UPDATES IN PREVALENCE, RISK FACTORS, MANAGEMENT AND OUTCOME OF TREATMENT OF ACUTE PANCREATITIS

Khalil Salameh Yakoub Al Neimat¹*, Abdulmalek Khaled Alserhany², Munif Eid Alanazi², Abdulaziz Alhumaidi Alanazi², Naif Eid Alanazi², Majed Ahmed Alanazi², Faisal Abdulaziz Almulhim², Ibrahim Ahmed Alazmi², Abdulmajeed Qasem Alanazi², Abdulrahman Saud Alsharari³, Meshal Mohammed Alsharari², Daham Abdullah Aldaham,³ Noor Hassan Alazmi²

Department of Internal Medicine, Alqurayat General Hospital, Alqurayat, Saudi Arabia. AlQurayat General Hospital, Alqurayat, Saudi Arabia. General practitioner, King Fasial Hospital, Alqurayat, Saudi Arabia.

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ABSTRACT

A frequent pancreatic condition is acute pancreatitis. It is unique of the main reasons of in hospice fatalities along with the greatest mutual gastrointestinal reason for admission. As of a moderate, self-limiting condition to a stark case of acute necrotizing pancreatitis marked by general consequences and multi organ failure, it can fluctuate in severity. Acute pancreatitis is often identified in a hospital setting, wherever the case will also get care and be kept under close observation for problems. Uncertainty the case has serious pancreatitis, the physician might inquire about his indicators and may even examine his abdomen, which will be quite sensitive.

Early intensive fluid therapy remains the basis for the management of acute pancreatitis. In the absence of additional contraindications, a bolus of 15-20 mL / kg lactated Ringer solution is recommended. Then, for the first 24 hours, administer at a rate of 3 mL/kg per hour (often 250-500 mL per hour). Monitor fluid resuscitation using a combination of blood urea nitrogen, hematocrit, and urine volume to change fluid volume during the first 24 hours of resuscitation.

Keywords: Acute pancreatitis, Prevalence, Risk factors, Management, Outcome of treatment

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Introduction

The most common gastrointestinal symptom that requires hospitalization in the US is acute pancreatitis, which is contagious. The virus can cause mild illness that only requires conservative care to severe, complex illness with increased morbidity and fatality rates. The diagnosis of an acute manifestation is straightforward, but forecasting how the illness will develop and manifest itself poses the most obstacle. Determine the equal of care using this [1].

Recently, the occurrence of acute pancreatitis (AP) has amplified Worldwide to roughly 34 bags per 100,000 persons annually [2].

Though gallstones and alcohol ingestion are the most common grounds of AP, hypertriglyceridemia, drugs, endoscopic backward cholangiopancreatography (ERCP), shock, obesity, diabetes, and infection are also well-known triggers of local and universal inflammation [3].

The therapeutic concept of AP is fundamentally changing, considering minimally invasive rapy over the dominant multidisciplinary participatory step-up approach [4].

The existence of one of the most common and severe gastrointestinal conditions requires a hospital entrance fee. In the USA, AP-related admissions cost nearly ~$2.6 billion yearly. However, the total global prevalence of AP ranges between 4.9 and 73.4 cases per 100,000 folks yearly [5].

The prevalence of AP is increasing with age in females and males, >60% of cases document in adults. Similarly, the frequency of AP is binary and three times higher in African-American populations compared to Caucasian populations [6].

Percutaneous tube drainage (PCD), endoscopy, small incision surgery, and video-assisted hospitals are key components of minimally invasive surgery that have gradually replaced open surgery [7]. In-hospital mortality is a life-threatening condition of about 15%, and undecorated mutants make up about 20-30% of patients. The 2012 edition of Atlanta Classification and Description based on global consensus is the most widely used classification system for severe pancreatitis. Two stages (early and late) are recognized in this classification. There are three levels of difficulty: light, medium, and basic. Mild pancreatitis (interstitial edematous pancreatitis) usually heals within the first week and has no organ failure or regional or systematic effects. Temporary organ failure (less than 48 hours), with local consequences, or exacerbation of associated illness, is categorized as moderate individuals who have continuous (above 48 h) structure failure consisting of the severe type of the illness [1, 8].

