DOI: 10.1148/rg.256055036
RadioGraphics 2005;25:1451-1468
© RSNA, 2005
Intraductal Papillary Mucinous Neoplasm of the Pancreas: Can Benign Lesions Be Differentiated from Malignant Lesions with Multidetector CT?1
Satomi Kawamoto, MD,
Karen M. Horton, MD,
Leo P. Lawler, MD,
Ralph H. Hruban, MD and
Elliot K. Fishman, MD
1 From the Russell H. Morgan Department of Radiology and Radiological Science (S.K., K.M.H., L.P.L., E.K.F.) and the Department of Pathology (R.H.H.), Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Hospital, Baltimore, Md. Presented as an education exhibit at the 2004 RSNA Annual Meeting. Received March 2, 2005; revision requested March 28 and received May 12; accepted May 13. All authors have no financial relationships to disclose.
Address correspondence to S.K., Department of Radiology, Johns Hopkins Hospital, JHOC 3235A, 601 N Caroline St, Baltimore, MD 21287 (e-mail: skawamo1{at}jhmi.edu).
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Abstract
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Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a distinct clinicopathologic entity that is being recognized with increasing frequency. In 25%–44% of IPMNs treated with surgical resection, associated invasive carcinoma has been reported. Surgical resection is the treatment of choice for most IPMNs. Preoperative determination of the presence or absence of associated invasive carcinoma is crucial. The prognosis is worse if there is associated invasive carcinoma; when invasive carcinoma is present, the surgical procedure may be modified to include resection of regional lymph nodes. The spectrum of appearances of IPMN, which includes adenoma, borderline lesion, and lesions with associated carcinoma in situ or invasive carcinoma, was studied with 16-section multidetector computed tomography (CT) and histologic correlation. CT was performed with dual-phase acquisition; the reconstructed images were reviewed on a workstation with axial scrolling and interactive multiplanar reformation and three-dimensional reformation techniques. Features predictive of invasive carcinoma in IPMN at CT and other imaging studies include involvement of the main pancreatic duct, marked dilatation of the main pancreatic duct, diffuse or multifocal involvement, the presence of a large mural nodule or solid mass, large size of the mass, and obstruction of the common bile duct.
© RSNA, 2005
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Describe the clinical and pathologic features of IPMN of the pancreas.
- Identify the spectrum of appearances of IPMN at CT.
- Discuss the CT and other imaging features that suggest the presence of associated malignancy in IPMN.
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Introduction
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Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a distinct clinicopathologic entity that is being recognized with increasing frequency (1–4). IPMNs were first reported more than 70 years ago, but their unique features were not appreciated until Ohhashi et al (5) reported on a series of mucin-producing tumors of the pancreas in 1982. IPMNs arise in the main pancreatic duct or one of its branches and are characterized by abundant extracellular mucin production, a papillary growth pattern, mucin retention in the pancreatic ducts, high resectability, and a good prognosis (5). In 1996, IPMN was defined by the World Health Organization as "an intraductal papillary mucin-producing neoplasm, arising in the main pancreatic duct or its major branches" (6).
IPMN represents a spectrum of disease from small benign adenomas through aggressive and lethal invasive carcinomas. IPMNs have a more favorable prognosis than do ductal adenocarcinomas of the pancreas (7). However, IPMNs are an important precursor to invasive adenocarcinoma of the pancreas. IPMNs with an associated invasive carcinoma have a significantly worse prognosis than do IPMNs without an associated invasive carcinoma (2,8).
IPMNs typically produce radiographically identifiable ductal dilatation secondary to production of large amounts of mucin, which may predominantly involve the main pancreatic duct, branch ducts, or both. Different imaging modalities including computed tomography (CT), magnetic resonance (MR) imaging or MR cholangiopancreatography, endoscopic retrograde cholangiopancreatography (ERCP), transabdominal ultrasonography (US), and endoscopic US have been used to evaluate IPMNs, and each modality has advantages and disadvantages (8–12). CT continues to be the primary technique used for evaluation of patients who are suspected to have pancreatic malignancy (13). Although it is generally believed that preoperative distinction between benign and malignant IPMNs is often difficult, prior studies reported that some morphologic features are associated with malignancy in IPMNs at preoperative imaging (4,8,9,12–20).
A wide variety of cystic lesions can occur in the pancreas, including pseudocysts, mucinous cystadenoma and cystadenocarcinoma, and serous cystadenoma. Differentiation of IPMN from other cystic pancreatic masses may be difficult at CT. The presence of a communication between the cystic lesion and the main pancreatic duct is one of the most reliable findings for the diagnosis of IPMN (14). Pancreatic pseudocysts also often communicate with the main pancreatic duct, and differentiation from branch duct type IPMN can be difficult. Mucinous cystadenoma, cystadenocarcinoma, and serous cystadenoma usually do not communicate with the main pancreatic duct. The presence of mural nodules projecting into the main pancreatic duct or cystic lesions are more suggestive of IPMN than of serous cystadenoma or pseudocyst (14,21). Cases of IPMN are often clinically associated with pancreatitis, and main duct type IPMN can be difficult to differentiate from chronic pancreatitis. Calcifications are often associated with chronic pancreatitis, although calcifications are also occasionally associated with IPMN (10,20). Protrusion of the major papilla into the duodenum in association with pancreatic duct dilatation suggests the diagnosis of IPMN (14,21,22).
