I would strongly support what you're already doing: get opinions from surgeons who specifically treat peritoneal disease and pancreatic cancer before assuming systemic chemotherapy is the only option. Her history is unusual—six years from diagnosis, long disease-free intervals, apparently very limited peritoneal disease, excellent performance status, and strong prior response/tolerance to FOLFIRINOX.

On the question about chemotherapy reaching the peritoneum: there is some scientific basis for that concern, but saying systemic chemotherapy simply “doesn't reach the peritoneum” is too strong. FOLFIRINOX and gemcitabine/nab-paclitaxel can and do produce responses in pancreatic cancer with peritoneal metastases. However, the peritoneal cavity can be a difficult compartment to treat, and intraperitoneal approaches can produce much higher local drug exposure. This is one reason HIPEC, NIPEC and PIPAC are being investigated.

The important issue is that CRS/HIPEC is not currently standard treatment for metastatic pancreatic adenocarcinoma. The evidence is still based largely on small studies and very carefully selected patients. Recent reviews nevertheless report encouraging long-term outcomes in selected patients with isolated, low-volume peritoneal metastases who can undergo complete cytoreduction. Researchers emphasize that we still don't know which patients truly benefit compared with systemic therapy alone.

Your mother's situation is exactly the kind of unusual case where I think asking about this makes sense. Before making a major decision, I would want the specialists to determine whether that 1.8-cm PET-positive nodule really is pancreatic cancer. If technically feasible, biopsy or surgical/laparoscopic confirmation could be important. “Consistent with peritoneal carcinomatosis” on PET isn't the same thing as pathology-confirmed carcinomatosis—particularly when we're talking about essentially one PET-positive lesion and an otherwise clear scan.

I'd also ask about a staging laparoscopy and Peritoneal Cancer Index (PCI). Imaging can underestimate small-volume peritoneal disease. A surgeon considering cytoreduction needs to know whether this really is one or two isolated implants or whether additional tiny deposits are present.

Her germline ATM mutation is another reason I'd want a pancreatic cancer precision-oncology specialist involved. ATM affects DNA-damage repair and makes platinum sensitivity and clinical trials particularly interesting, although ATM does not have the same established pancreatic-cancer indication for PARP maintenance that germline BRCA1/2 does.

There is active research in this area, which reinforces that your questions aren't unreasonable. Current studies are evaluating cytoreductive surgery plus HIPEC in highly selected pancreatic cancer patients with peritoneal involvement, typically requiring favorable biology and disease that remains controlled with systemic therapy.

So I would go into the Cleveland Clinic and Dr. Bartlett consultations asking one central question: “Is this truly widespread carcinomatosis, or is this an oligometastatic/very-low-volume peritoneal recurrence that could reasonably be approached with curative-intent or prolonged-disease-control treatment?”

Given her unusually long history and limited apparent recurrence, I would absolutely want that question answered by more than one experienced team before closing the door on an aggressive approach.