ABSTRACT
Background:
Pancreatic fluid collections (PFCs) are the most common local complications of pediatric pancreatitis. Evidence in children is limited, with most evidence extrapolated from adult studies.
Materials and Methods:
A retrospective study was conducted at a tertiary pediatric surgical center between 2013 and 2024. Children with acute pancreatitis (AP), acute recurrent pancreatitis, or acute-on-chronic pancreatitis (ACP) who developed PFCs were included. PFCs were classified according to the revised Atlanta classification.
Results:
Fluid collections were noted in 92 (40%) children. Acute peripancreatic fluid collection (APFC) was the most common type (70%). Acute necrotic collections (ANCs) occurred more frequently in older children (P = 0.013) and presented earlier than APFCs (3.5 ± 2.7 vs. 6.2 ± 5.1 days, P = 0.04). APFCs were more commonly associated with ACP, whereas ANCs predominated in AP (P = 0.004). Fifty-three percent of APFCs progressed to pancreatic pseudocysts (PPCs), and 54% of ANCs progressed to walled-off necrosis (WON). APFC diameter >6 cm and pancreatitis phenotype independently predicted progression to PPC, while PPC diameter >6 cm, ascites, and increasing age predicted the need for intervention. Most children were managed conservatively; symptomatic PPCs and WONs required drainage, predominantly via a percutaneous approach.
Conclusion:
PFCs occurred in approximately 40% of children with pancreatitis, most commonly as APFCs. Collections >6 cm in diameter were more likely to progress and require intervention. Percutaneous drainage was a safe and effective modality for symptomatic collections in this cohort.
KEYWORDS: Acute necrotic collection, acute peripancreatic fluid collection, pancreatic fluid collection, pancreatic pseudocyst, pancreatitis, walled-off necrosis
INTRODUCTION
Acute pancreatitis (AP) is one of the most devastating conditions in children, with an increasing incidence worldwide.[1,2,3] Although it is less morbid and less fatal than its adult counterpart, pediatric AP can present with complications in up to 50% of cases.[2,3] Fluid collection is the most common complication of pancreatitis, occurring due to pancreatic inflammation and enzyme activation.[2,3] According to the revised Atlanta classification, these fluid collections are categorized as acute peripancreatic fluid collection (APFC) or pancreatic pseudocyst (PPC) in interstitial edematous pancreatitis, and as acute necrotic collections (ANC) or walled-off necrosis (WON) in necrotizing pancreatitis.[4] The classification is based on the nature and duration of collections.[4,5]
Classifying fluid collections is essential for prognostication and effective management of children with pancreatitis.[4,5,6] APFC is usually self-limiting, with a spontaneous resolution rate of 80%–90%, and is managed conservatively with supportive care.[4,5,6] PPC represents a moderately severe disease, with a resolution rate of 30%–60%. Only symptomatic PPCs require drainage, which may be performed by endoscopic, percutaneous, or surgical approaches.[4,5,6] ANC represents severe pancreatitis and carries high morbidity and mortality, especially if infected.[4,5,6,7,8] ANC can lead to severe sepsis and multiorgan dysfunction. Management of ANC follows a step-up approach, ranging from initial treatment to open necrosectomy as a last resort.[4,5,6,7,8] WON is a mature, encapsulated collection of necrotic pancreatic tissue and inflammatory fluid.[4,5,6,7,8] WON carries a higher risk of bleeding, rupture, and infection; hence, it usually requires intervention using a step-up approach, as delayed management is associated with a poor prognosis.[4,5,6,7,8]
However, literature on pancreatic fluid collections (PFCs) in children remains limited, with most evidence extrapolated from adult studies, particularly those applying the revised Atlanta classification.[2,4,5,6,7,8] Hence, a study was conducted to evaluate the clinical spectrum, natural history, management, and outcomes in children with PFCs.
MATERIALS AND METHODS
Study design and setting
A retrospective study was conducted in the Department of Pediatric Surgery at a tertiary care government hospital over 12 years (January 2013–December 2024). The study was conducted in accordance with the Declaration of Helsinki. Ethical clearance was obtained from the Institute Ethics Committee prior to initiation of the study (BMCRI/PS/226/22-23). A waiver of informed consent was granted by the Ethics Committee. The study was reported in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology guidelines.
Patient selection
Children under 18 years of age admitted with a diagnosis of AP, acute recurrent pancreatitis (ARP), or acute-on-chronic pancreatitis (ACP) and with any form of PFC were included in the study.
AP was defined as the presence of at least two of the following three criteria: Abdominal pain suggestive of AP, imaging findings suggestive of AP, and serum lipase and/or amylase ≥3 times the normal upper limit.[9] ARP was defined as the occurrence of at least two episodes of AP, with complete resolution of pain or complete normalization of amylase and lipase between episodes for at least 1 month.[9] Chronic Pancreatitis (CP) was defined as at least one of the following three criteria: abdominal pain consistent with pancreatic origin with imaging features suggestive of CP, endocrine pancreatic insufficiency with imaging features suggestive of CP, and exocrine pancreatic insufficiency with imaging features suggestive of CP.[9]
Children who had undergone intervention(s) at other centers and were later referred to our center were excluded. Children with incomplete medical records were also excluded. Demographic details, clinical presentation, management details, and outcomes were retrieved from inpatient and outpatient hospital records.
