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Acute pancreatitis

Acute pancreatitis is a sudden and often severe inflammation of the , the organ responsible for producing and hormones like insulin, typically resulting from the premature activation of these enzymes that leads to autodigestion of pancreatic tissue. It manifests abruptly with intense upper that may radiate to the back, accompanied by , , fever, and elevated levels of pancreatic enzymes such as and in the blood. While most cases are mild and resolve with supportive care within a few days, severe forms can lead to life-threatening complications like pancreatic , , or organ failure, with overall mortality ranging from 1-2% in mild cases to higher in severe ones. The condition accounts for approximately 300,000 hospital admissions annually , with incidence rates increasing over recent decades, particularly among adults in their 40s to 60s, though cases in children and the elderly are also rising. The two leading causes are gallstones, which account for 35-40% of cases by obstructing the , and heavy consumption, responsible for 17-25% of episodes through toxic effects on pancreatic cells. Other notable etiologies include (high blood fat levels), certain medications, , infections, high calcium levels (hypercalcemia), and genetic factors such as mutations in genes like PRSS1 or CFTR. Risk factors that elevate susceptibility include (BMI ≥ 30), cigarette smoking (which triples the risk), , and a family history of pancreatitis or gallstones, with men and Black individuals facing higher incidence rates. In severe cases, complications may involve , acute respiratory distress, or pseudocysts, necessitating intensive care. Initial management typically involves hospitalization for intravenous fluids, pain control, and nutritional support, with interventions like endoscopic procedures to remove gallstones or antibiotics for infections as needed. Early recognition is critical, as prompt treatment improves outcomes and prevents progression to in recurrent cases.

Introduction

Definition and Classification

Acute pancreatitis is defined as a sudden inflammatory process of the pancreas characterized by reversible parenchymal injury and potential necrosis of peripancreatic fat, which typically resolves within six months without leading to permanent structural changes. This condition arises from premature activation of pancreatic digestive enzymes, resulting in autodigestion of the gland and surrounding tissues, distinguishing it from chronic pancreatitis, which involves irreversible fibrosis. The Revised Classification, established in through an international , provides a standardized framework for assessing the severity of acute pancreatitis based on the presence of organ failure and complications. It categorizes the disease into three severity levels: mild acute pancreatitis, which lacks organ failure or local/systemic complications and generally resolves without intervention; moderately severe acute pancreatitis, characterized by transient organ failure lasting less than 48 hours or the presence of local or systemic complications without persistent failure; and severe acute pancreatitis, defined by persistent organ failure exceeding 48 hours, often associated with higher mortality risk. This system divides the disease course into an early phase (first week, driven by systemic inflammatory response) and a late phase (after the first week, potentially involving local complications). Morphologically, acute pancreatitis is classified into interstitial edematous pancreatitis, involving pancreatic l edema without , and necrotizing pancreatitis, which includes of the pancreatic , peripancreatic tissues, or both. Necrotizing pancreatitis is further subdivided into sterile , which does not involve , and infected , a critical complication that significantly worsens and often requires . These morphologic distinctions guide and decisions, with computed commonly used to identify after 72 hours from onset. The evolution of classification systems reflects advances in understanding the disease's clinical and radiologic features, progressing from the 1963 Marseille classification—which distinguished acute edematous from acute necrotizing pancreatitis based primarily on —to the Marseille update incorporating relapsing forms, and then to the 1992 Atlanta symposium's clinically oriented criteria emphasizing organ failure and local complications. The 2012 revision of the Atlanta system incorporated evidence from prospective studies and refined definitions to improve prognostic accuracy and interobserver reliability, replacing outdated terms like "pancreatic abscess" with more precise descriptors of infected collections.

Epidemiology

Acute pancreatitis affects an estimated 13 to 45 individuals per 100,000 population annually worldwide, with pooled global incidence rates from systematic reviews indicating approximately 34 cases per 100,000. According to the 2021, the number of incident cases reached approximately 2.75 million globally, reflecting an increase from 1.73 million in 1990, though age-standardized incidence rates have remained relatively stable around 34 per 100,000 due to . The increasing trends in case numbers are largely attributed to rising of risk factors such as , disease, and consumption, which have driven a gradual upward trajectory over recent decades. Demographic patterns reveal a higher overall incidence in men compared to women, with a male-to-female ratio of approximately 1.5:1 to 2:1, primarily due to as a predominant etiological factor in males. In contrast, women experience elevated rates linked to s, which account for a larger proportion of cases in this group. The condition peaks in incidence between the ages of 40 and 60 years, though rates rise with advancing age, particularly beyond 75 years where biliary causes dominate. Geographically, incidence rates are notably higher in developed countries, ranging from 30 to 50 cases per 100,000 in and the , compared to lower figures of 5 to 20 per 100,000 in parts of and . These disparities are tied to socioeconomic factors, including greater consumption and prevalence in high-income regions, alongside differences in gallstone disease patterns influenced by and .

