create resources that could detect the morphologic changes that occur in the pancreas. As developing countries are advancing slowly, it is leading to an increase in alcohol consumption, which increases the risk of acquiring pancreatitis in those countries. However, countries like North America and European countries have found a generally stable or decrease in the consumption of alcohol. Even though acute pancreatitis has a higher incidence and prevalence chronic pancreatitis which is lower in incidence and prevalence, they both play a significant part in affecting a patient’s life and the quality of it.
The pancreas plays a major deal in the nutrient digestion. It is known that the nutritional management of a patient with pancreatitis depends on the underlying disease. The nutritional implications of an individual with pancreatitis deals with a numerous amount of implications depending on the severity and stage of pancreatitis. Chronic pancreatitis affects the normal digestion and absorption of nutrients. Maldigestion tends to be a late complication that is seen in individuals with chronic pancreatitis. With this, it results in frequent nutrient deficiencies that can be derived from risk factors like diabetes and alcoholism etc. The nutritional implications given to a patient that has pancreatitis are started by a nutrition screening.
The reason for this is because the nutritional risk is a significant part of the nutritional risks that the patient falls into. The nutritional screening is simple and generally identifies to see if the patient is at actual nutritional risk. Once the screening and assessment are completed it is then when the individual goes into an evaluation to create nutritional requirements and plans for nutrition therapy and care. Some patients are advised to fast a couple of days. During this fasting state, since there is an absence of the stimulatory nutrients that is within the gastrointestinal lumen, the pancreas is not inactive. Daily intake of carbohydrates is about 300 grams corresponding to about half the caloric intake per day. About half of the caloric intake is carbohydrates and 30% are sucrose (Holst, 2013). A specific diet plan is given to the individual which includes detailed information about their protein, energy, fat etc. intake.
A protein diet of 1.0-1.5 g/kg body weight/d is generally sufficient and well-tolerated. Usually, if 30%-40% of the calories are given as fat this is well tolerated, especially when the foods are rich in vegetable fats (Holst, 2013). It is also advised that a low fiber diet is adapted into the diet plan. The fiber may absorb enzymes which then can delay the absorption of nutrients. Pancreatitis and the medical interventions of nutritional implications affect the nutritional status by increasing it. According to the definition, the severity of malnutrition is correlated with two major factors: depletion of nutrients (alcoholism and pain) and malabsorption causes impaired nutritional status and increased metabolic activity due to the inflammatory component of CP (severity of disease) (Holst, 2013).
If any obstruction to the diet, it can cause complications which can lead to malnutrition which leads to weight loss and the complications can result in the individual experiencing a great deal of pain. An inadequate nutritional diet for an individual with pancreatitis can lead to enteral nutrition and increase nutritional status it is recommended to give nutrition through a nasojejunal tube. Medical nutrition therapy is given to an individual with pancreatitis which includes the recommendations of two treatments that is based on the severity of the disease overall. When nutritional support is necessary then the early use of enteral feeding is done to patients which then decreases the severity of the disease.
However, if the severity of the disease is much greater, and nutritional support cannot be possible, it is then advised and predicted that the patient would benefit from nutritional therapy. In most cases, nutritional support is essential to patients that have severe pancreatitis. The patient’s tolerance affects the determination of how the nutrients will be delivered to the patient. With severe pancreatitis, patients most of the time require both enteral and parenteral nutrition. Nutritional goals can be reached by the combination of both the enteral and parenteral nutrition. There are not many prospective data that could form a fundamental for an evidence-based guideline.
In conclusion, there are guidelines published, however, there is a need for them to get a high-quality update. The American Pancreatic Association (APA) had to handle the need to revise these guidelines using an evidence-based approach. A group of ‘expert referees’ (see Collaborator section) was identi?ed based on relevant publications in the ?eld of clinical acute pancreatitis and input during the IAP/APA meeting. This group reviewed the guidelines in the ?nal stages. After the last round of discussion within the executive committee, the working plan was ?nalized to include 12 main topics and 38 clinical questions concerning key aspects of medical and surgical management of acute pancreatitis (Lerch, 2015).

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