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Peritoneal metastasis of pancreas cancer mimicking the local recurrence of colon cancer after laparoscopic colectomy A previously healthy 67-year-old man presented with gross haematochezia. Colonoscopy revealed a 30-mm adenocarcinoma at the hepatic flexure. No enlarged lymph nodes, distant metastases or other significant findings were noted on computed tomography or fluorodeoxyglucose positron emission tomography. Physical examination was unremarkable, and laboratory data, including tumour makers, were within normal limits. He underwent laparoscopyassisted right hemicolectomy. Pathology showed adenocarcinoma with subserosal invasion. Surgical margins and lymph nodes were negative (pT3N0M0 Stage II). Immunostaining was positive for CK20 and CDX-2 but negative for CK7. Despite the presence of vascular invasion, the patient chose observation. Three months post-operatively, he presented with abdominal pain. Computed tomography revealed enhanced wall thickening and stricture of the ileo-colonic anastomosis. It also revealed irregularly shaped nodules at the previous port sites and a 30-mm low-density lesion in the pancreatic body. Strong fluorodeoxyglucose uptake was noted in all of these lesions (Fig. 1). Blood tests showed mild leucocytosis (10 000/μL). Tumour marker levels were as follows: carcinoembryonic antigen, 4.5 ng/mL (upper limit of normal (ULN)
< 5.0); carbohydrate antigen 19-9, 1343 U/mL (ULN < 37); Duke pancreatic adenocarcinoma cell 2, 647 U/mL (ULN < 150); and s-pancreas-1, 151 U/mL (ULN < 30). The patient underwent needle biopsy of the subcutaneous tumours and endoscopic ultrasound-guided fine needle biopsy of the pancreatic lesion. Both showed adenocarcinoma positive for CK7 but negative for CK20 and CDX2. This immunostaining profile led to the final diagnosis of primary pancreatic cancer with metastases to the anastomosis and port sites of the previous laparoscopic colectomy. Retrospective review of the preoperative images did not reveal significant radiological findings in the pancreas. Multiple liver metastases appeared within a month; the patient died two months later. Several studies have reported the recurrence of completely resected tumours, or the recurrence of unexpected malignant lesions in an organ resected for benign disease (e.g. recurrence of gallbladder carcinoma after laparoscopic cholecystectomy for cholelithiasis). However, this case is unique and challenging because peritoneal metastases of occult cancer became evident after oncological surgery for a seemingly unrelated organ and the
Fig. 1. Computed tomography (a–c) and positron emission tomography (d–f) 3 months after laparoscopic colectomy. They revealed enhanced wall thickening and stricture of the ileo-colonic anastomosis (a), irregularly shaped nodules at the previous port sites (b) and a 30-mm low-density lesion in the pancreatic body (c). Strong fluorodeoxyglucose uptake was noted in all of these lesions (d–f).
© 2015 Royal Australasian College of Surgeons
ANZ J Surg •• (2015) ••–••
2
radiographic features of this case were confusingly similar to that of local recurrence of the primary tumour. A PubMed search revealed six cases with a similar clinical history, but all exhibited port-site metastasis only. The preceding operation was laparoscopic cholecystectomy in all cases and the origins of malignancy were the ovary,1 colon,1,2 and undetected3–5 in one, two and three patients, respectively. There are two possible scenarios to explain the clinical course of this patient as peritoneal washing cytology was not performed. The first scenario is that laparoscopic colectomy spread pancreatic cancer cells to the peritoneal cavity; the second scenario is that the operation promoted the progression of already existing intraperitoneal-free malignant cells. The first scenario could have occurred with mobilization of the right colon. Although direct manipulation of a pancreatic tumour was unlikely, the procedure could facilitate tumour dissemination by retroperitoneal dissection and exposure of the pancreatic head. Injury to the peritoneum could also promote tumour proliferation through the formation of blood clots with fibrin that can trap intraperitoneal-free cancer cells, or through the formation of inflammatory, growth and angiogenic factors. Although not proven histologically, the anastomotic stenosis may have been due to the implantation of cancer cells into the anastomotic site. Other potential mechanisms for tumour seeding have been proposed, such as an effect of carbon dioxide, pneumoperitoneum5 or aerosolization of tumour cells, but these mechanisms remain unproven.
Images for surgeons
References 1. Rieger N, McIntosh N. Port site metastasis from synchronous primaries of the colon and ovary following laparoscopic cholecystectomy. Eur. J. Surg. Oncol. 1998; 24: 144–5. 2. Azevedo JL, Mattos D, Ricci M, Azevedo O. Dissemination of latent colon adenocarcinoma after laparoscopic cholecystectomy. Endoscopy 1999; 31: 828–30. 3. Mintz Y, Lotan C, Goitein D, Muggia-Sullam M. Laparoscopic port site metastasis of an undetected primary tumor. Surg. Laparosc. Endosc. 1999; 9: 68–9. 4. Yildirim S, Ezer A, Colakoglu T et al. An unusual case of port site metastasis after laparoscopic cholecystectomy in a renal transplant patient: a case report. Transplant. Proc. 2006; 38: 1369–70. 5. Rao S, Rathod A, Kamble A, Gupta D. Delayed presentation of port-site metastasis from an unknown gastrointestinal malignancy following laparoscopic cholecystectomy. Singapore Med. J. 2014; 55: e73–6.
