Clinical Characteristics and Risk factors of Acute Pancreatitis in Paediatric Patients in Oman: An 11-year experience from a tertiary centre

Summary

Objectives:

The incidence of acute pancreatitis (AP) in the paediatric population has increased over the past two decades, with an estimated annual rate of 0.78 per 100,000 children. This study aimed to describe the risk factors and characteristics of AP in Omani children.

Methods:

A retrospective cohort study was conducted, including all children <14 years who were admitted and treated with AP at Sultan Qaboos University Hospital in Muscat, Oman, from January 2010 to December 2020. Case presentations, aetiology, management, and outcomes were reviewed.

Results:

During the 11-year study period, 55 cases were identified (male: female, 1.2:1). The most frequently reported risk factors were toxic/metabolic (49.1%). Abdominal pain was the predominant symptom (76.4%). Conservative treatment was administered in 74.5% of cases, while the remaining patients required surgery or endoscopic retrograde cholangiopancreatography. Of the 55 patients, 51 fully recovered. The number of risk factors per case was not associated with patient outcomes or length of hospital stay.

Conclusion:

Future multicentre and prospective studies with comprehensive data collection are crucial to further understand paediatric AP in Oman and inform potential modifications to treatment guidelines.

Advances in Knowledge

• The findings revealed that toxic/metabolic factors were the most common (49.1%), followed by obstructive causes (23.6%).

• This study reported a high recurrence rate of acute pancreatitis in our group, reaching 20%.

• This study showed that patients with more risk factors of AP have shorter duration of admission.

Application to Patient Care

• This study provided further evidence suggests an association between inborn error of metabolism, particularly between organic acidemias and acute pancreatitis.

• Future multicentre and prospective studies are crucial to further understand paediatric AP in Oman.

1. Introduction

Acute pancreatitis (AP) is an inflammatory condition resulting from the conversion of trypsinogen to trypsin, leading to autolysis of the pancreas.¹ Recent studies have shown an increased incidence of AP across all paediatric age groups over the last two decades.² Although AP is considered a rare disease in children, it has been diagnosed more frequently in recent years. A study conducted in the UK found that the incidence of AP in children under 15 years of age was 0.78 per 100,000.³ This rise in incidence is not fully understood and it may be attributed to increased awareness of the disease within the paediatric population.¹ A recently published study in Saudi Arabia reported an average incidence of 2–3 cases per year, which is also considered uncommon.⁴

According to the International Study Group of Pediatric Pancreatitis: In Search for a Cure (INSPPIRE), the diagnosis of AP requires the presence of two out of the following three criteria: classical abdominal pain, amylase and/or lipase levels that are at least three times higher than the upper normal limit, and radiological imaging consistent with AP.⁵ Although contrast-enhanced computed topography (CT) is the gold standard radiological test for diagnosing AP, ultrasound is preferred as the initial imaging modality.⁶

There are several aetiologies of AP in children. The most common causes include biliary system obstruction, metabolic diseases, medications, structural anomalies, blunt abdominal trauma, hereditary pancreatitis, and systemic diseases such as Crohn's disease, autoimmune pancreatitis, diabetes mellitus, haemolytic uraemic syndrome, and Henoch-Schönlein purpura. Therefore, it is essential to identify the aetiology of AP in paediatric patients for appropriate disease management.⁷ The management of AP is determined by its aetiology and primary involves pain control, hydration and nutrition. Surgical or endoscopic interventions are rarely required in children.⁸ Most children with AP recover fully, although some may develop acute recurrent pancreatitis and others may progress to chronic pancreatitis.⁶

As there is currently no available data on AP in Oman, this study aimed to fill this gap by examining the clinical characteristics and aetiologies of AP in Omani children presenting to a single hospital. The study seeks to identify potential causes of AP and compare these with international findings to gain insights into the aetiology and characteristics of the condition within this demographic.

2. Methods

A retrospective cohort study was conducted to describe the clinical characteristics of AP in Omani children treated at Sultan Qaboos University Hospital (SQUH), Muscat, Oman. The study investigated possible aetiologies and compared them with data published internationally. Data was collected by reviewing the patients' medical records from the Hospital Information System after obtaining institutional ethical approval.