Alcohol and gallstones are the two main causes of acute pancreatitis (gallstones). There are clear differences between the number of people who develop pancreatitis due to gallstones or alcohol in different countries and regions. Heavy drinking is related to a higher risk of severe alcoholic pancreatitis. Men were more likely to develop alcoholic pancreatitis than women, although after accounting for alcohol intake, the risk was the same in both sexes. Other related risk factors comprise endoscopic retrograde cholangiopancreatography, surgery, medications, HIV infection, hyperlipidemia, and biliary system abnormalities [9].

From mild, self-limited disease to severe acute necrotizing pancreatitis with generalized consequences and multi-organ failure, the severity varies. Nearly 20% of people with acute pancreatitis develop severe cases, which can be associated with multi-organ failure (respiratory, circulatory, and renal). AKI, a common consequence of severe pancreatitis, often presents at night during the illness after another organ failure. Its prognosis is extremely poor with a mortality rate of 75%, especially if renal replacement therapy is required. Although the exact pathogenesis of AKI in acute pancreatitis remains unclear, it appears to begin with impaired capacity and then be influenced by complex vascular and humoral mechanisms. We describe the epidemiology, pathophysiology, etiology, and use of AKI in this section in patients with severe acute pancreatitis [10].

Study Objective

The study aims to summarize current evidences regarding the prevalence, risk factors, management and outcome of treatment of acute pancreatitis.

Materials and Methods

Study Design

Integrative Literature Review (ILR).

Study Duration 

Data was collected during the period from 1– 29 May, 2022.

The papers that had the same goal as our study were reviewed in depth after searching and defining the sample.

PubMed and EBSCO Information Services were chosen as the exploration databases for the publications used in the study due to their reputation as trustworthy resources. The National Center for Biotechnology Information (NCBI), a component of the National Library of Medicine of the United States, developed PubMed, one of the largest online digital libraries. The prevalence, risk factors, management, and results of treatment for acute pancreatitis were the topics used to produce the article. The established papers' subjects and summaries were carefully examined.

The addition of the subjects was determined by their relevance to the research, which had to include at least one of the following topics: prevalence, risk factors, management, treatment outcomes, and acute pancreatitis.

Exclusion Criteria

All additional papers, recurring researches, and reviews of research which do not possess one of these themes as their major end were disregarded.

Analysis of Statistics

There was no programme used to analyse the data. The data was extracted from a predefined form that also contained the research subject, author's title, goal, executive summary, findings, and outcomes. The outcomes of each affiliate were double-revised in order to ensure reasonableness as well as to cut down on inaccuracies.

Studies were double-reviewed during the article selection process to verify that the research we included is pertinent to the target line of our study and to prevent or lessen slippage in the results.

Etiology

Gallstones, hypertriglyceridemia, and alcohol consumption are the greatest mutual reasons for spartan acute pancreatitis. Each cause of severe acute pancreatitis has a different incidence, which varies by geographic region and socioeconomic class. Alcohol consumption, gallstones, hypertriglyceridemia, drug-induced acute pancreatitis, and triglycerides are common causes of acute pancreatitis. Following procedure (endoscopic retrograde cholangiopancreatography or abdominal surgery), canal stenosis previously defined as sphincter of Oddi dysfunction type I, autoimmune pancreatitis type I (associated with systemic IgG4 disease) and type II, viral infections  (Coxsackie, Cytomegalovirus, Echovirus, Epstein-Barr virus, hepatitis A/B/C, HIV, mumps, rubella, varicella), leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis, mycoplasma, shock, bacterial infections (Campylobacter jejuni, Legionella, abnormal birth defects (annular pancreas), hypercalcemia, hereditary diseases (including hereditary pancreatitis, cystic fibrosis, and alpha 1-deficiency) antitrypsin), kidney disease (hemodialysis), toxin poisoning (scorpion organophosphates) and vasculitis (multinodal inflammation, systemic lupus erythematosus) and parasitic infections (Ascaris lumbricoides, Cryptosporidium, Chlorine norchis sinensis, microsporidia) [8-11].