Diagnostic evaluation
All children underwent biochemical evaluation, including serum amylase, serum lipase, blood sugar monitoring, liver function tests, lipid profile, serum calcium, and complete blood count. AP, ARP, and CP were diagnosed according to the INSPPIRE criteria.[9] Initial imaging was performed using abdominal ultrasonography to assess the pancreatic morphology and identify fluid collections. Children with suspected necrotizing pancreatitis underwent contrast-enhanced computed tomography to determine the presence and degree of necrosis, the nature of the collection, and associated complications. Features of chronic pancreatitis, if found, were also noted. Magnetic resonance cholangio-pancreatography was performed selectively in children with ARP or ACP to evaluate ductal anatomy and structural abnormalities, and to characterize collections.
Classification of fluid collections
Fluid collections were classified according to the revised Atlanta classification, based on the duration (≤ or >4 weeks) and nature of the collection (necrotic or non-necrotic).[4,5] Collections of ≤4 weeks duration and having clear contents were defined as APFCs, while collections persisting beyond 4 weeks with clear contents were classified as PPCs. Collections of ≤4 weeks duration containing necrotic contents were defined as ANCs, and those persisting beyond 4 weeks containing necrotic debris were classified as WON. The size, location, wall thickness, and relation to the adjacent viscera were documented for all cases.
Management protocol
Children were initially stabilized hemodynamically with intravenous fluids and administered adequate analgesia. Oral feeds were resumed once the ileus had resolved. Antibiotics were reserved for children with severe necrotizing pancreatitis, persistent fever (>2 days), or clinical evidence of sepsis due to an infected collection. Only symptomatic PFCs underwent intervention. Symptomatic collections were defined as collections associated with persistent and severe abdominal pain, features of gastric outlet obstruction (persistent vomiting and intolerance to enteral feeds) or biliary obstruction (jaundice), evidence of infection (persistent fever and raised inflammatory markers), or sepsis (hemodynamic instability). Weight loss or failure to thrive during follow-up was also considered a symptomatic collection. No interventions were performed based on radiological findings (such as the size of the collection).
Children with symptomatic PPCs suitable for internal drainage underwent endoscopic or open cystogastrostomy. Those with trauma-related PPCs and ductal disruption were treated with endoscopic retrograde cholangio pancreatography (ERCP) and stent placement, when feasible. If ERCP was not possible or failed, cystogastrostomy or percutaneous drainage was performed.
Children with ANCs were managed conservatively with analgesics and antibiotics; nonresponders underwent percutaneous drainage. WON was primarily managed by percutaneous drainage using a step-up approach. Children with splenic vein thrombosis were treated conservatively and followed up. Enoxaparin was used for anticoagulation if thrombus extension into the portal vein or associated ascites was detected.
Follow-up
Children with asymptomatic fluid collections were followed up two-weekly for a month, monthly for 3 months, 6-monthly for 1 year, and then yearly. For children who required intervention, follow-up was tailored to the procedure. Children who underwent percutaneous drainage were followed weekly for output and patency. In contrast, children who underwent endoscopic or surgical intervention were reviewed as clinically indicated to monitor for recurrence or stent-related issues.
Outcome measures
The primary outcome measures of the study were the incidence and spectrum of PFC (APFC, ANC, PPC, and WON) in pediatric pancreatitis, classified according to the revised Atlanta classification. The secondary outcome measures included the clinical presentation of children with PFCs, the need for intervention (conservative, percutaneous, endoscopic, or surgical), factors associated with progression of collections, procedure-related complications, and the need for reintervention.
Sample size calculation
No a priori sample size or power calculation was performed due to the retrospective study design. The study comprised all children with AP, ARP, or ACP who developed PFCs. The final cohort size was comparable to previously published pediatric studies considered adequate for descriptive analysis and for evaluating factors associated with progression of collections and the need for intervention.[3,6]
Statistical analysis
Statistical analysis was performed using SPSS version 27.0 (IBM Corp., Armonk, NY). Categorical variables were expressed as frequencies and percentages, and continuous variables as mean ± standard deviation or median (range), depending on the data distribution. Group comparisons (APFC vs. ANC, progressed vs. resolved APFC, progressed vs. resolved ANC, and conservative vs. need for intervention) were performed using the Chi-square test, Fisher’s exact test, or Fisher–Freeman–Halton exact test for categorical variables, and the independent samples t-test or Mann–Whitney U test for continuous variables. A two-tailed P < 0.05 was considered statistically significant.
Logistic regression analysis was performed to identify factors predicting progression to PPC and the need for intervention. To minimize model overfitting, given the relatively small sample size, predictors included in multivariable models were limited to those with clinical relevance and univariable significance. Receiver operating characteristic (ROC) analysis was used to determine the cutoff diameter predicting progression to PPC and the need for intervention. Two optimal thresholds were identified using the Youden index (J = Sensitivity + Specificity– 1), and a higher-specificity threshold of 6 cm was also evaluated for clinical decision making. Regression analysis of progression and intervention in WON was not performed due to the small subgroup size. Children with missing data were minimal and were excluded from the analysis.
