Ovarian cancer most commonly spreads within the peritoneal cavity, often along surfaces within the abdomen and pelvis, rather than primarily through the bloodstream. The typical pattern involves direct extension and shedding of cancer cells into the peritoneal fluid, leading to implantation on peritoneal surfaces, the omentum, and diaphragmatic surfaces. Lymphatic spread and, less commonly, hematogenous (blood-borne) spread can occur as secondary routes, but intracavitary/peritoneal dissemination is the hallmark pattern for most epithelial ovarian cancers. This peritoneal spread can result in widespread small tumor implants and ascites, particularly when the disease involves the omentum and peritoneal surfaces. Key spread patterns to know:
- Intracavitary/peritoneal spread: cancer cells disseminate within the peritoneal cavity, implanting on serosal surfaces (e.g., omentum, peritoneum, diaphragmatic surfaces), often with ascites.
- Direct extension: local invasion into adjacent pelvic organs such as the uterus, bladder, rectum, or colon.
- Lymphatic spread: involvement of regional lymph nodes can occur and may precede or accompany peritoneal spread.
- Hematogenous spread: less common as an initial pattern, but distant metastases via blood can occur, especially in advanced disease.
Clinical implications:
- Symptoms often reflect peritoneal involvement (abdominal distension from ascites, weight loss, abdominal pain).
- Staging and prognosis frequently depend on the extent of peritoneal tumor implants and involvement of omentum and diaphragmatic surfaces.
- Treatments (surgery and platinum-based chemotherapy) are typically planned with the goal of debulking peritoneal disease to minimize tumor burden.
If you’d like, I can tailor this to a specific subtype (e.g., high-grade serous ovarian cancer) or summarize how spread patterns influence staging and treatment decisions.