**2. Acute pancreatitis**

Acute pancreatitis (AP) is an acute inflammatory condition with a range of severity and various local and systemic complications. The main etiologies are the presence of gallstones or alcohol abuse (75–80%); other causes are pancreatic tumors, traumatic or iatrogenic damage and drugs (thiazide diuretics, steroids, azathioprine). In 10–15% of patients, the cause is not identified [1].

The 2012 Revised Atlanta Criteria is an update of the 1992 original classification of AP and is aimed to clarify and improve the terminology of severity grading and local complications. AP is now divided into two distinct subtypes based on the presence or

the absence of parenchymal necrosis: necrotizing pancreatitis (NP) and interstitial edematous pancreatitis (IEP). Patients can develop four distinct collection subtypes that are identified based on the presence of pancreatic necrosis and the time elapsed since the pancreatitis onset (with 4 weeks as a threshold). Acute peripancreatic fluid collections (APFCs; <4 weeks) and pseudocysts (PSCs: >4 weeks) occur in IEP and contain fluid only. Acute necrotic collections (ANCs; <4 weeks) and walled-off necrosis (WONs: >4 weeks) occur only in NP and contain fluid with necrotic debris. APFCs and ANCs are acute complications and they may either resolve or persist, developing a mature wall to become delayed complications such as PSCs or WONs, respectively. In addition, any collection subtypes may become infected and may lead to other local or systemic complications [2, 3].

The pancreatitis severity scale has also been updated to improve the stratification and the management of patients; to the original categories of mild and severe AP, based on the presence of organ failure, a third moderately severe AP category has been added for patients with local complications, substantial morbidity and low mortality. A variety of imaging-based scoring systems can be applied to predict severity although they do not account for risk factors like obesity. The computed tomography severity index (CTSI) is the most commonly used and recommended scoring system, it combines the Balthazar grade with the extent of the pancreatic necrosis on a 10-point severity scale as shown in **Table 1**.

Radiological examinations offer various imaging modalities which play specific roles in the different phases of acute pancreatitis. In the early phase, during the first week after onset, imaging aims to establish the diagnosis, determine the etiology and stage the severity; in the late phase, imaging is needed to establish and monitor complications and to guide interventional procedures.

### **2.1 Imaging in the early phase**

The onset of pancreatitis is considered to coincide with the first day of pain; in the first week after onset, the imaging findings correlate poorly with the clinical severity, but they may be useful in assessing the cause of acute pancreatitis [1].

The 2012 Revised Atlanta Classification requires two or more of the following criteria to make a diagnosis of AP: a) abdominal pain suggestive of pancreatitis, b)


### **Table 1.** *Imaging-based scoring systems.*

### *Imaging of Pancreatitis DOI: http://dx.doi.org/10.5772/intechopen.106764*

serum amylase or lipase level greater than three times the upper normal value, c) characteristic imaging findings.

Thus, imaging in the initial diagnosis of AP is requested only if the other criteria are not conclusive for the diagnosis but is still necessary in the assessment of the cause of AP.

Ultrasound (US) is the primary imaging technique for the assessment of the biliary tract and should be performed in every patient to rule out gallstones; the examination can also show pancreatic swelling, dilatation of the pancreatic duct or secondary findings like gallbladder or choledochal wall thickening, pericholecystic fluid or fat stranding. The major disadvantage of US is the limited visibility of the pancreatic region because of the presence of overlying bowel gas; moreover, US is poorly accurate in delineating extra pancreatic inflammatory spread and in detecting intrapancreatic necrosis [4, 5].

The American College of Gastroenterology and the American College of Radiology appropriateness criteria recommend performing contrast-enhanced computed tomography or magnetic resonance imaging only in patients with an unclear diagnosis or who do not improve within 48–72 hours of admission [1]. In fact, early CT is indicated if a complication is suspected, even if parenchymal necrosis may be misdiagnosed due to edema and vasoconstriction. The use of a contrast medium is essential for detecting parenchymal necrosis and vascular complications; the standard examination includes an unenhanced phase, a pancreatic phase (delay of 40–50 s) and a portal venous phase (delay of 60–70 s). A monophasic CT protocol is usually sufficient for the diagnosis and the progression assessment, while dual-phase studies (arterial and portal venous) are recommended in case of suspicion of hemorrhage, mesenteric ischemia or arterial pseudoaneurysm or pancreatic mass [3, 5, 6]. In IEP imaging shows a focal or diffuse pancreatic enlargement and an entire parenchymal enhancement with no unenhanced areas (**Figure 1**), although enhancement may be less avid than that of the normal pancreas due to the interstitial edema.