In all cases of severe pancreatitis, the extent of pancreatitis elicited by alcohol and gallstones differs greatly between nations and regions. Prevalence of alcoholic pancreatitis is 1.5 times greater in Hungary as compared to gallstone pancreatitis, and the high frequency of acute intoxication pancreatitis is thought to be linked to heavy alcohol use [12].

In contrast, in Greece, Italy, and Norway, the prevalence of gallstone pancreatitis is significantly greater compared to alcoholic pancreatitis. Acute alcoholic pancreatitis is more frequent than gallstone pancreatitis in France, Germany, and Korea, but this is not the case in Mexico and Sweden [13].

AP, or pancreatic inflammation, is frequently accompanied by systemic inflammatory response syndrome (SIRS), which may compromise the function of other organs. In between 75% and 85% of instances, the cause of AP is easily discernible [14].

The American Gastroenterological Association (AGA) offers a thorough manual to control the causes of pancreatitis. The estimation would instigate thru a detailed past converging on indicators and appearance. The exploration is required to pay much attention to the assessment of any previously documented gallstones, alcohol use, past hypertriglyceridemia or hypercalcemia, family history of pancreatic illnesses, prescription/non-prescription drug history, history of trauma, and presence of autoimmune illness [15].

Epidemiology

Overall, the Joint States and the rest of the world have seen an increase in the prevalence of acute pancreatitis. It is difficult to tell if this trend reflects an actual rise in incidence or only increased detection. With several rumors presenting an increase in acute pancreatitis subservient to hypertriglyceridemia, the rise in incidence is thought to be partially caused by enhanced hypertriglyceridemia and metabolic syndrome [1, 8].

Between 15.9 and 36.4 cases of AP occur annually per 100,000 persons. It is expected that the cost of disease on the use of healthcare resources would rise in the near future. Regardless of the advancements in imaging technologies, therapies, and admittance to healthcare, AP continues to have considerable disease and suffering that has generally been unaltered throughout time. The total mortality rate was between 5 and 17 percent in cases of severe AP and 1.5 percent in cases of mild AP [16].

Pathophysiology

The confined demolition of the pancreas and the general inflammatory response are mutual constituents of pancreatitis' pathogenesis. The initial activation of trypsinogen to trypsin within the acinar cell in contrast to the duct cavity is the initiating incident. This is thought to be related to issues with calcium homeostasis, pH, and high ductal weights (such as those found in duct obstruction). It is believed that numerous poisons responsible for pancreatitis (comprising alcohol) encompass ATP drop occasioning in raised intra-acinar calcium courtesies that arouse the first initiation of trypsinogen to trypsin, it triggers enzymes for instance elastase then phospholipases. Calcium transference is an ATP-compelled practice, predominantly for repossession in the smooth endoplasmic reticulum [1, 17].

Diagnosis

The case will frequently report nausea, and anorexia, in addition to reasonable to serious epigastric stomach discomfort. The generous of ache might fluctuate depending on whether a biliary blockage or a metabolic or toxicologic is to be blamed. While metabolic and toxicologic causes, like alcohol, might have lethargic beginning with more dull and broad pain, the biliary etiology is more frequently reported as having a sharper pain that radiates through to the backbone with a more abrupt onset [18].

Acute pancreatitis is usually diagnosed in a hospital, where people are treated and monitored for complications. The doctor will ask the patient regarding symptoms and may touch the abdomen - it may be tender if preserving has acute pancreatitis. A blood test will be performed, and occasionally a CT scan to assist in the diagnosis. Initially, it can be challenging to identify if acute pancreatitis is mild or severe. He will be monitored closely for signs of grave problems, such as organ failure. The updated Atlanta structure for AP aids in uniforming AP diagnosis. The categorization system defines pancreatitis as occurring in the enduring when any two of the following three characteristics are present: Abdominal discomfort that is consistent with AP, serum amylase and/or lipase levels that are 3 times greater than the highest limit of normal and abdominal cross-sectional imaging findings that exhibit AP features [19, 20].