RESULTS
A total of 270 children presented with pancreatitis during the study period, 232 were included in the study, and 92 (40%) of them developed PFCs [Figure 1]. The demographic and clinical profiles of children with PFC are presented in Table 1. The duration of follow-up ranged from 1 year to 13 years.
Figure 1.
Flow diagram showing patient selection, classification of pancreatic fluid collections, and their clinical outcomes
Table 1.
Demographic and clinical profile of children with pancreatic fluid collections
| Parameters | Total (n=92), n (%) | APFC (n=64), n (%) | ANC (n=28), n (%) | P |
|---|---|---|---|---|
| Age (years), mean | 11.3±4.3 | 11.1±4.3 | 11.6±4.1 | 0.6@ |
| Age group (years) | ||||
| <5 | 16 (17) | 10 (16) | 6 (21) | 0.013* |
| 5–10 | 20 (22) | 19 (30) | 1 (4) | |
| 10–15 | 41 (45) | 23 (36) | 18 (64) | |
| >15 | 15 (16) | 12 (19) | 3 (11) | |
| Boys | 60 (65) | 40 (63) | 20 (71) | 0.4* |
| Type of pancreatitis | ||||
| Acute pancreatitis | 48 (52) | 27 (42) | 21 (75) | 0.004* |
| Acute recurrent pancreatitis | 12 (13) | 8 (13) | 4 (14) | |
| Acute on chronic pancreatitis | 32 (35) | 29 (45) | 3 (11) | |
| Etiology | ||||
| Idiopathic | 78 (85) | 52 (81) | 26 (93) | 0.20$ |
| Trauma | 8 (9) | 6 (9) | 2 (7) | |
| Gall stones | 4 (4) | 4 (6) | 0 | |
| Pancreatic divisum | 1 (1) | 1 (2) | 0 | |
| Drug induced | 1 (1) | 1 (2) | 0 | |
| Duration of symptoms at presentation (days) | 5.4±4.6 | 6.2±5.1 | 3.5±2.7 | 0.04@ |
| Symptoms | ||||
| Abdominal pain | 92 (100) | 64 (100) | 28 (100) | 1* |
| Vomiting | 79 (86) | 54 (83) | 25 (89) | 0.53* |
| Anorexia | 9 (10) | 6 (9) | 3 (11) | 1# |
| Loss of weight | 7 (8) | 6 (9) | 1 (4) | 0.67# |
| Cyst rupture | 1 (1) | 1 (2) | 0 | 1# |
| Diameter >6 cm | 25 (27) | 17 (27) | 8 (29) | 0.96* |
| Communication with MPD | 15 (16) | 13 (20) | 2 (7) | 0.14# |
| MPD disruption | 6 (7) | 5 (8) | 2 (7) | 0.1# |
| Dilated MPD | 15 (16) | 12 (19) | 3 (11) | 0.54# |
| Splenic vein thrombosis | 11 (12) | 6 (10) | 5 (18) | 0.3# |
| Ascites | 50 (54) | 30 (47) | 20 (71) | 0.03* |
| Pleural effusion | 15 (16) | 9 (14) | 6 (21) | 0.06# |
*Chi-square test, #Fisher’s exact test, @Independent sample t-test, $Fisher’s–Freeman–Halton exact test. APFC: Acute peripancreatic fluid collection, ANC: Acute necrotic collection, MPD: Main pancreatic duct
Acute peripancreatic fluid collections
APFCs were identified in 64 (70%) children, with boys accounting for 63%. The mean age at presentation was 11.1 ± 4.3 years, and APFCs were detected at a mean of 6.2 ± 5.1 days after the pancreatitis episode. ACP accounted for 45% of cases. Communication with the main pancreatic duct (MPD) was identified in 13 (20%) children, while ascites and pleural effusion were present in 30 (47%) and nine (14%) children, respectively [Table 1]. All children were managed conservatively.
Acute necrotic collections
ANCs were noted in 28 (30%) children; 64% of them were 10–15 years old. AP accounted for 75% of cases of ANCs. The mean time to presentation was 3.5 ± 2.7 days after the symptom onset [Table 1]. All children were treated conservatively. Thirteen (46%) ANCs resolved spontaneously, while 15 (54%) progressed to WON.
Comparison between acute peripancreatic fluid collection and acute necrotic collection
Children with ANC presented earlier than those with APFC (3.54 ± 2.73 days vs. 6.17 ± 5.05 days; P = 0.04, independent-samples t-test). Age group was significantly associated with the type of fluid collection (χ2 [3, n = 92] = 10.77, P = 0.013, Cramer’s V = 0.34 [moderate association]). ANC was most frequent in children aged 10–15 years, whereas APFC predominated in other age groups. There was also a significant association between the type of pancreatitis and the type of fluid collection (χ2 [2, n = 92) = 10.77, P = 0.004, Cramer’s V = 0.34 [moderate association]). Children with AP were more likely to develop ANC, whereas those with ACP more frequently developed APFC. There was no difference in the etiological distribution between the APFC and ANC groups (Fisher–Freeman–Halton exact test, P = 0.20). Ascites was more commonly found in children with ANC (71% vs. 47%, P = 0.03, Chi-square test) than in those with APFC [Table 1].
