Fig. 16.1
Acute pancreatitis—Classic appearance on imaging of the pancreatic gland after the first days of edematous acute pancreatitis in different patients. (a) US transverse scan showing an enlarged pancreatic gland with convex contours. (b) CE-CT showing a swollen homogenous pancreatic gland with convex contours. Some effusion is visible. (c) MR imaging T2-weighted sequence showing an enlarged pancreatic gland with convex contours
16.3.1.1 On Ultrasound
Analysis of the pancreatic echotexture compared to the liver is usually not helpful for the diagnosis. During AP, the pancreas remains hypo or isoechoic or can even be hyperechoic. Chao et al. reported that a pancreatic duct larger than 1.5 mm in children between 1 and 6 years, larger than 1.9 mm at ages between 7 and 12 years, and larger than 2.2 mm at ages between 13 and 18 years was significantly associated with AP, mainly idiopathic [20]. However, the caliber of the pancreatic duct is also variable depending on the etiology (obstructive vs non-obstructive). The duct can be compressed by the swollen gland (Fig. 16.2) or distended, secondary to its obstruction or due to underlying chronic pancreatitis. Evaluation of the peri-pancreatic collections content (debris, gas bubbles, septations) is better demonstrated with US.
Fig. 16.2
Acute pancreatitis. Consequences on pancreatic duct. (a) The pancreatic duct is visible as two separate parallel lines in the pancreatic head. (b) It is compressed by the edematous gland at the junction between the isthmus and body of the pancreas (yellow arrow)
16.3.1.2 On CT
The main advantages of CT compared to US are to visualize accurately the entire gland whatever the bowel distension and to differentiate, thanks to contrast injection, edematous reaction from necrosis of the gland. Additional positive findings include enlargement either diffuse or focal, irregular and ill-defined contours of the gland, ductal distension, infiltration of the peripancreatic fat, thickening of the adjacent fascial planes, detection and analysis of the peripancreatic fluid collections (size, density, contains, wall) (Fig. 16.3).
Fig. 16.3
Acute edematous pancreatitis on CE-CT: Homogenous swollen pancreatic gland with surrounding homogenous hypodense fluid collections
16.3.1.3 On MR Imaging
MR exploration has the same advantages and ability to detect AP than CT without the inconvenience of ionizing radiation but with a longer time of examination as well as the need for sedation in patients younger than 5 years. Inflammation is responsible for a diffuse or focal loss of the normal T1-weighted hypersignal of the pancreatic gland and a heterogeneous appearance in T2-weighted sequences. Focal increased hyperintensity on T1 is present in case of hemorrhage. Gadolinium injection is not necessary to confirm the presence of an AP but allows the differentiation between viable pancreatic tissue and necrosis (Fig. 16.4).
Fig. 16.4
Acute edematous pancreatitis on MR imaging in a 5-year-old child. (a) T2-weighted fat saturation sequence showing a homogenous swollen pancreatic gland. (b) T1 gadolinium fat saturation showing a homogenous swollen pancreatic gland
16.3.2 Positive Diagnosis of the Causes of AP
Determining the cause is mandatory in order to prevent recurrent episodes. Imaging plays an important role for this purpose and helps to define the therapeutic strategy. Some of the causes are obvious (known trauma), others must be searched carefully to be treated immediately (obstructive lithiasis) or at distance of the AP. Resolution of the pancreatic gland edema several days or weeks after the beginning of AP allows to appreciate more easily the presence of congenital duct malformations (common pancreato-biliary canal, pancreas divisum, etc.) or signs of chronic pancreatitis [19].
16.3.2.1 Trauma
Causes of traumatic AP include accidental, post-surgical, post-endoscopic, and non-accidental trauma. The latter will not display any specific finding on imaging but must be considered as potential cause. Additional dedicated imaging explorations related to clinical symptoms and children’s age must be performed (i.e., brain CT, skeletal survey) as required. In case of polytrauma, CT is the imaging of choice allowing a full work-up of all the organs. Rupture of pancreatic duct is an important issue which could be visualized either on CT or MR imaging (Fig. 16.5). This rupture must be treated, either surgically and/or endoscopically in order to restore duct continuity and suppress the enzymatic leak.
Fig. 16.5
Fracture of the pancreas in a 5-year-old boy. (a) CE-CT 3 mm cut reveals a hypodense fracture in the mid-body of the pancreas. (b) MR imaging T2-weighted FS: the contrast between normal pancreatic tissue and fracture is better seen on the 4 mm T2 FS. (c) MR imaging T1-weighted fat saturation postgadolinium injection
16.3.2.2 Biliary Lithiasis
Stones within the biliary tract appear on US hyperechoic with or without shadowing depending on their size and their content. On CT, the stones are either hyperdense or isodense. On MR imaging, they are better visualized on T2 sequences as hyposignal nodular structures in a dependent position. On T1-weighted sequences, depending on their composition, the signal can be highly variable (Fig. 16.6).
