J. Newman, et al. Surg Chron 2012; 17(3): 223-224.

Pancreatic Tail Adenocarcinoma Presenting with Haematuria and Bowel Obstruction
James Newman1, James Edward Frankland Fitzgerald 1, Adam P. Levene 2 ,Rajesh Aggarwal 3, Timothy George AllenMersh 3
1 2

Chelsea & Westminster NHS Hospital Trust, 369 Fulham Road, London, SW10 9NH Department of Histopathology, St Mary’s Hospital, Praed Street, London W2 1NY 3 Division of Surgery, Oncology, Reproductive Biology and Anaesthetics, Imperial College, London, SW7 2AZ

Pancreatic carcinoma has the eighth highest incidence of all cancer world-wide, and has the highest case mortality when 5-year incidence is compared to 5-year mortality (ratio 0.977).[1] This high mortality is partly attributable to late presentation arising from difficulty in early detection and diagnosis, with approximately 50% of cases presenting with distant metastases at the time of diagnosis[2]. Localised adenocarcinoma may progress to local invasion of surrounding vasculature and organs, typically duodenum, bile duct, stomach and spleen. Metastases commonly occur in liver, peritoneum, and lung although may occur in any abdominal organ via peritoneal spread. Cases where initial presentation is due to symptoms from metastasis to small bowel[3], bladder[4], and direct invasion of the splenic flexure[5] have been reported. To the best of our knowledge, this is the first case in the literature of pancreatic carcinoma presenting as haematuria from metastasis to bladder with synchronous large bowel obstruction due to direct tumour infiltration. A 62-year-old male heavy smoker was seen in the Urology outpatient clinic with a short history of haematuria. A further one-month history of central abdominal and lower back pain, 6kg weight loss, and 10-day history of constipation was elicited. A computerised tomography scan reported an enhancing nodule at the superior aspect of the bladder. It also showed a partially constricting annular lesion of the splenic flexure with lesions suspicious for malignant metastases abutting the pancreatic tail and greater curve of the stomach. Numerous liver metastases and generalised peritoneal nodularity were also noted. One-week post-CT scan, he presented to the emergency department with acute abdominal pain. Plain abdominal radiograph suggested large bowel obstruction with competent ileocaecal valve and free air was present under the diaphragm. At emergency laparotomy, caecal perforation was found with multiple peritoneal metastases. There was a fixed, indurated area at the splenic flexure with appearances suggestive of a primary colonic tumour that appeared to be directly infiltrating the spleen; visualisation of the pancreas was not attempted. A right hemicolectomy with defunctioning ileostomy was performed to excise the ischaemic caecum; the tumour was left in situ as it was assessed as clinically non-resectable by the operating surgeon. Post-operatively the patient developed a perihepatic collection containing faecal material which was drained percutaneously under radiological guidance. Despite prophylactic low molecular weight heparin he developed a

deep vein thrombosis with subsequent massive pulmonary embolus and was placed on a palliative care pathway. The histopathology (figs 1-3) showed bowel mucosa with patchy ulceration associated with active chronic inflammation. Within the muscularis propria and the serosa there was focal infiltration by a moderately differentiated adenocarcinoma which did not arise from the mucosa. The tumour was associated with full-thickness mural necrosis and marked fibrinopurulent peritoneal deposits, with bowel perforation. The tumour cells stained strongly positive for cytokeratin 7 (CK7) and negative for cytokeratin 20 (CK20). The tumour cells also showed strong positivity for carcinoembryonic antigen (CEA).