Pancreatic pseudocysts
Thirty-four (53%) of 64 APFCs progressed to PPC, with a mean interval of 6.5 ± 5.5 months from the acute episode [Table 2]. Twenty-six (76%) cysts were located in the pancreatic body or tail. The type of pancreatitis significantly influenced progression (χ2 [2, n = 92] = 10.45, P = 0.005, Cramer’s V = 0.40 [moderate-to-large association]), with APFCs secondary to AP and ARP being more likely to resolve. In contrast, those associated with ACP were more likely to progress to PPC [Table 2]. APFCs measuring >6 cm in diameter were more likely to evolve into PPC [47% vs. 3%, P < 0.001, Fisher’s exact test; Table 2].
Table 2.
Clinical profile of children with progressed versus resolved acute peripancreatic fluid collections
| PPC (n = 34), n (%) | Resolved APFC (n = 30), n (%) | P | |
|---|---|---|---|
| Age (years), mean | 11.6 ± 4.2 | 10.6 ± 4.4 | 0.38@ |
| Age group (years) | |||
| <5 | 5 (15) | 5 (17) | 0.83* |
| 5–10 | 9 (27) | 10 (33) | |
| 10–15 | 14 (41) | 9 (30) | |
| >15 | 6 (18) | 6 (20) | |
| Boys | 22 (65) | 18 (60) | 0.7* |
| Type of pancreatitis | |||
| Acute pancreatitis | 12 (35) | 15 (50) | 0.005* |
| Acute recurrent pancreatitis | 1 (3) | 7 (23) | |
| Acute on chronic pancreatitis | 21 (62) | 8 (27) | |
| Etiology | |||
| Idiopathic | 27 (79) | 25 (83) | 0.30$ |
| Trauma | 5 (15) | 1 (3) | |
| Gall stones | 1 (3) | 3 (10) | |
| Pancreatic divisum | 0 | 1 (3) | |
| Drug induced | 1 (3) | 0 | |
| Symptoms | |||
| Abdominal pain | 34 (100) | 30 (100) | 1* |
| Vomiting | 30 (88) | 24 (80) | 0.37* |
| Anorexia | 4 (12) | 2 (7) | 0.49# |
| Loss of weight | 6 (18) | 0 | 0.03# |
| Cyst rupture | 0 | 1 (3) | 1# |
| Diameter >6 cm | 16 (47) | 1 (3) | <0.001# |
| Communication with MPD | 10 (30) | 3 (10) | 0.07# |
| MPD disruption | 4 (12) | 1 (3) | 0.36# |
| Dilated MPD | 9 (26) | 3 (10) | 0.12# |
| Splenic vein thrombosis | 4 (12) | 2 (7) | 0.68# |
| Ascites | 16 (47) | 14 (47) | 0.83* |
| Pleural effusion | 6 (18) | 3 (10) | 0.48# |
*Chi-square test, @Independent sample t-test, $Fisher’s–Freeman–Halton exact test, #Fisher’s exact test. APFC: Acute peripancreatic fluid collection, PPC: Pancreatic pseudocyst, MPD: Main pancreatic duct
Multivariable logistic regression demonstrated that APFC diameter >6 cm (odds ratio [OR] 22.1, 95% confidence interval [CI] 2.4–204.9, P = 0.006) and type of pancreatitis (OR 4.89, 95% CI 1.43–16.76, P = 0.012) were independent predictors of progression (Hosmer–Lemeshow χ2 = 6.93, P = 0.545; Nagelkerke R2 = 0.467). Age and communication with MPD were not significant predictors. ROC analysis demonstrated that the APFC diameter predicted progression to PPC (area under the curve [AUC] 0.820, 95% CI: 0.718–0.922; P < 0.001). A cutoff of 3.5 cm yielded 62% sensitivity and 90% specificity (J = 0.518), whereas 6 cm yielded 44% sensitivity and 97% specificity [J = 0.408; Figure 2a].
Figure 2.
(a) Receiver operating characteristic curve analysis for the diameter of acute peripancreatic fluid collection as a predictor of progression to pancreatic pseudocyst. (b) Receiver operating characteristic curve analysis for diameter as a predictor for the need for intervention in pancreatic pseudocyst
Twenty (59%) children with PPC required intervention. ERCP with sphincterotomy was attempted in 12 (35%) children and was successful in nine, including five who underwent pancreatic duct (PD) stenting. Among the three failed ERCPs, one was managed with percutaneous drainage, one with open cystogastrostomy (due to the cyst’s proximity to the splenic vessels), and one resolved spontaneously. The child who underwent open cystogastrostomy developed complete blockage of the cystogastrostomy within 2 months, which was successfully treated by percutaneous drainage. Endoscopic cystogastrostomy was attempted in two children; one was successful, and the other resolved spontaneously on follow-up. One child with splenic PPC underwent marsupialization. Five (15%) children underwent percutaneous drainage; one developed a cysto-cutaneous fistula that healed spontaneously in 6 weeks.