In this article, we discuss and illustrate the spectrum of appearances of IPMN on CT images obtained with a 16-section multidetector CT scanner with a dual-phase acquisition. To our knowledge, there were no prior studies that directly compared single-detector spiral CT and multidetector CT in evaluation of IPMN. However, it is expected that multidetector CT is higher in spatial resolution, particularly in the z-axis direction, and multiplanar reformatted images and three-dimensional images may provide greater information compared with single-detector spiral CT. Images were reconstructed on a workstation and evaluated with axial scrolling and interactive multiplanar reformation and three-dimensional reformation techniques. The objectives of this article are to discuss and illustrate the spectrum of appearances of IPMN at multidetector CT with histologic correlation, including adenoma, borderline lesion, and lesions associated with carcinoma in situ and invasive carcinoma, and to discuss and illustrate the morphologic features suggestive of invasive carcinoma in IPMN at multidetector CT and other imaging modalities reported in the literature. A brief discussion of the pathologic features of IPMN and treatment considerations, the CT technique, and the clinical features suggestive of malignancy associated with IPMNs is also included.
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Pathologic Features of IPMN
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In contrast to mucinous cystic neoplasms, IPMNs involve the main pancreatic duct or its major branches, and they lack an associated ovarian-type stroma. IPMNs communicate with the pancreatic ductal system, whereas mucinous cystic neoplasms typically do not. The papillary epithelial component and the degree of mucin secretion, cystic dilatation, and invasiveness are variable, and the macroscopic appearance of IPMN and consequent imaging findings of the tumor vary according to the site of origin and the ductal involvement of the disease (4,21). IPMNs may arise in the main pancreatic duct, a branch duct, or a combination of the main and branch ducts, and they typically produce radiographically identifiable ductal dilatation (23).
IPMNs represent a spectrum of disease from small benign adenomas through aggressive and lethal malignancy. IPMNs can be divided into three categories depending on the degree of cytologic and architectural atypia according to the criteria established by the World Health Organization (24). These categories are IPMN adenoma, IPMN borderline lesion, and intraductal papillary mucinous carcinoma. Papillary mucinous carcinoma is the usual designation for an IPMN with an associated invasive carcinoma (24). A single IPMN can have varying histologic features, with different areas of the same tumor showing dramatically different degrees of dysplasia. IPMNs are generally graded based on the greatest degree of atypia present. A sequential progression from adenoma to carcinoma in IPMN has been suggested by histologic and immunohistochemical studies (25). In prior studies of patients with IPMN who were treated with surgical resection, the prevalence of carcinoma in situ associated with IPMN was 7%–34% and the prevalence of invasive carcinoma associated with IPMN was 25%–44% (2,3,8,13–15).
In IPMN adenoma, the papillae are architecturally simple and the epithelium is composed of tall columnar cells with abundant apical cytoplasmic mucin and basally oriented uniform nuclei with no or slight atypia. The epithelium maintains a high degree of differentiation (Fig 1). IPMNs with moderate dysplasia are placed in the borderline category. The epithelium shows no more than moderate loss of polarity, nuclear crowding, nuclear enlargement, pseudostratification, and nuclear hyperchromatism. Noninvasive IPMNs with severe dysplastic epithelial change are considered carcinoma in situ (Fig 2). They can be papillary or micropapillary. Cribriform growth, atypical mitoses, and budding of small clusters of epithelial cells into the lumen support the diagnosis of carcinoma in situ. When invasive, an IPMN may be called papillary mucinous carcinoma since it is no longer only intraductal. Approximately half of the invasive carcinomas associated with IPMNs are colloid (mucinous noncystic) carcinomas (Fig 3), and most of the remainder are conventional tubular adenocarcinomas (23,26,27). IPMNs with an associated colloid type invasive carcinoma have a better prognosis than do IPMNs with an associated tubular type invasive carcinoma (2,26).
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Figure 1a. IPMN adenoma. Photomicrographs (original magnification, x 100 [a] and x 250 [b]; hematoxylineosin stain) of a surgical specimen. The papillae are architecturally simple, and the epithelium is composed of tall columnar cells with abundant apical cytoplasmic mucin and basally oriented nuclei without significant dysplasia. The epithelium maintains a high degree of differentiation.
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Figure 1b. IPMN adenoma. Photomicrographs (original magnification, x 100 [a] and x 250 [b]; hematoxylineosin stain) of a surgical specimen. The papillae are architecturally simple, and the epithelium is composed of tall columnar cells with abundant apical cytoplasmic mucin and basally oriented nuclei without significant dysplasia. The epithelium maintains a high degree of differentiation.
