I’ll write a more detailed post when I have some time, but our visit to Yale on Tuesday yielded unexpected hope and cleared away much confusion. Dr. Kliman clarified the diagnosis as massive perivillous fibrin deposition, not maternal floor infarction, related to inflammation (intervillositis) of the placenta’s intervillous space, caused by invading white blood cells from my immune system. In maternal floor infarction, the fibrin, or clotting material, is limited to the area of the placenta closest to the mother’s side. In my case, fibrin built up throughout the intervillous space, obliterating it.
For some reason not clearly understood by science, in cases like mine the placenta fails its job of keeping the baby “invisible” so that the mother’s immune system doesn’t attack it, as any mother’s would otherwise do. Dr. Kliman felt the condition was present from the beginning of the pregnancy and not one that developed toward the end, as I had previously written. He also doesn’t believe an autoimmune disorder was involved and thinks it was a response to Luke’s particular genetic makeup—which helps explain my prior uncomplicated, full-term pregnancy.
Dr. Kliman had hope for a subsequent pregnancy as Luke fared well and strong under the circumstances despite a small and failing placenta, as evidenced by his weight, his survival to 37 weeks, and the fact that he even tried to make some of his own red blood cells. We discussed treatment and monitoring methods and his research, and for the first time in a long time I felt I had met a medical professional who truly cares and is trying to make a difference.