Clinical Presentation

Signs and Symptoms

The cardinal symptom of acute pancreatitis is severe epigastric pain that typically radiates to the back, often described as constant, deep, burning, or stabbing in nature, with sudden onset and worsening after eating; this pain usually persists for hours to days. Patients commonly report associated symptoms including , non-bilious , and anorexia, which contribute to and discomfort. On , findings include abdominal tenderness in the epigastric region, often with guarding or mild rigidity, diminished bowel sounds suggestive of , and possible in more severe presentations. may reveal fever and , reflecting the inflammatory process; in severe cases, and altered mental status can indicate hemodynamic instability. Rare hemorrhagic manifestations, such as (periumbilical ecchymosis) or (flank ecchymosis), occur in cases of retroperitoneal or intraperitoneal bleeding and are uncommon, appearing in fewer than 3% of patients. In mild cases, symptoms typically resolve within 3 to 7 days with supportive care, representing about 80% of presentations. Severe cases, however, may progress to (SIRS), characterized by persistent fever, , and , potentially leading to multi-organ involvement if untreated.

Complications

Acute pancreatitis can lead to a range of local and systemic complications that significantly impact patient outcomes, with local complications occurring in approximately 10-20% of cases and systemic complications in 15-25%, though rates are substantially higher in necrotizing pancreatitis.31310-6/fulltext) These complications often determine the transition from mild to moderately severe or severe disease, as defined by the revised Atlanta classification, and may require interventional management to prevent progression to multi-organ failure or death. Local complications primarily involve peripancreatic structures and evolve over time based on the disease phase. Acute peripancreatic fluid collections (APFC) form within the first 4 weeks after onset and consist of homogeneous collections of enzyme-rich fluid adjacent to the in the setting of edematous , without non-viable pancreatic tissue; they are often but can cause or if persistent. After 4 weeks, APFCs may mature into pancreatic pseudocysts, which are well-circumscribed, encapsulated collections of fluid devoid of solid necrotic debris, occurring in up to 10-20% of cases and potentially leading to symptoms such as , , or rupture if untreated. In necrotizing , acute necrotic collections (ANC) develop in the first 4 weeks as heterogeneous collections containing both fluid and non-viable pancreatic or peripancreatic tissue, carrying a of . These can progress to walled-off necrosis (WON) after 4 weeks, forming encapsulated necrotic collections that are clinically significant due to their association with , hemorrhage, or disconnection of viable pancreatic tissue, often necessitating drainage. Additional local issues include , resulting from inflammatory or pseudocyst compression on the , and , arising from extrinsic compression or direct inflammatory extension, both of which can lead to or portal hypertension.04916-3/fulltext) Systemic complications arise from the inflammatory cascade and are more ominous, often defining severe disease. Persistent organ failure, lasting beyond 48 hours, commonly affects the (e.g., via ), cardiovascular system (e.g., shock), or renal system (e.g., ), occurring in about 20% of all cases and driving much of the 15-30% mortality in severe .30102-7/fulltext) Infected pancreatic necrosis develops in 20-30% of severe cases, typically after the third week when gut bacteria translocate into necrotic tissue, manifesting as fever, worsening , and high mortality rates up to 30% despite antibiotics and . Complications are temporally divided into early and late phases to guide prognosis and intervention. Early complications, within the first week, include systemic inflammatory response syndrome (SIRS), characterized by widespread inflammation leading to fever, , and , and acute respiratory distress syndrome (ARDS), which impairs gas exchange and requires ventilatory support in up to 20% of severe cases. Late complications, beyond the first week, encompass multi-organ dysfunction syndrome (MODS), involving failure of two or more organ systems due to ongoing inflammation, and a persistent inflammatory response that exacerbates tissue damage and increases risk. Overall, these early and late events highlight the need for vigilant monitoring, as persistent systemic issues portend worse outcomes compared to transient ones.

