Imaging and Intervention in Acute Pancreatic Conditions 5.6

Chapter

G. Mansueto, D. Cenzi, A.A. Gumbs, M. D’Onofrio

Contents 5.6.2 Pancreatic Infections 5.6.1 Introduction ...... 493

5.6.2 Pancreatic Infections ...... 493 Infection is the most serious risk factor in patients suffer- 5.6.2.1 Diagnosis of Pancreatic Infection ...... 493 ing from pancreatic inﬂammatory diseases. The early de- 5.6.2.2 Percutaneous Management tection of this complication is extremely important, be- of Pancreatic Infection ...... 499 5.6.2.3 Results of Percutaneous Management cause interventional or surgical rather than medical treat- of Pancreatic Infection ...... 502 ments are necessary (Farthmann 1993).

5.6.3 Involvement of Adjacent Organs, Structures and Spaces ...... 503 5.6.3.1 Gastrointestinal Obstruction ...... 503 5.6.2.1 Diagnosis of Pancreatic Infection 5.6.3.2 Splenic Involvement ...... 504 5.6.3.3 Pancreatic Fistulas ...... 504 Infected pancreatic necrosis, pancreatic abscess, and infected pseudocyst are three different forms of pancreatic 5.6.4 Vascular Involvement ...... 510 5.6.4.1 Diagnosis and Embolization Therapy infection (Procacci et al. 2002). They differ in etiological of Arterial Lesions ...... 510 clinical and pathological characteristics (Bradley 1993), 5.6.4.2 Diagnosis and Management and this distinction is important as it inﬂuences the thera- of Venous Complications ...... 517 peutic management (Morgan et al. 1997). References ...... 519

Infected Pancreatic Necrosis Infected pancreatic necrosis is defined as infected pancre- 5.6.1 Introduction atic and/or peri-pancreatic tissue (Balthazar et al 1994). It can occur only in those patients suffering from severe Non-traumatic pancreatic emergencies can occur as a con- acute pancreatitis. Its incidence varies between 30 and 70% sequence of primary pancreatic pathologies (acute and (Beger et al. 1997), but 80% of patients affected by acute chronic pancreatitis,tumors) or secondary to intervention- pancreatitis (AP) die secondary to septic complications al or surgical therapy. following infection of the pancreatic necrotic tissue (Beger Acute pancreatic conditions are represented by pancre- et al. 1997; Robinson and Sheridan 2000). Infection is due atic infections, involvement of adjacent organs, structures mainly to Gram-negative bacteria, especially E. Coli and and spaces, and vascular complications. The role of radiol- Enterococcus. Infections from anaerobic bacteria or fungi ogy in the management of these complications is twofold: are much less common (Beger et al. 1997). Contamination firstly, it must identify the lesion, diagnose and define the is usually due to diapedesis through the colonic wall, lesion’s topographic characteristics; then it must proceed whereas hematogenous or biliary infection due to bile re- with treatment. Specifically, whenever an interventional flux in the pancreatic duct is rare (Reber 2001). Infection procedure is preferable to surgery or when it would opti- rates correlate proportionately with the seriousness of the mize surgical results. acute pancreatitis,as measured by Ranson’s criteria and CT In this chapter, all pancreatic complications with “emer- findings. Infection in acute pancreatitis has been reported gency” characteristics are taken into account with the ex- to be as high as 58% in cases with five or more Ranson’s ception of hepatobiliary involvement, which is discussed in criteria signs (Laws and Kent 2000). a previous chapter. Because infected pancreatic necrosis reaches a peak 15–20 days after the onset of clinical acute pancreatitis (Laws and Kent 2000), it is, therefore, clinically important to 494 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 1a–d. Infected pancreatic ﬂuid collection. a, b Axial ultra- phase, displays a large collection, surrounding the pancreas and sound scans highlight a hypoechoic collection (calipers) with occupying the lesser sac (c) and the left anterior pararenal space necrotic debris (arrow) in front of the pancreas (P) c, d Another (arrows in d). (From Procacci et al. 2002) case. Computed tomography, in the arterial contrastographic

suspect it. If the infection sets in earlier, the septic phase su- a dilated gallbladder when located in the latter’s area. The perimposes the toxemic one so that the two are clinically in- CT can indicate the presence and the extent of the necrotic distinguishable; however, fever with acute necrotic pancre- collections, as well as their topographic location (Balthazar atitis must lead to the suspicion of infection.A prompt diag- 1989; Laws and Kent 2000; Siegel and Sivit 1997). The site nosis is mandatory to prevent septic shock, which is the and extent of the necrosis correlates with the seriousness of natural evolution of untreated infection. Septic patients die the disease (Kemppainen et al. 1996). The CT shows one or of multiple organ failure (MOF). The death rate of nontreat- more hypodense collections which do not change after ed infected necrosis is 100% (Lumsden and Bradley 2000). contrast medium administration (Fig. 2a). Infection is Ultrasonography can demonstrate the collection suspected only in the presence of gas bubbles within the (Fig. 1a,b), but the exploration of the pancreatic area is collections (Fig. 3a,b). Nevertheless, this sign is not patho- often hindered by intestinal meteorism. A CT exam is the gnomic of this complication, and it occurs in no more than gold standard imaging technique in acute pancreatitis: the 20% of cases as a consequence of infection due to anaero- collections have an irregular morphology, conform to the bic bacteria (Balthazar 1989; Siegel and Sivit 1997; Laws anatomic space in which they reside, and frequently cross and Kent 2000). Furthermore, the presence of gas related to the lesser sac, the left anterior pararenal space, the trans- sterile necrosis has also been reported, even though it is an verse mesocolon or the mesenteric root (Fig. 1c,d). False- extremely rare condition (Gandini et al. 1996). A definitive negative exams are extremely rare: a fluid collection is very diagnosis of infected pancreatic necrosis can only be ob- seldom misinterpreted as a fluid-filled intestinal loop or as tained by means of needle aspiration (Fig. 3c). When the Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 495

Fig. 2a–c. Infected pancreatic necrosis. a A CT scan in the contrastographic phase demonstrates a hypodense area (arrow) in the cephalic site, hypovascul- arized, compatible with necrosis. b, c On a T2-weighted MR sequence, it is possible to distinguish the hyperintense ﬂuid component from the hypointense necrotic tissue (arrowheads)

purulent nature of the aspirated ﬂuid is not clear, a culture to establish the collection’s degree of ﬂuidity. In fact, the must be carried out (Balthazar 1989; Farthmann 1993; presence of necrotic debris or of actual infected parenchy- Siegel and Sivit 1997; Apte et al. 1999; Laws and Kent 2000). mal sequestrations makes surgery necessary, since it is im- In order to make a therapeutic decision, it is also necessary possible to remove them by means of percutaneous 496 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 3a–c. Infected pancreatic necrosis. a, b The CT scans in the contrastographic phase show a large ﬂuid collection occupying pancreatic body and tail. The presence of multiple gas bubbles demonstrate the infection of pancreatic necrosis. c Another case. A CT-guided needle aspiration of a small collection without gas, located under the pancreatic head (c). (From Procacci et al. 2002) Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 497

