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Imaging and Intervention in Acute Pancreatic Conditions 5.6 Chapter Imaging and Intervention in Acute Pancreatic Conditions 5.6 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 in- fected 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 hypo- dense area (arrow) in the cephalic site, hypovascul- arized, compatible with necrosis. b, c On a T2-weight- ed 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.
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