Etiology

Common Causes

The two most common causes of acute pancreatitis are and consumption, accounting for the majority of cases worldwide. Percentages vary by region; for example, accounts for a higher proportion (up to 40%) in compared to 17-25% in the . pancreatitis arises from the migration of into the , causing transient biliary obstruction and subsequent reflux of into the , which triggers premature activation of pancreatic enzymes and autodigestion of the . This etiology accounts for 35 to 40 percent of acute pancreatitis cases, with higher prevalence in women over 50 years of age due to the demographic distribution of disease. Key risk factors include , female gender, rapid , and older age, though only 3 to 7 percent of individuals with develop pancreatitis. Alcoholic pancreatitis results from chronic heavy alcohol use, involving mechanisms such as direct toxicity to acinar cells, from , and dysfunction of the leading to ductal and . It comprises 17 to 25 percent of cases and typically requires prolonged heavy consumption, such as more than 5 drinks per day for over 5 years, with often serving as an acute precipitant. This cause is more prevalent in men aged 30 to 50 years, and cigarette synergistically increases risk by potentiating pancreatic injury. In approximately 10 percent of cases, both gallstones and contribute to the .

Less Common Causes

Hypertriglyceridemia accounts for approximately 1-10% of acute pancreatitis cases, with higher incidences reported in certain populations. It typically occurs when serum levels exceed 1000 mg/dL, though levels above 2000 mg/dL confer a substantially elevated risk of up to 10-20%. The mechanism involves the of triglycerides into free fatty acids, which exert direct toxic effects on pancreatic acinar cells, leading to . Management strategies include aggressive lipid-lowering therapies, such as insulin infusion or , to rapidly reduce levels and mitigate severity. Post-endoscopic cholangiopancreatography (ERCP) is an iatrogenic complication occurring in 3-10% of procedures, representing a notable procedural . Incidence rises with factors such as sphincterotomy, difficult biliary cannulation, or characteristics like female sex and younger age. Preventive measures, including rectal nonsteroidal drugs and adequate , are recommended to lower this in high-susceptibility cases. Drug-induced acute is rare, comprising less than 2% of cases, and often results from idiosyncratic reactions rather than dose-dependent toxicity. Commonly implicated medications include , valproic acid, and statins, with early pharmacovigilance data raising concerns for glucagon-like peptide-1 receptor agonists such as liraglutide and ; however, 2025 analyses indicate no increased and suggest safe use even in with a history of . High-risk drugs also encompass and , necessitating immediate discontinuation upon suspicion and careful rechallenge assessment. Other less common etiologies include hypercalcemia, often secondary to , which accounts for 1-7% of cases through calcium-mediated activation of pancreatic enzymes. Traumatic injury, such as blunt , can precipitate pancreatitis via direct glandular disruption, though it is infrequent outside of surgical or accidental contexts. Infectious causes, including viral agents like or , are rare triggers, typically in pediatric or immunocompromised patients. , particularly , represents about 1-6% of chronic cases but can present acutely, characterized by lymphoplasmacytic infiltration responsive to corticosteroids. Idiopathic acute pancreatitis, where no etiology is identified after initial , comprises 10-30% of cases and may reflect occult or sphincter of Oddi dysfunction upon further investigation. While gallstones and alcohol remain the predominant causes overall, these less common factors highlight the need for comprehensive etiological assessment to guide targeted interventions.

Pathology

Acute pancreatitis is initiated by the premature activation of to within pancreatic acinar cells, which bypasses normal protective mechanisms such as trypsin inhibitor proteins and compartmentalization in granules. This aberrant activation occurs intracellularly, often triggered by factors like lysosomal hydrolase or altered intracellular , leading to the loss of acinar cell integrity. The activated then catalyzes the conversion of other proenzymes, including prophospholipase A2, proelastase, and prolipase, into their active forms, setting off a proteolytic cascade. This local autodigestion process promotes the release of inflammatory mediators, including cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor factor-alpha (TNF-α), from damaged acinar and immune cells. These cytokines drive infiltration into the pancreatic , exacerbating microvascular injury through endothelial activation and increased . Locally, the effects manifest as interstitial edema from fluid leakage, parenchymal due to ongoing enzymatic destruction, and fat where activated lipases hydrolyze peripancreatic into soaps. Systemically, the amplified inflammatory response creates a that induces (SIRS), characterized by widespread and activation of coagulation pathways. The further compromises distant organs, notably through gut barrier failure, where increased allows bacterial translocation from the into the bloodstream or peripancreatic spaces. Recent 2025 research indicates that contributes to this process, worsening severity and risk in necrotizing cases through shifts in microbial composition. This translocation contributes to multi-organ dysfunction, including and , by perpetuating the inflammatory cascade. Acute pancreatitis is classified into edematous () and necrotizing forms; the latter involves pancreatic or peripancreatic tissue death and initially presents as sterile , but up to 30-40% progress to infected via bacterial translocation. These pathophysiological processes result in characteristic histological appearances of acinar cell dropout and inflammatory infiltrates.

