Letter to the Editor: Ascites in acute pancreatitis: Prognostic considerations

Abstract

Ascites in acute pancreatitis (AP) has long been regarded as a nonspecific epiphenomenon of the inflammatory process. However, accumulating clinical and experimental evidence increasingly supports the view that ascites represents a clinically meaningful and readily accessible marker of disease severity. Building on our previously published study by Zerem et al, published in the recent issue of the World Journal of Gastroenterology on ascites in AP, this letter reframed ascites as an integrated pathophysiological signal that reflects both pancreatic structural disruption and systemic inflammatory activation. Early identification and dynamic monitoring of ascitic fluid may offer a valuable prognostic window into the evolving course of AP, particularly during the early phase of the disease when uncertainty regarding severity and outcome is greatest. Rather than proposing ascites as a replacement for established severity scoring systems, we argued that its presence, volume, and temporal evolution may complement existing risk stratification tools and enhance bedside clinical judgment. Finally, this article provided a conceptual framework to support future validation studies and to inform more nuanced, pathophysiology-driven clinical decision making in the management of AP.

Key Words: Acute pancreatitis; Ascites; Prognosis; Biomarkers; Severity assessment

Core Tip: Ascites in acute pancreatitis is a heterogeneous and dynamic clinical finding that may reflect the extent of pancreatic injury and the intensity of systemic inflammation. When detected early and interpreted cautiously, ascites can serve as a complementary prognostic signal that enhances bedside risk stratification without supplanting established scoring systems. Clear operational definitions and recognition of evidence limitations are essential to avoid over-interpretation.

TO THE EDITOR

I read with interest the study by Zerem et al[1], published in the current issue of the World Journal of Gastroenterology, which aimed to clarify early risk stratification remains a central challenge in the management of acute pancreatitis (AP). Despite the availability of multiple prognostic systems (such as the Bedside Index of Severity in Acute Pancreatitis and the Acute Physiology and Chronic Health Evaluation and CT-based indices), no single prognostic score fully captures the dynamic interaction between local pancreatic injury and the evolving systemic inflammatory response during the early phase of the disease[1-3]. Ascites is a frequent finding in AP but is often interpreted as a nonspecific byproduct of inflammation rather than as a clinically informative signal. However, emerging evidence suggests that ascites may reflect clinically relevant pathophysiological processes, including pancreatic parenchymal disruption, ductal leakage, and inflammatory microvascular injury[4-6]. This article expanded on these observations by offering a clinically oriented perspective on ascites as a complementary prognostic signal in AP while explicitly acknowledging current evidence limitations.

PATHOPHYSIOLOGICAL BASIS AND HETEROGENEITY OF ASCITES IN AP

In accordance with the Revised Atlanta Classification, it is important to distinguish generalized intraperitoneal ascites from localized acute peripancreatic fluid collections, which are confined to the peripancreatic space and are common in interstitial and necrotizing pancreatitis[5]. The present discussion refers specifically to generalized ascites or fluid extending beyond the peripancreatic region rather than localized acute peripancreatic fluid collections[5]. Ascites formation in AP results from multiple, often overlapping pathophysiological mechanisms, including increased microvascular permeability mediated by inflammatory cytokines, enzymatic leakage from injured pancreatic parenchyma, and disruption of pancreatic ductal integrity[1,3]. Importantly, AP-related ascites is not a homogeneous entity but encompasses a spectrum ranging from reactive inflammatory exudate to enzyme-rich fluid associated with ductal disruption or evolving pancreatic necrosis.

Reactive inflammatory ascites most commonly reflects an early systemic inflammatory response, whereas enzyme-rich or persistent ascites is more frequently associated with extensive pancreatic injury, progressive necrosis, or overt ductal disruption[5,7]. These distinct ascitic phenotypes differ in their biochemical composition, clinical course, and prognostic implications, underscoring the need for contextual and pathophysiology-driven interpretation rather than reliance on volume-based assessment alone.

OPERATIONAL DEFINITION OF ASCITES IN AP

For pragmatic clinical interpretation ascites in AP may be defined as free intraperitoneal fluid detected by ultrasound or CT beyond physiological pelvic recesses and extending outside the immediate peripancreatic region with interpretation guided by clinical context rather than volume alone[3,8]. Minimal pelvic fluid without extrapelvic extension may be physiologic or clinically negligible and should not be over-interpreted. Particular relevance may be attributed to ascites detected within the first 72 hours of symptom onset, a period during which conventional imaging and scoring systems may underestimate disease severity. Fluid distribution, persistence, and biochemical characteristics may further refine prognostic interpretation although standardized integration into routine practice requires prospective validation.

ASCITES AS A COMPLEMENTARY PROGNOSTIC SIGNAL

Several observational studies have demonstrated associations between the presence of ascites and adverse clinical outcomes, including persistent organ failure, pancreatic necrosis, subsequent infected collections, and mortality[3,6,9]. These associations suggest that ascites may serve as a composite signal integrating local pancreatic injury and systemic inflammatory burden. Importantly, ascites should be viewed as a complementary clinical finding rather than as a substitute for established prognostic systems such as the Bedside Index of Severity in Acute Pancreatitis and the Acute Physiology and Chronic Health Evaluation or CT-based indices[3,10]. Its potential value lies in its early bedside detectability, and its dynamic behavior (persistence, progression, or re-accumulation) may offer additional insight into disease trajectory.

CLINICAL IMPLICATIONS AND CAUTIONS

From a practical standpoint the detection of ascites in early AP may justify closer hemodynamic and respiratory monitoring, particularly given its role as a marker of third-space fluid loss and potential intravascular volume depletion. Significant or progressive ascites may therefore have implications for early fluid resuscitation strategies and monitoring intensity although management decisions should remain individualized and guideline-concordant. In selected cases diagnostic paracentesis can provide additional information regarding ductal integrity or infection risk[7,11]. However, any consideration of therapeutic drainage must remain individualized and aligned with current international guidelines. Potential risks include bleeding, infection, and fluid shifts, reinforcing the need for indication-driven rather than routine intervention[3].

LIMITATIONS AND FUTURE DIRECTIONS

The concepts discussed herein are primarily derived from observational data and pathophysiological reasoning. Prospective studies are needed to standardize ascites definitions, timing of assessment, biochemical profiling, and integration with existing severity frameworks. Head-to-head comparisons with established prognostic scores will be essential before ascites can be formally incorporated into severity assessment algorithms.

CONCLUSION

Ascites in AP should not be dismissed as a passive epiphenomenon. When interpreted within a structured clinical framework, it may provide complementary prognostic insight during the early phase of the disease. This clinical perspective underscores that only through standardized operational definitions, strict distinction from localized peripancreatic collections, and cautious, context-driven interpretation can ascites evolve from an overlooked epiphenomenon into a meaningful complementary signal within early risk stratification frameworks for AP.