Fig. 4. Pancreatic abscess. A CT scan, in the contrastographic phase, highlights a voluminous mainly liquid hypodense collection bordered by a thin dense capsule; within it, multiple gas bubbles are seen

drainage (Bassi 1994; Rau et al. 1997). Defining the collec- et al.1997; Siegel and Sivit 1997; Gervais et al 2001).To date, tion’s content is difficult with CT (Fig. 2a), whereas it is MR is the most reliable investigation in this respect, as it more easily obtainable with MR (Fig. 2b,c). On T2-weight- can better characterize the internal consistency of collec- ed sequences it is possible to distinguish the hyperintense tions (Fig. 3b,c) (Morgan et al. 1997). infected fluid from the necrotic tissue,which appears clear- The post-operative abscess occurs as a complication of ly hypointense (Morgan et al. 1997). the dehiscence of intestinal or biliary pancreatic anasto- moses and has the same imaging features (Berberat et al. 1999; Gervais et al 2001). A pancreatic abscess complicates Pancreatic Abscess the post-operative course in 10% of patients who undergo A pancreatic abscess is defined as a well-circumscribed pus pancreatoduodenectomy. Post-operative abscesses can collection that occurs in areas of limited pancreatic necro- have a peripancreatic location or develop in the peritoneal sis, which has become infected (Farthmann 1993; Siegel spaces, and can be found in the sub-diaphragmatic, sub- and Sivit 1997; Ferrucci and Mueller 2003; Maher et al. hepatic, or pelvic space (Berberat et al. 1999; Gervais et al 2004). Multiple abscesses occur in about 30–39% of cases. 2001). Abscesses can arise as a consequence of acute pancreatitis or pancreatic surgery. It occurs in about 3% of patients affected by severe acute pancreatitis, so that it is much less Infected Pseudocyst common than infected necrosis (Bradley 1993). Infected pseudocyst is a collection of infected fluid within An abscess secondary to acute pancreatitis probably a fibrous capsule located in the pancreatic area. The supra- starts off as infected pancreatic necrosis. The pathogenic infection of a pseudocyst is an uncommon condition and a agents are mainly of intestinal origin, as in infected necro- high index of clinical suspicion is extremely important for sis. The progressive necrotic tissue liquefaction leads to the the definitive diagnosis.Most of the patients suffering from formation of a mainly liquid collection of pus and pancre- infected pancreatic pseudocyst are septic. Pseudocyst can atic secretion. be recognized by ultrasound (Fig. 5a) or CT (Fig. 5b). Diag- An abscess appears later than infected necrosis, usually nosis of infection is possible at imaging if gas bubbles are after the fourth week with fever and leukocytosis (Farth- present in the pseudocyst (Fig. 5c,d). When there are no mann 1993; Beger et al. 1997; Siegel and Sivit 1997), and is gas bubbles inside the fluid collection, only fluid aspiration usually preceded by a period of relative well-being, albeit can provide the exact diagnosis. short. Pseudocysts can communicate with the pancreatic duc- Computed tomography shows a mainly liquid hypo- tal system. Demonstrating this communication, by means dense collection on the pancreatic gland, outlined by a of CT or endoscopic retrograde cholangiopancreatograph- thin, dense wall (Fig. 4). The differential diagnosis between ic (ERCP) examinations (Fig. 6), is important for therapeu- infected necrosis and the abscess is important, since the tic planning, negatively influencing the results of percuta- latter has a better prognosis and most often can be success- neous treatment (Bradley and Warshaw 1993; Mithöfer et fully treated with percutaneous catheter drainage (Morgan al. 1997). 498 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 5a–d. Infected pseudocyst. a–b On axial US (a) and CT (b) wall. c, d Another case. On CT scans carried out in the venous con- scans, taken at the pancreatic tail level, a bilobed anechoic forma- trastographic phase,a large pseudocyst with gas bubbles is present tion with well-deﬁned margins is seen, delimited by a thin ﬁbrous in front of the pancreas. (From Procacci et al. 2002)

Fig. 6 a–c. Infected pseudocyst communicating with the main and uncinate process, with thick walls, are evident. An ERCP (c) duct. On contrast-enhanced CT scans (a, b) a slight dilation of the displays the communication between the duct of Wirsung (arrow) duct of Wirsung (arrow),and a voluminous pseudocyst of the head and the infected pseudocyst (asterisk). (From Procacci et al. 2002) Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 499

(Lee et al. 1998; Laws and Kent 2000). However, the percuta- 5.6.2.2 Percutaneous Management neous approach is awarded an important additional role, of Pancreatic Infection since, when used as a first step, it can make the subsequent surgical “debridement,” if required, definitive (Baril et al. Percutaneous catheter drainage is a well-established inter- 2000). ventional option in the management of pancreatic infection. As a general rule, the more infected pancreatic collection contents are viscous and corpuscular, necessitating Pancreatic Abscess and Infected Pancreatic Pseudocyst larger-sized catheters, preferably with a double-lumen Percutaneous drainage under the guidance of imaging is sump and large-bore diameter (vanSonnenberg et al. 1991; highly efficient in the treatment of both pancreatic abscess vanSonnenberg et al. 1997; vanSonnenberg et al. 2001; Fer- and infected pseudocyst (Siegel and Sivil 1997; Morgan et rucci and Mueller 2003; Maher et al. 2004; Shankar et al. al. 1997; Laws and Kent 2000; Robinson and Sheridan 2004). 2000). The mainly fluid content and the fact that this lesion is frequently solitary explains the great clinical success of this procedure. Percutaneous drainage can be carried out Infected Pancreatic Necrosis under US or CT guidance (Berberat et al. 1999), although In cases of infected pancreatic necrosis, surgical “debride- CT is usually preferable, especially where deep lesions are ment” should be the treatment of choice. Percutaneous ap- concerned (Fig. 9c,d). On the whole, the shortest and most proaches should be considered in patients at high surgical direct access route to the pancreas is preferable, avoiding risk. It is difficult to completely remove the infected necrot- involvement of the neighboring structures. When going ic debris and the parenchymal sequestrations by means of through a viscus is inevitable, the trans-gastric approach percutaneous drainage (Farthmann 1993; Morgan et al. is preferable. Positioning of the drain, usually single, can 1997; Beger et al. 1997; Robinson and Sheridan 2000; Laws be carried out with the Trocar technique, or, less often, and Kent 2000; Ferrucci and Mueller 2003). The treatment the Seldinger technique (Gervais et al. 2001). The latter is must be planned and carried out under CT guidance. At better for positioning larger-sized catheters. Usually, we least two collection catheters have to be placed in the most start with a small catheter, substituting it with a larger appropriate positions to obtain a combined washout one later. The size of the catheters used varies from 12 (Fig. 7). The Trocar technique is the best, initially using to 14 F, preferably of the double lumen type (Lee et al. 8 to 10 F catheters.When the subcutaneous drainage chan- 1998). The timing of catheter removal is decided on by nel has consolidated, it is easier to position larger catheters evaluating the drainage parameters (reduction of the out- with the Seldinger technique under fluoroscopic control put) and the imaging aspects (considerable reduction or (Fig. 8).The size of the catheters used varies from 20 to 24 F collapse of the cavity). Even in the remission period, before (Lee et al. 1998), up to 30 F (Fig. 9a,b) (Balthazar et al. removing the drainages, fluoroscopic or CT contrasto- 1994). The “debridement”procedure typically needs a great graphic study through the drainages must be performed to deal of washout fluid. A long-term aftercare catheter detect any communication with the main pancreatic duct. drainage follows with frequent irrigation, periodic de- The presence of a connection would considerably increase bridement and strict monitoring of the catheter output the risk of relapse (Gervais et al.2001; Ferrucci and Mueller (Freeny et al. 1998; Echenique et al. 1998; Ferrucci and 2003). Mueller 2003; Shankar et al. 2004; Maher et al. 2004); how- A sample of the fluid is taken during the procedure to ever, even with several large-sized catheters, further de- assess for the presence of amylase,which would indicate a bridement and scrupulous aftercare catheters, the necrotic communication with the duct of Wirsung. The presence component is always difficult to remove completely and the and the extent of the communication with the main pan- necrotic debris often perpetuates the infection and hence creatic duct have important consequences for the percuta- the septic condition. Early studies in selected patients have neous treatment. A slight communication with the sec- shown promise using percutaneous basketing (or other ondary ducts indicates that watchful waiting may lead to percutaneous devices such as snares and forceps) and me- resolution of the lesion, whereas communication with the chanical removal of solid debris to treat necrosis. Clinical duct of Wirsung that is associated with a downstream ob- success rates have generally varied between 40 and 60%, struction can lead to the development of an external pan- but they require refinement and evaluation in larger pa- creatic fistula and/or a relapse in the pancreatic collection. tient populations before they can be widely used in clinical In these cases the surgical approach is mandatory (Lee et practice (Shonnard et al. 1997; Carter et al. 2000; Maher et al. 1998). In treating pancreatic abscess or infected pseudo- al. 2004; Shankar et al. 2004). For this reason, both the sur- cyst communicating with the main pancreatic duct, the gical and radiological literature are in general agreement endoscopic approach by means of trans-papillary drainage that surgical debridement is the best treatment modality has been reported (Venu et al. 2000). 500 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 7a–e. Combined percutaneous and endoscopic drainage of infected ﬂuid collection. a, b Computed tomography, carried out in the venous contrastographic phase, shows a huge pancreatic necrotic collection extending from the lesser sac to the left anterior para-renal space. c–e After combined percutaneous and endoscopic treatment, the CT scan in the cranial position (c) demonstrates the transgastric catheter, introduced endoscopically inside the collection which appears notably reduced in size. In the caudal scan (d), the catheter placed percutaneously under CT guidance in the more sloping portion of the collection is recognizable. The position of the two drainages is better deﬁned in the CT topogram (e). (From Procacci et al. 2002) Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 501