Histopathology

Acute pancreatitis manifests histopathologically in two primary forms: interstitial edematous pancreatitis and necrotizing pancreatitis, distinguished by the extent of tissue damage and . In the edematous form, the milder variant, the exhibits diffuse interstitial with scant inflammatory infiltrates composed predominantly of neutrophils and macrophages, alongside acinar vacuolization but minimal and preservation of overall lobular architecture. is limited, and gross examination reveals a swollen, organ without significant hemorrhage. The necrotizing form, indicative of severe disease, involves extensive of acinar cells and surrounding , accompanied by prominent characterized by —the formation of calcium soaps from lipid breakdown. Microscopically, this is marked by dense leukocytic infiltrates, vascular , and parenchymal destruction, while grossly, the tissue appears friable, dark red to black, and hemorrhagic in advanced cases. These changes reflect the progression from localized injury to widespread tissue death. Histopathological evolution occurs in phases: early within hours, featuring premature enzyme activation and initial acinar disruption; intermediate over days, with and dominating; and late over weeks, potentially leading to and scarring if the inflammation persists unresolved. Biopsy of pancreatic tissue is rarely performed due to risks, but when obtained, it reveals loss of lobular architecture, ductal disruption, and variable inflammatory patterns.

Diagnosis

The diagnosis of acute pancreatitis requires at least two of the following three features according to the revised Atlanta classification: characteristic , serum or elevated to at least the upper limit of , and characteristic findings of acute pancreatitis on .

Laboratory Evaluation

Laboratory evaluation plays a crucial role in confirming the of acute pancreatitis and assessing its severity through specific biomarkers and tests for . The primary diagnostic enzymes are serum and , which should be elevated to at least the upper limit of (ULN) to support the when combined with clinical features. is more specific than for acute pancreatitis and remains elevated longer, typically for 8 to 14 days after symptom onset compared to 3 to 5 days for . However, levels of these enzymes within the first 48 hours of symptom onset do not rule out the condition, as elevations may occur later. Inflammatory markers provide prognostic information regarding disease severity. C-reactive protein (CRP) is the gold standard for predicting severe acute pancreatitis, with levels exceeding 150 mg/L at 48 hours after admission indicating a higher of complications. Procalcitonin (PCT) is useful for detecting infection, particularly in cases of pancreatic , where levels >1.0 ng/mL are associated with a higher of infected . Evaluation of organ function involves several key tests to identify early signs of multiorgan involvement. (BUN) and levels assess renal function; an elevated BUN >20 mg/dL on admission is associated with severe disease and poor outcomes. A decrease in from baseline, often >10%, signals significant fluid sequestration and . , typically with serum calcium <8 mg/dL, occurs in up to 20% of severe cases due to saponification of fats and is a marker of systemic inflammation. Additional laboratory tests help identify etiology and monitor systemic effects. Elevated liver enzymes, particularly alanine aminotransferase (ALT) >3 times ULN (e.g., >150 IU/L), strongly suggest gallstone-related pancreatitis with a predictive probability of approximately 95%. triglycerides >1000 mg/dL confirm as the causative factor in 1-4% of cases. Hematologic evaluation reveals , with (WBC) count >12,000/mm³ contributing to the diagnosis of (SIRS), while >16,000/mm³ indicates increased severity risk per Ranson's criteria.