Children requiring intervention were older (12.9 ± 3.9 years vs. 9.9 ± 4.2 years, P = 0.036, independent sample t test) and more likely to have PPCs >6 cm (14/20 vs. 2/14, P = 0.002, Fisher’s exact test). Although all traumatic PPCs required intervention, this was not statistically significant. Etiology and pancreatitis type were not associated with intervention [Table 3].
Table 3.
Clinical profile of pancreatic pseudocysts according to the management
| Parameters | Intervention (n=20), n (%) | Conservative (n=14), n (%) | P |
|---|---|---|---|
| Age (years), mean | 12.9±3.9 | 9.9±4.2 | 0.036@ |
| Duration at presentation (months) | 3.4±2.2 | 4.5±2.3 | 0.14@ |
| Age group (years) | |||
| <5 | 2 (10) | 3 (21) | 0.2* |
| 5–10 | 4 (20) | 5 (36) | |
| 10–15 | 9 (45) | 5 (36) | |
| >15 | 5 (25) | 1 (7) | |
| Boys | 14 (70) | 8 (57) | 0.38* |
| Type of pancreatitis | |||
| Acute pancreatitis | 7 (35) | 5 (36) | 1$ |
| Acute recurrent pancreatitis | 1 (5) | 0 | |
| Acute on chronic pancreatitis | 12 (60) | 9 (64) | |
| Etiology | |||
| Idiopathic | 14 (70) | 13 (93) | 0.17$ |
| Trauma | 5 (25) | 0 | |
| Gall stones | 0 (3) | 1 (7) | |
| Pancreatic divisum | 0 | 0 | |
| Drug induced | 1 (3) | 0 | |
| Symptoms | |||
| Abdominal pain | 20 (100) | 14 (100) | 1# |
| Vomiting | 18 (90) | 12 (86) | 1# |
| Anorexia | 4 (20) | 0 | 0.13# |
| Loss of weight | 4 (20) | 2 (14) | 1# |
| Cyst rupture | 0 | 0 | 1# |
| Diameter >6 cm | 14 (70) | 2 (14) | 0.002# |
| Communication with MPD | 7 (35) | 3 (21) | 0.47# |
| MPD disruption | 4 (20) | 0 | 0.13# |
| Dilated MPD | 7 (35) | 2 (14) | 0.25# |
| Splenic vein thrombosis | 3 (15) | 1 (7) | 0.63# |
| Ascites | 12 (60) | 4 (29) | 0.09# |
| Pleural effusion | 2 (10) | 4 (29) | 0.20# |
*Chi-square test, $Fisher’s–Freeman–Halton exact test, #Fisher’s exact test, @Independent sample t-test. MPD: Main pancreatic duct
On multivariable logistic regression analysis, PPC diameter >6 cm in diameter (OR 139.2, 95% CI 5.5–3502.1, P = 0.003), presence of ascites (OR 18.87, 95% CI 1.1–316.4, P = 0.041), and the age of the child (OR 1.47, 95% CI 1.1–2.2, P = 0.049) independently predicted the need for intervention (Hosmer–Lemeshow χ2 = 2.69, P = 0.952; Nagelkerke R2 = 0.763). ROC analysis demonstrated that PPC diameter predicted intervention (AUC 0.704, 95% CI: 0.522–0.885; P = 0.046). A cutoff of 6.5 cm yielded 60% sensitivity and 93% specificity (J = 0.529), while 6 cm yielded 63% sensitivity and 86% specificity [J = 0.483; Figure 2b].
Walled-off necrosis
Fifteen (54%) out of 28 ANCs progressed to WON. The mean age at presentation was 10.3 ± 4.3 years, with a mean interval of 1.6 ± 0.6 months after the acute episode. AP was the most common cause of WON [Table 4]. Children with ANC aged <5 years were more likely to progress to WON [40% vs. 0%, P = 0.02, Fisher’s exact test; Table 4]. Six (40%) children underwent percutaneous drainage, and one underwent ERCP with sphincterotomy. WONs measuring >6 cm in diameter were associated with an increased need for intervention [71% vs. 13%, P = 0.04, Fisher’s exact test; Table 5].
Table 4.