### **Figure 1.**

*F, 64 yo, affected by an acute interstitial edematous pancreatitis; At CT a homogeneous decreased enhancement of the entire pancreas is appreciable with no evidence of non-enhancing areas (a); at the level of the tail, a peripancreatic collection is noticeable (b).*

**Figure 2.**

*F, 78 yo, affected by a biliary NP. The patient underwent a CT follow-up that showed a progressive lack of enhancement in the body-tail of the pancreas with large necrotic collections.*

Necrotizing pancreatitis (NP) account for 5–10% of all AP and in the early phase, pancreas can appear edematous and hypoenhancing like in IEP, then non-enhancing areas appear as a sign of pancreatic necrosis, which evolves over time (**Figure 2**). There are three subtypes of NP based on the distribution of the necrotic areas: pancreatic NP (5%) without peripancreatic collections, peripancreatic NP (20%) showing peripancreatic necrosis with collections of fluid and components, combined NP (75%) characterized by non-enhancing pancreatic areas and heterogeneous peripancreatic collections [1]. The different subtypes of NP can be observed in the same patient at different times (**Figure 2**).

CT shows the extension of the inflammatory process, but it has a limited capability of differentiating homogeneous fluid collection from debris within collections; moreover, CT has a limited capability of differentiating small necrotic areas from local effusions or focal adipose depositions in elderly people [7].

MRI is an alternative imaging technique especially indicated in case of renal failure, young patients and pregnant women; it is superior to CT in the characterization of pancreatic collections identifying the presence of debris or necrotic material, although its longer scanning time makes its use difficult in uncooperative patients. Moreover, it is useful in the diagnosis of AP when other criteria are inconclusive and US is still uncertain, thanks to its superior sensitivity to pancreatic edema (**Figure 3**). MRI, especially with cholangiopancreatography (MRCP) shows high sensitivity and specificity for choledocholithiasis or congenital anomalies which can explain the AP.

MRI features of IEP include a slight parenchymal hypointensity on T1WI and hyperintensity on T2WI. There may be acute peripancreatic fluid collections showing patchy-like hyperintensity on T2WI in the peripancreatic region, pararenal spaces and lesser omental bursa. Diffusion-weighted imaging (DWI) technique allows a better appreciation of slight pancreatic edema (**Figure 3**).

After contrast agent administration, the pancreas shows homogeneous enhancement. In NP the necrotic areas are hypointense on T1WI, hyperintense on T2WI and have no enhancement after contrast medium. Collections around the pancreas show mixed intensity on T1WI and T2WI, but no enhancement [3, 8].

### **2.2 Imaging in the late phase: follow up and complications**

Imaging is most useful if performed 5–7 days after the onset of AP, when pancreatic necrosis, collections and local complications are distinguishable. The Revised Atlanta

### **Figure 3.**

*F, 74 yo with the diagnosis of IEP. Patient with 8x increase of lipase and amylase, pain, gallbladder calculi (a) but a normal-sized pancreas at US (b). At CT (c) no significant alterations of the pancreatic parenchyma are appreciable, but a slight peripancreatic fluid collection in the tail. At MRI, a slight peripancreatic fluid collection is appreciable with different sequences: T2 (d), DWI and ADC map (f, g, h), while pancreatic parenchyma does not show significant alterations at T1WI (e). With DWI, slight parenchymal edema is appreciable in the tail; gallbladder calculi (i).*

Criteria distinguishes the collections that contain purely fluid in IEP from the collections that contain also necrotic debris in NP. The distinctions for classifying collections are the time course (≤ 4 or > 4 weeks from the onset of pain) and the presence of necrosis at imaging [1].

APFCs are diagnosed during the first four weeks in patients with IEP; they are peripancreatic homogeneous fluid collections without a wall and tend to conform to the retroperitoneal spaces (**Figure 4**). When a similar collection is seen within the pancreatic parenchyma, it is by definition an ANC and the diagnosis is NP. At MRI APFCs are homogeneously hypointense on T1WI and hyperintense on T2WI [1, 8]. Most APFCs resolve spontaneously, the drainage should not be performed because of

### **Figure 4.**

*M, 49 yo. CT images show acute peripancreatic fluid collections (a) within four weeks from the onset of interstitial edematous pancreatitis and the development of a pseudocyst four weeks later (b).*

the risk of infecting a sterile collection. Pseudocyst develops in fewer than 10% of IEP when an APFC does not resolve within four weeks and becomes more organized with a wall containing only fluid (**Figure 4**); it is called pseudocyst because lacks a true epithelial tissue. At MRI pseudocysts are uniformly hyperintense on T2WI, with no solid components or debris, and have a thin smooth wall; they may have a connection to the ductal system.

