A 65-year-old woman with a past medical history
significant for depression and anxiety disorder presented in 1991 with
abdominal distension and increasing girth. Imaging studies revealed bilateral
ovarian masses, and she underwent a total abdominal hysterectomy and bilateral
salpingo-oophorectomy and debulking surgery for a stage IIb ovarian epithelial
Adjuvant chemotherapy with carboplatin and
cyclophosphamide was given for a total of six cycles. Her disease remained
indolent, and she was monitored with surveillance scans and blood work. In
1998, she was found to have an isolated relapse in the spleen. The patient
underwent splenectomy. Chemotherapy was not administered after the surgery.
In October 2000, it was noted that her CA-125 started to
slowly increase with a negative CT scan. She had no complaints of symptoms. She
was again monitored with surveillance scans and blood work. In February 2002,
she developed left supraclavicular metastasis as the only site of disease.
Treatment with tamoxifen at that time failed. Her lymphadenopathy became
painful and enlarged further in early 2003, and she was treated with five
cycles of carboplatin and paclitaxel with an excellent response.
Figure 1. (Clockwise from top left CT image, PET image,
whole body maximum intensity projection PET image, CT/PET fusion image). There
is progression of lymphadenopathy in the left supraclavicular station (arrow
Photos courtesy of M. Ghesani
She had recurrence of the supraclavicular lymph nodes in
December 2005 and received seven doses of doxorubicin. She had a good partial
response, but treatment was stopped because of severe skin toxicity. She then
received docetaxel/cisplatinum, resulting in a marked decrease in the size of
her neck nodes to less than 1 cm and a drop in the CA-125 from 170 in November
2006 to 19 on January 2007.
Her left neck/supraclavicular lymphadenopathy, again,
became enlarged and symptomatic with pain. She completed a course of RT to the
left neck/supraclavicular area with slow regrowth during 13 months,
subsequently. At that time, chemotherapy was restarted with cisplatin and
cyclophosphamide in April 2010. She received two cycles in that month, 21 days
apart. The third cycle, given in May, was interrupted because of platinum
allergic reaction. Repeat CT scan of the neck and the physical examination
showed no change in her neck nodes.
She received gemcitabine hydrochloride from June to October. She did not
tolerate treatment well, showing abnormal liver function tests and significant
fatigue. She did not respond to chemotherapy, and bulky disease progressed in
the left neck. Salvage chemotherapy with weekly vinorelbine started last month.
Figure 2. Display convention, same as Figure 1. There is
progression of lymphadenopathy in the left tracheoesophageal groove (arrow
Ovarian cancer is one of the most treatable solid
tumors; most patients will respond temporarily to surgery and cytotoxic agents.
The disease, however, frequently persists and recurs, having the highest
fatality-to-case ratio of all the gynecologic cancers. Ovarian cancer
represents one-fourth of the malignancies of the female genital tract, but it
is the most common cause of death among women who develop cancers of
gynecologic origin. Ovarian carcinomas account for 4% of the total cancers in
women in the US, ranked behind malignant neoplasms of the lung, breast, colon
and uterus. Annually in the US, approximately 21,550 new cases are diagnosed
and 14,600 ovarian cancer-related deaths occur. Despite discouraging
statistics, improvement in 5-year survival has occurred steadily during the
past 3 decades because of more aggressive surgical management and the
development of more effective chemotherapy. Five-year survival in the US has
improved significantly, from 37% in 1974-1976 to 52% in 1992-1998.
Ovarian carcinoma can spread by local extension,
lymphatic invasion, intraperitoneal implantation, hematogenous dissemination
and transdiaphragmatic passage. Intraperitoneal dissemination is the most
common and recognized characteristic of ovarian cancer. In contrast,
hematogenous spread is clinically unusual early on in the disease process,
although it is not infrequent in patients with advanced disease. It has been
demonstrated that the earliest mode of spread is by exfoliation of cells that
implant along the surfaces of the peritoneal cavity. The cells follow the
circulatory path of peritoneal fluid, often moving with the forces of
respiration from the pelvis, up the paracolic gutters (especially on the
right), along the intestinal mesentery, to the right hemidiaphragm. These
implanted cells give rise to metastatic foci in the posterior cul-de-sac, the
paracolic gutters, on the diaphragmatic surface, the liver capsule, the surface
of the intestines, and the omentum. This progressively agglutinates loops of
bowel, leading to functional intestinal obstruction, or carcinomatous ileus.
Figure 3. Display convention, same as Figure 1. New metabolic
lymphadenopathy in the left periparotid region (arrow 3); suspicious for
metastatic ovarian carcinoma. Note that metastatic disease is limited to the
left neck. There was no evidence of metastatic disease in the lungs, abdomen,
pelvis or skeleton.
Lymphatic dissemination to the pelvic and para-aortic
lymph nodes is most common, particularly in advanced disease. Spread through
the lymphatic channels of the retroperitoneal lymph nodes and the diaphragm can
lead to dissemination of disease into the supraclavicular lymph nodes and
pleural space. Apparent stage I and II tumors have retroperitoneal lymphatic
dissemination in about 5% to 10% in most series, whereas lymphatic
dissemination in stage III has been reported to be as high as 42% to 78% in
carefully explored patients. Most of these lymph nodes are not enlarged but are
microscopically positive for malignant cells. Spread through the
retroperitoneal and diaphragmatic lymphatics can result in metastasis to the
supraclavicular lymph nodes. Hematogenous dissemination at the time of
diagnosis is uncommon, with only a small percent of patients who are found to
have parenchymal involvement of the lungs or liver. Brain metastases are
Munir Ghesani, MD, is an attending radiologist at St.
Lukes-Roosevelt Hospital Center, and Beth Israel Medical Center and a
HemOnc Today section editor. He is an associate clinical professor
of radiology at Columbia University College of Physicians and Surgeons.
Amit Patel, MD, is a fellow in oncology at St. Lukes-Roosevelt
Gabriel Sara, MD, is an oncology attending at St.
For more information:
- Burghardt E. Am J Obstet Gynecol.
- Cannistra SA. N Engl J Med. 2004;351:2519-2529.
- Chen SS. Gynecol Oncol. 1983;16:95-100.
- Dauplat J. Cancer. 1987;60:1561-1566.
- Jemal A. CA Cancer J Clin. 2009;59:225-249.