Clinical profile of children with progressed versus resolved acute necrotic collections
| Parameters | WON (n=15), n (%) | Resolved ANC (n=13), n (%) | P |
|---|---|---|---|
| Age (years), mean | 10.3±4.3 | 13.1±2.3 | 0.08@ |
| Age group (years) | |||
| <5 | 6 (40) | 0 | 0.02# |
| 5–10 | 0 | 1 (8) | 0.46# |
| 10–15 | 8 (53) | 10 (77) | 0.37# |
| >15 | 1 (7) | 2 (15) | 0.58# |
| Boys | 12 (80) | 8 (62) | 0.41# |
| Type of pancreatitis | |||
| Acute pancreatitis | 9 (60) | 12 (77) | 0.6$ |
| Acute recurrent pancreatitis | 3 (20) | 1 (8) | |
| Acute on chronic pancreatitis | 3 (20) | 0 (8) | |
| Etiology | |||
| Idiopathic | 14 (93) | 12 (92) | 1# |
| Trauma | 1 (7) | 1 (8) | |
| Gall stones | 0 | 0 | |
| Pancreatic divisum | 0 | 0 | |
| Drug induced | 0 | 0 | |
| Symptoms | |||
| Abdominal pain | 15 (100) | 13 (100) | 1# |
| Vomiting | 14 (93) | 11 (85) | 0.58# |
| Anorexia | 2 (13) | 1 (8) | 1# |
| Loss of weight | 1 (7) | 0 | 1# |
| Cyst rupture | 0 | 0 | 1# |
| Diameter >6 cm | 6 (40) | 2 (15) | 0.39# |
| Communication with MPD | 1 (7) | 1 (8) | 1# |
| MPD disruption | 1 (7) | 1 (8) | 1# |
| Dilated MPD | 2 (13) | 1 (8) | 1# |
| Splenic vein thrombosis | 3 (20) | 2 (15) | 1# |
| Ascites | 11 (73) | 9 (69) | 1# |
| Pleural effusion | 3 (20) | 3 (23) | 1# |
@Independent sample t-test, $Fisher’s–Freeman–Halton exact test, #Fisher’s exact test. ANC: Acute necrotic collection, WON: Walled off necrosis, MPD: Main pancreatic duct
Table 5.
Clinical profile of walled-off necrosis according to the management
| Parameters | Intervention (n=7), n (%) | Conservative (n=8), n (%) | P |
|---|---|---|---|
| Age (years), mean | 11.9±4.8 | 9±4.9 | 0.28@ |
| Duration at presentation (months) | 1.6±0.5 | 1.6±0.6 | 0.88@ |
| Age group (years) | |||
| <5 | 2 (29) | 4 (50) | 0.61# |
| 5–10 | 0 | 0 | 1# |
| 10–15 | 4 (57) | 4 (50) | 1# |
| >15 | 1 (14) | 0 | 1# |
| Boys | 6 (86) | 6 (75) | 1# |
| Type of pancreatitis | |||
| Acute pancreatitis | 4 (57) | 5 (63) | 0.8$ |
| Acute recurrent pancreatitis | 1 (14) | 2 (25) | |
| Acute on chronic pancreatitis | 2 (28) | 1 (13) | |
| Etiology | |||
| Idiopathic | 7 (93) | 7 (92) | 1# |
| Trauma | 0 (7) | 1 (8) | |
| Gall stones | 0 | 0 | |
| Pancreatic divisum | 0 | 0 | |
| Drug induced | 0 | 0 | |
| Symptoms | |||
| Abdominal pain | 7 (100) | 8 (100) | 1# |
| Vomiting | 6 (86) | 8 (100) | 0.47# |
| Anorexia | 0 | 2 (25) | 0.47# |
| Loss of weight | 0 | 1 (13) | 1# |
| Cyst rupture | 0 | 0 | 1# |
| Diameter >6 cm | 5 (71) | 1 (13) | 0.04# |
| Communication with MPD | 0 | 1 (13) | 1# |
| MPD disruption | 0 | 1 (13) | 1# |
| Dilated MPD | 0 | 2 (25) | 0.47# |
| Splenic vein thrombosis | 0 | 3 (0) | 0.20# |
| Ascites | 7 (100) | 4 (50) | 0.08# |
| Pleural effusion | 0 | 3 (38) | 0.20# |
@Independent sample t-test, $Fisher’s–Freeman–Halton exact test, #Fisher’s exact test. MPD: Main pancreatic duct
Complications and re-interventions
Of the 27 (29%) children who required intervention for PFCs, postprocedural complications occurred in 2 (7%): a cysto-cutaneous fistula following percutaneous drainage of PPC, which healed with conservative management, and a blocked cystogastrostomy for PPC, which was managed by percutaneous drainage. No procedural mortalities were recorded. There were no late recurrences – all children who underwent intervention achieved clinical symptomatic relief prior to discharge and remained asymptomatic during follow-up.
Mortality and genetic evaluation
There were two deaths out of all children with pancreatitis, but none among those with PFCs. Genetic analysis is currently underway to identify mutations in children with ARP and CP.
DISCUSSION
Fluid collection is the most common complication of pancreatitis.[2,3,6] Despite its frequency, the available literature regarding the etiology, diagnosis, and management of PFCs in children remains limited and is largely derived from adult studies.[2,6,8,10,11,12] The present study was conducted to expand the pediatric evidence base by examining the spectrum, evolution, and management of PFCs in children.