Fig. 8 a–e. Percutaneous drainage of pancreatic infection. a The CT guidance with a larger-sized one (14 F) using the Seldinger CT scan shows percutaneous drainage (arrow), of small caliber technique under ﬂuoroscopic control in the latero-lateral projec- (8 F), placed under CT guidance in the collection located at the tail tion. (From Procacci et al. 2002) of the pancreas. b–e Exchange of the drainage positioned under 502 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 9 a–d. Percutaneous drainage of pancreatic infection. a, b First pseudocyst of the pancreatic tail in which the distal extremity of case. The CT scans show large caliber percutaneous drainage posi- the percutaneous drainage is seen (arrows). In the more caudal tioned through anterior transgastric access, and with its extremity scan (d) it is evident that the CT guidance has allowed for the po- lodged inside the infected necrotic collection located at the left an- sitioning of the drainage through the only possible pathway above terior para-renal space. c, d Another case. Computed tomography, the left colic ﬂexure. (From Procacci et al. 2002) in scans carried out in the contrastographic phase, shows infected

5.6.2.3 Results of Percutaneous Management the percutaneous treatment of pancreatic abscess vary of Pancreatic Infection from 32 to 90%, and is <50% in infected necrosis (Table 1). The percutaneous approach under radiographic guidance has a low occurrence of complications (Ferrucci and The results of radiological treatment reported in the litera- Mueller 2003). The worst is acute bleeding caused by the ture vary greatly depending on the different types of loss of the compression that the distended collection had lesions treated. The ﬂuidity of the infected contents ex- on the arterial and venous vessels involved. Location and plains the different success rates reported in the literature. treatment of this acute vascular complication is often pos- Percutaneous drainage of infected pseudocysts has a clini- sible during an angiographic examination, as described cal success rate of more than 90%, whereas the results for later.

Table 1. Clinical success rates of percutaneous drainage for pancreatic infection

No. of patients No. of necroses No. of abscesses No. of pseudocysts Success (%)

Freeny et al. (1998) 34 34 – – 47 Carter et al. (2000) 14 14 – – 86 Steiner et al. (1988) 25 – 25 – 32 Lee et al. (1992) 30 – 41 – 47 Stanley et al. (1988) 14 – 16 – 64 Freeny et al. (1988) 23 – 23 – 65 Adams et al. (1990) 58 – 58 – 79 vanSonnenberg (1997) 59 – 80 – 86 vanSonnenberg et al. (1989) 48 – – 48 94 Cantasdemir et al. (2003) 30 – – 30 96 Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 503

Bowel involvement can occur via a compressive mecha- 5.6.3 Involvement of Adjacent Organs, nism, usually due to a voluminous collection or pseudocyst Structures and Spaces (Fig. 10a,b). If the diameter is particularly large, the compression can be marked: in this case, radiology is necessary Pancreatic inflammatory diseases often involve adjacent or- to not only demonstrate the cause of obstruction, but also gans and structures. The strict relationship of the pancreat- to proceed with percutaneous drainage (Fig. 10c,d), as a ic head with the duodenum and the common bile duct, of temporary solution while awaiting surgery. the pancreatic body with the anteriorly lying transverse Visceral stenosis can be a sign of neoplastic infiltration colon, the splenic flexure to the left, and of the pancreatic of the viscus, more commonly due to ductal adenocarcino- tail with the splenic vessels and hilum explains the frequent ma or the late complication of a severe AP. In this latter involvement of these structures in pancreatic diseases. condition,stenosis can occur secondary to the fibrous reaction of the viscus on reabsorbing the fluid collection located in the transverse mesocolon or in the left anterior 5.6.3.1 Gastrointestinal Obstruction pararenal space. In the past, diagnosis of stenosis or obstruction was obtained by direct examination of the ab- An acute intestinal obstruction, high or low depending on domen (signs of intestinal blockage) and/or with the con- the structure involved, is very rare in pancreatic diseases. trastographic study of the digestive tract. It was possible to Stenosis of the digestive tract with the consequent delayed show not only the compression due to voluminous masses, emptying is more common (Safrit and Rice 1989). but also the nature of the stenosis, whether fibrotic (un-

Fig. 10a–d. Percutaneous drainage of the pseudocyst responsible percutaneous drainage, show the considerable reduction in vol- for duodenal stenosis. a, b The CT scans show a voluminous pan- ume of the pseudocyst within which the end of the drainage is vis- creatic pseudocyst, causing compression of the duodenal route ible (arrow). The drainage runs between the liver and the stomach. (arrowheads). c, d The CT scans, carried out after positioning the (From Procacci et al. 2002) 504 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

