General Aspects of Obstetric VasculopathiesCHAPTER 1

As a junior resident in the labor ward I once received two mothers of Pregnancy-induced Hypertension (PIH) back-to-back. First one was 37 weeks pregnant, had a BP of 150/100, had edema and trace of albuminuria. The second subject had only 22 weeks pregnancy, a BP of 160/110, edema and very high albuminuria. The first subject went on to deliver normally a 2.9 kg child who was healthy and alive. The second subject of the same disease had to be induced as her BP progressively got more dangerous. The baby could not be salvaged and she took a long time to get her BP pulled back to normal. She stayed in the hospital for nearly 3 months. Many such patients came and went and each time I got challenged, “Why she had this outcome? Why not the others”?

As a couple of years rolled by, I started getting these mothers for subsequent obstetric performances. In her next pregnancy, the first mother who had a milder form of the disease came with no PIH or any other high-risk factor. She delivered vaginally uneventfully and left. The second mother (who had a severe form of the disease and that too very early in pregnancy) came in her next pregnancy with a fetal demise at 10 weeks of pregnancy. The third time she had an IUGR with accidental hemorrhage. She incidentally managed to reach 34 weeks. She had to be sectioned out (LSCS) and went home after nearly a month of stay with us. Her BP had shot up nearing delivery and took nearly a month again for it to come back 2to normal. Concurrently her baby too needed on initial admission in the neonatal intensive care unit (NICU) as we used to call and then a close monitoring. The silver lining was that the mothers did go home with this live baby.

Seemingly diverse obstetric conditions: Severe PIH remote from term, IUGR, accidental hemorrhage and fetal demise all occurred in the same mother in different pregnancies. Are those interlinked conditions? If yes what way they are interlinked? What binds them together? Do they have some long-term effects? Above all, what causes them? How does one treat them?

Those were the early years of the decades of 80s. The institution where, I worked did not have any facilities for ultrasound leave aside a color Doppler then. Aspirin was still scoffed at. We had just begun to use magnesium sulfate to treat eclampsia. There were no computers to manage the data and at best we had calculators to calculate the statistical indices. Our first study on this matter titled preeclampsia remote from term was presented at the All India Conference of Obstetrics and Gynecology at Jaipur. It showed interesting results. This was the harbinger of more than two decades of diligent and dedicated study of these conditions which are now clubbed as obstetric vasculopathy.

Obstetric vasculopathy is not the vasculopathy that occurs in the maternal vascular system. It is the vasculopathy that occurs at the fetomaternal interface. Inherited probably by the genetic propensity at the fetomaternal system, there occurs a series of changed at this interface which invites seemingly totally diverse and apparently unrelated conditions.

In early understandings it was perceived that one condition leads to the other. But as advances in understanding increased, it became clear that this is not a cause-effect relationship but are fruits of the same pathology. In the initial years, only a few conditions were attributed to obstetric vasculopathy viz,

Newer additions also continued which included hyperhemocystenemia. SLE associated pregnancies are a special class. They have a magnified manifestation of vasculopathy thereby enabling a closer look at this miraculous but mysterious phenomenon. While still on lupus, I am reminded of a very thought provoking incidence that took place with me in 1980. It was during my internship in internal medicine that we were allowed to attend a PG case presentation. Incidentally in one of these presentations, one guest from abroad who was visiting my institution was also present. The case being presented was that of SLE. This subject was not pregnant. A professor in internal medicine remarked that this was a rare case. The visiting guest did not agree. He said that he wanted to visit the clinical wards. To the surprise of many of us, he pointed out so many admissions that could be having lupus in association. I do not know if this was followed up with any further investigations or was just scoffed at. I, too, had completely forgotten this incidence. It was nearly a decade later that I suddenly recollected the event when more and more diverse obstetric conditions started associating with obstetric vasculopathy. Lest I may be misunderstood, I wish to clarify that all obstetric vasculopathies are not SLE but SLE does produce obstetric vasculopathy. I would however like to highlight that immunology of and its disturbances have indeed a big role to play in obstetric vasculopathy.