Incidence
The incidence of fluid collection in our study was 40%, which lies within the wide range of 1.6% to 79.9% reported in previous studies.[2,3,6,10,11,12] Previous pediatric studies by Lal et al., Mirza et al., and Bolia et al. reported incidences of 61%, 20%, and 59%, respectively.[6,13,14] However, these studies had smaller sample sizes and included only children with AP. In contrast, our study included children with AP, ARP, and chronic pancreatitis (CP) presenting with an acute episode, as defined by the INSPPIRE criteria.[9,15] Fluid collections arise from inflammatory injury to the pancreas and peripancreatic tissues mediated by enzymatic activity.[4,7]
AP was the most common type of pancreatitis associated with PFCs in our study, as children with AP typically experience a single severe attack, unlike those with ARP and ACP.[16,17] In ACP, pancreatic fibrosis reduces the lipolytic flux between adipocytes and acinar cells, thereby limiting the acinar adipokine levels and decreasing parenchymal injury and necrosis.[4,17,18,19,20]
Sex differences
The majority of our patients were boys, consistent with the findings of Lal et al., Mirza et al., and Bolia et al.[6,13,14] The reasons for male predominance remain unclear but may be related to the higher incidence of pancreatitis and pancreatic trauma among boys, and the protective action of Estrogen in girls.[21,22,23]
Clinical presentation
Abdominal pain was the most common presenting symptom, noted in all participants, similar to previous pediatric and adult studies.[13,14,21] The pain likely results from peripancreatic irritation, enzymatic inflammation of the retroperitoneum, stretching of the pancreatic capsule, and compression of adjacent viscera by the collection.[6,7,17,21] Other symptoms included vomiting, anorexia, fever, and weight loss.[6,13,14] Children with biliary pancreatitis occasionally present with jaundice.[6,13,14] Ascites was observed in 54% of our patients, attributed to leakage from collections, cyst rupture, or PD disruption.[24]
Etiology of pancreatitis
In the majority (85%) of our study population with PFCs, no identifiable etiology could be determined. This aligns with reports from previous pediatric pancreatic pancreatitis, where idiopathic pancreatitis ranges from 21% to 82%.[3,6,9,14] We could not find an association between the etiology and the type of PFC or the need for intervention, similar to previous pediatric studies.[3,6,9,14]
Acute peripancreatic fluid collection versus acute necrotic collection
APFC was the most common local complication, consistent with prior pediatric studies.[13,14,18,25] This contrasts with adult studies, where ANCs predominate.[10,11,12] The difference likely reflects the less severe and more interstitial nature of pediatric AP compared with adults, who more often develop necrotizing pancreatitis.[7,17,21] Unlike adult pancreatitis, pediatric pancreatitis is often idiopathic, characterized by transient enzyme activation with rapid resolution. The better pancreatic microcirculation in children and the absence of comorbidities such as obesity, diabetes, and atherosclerosis further reduce ischemic risk.[26] All APFCs in our study were managed conservatively, consistent with previous reports.[6,11,12,14] APFCs are typically sterile, self-limiting, and resolve spontaneously as inflammation subsides.[17,21] Drainage is required only if symptomatic or infected.[4,7,21]
ANCs were more frequent among children aged 10–15 years (mean age 11.6 ± 4.1 years), similar to the findings of Raizner et al. (mean 12.8 years).[27] Older children are more prone to trauma and biliary disease and have near-adult levels of pediatric enzyme activity, predisposing them to necrotizing pancreatitis and ANC formation.[27,28,29] In our study, children with ANCs presented earlier than those with APFCs, likely due to the systemic inflammatory response and organ dysfunction associated with necrosis.[27]
APFCs were more common in children with ACP, whereas ANCs predominated in AP. In ACP, the pancreas is fibrotic and scarred, with patches of viable acinar tissue that leak pancreatic enzymes, leading to APFCs without extensive necrosis. In contrast, AP affects a structurally normal pancreas, resulting in microvascular injury, intense autodigestion, and necrosis.[4,17,18,19,20] The ischemic insult is more severe in AP because of active vascular injury, while the fibrotic tissue in ACP limits the enzyme activation.[18,19,20] In ACP, the ductal dilatation and irregularity promote enzyme leakage into peripancreatic tissue, leading to sterile APFCs. In contrast, in AP, the duct integrity is usually intact in the initial phase, with predominant parenchymal and vascular injury, leading to ANC.[17,18,19,20] The inflammatory cytokine surge involving tumor necrosis factor-alpha, interleukin-6 (IL-6), and IL-1 β in AP contributes to necrosis and ANC development, which is less pronounced in ACP.[30]
Predictors of progression of acute peripancreatic fluid collections
In our study, 53% of APFCs progressed to PPCs, comparable to Lal et al. (52%) and Bolia et al. (65%).[6,13] On multivariable logistic regression analysis, the diameter of APFCs and the type of pancreatitis emerged as independent predictors of progression to PPCs. The children with APFCs secondary to ACP were found to have five times higher odds of progression to PPC. Kim et al. similarly reported higher pseudocyst formation in ACP.[31] ACP causes ductal injury, disruption, or stricture, leading to continuous pancreatic leakage and pseudocyst formation.[31,32] ACP also promotes fibroinflammatory reaction and capsule formation, increasing PPC risk.[32] APFCs measuring >6 cm were associated with 22 times higher odds of progression to PPCs, likely due to persistent enzymatic leakage or ductal disruption, along with compression-induced venous and lymphatic stasis, which facilitate encapsulation.[31,32] ROC analysis further demonstrated good discriminatory ability of APFC diameter for predicting progression (AUC = 0.82). While a threshold of 3.5 cm provided a balance between sensitivity and specificity, a 6 cm cutoff showed high specificity, suggesting that larger collections are particularly prone to evolving into pseudocysts.