Fig. 16.6
Pancreatitis secondary to biliary lithiasis in a 7-year-old girl. (a) US: transverse scan through the head of the pancreas; the lithiasis appears as a hyperechoic pseudo-tumor with a large and layered structure with no posterior shadowing. (b) MR imaging T2- weighted sequence reveals a two layered hyposignal lesion within the distal common bile duct in the head of the pancreas
An underlying pathology is frequently associated, including congenital malformation of the bile ducts, hemoglobinopathies, parenteral nutrition, or short bowel syndrome.
16.3.2.3 Malformations
MRCP is the imaging technique of choice.
Pancreaticobiliary Junction Anomaly
A common biliopancreatic channel is defined by a junction of the common bile duct and the pancreatic duct outside the duodenal wall. Reflux of bile or stenosis of the pancreatic duct is responsible for the AP. US and MR imaging can demonstrate the anomalous junction within the head of the pancreas especially when the ducts are dilated [22] (Figs. 16.7 and 16.8).
Fig. 16.7
Acute pancreatitis secondary to common biliopancreatic canal (CBPC) in a 3-year-old girl. (a) US: Small arrow and small dashed arrow show the pancreatic ducts (main and accessory) joining the dilated common bile duct within an enlarged head of pancreas; large yellow arrow points to a small associated lithiasis within the CBD. (b) Percutaneous cholecystography confirms the CBPC with two separate abnormal junctions of the main and accessory ducts within a choledochal cyst. Note the associated congenital cystic duct dilatation
Fig. 16.8
MR imaging axial T2-weighted sequence on a 7-year-old boy with CBPC: The pancreatic and bile ducts jointo a CBPC (small yellow arrow) far from the ampulla, within the pancreatic head. Small dashed arrow reveals a lithiasis in hyposignal in a dependent position within the common bile duct
Pancreas Divisum
Absence of fusion between the ventral and dorsal pancreatic anlages results in absence of connection between the dorsal Santorini canal and the ventral main pancreatic duct. The Santorini drains the body and tail of the pancreas and ends within the minor papillae (Fig. 16.9). This anomaly is more prone to provoke AP.
Fig. 16.9
Pancreas divisum on MRCP. Coronal reconstruction. The main pancreatic duct joins the minor papilla while the common bile duct with the ventral pancreatic canal joins the major papilla in the duodenum wall
Duplication
Pancreatic duplication is a very rare malformation where the canal of the duplicated gland can be stenotic and responsible for AP. Imaging, either CT (Fig. 16.10) or MR imaging allows to ascertain the diagnosis.
Fig. 16.10
Duplication cyst connected to an ectopic pancreas as cause of recurrent acute pancreatitis—6-year-old girl. (a) US transverse scan showing a cystic mass with layered wall. (b) CE-CT—Reformatted coronal view—visualizes an abnormal duct with thickened wall below the pancreatic gland. (c) Percutaneous opacification of the duplication prior to surgery confirms a complete duodeno-pancreatic duplication with a duplicated pancreatic duct starting from the duplication cyst and joining the main duct in the tail of the pancreas
Annular Pancreas
This pathology can exceptionally be revealed by an AP. The visualization of pancreatic tissue around or on the right lateral side of the duodenum suggests the diagnosis. An abnormal pancreatic canal encircling the duodenum can also be demonstrated [23]. Lin et al. report [24] a review of 15 children with annular pancreas. In their series, 80% of patients presented associated malformations including malrotation (40%), intrinsic duodenal obstruction (33%), trisomy 21 (27%), and duodenal bands (27%).
16.3.2.4 Autoimmune Pancreatitis
Less than 30 cases of autoimmune pancreatitis have been published in children. Two types have been described. Type 2 is the most frequent in children and is associated with ulcerative colitis and a normal serum level of IgG4. It occurs in a younger population than in type 1. CT and MR imaging demonstrate a diffuse enlargement of the pancreatic gland, multifocal pancreatic duct narrowing, peripancreatic hypointense or hypodense rim, respectively, on MR imaging or CE-CT [25]. Other reported associated abnormalities include sclerosing cholangitis, renal mass or nephritis, retroperitoneal fibrosis, and submandibular masses. Rapid regression of imaging abnormalities under steroid therapy may confirm the etiological diagnosis.
16.3.3 Complications
16.3.3.1 Acute Complications
Within 4 weeks after the beginning of the AP.
A new classification of the complications based on their presentation before and after 1 week of the beginning of the AP is now in use in adults [27] but is not yet applied in pediatric practice.
Fluid Collections
Fluid collections present on imaging without a well-defined surrounding limit and with or without internal tissues. They are located close or at distance of the pancreatic bed.
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