Imaging Modalities

Abdominal serves as the first-line imaging modality in suspected acute pancreatitis, particularly for identifying gallstones as an underlying , with a reported of 70-90%. However, its utility is constrained by overlying bowel gas, which often obscures direct visualization of the itself, limiting its role to etiological assessment rather than detailed pancreatic evaluation. Contrast-enhanced computed tomography (CECT) is considered the gold standard for diagnosing and staging acute pancreatitis, providing comprehensive assessment of pancreatic inflammation, , and peripancreatic complications. The scoring system, integrated into the CT severity index, grades the degree of glandular and extrapancreatic involvement based on morphological changes such as edema, fluid collections, and tissue heterogeneity. is identified by lack of contrast enhancement in the pancreatic , with severity graded as none (0%), <30% (2 points), 30-50% (4 points), or >50% (6 points) in the CT severity index, while fluid collections appear as non-enhancing areas surrounding the gland. To optimize accuracy in detecting the full extent of and avoid early overestimation or underestimation of severity, CECT is typically performed at least 72 hours after symptom onset. Magnetic resonance imaging (MRI), often combined with magnetic resonance cholangiopancreatography (MRCP), is particularly useful for evaluating pancreatic ductal abnormalities, such as disruptions or strictures, in equivocal cases or when radiation exposure is a concern. MRCP excels in delineating the biliary tree and without , making it superior for confirming biliary etiologies like choledocholithiasis when findings are inconclusive. Its multiplanar capabilities also allow for better characterization of collections and parenchymal changes compared to in select patients. Endoscopic ultrasound (EUS) offers high-resolution of the pancreas and surrounding structures, making it ideal for detecting subtle findings such as or early necrotic changes in idiopathic or recurrent acute pancreatitis. With its proximity to the gland via endoscopic access, EUS achieves superior sensitivity for microlithiasis—often missed by transabdominal ultrasound—and avoids , though it requires and expertise. It is especially valuable in cases where noninvasive is nondiagnostic, providing targeted of ductal variants or small tumors.

Differential Diagnosis

The differential diagnosis for acute pancreatitis encompasses a range of intra-abdominal, thoracic, and systemic conditions that can present with acute epigastric or upper , , , and systemic inflammatory signs, necessitating prompt evaluation to avoid misdiagnosis. Distinguishing features often rely on clinical history, , targeted tests, and to identify alternative pathologies while confirming or excluding pancreatic involvement. Gastrointestinal conditions commonly mimic acute pancreatitis due to overlapping abdominal symptoms. Perforated peptic ulcer typically causes sudden, severe generalized abdominal pain with signs of peritonitis and is differentiated by the presence of free subdiaphragmatic air on upright chest radiography or computed tomography (CT). Acute cholecystitis presents with right upper quadrant tenderness, fever, and a positive Murphy's sign on palpation; ultrasound revealing gallstones, pericholecystic fluid, or gallbladder wall thickening helps confirm this entity. Appendicitis is suggested by right lower quadrant pain that may migrate from the periumbilical region, accompanied by anorexia and rebound tenderness, and is verified through clinical scoring systems like Alvarado criteria combined with CT findings of appendiceal inflammation. Vascular disorders must be considered in patients with severe, atypical pain patterns. Aortic dissection often manifests as abrupt, tearing chest or radiating to the , with deficits or disparities; urgent is diagnostic. Mesenteric ischemia features disproportionate relative to findings, potentially with bloody and elevated serum lactate; contrast-enhanced or mesenteric identifies vascular occlusion. Other mimics include cardiopulmonary and metabolic emergencies. may simulate epigastric discomfort, particularly in inferior wall involvement, but electrocardiographic changes (e.g., ST-segment elevation) and elevated cardiac troponins distinguish it. Lower lobe can refer to the upper via diaphragmatic irritation, with respiratory symptoms and chest infiltrates providing differentiation. (DKA) presents with diffuse abdominal , dehydration, and vomiting in hyperglycemic patients; blood glucose exceeding 250 mg/dL, ketonemia, and arterial pH below 7.3 on blood gas analysis are confirmatory. Key discriminators for acute pancreatitis include serum lipase levels elevated more than the upper limit of normal, which offers higher specificity than for pancreatic origin, alongside imaging (e.g., ) demonstrating pancreatic parenchymal inflammation or peripancreatic fluid without evidence of alternative pathologies. Cases remaining undiagnosed after exhaustive exclusion of common etiologies are termed idiopathic acute pancreatitis.