Risk Factors

Numerous research has endeavored in estimating the hazard of unadorned alcoholic pancreatitis since alcohol is among 2 primary etiological variables for serious pancreatitis [21].

Another significant etiological cause of severe pancreatitis is cholelithiasis. According to U.S. research, the relative risk (RR) for acute pancreatitis in cholelithiasis individuals was 14/35 for males and 12/25 for females. 3.4 percent of 2583 cholelithiasis patients had pancreatitis throughout the follow-up retro [22].

One of the most common side effects of endoscopic retrograde cholangiopancreatography is acute pancreatitis (ERCP). Acute pancreatitis following diagnostic ERCP occurred somewhere between 0.4 percent and 1.5 percent of the time (Near 2c), based on the intelligence reports from the United States and Europe [23].

After surgeries close to the pancreas, like biliary tract processes, gastric operations, splenectomies, and splenorenal shoves (Level 4), the likelihood of developing postoperative pancreatitis is substantial [24].

Numerous studies have hypothesized links between drug usage and the incidence of acute pancreatitis, but only a few medications have been directly linked to the condition [25].

Acute pancreatitis risk is thought to increase with blood triglyceride levels above 1000–2000 mg/dl [26].

One of the most common consequences of learned immunodeficiency syndrome is acute pancreatitis (4 percent to 22 percent of cases), and the risk rises as HIV infection progresses [27].

Irrespective of the nation, the area, or the case series, idiopathic causes of acute pancreatitis rank 3rd utmost frequently behind gallstones and alcohol. Acute pancreatitis with an undetermined etiology is referred to as severe idiopathic pancreatitis [28].

Management

Early, violent fluid resuscitation continues to be the cornerstone of treating acute pancreatitis. If there are no other present contraindications, lactated Ringer's solution should be administered, with an initial bolus of 15 to 20 mL/kg and successive rates of 3 mL/kg per hour (often 250 to 500 mL per hour) for the first 24 times. In the first 24 hours of resuscitation, nursing is performed every 4 to 6 hours to change the fluid rate. The resuscitation of fluid is observed by a combination of blood urea nitrogen, hematocrit, and urine output. A high chance of developing MODS is indicated by sustained non-response, which justifies raising the degree of treatment. Antibiotics for prevention are not required. Empiric antibiotics are recommended if contagion is suspected until cultures show their results. The signal for antibiotics is restricted to the appearance of necrosis [29].

Early venous hydration aggressively, sufficient nutrition, essential therapies, and pain control are the foundations of AP care. The most recent and available AP therapy possibilities are reviewed. It is not advised to continuously use prophylactic antibiotics except if there is clear evidence of a current infection. Nephrotoxic antibiotics would not be administered if supplied. To limit the hazard of different nephrotoxicity, not all patients with acute pancreatitis prerequisite to requiring contrast-enhanced computed tomography, especially those with minimal pancreatitis and those who recover quickly. Although gadolinium injection has been linked to the development of nephrogenic universal fibrosis, magnetic resonance imaging can be an option since it provides excellent soft tissue contrast [30].

Initial Valuation

Preliminary evaluation and triage to the proper hospital environment are important prompt steps in the care of individuals with AP. This has to be discussed as soon as possible during the hospital stay to permit a proper organization [31].

Fluid Restoration

The existing strategies concerning fluid restoration in dealing with cases of AP are emergent. Regardless of these fluctuations, there remains to be an agreement on the rank and vital of durable early fluid recovery [32] Several sorts of fluids are presently used for fluid resuscitation, which mainly comprises crystalloid and colloidal keys. With an increased risk of mortality and kidney failure needful renal replacement treatment has been observed when using hydroxyethyl arrowroot instead of crystalloid solution [33]. At present, the use of crystal fluids for fluid revival is usually preferred, with colloidal fluids playing an auxiliary part [34].