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Figure 2a. Carcinoma in situ arising in IPMN. Photomicrographs (original magnification, x 100 [a] and x 160 [b]; hematoxylineosin stain) of a surgical specimen show severe dysplastic epithelial changes in IPMN. There is cribri-form growth and budding of small clusters of epithelial cells into the lumen. Note the severe cytologic atypia including loss of polarity, loss of differentiated cytoplasmic features including diminished mucin content, cellular and nuclear pleomorphism, nuclear enlargement, and the presence of mitoses.
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Figure 2b. Carcinoma in situ arising in IPMN. Photomicrographs (original magnification, x 100 [a] and x 160 [b]; hematoxylineosin stain) of a surgical specimen show severe dysplastic epithelial changes in IPMN. There is cribri-form growth and budding of small clusters of epithelial cells into the lumen. Note the severe cytologic atypia including loss of polarity, loss of differentiated cytoplasmic features including diminished mucin content, cellular and nuclear pleomorphism, nuclear enlargement, and the presence of mitoses.
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Figure 3. Invasive carcinoma (colloid carcinoma) arising from IPMN. Photomicrograph (original magnification, x 100; hematoxylineosin stain) of a surgical specimen shows well-defined pools of mucin embedded in the stroma of the gland, with malignant epithelial cells floating within the mucin in clusters.
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Genetic alterations that occur in IPMNs are under intense investigation. Genetic analyses of IPMNs have disclosed abnormalities in many of the same genes altered in conventional ductal adenocarcinoma, including mutations of the KRAS2 (28,29), TP53 (29), and p16/CDKN2A genes (30), although the incidence of mutations in these genes appears to be lower in IPMNs than in ordinary ductal adenocarcinoma (31). Inactivation of the DPC4 gene is relatively uncommon in IPMNs, in contrast to ductal adenocarcinomas, and is primarily confined to those neoplasms with high-grade dysplasia or an invasive carcinoma (2,32). Approximately 25% of IPMNs harbor mutations in the Peutz-Jeghers gene (STK11/LKB1) (33).
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Treatment Considerations
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Surgical resection is the treatment of choice for IPMNs because of their malignant potential, and IPMNs resected before the development of invasive carcinoma are highly curable (1,2). The prognosis is significantly worse if there is associated invasive carcinoma (2,8), particularly if there are lymph node metastases (1,2).
The presence of invasive carcinoma is the single strongest adverse predictor of survival (2). Preoperative determination of the presence or absence of associated invasive carcinoma is crucial in this disease. When invasive carcinoma is present, the surgical procedure may be modified to include resection of regional lymph nodes. ERCP and/or endoscopic US can be used for evaluation of patients with equivocal cross-sectional imaging findings or for transpapillary sampling of mucin, the pancreatic duct wall, and mural nodules to help differentiate malignant and benign lesions (7,17).
The surgical resection must ideally include the entire neoplasm with negative margins. It is important to correctly evaluate the extent of IPMN to determine the extent of pancreatectomy and guide surgical treatment. However, extension of the disease along the main pancreatic ducts may be difficult to assess preoperatively because the extent of main pancreatic duct involvement may be overestimated or underestimated at preoperative imaging (13). Planned surgical resection could be modified by intraoperative frozen section analysis to yield negative margins for invasive disease and for noninvasive disease with significant dysplasia (2). Patients with resected invasive and noninvasive IPMNs should undergo careful follow-up and surveillance, as they remain at risk for the development of recurrent disease (2,34).
The natural history of IPMN is poorly understood, and there are controversies regarding optimal treatment of these neoplasms. Improved imaging techniques and improved understanding of the nature of this disease have resulted in an increasing prevalence of branch duct type IPMN (4). Patients with branch duct type IPMNs are often elderly and free of symptoms. Some surgeons recommend surgical resection as soon as IPMN is suspected because of a lack of reliable markers of malignancy (8); however, for a patient with an asymptomatic small branch duct type lesion without evidence of malignancy (no mural nodule, absence of main pancreatic duct dilatation), some authors have performed close follow-up with meticulous serial imaging studies instead of surgery (7,35–37). Further understanding of the long-term natural history of this disease is needed to determine which approach is better.
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CT Technique
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For evaluation of the pancreas with a 16-section multidetector CT scanner, we use a detector collimation of 16 x 0.75 mm to obtain a 0.75-mm section thickness. The data were reconstructed at 0.5-mm intervals (0.25-mm overlap). The parameters were as follows: table speed, 12 mm per rotation; gantry rotation speed, 0.5 second; 120 kVp; and 130–200 mAs. After fasting for at least 2–3 hours, each patent ingested 750–1000 mL of water over a 15–20-minute period before scanning began. We injected 120 mL of iohexol (Omnipaque 350; Amersham Health, Princeton, NJ) through a peripheral venous line at 3 mL/sec. Then, arterial and venous phase images were acquired at 25 seconds and 50–60 seconds from the start of the intravenous contrast material injection. A precontrast scan is helpful to distinguish between mucin globs and mural nodules in IPMN (4,22).
All image data were reconstructed with the body soft-tissue algorithm and sent to a workstation (Leonardo; Siemens Medical Solutions, Malvern, Pa) in the original resolution of 512 x 512. InSpace software (Siemens Medical Solutions) was used for data analysis; this was the volume imaging application for interactive viewing of volume data that was available on the workstation. The images were evaluated by using real-time scrolling and interactive multiplanar reformation and three-dimensional rendering techniques.