The study included children aged <14 years who were admitted and treated in the paediatrics wards at SQUH (patients aged 14 years and older are managed in the adult wards). The sample included all cases from January 2010 to December 2020 who were managed for AP. Only the first episodes of AP were included after filtering the data.

Data were collected from the patients' electronic medical records and included variables such as date of birth, date of presentation, date of resolution, gender, symptoms and their duration, number of recurrences and details of admission (duration, admission to intensive care unit). Blood investigations, including inflammatory markers (white cell counts [WCC], C-reactive protein [CRP]), amylase and lipase levels, genetic testing, as well as imaging modalities and their findings, were recorded. Management details—including nil per os (NPO) duration, medications used, surgeries, procedures required and outcomes—were also included.

Cases with recurrent AP were recorded as a single case. Recurrence was defined as a distinct episode of AP occurring after one month of complete resolution of the first episode. Resolution was defined as the resolution of pain and normalisation of pancreatic enzymes. Cases presented in 2020 were followed up until December 2023 for recurrences monitoring.

Predisposing factors were recorded and categorised into hereditary pancreatitis, biliary, toxic, metabolic, autoimmune, traumatic and iatrogenic. These factors were identified based on previously mentioned risk factors in the literature.

Hereditary pancreatitis refers to pancreatitis due to pathologic genetic variants predisposing patients to the development of pancreatitis. These conditions include genetic mutations in certain genes such as Protease serine 1, serine protease inhibitor Kazal type 1 (SPINK1), cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsin C (CTRC) and carboxypeptidase A1 (CPA1). Toxic pancreatitis is defined as pancreatitis triggered by exposure to harmful substances, including medications, alcohol, high urea or environmental toxins. Metabolic causes of pancreatitis include hypertriglyceridemia, hyperglycaemia and inborn errors of metabolism (IEM). Iatrogenic pancreatitis is pancreatitis caused by medical or surgical interventions, typically unintended, including procedures such as ERCP or surgeries.

Data analysis was performed using the Statistical Package for the Social Sciences (SPSS) software, Version 23 (IBM Corp., Armonk, New York, USA). After recording the data in SPSS, variables were categorised as continuous or categorical. Each group of categorical variables was coded numerically, depending on the number of groups. Descriptive statistics (mean, median, mode, standard deviation) were used to represent the continuous variables (age, duration of admission, duration of NPO, WCC, CRP, amylase and lipase levels). Frequencies of symptoms, imaging performed, positive imaging findings and risk factors were obtained and reported.

3. Results

Over an 11-year period (2010–2020), 55 children presented with AP, of whom 54.5% were male and 45.5% were female. The youngest child was 8 months old and the oldest was 14 years old, with a mean age of 7.6 years (7.7 years for males and 7.5 years for females). Abdominal pain was the most commonly reported symptoms, occurring in 42 out of 55 cases (73.3% of males and 80.0% of females). Vomiting was observed in 63.3% of males and 72.0% of female, while nausea was present in 60.0% of all patients. There was no statistically significant difference between males and females in the occurrence of symptoms (P >0.05). The mean duration of symptoms was 4.2 days [Table 1].

Table 1.

Demographic data of patients with acute pancreatitis (N = 55).

	Male	Female	Total	P-Value
		n (%)
Gender	30 (54.5)	25 (45.5)	55 (100)
Mean age ± SD in years	7.65 ± 4.29	7.53 ± 3.83	7.6 ± 4.0
Clinical presentation
Abdominal pain	22 (73.3)	20 (80.0)	42 (76.4)
Vomiting	19 (63.3)	18 (72.0)	37 (67.3)
Nausea	13 (43.3)	9 (36.0)	22 (40.0)
Asymptomatic	3 (10.0)	2 (8.0)	5 (9.1)
Mean duration of symptoms in days	2.97	5.56	4.17
Recurrence	4 (13.3)	7 (28.0)	11 (20.0)	0.176
Mean time till first recurrence in months	6.00	18.86	14.18
Mean duration of admission in days	7.33	11.42	9.19
Patients requiring ICU	3 (10.0)	3 (12.0)	6 (10.9)

SD = standard deviation; ICU = intensive care unit.

