Discussion
       Endometrial cancer is the most common gynecological malignancy, but accounts for only 18% of deaths resulting from female genital tract cancer.⁴ Most relapses of endometrial cancers are either pelvic or distant metastasis and occur within the first 2 years after hysterectomy.⁵ Cutaneous spread is quite unusual,^6,7 and implantation of endometrial cancer in the previous scar is even more rare. Only 6 cases of recurrent endometrial cancer in the incision site have been reported.^8–12,13
       The authors believe this case is one of abdominal wound tumor implantation at the time of hysterectomy. The 5-year disease-free interval and the solitary recurrence in the abdominal scar without other concomitant metastases suggests that the tumor probably recurred from cells implanting directly in the wound and then growing slowly, rather than being spread via blood or lymphatic vessels from the initial tumor. Unlike instances of laparotomy wound implantation, skin metastases of endometrial cancer outside the laparotomy wound typically appear as multiple firm nodules that grow quickly in various sites within the body along with coexistent metastases in different organs.¹⁴ This reflects a generalized spread through lymphatics and blood vessels.
       Macias et al¹³ have discussed 2 possible mechanisms to explain how tumor cells may reach the abdominal wall. First, they may penetrate the thickness of the uterine wall or the fallopian tube and spread intraperitoneally through the laparotomy wound. Second, the cells may spill through the cervix during hysterectomy and implant directly in the incision. The tumor cells may or may not remain viable depending on factors, such as the immune status of the patients. Although the effectiveness of suture closure of the uterine cervix before hysterectomy to prevent tumor implantation is not clear, the authors routinely perform this procedure. This patient had deep myometrial invasion and positive peritoneal washings, so the first of these mechanisms is more probable. Two other important mechanisms that were not mentioned are the transference of malignant cells to the abdominal wall by way of surgical gloves or instruments and abdominal washings. Since the peritoneal cavity contains malignant cells, the surgeon’s gloves could likely pick up a few cells and be “transplanted” to the subcutaneous tissue. The same is true with the irrigation fluid from the peritoneal cavity. It is possible that some fluid carrying malignant cells could be left in the subcutaneous tissue. These cells would later implant and cause a problem. These cells would be somewhat resistant to chemotherapy because at the time the chemotherapy is given, they would not have a significant blood supply and consequently would not be exposed to a high level of chemotherapy.
       The clinical features of 7 patients reported with laparotomy wound implantation following endometrial cancers (including the patient in the present study), are summarized in Table 1. Five patients had early stage uterine cancers, and 2 had concomitant metastases in the vagina⁸ and para-aortic lymph nodes.⁹ However, the other 2 patients had advanced stage uterine cancers but no concomitant metastases. The presence of cancer in these sites shows an unusual pattern of dissemination. Espinos et al⁹ suggested that alternative channel formation or possible retrograde flow caused by blockage of the lymph flow during operation as a possible explanation for this dissemination pattern.
       In all patients, the metastases appeared after age 50. Subcutaneous nodules, abdominal pain, incisional pain, and bulging were the first clinical symptoms. The disease-free interval ranged from 1 month to 7 years. The size of the tumor in the laparotomy scar ranged from 4 cm to 12 cm. In 2 patients with advanced stage endometrial cancers (including the patient in the present study), neither received hormonal therapy postoperatively. The effect of hormonal therapy is not clear and it does not appear to alter disease-free survival. Theoretically, continuous combined therapy may be the most appropriate for patients with persistent climacteric symptoms despite using low dose progestin. Patients should be managed on an individual basis and deserve a comprehensive explanation that balances any potential risks with benefits. Kelley and Baker¹⁵ first described the beneficial effect of progestogens in treating metastatic endometrial carcinomas. Although popular, further trials have not shown endocrine therapy to be effective as adjuvant treatment for the primary disease.¹⁶ Progesterone receptors may inhibit the stimulatory effect of estrogens as mitogens in endometrial carcinomas, and hormonal therapy has a place in the management of recurrent disease, particularly where vaginal bleeding is distressing.
       Each of the 7 patients was treated in a different way, including mass resection, EBRT (alone or postoperatively), brachytherapy, chemotherapy, and hormonal therapy. The rarity of this clinical presentation prevents establishing an optimal treatment combination. In the absence of metastases, surgery may be performed as initial treatment if the abdominal mass seems resectable. Postoperative EBRT was administered to solitary laparotomy wound implantation to avoid secondary abdominal scarring for 2 of the patients. Chao et al¹⁷ suggested a dose of about 70–75 Gy focused on the abdominal wound, which is similar to that used for curative treatment of vaginal cuff scar recurrence. Given the documented reduction of tumor volume, even with moderate doses,⁹ EBRT with concomitant hormonal therapy may be used in palliative and preoperative treatments.