damaged mucosa) or neoplastic (parietal infiltration). ered an emergency because of the severity of the basic dis- Presently, CT can demonstrate the cause of obstruction ease (severe AP, ductal adenocarcinoma) or the clinical and its relationship to the viscus involved. condition (sepsis), even though it often represents a serious complication. There are also fistulas that can appear acute, such as the pancreo-mediastinal and pancreo-pleur- 5.6.3.2 Splenic Involvement al fistulas, characterized by thoracic pain and dyspnea; or the intra-peritoneal fistula, which gives acute abdominal During pancreatic inflammatory disease, splenic involve- pain and ascites (Cole and Bradley 1992). ment is rare (from 1 to 5%) and includes intrasplenic Pancreatic fistulas can be distinguished into two differ- pseudocyst, abscess, hemorrhage, infarction and splenic ent groups: internal and external ones, characterized by rupture (Fishman et al. 1995). Since these complications different etiological mechanisms and clinical manifesta- can be life threatening, the extent and course of the disease tions. The radiological approach to pancreatic fistulas dif- are closely followed up with CT, to determine if, and when, fers significantly when dealing with internal or external aggressive intervention is necessary to avoid catastrophic ones. Internal fistulas are often an incidental finding at clinical outcomes (Fishman et al. 1995). Both mechanisms imaging, even though they are characterized by serious of splenic involvement in pancreatitis are possible: indirect symptomatology, whereas external fistulas can be diag- and direct. Indirect involvement of the spleen may occur nosed by examination of the quantitative and qualitative either by damage to splenic vessels (vascular involvement) characteristics of the fluid and require imaging to supply or by lytic action of necrotic hemorrhagic collections on the extension of the lesion (Pistolesi et al. 1992). The thera- the peritoneal layer of the spleen (Fig. 11). Direct involve- peutic approach is also different for both cases (Sunder- ment of the spleen is less common (Pistolesi et al.1987) and land and Imrie 1992). occurs through the lieno-pancreatic ligament, which is the only pathway through which both acute and, above all, chronic pancreatic processes directly penetrate into the Internal Pancreatic Fistula spleen (Fig. 12a–c). Internal pancreatic fistula is quite rare and due to the com- Intrasplenic pseudocyst is a homogeneous fluid collec- munication of the pancreatic duct with other structures tion at the central or sub-capsular location. Diagnosis and spaces (Cole and Bradley 1992). is easy with CT, which demonstrates the fluid density The digestive fistula, pancreatico-digestive fistula, is (Fig. 12d–f). more common.In this case,the proteolytic action of the ac- Splenic hemorrhage and hematoma arise from erosion tivated pancreatic enzymes, coming out of the duct or pre- by activated pancreatic enzymes of small intrasplenic ves- sent in a peripancreatic collection, are the cause of intesti- sels, preserving capsule integrity. In this case, faced with an nal wall erosion. This is sometimes due to necrosis, sec- ultrasound diagnosis of an intra- or peri-splenic fluid col- ondary to inflammatory thrombosis. The pancreatico-colic lection, CT and MR immediately demonstrate the hemor- fistula is clinically the worst due to frequent infection and rhagic content of the collection (Fig. 13).If the hemorrhage bleeding complications, with a mortality rate of around is massive, laceration and capsular disruption may occur. 50%. On the contrary,the pancreatico-gastric or pancreati- Splenic rupture results from the erosion of the capsule co-duodenal fistula can paradoxically appear with an im- by activated pancreatic enzymes, and appears with hemo- provement in the clinical picture (De Baker et al. 2001). peritoneum. Although small splenic parenchymal lesions, Demonstration of the pancreatico-digestive fistula is such as small intra-splenic pseudocysts or subcapsular achievable during a contrast study of the digestive tract.This hematomas, probably heal themselves spontaneously, the investigation can be justified by the suspicion of such a com- risk of splenic disruption requires surgery. The early detec- plication on the basis of symptoms and, above all, CT recog- tion of direct splenic involvement is extremely important nition of gas in the pancreatic collection (Fig. 14a) in the ab- to determine the need for immediate splenectomy, thus, sence of sepsis (Pistolesi et al. 1992). Currently, diagnostic avoiding hemorrhagic life-threatening complications. confirmation with ERCP can be made with MRCP,especially using secretin stimulation, which demonstrates the site of the ductal rupture and eventually the fluid collection and/or 5.6.3.3 Pancreatic Fistulas the viscus involved (Fig. 14b,c) (Bohlman et al. 1976). Intra-peritoneal fistula results from the pancreatic col- Fistulas are increasing in incidence as a consequence of the lection’s erosion through the peritoneal parietal layer and considerable increase in the number of major pancreatic can cause the intra-peritoneal spreading of pancreatic juice surgical procedures. Furthermore, the improvement in (Cole and Bradley 1992) , with the appearance of pancreat- imaging techniques, especially CT, can give the diagnosis ic ascites. The hepatic origin of ascites can be excluded or at least the suspicion of pancreatic fistula. This is partic- with paracentesis and amylase dosage (Cameron et al. ularly true for internal fistulas, which often went unrecog- 1976). At imaging the drastic and sudden volumetric re- nized in the past. Pancreatic fistula is not usually consid- duction of an intra- or peripancreatic pseudocyst, in the Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 505

Fig. 11a–f. Indirect involvement of the spleen. a–c In the scheme hilum of the enlarged spleen. d–f In the scheme (d) ﬂuid collection (a) the pseudocyst of the pancreatic tail compresses the splenic of the pancreatic tail surrounds the splenic vessels. The CT scans vascular penducle. The CT scans in the arterial contrastographic in the arterial contrastographic phase (e, f) display a necrotic col- phase (b, c) highlight a pseudocyst at the pancreatic tail, causing lection without capsule, involving the splenic hilum and the lower dislocation and compression of the vascular structures of the pole of the spleen (a,d–f). (From Procacci et al. 2002)

Fig. 12a–f. Direct involvement of the spleen. a–c In the scheme (a) ment, with development of intra-splenic pseudocyst. The CT scans, the collection dissects, through the spleno-pancreatic ligament, the in the arterial contrastographic phase,highlight a pseudocyst at the visceral peritoneal layer, settling itself in the subcapsular area. The pancreatic tail,causing dislocation and compression of the vascular CT scans in the venous contrastographic phase (b, c) show the sub- structures of the hilum of the spleen (e). A ﬂuid hypodense collec- capsular ﬂuid collection. d–f In the scheme (d) the collection pene- tion is inside the spleen, inducing the suspicion of development of trates the splenic parenchyma through the spleno-pancreatic liga- an intrasplenic pseudocyst (f) (From Procacci et al. 2002) 506 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 13a–f. Intrasplenic pseudocyst and pancreatic tail bleeding tensity is due to the hemorrhagic content. In fact, the pancreatic pseudocyst in chronic pancreatitis (same case as in Fig. 12e,f). a–d tail pseudocyst has eroded the left gastroepiploic artery and has In MR sequences, a pancreatic tail pseudocyst has eroded the been transformed into a bleeding pseudocyst. The arterial lesion splenic hilum creating a voluminous intra- and peri-splenic ﬂuid (arrow) is clearly highlighted at angiography, which also demon- collection, which appears hyperintense both on T1-weighted fat strates the subcapsular location of intrasplenic pseudocyst (aster- suppression (a, b) and on T2-weighted images (c, d). The hyperin- isks in e, f) Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 507

Fig. 14 a–c. Pancreo-digestive internal fistula. a A CT scan in the arterial contrastographic phase demonstrates voluminous pancreatic collection with gas bubbles in a nonseptic patient, a direct sign of pancreo-digestive fistula. b, c Another case. The MRCP,carried out after secretin stimulation, highlights well the duct of Wirsung 1 min after stimulation (b), and the colon at the splenic flexure level 15 min after stimulation (c), confirming the communication between the main pancreatic duct and the viscus. (From Procacci et al. 2002) 508 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 15a–f. Complicated retroperitoneal internal fistulas. a–c Pan- pancreas which imprints the kidney; 2 years later, CT scan (e) creo-pleural fistula. Computed tomography scans carried out in shows the persisting pseudocyst impression on the kidney. There the cranio-caudal direction after contrast medium administration is concomitant dilation of the duct of Wirsung and a large calcifi- document the presence of pleuritis which assumes a sac-like ap- cation at the body–tail passage. After 4 years, CT (f) highlights the pearance in the para-mediastinal area (a),and the fluid-containing kidney’s direct involvement with the pseudocyst situated inside fistulous link situated between the diaphragm (b) and the body of the renal capsule and the consequent serious parenchymal com- the pancreas (c). d–f Pancreo-renal fistula. A CT scan in the con- pression. (From Procacci et al. 2002) trastographic phase (d) highlights a pseudocyst at the tail of the

presence of ascites,should induce the suspicion of an intra- pleura with the onset of a pancreatico-pleuro-bronchial peritoneal fistula. The ERCP,when able to directly demon- fistula (Iglehart et al. 1986). strate the rupture of the duct of Wirsung into the peri- Small retroperitoneal fistulas can be found by chance at toneum, is definitive for the diagnosis. CT examination required to define the cause of acute pain; Sometimes the fistula can develop in the retro-peri- US diagnosis is much more difficult. The lesion, constantly toneum. The retroperitoneal fistula can involve the kidney, refilled, can become a pseudocyst. Its rupture can occur in the ureter or the psoas muscle. During its development, it an abdominal organ such as the spleen, the liver, or, more can go back and up reaching through the esophageal or the rarely, the kidney, causing a subcapsular collection aortic hiatus into the mediastinum (Fig. 15a–c).At this lev- (Fig. 15d–f) that is often hemorrhagic (Pistolesi et al. el pancreatico-mediastinal fistulas and mediastinitis can 1992). In this case US can highlight the fluid collection, but set in with catastrophic complications when the pancreatic the lesion’s characteristics and their relationship with the enzymes are activated (Pistolesi et al. 1978; Alexander et al. pancreatic gland are better documented by CT. In the past, 1982). Pseudocyst or erosion into the esophagus or the diagnostic confirmation was only obtainable with ERCP, pericardium is also possible (Procacci et al. 1987). Erosion which showed the communication between the duct of of the parietal pleura – pancreatico-pleural fistula – more Wirsung and the fistula (Pistolesi et al. 1992). Currently, a commonly causes pancreatic pleuritis (Fig.16a), which can definitive role in the study of this disease is carried out by be the cause of acute dyspnea in relation to the massive ef- MRCP,especially using secretin stimulation, which appears fusion. Much more rare is the erosion into the visceral to be alternative to ERCP. Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 509

