Thank you for all for your responses. You're certainly not bursting my bubble, Betsy; I think I've read nearly all the published French, Italian, and English literature on treating peritoneal disease in the context of colorectal cancer. (I only felt comfortable playing Pollyanna when no one else would.) That said, I am curious about the scientific rationale for the oncologists' and surgeons' newfound optimism. Throughout this ordeal, I have unfortunately had a very hard time finding any comparable presentations to my wife. On this board, for example, I can't even find a single case of massive ascites that wasn't caused by either extensive carcinomatosis or liver failure. (Nicopia's
is probably the closest case to my wife's, although her met was metachronous, followed by Skifletch and rheaeliza, although her cancer's spread was much more extensive and cytoreduction more extreme; alan b's
case has similarities, but the signet cell ring histology makes comparison difficult.) The only substantial literature reviews of pseudo-Meigs' syndrome in colorectal cancer I've found are the following: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5109729
. (I have a hard time even finding solidly documented case reports of CRC patients diagnosed with isolated
ovarian metastases.) Remarkably, among the vanishingly few reported cases of pseudo-Meigs', a majority of those with long follow-ups (i.e., a handful, which obviously isn't much to go on) remained alive without disease. (Maybe that means there's something unique about the biological and pathophysiological features of cancers that provoke this rare syndrome . . .)
The real question is, Where is my wife likely to recur and will conventional imaging modalities be able to detect a recurrence in a therapeutically timely fashion? Before my wife's exploratory laparotomy and HIPEC in December, I conjectured that her remaining ovary and peritoneum were the most vulnerable potential sites of metastasis. My wife had a normal transvaginal ultrasound about a year before the 22 cm mass was discovered in her left ovary (which was a well-differentiated adenocarcinoma), so it stands to reason that metastasis occurred not long before her dx and grew prodigiously in a short span of time and therefore the ovary represents a preferential site of metastasis in her disease. As her right ovary appeared normal at second-look laparotomy over eight months after her previous operation, if the metastatic pathway to her left ovary was transcoelomic (which is likely since the primary was t4 and the spread was unilateral) rather than hematogenous, there should be a very high likelihood that her right ovary is not microscopically infested. What's more, while not discounting the possibility that pelvic/abdominal adhesions might have insulated the remaining ovary, the fact that her remaining ovary was not obviously infested may have further prognostic significance and serve as an indication that her abdominal/pelvic cavities are largely free from any residual cancer cells—and it's to be hoped that the HIPEC wash eliminated any remaining cells. Even still, if she were to recur in her right ovary, past experience suggests that CA-125 would be markedly elevated, so quarterly serum testing should be at least as effective as pelvic CTs.
Since my wife's PCI turned out to be 0 in her second-look laparotomy, I'm not especially concerned right now about the possibility of peritoneal mets. Preliminary results from trials on prophylactic HIPEC (as well as, I believe, Sugarbaker's anecdotal observations in Peritoneal Carcinomatosis: Principles of Management
) indicate that patients who are macroscopically free of peritoneal surface malignancy at second-look laparotomies scheduled six months or more after primary intervention are very unlikely to subsequently develop carcinomatosis (see, e.g., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291843
). At any rate, CT, PET, and MRI are astonishingly bad at identifying carcinomatosis while it is still surgically treatable, so I'm not convinced that more frequent scans would make a meaningful difference at the end of the day.
Then there's the possibility of liver mets, which is easily the most daunting. But there, too, my wife's case is a bit unusual. First, there has never been any indication of hepatic involvement (unlike, say, rheaeliza or perhaps even Skifletch, who reported that his surgeon discovered friable necrotic material on the dome of his liver). Second, my wife's HIPEC surgeon thoroughly palpated her liver (which can be more effective than radiology in identifying very small superficial lesions) and did discover what he thought was a lesion in her left lobe, so he ended up performing what turned out to be an unnecessary wedge resection, which afforded an opportunity for microscopic evaluation. Third, my wife's one possibly affected lymph node from her primary resection was infested through direct invasion. While the issue is somewhat contentious, there is a good case to be made that direct-invasion-only lymph node status is prognostically intermediate between N0 and N1 status. Last, assuming a clean scan in May, she will be 13.5 months NED. For the sake of assessing the probably of hepatic recurrence, since my wife only had an isolated intraperitoneal met, it makes most sense to compare her odds with stage IIIa patients. If memory serves (I'd have to go through my files to find the precise studies), at least 40 percent of recurrences (at any location) for colon cancer (not rectal cancer) occur within a year. Since only around 15 percent of stage IIIa patients with my wife's tumor histology and the like (although obviously without the ovarian met) will ever develop hepatic metastases, my wife's odds of belonging to the cohort of patients who will never develop hepatic metastases is still somewhat better than even when one widens the confidence interval to account for the admittedly prejudicially skewed data. It's conceivable that this consideration combined with the aforementioned other factors is enough to substantiate the opinion that my wife's probable oncological outcome is at least as good as a stage IIIa patient and justify treating/monitoring her accordingly.
Last, there's a possibility of lung mets, but I think that's fairly remote with my wife's primary location and nodal status. Are six-monthly chest CTs appreciably better at detecting lung mets in a therapeutically timely manner than annual CTs and quarterly serum panels? If my wife were to get a lung met, since her primary was a well-differentiated adenocarcinoma, I would expect it to be pretty slow growing. It's hard to know for sure if CEA is a reliable marker for my wife (owing to the ascites/pleural at the time of her dx), but I tend to think it probably is since it isn't usually elevated with normal Meigs' syndrome, and her level promptly plummeted upon resection of the primary even though she remained septic and her inflammation markers were through the roof.
So, in conclusion, I suppose I'm coming around on this annual CT scan idea. I do like rp1954's idea of adding more indirect markers and have been prevailing upon my wife's doctor to add back in the CA19-9 test (which they don't want to do primarily because it's expensive and probably superfluous—the slightly elevated but still "normal" CA19-9 value at dx can easily be chalked up to peritoneal/pleural irritation); we have something like two dozen biochemical, cytokine, and endocrine panels (still haven't been able to work out why a colonic primary would significantly elevate her testosterone levels) from the months leading up to her diagnosis that were taken in the context of an infertility workup. We will probably be going back to the fertility doctor in the coming months, so it will be easy to add some complementary blood work.