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Clinical Features Suggestive of Invasive Carcinoma in IPMN
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Prior studies have evaluated clinical features that suggest a malignant IPMN. Reported clinical predictive signs of malignancy in IPMN include diabetes mellitus (9,13), a history of alcohol abuse (38), short duration of symptoms (3), nausea and vomiting (2), weight loss (2), obstructive jaundice (2,3,16,38), elevated results of liver function tests (3), and elevated serum levels of cancer antigen 19-9 (CA 19-9) (3). However, some of these features remain controversial; in addition, some studies include carcinoma in situ and invasive carcinoma as malignancy, whereas some studies include only invasive carcinoma as malignancy.
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CT and Other Imaging Features Suggestive of Invasive Carcinoma in IPMN
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Predictive features for the presence of invasive carcinoma at preoperative CT and other imaging studies include involvement of the main pancreatic duct, marked dilatation of the main pancreatic duct, diffuse or multifocal involvement, the presence of a large mural nodule or solid mass, large size of the mass, calcified intraluminal contents, and obstruction of the common bile duct (Table).
Involvement of the Main Pancreatic Duct
IPMNs are divided into three types according to the pattern of ductal involvement: (a) the main pancreatic duct type, in which the main pancreatic duct is dilated and the tumor predominantly exists in the main pancreatic duct (Figs 4, 5); (b) the branch duct type, in which only branches are dilated and the tumor does not involve the main pancreatic duct (Figs 6–8); and (c) the combined type, in which the tumor involves both the main pancreatic duct and its branches (Figs 9–11) (24). In cases of branch duct type or combined type IPMN, branch duct lesions are most often seen in the uncinate process or head of the pancreas (39) (Figs 6, 8, 12) but occasionally are seen in the body or tail of the gland (Fig 7).
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Figure 4a. Main duct type IPMN borderline lesion. Oblique axial (a) and oblique coronal (b) venous phase reformatted images show marked dilatation of the main duct in the pancreatic body and tail. Although there is significant dilatation of the main pancreatic duct, pathologic analysis demonstrated an IPMN borderline lesion. No invasive carcinoma was identified in the entire specimen.
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Figure 4b. Main duct type IPMN borderline lesion. Oblique axial (a) and oblique coronal (b) venous phase reformatted images show marked dilatation of the main duct in the pancreatic body and tail. Although there is significant dilatation of the main pancreatic duct, pathologic analysis demonstrated an IPMN borderline lesion. No invasive carcinoma was identified in the entire specimen.
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Figure 5a. Main duct type IPMN with associated invasive carcinoma. Oblique axial (a) and oblique coronal (b) venous phase reformatted images show a markedly dilated main duct in the pancreatic body and tail with an ill-defined soft-tissue mass in the pancreatic head (arrows). There is obstruction of the common bile duct by the mass; a common bile duct stent is in place. Pathologic analysis demonstrated an infiltrating moderately differentiated ductal adenocarcinoma associated with IPMN with carcinoma in situ. There was associated chronic pancreatitis and invasion of the duodenal wall and distal common bile duct. Metastases were found in four of 10 regional lymph nodes.
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Figure 5b. Main duct type IPMN with associated invasive carcinoma. Oblique axial (a) and oblique coronal (b) venous phase reformatted images show a markedly dilated main duct in the pancreatic body and tail with an ill-defined soft-tissue mass in the pancreatic head (arrows). There is obstruction of the common bile duct by the mass; a common bile duct stent is in place. Pathologic analysis demonstrated an infiltrating moderately differentiated ductal adenocarcinoma associated with IPMN with carcinoma in situ. There was associated chronic pancreatitis and invasion of the duodenal wall and distal common bile duct. Metastases were found in four of 10 regional lymph nodes.
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Figure 6a. Branch duct type IPMN adenoma. Axial (a) and oblique coronal (b) venous phase reformatted images show a small cystic mass with minimal septa in the uncinate process of the pancreas (arrow in a, large arrow in b). The main pancreatic duct (arrowhead in b) and common bile duct (small arrow in b) are not dilated. Pathologic analysis demonstrated a 1-cm-diameter branch duct type IPMN adenoma. No invasive carcinoma was identified.
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Figure 6b. Branch duct type IPMN adenoma. Axial (a) and oblique coronal (b) venous phase reformatted images show a small cystic mass with minimal septa in the uncinate process of the pancreas (arrow in a, large arrow in b). The main pancreatic duct (arrowhead in b) and common bile duct (small arrow in b) are not dilated. Pathologic analysis demonstrated a 1-cm-diameter branch duct type IPMN adenoma. No invasive carcinoma was identified.
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Figure 7a. Branch duct type IPMN adenoma. Axial (a) and coronal (b) venous phase reformatted images show a small unilocular cystic mass in the pancreatic body (arrow). There is no pancreatic duct dilatation. Pathologic analysis demonstrated a 1.2-cm-diameter IPMN adenoma. No invasive carcinoma was identified.