Fig. 16a–d. External pancreatic fistula. a, b The fistulography by fied through the surgical drainages, is in communication with the means of surgical drainage highlights the pancreatic collection right colon (asterisks) and the duct of Wirsung: complicated pan- (asterisk), in communication with the pancreatic duct (arrows): creatic fistula. (From Procacci et al. 2002) simple pancreatic fistula. c, d Another case. The collection, opaci-

There are few reports in the literature which are consis- pathway of the drain inserted during the operation. This tent with the rarity of this pathology (Kay et al.1997; Fulcher complication may follow surgical resection (pancreatico- et al.1999; Materne et al.2000).Massive pleural effusions can duodenectomy, distal pancreatectomy; Papachristou et al. be seen on imaging without being able to define their origin. 1981; Lerut et al.1985; Sheiman et al.2001) or drainage pro- The diagnosis of pancreatico-pleural fistula can immediate- cedures (pancreatico-jejunostomy or cysto-jejunostomy). ly be assessed by the amount of amylase in the pleural fluid In most cases, it is caused by the dehiscence of the pancre- (Cole and Bradley1992). Both ERCP and MRCP can docu- atico-digestive anastomosis or, in the absence of this, a ment retroperitoneal fistula and/or the mediastinal pseudo- leakage at the pancreatic stump. The fistula can complicate cyst without, however, being able to confirm the direct rela- the drainage of a simple pancreatic collection (Fotoohi et tionship with the pleural cavity or the bronchial tree. al. 1999) or other surgical abdominal procedures: such as Treatment of the internal fistula is almost exclusively after surgery for a gastric or duodenal ulcer, which pene- surgical. Only in selected cases, such as when infection trates into the pancreas or after an emergency splenecto- complicates the fistula, might it be necessary to insert a my, or after a left nephrectomy secondary to excessive sur- percutaneous drain (Cole and Bradley 1992). gical handling of the pancreatic tail (Spirnak et al. 1984). The external fistula may be simple, with direct communication of the duct of Wirsung with the skin (Fig. 16a,b) or External Pancreatic Fistula complicated by the involvement of other structures, partic- External pancreatic fistula is more common, as a conse- ularly the digestive tract (Fig. 16c,d) (Pistolesi et al. 1992). quence of surgery or, much less commonly, due to a pan- Diagnosis is mostly clinical, since evaluation of the out- creatic biopsy (Iglehart et al. 1986). It develops along the put and analysis of the fluid leads to the diagnosis of fistu- 510 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

la and also to an indication of the viscus involved. To date, the pancreatic tail, next to the spleen hilum or at the head fistulography is the primary investigation and often the of the pancreas. The more commonly involved vessels are only one carried out, to define the viscus involved (Pistole- the splenic artery,the gastroduodenal artery,the pancreati- si et al. 1992). A study of the digestive tract should be con- co-duodenal arcades, and lastly, the left gastric artery. sidered in cases of complex fistulas, to better define the ex- Anatomy explains these clinical presentations.On the left tent of its involvement. In selected cases, a CT examination side, arterial lesions usually involve the last tract of the with the opacification of the fistula may be useful to splenic artery, immediately upstream the origin of the left achieve more exact information as to the spatial extension. gastroepiploic artery and the collateral omental branches.At Usually, when there are low-output fistulas, sponta- this site, retroperitoneal splenic branches become intraperi- neous closure is expected in 68–100% of cases after toneal, so they are more mobile and may induce traction on- 6–26 days (Pederzoli et al. 1986) and medical therapy al- to the stable retroperitoneal vessels until they break down most always resolves the problem (Sunderland and Imrie (Fig. 17a,b). The same mechanism can be observed on right 1992). High-output external fistulas (>200 ml/24 h) require sided bleeds. We look for arterial lesions at the point in a different therapeutic modality, as they are less inclined to which the gastroduodenal artery divides into the right gas- spontaneous closure. Standard management includes total troepiploic artery and the pancreatico-duodenal branches, parenteral nutrition,somatostatin analogues,and,more re- as this site corresponds to a “locus minori resistentiae,” in cently, endoscopic stent placement in the pancreatic duct which the artery enters from the retroperitoneum into the (Saeed et al. 1993; Bassi et al. 1996; Falconi et al. 1999; Bassi omental root and becomes intraperitoneal (Fig. 17d,e). et al. 2000; Boerma et al. 2000; Costamagna et al. 2001) or percutaneous radiological catheterization of the main pancreatic duct (Cabay et al. 1998), with the aim of aiding the Pseudoaneurysm physiological efflux of the pancreatic juice. Surgery is indi- When pancreatitis is associated with a pseudocyst, both the cated when this therapy has failed. Although some authors progressive enlargement and the mechanic decubitus of the have observed that high-output fistulas show a greater ten- pseudocyst cause necrotizing arteritis, with maceration of dency to cause complications, Bassi et al. observed neither the vessel walls and hemorrhage into it. The hemorrhage is a greater nor a lesser infection tendency in fistulas in rela- initially contained by a fibrous tissue capsule that progres- tion to output, but rather a greater bacterial concentration sively enlarges due to the unrelenting arterial pressure. (and enhanced risk of the clinical onset of infection) in The size of the pseudocyst depends on the type of the low-output fistulas, perhaps caused by a reduced intrinsic lesion developed: bleeding in a small pseudocyst is con- washout mechanism. This mechanism is rapidly interrupt- tained and more commonly ends up as a pseudoaneurysm. ed by inhibitory therapy and may account for the occur- In the case of a larger pseudocyst, the arterial lesion is de- rence of so-called false closure of the fistula (Bassi 1992). fined as a bleeding pseudocyst and, therefore, has a signifi- cant risk of rupture in the gastrointestinal tract or into the peritoneal and/or retroperitoneal cavities. Angiography demonstrates the presence of pseudoaneurysm, without 5.6.4 Vascular Involvement bleeding, in 10–21% of patients with chronic pancreatitis (Burke et al. 1986). The occurrence is higher (10–31%) in The erosive action of activated pancreatic proteolytic en- patients with pseudocyst (Kiviluoto et al. 1989; Frey et al. zymes in acute pancreatitis, the decubitus of a pseudocyst 1992). Hemorrhagic complications are expected in 6–31% and the drainage in the surgically treated pancreas can of patients with pancreatic pseudocyst (Sankaran and Walt involve pancreatic or peri-pancreatic vessels. The result of 1975) and in 7–14% of those suffering from chronic pan- these conditions are arterial lesions, such as pseudo- creatitis (Bresler et al. 1991). The preventive vascular study aneurysm or disruption, and venous complications, in par- of patients with pancreatic pseudocyst must be carried out ticular, venous thrombosis. since arterial pseudoaneurysm, although infrequent, is a potentially catastrophic complication. Currently, noninvasive vascular imaging (Doppler US, MSCT, MRA) is almost 5.6.4.1 Diagnosis and Embolization Therapy as sensitive as angiography and should be chosen as the of Arterial Lesions first choice in asymptomatic patients (Ammori et al. 1998). Asymptomatic pseudoaneurysm is occasionally report- Major severe hemorrhagic arterial complications in pan- ed in the course of an ultrasound examination. Duplex creatitis are infrequent but life-threatening conditions Doppler ultrasonography immediately recognizes the (Frey et al. 2002; Procacci et al. 2002). Massive bleeding may blood flow inside the pseudoaneurysm and, in some be due to pseudoaneurysm or arterial disruption. Usually cases, may identify the vessel of origin.A bleeding pseudo- it occurs late in the disease course and in post-operative cyst may be suspected at ultrasound if a cystic pancreatic patients (Beattie et al. 2003). According to our experience, mass rapidly enlarges or suddenly changes echogenicity spontaneous bleeding always occurs in the same sites, at (Fig. 18a). Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 511