Risk factors were classified into hereditary, metabolic, toxic, obstructive, autoimmune, and other categories (such as trauma or iatrogenic causes). The majority of patients exhibited at least one identifiable risk factor [Table 2]. The most frequently observed were toxic/metabolic factors (49.1%), followed by obstructive factors (23.6%) [Table 3]. The most common single cause was gallstones, reported in 9 patients. Metabolic aetiologies were predominant, with 22 cases identified, of which 12 were attributed to organic acidemias and MUSD. Reported hereditary causes included heterozygous cystic fibrosis transmembrane conductance regulator (CFTR) variant (n = 2) and variants in serine peptidase inhibitor Kazal type 1(SPINK1) gene (n = 2). Six patients developed drug-induced pancreatitis, attributed to agents such as L-asparaginase, chloroquine, azathioprine, and prednisolone. Additionally, one patient developed iatrogenic pancreatitis following an ERCP procedure. Among the 6 patients who have two risk factors, combinations included hereditary and toxic risk factors (n = 2) and hereditary and obstructive factors (n = 2) [Table 2]. Eight patients (14.5%) have no discernible risk factors.

Table 2.

Number of risk factors found in each patient with acute pancreatitis (N = 55).

Number of Risk Factors	n (%)
No risk factors	8 (14.5)
1 risk factor	41 (74.5)
2 risk factors	6 (10.9)
Genetic and toxic	2 (3.6)
Genetic and obstructive	2 (3.6)
Toxic and autoimmune	1 (1.8)
Toxic and obstructive	1 (1.8)

Table 3.

Risk factors of acute pancreatitis, including patients with multiple risk factors (N = 55).

Risk factors	n (%)
Toxic	7 (12.7)
Medications	6 (85.7)
Chronic kidney disease	1 (14.3)
Metabolic	22 (40.0)
Diabetic ketoacidosis	4 (18.2)
Hypertriglyceridemia	1 (4.5)
Organic acidaemia
Propionic acidaemia	4 (18.2)
Isovaleric acidaemia	1 (4.5)
Methylmalonic acidaemia	1 (4.5)
MSUD	6 (27.4)
Glycogen storage disease	2 (9.1)
Mitochondrial disease	2 (9.1)
HMG CoA lyase deficiency	1 (4.5)
Obstructive	15 (27.3)
Acquired	9 (60.0)
Anatomical (divisum, dilated duct, etc)	6 (40.0)
Hereditary pancreatic diseases	4 (7.3)
CFTR*	2 (50.0)
SPINK1†	2 (50.0)
Autoimmune	5 (9.1)
Systemic lupus erythematosus	3 (60.0)
Ulcerative colitis	1 (20.0)
Primary sclerosing cholangitis	1 (20.0)
Other	7 (12.7)
Iatrogenic	1 (14.3)
Infection	4 (57.1)
Traumatic	2 (28.6)

^*Cystic fibrosis transmembrane conductance regulator;

^†Serine Peptidase Inhibitor Kazal Type 1.

The mean highest lipase level was 1,388.3 IU/L, with a range of 99–8,479 IU/L. CRP was elevated in 28 patients (50.9%), occurring in 60.7% of males and 39.3% of females. Leucocytosis was observed in 16 cases (29%) [Table 4].

Table 4.

Laboratory results of the patients with acute pancreatitis (N = 55).

	Male	Female	Total
		n (%)
Amylase >3 times upper normal (25–125)	12 (57.1)	9 (42.9)	21 (38.2)
Lipase >3 times upper normal (3–216)	18 (56.3)	14 (34.7)	32 (58.2)
WBCs >12 × 109/L	9 (56.3)	7 (43.8)	16 (29.1)
CRP >10 mg/L	17 (60.7)	11 (39.3)	28 (50.9)

WBCs = white blood cells count; CRP = C-reactive protein.