Management

Supportive Care

Supportive care forms the cornerstone of initial management for acute pancreatitis, focusing on stabilizing the patient through hydration, analgesia, and gastrointestinal rest while preventing complications from . Fluid resuscitation is prioritized to address and maintain organ , with goal-directed recommended to guide administration based on clinical response. According to the 2024 American College of Gastroenterology (ACG) guidelines, moderately aggressive hydration using lactated Ringer's solution at an initial rate of 1.5 mL/kg per hour for the first 24 hours is advised for most patients, with additional boluses of 10 mL/kg if is evident. This approach has been shown to reduce the risk of persistent organ failure compared to less aggressive strategies. Monitoring during fluid resuscitation is essential to ensure adequacy without excess, targeting urine output greater than 0.5 mL/kg per hour, a decrease in (), and levels below 35-44%. Over-resuscitation should be avoided, as it can lead to complications such as , particularly in severe cases. Patients with predicted severe disease may require () admission for close hemodynamic monitoring, including and . Pain management is critical given the severe abdominal discomfort associated with acute pancreatitis, typically achieved with intravenous opioids as first-line therapy. or are preferred agents, administered via (PCA) pumps for titrated relief, while meperidine is avoided due to its neurotoxic metabolite normeperidine. Adjunctive non-opioid analgesics, such as acetaminophen, can be used to minimize opioid requirements. Patients are initially kept nil per os (NPO) to reduce pancreatic stimulation, but recent guidelines emphasize early oral feeding in mild cases to promote recovery. The 2025 International Association of Pancreatology (IAP) update recommends initiating oral intake within 24 hours if tolerated, rather than prolonged NPO, as this approach shortens hospital stays without increasing complications. For those unable to tolerate oral feeding, a brief transition to enteral may be considered, but supportive care prioritizes resuming oral diet as soon as possible in non-severe presentations.

Interventional Therapies

(ERCP) is recommended for acute pancreatitis patients with concomitant cholangitis or persistent biliary obstruction, with urgent intervention ideally performed within 24 hours for cholangitis and within 72 hours for obstruction without infection. In contrast, routine early ERCP is not advised for predicted severe gallstone pancreatitis without cholangitis, as it does not improve outcomes and may increase the risk of complications. These recommendations from the 2024 American College of Gastroenterology (ACG) guidelines emphasize targeted use to address specific biliary complications. Prophylactic antibiotics are not recommended in severe acute pancreatitis or sterile necrosis, as they do not reduce infection rates or mortality and may promote resistant organisms. Therapeutic antibiotics are indicated for confirmed or suspected infected pancreatic necrosis, with agents such as carbapenems (e.g., imipenem or ) or piperacillin-tazobactam preferred due to their ability to penetrate necrotic tissue; selection should be guided by culture results and local resistance patterns. Nutritional support is a key interventional component, with enteral nutrition preferred over parenteral to reduce infectious complications and length of stay in patients unable to tolerate oral intake. Nasojejunal tube placement is considered if gastric feeding is not tolerated, while in mild cases, early oral feeding with a low-fat solid diet should begin within 24-48 hours as tolerated to promote recovery. Parenteral nutrition is reserved for cases where enteral routes are contraindicated or ineffective. For symptomatic peripancreatic fluid collections or walled-off necrosis, percutaneous drainage serves as an initial minimally invasive option in the step-up approach, particularly when infection is suspected, to alleviate symptoms and delay more invasive procedures. Anti-emetic therapy, such as , is commonly used to manage associated and , with suggesting improved short-term outcomes in hospitalized patients. These targeted interventions complement foundational supportive care to address complications effectively.

Surgical Interventions

Surgical interventions in acute pancreatitis are primarily reserved for complications in severe cases, particularly when conservative and interventional therapies fail to control infection or symptoms. The step-up approach, endorsed by the 2012 International Association of Pancreatology/American Pancreatic Association (IAP/APA) guidelines and reaffirmed in subsequent updates including the 2024 American College of Gastroenterology (ACG) guidelines, emphasizes delaying invasive procedures to allow necrosis to become walled-off, typically for at least 4 weeks in stable patients. This strategy begins with percutaneous catheter drainage under radiological guidance for infected collections, followed by minimally invasive necrosectomy if drainage alone is insufficient. Minimally invasive techniques, such as video-assisted retroperitoneal debridement (VARD), involve small incisions to access and remove necrotic tissue, reducing morbidity compared to traditional open methods. Indications for surgical intervention include infected pancreatic necrosis that does not respond to antibiotics and percutaneous drainage, leading to persistent or organ failure. Disconnected pancreatic duct syndrome, a complication of necrotizing , may necessitate in symptomatic cases, such as recurrent fluid collections or pain unrelieved by endoscopic stenting. Symptomatic pseudocysts larger than 6 cm persisting beyond 6 weeks, causing compression of adjacent structures like the stomach or , also warrant surgical drainage or resection if endoscopic approaches fail.01067-6/fulltext) Open necrosectomy, involving for of necrotic tissue followed by closed or continuous lavage, is now reserved for cases where minimally invasive methods are not feasible or have failed, such as in patients with extensive anterior or hemodynamic requiring immediate source control. This procedure carries higher risks, with mortality rates reported between 15% and 25% in contemporary series, largely due to postoperative complications like and enterocutaneous fistulas. For etiology-specific , laparoscopic is recommended during the index admission for mild gallstone-related acute pancreatitis to prevent recurrence, as per the 2024 ACG guidelines.