A

B

Figure 1: Adenocarcinoma on serosal surface (A) demonstrating staining for CEA (B) and CK7 (C) (10x)

The consensus opinion of the lower gastrointestinal cancer multidisciplinary team meeting in view of the immunohistochemistry results and after review of the imaging at the local specialist centre was that of a primary tail of pancreas adenocarcinoma with direct invasion of the spleen and local spread to the splenic flexure with disseminated malignancy. The lesion on the bladder was shown to be an infiltrating metastasis from the pancreatic carcinoma with full thickness invasion of the bladder wall. Timely clinical diagnosis of pancreatic cancer can be difficult due to the variable and often non-specific early symptoms. This unique presentation was that of haematuria, with a subsequent emergency presentation consistent with an obstructing colonic primary at the splenic flexure. Histopathology was essential in establishing the final diagnosis. Histopathology revealed the tumour to be + CK7 /CK20 and strongly positive for CEA which in this clinical setting favoured a pancreatico-biliary origin for the tu+ mour. The immunoprofile CK7 /CK20 has been variously reported as positive in 26-65% of carcinomas of pancreatico-billary origin[6-8] although may also occur in upper gastrointestinal, lung, thyroid and breast carcinoma. The negative CK20 staining was useful in this case in ruling out a co223

J. Newman, et al. Surg Chron 2012; 17(3): 223-224.

lonic carcinoma. The immunohistochemistry was therefore important for the diagnosis and subsequent management of the patient. The presentation of painless haematuria in a male should always include malignancy within the differential th diagnoses, as bladder carcinoma is the 7 most common carcinoma in males[1]. Tumour induced haematuria may be caused by metastatic spread and invasion of any part of the urinary tract[9] and is often associated with late stage, advanced metastasis. Haematuria is a rare presenting symptom for pancreatic carcinoma and has been infrequently reported[4] as symptomatic metastasis to the bladder is rare due to the fact that metastatic carcinoma does not commonly invade the bladder mucosa[4]. This unique presentation serves to highlight the importance of early detection and treatment of annular constricting lesions of the large bowel, and the need for a wide differential when considering causes of painless haematuria and bowel obstruction. In this case, histopathological analysis of the tissue was essential to correctly identifying the tissue origin of the tumour and informing the subsequent management plan and discussions with the patient. References
1. Parkin DM, Bray F, Ferlay J, Pisani P. Global Cancer Statistics, 2002. CA Cancer J Clin. 2005 March 1;55(2):74-108.

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Kalser MH, Barkin J, Macintyre JM. Pancreatic cancer. Assessment of prognosis by clinical presentation. Cancer 1985;56(2):397-402. Takase K, Imanishi K, Murao S, Kamamaru T, Yamamoto M. A Case of Perforation of the Small Bowel Due to a Metastatic Small Intestinal Tumor From Pancreatic Cancer. -Analysis and Report of this Disease in Japan-. Pancreas 2009 July;38(5):490. Chiang KS, Lamki N, Athey PA. Metastasis to the bladder from pancreatic adenocarcinoma presenting with hematuria. Urol Radiol 1991;13(1):187-189. Slam KD, Calkins S, Cason FD. LaPlace's law revisited: Cecal perforation as an unusual presentation of pancreatic carcinoma. World J Surg Oncol 2007;(5):14. Wang NP, Zee S, Zarbo RJ, Bacchi CE, Gown AM. Coordinate expression of cytokeratin-7 and cytokeratin-20 defines unique subsets of carcinomas. Appl Immunohistochem 1995;3(2):99-107. Alexander J, Krishnamurthy S, Kovacs D, Dayal Y. Cytokeratin profile of extrahepatic pancreaticobiliary epithelia and their carcinomas. Appl Immunohistochem 1997;5(4):216-222. Tot T. Adenocarcinomas metastatic to the liver. The value of cytokeratins 20 and 7 in the search for unknown primary tumors. Cancer 2000;85(1):171-177. Martino L, Martino F, Coluccio A, Mangiarini MG, Chioda C. Renal metastasis from pancreatic adenocarcinoma. Arch Ital Urol Androl. 2004;76(1):37-39.

Author for correspondence: James Newman Chelsea & Westminster NHS Hospital Trust, 369 Fulham Road, London, SW10 9NH Email: james.newman@some.oxon.org Telephone: +44 (0) 7929 721929

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