LETTERS TO THE EDITOR
Incidental Regression of a Suspected Pancreatic Intraductal Papillary Mucinous Neoplasm after Nontarget Embolization From: Jeffrey Forris Beecham Chick, MD, MPH James X. Chen, MD Shelby J. Bennett, MD Nikunj Rashmikant Chauhan, MD Shilpa N. Reddy, MD Terence Gade, MD, PhD Micah M. Watts, MD Gregory J. Nadolski, MD Department of Radiology Division of Interventional Radiology Hospital of the University of Pennsylvania Perelman School of Medicine 1 Silverstein 3400 Spruce Street Philadelphia, PA 19104
Editor: Intraductal papillary mucinous neoplasm (IPMN) is a cystic neoplasm of the pancreas characterized by dysplastic mucinproducing epithelial cells that arise from either the main pancreatic duct or its branches. IPMNs are more commonly seen in men 60–70 years old, with an estimated incidence of 4.3 per 100,000 persons (1). These tumors may cause pain or mimic chronic pancreatitis, although many are detected incidentally on high-resolution abdominal imaging. IPMNs manifest with varying degrees of malignancy with either carcinoma in situ or invasive carcinoma seen in 62% of main-branch and 26% of side-branch IPMNs (2). Although certain imaging features, such as dilatation of the main pancreatic duct or mural nodularity, are concerning for malignancy, imaging alone cannot distinguish benign from malignant subtypes. International consensus guidelines recommend resection for all patients deemed fit for surgery with main-duct IPMNs, but the management of side-branch IPMNs is controversial (2). Furthermore, limited options are available for managing IPMNs in patients who are not ideal surgical candidates, warranting investigation into minimally invasive treatment options. Transarterial chemoembolization is a minimally invasive procedure that has been used in the treatment of unresectable hepatocellular carcinoma. Nontarget embolization and extrahepatic deposition of chemoembolic agents during transarterial chemoembolization is a well-recognized consequence. Specifically, nontarget embolization of the pancreas during transarterial chemoembolization is common and often asymptomatic, although it may cause acute None of the authors have identified a conflict of interest. http://dx.doi.org/10.1016/j.jvir.2015.12.758
pancreatitis in 2%–15% of patients (3). To our knowledge, nontarget embolization resulting in involution of pancreatic cystic masses has not been reported. We report a case of complete regression of a pancreatic IPMN after nontarget embolization during transarterial chemoembolization. Institutional review board approval was not required for this report. A 66-year-old African American man with wellcompensated hepatitis C cirrhosis and hepatocellular carcinoma status post left lateral segmentectomy presented with a recurrent tumor in segment 4. Magnetic resonance (MR) imaging performed before treatment demonstrated multifocal hepatocellular carcinoma confined to segment 4. An incidental finding was a 4.2 cm 3.0 cm T2 hyperintense, nonenhancing, multilobulated cystic lesion in the pancreatic head with suggestion of side-branch pancreatic duct communication (Fig 1). There was no main pancreatic duct dilatation. This cystic pancreatic mass had increased slightly in size from 2009, at which time it measured 3.5 cm 2.4 cm, but was otherwise unchanged in appearance. The remainder of the pancreas was normal without atrophy or calcifications to suggest chronic pancreatitis. The MR imaging appearance of the pancreatic cystic mass, overall stability of the mass, and demographics of the patient were all consistent with a diagnosis of a side-branch pancreatic IPMN. The patient underwent selective segment 4 hepatic artery chemoembolization using 100–300 μm drug-eluting embolic agents loaded with 75 mg doxorubicin (LC Beads; BTG, Conshohocken, Pennsylvania) (Fig 2). The patient was discharged after overnight observation, but returned 2 days later with worsening left upper quadrant pain and melena. Laboratory evaluation showed a lipase 27 U/L (normal range, 11–82 U/L) and hemoglobin 11.6 g/dL (normal range,
Figure 1. Axial T2-weighted MR image demonstrating a 4.2 cm 3.0 cm T2 hyperintense multilobulated cystic lesion within the pancreatic head adjacent to the pancreaticoduodenal groove (arrows), compatible with a side-branch pancreatic intraductal papillary mucinous neoplasm or a mucinous cystic neoplasm of the pancreas.
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13.5–17.5 g/dL). Esophagogastroduodenoscopy confirmed sequelae of gastric ischemia from nontarget embolization, including multiple gastric and pyloric ulcers (Fig 3). Omeprazole and hydromorphone provided symptomatic relief, and the patient was discharged home.
Figure 4. Axial T2-weighted MR image showing complete involution of the previously seen cystic lesion within the pancreatic head adjacent to the pancreaticoduodenal groove (arrows).
Figure 2. Selective segment 4 hepatic artery chemoembolization demonstrating embolic material traveling inferolateral to the expected location of the residual left hepatic lobe (solid arrow), likely within the gastrohepatic ligament, concerning for nontarget embolization. In retrospect, contrast agent staining adjacent to the microcatheter (dashed arrow) may represent the pancreas. A Simmons 1 (Cook, Bloomington, Indiana) catheter is seen within the celiac artery and a Renegade HI-FLO Microcatheter (Boston Scientific, Marlborough, Massachusetts) is seen within the segment 4 hepatic artery.
Repeat MR imaging performed 1 month after the chemoembolization procedure demonstrated complete treatment response of the segment 4 hepatocellular carcinomas. This MR imaging also showed complete involution of the pancreatic IPMN (Fig 4). Given the esophagogastroduodenoscopy findings of gastric ischemia from nontarget embolization, interval regression of the pancreatic IPMN was also thought to be a result of nontarget embolization. Although the pancreatic body and tail have extensive collateral vascular supplies from the pancreatica magna, dorsal pancreatic, and transverse pancreatic arteries, the pancreatic head is vulnerable to injury, as the supplying pancreatoduodenal arcades are terminal vessels (4). In this case, we theorize that reflux of chemoembolic materials into the gastroduodenal artery resulted in nontarget embolization of the pancreaticoduodenal arterial arcade as well as the posterior superior pancreaticoduodenal, anterior superior pancreaticoduodenal, and right gastroepiploic arteries, manifesting in the described findings in the pancreatic head, pylorus, and greater curvature of the stomach (4). In conclusion, although embolization of the pancreatic IPMN was unintentional in this case, it raises the question of whether intentional embolization of IPMNs may become an efficacious form of locoregional therapy. Long-term surveillance of this patient is necessary to assess the durability of the results.
REFERENCES
Figure 3. Photograph from an esophagogastroduodenoscopy showing a 3-cm ulcer with black eschar on the greater curve of the stomach (arrows), consistent with gastric ischemia from nontarget embolization.
1. Klibansky DA, Reid-Lombardo KM, Gordon SR, Gardner TB. The clinical relevance of the increasing incidence of intraductal papillary mucinous neoplasm. Clin Gastroenterol Hepatol 2012; 10:555–558. 2. Tanaka M, Fernández-del Castillo C, Adsay V, et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pancreatology 2012; 12:183–197. 3. López-Benítez R, Radeleff BA, Barragán-Campos HM, et al. Acute pancreatitis after embolization of liver tumors: frequency and associated risk factors. Pancreatology 2007; 7:53–62. 4. Walker TG. Mesenteric vasculature and collateral pathways. Semin Interv Radiol 2009; 26:167–174.