       Irradiation of the pelvis after hysterectomy is a common practice to prevent the local recurrence of endometrial cancers. A dose of 45–50 Gy is considered sufficient to treat microscopic disease.¹⁷ As shown in Table 1, 4 of the 7 patients were irradiated after hysterectomy but developed the wound implant 1.5–5 years later. Macias et al¹³ suggested 2 possible reasons for these laparotomy wound implantations. First, the laparotomy wound may be underdosed as a way to avoid significant toxicity. Second, the cranial part of the laparotomy wound may not be included in the irradiation field. In the authors’ opinion, the current radiation therapy plan should not be modified because the acute and chronic toxicity (mainly intestinal) is likely to be greater than the theoretical benefit of preventing this rare type of spread. One patient found in the literature search had their laparotomy scar irradiated after previous radiotherapy of the pelvis. This technique cannot be used again because the small intestine will have already received 50 Gy, which is close to the limit of tolerance.
       A MEDLINE search revealed no reported cases (since 1966) of abdominal wall abscesses that occurred more than a few years after hysterectomy. The patient’s acute lower abdominal pain was similar to the symptoms of an abdominal wall abscess. An abdominal CT scan showed a localized anterior abdominal wall mass in the previous midline incision. Making a differential diagnosis between an abdominal wall abscess and laparotomy wound implantation is sometimes difficult to accomplish clinically. Ultrasonography is a useful tool for making an accurate preoperative diagnosis of an abdominal wall abscess,¹⁸ but it did not help in this case. When cancer cells or abscess definitively invade the abdominal wall, it is difficult to clinically evaluate the degree of vertical invasion to the peritoneum, deep muscle, fascia, and fat layer. In such cases, en bloc full-thickness excision of the anterior abdominal wall may be the most appropriate diagnostic and curative procedure.^10,11
       The diagnosis of laparotomy wound implantation remains a challenge to physicians providing primary care. Laparotomy wound implantation, particularly in its initial phase, often enlarges slowly and has an uncharacteristic presentation. Furthermore, its later symptoms are similar to other frequent and often harmless diseases, such as abdominal wall abscesses. To confront these difficulties, clinicians should pay close attention to those patients in whom the presence of an abdominal wall mass is suspected. Clinical features such as abdominal pain, history of previous surgery, elevated levels of tumor markers, or abnormal histopathology, should be considered.

References

1. Jin F, Devesa S, Chow WH, et al. Cancer incidence trends in urban Shanghai, 1972–1994: an update. Int J Cancer. 1999;83(4):435–440.
2. Rosen T. Cutaneous metastases. Med Clin North Am. 1980;64(5):885–900.
3. Amant F, Moerman P, Neven P, Timmerman D, Van Limbergen E, Vergote I. Endometrial cancer. Lancet. 2005;366(9894):491–505.
4. Boring CC, Squires TS, Tong T. Cancer statistics, 1993. CA Cancer J Clin. 1993;43(1):7–26.
5. Perez CA, Bedwinek JM, Breaux SR. Patterns of failure after treatment of gynecologic tumours. Cancer Treat Symp. 1983;2:217.
6. Mustafa MS, Al-Nuaim L, Inayat-Ur-Rahman N. Scalp and cranial bone metastasis of endometrial carcinoma: a case report and literature review. Gynecol Oncol. 2001;81(1):105–109.
7. Giardina VN, Morton BF, Potter GK, Mesa-Tejada R, Waterfield WC. Metastatic endometrial adenocarcinoma to the skin of the toe. Am J Dermatopathol. 1996;18(1):94–98.
8. Chapman GW Jr, Fabacher P, Thompson H. Incisional recurrence of endometrial carcinoma. J Nat Med Assoc. 1998;80(3):350–351.
9. Espinos JJ, Garcia-Patos V, Guiu XM, Delgado E. Early skin metastasis of endometrial carcinoma: case report and review of literature. Cutis. 1993;52(2):109–111.
10. Curtis MG, Hopkins MP, Cross B, Tantri MD, Jenison EL, Rehmus E. Wound seeding associated with endometrial cancer. Gynecol Oncol. 1994;52(3):413–415.
11. Kotwall CA, Kirkbride P, Zerafa AE, Murray D. Endometrial cancer and abdominal wound recurrence. Gynecol Oncol. 1994;53(3):357–360.
12. Khalil AM, Chammas MF, Kaspar HJ, Shamseddine AI, Seoud MA. Case report: endometrial cancer implanting in the laparotomy scar. Eur J Gynaecol Oncol. 1998;19(4):408–409.
13. Macias V, Baiotto B, Pardo J, Munoz F, Gabriele P. Laparotomy wound recurrence of endometrial carcinoma. Gynecol Oncol. 2003;91(2):429–434.
14. Elit L, Lukka H, Friedman E. Cutaneous metastasis of papillary serous uterine cancer. Gynecol Oncol. 2001;82(1):208–211.
15. Kelley RM, Baker WH. Progestational agents in the treatment of carcinoma of the endometrium. N Engl J Med. 1961;264:216–222.
16. MacDonald RR, Thorogood J, Mason MK. A randomised trial of progestogens in the primary treatment of endometrial carcinoma. Br J Obstet Gynaecol. 1988;95(2):166–174.
17. Endometrium. Chao KSC, Perez CA, Brady LW, eds. Radiation oncology: management decisions. Philadelphia, Pa: Lippincott-Raven; 1999:513–514.
18. Weiner CI, Diaconis JN. Primary abdominal wall abscess diagnosed by ultrasound. Arch Surg. 1975;110(3):341–342.