**1. Introduction**

## **1.1 Definition and incidence**

Acute pancreatitis (AP) refers to the sudden inflammation of the pancreas, and it may be confined to the pancreas, or more life-threatening, affecting all organs and systems [1–5]. Recurrence is experienced in 15–30% of patients, and 5–25% can develop chronic pancreatitis. It progresses mildly in 80% of patients and resolves with treatment, but in cases of severe AP, complications such as organ failure and pancreatic necrosis may develop, with mortality of around 30% recorded in this group [2, 4, 5]. AP is an acute gastrointestinal disease that requires hospitalization, and is the most common cause of admission to the emergency room worldwide [1, 6, 7]. Hospital admissions for AP in the United States are in the region of 270,000/year, with a mortality rate of 30% in severe cases. Death is due to systemic inflammatory response syndrome (SIRS) and organ failure in the first two weeks, while death after two weeks can be attributed to sepsis and complications [3, 6, 8, 9].

### **1.2 Etiology**

Gallstones are the most common etiology of AP, being responsible for 40–70% of AP cases [10–12]. The ease at which small gallstones can pass into the bile duct make

AP more common in this patient group [13]. Although alcohol is commonly blamed as the second most common cause, the link between alcohol and AP is unclear, as AP is seen in only a small number of alcoholics [2, 14, 15]. Recent studies have suggested that alcohol increases the oxidative metabolism in the acinar cells of the pancreas, thereby causing mitochondrial dysfunction and cell death. This increases also the production of acetaldehyde in the pancreatic stellate cells, and increases circulating lipopolysaccharide and tumor necrosis factor alpha (TNFα), leading to fibrosis in the pancreas [16, 17]. Alcohol has also been reported to increase the viscosity of pancreatic juice and to cause ductal obstructions. That said, it has also been suggested that genetic factors play a role in the development of AP,based on the low incidence of AP in people with chronic alcohol consumption [2, 15, 18]. Other causes have been identified as Hypertriglyceridemia (HTR), and diabetes, hypothyroidism, pregnancy and obesity that cause HTR [1]. Patients with a body mass index (BMI) >35 are at risk of both HTR and AP, while those with serum triglyceride levels >1000 mg/dl are at greater risk [19–21]. Following endoscopic retrograde cholangiopancreatography (ERCP) performed by inexperienced practitioners, patients with Sphincter of Oddi dysfunctions may develop AP following ERCP due to difficult cannulation [22].

AP can also occur due to drugs at a rate of 0.1–0.5% [2, 23–25]. Many drugs have been identified that cause acute pancreatitis. Drugs cause AP by different mechanisms. While some drugs cause direct toxicity to the pancreas (eg, diuretics, sulfonamides), some drugs cause acute pancreatitis by causing an immunological reaction (eg, 6-mercaptopurine, amino salicylates, sulfonamides). Diuretics and azothiopurine cause direct ischemia, while hormones such as steroids and estrogen cause vascular thrombosis or ischemic pancreatitis by decreasing the viskosity of the pancreatic juice. Toxic metabolites of drugs such as valproic acid and tetracycline may accumulate in the pancreas and cause pancreatitis [2, 26, 27].

AP cases have been reported associated with such infectious diseases as Mumps, Coxsackievirus, Hepatitis B, Cytomegalovirus, Varicella-Zoster, herpes simplex and human immunodeficiency virus (HIV) among the viruses; with Mycoplasma, Legionella, Leptospira and Salmonella among the bacteria; with Aspergillus among the fungi; and with Toxoplasma and Cryptosporidium among the parasites [2, 27, 28]. There have been reports of cases of AP with the recent SARS-CoV-2 infection at the heart of the current global pandemic [29, 30]. In a review of current literature, AP was found to be detected in 17% of patients hospitalized due to Covid-19 [29]. Although tests for specific infectious agents are not generally recommended in AP patients, Covid-19 infection should also be kept in mind in AP cases during the pandemic [30].

Concerning other rare causes, pancreatic injury following trauma is an extremely rare condition due to its retroperitoneal nature. Pancreatic duct injuries may occur due to blunt or penetrating traumas [31], while AP may occur due to gallbladder sludge, tumors, autoimmune pancreatitis, hypercalcemia, anatomical and physiological anomalies (pancreatic divisum, biliary cysts, pancreaticobiliary malunion, large juxta-ampullary diverticula, annular pancreas and Sphincter of Oddi dysfunction), and vasculitis [27, 32–36]. Ischemic AP can also be seen after major cardiovascular operations [27, 37, 38]. Patients with an unknown etiology after history-taking, physical examination, laboratory tests, imaging methods and advanced tests are classified as idiopathic. In the event of recurrent AP attacks in this patient group and AP at a young age, genetic factors should be investigated [27, 39].

### **1.3 Pathogenesis**

As its main mechanism, AP blockades the secretion of enzymes while the synthesis of enzymes continues [2, 40]. Under normal conditions, trypsinogen is *Emergency Management of Acute Pancreatitis DOI: http://dx.doi.org/10.5772/intechopen.95986*

produced in the pancreas and secreted into the duodenum where it is converted into protease trypsin, but in cases where secretion is blocked, trypsin continues to be produced in pancreatic acinar cells. While activation continues, elimination is inhibited, and the active trypsin damages the vascular endothelium, interstitium and acinar cells [2, 40, 41]. As a result, autodigestion begins in the pancreas,and ischemia occurs at a tissue level in the pancreas due to the vasoconstriction and stasis of the capillary vessels. The activation of granulocytes and macrophages in response to these events causes a release of proinflammatory cytokines (tumor necrosis factor, interleukins 1, 6 and 8), arachidonic acid metabolites (prostaglandins, platelet activating factor and leukotrienes), proteolytic and lipolytic enzymes, and reactive oxygen metabolites [2, 27, 42, 43]. All of these factors together cause damage to the pancreatic tissue. In general, the inflammation is locally self-limiting, buton occasions, inflammatory agents may cause a systemic response, leading to the damage and failure of distant organs. This, in turn, may result in Acute Respiratory Distress Syndrome (ARDS), pleural effusion, acute renal failure, shock, and even death [2, 27, 44, 45].
