Materials and Methods
A.
Patient Data
The archives of the paediatric radiology department were reviewed for AP patients,
documented between 2007 and 2018.
The search yielded 74 patients (32 Male,
42 Female; age of diagnosis ranging between 1-18 years; mean age was 9 ± 4.9 years. We observed slight female preponderance with a ratio of 1.3:1.
The number of hospitalization over the years is shown in Fig. 9.
In recent years,
many studies have drawn attention to the increasing incidence of AP over the years in children.
This issue was described firstly by Lopez [18],
which has been confirmed with various other studies [19-21].
In our 12-year study,
the incidence of acute pancreatitis was increasing in a similar manner especially after 2012 over the years.
Previous studies pointed that the probable reasons of this incline are,
increasing body mass index of the paediatric population,
increased clinical awareness about AP and increased referral to the tertiary care hospitals.
B.
Etiology
The overall etiology of the AP is exhibited in Fig. 10.
Most common causes of AP were pancreaticobiliary ductal anomalies (24.3 %),
followed by gallstones (12.1 %) Fig. 11 and cystic fibrosis(10.8 %).
All of the pancreaticobiliary ductal anomalies were diagnosed by MR cholangiopancreatography (MRCP).
If the etiologies were revealed more detailed,
11 (61.1 %) of the pancreaticobiliary ductal anomalies were pancreas divisum Fig. 12.
Upon 6 (8.1 %) patients with drug induced pancreatitis,
5 patients were due to L-asparaginase for acute lymphoblastic leukemia,
1 patient was due to teriflunomide treatment due to multiple sclerosis.
In 5 (6.8 %) hyperlipidemia patients,
2 type I,
2 type III and 1 type V hyperlipidemia were seen.
In 3 patients different types of choledocal cysts were revealed with MRCP Fig. 13.
Most of the studies indicated no clear etiology for most of the patients in contradiction to our study which revealed pancreaticobiliary ductal anomalies as the most common cause [1,2,4-6].
This is probably due to inclusion of patients only with cross-sectional imaging in our study. Regarding to this results,
we suggested that recent increase of examination with US or MRCP at the onset of disease immediately after the approach to the emergency might be another probable reason of this increased diagnosis over the years.
C.
Clinical Findings
Most common presenting symptom was epigastric pain in 67 patients (90.5 %),
followed by nausea and vomiting.
16 patients (21.6 %) had negative laboratory findings (more than 3 times increase of normal range of pancreatic amylase and lipase) for AP.
The etiology of these patients were,
autoimmune pancreatitis (3),
hyperlipidemia (2),
gallstones (2),
L-asparaginase related (1),
cystic fibrosis (1),
pancreaticobiliary ductal anomalies (3) and idiopathic (4).
Although amylase and lipase levels were in normal range,
IgG4 level was high in all of the patients with IgG4 related pancreatitis Fig. 14.
Radiologic Results
All of the patients have initially evaluated with US and 30 (40.5 %) of them had positive findings (pancreatic swelling and/or peripancreatic fluid) for AP.
Within first month,
57 (77 %) patients were evaluated with only MR/MRCP imaging,
only CT was performed to 8 (10.8 %),
both CT and MR/MRCP were performed to 8 (10.8 %) and 1 patient was followed with only initial US images.
49 (66.2 %) had positive radiologic findings for acute pancreatitis on MR and/or CT.
Pancreatic swelling was demonstrated in 38 (51.3 %),
fluid collection was seen in 26 (35.1 %) and lack of contrast enhancement was shown in 3 (4.1 %).
The follow-up CT/MR scans performed at least 1 month after the initial imaging were evaluated for the presence of the following residual findings or complications which showed WON in 5 (6.8 %),
pseudocyst in 4 (5.4 %) and parenchymal necrosis in 2 (2.7 %) patient.
In 8 of the patients follow up images revealed irregular dilatation of pancreatic duct along with parenchymal atrophy suggestive of chronic pancreatitis.
The number of the imaging features were outlined in Fig. 15.
Discussion
Although,
the typical symptoms of AP,
such as abdominal pain and vomiting along with elevated lipase generally establish the diagnosis,
in up to 5% of cases without diagnostic imaging,
AP may be missed [22].
Imaging findings is not only the crucial part of diagnostic algorithm,
but also important to find out etiology and determine the complications.
The imaging features of AP in paediatric patients,
which are similar to those seen in adults,
are pancreatic swelling due to edema,
peripancreatic inflammation,
collections and necrosis of the pancreatic parenchyma and peripancreatic fat [10].
US is the initial imaging method for AP followed by CT [23].
Recent studies revealed that the sensitivity of CT for the diagnosis of AP is estimated at 47–81% [3,20,22,23].
Therefore,
concerns about radiation exposure and its close sensitivity with US in diagnosing pancreatitis justify a minimal role for CT scanning in the diagnosis of AP in children.
Besides,
CT has limited benefit either for visualizing biliary ductal system which is the most common cause of AP in our cohort or characterizing the content of peripancreatic fluid collection Fig. 16. Likewise,
according to revised Atlanta criteria,
CT is not recommended in the first phase of acute edematous pancreatitis,
however,
it should be performed when pancreatic necrosis is suspected [16].
Based upon all of these findings,
we recommend MR and MRCP as a second option when initial US is inconclusive.
Early detection of pancreatic necrosis is challenging,
because both necrotic and edematous parenchyma exhibit heterogeneous enhancement on contrast-enhanced imaging [9].
As applicable,
imaging should be performed at least 72 hours after initial symptoms.
One important point is,
intraparenchymal collections due to pancreatitis are referred to as ANC or WONs,
not as pseudocysts Fig. 17 [8].
We have only 2 patients with parenchymal necrosis both confirmed surgically.
The etiology of these patients were trauma and parenchymal necrosis was demonstrated with CT in the first week.
Also in one girl with the age of 14 years old,
initial MR imaging which was performed 6 days after the onset of symptoms,
revealed lack of contrast enhancement.
However,
control imaging after 1 month revealed normal enhancement pancreas parenchyma with walled of necrosis.
These findings may be suggestive of over diagnosis for contrast enhanced MR and CT in early phase (< 1 week) regarding to parenchymal necrosis.