Most patients underwent diagnostic imaging (n = 48, 87.3%), with abdominal ultrasound being the most frequently employed modality (41.7%).

The length of hospital stay ranged from 12 hours to 10.7 weeks (mean 9.2 days, median 5 ± 14.0 days). Children with none or one risk factor for AP had a longer mean hospital stay (9.7 days) compared to those with two or more risk factors (4.7 days); however, this difference was not statistically significant (P >0.05) [Table 5]. Six children (11.5%) required admission to the intensive care unit (ICU). Over the 11-year study period, 11 patients (20.0%) experienced recurrence within 3 years of follow-up, with a mean time to first recurrence of 14.2 months.

Table 5.

Number of risk factors by the length of hospital stay for all of the patients (N = 55).

	Duration of admission in days
	n (%)	Mean ± SD	P-value*
0 or 1 risk factor	49 (89.1)	9.74 ± 14.78	0.221
2 risk factors	6 (10.9)	4.67 ± 2.42

SD = standard deviation.

^*Independent sample test.

Conservative management was the predominant treatment approach, applied in 41 of 55 patients (74.5%). Surgery was performed for 5 patients, ERCP in 7, and a combination of surgery and ERCP in 2 patients. Among those receiving conservative treatment, all were administered intravenous fluids, and all except 2 patients were kept nil per os for a mean of 15.4 ± 24.4 hours (range: 0–96). Seventeen patients received antibiotics, and 34 received analgesia, most commonly paracetamol (75.6%), followed by tramadol (19.5%) and morphine (9.8%).

Overall, 51 patients (92.7%) achieved full recovery by discharge, while 4 (7.3%) died during admission. Three of these deaths were attributable to their primary illnesses—Maple Syrup Urine Disease (MSUD), methylmalonic acidaemia, and congenital lactic acidosis—whereas one death was directly due to AP. This latter case involved a patient who had recently undergone haematopoietic stem cell transplantation, was severely immunosuppressed and developed severe pancreatitis complicated by multiorgan failure. Despite supportive care, the patient's condition deteriorated rapidly due to his fragile immune status.

The relationship between risk factors and outcomes was examined using the Chi-squared test, with a two-sided P-value of <0.05 considered statistically significant. There was no significant association between the number of risk factors per case and patient outcomes (P > 0.05) [Table 6]. Similarly, no significant differences in outcomes were observed when comparing cases with elevated white cell count (WCC) and CRP levels. However, WCC >12 × 10⁹/L and CRP >10 mg/L were associated with a higher likelihood of ICU admission (P = 0.32 and 0.35, respectively).

Table 6.

Number of risk factors x outcome (N = 55).

	Recovered	Died	Total
		n (%)		P-value*
0 or 1 risk factor	45 (91.8)	4 (8.2)	49 (89.1)	0.467
2 risk factors	6 (100.0)	0 (0)	6 (10.9)
Total	51 (92.7)	4 (7.3)	55 (100.0)

^*Pearson Chi-squared test.

4. Discussion

This study aimed to describe the clinical characteristics and possible aetiologies of AP in Omani children and to compare the findings with published international data, taking into account the reported increase in paediatric AP incidence in recent years. The phenomenon of increasing AP incidence was first described by Lopez in a children's hospital in Dallas, where cases rose from 5 to 113 per year between 1993 and 1998.⁹

Over the 11-year study period, the annual number of AP cases at our institution (excluding recurrences) ranged from 1 to 11, with fluctuations observed across the years and a general upward trend in the later period. A single-centre study from Saudi Arabia reported an incidence of 2–3 cases per year.⁴ The observed increase in the current setting is likely related to heightened diagnostic awareness and greater utilisation of serum amylase and lipase testing in paediatric patients presenting to the emergency department. Furthermore, a trend towards routine testing of admitted patients has emerged, leading to diagnoses in some asymptomatic individuals based solely on laboratory and imaging findings. These observations align with explanations provided in earlier studies, which also highlighted the impact of increased referrals to tertiary care centres.² This rise may also be multifactorial, involving factors such as higher referral rates and environmental influences, including increasing rates of obesity—a recognised risk factor for biliary pancreatitis.²