Fig. 17a–f. Arterial involvement in pancreatitis. a–c The scheme and vulnerable to lesion (circle). d–f Right side vascular anatomy is highlights pancreatic left side arterial anatomy(a): arterial lesions shown in the scheme (d).At this site the “locus minori resistentiae” usually occur in the last tract of splenic artery, immediately up- is the point in which the gastroduodenal artery divides into the stream the origin of the left gastroepiploic artery and the collater- right gastroepiploic artery and the pancreatico-duodenal branch- al omental branches (scheme) (b). Selective angiography of es (scheme) (e). Selective angiography of coeliac trunk demon- splenic artery in an oblique projection (c) displays how these strates arterial branches becoming intraperitoneal (circle; f) retroperitoneal branches become intraperitoneal, so more mobile

Pseudoaneurysm identification more often occurs in a pancreatic inflammatory disease and of a pseudo- during CT examination (Fig. 18b,c), carried out following aneurysm on CT examination (Fig. 19a), ERCP has the task complaints of acute, usually gastrointestinal, pain associat- of looking for an abnormal communication between the ed with or without bleeding. Multiple recurrences of gas- main pancreatic duct and the pseudoaneurysm,with direct trointestinal hemorrhage, especially in association with endoscopic visualization of wirsungorrhage or indirect transient pancreatic pain, must lead to the suspicion of a confirmation due to the opacification of the pseudo- pseudoanuerysm or a bleeding pseudocyst, expecially aneurysm (Fig. 19b). when endoscopic examinations are negative for concurrent Regarding symptomatic pseudoaneurysms and chronic peptic diseases. gastrointestinal bleeding, the acute bleeding is a conse- The intermittence of the bleeding is characteristic of quence of the pseudoaneurysm or ruptured bleeding “wirsungorrhage” or “hemosuccus pancreaticus.” De- pseudocyst.As already stated, the progressive expansion of scribed for the first time by Lower and Farrell in 1931 the arterial lesion, owing to unrelenting arterial pressure, (Lower and Farrell 1931), it appears as intermittent hemor- can result in a sudden and immediate rupture in the gas- rhagic flow from the major papilla, a rare finding but trointestinal tract, the peritoneal cavity, or the retroperi- pathognomonic for pancreatic arterial hemorrhage (Nabi toneal space. Its clinical presentation is characterized by Yattoo et al. 1999; Dasgupta et al. 2002; Feng and Mauro sudden hemorrhagic shock, with a mortality rate of 50% 2003). In the presence of chronic gastrointestinal bleeding (Lendrum 1994). Computed tomography can highlight the 512 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 18a–f. Bleeding pseudocyst of the left gastroepiploic artery, ra- frontward (arrow). There is a vast infarcted area in the spleen. Selec- diologically and surgically treated. The ultrasound examination (a) tive angiography of the splenic artery (d) shows the pseudoa- highlights a voluminous pseudocyst of the tail of the pancreas with neurysm (asterisk) slightly downstream of the left gastroepiploic a ﬁnely corpuscular hyper-echoic content. The CT scans in the arte- artery origin (arrowhead). Selective angiography after placing coils rial contrastographic phase (b, c) demonstrate the pancreatic tail at the pseudoaneurysm afferences (e) demonstrates its complete ex- pseudocyst (asterisk) compressing the splenic artery. In front of the clusion. Axial CT scans (f), carried out following splenectomy and pseudocyst, a small pseudoaneurysm is visible (arrowhead), adher- cysto-jejunostomy demonstrate that the arterial embolizing materi- ing to the left gastroepiploic artery,which is stretched and displaced al placed radiologically is still in position.(From Procacci et al.2002) Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 513

Fig. 19a–e. Pseudoaneurysm in chronic pancreatitis, radiological- pseudoaneurysm (asterisk) is fed by the gastroduodenal artery ly treated. The axial CT scan in the arterial phase (a) demonstrates and the pancreato-duodenal arcades. The coils (arrows) mimic the the presence of a pseudoaneurysm (asterisk) embedded the pan- course of the embolized vessels (d) recreating their anatomy. The creatic head; ERCP (b) reveals the passing of contrast medium axial CT scan (e), carried out a year later, shows the collapse of the from the main pancreatic duct (arrow) to the lumen of the aneurysmatic sac with the coils positioned in the arcade. (From pseudoaneurysm (arrowheads). Angiography (c) shows that the Procacci et al. 2002)

pseudoaneurysm and its contiguity with the gastrointesti- coils; both the coaxial technique and the micro-coils lead to nal tract or the presence of hemoperitoneum. a particularly high success rates.The occlusion of all the ef- To date, MSCT, with image reconstruction programs ferents and, therefore, all of the afferents to the lesion with (MPR, MIP,SSD,VR), or MR, with 3D sequences in contrast coils is technically similar to surgical tying, but it is clearly phases, are extremely sensitive in defining a detailed arter- much less invasive. It is better not to place coils inside the ial map of the pancreatic region as well as the site of the pseudoaneurysm, unless this is required to occlude the arterial lesion. efferent vessels, which would otherwise be inaccessible Angiography, therefore, plays no role in the diagnostic (Schoder et al. 2000). Notably, pseudoaneurysms have a phase but is immediately used for treating lesions identi- pseudo-wall of variable thickness that can derive from the fied with noninvasive imaging. Embolization, in particular, fibrotic wall of the pseudocyst. Moreover, without coils in- has high success rates in the treatment of these lesions side the pseudoaneurysm, CT can better demonstrate the (Beattie et al. 2003; Deshmukh et al. 2004; Bergert et al. reduction of the sac until it collapses during follow-up. 2004, 2005). Initially, all the afferent and efferent arteries This is because it is not hidden by the artifacts (Fig. 19e). involved must be defined (Fig. 19c). Only the occlusion of When the pseudoaneurysm is ruptured, the emergency all of them results in the complete and definite exclusion of condition can justify the use of acrylic glue together with the pseudoaneurysm or bleeding pseudocyst from the coils (Schoder et al. 2000; Yamakado et al. 2000) to obtain a arterial flow, with its resultant progressive collapse quicker occlusion of the bleeding vessel, as described later. (Fig. 19d,e). The best embolizing materials are Gianturco Recently, a direct US and/or CT guided percutaneous em- 514 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