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Figure 7b. Branch duct type IPMN adenoma. Axial (a) and coronal (b) venous phase reformatted images show a small unilocular cystic mass in the pancreatic body (arrow). There is no pancreatic duct dilatation. Pathologic analysis demonstrated a 1.2-cm-diameter IPMN adenoma. No invasive carcinoma was identified.
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Figure 8. Branch duct type IPMN adenoma. Coronal venous phase reformatted image shows a unilocular cystic mass in the pancreatic head (large arrow). The main pancreatic duct (small arrow) and common bile duct (arrowhead) are not dilated. Pathologic analysis demonstrated a 1.4-cm-diameter branch duct type IPMN adenoma. No invasive carcinoma was identified.
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Figure 9a. Combined type IPMN borderline lesions. Coronal venous phase reformatted images show multiple cystic lesions with multiple thin septa predominantly involving the pancreatic head and body (arrow). The main pancreatic duct is minimally dilated (arrowhead in b). Pathologic analysis demonstrated IPMN borderline lesions. No in situ or invasive carcinoma was identified.
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Figure 9b. Combined type IPMN borderline lesions. Coronal venous phase reformatted images show multiple cystic lesions with multiple thin septa predominantly involving the pancreatic head and body (arrow). The main pancreatic duct is minimally dilated (arrowhead in b). Pathologic analysis demonstrated IPMN borderline lesions. No in situ or invasive carcinoma was identified.
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Figure 10a. Combined type IPMN borderline lesion. Axial (a), coronal (b), and sagittal (c) venous phase reformatted images show dilatation of the main duct in the pancreatic tail (arrowhead in a) and a 3.5-cm-diameter cystic mass with multiple septa (arrows). An incidentally found old hematoma with peripheral calcification (* in a and b) is seen superior to the right kidney. Pathologic analysis demonstrated an IPMN borderline lesion. There was no invasive carcinoma.
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Figure 10b. Combined type IPMN borderline lesion. Axial (a), coronal (b), and sagittal (c) venous phase reformatted images show dilatation of the main duct in the pancreatic tail (arrowhead in a) and a 3.5-cm-diameter cystic mass with multiple septa (arrows). An incidentally found old hematoma with peripheral calcification (* in a and b) is seen superior to the right kidney. Pathologic analysis demonstrated an IPMN borderline lesion. There was no invasive carcinoma.
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Figure 10c. Combined type IPMN borderline lesion. Axial (a), coronal (b), and sagittal (c) venous phase reformatted images show dilatation of the main duct in the pancreatic tail (arrowhead in a) and a 3.5-cm-diameter cystic mass with multiple septa (arrows). An incidentally found old hematoma with peripheral calcification (* in a and b) is seen superior to the right kidney. Pathologic analysis demonstrated an IPMN borderline lesion. There was no invasive carcinoma.
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Figure 11a. Combined type IPMN borderline lesions. Oblique axial (a) and coronal (b, c) venous phase reformatted images show diffuse moderate dilatation of the main pancreatic duct (arrowheads) and multiple cystic lesions communicating with the main duct throughout the pancreas. Pathologic analysis demonstrated IPMN borderline lesions. No in situ or invasive carcinoma was identified.
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Figure 11b. Combined type IPMN borderline lesions. Oblique axial (a) and coronal (b, c) venous phase reformatted images show diffuse moderate dilatation of the main pancreatic duct (arrowheads) and multiple cystic lesions communicating with the main duct throughout the pancreas. Pathologic analysis demonstrated IPMN borderline lesions. No in situ or invasive carcinoma was identified.
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Figure 11c. Combined type IPMN borderline lesions. Oblique axial (a) and coronal (b, c) venous phase reformatted images show diffuse moderate dilatation of the main pancreatic duct (arrowheads) and multiple cystic lesions communicating with the main duct throughout the pancreas. Pathologic analysis demonstrated IPMN borderline lesions. No in situ or invasive carcinoma was identified.
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Figure 12a. Small invasive carcinoma associated with IPMN with extensive carcinoma in situ. Axial (a) and oblique coronal (b) venous phase reformatted images show a small cystic mass in the pancreatic head (arrowhead) with diffuse mild dilatation of the main pancreatic duct. Pathologic analysis demonstrated a 1.1-cm-diameter IPMN with extensive carcinoma in situ and an associated infiltrating moderately differentiated ductal adenocarcinoma (0.6 cm in diameter) just proximal to the ampulla.
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Figure 12b. Small invasive carcinoma associated with IPMN with extensive carcinoma in situ. Axial (a) and oblique coronal (b) venous phase reformatted images show a small cystic mass in the pancreatic head (arrowhead) with diffuse mild dilatation of the main pancreatic duct. Pathologic analysis demonstrated a 1.1-cm-diameter IPMN with extensive carcinoma in situ and an associated infiltrating moderately differentiated ductal adenocarcinoma (0.6 cm in diameter) just proximal to the ampulla.