Nourishment

As opposed to the traditional nil per oral approach used in the past, early start of nutritious supplements is now the norm when discussing nutrition in AP. The AGA now recommends starting first oral feedings in individuals with mild AP (within 24 hours) [35, 36].

 

Dealing with Pain

In order to effectively treat AP, pain management is still crucial. Uncontrolled pain might cause hemodynamic instability, which can have more serious effects [37, 38].

Antibiotics

Prophylactic antibiotics have no place in treating AP patients. Recent studies have revealed no connection between the start of antibiotic therapy in AP and straightforward outcomes such as organ failure, necrosis, or death [39, 40].

Endoscopy

Patients with AP who develop synchronous cholangitis or biliary blockage may consider endoscopic intervention. Tenacious choledocholithiasis can become obstructive in a limited subset of individuals and cause a pancreatic/biliary sapling obstruction [41].

Surgery

The starring role of surgery in the diagnosis of acute pancreatitis is minimal. The most common reason for intervention in acute pancreatitis is to treat sequelae, particularly infected walled-off necrosis. The step-up strategy has been recognized in this setting, with prior draining (endoscopic or percutaneous), a wait for the wall to mature, and finally debridement using endoscopic or minimally invasive surgical approaches. Only when all other options have failed is open surgery recommended. Acute compartment syndrome, non-occlusive intestinal ischemia and necrosis, enterocutaneous fistulae, vascular complications, and pseudocyst are among the other reasons for surgery in acute pancreatitis. By performing a cholecystectomy, surgery can help avoid recurring acute pancreatitis [41, 42].

Alcohol Cessation

All patients with known AP should receive abstinence counseling [43]. A randomized controlled trial showed that abstinence counseling during AP reduced the recurrence rate of AP over 2 years [44].

Prognosis

Organ failure and pancreatic necrosis are two factors that influence the prognosis of acute pancreatitis and represent the severity of the condition. Dynamic contrast-enhanced computed tomography (CT) scanning can be used to diagnose pancreatic necrosis. According to the definitions from the 1992 Atlanta Conference, the following elements are necessary for a structure to fail: (1) shock — systolic blood pressure less than 90 mmHg, (2) respiratory failure — PaO2 less than 60 mmHg, (3) renal failure — serum creatinine more than 2 mg/dl after hydration, and (4) gastrointestinal hemorrhage — blood loss more than 500 ml/24 hours [45]. The study group sponsored by JMHW has developed an independent measure for defining the severity,162 and the parameters comprise dyspnea, shock, illnesses of the central nervous system, a tendency to bleed, an undesirable base excess, and indications of organ failure, comprising an increase in blood urea nitrogen level and the creatinine equal [46].

Acute pancreatitis generally has a fatality rate of one-two percent, whereas severe pancreatitis has a substantially higher but unclear mortality rate. Prognostication and severity analysis is crucial for controlling the degree of treatment. Several clinical prediction measures have been created and proven effective. Maximum is difficult to compute and requires 48-hour information [28, 46]. 

AKI Associated with Acute Pancreatitis

Acute Kidney Injury (AKI) develops later with the progress of the illness, more often next to the failure of other organs, in addition, it is considered a common consequence of serious acute pancreatitis. It has an extremely bleak outlook, especially if kidney transplant treatment is necessary, with fatality rates above 75%. AKI in acute pancreatitis has complicated pathogenesis that is yet unclear, however, it appears to be caused by volume depletion initially, and then complex vascular and humeral problems [10, 31].

Conclusion

HTG is known to be among the most significant risk factors for AP, more specifically in patients who have diabetes. According to this study's results, there is a significant relationship among AP and poor glycemic control (measured by HbA1c levels and fasting and postprandial glycemic values), elevated TG values, the existence of AHT, and the initiation and development of diabetic chronic issues.

Acknowledgments: Many thanks to Khalil Salameh Yakoub Al Neimat; Consultant of Internal Medicine, Alqurayat General Hospital, for his continuous help, support and encouragement to complete this work.

Conflict of interest: None

Financial support: None

Ethics statement: None