bolization of pseudoaneurysms with thrombin has been bolization is control of the vessel proximally and distally to proposed as an alternative to endovascular embolization the site of bleeding (Fig. 20c–e). with glue (Sparrow et al. 2003; Puri et al. 2003; Geoghegan Embolization of the vessel with spongostan has a high et al. 2004; Krueger et al. 2005). In the presence of a copi- rate of rebleeding. This is because the fibrin sponge is sen- ously bleeding pseudocyst, radiological treatment is a pri- sitive to the lytic action of the activated pancreatic en- ority, but not mandatory. By proceeding in this manner, the zymes (Golzarian et al. 1997) and the vessel is practically hemorrhage can be stopped and the patient can proceed to without walls at the disruption site, as a result, its plugging surgery in a controlled and hemodynamically stable condi- is useless since the re-establishment of the pressure system tion (Fig. 18d–f). In acute hemorrhage, the surgical ap- would re-open the arterial breach. For the same reason, proach is in fact subject to a high mortality rate, varying stopping the bleeding following an accidental proximal from 12 to 64% (Stabile et al. 1983; El Hamel et al. 1991). dissection of an arterial vessel is rarely definitive. Metal coils can completely embolize the arterial lesion only when they are placed up and downstream of the breach in the Arterial Disruption bleeding arterial vessel, where the wall is not affected by Arterial disruption is one of the most serious emergency enzymatic erosion. conditions in pancreatic pathology. It is an uncommon According to our experience, acrylic glue has proved complication of inflammatory pancreatic disease, but mor- to be the most efficient embolizing agent when hemody- tality is >50%. Survival depends greatly on quick and accu- namic instability requires rapid embolic action, or when rate diagnostic and therapeutic views. catheterization of the vessel downstream of bleeding is Clinical presentation is characterized by hemorrhagic impossible (Yamakado et al. 2000). Injected upstream of shock at the moment of diagnosis. Bleeding can occur in the arterial lesion and correctly diluted, the glue is able to the gastrointestinal lumen, the peritoneal cavity, the reach the arterial tract downstream and, with its progres- retroperitoneum, or simultaneously in several anatomic sive polymerization, brings about the proximal and distal cavities. occlusion. Another useful advantage is that the glue’s poly- Arterial disruption in acute pancreatitis follows the merization has an exothermic reaction, which creates a powerful proteolytic action of activated enzymes present germicidal action in the usually infected collection. When- in the inflammatory pancreatic fluid combined with mac- ever possible, it is better to precede the injection of the glue eration of the arterial wall. The most commonly involved with partial embolization with coils.This is in order to slow arterial vessel is the splenic artery, but all the peripancreat- down the arterial flow and avoid distal progression of the ic vessels can be involved, depending on the location of the embolizing material,whose polymerization time cannot be fluid collection. Bleeding from the right and middle colic calculated accurately. arteries is common when the collection occupies the The incidence of hemorrhagic complications due to ar- mesenteric root. Superior mesenteric artery and the celiac terial disruption after pancreatic surgery, especially pan- trunk can also be involved, but to a lesser degree.When he- creatoduodenectomy, has not changed in the past 20 years morrhagic shock occurs, spiral CT is first imaging tech- (2–18%) (Rumstadt et al. 1998). Bleeding is a serious com- nique: it can highlight the collections that completely sur- plication, the second most frequent after sepsis due to de- round the arterial vessels and often when there is hemody- hiscence of the pancreatic anastomosis. In the first 2 weeks, namic instability, it can identify the spreading hemorrhage early bleeding can be due to insufficient intra-operative he- inside the collection (Fig. 20a) and its vessel of origin. Nev- mostasis at the abdominal vessel level or in correspon- ertheless, diagnosis remains the great challenge, as it may dence with the anastomosis and requires a second laparo- fail in emergency conditions and immediate treatment is tomy.After the first to second week,late bleeding can occur. required. In such situations, the gold standard imaging Its diagnosis as well as its treatment are often a challenge. technique is angiography,which has the advantage of being The dehiscence of the pancreato-jejunal anastomosis can diagnostic and therapeutic at the same time (Fig. 20b–g). cause the liberation of lytic enzymes activated by the en- Arterial bleeding in acute pancreatitis is a dramatic oc- teric contents, with consequent arterial disruption with currence that is subject to a high mortality rate. Stopping it massive hemorrhage. More than 2 weeks following surgery, may be very difficult both surgically and radiologically. even modest bleeding must be considered a potential sign Emergency surgery is associated with a high degree of fail- of anastomotic dehiscence. This initial bleed is known ure and mortality. A >80% recurrence rate of bleeding has as “sentinel bleeding” because it often precedes massive been reported in the literature (Stanley et al.1976; Stabile et hemorrhage from erosion of a large arterial branch by 6 h al. 1983; El Hamel et al. 1991). Surgical resection has a more to 10 days. Rumstadt et al. suggest that when “sentinel than 50% mortality (Bresler et al. 1991). bleeding” appears at the drainage or the gastrointestinal The radiological treatment of arterial disruption in tract, immediate surgical intervention with a revision “necrotic hemorrhagic” pancreatitis can fail due to the of the pancreatic–digestive anastomosis should be un- excessive extent of the maceration of the vessel or the dertaken (Rumstadt et al. 1998). When dehiscence of the involvement of multiple arterial branches. The goal of em- anastomosis occurs, the massive hemorrhage results in Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 515

Fig. 20a–h. Emergency radiological treatment of arterial disrup- upstream to the arterial lesion (arrows), at the origin of gastroepi- tion in bleeding pancreatitis. a Contrast-enhanced CT scan high- ploic artery, superior pancreatico-duodenal artery and into gas- lights a fluid collection at the site of pancreatic head, almost com- troduodenal artery till the origin of common hepatic artery (c). pletely destroyed by necrosis. A tiny hyperdensity inside the col- Selective angiography of superior mesenteric artery is then per- lection induces the suspicion of arterial disruption, even though formed and coils are positioned along the inferior pancreato-duo- bleeding source cannot be clearly identified. b Selective angiogra- denal arcades (arrows), to definitely exclude the arterial lesion and phy demonstrates an active bleeding from gastroduodenal artery, reduce the risk of rebleeding (d, e). f–g At the end of the procedure, immediately before the origin of right gastroepiploic artery. The digital subtraction angiography angiographies of superior mesen- angiographic image is pathognomic of an arterial disruption in teric artery (f) and coeliac trunk (g) confirm the complete em- acute pancreatitis with contrast medium spreading directly into bolization of arterial lesion. h At 15 days CT control coils are clear- the peripancreatic fluid collection. c–e Emergency radiological ly demonstrated and there is no evidence of arterial bleeding re- treatment is carried out positioning microcoils downstream and currence mortality in 15–58% of cases (Rumstadt et al. 1998; Sato et greater amount of bleeding is noted from the drains, al. 1998). and/or the gastrointestinal tract, CT is usually effective in If the patient is hemodynamically stable, CT examina- revealing the site of hemorrhage, but in this case the unsta- tion may fail to demonstrate the source of bleeding,but it is ble hemodynamic condition of the patient makes it prefer- very useful for highlighting peri-anastomotic collections, able to perform angiography immediately because it can which could be responsible for the arterial lesion. When a diagnose and treat the site of bleeding. Bleeding associated 516 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 20a–h. (continued)

with anastomotic dehiscence requires an embolization The arterial disruption in neoplastic pathology is the technique similar to that used in acute pancreatitis. The result of infiltration of the pancreatic and peri-pancreatic most commonly involved vessels are the gastroduodenal vessels. Arterial bleeding is, however, an uncommon com- artery and the common hepatic artery (Aranha et al. 1984; plication of the very advanced stages, when even palliative Brodsky and Turnbull 1991; Balladur et al. 1996; Rumstadt treatment loses its effectiveness. Neuroendocrine tumors et al. 1998; Sato et al. 1998). Embolization with coils leads to at the cephalo-pancreatic site are an exception: they grow definite stoppage of the bleeding only when the gastroduo- slowly and require response to chemotherapy.Their bleed- denal artery is occluded in a tract not involved by septic ing is usually due to infiltration of the duodenal wall, maceration or, alternatively, the common hepatic artery is so endoscopic examination can make the definite diagno- directly occluded. Embolization is sometimes used as a sis. Palliative treatment consists of embolization of the ar- temporary procedure to stop or slow down bleeding so that terial vessels involved. The best embolizing material is a patient can be operated on electively rather than emer- spongostan or microspheres of polyvinyl alcohol, whereas gently (Vujic 1989). There are few articles in the literature the afferent arteries to the neoplasm are occluded with that report late hemorrhage following a pancreatoduo- coils. denectomy treated with embolization. Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 517