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When the main pancreatic duct is involved (combined type [3,7,13,15,16,18,20,38,40] or main duct type [7,9,15,16,19,39,40]), there is a higher risk of associated malignancy than in the branch duct type. Although malignant lesions can be encountered in the form of a unilocular cystic mass (14), small branch duct type lesions of simple cystic appearance are usually not associated with malignancy (Figs 7 , 8). In a series of 13 patients with branch duct type lesions who were evaluated surgically, Terris et al (39) reported carcinoma in situ in two patients (15%) with no invasive carcinoma; in contrast, among 30 patients with main duct type lesions, 11 (37%) had invasive carcinoma and six (20%) had in situ carcinoma.
In branch duct type lesions, communication between the cystic mass and the main pancreatic duct is often visualized with multidetector CT by using axial scrolling or multiplanar reformation imaging and the diagnosis of IPMN is suggested (4). Fukukura et al (11) compared ERCP, thin-section (3–5-mm) helical CT, dynamic MR imaging, and MR cholangiopancreatography in detection of a communicating duct between the main pancreatic duct and the cystic lesion in IPMN; they reported that the communication was visualized in 80.8% of cases with ERCP, in 53.8% with CT, in 42.3% with MR imaging, and in 55.7% with MR cholangiopancreatography. Using MR cholangiopancreatography, Choi et al (18) found that the caliber of the communicating tract was significantly larger in malignant IPMNs (6.8 mm ± 4.4) than in benign IPMNs (3.2 mm ± 1.3).
Marked Dilatation of the Main Pancreatic Duct
Marked dilatation of the main pancreatic duct has been associated with malignancy in IPMN (9,12–20) (Fig 5), although a study that analyzed surgical specimens did not confirm this finding (40). Prior studies have proposed different size thresholds for use with CT, transabdominal US, endoscopic US, ERCP, and MR imaging, including greater than 7 mm (16), 8 mm (17), 10 mm (7,9,13,14), and 15 mm (15,19). At helical CT, dilatation of the main pancreatic duct to greater than 10 mm has a reported specificity of 92% and sensitivity of 78% for the presence of malignancy (13).
In our retrospective study using four-section multidetector CT in 36 patients with known IPMN, a markedly dilated main pancreatic duct was associated with invasive carcinoma, and the sensitivity and specificity of multidetector CT in the diagnosis of associated invasive carcinoma were dependent on the threshold value. When a threshold value of 15 mm was used, the sensitivity and specificity were 20% and 95%, respectively. When a threshold value of 10 mm was used, they were 33% and 86%, respectively. When a threshold value of 6 mm was used, they were 73% and 81%, respectively (20).
Diffuse or Multifocal Involvement
Extensive dilatation of the main pancreatic duct at MR cholangiopancreatography has been reported to be associated with malignancy (18,19). Choi et al (18) evaluated 45 patients with IPMN using MR cholangiopancreatography and MR angiography; they reported that dilatation of the main pancreatic duct affecting more than 50% of the extent was associated with malignant IPMN including borderline lesions (which were defined as tumors that are not overtly malignant but have some foci of severe cellular atypia). In another study, when lesions were located throughout the entire pancreas (diffuse involvement) or in more than one segment (head and/or uncinate process, body, tail) at CT, they were more likely associated with invasive carcinoma (specificity, 77%; sensitivity, 56%) (13).
Presence of a Large Mural Nodule or Solid Mass
The presence of a large mural nodule or solid mass is suggestive of malignancy in IPMN (9,12,13,15,16,18–20,40). Large mural nodules with different size criteria (
3 mm in diameter at preoperative imaging [16], 5.4 mm in height at endoscopic US [12], 10 mm in mean diameter at preoperative imaging and best evaluated with endoscopic US [9]) have been found to be associated with malignancy. Fukukura et al (11) compared helical CT, dynamic MR imaging, and MR cholangiopancreatography for detectability of mural nodules and reported that papillary neoplastic proliferation measuring 3 mm or larger in the main pancreatic duct or a cystic lesion, found in seven of 25 patients with IPMN (28%), was equally depicted with these modalities.
Using helical CT, Taouli et al (13) reported that the most specific predictive sign of invasive carcinoma was the presence of a solid mass (specificity, 96%; sensitivity, 67%). An apparent soft-tissue mass (Figs 5, 13–15) and a large mural nodule within the dilated duct or a soft-tissue component within a cystic mass (Fig 16) are both highly suggestive of an associated invasive carcinoma. Thick walls (Fig 17) and/or thick septa (Fig 18) suggest malignant degeneration (4,18); however, they are not specific and may be seen in nonmalignant lesions (Fig 10 ). At CT, carcinoma in situ and small invasive carcinoma remain difficult to detect (Fig 12). Fukukura et al (14) reported that invasion into the pancreatic parenchyma was not depicted at thin-section helical CT in any of nine patients with malignant IPMN including carcinoma in situ and invasive carcinoma, as all of them had chronic pancreatitis and the invasion was minimal.
