Laparoscopic port site recurrence in the absence of intra-abdominal disease

A case is reported of a patient who presented with recurrent tumour at the site of a laparoscopy port where there had been no evidence of intra-abdominal tumour. Possible mechanisms of recurrence are postulated including a haematogenous spread of the primary tumour and the implantation at the port site.

Laparoscopy and laparoscopic ultrasonography significantly improve the accuracy of staging upper gastro-intestinal malignancy. However, the risk of port site tumour recurrence is a potential complication.^1,2 The incidence is relatively low in diagnostic laparoscopy and may be increased in procedures, which involve tumour manipulation.² In the majority of cases it is likely that direct implantation of tumour cells from instruments or indirect implantation from an aerosol of cells in the pneumoperitoneum account for laparoscopic port site recurrences.² In this report, we describe the development of a port site recurrence in a patient in whom there was no intra-abdominal tumour and neither direct nor indirect tumour implantation can be implicated as a cause for the observed port site metastasis.

A 69-year-old woman presented with a 3-month history of progressive dysphagia. A barium swallow and endoscopy demonstrated the presence of a mid-oesophageal stricture, which on biopsy was found to be due to a primary small cell carcinoma of the oesophagus. A computerised tomography (CT) scan of the chest and abdomen showed no direct extension of the tumour and no mediastinal or abdominal lymphadenopathy and a laparoscopy showed no evidence of intra-abdominal disease. Laparoscopic ultrasonography demonstrated a 0.7 mm lymph node in the coeliac region that was thought suspicious of a metastasis. The patient underwent an oesophagogastrectomy with an uneventful recovery.

Pathology confirmed the presence of a small cell carcinoma that had been completely resected, three out of seven mediastinal lymph nodes were involved with tumour but the nodes from the coeliac axis (submitted seperately) were free of tumour.

Eight months post-operatively the patient presented with weight loss and recurrent dysphagia. On examination, there was a solid nodule at the site of insertion of the port used for the laparoscopic ultrasound probe. A CT scan demonstrated extensive intra-abdominal recurrence of the tumour in the retroperitoneum and hepatic metastases (Figure 1). Fine needle aspiration cytology on the subcutaneous nodule showed features of a small cell carcinoma compatible with the previously excised primary tumour (Figure 2). The patient’s general condition deteriorated rapidly and she died 2 weeks later.

Figure 1: CT scan of patient at the time of recurrent tumour showing hepatic metastases, extensive retroperitoneal tumour recurrence and a nodule on the anterior abdominal wall at the site of a previous port site used for laparoscopic ultrasonography

Figure 2: Fine needle aspiration cytology from a cutaneous skin nodule, at the site of a laparoscopic port, showing typical features of a recurrent small cell carcinoma on a background of necrotic tissue

In the majority of patients with laparoscopic port site metastases the implantation of exfoliated malignant cells is thought to be responsible for this. In this patient, haematogenous spread is the likely mechanism by which tumour cells gained access to the wound as the recurrence was in a body cavity originally uninvolved by tumour. However, wound site recurrences are uncommon following open surgery, when there must be the same opportunity for malignant cells to enter the circulation. Additional factors, therefore, must be implicated in the laparoscopic wound recurrences. Experimental animal models suggest that a pneumoperitoneum may predispose to an altered pattern of tumour growth favouring wound implantation.^2,3 In addition, malignant cells have been demonstrated to grow preferentially in areas of high cellular proliferation such as during repair at a port site wound, this may in part relate to the presence of inflammatory mediators.^{4, 5} In this particular case, it is proposed that the natural history of the cell type may have potentiated haematogenous spread of tumour cells, which have preferentially seeded at the site of the laparoscopic port due to local tissue factors and the presence of a pneumoperitoneum.

Correspondence: Professor K.G.M. Park, Ward 33, Aberdeen Royal Infirmary, Foresterhill, Aberdeen AB25 2ZD, UK

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