Embolization Therapy Complications tibiotic therapy is necessary if the fever persists over the Complications due to embolization therapy in the pancre- sixth day. If imaging displays the presence of a collection in atic and visceral area are limited. Often patients complain the embolized area, it is possible to perform percutaneous of the so-called postembolization syndrome, in which drainage. there is a modest rise in temperature, leukocytosis, pain and nausea. Symptoms usually resolve in a few days with anti-inflammatory and anti-emetic therapy and intra- 5.6.4.2 Diagnosis and Management venous resuscitation. The risk of ischemia is minimal in of Venous Complications the upper gastrointestinal tract if the normal collateral pathways are patent and the appropriate embolic agents Venous Thrombosis of the Peripancreatic Tributaries are used. In this region, the left gastric, gastroduodenal, of the Portal Vein gastroepiploic, and pancreaticoduodenal arteries can be Venous thrombosis is a frequent complication of pancre- safely embolized (Rosen and Sanchez 1994). Using a tech- atitis. Thrombosis of the splenic vein is the most common nique that leads to the most proximal occlusion possible vascular complication of pancreatitis.This is because of its with coils or fast polymerization acrylic glue, the recruit- location in a groove along the upper posterior border of ment of collateral circulation downstream allows for the the pancreas. It has been reported to be occluded in up to re-vascularization of the occluded vessel. Splenic artery 45% of patients with pancreatitis (Vujic 1989). Chronic occlusion determines the onset of sectorial infarcts, which pancreatitis, especially when calcified, is the most com- usually resolve with no further consequences.Occlusion of mon cause of splenic vein thrombosis with 5–37% of pa- a short tract up- and downstream of the bleeding of arter- tients affected. All the signs of pre-hepatic segmental por- ial branches, such as the middle colic artery, is tolerated. tal hypertension are also present. Compression and/or ve- Occlusion of the common hepatic artery, with normal pa- nous infiltration induces thrombosis that leads to the tency of the portal vein, has no clinical consequences. Em- formation of esophageal or gastric varices, which can be bolization is inadvisable in the presence of thrombosis or responsible for acute bleeding. The development of compression of the portal vein (Cardella et al. 1997). Treat- esophageal varices occurs in >50% of patients with ment of bleeding from the common hepatic artery or from splenic artery thrombosis, whereas gastric varices can the short stump of the gastroduodenal artery following a bleed in 45–69% of patients with splenic vein thrombosis pancreatoduodenectomy is often problematic for the sur- (Moossa and Gadd 1985). Ultrasound and/or CT imaging geon. In fact, after surgery, there is a reduction in the num- can easily demonstrate the presence of varices but not ac- ber of arteries available for collateralization. Moreover, tual bleeding. Diagnosis is the task of endoscopy, which is compression, even as far as thrombosis, of the portal vein also often required to carry out sclerotherapy. Splenic vein is common due to the adjacent hematic collection. In these thrombosis and sinistral hypertension may be treated by cases the alternative treatment to embolization is the splenectomy (Vujic 1989). placement of covered stents, which maintain the patency of the hepatic artery in emergencies. There are still only a few reports in the literature concerning the use of Pancreatic Duct/Portal Vein Fistula this technique in repairing the hepatic artery (Bürger Pancreatic duct/portal vein fistula results from a sponta- et al.2000; Paci et al.2000).Occlusion of the stent over time neous rupture of a pancreatic pseudocyst into the portal due to intimal hyperplasia is predictable. Nevertheless, vein. The onset of this venous complication is very unusu- the treatment stops the bleeding immediately and main- al: only a few cases have been reported in the literature tains the blood flow to the liver. The slow occlusion of the (Procacci et al. 1995; Yamamoto et al. 1999; Ko et al. 2003; stent can then be compensated by the recruitment of col- Riddel et al. 2005). The diagnosis of the fistula cannot be lateral intra-hepatic arterial circulation and the return to obtained by angiography because the portal tree is exclud- normal portal flow or the growth of a collateral portal net- ed from the systemic circulation and it develops a cystic work. transformation. The ERCP can highlight the fistula if the A rare complication of interventional treatment is infec- latter directly involves the pancreatic duct (Willis and tion. This is related to the introduction of foreign embolic Brewer 1989).Whenever the fistula is induced by a pseudo- material or the covered stents. Preventive treatment is cyst, ERCP may not be diagnostic. On contrast-enhanced therefore advisable by administering a second-generation CT, the portal lumen is easily recognizable with a liquid- cephalosporin on the day of the procedure. If fever or type density (Fig. 21).Sometimes,communication between leukocytosis appear in the immediate post-procedure peri- the venous lumen and the pseudocyst can be demonstrat- od, the differential diagnosis between post-embolization ed. Confirmation of the fistula is obtainable by trans-he- syndrome and infection can be difficult. Gas bubbles in the patic portography carried out under US or CT guidance. infarcted foci are not a definite sign of infection. If fever Presently, magnetic resonance can also diagnose the devel- persists, the suspicion of infection is more certain.A blood opment of pancreatic duct/portal vein fistula (Riddel et al. culture usually confirms the diagnosis. Nevertheless, an- 2005). 518 G.Mansueto,D.Cenzi,A.A.Gumbs,M.D’Onofrio

Fig. 21a–d. Pancreatic duct/portal vein ﬁstula.The CT scans,carried tree (arrowheads), involved by a voluminous pseudocyst of the pan- out in the cranio-caudal direction in the contrastographic phase, creatic body (asterisk). The lumen of the portal vessels has the same show hypodense hepatic areas, due to the reduced contribution of liquid density of the pseudocyst, as a consequence of its sponta- the hematic portal ﬂow caused by the total thrombosis of the portal neous rupture into the portal vein. (From Procacci et al. 2002)

Thrombophlebitis of the Peripancreatic Tributaries appear as badly deﬁned hypodense collections, which may of the Portal Vein or may not contain small gas bubbles (Fig. 22a–c). The ear- Thrombophlebitis of the peripancreatic tributaries of the ly detection of septic ascending thrombophlebitis and its portal vein is deﬁned as acute infection of the portal system adequate treatment (Fig. 22d–f) may decrease the mortality associated with hepatic involvement. It can arise from the rate and the serious prognosis reported in the surgical liter- extension of pancreatic necrosis infection along the portal ature (Balthazar and Gollapudi 2000). venous tree. The pyogenic diffusion through the portal system is followed by hepatic involvement, with the formation Acknowledgement. The authors dedicate this chapter to the of one or more abscesses. At CT, the intra-hepatic abscesses memory of Prof. Carlo Procacci. Chapter 5.6 Imaging and Intervention in Acute Pancreatic Conditions 519

Fig. 22a–f. Pylephlebitis in chronic pancreatitis. a–c Contrast-en- drainage of liver abscesses can contribute to the definite diagnosis hanced CT scans show portal thrombosis (arrowheads in a) and and treatment. It was carried out with a fine needle (d) then ex- adjacent hypodense hepatic areas with hyperdense walls (arrows changed by a percutaneous catheter. The communication between in b, c), liver abscesses consequent to the pyogenic diffusion fluid collections and thrombosed portal vein is demonstrated by through the portal system. d–f Percutaneous transhepatic the spreading of contrast medium directly into portal tree (e, f)

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