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Figure 13a. Invasive carcinoma associated with IPMN. Axial (a) and coronal (b) venous phase images show an apparent solid mass in the pancreatic head (large arrow in b) that involves the distal common bile duct. A biliary stent is in place. There is diffuse dilatation of the main pancreatic duct (small arrow in b) and a large pseudocyst in the lesser sac (*), which is secondary to pancreatitis and compresses the stomach. Pathologic analysis demonstrated an infiltrating moderately differentiated ductal adenocarcinoma arising in IPMN. The carcinoma infiltrated into the wall of the distal common bile duct. Metastatic carcinoma was found in six of 14 lymph nodes.
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Figure 13b. Invasive carcinoma associated with IPMN. Axial (a) and coronal (b) venous phase images show an apparent solid mass in the pancreatic head (large arrow in b) that involves the distal common bile duct. A biliary stent is in place. There is diffuse dilatation of the main pancreatic duct (small arrow in b) and a large pseudocyst in the lesser sac (*), which is secondary to pancreatitis and compresses the stomach. Pathologic analysis demonstrated an infiltrating moderately differentiated ductal adenocarcinoma arising in IPMN. The carcinoma infiltrated into the wall of the distal common bile duct. Metastatic carcinoma was found in six of 14 lymph nodes.
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Figure 14a. Invasive carcinoma associated with IPMN. Axial (a), coronal (b, c), and sagittal (d) venous phase images show a large cystic mass with a solid component (arrowheads in b and c) in the pancreatic head. There are fistulous tracts between the mass and duodenum (large arrow in b, arrow in d) and between the mass and common bile duct (small arrow in b). In addition, there are small air bubbles within the mass and diffuse dilatation of the main pancreatic duct. Pathologic analysis demonstrated an infiltrating moderately differentiated adenocarcinoma with prominent extracellular mucin production arising in association with IPMN with carcinoma in situ. The infiltrating carcinoma involved the wall of the duodenum.
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Figure 14b. Invasive carcinoma associated with IPMN. Axial (a), coronal (b, c), and sagittal (d) venous phase images show a large cystic mass with a solid component (arrowheads in b and c) in the pancreatic head. There are fistulous tracts between the mass and duodenum (large arrow in b, arrow in d) and between the mass and common bile duct (small arrow in b). In addition, there are small air bubbles within the mass and diffuse dilatation of the main pancreatic duct. Pathologic analysis demonstrated an infiltrating moderately differentiated adenocarcinoma with prominent extracellular mucin production arising in association with IPMN with carcinoma in situ. The infiltrating carcinoma involved the wall of the duodenum.
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Figure 14c. Invasive carcinoma associated with IPMN. Axial (a), coronal (b, c), and sagittal (d) venous phase images show a large cystic mass with a solid component (arrowheads in b and c) in the pancreatic head. There are fistulous tracts between the mass and duodenum (large arrow in b, arrow in d) and between the mass and common bile duct (small arrow in b). In addition, there are small air bubbles within the mass and diffuse dilatation of the main pancreatic duct. Pathologic analysis demonstrated an infiltrating moderately differentiated adenocarcinoma with prominent extracellular mucin production arising in association with IPMN with carcinoma in situ. The infiltrating carcinoma involved the wall of the duodenum.
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Figure 14d. Invasive carcinoma associated with IPMN. Axial (a), coronal (b, c), and sagittal (d) venous phase images show a large cystic mass with a solid component (arrowheads in b and c) in the pancreatic head. There are fistulous tracts between the mass and duodenum (large arrow in b, arrow in d) and between the mass and common bile duct (small arrow in b). In addition, there are small air bubbles within the mass and diffuse dilatation of the main pancreatic duct. Pathologic analysis demonstrated an infiltrating moderately differentiated adenocarcinoma with prominent extracellular mucin production arising in association with IPMN with carcinoma in situ. The infiltrating carcinoma involved the wall of the duodenum.
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Figure 15a. Invasive carcinoma associated with IPMN. (a) Oblique coronal venous phase reformatted image shows a markedly dilated main duct in the pancreatic body and tail (arrow). (b–d) Axial (b), oblique coronal (c), and sagittal (d) venous phase reformatted images show that the dilatation of the main duct abruptly ends at the pancreatic body, where there is a soft-tissue mass (arrow in c, white arrows in d). There is also irregularity and narrowing of the adjacent splenic vein (arrows in b, black arrow in d). Pathologic analysis demonstrated an invasive poorly differentiated adenocarcinoma with anaplastic features arising in association with IPMN. The carcinoma invaded the splenic vein. Metastatic carcinoma was found in one of 14 lymph nodes.
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Figure 15b. Invasive carcinoma associated with IPMN. (a) Oblique coronal venous phase reformatted image shows a markedly dilated main duct in the pancreatic body and tail (arrow). (b–d) Axial (b), oblique coronal (c), and sagittal (d) venous phase reformatted images show that the dilatation of the main duct abruptly ends at the pancreatic body, where there is a soft-tissue mass (arrow in c, white arrows in d). There is also irregularity and narrowing of the adjacent splenic vein (arrows in b, black arrow in d). Pathologic analysis demonstrated an invasive poorly differentiated adenocarcinoma with anaplastic features arising in association with IPMN. The carcinoma invaded the splenic vein. Metastatic carcinoma was found in one of 14 lymph nodes.