Risk factors for AP in children are heterogeneous. In the current cohort, toxic/metabolic factors were the most common (49.1%), followed by obstructive causes (23.6%). In a 10-year study at Hospital de Braga, biliary causes accounted for 24.3% of AP cases, followed by trauma (16.2%).¹⁰ In the current series, 14.5% of patients had no identifiable risk factors, compared to 42% in the aforementioned Saudi study.⁴ Cases in the current cohort were labelled as idiopathic only after comprehensive clinical evaluation and appropriate diagnostic testing excluded common causes such as biliary disease, medication exposure, trauma or metabolic disorders. Nonetheless, due to the retrospective nature of the current work and variability in the extent of investigations—particularly in milder or rapidly resolving cases—some aetiologies may have gone undetected. This reinforces the need for paediatricians to investigate all possible causes before designating a case as idiopathic.⁴

A distinctive finding in the current cohort was the high prevalence of metabolic causes, particularly organic acidemias, compared with international reports. Reviews of paediatric AP generally cite metabolic causes in 2–7% of cases, most often due to diabetic ketoacidosis;¹¹ in contrast, organic acidaemias predominated in the current series. The association between AP and organic acidaemias was first described by Kahler et al. in 1994, who reported 9 children with organic acidaemia, including 7 with acute and 2 with chronic pancreatitis, among 108 affected patients.¹¹ A more recent UK study reported organic acidaemia in 13% of AP cases.³ The prominence of metabolic aetiologies in the current population likely reflects the high incidence of inborn errors of metabolism (IEM) in Oman, related to high rates of consanguinity, as documented by Al-Thihli et al. in 2014.¹² In addition, our institution serves as the main national referral centre for IEM.

The current study also highlights the occurrence of multiple concurrent risk factors in paediatric AP, reflecting the multifactorial nature of the disease, as observed in prior studies.^13,14

Another notable finding was the high recurrence rate of 20%, with females accounting for 28% of recurrent cases. Reported recurrence rates in other studies vary from 15% to 34.5%.¹⁵ Acute recurrent pancreatits has been associated with hereditary, metabolic and obstructive causes.¹⁴ In the current cohort, obstructive causes (acquired or congenital) were present in 7 of the recurrent cases, and both patients with pathogenic genetic variants (SPINK1 and CFTR) developed acute recurrent pancreatitis. These variants have been linked to both acute recurrent pancreatitis and chronic pancreatitis.¹⁴

According to the INSPPIRE criteria, paediatric AP is diagnosed based on typical abdominal pain, elevated serum pancreatic enzymes (>3 × the upper limit of normal [ULN]), and radiological evidence. As anticipated, abdominal pain was the most frequently reported symptom in the current study, followed by vomiting (76.4% and 67.3%, respectively), consistent with previous reports.¹ Fever was not described as a presenting symptom in the current cohort, as it is considered uncommon; however, it has been reported in other studies, including Grzybowska-chlebowczyk et al. (3.8%), Sanchez-Ramirez et al. (27%) and Kandula and Lowe (40%).^1,15,16

The key laboratory indicators for AP diagnosis are amylase and/or lipase levels exceeding three times the ULN. In the current cohort, amylase levels were >3 × ULN in 42% of cases, which is in line with findings from studies conducted in the US and UK.^17,18 This reflects the lower sensitivity of amylase compared with lipase in diagnosing AP.