Hiroshi Nagata, MD Hironori Yamaguchi, MD, PhD Toshiaki Watanabe, MD, PhD Department of Surgical Oncology, The University of Tokyo, Bunkyo, Tokyo, Japan doi: 10.1111/ans.13015
© 2015 Royal Australasian College of Surgeons
Peritoneal metastasis of pancreas cancer mimicking the local recurrence of colon cancer after laparoscopic colectomy A previously healthy 67-year-old man presented with gross haematochezia. Colonoscopy revealed a 30-mm adenocarcinoma at the hepatic flexure. No enlarged lymph nodes, distant metastases or other significant findings were noted on computed tomography or fluorodeoxyglucose positron emission tomography. Physical examination was unremarkable, and laboratory data, including tumour makers, were within normal limits. He underwent laparoscopyassisted right hemicolectomy. Pathology showed adenocarcinoma with subserosal invasion. Surgical margins and lymph nodes were negative (pT3N0M0 Stage II). Immunostaining was positive for CK20 and CDX-2 but negative for CK7. Despite the presence of vascular invasion, the patient chose observation. Three months post-operatively, he presented with abdominal pain. Computed tomography revealed enhanced wall thickening and stricture of the ileo-colonic anastomosis. It also revealed irregularly shaped nodules at the previous port sites and a 30-mm low-density lesion in the pancreatic body. Strong fluorodeoxyglucose uptake was noted in all of these lesions (Fig. 1). Blood tests showed mild leucocytosis (10 000/μL). Tumour marker levels were as follows: carcinoembryonic antigen, 4.5 ng/mL (upper limit of normal (ULN)
< 5.0); carbohydrate antigen 19-9, 1343 U/mL (ULN < 37); Duke pancreatic adenocarcinoma cell 2, 647 U/mL (ULN < 150); and s-pancreas-1, 151 U/mL (ULN < 30). The patient underwent needle biopsy of the subcutaneous tumours and endoscopic ultrasound-guided fine needle biopsy of the pancreatic lesion. Both showed adenocarcinoma positive for CK7 but negative for CK20 and CDX2. This immunostaining profile led to the final diagnosis of primary pancreatic cancer with metastases to the anastomosis and port sites of the previous laparoscopic colectomy. Retrospective review of the preoperative images did not reveal significant radiological findings in the pancreas. Multiple liver metastases appeared within a month; the patient died two months later. Several studies have reported the recurrence of completely resected tumours, or the recurrence of unexpected malignant lesions in an organ resected for benign disease (e.g. recurrence of gallbladder carcinoma after laparoscopic cholecystectomy for cholelithiasis). However, this case is unique and challenging because peritoneal metastases of occult cancer became evident after oncological surgery for a seemingly unrelated organ and the
Fig. 1. Computed tomography (a–c) and positron emission tomography (d–f) 3 months after laparoscopic colectomy. They revealed enhanced wall thickening and stricture of the ileo-colonic anastomosis (a), irregularly shaped nodules at the previous port sites (b) and a 30-mm low-density lesion in the pancreatic body (c). Strong fluorodeoxyglucose uptake was noted in all of these lesions (d–f).
© 2015 Royal Australasian College of Surgeons
ANZ J Surg •• (2015) ••–••
2
radiographic features of this case were confusingly similar to that of local recurrence of the primary tumour. A PubMed search revealed six cases with a similar clinical history, but all exhibited port-site metastasis only. The preceding operation was laparoscopic cholecystectomy in all cases and the origins of malignancy were the ovary,1 colon,1,2 and undetected3–5 in one, two and three patients, respectively. There are two possible scenarios to explain the clinical course of this patient as peritoneal washing cytology was not performed. The first scenario is that laparoscopic colectomy spread pancreatic cancer cells to the peritoneal cavity; the second scenario is that the operation promoted the progression of already existing intraperitoneal-free malignant cells. The first scenario could have occurred with mobilization of the right colon. Although direct manipulation of a pancreatic tumour was unlikely, the procedure could facilitate tumour dissemination by retroperitoneal dissection and exposure of the pancreatic head. Injury to the peritoneum could also promote tumour proliferation through the formation of blood clots with fibrin that can trap intraperitoneal-free cancer cells, or through the formation of inflammatory, growth and angiogenic factors. Although not proven histologically, the anastomotic stenosis may have been due to the implantation of cancer cells into the anastomotic site. Other potential mechanisms for tumour seeding have been proposed, such as an effect of carbon dioxide, pneumoperitoneum5 or aerosolization of tumour cells, but these mechanisms remain unproven.
Images for surgeons
References 1. Rieger N, McIntosh N. Port site metastasis from synchronous primaries of the colon and ovary following laparoscopic cholecystectomy. Eur. J. Surg. Oncol. 1998; 24: 144–5. 2. Azevedo JL, Mattos D, Ricci M, Azevedo O. Dissemination of latent colon adenocarcinoma after laparoscopic cholecystectomy. Endoscopy 1999; 31: 828–30. 3. Mintz Y, Lotan C, Goitein D, Muggia-Sullam M. Laparoscopic port site metastasis of an undetected primary tumor. Surg. Laparosc. Endosc. 1999; 9: 68–9. 4. Yildirim S, Ezer A, Colakoglu T et al. An unusual case of port site metastasis after laparoscopic cholecystectomy in a renal transplant patient: a case report. Transplant. Proc. 2006; 38: 1369–70. 5. Rao S, Rathod A, Kamble A, Gupta D. Delayed presentation of port-site metastasis from an unknown gastrointestinal malignancy following laparoscopic cholecystectomy. Singapore Med. J. 2014; 55: e73–6.
Hiroshi Nagata, MD Hironori Yamaguchi, MD, PhD Toshiaki Watanabe, MD, PhD Department of Surgical Oncology, The University of Tokyo, Bunkyo, Tokyo, Japan doi: 10.1111/ans.13015
© 2015 Royal Australasian College of Surgeons