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Figure 15c. Invasive carcinoma associated with IPMN. (a) Oblique coronal venous phase reformatted image shows a markedly dilated main duct in the pancreatic body and tail (arrow). (b–d) Axial (b), oblique coronal (c), and sagittal (d) venous phase reformatted images show that the dilatation of the main duct abruptly ends at the pancreatic body, where there is a soft-tissue mass (arrow in c, white arrows in d). There is also irregularity and narrowing of the adjacent splenic vein (arrows in b, black arrow in d). Pathologic analysis demonstrated an invasive poorly differentiated adenocarcinoma with anaplastic features arising in association with IPMN. The carcinoma invaded the splenic vein. Metastatic carcinoma was found in one of 14 lymph nodes.
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Figure 15d. Invasive carcinoma associated with IPMN. (a) Oblique coronal venous phase reformatted image shows a markedly dilated main duct in the pancreatic body and tail (arrow). (b–d) Axial (b), oblique coronal (c), and sagittal (d) venous phase reformatted images show that the dilatation of the main duct abruptly ends at the pancreatic body, where there is a soft-tissue mass (arrow in c, white arrows in d). There is also irregularity and narrowing of the adjacent splenic vein (arrows in b, black arrow in d). Pathologic analysis demonstrated an invasive poorly differentiated adenocarcinoma with anaplastic features arising in association with IPMN. The carcinoma invaded the splenic vein. Metastatic carcinoma was found in one of 14 lymph nodes.
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Figure 16a. Invasive carcinoma arising in IPMN. Axial (a, b), coronal (c), and sagittal (d) venous phase reformatted images show a large complex cystic mass with calcifications and an apparent solid component (arrowhead in a, top arrowhead in b, arrowheads in c and d) in the pancreatic body and tail. The main pancreatic duct is markedly dilated. An enlarged, hypoattenuating celiac lymph node is also seen (black arrow in a). There is a small peripancreatic fluid collection and ascites. There is also splenic vein occlusion with gastroepiploic collateral veins (white arrows in a) and a small splenic infarct (bottom arrowhead in b). Pathologic analysis demonstrated colloid carcinoma arising in IPMN and extending into the peripancreatic soft tissue. Multiple metastatic carcinoma involved peripancreatic and celiac lymph nodes. There was mucinous and necrotic debris with focal calcifications within the mass.
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Figure 16b. Invasive carcinoma arising in IPMN. Axial (a, b), coronal (c), and sagittal (d) venous phase reformatted images show a large complex cystic mass with calcifications and an apparent solid component (arrowhead in a, top arrowhead in b, arrowheads in c and d) in the pancreatic body and tail. The main pancreatic duct is markedly dilated. An enlarged, hypoattenuating celiac lymph node is also seen (black arrow in a). There is a small peripancreatic fluid collection and ascites. There is also splenic vein occlusion with gastroepiploic collateral veins (white arrows in a) and a small splenic infarct (bottom arrowhead in b). Pathologic analysis demonstrated colloid carcinoma arising in IPMN and extending into the peripancreatic soft tissue. Multiple metastatic carcinoma involved peripancreatic and celiac lymph nodes. There was mucinous and necrotic debris with focal calcifications within the mass.
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Figure 16c. Invasive carcinoma arising in IPMN. Axial (a, b), coronal (c), and sagittal (d) venous phase reformatted images show a large complex cystic mass with calcifications and an apparent solid component (arrowhead in a, top arrowhead in b, arrowheads in c and d) in the pancreatic body and tail. The main pancreatic duct is markedly dilated. An enlarged, hypoattenuating celiac lymph node is also seen (black arrow in a). There is a small peripancreatic fluid collection and ascites. There is also splenic vein occlusion with gastroepiploic collateral veins (white arrows in a) and a small splenic infarct (bottom arrowhead in b). Pathologic analysis demonstrated colloid carcinoma arising in IPMN and extending into the peripancreatic soft tissue. Multiple metastatic carcinoma involved peripancreatic and celiac lymph nodes. There was mucinous and necrotic debris with focal calcifications within the mass.
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Figure 16d. Invasive carcinoma arising in IPMN. Axial (a, b), coronal (c), and sagittal (d) venous phase reformatted images show a large complex cystic mass with calcifications and an apparent solid component (arrowhead in a, top arrowhead in b, arrowheads in c and d) in the pancreatic body and tail. The main pancreatic duct is markedly dilated. An enlarged, hypoattenuating celiac lymph node is also seen (black arrow in a). There is a small peripancreatic fluid collection and ascites. There is also splenic vein occlusion with gastroepiploic collateral veins (white arrows in a) and a small splenic infarct (bottom arrowhead in b). Pathologic analysis demonstrated colloid carcinoma arising in IPMN and extending into the peripancreatic soft tissue. Multiple metastatic carcinoma involved peripancreatic and celiac lymph nodes. There was mucinous and necrotic debris with focal calcifications within the mass.
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Abstract
LEARNING OBJECTIVES