Given that most patients presented with abdominal pain, abdominal ultrasound was frequently performed, yielding suggestive findings of AP in 20% of cases. In the current study, imaging played a crucial role in confirming the diagnosis. Ultrasound was typically employed as the first-line modality to exclude biliary causes, especially gallstones. Conversely, computed tomography (CT) detected AP in 80% of patients who underwent the scan and was instrumental in identifying complications such as pancreatic necrosis or fluid collections, which influenced clinical decisions regarding surgical intervention or intensive monitoring. Nonetheless, CT was not routinely recommended if both INSPPIRE clinical and biochemical criteria were fulfilled.¹⁹ It remains advisable to perform CT when pancreatic necrosis is suspected.²⁰ The reported sensitivity of CT ranges from 47% to 81%, which is generally higher than that of ultrasound.²¹ Despite this, CT usage is often less frequent due to concerns about radiation exposure in children.²¹

The median length of stay (LOS) for the current patients was 5 days (range: 0.5–75 days), comparable to reports from Saudi Arabia (5 days) and Jordan (4 days).^5,22 Variability in LOS likely reflects differences in the underlying systemic illnesses of patients. Notably, in the current study, patients with more risk factors for AP had shorter admissions. This may be explained by the possibility that families of children with known risk factors have a lower threshold for seeking early medical attention, resulting in quicker treatment initiation and recovery. However, statistical analysis did not demonstrate a statistically significant association between the number of risk factors and LOS.

These findings align with Rivera-Suazo and Vázquez-Frias, who demonstrated that early feeding—rather than age, recurrence, severity grade, aetiology, comorbidities, complications, fluid resuscitation, parenteral nutrition, or initial biochemical profiles—had the greatest influence on LOS in children with AP.²³

Most paediatric AP cases are mild, resolve without complications and have low mortality rates.¹¹ This was confirmed in the current study, in which 51 patients achieved complete recovery at discharge. Of the four deaths observed, only one was directly attributable to AP, occurring in a high-risk, immunocompromised patient. Earlier recognition and aggressive supportive management may have provided a narrow window for intervention in such cases, underscoring the importance of heightened vigilance and multidisciplinary management in high-risk populations.

Although this is the first study to characterise AP in Omani children, it has several limitations. First, its retrospective design limits the ability to establish causal relationships between risk factors and AP development. Second, as this was a single-centre study, the findings may not represent the national picture and could under-represent milder cases managed in primary or secondary care, introducing referral bias and possibly leading to overestimation of moderate to severe cases. Finally, reliance on medical records means that certain clinical or demographic details may have been omitted or incompletely documented, which could affect the comprehensiveness of risk factor identification. Future research employing larger, multicentre, prospective designs with standardised and complete data collection would enhance understanding of paediatric AP in Oman and provide a stronger evidence base to inform local guidelines.

5. Conclusion

This study demonstrated an increasing number of AP cases among Omani children, possibly attributable to heightened clinical awareness, increased metabolic testing and other environmental factors such as diet and obesity. Metabolic/toxic factors—particularly organic acidaemias—were the most common aetiology, a finding that differs from patterns reported in other populations. A recurrence rate of 20% was observed, with females appearing more susceptible and obstructive or hereditary factors being key contributors. The low mortality rate aligns with the generally mild clinical course of paediatric AP. These findings provide important insights into the epidemiology, aetiology and outcomes of paediatric AP in Oman, and may inform future diagnostic and management strategies.

Authors' Contribution

Shurooq S. Al Shereiqi: Data Curation, Writing- Original Draft, Writing - Review & Editing. Aisha Al Fudhaili: Data Curation, Writing- Original Draft. Dafalla Rahmatalla: Methodology, Data Curation. Ravi Chandra: Methodology, Data Curation. Sanjay Jaju: Methodology, Data Curation. Ahmed Al Adawi: Data Curation. Adawiya Al Jamei: Data Curation. Yusriya Al Rawahi: Conceptualization, Methodology, Data Curation, Writing- Original Draft, Writing - Review & Editing.

Acknowledgement

The authors would like to acknowledge the support of the Sultan Qaboos University Hospital Information System for their assistance in data collection used in this study.

Ethics statement

Ethical approval for this study was obtained from the Medical Research Ethics Committee at the Sultan Qaboos University (MREC# 2401)

Conflict of Interest

The authors declare no conflicts of interest.

Funding

No funding was received for this study.

Data Availability

Data is available upon reasonable request from the corresponding author.