Severity Assessment

Clinical Scoring Systems

Clinical scoring systems are essential bedside tools used to predict the severity of acute pancreatitis, stratify patients for intensive care, and guide therapeutic decisions early in the disease course. These systems integrate clinical, laboratory, and physiological parameters to estimate the risk of complications such as organ failure and mortality, allowing for timely intervention. Widely adopted systems include the Ranson score, , BISAP, and /Imrie score, each with distinct parameters and timing for assessment. The Ranson score, developed in , evaluates 11 parameters to prognosticate outcomes in acute pancreatitis. Five parameters are assessed at admission: age greater than 55 years, count exceeding 16,000 cells/μL, blood glucose above 200 mg/dL, level greater than 350 IU/L, and aspartate aminotransferase greater than 250 IU/L. An additional six parameters are measured at 48 hours: drop of more than 10%, rise exceeding 5 mg/dL, serum calcium below 8 mg/dL, arterial of oxygen less than 60 mmHg, deficit greater than 4 mEq/L, and estimated sequestration surpassing 6 L. A score of 3 or higher indicates severe disease with increased risk of mortality. The score, originally introduced in for general critical illness severity, has been validated for acute pancreatitis, particularly in intensive care settings. It comprises 12 physiological variables (including temperature, mean arterial pressure, heart rate, respiratory rate, oxygenation, arterial pH, serum sodium, serum potassium, creatinine, hematocrit, white blood cell count, and ), plus points for age and chronic health status. A score greater than 8 at admission or within 24 hours predicts severe pancreatitis and higher mortality risk, with advantages in dynamic monitoring over time. The BISAP score is a simplified five-point system designed for early risk stratification within 24 hours of admission. It assigns one point each for blood urea nitrogen greater than 25 mg/dL, impaired mental status ( <15), presence of ic inflammatory response syndrome (meeting ≥2 criteria), age over 60 years, and pleural effusion on imaging. A score of 3 or higher identifies patients at high risk for in-hospital mortality and severe disease, offering ease of use compared to more complex systems. The Glasgow/Imrie score, a modification of earlier criteria introduced in 1984, uses eight parameters assessed at admission or within 48 hours to predict severity. These include age over 55 years, white blood cell count greater than 15,000 cells/μL, blood glucose above 180 mg/dL, serum calcium below 8 mg/dL, partial arterial oxygen pressure less than 60 mmHg, urea above 45 mg/dL, lactate dehydrogenase greater than 600 IU/L, and alanine aminotransferase greater than 100 IU/L. Similar to the , a total of 3 or more points signifies severe acute pancreatitis with elevated complication rates.