ANCs are poorly organized necrotic collections that develop in NP within the first four weeks of symptoms; they are usually found in the lesser sac, in the pararenal spaces or extended into the pancreatic parenchyma with a lobulated appearance and containing solid or fat debris (**Figure 5**). Any collection associated with an NP should be termed an ANC, even if it is homogeneous without debris. At MRI, ANCs show mixed signals on T1WI and T2WI, with flocculent unenhanced low signal necrotic areas [1, 3, 8]. WON is an ANC that after four weeks develops a thick enhancing wall containing fluid and debris of necrotic fat or pancreatic tissue (**Figure 5**); it may be confined to the pancreatic parenchyma or be in the peripancreatic space. At MRI, a WON shows a well-defined T2-hypointense, gadolinium-enhancing wall and contains non-liquid substances floating [1, 3, 8]. Differentiating a pseudocyst from a WON is important because WON does not respond to endoscopic cyst gastrostomy, but requires surgical debridement [3]. A pseudocyst is peripancreatic with homogeneous

### **Figure 5.**

*F, 83 yo. CT follow-up of a patient with necrotizing pancreatitis showing the progression over time from an acute necrotic collection (a) to walled-off necrosis (b); the late infection of the collection (c) required surgical intervention.*

### *Imaging of Pancreatitis DOI: http://dx.doi.org/10.5772/intechopen.106764*

fluid, while WON contains necrotic material and can involve both pancreatic and peripancreatic tissue. MRI outperforms CT in the assessment of fluid and necrotic debris in the collections for planning interventions [7].

Any collection can be sterile or infected, the only imaging finding of infection is the presence of gas appearing as multiple small bubbles scattered throughout the collection (**Figure 5**). According to some authors, MRI with DWI shows high sensitivity (100%) and specificity (91%) in detecting infection of collections, even when CT is doubtful due to the lack of bubble gas. On the ADC map the collection shows a target appearance, bright at the center and black at the periphery of the collection, with a similar appearance to a hepatic abscess [9].

The imaging-guided aspiration of fluid collections or the fine-needle aspiration of necrotic tissue can help to diagnose the infection before invasive surgery but can cause iatrogenic infection. Percutaneous drainage is preferred to the fine-needle aspiration because the culture of the fluid can be easily performed; the fine-needle aspiration remains helpful when clinical and imaging findings are confusing [1, 3].

### **Figure 6.**

*F, 56 yo with upper gastrointestinal bleeding a month after acute pancreatitis onset; CT detected a pseudoaneurysm of the superior pancreaticoduodenal artery due to walled-off necrosis (a, b). The patient underwent an emergent percutaneous angiography that confirmed the extravasation of the contrast medium (c) and selective embolization of the culprit branches (d).*

Pancreatic collections may have an extrapancreatic spread resulting in intrasplenic collection or abscess, splenic infarction or intrasplenic hemorrhage; similar complications may occur in the liver. In these cases, the pancreatic enzymes may extend into the mesenteries and can cause bacterial translocation, bowel ischemia and perforation. Moreover, necrotic collections can erode the bowel wall (especially the wall of the colon and duodenum in 4% of NP) and create a pancreatic-enteric fistula that also manifests gas bubbles in infected collections. Renal involvement is usually due to the inflammatory spread to pararenal spaces, the left space is the one commonly involved by vascular abnormalities [10].

Other main complications are due to the involvement of vascular structures and can lead to developing portal system thrombosis or arterial pseudoaneurysms. Splenic vein thrombosis is the most common complication and may result in gastric varices or splenomegaly [3]. Arterial pseudoaneurysms can lead to life-threatening hemorrhages when the extravasated pancreatic enzymes erode the walls of splenic, pancreaticoduodenal or gastroduodenal arteries [3]. In these cases, the interventional radiology approach is recommended to perform fast and selective vessel embolization with coils or glue (**Figure 6**).