Predictors of interventions in pancreatic pseudocysts
Among children who developed pseudocysts, 59% required intervention, consistent with Poddar et al. (67%).[21] Asymptomatic PPCs can safely be followed up, whereas symptomatic ones require percutaneous, endoscopic, or surgical drainage.[14,17] On multivariable analysis, PPC diameter >6 cm, presence of ascites, and increasing age of the child were independently associated with the need for intervention. Larger PPCs tend to cause persistent abdominal pain, compressive symptoms, and may also reflect ongoing pancreatic ductal leakage or impaired drainage, thereby necessitating therapeutic intervention. The presence of ascites may reflect more severe pancreatic inflammation, and therapeutic drainage may be necessary to control symptoms or complications. ROC analysis demonstrated that a diameter threshold of 6–6.5 cm provided high specificity, suggesting that larger pseudocysts were likely to require intervention. All trauma-related PPCs required drainage, as reported previously.[14,21]
Progression of acute necrotic collections and interventions in walled-off necrosis
In our study, 54% of ANCs progressed to WON, a rate similar to that reported by Lal et al. (68%).[6] Children under 5 years were more likely to progress to WON, possibly due to higher rates of malnutrition and consequent immune compromise.[33] Unlike Lal et al., we found no significant difference in the intervention rates between WON and PPC (P = 0.43), likely because only symptomatic WONs were drained.[6] WONs >6 cm were more likely to require drainage due to greater necrotic burden, reduced clearance by macrophages, higher infection risk, and compressive symptoms.[7,8,32]
Adult literature describes several endoscopic techniques for the management of WON, including nasocystic irrigation, the multiple transluminal gateway technique, direct endoscopic necrosectomy, the development of novel metal stents, such as fully covered self-expanding metal stents and lumen-apposing metal stents (LAMS), dual-modality drainage, and the endoscopic step-up approach.[34] The clinical success rates with these procedures ranged from 75% to 100%.[34] However, their pediatric use is limited due to equipment size and expertise constraints.
Percutaneous drainage
In our cohort, percutaneous drainage was the preferred treatment for symptomatic PFCs, reflecting both institutional protocol and specific resource constraints. Advanced pediatric endoscopic instruments and LAMS were unavailable at our center. In addition, percutaneous drainage offers high technical success and flexibility in smaller children, where the gastric wall-to-cyst distance may be suboptimal for endoscopic intervention. Although our study supports the safety and feasibility of this approach, the lack of a comparative control group precludes conclusions regarding the superiority of one modality over another.
Genetic evaluation
While genetic mutations, such as PRSS1, CFTR, and SPINK1, are known to play a significant role in the etiology of pediatric ARP and ACP, there is no evidence of their role in fluid collections. Our study on genetic mutations is still in the preliminary stage, and we have not yet completed it or drawn conclusions at this point in time.
Clinical implications
The findings of this study have several clinical implications. Most PFCs in children resolve spontaneously and can be managed conservatively with close clinical and radiological monitoring. However, larger collections (>6 cm) appear to have a higher likelihood of progression and require closer surveillance to allow timely intervention when clinically indicated. Percutaneous drainage was a safe and effective treatment modality in our cohort, particularly relevant for sick children and in centers where advanced pediatric endoscopic interventions may not be readily available.
Strengths and Limitations
The strengths of this study include a relatively large pediatric cohort and a detailed characterization of PFCs according to the revised Atlanta classification. The study also provides clinically relevant data on predictors of progression and interventions in children with PFCs, an area where the existing pediatric literature remains limited.
The study has several limitations. Its retrospective study design limits the ability to establish robust causal relationships. Severity grading of pancreatitis (mild, moderately severe, and severe) could not be performed because these data were inconsistently recorded in the medical records. Imaging follow-up was guided by clinical conditions rather than a standardized protocol, which may have introduced potential classification bias in evaluating the evolution of PFCs. As this was a single-center study conducted at a tertiary referral institution, the cohort may include a higher proportion of complex cases, potentially limiting generalizability. The relatively small number of children in certain subgroups also resulted in wide confidence intervals for some predictors. In addition, genetic evaluation was not available for all children, and advanced pediatric endoscopic instruments were unavailable at our center. Despite these limitations, the study provides important insights into the natural history and management of PFCs in children.
CONCLUSION
Fluid collections occurred in approximately 40% of children with pancreatitis, most commonly as APFCs. ANCs occurred more frequently in older children and presented earlier than APFCs. AP was more often associated with ANCs, whereas ACP and ARP were associated with APFCs. APFCs secondary to AP and ARP were more likely to resolve, whereas those secondary to ACP were more likely to progress to PPCs. Older children with APFCs were more likely to develop PPCs, whereas younger children (<5 years) with ANCs were more prone to WON. Collection diameter and pancreatitis phenotype were key determinants of progression of APFCs to PPCs, while PPC diameter, ascites, and increasing age predicted the need for intervention. Collections measuring greater than 6 cm were particularly prone to progression and intervention. In our experience, percutaneous drainage demonstrated safety and effectiveness as a primary intervention.
Conflicts of interest
There are no conflicts of interest.
Funding Statement
Nil.
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