Imaging-Based Scoring

Imaging-based scoring systems for acute pancreatitis primarily rely on computed tomography (CT) findings to quantify pancreatic parenchymal damage, peripancreatic inflammation, necrosis, and extrapancreatic complications, providing prognostic information independent of clinical parameters. These scores help stratify patients into mild, moderate, or severe categories, guiding decisions on intensive care needs and intervention timing, with CT preferred due to its widespread availability and validated correlation with outcomes such as mortality and length of hospital stay. These imaging scores complement the , which primarily uses the presence and duration of organ failure (persistent >48 hours) to define severity: mild (no organ failure), moderately severe (transient or persistent organ failure without local complications, or local complications without organ failure), and severe (persistent organ failure). The CT severity index (CTSI), introduced in , is a widely adopted 10-point scale combining pancreatic (graded 0-4 points: grade A normal =0; grade B enlargement or contour abnormality=1; grade C glandular and mild peripancreatic =2; grade D single fluid collection=3; grade E two or more fluid collections or gas=4) with the extent of (0 points for none; 2 for <30%; 4 for 30-50%; 6 for >50%). Scores of 0-3 indicate mild , 4-6 moderate, and 7-10 severe, with scores greater than 5 associated with severe and increased mortality risk (up to 17% for scores 7-10). This index correlates strongly with clinical outcomes, including organ failure and , outperforming earlier grading systems alone. The modified CT severity index (mCTSI), proposed in 2004, refines by simplifying scoring and incorporating extrapancreatic findings for a total of 10 points: pancreatic (0: normal ; 2: focal or diffuse glandular abnormalities with or without peripancreatic inflammatory changes; 4: single or multiple fluid collections or gas in or adjacent to ), (0: none; 2: ≤30%; 4: >30%), and extrapancreatic complications (2: one or more, e.g., , , vascular or parenchymal complications). Mild disease scores 0-2, moderate 4-6, and severe 8-10, with severe scores indicating high risk for persistent organ failure, , and need for . This reduces interobserver variability and better predicts complications compared to the original CTSI. Ultrasound and (MRI) lack fully standardized severity scores like but are valuable for assessing fluid collections and , particularly in contraindications to . evaluates collection size and symptoms, with peripancreatic fluid collections >6 cm often indicating need for intervention if symptomatic or persistent beyond 4-6 weeks. MRI, using T1- and T2-weighted sequences, can quantify and collections with high soft-tissue contrast, showing moderate correlation with clinical severity (e.g., MRSI scores 0-10 based on signal intensity and collections), though it is less routinely used due to cost and availability. Optimal timing for contrast-enhanced is 48-72 hours after symptom onset to accurately assess development, as earlier scans may underestimate extent. involving >30% of the gland, visible on these scans, predicts higher risk and worse outcomes, prompting vigilant monitoring for infected pancreatic .

Prognosis

Short-Term Outcomes

The short-term outcomes of acute pancreatitis are primarily determined by disease severity, with overall mortality rates ranging from 1% to 5%. In mild cases, mortality is less than 1%, while severe acute pancreatitis carries a 20% to 30% mortality risk, escalating to 15% to 35% in instances of infected pancreatic . These rates reflect a substantial improvement from historical figures of 10% to 20%, attributable to advancements like the step-up approach, which prioritizes minimally invasive interventions over immediate open . Hospital length of stay differs markedly by severity: mild cases typically resolve within 3 to 7 days, whereas severe cases often extend to 4 to 8 weeks due to complications requiring intensive monitoring and support. Approximately 15% to 20% of patients face readmission within 30 days, most commonly for persistent symptoms or secondary issues like fluid collections. Organ failure plays a in , with transient failure (lasting under ) resolving successfully in about 80% of affected patients, often without long-lasting sequelae. In contrast, persistent organ failure beyond strongly predicts adverse short-term outcomes, including higher mortality and prolonged . Early intervention strategies, as outlined in the 2025 International Association of Pancreatology guidelines, have been shown to reduce mortality by addressing complications promptly in high-risk cases. as an is linked to worse short-term outcomes, including increased severity and higher rates of organ failure compared to biliary causes. Severity assessment tools, such as those in the Revised Atlanta classification, aid in forecasting these outcomes by stratifying risk early in the disease course.

Long-Term Consequences

Acute pancreatitis can lead to persistent in approximately 20-30% of survivors, manifesting as due to inadequate production and . This condition often necessitates lifelong pancreatic replacement to mitigate nutritional deficiencies and . The risk is notably elevated following necrosectomy in severe cases, where pancreatic tissue loss exacerbates insufficiency, with prevalence reaching up to 33% in severe acute pancreatitis compared to 19% in mild forms. Endocrine dysfunction is another common long-term sequela, with new-onset mellitus developing in 10-50% of patients, particularly those with severe disease or extensive pancreatic resection such as total , where rates approach 100%. Impaired glucose tolerance may precede overt , contributing to metabolic complications that require ongoing monitoring and management. Additionally, recurrent acute pancreatitis occurs in 20-30% of cases if the underlying etiology remains unaddressed, such as gallstones without , potentially evolving into in about 10% of affected individuals. Survivors may also experience chronic abdominal pain in 5-10% of cases, alongside pseudocyst recurrence that can necessitate repeated interventions. These issues contribute to a diminished quality of life, with studies showing reduced SF-36 scores across physical and mental health domains compared to general populations. Recent 2024 reviews highlight an increased risk of pancreatic cancer following acute pancreatitis, with odds ratios ranging from 2 to 5, underscoring the need for vigilant long-term surveillance. Long-term mortality among survivors is elevated compared to the general population. A 2025 population-based study found a cumulative mortality of 37.7% in acute pancreatitis patients versus 29.8% in matched controls over extended follow-up, attributed to increased risks of , infections, and malignancies.