My treatment plan

I’ve been pretty neglectful of this blog, but I wanted to share some details of the treatment plan for my current pregnancy, particularly for other sufferers of MPFD/MFI/VUE/CHI who may come across these writings.

As a refresher, the issue in Luke’s pregnancy was a condition known variously as massive perivillous fibrin deposition, maternal floor infarction, chronic hystiocitic intervillositis, and villitis of unknown etiology. Essentially, for some reason my immune system was able to recognize his placenta where normally it would be “invisible.” His placenta was also expressing something incompatible to my immune system, which consequently attacked the spaces in between the villi, the fingerlike projections of the placenta that are responsible for keeping blood flowing in the placenta. (In cases of villitis, the immune system attacks the villi themselves, but in my case immune cells were found between the villi, hence the intervillositis diagnosis.) As a result, massive clots built up in the placenta (AKA massive perivillous fibrin deposition) and by the time Luke was born, the placenta was in the 0.01 percentile, meaning it was smaller than 99.99 placentas of the same gestational age.

MPFD et al. is characterized in medical journals as incredibly rare and poorly understood. It’s not understood why the placenta isn’t being kept invisible or what genetic factors make the placenta and immune system incompatible—i.e., a simple blood test from Mom & Dad & baby won’t predict whether the doomed combination is present (the placenta comes from paternal DNA, and interestingly, there is a significant history of stillbirth on my husband’s side of the family, for which we don’t know if there is any association). MPFD is said to have a high chance of recurrence (I’ve seen as high as 67 percent), but in truth the condition is so little studied that the actual percentage of recurrence is basically unknown. I belong to a couple of different support groups for MPFD and I’ve met women who’ve lost multiple pregnancies to the condition, including miscarriages, women who’ve had only one loss (often sandwiched in between successful pregnancies), and everywhere in between. There has been some development of a therapy that would suppress the immune system response, but it’s not really available in the U.S., and while it has shown good early results, there hasn’t been enough research to validate it as the treatment of choice. As a result, most of the treatment focuses on treating the clotting that could arise from an immune system response, although some women opt to go on no treatment at all, since the clotting treatments haven’t always proven successful either.

In my case, I found out through testing after Luke’s death that I have a common copy of a mutation in the MTHFR gene, which aids in clotting prevention. Something like 75 percent of the population has this mutation. But given the MPFD diagnosis and this additional information, I decided with my doctors and Dr. Harvey Kliman, a placental pathologist at Yale, to begin taking baby aspirin (81 mg daily) as soon as I had a positive pregnancy test. At around 10 weeks I began seeing a maternal fetal medicine specialist, who also prescribed a prenatal containing folate, as well as additional folate, since those with the MTHFR mutation are unable to properly process folic acid, which is contained in most “regular” prenatal vitamins.

I also had clotting tests redone at around 10 weeks, since some clotting disorders can arise only during pregnancy, and was indeed found to have a deficiency in the Protein S clotting factor. Thus I began a daily self injection of enoxaparin, the generic version of Lovenox, a blood thinner similar to heparin. I started at a dose of 40 mg/ml and was retested periodically to make sure the levels were still high enough in my blood, since enoxaparin is a weight-based medication. At 29 weeks, I indeed had to increase the dose to 60 mg/ml. At 33 weeks, I was retested and remained on the 60 mg/ml dose. I will come off the enoxaparin 24 hours before scheduled induction at 37 weeks, and then I’ll need to go back on it for about a month after delivery so that I myself do not develop clots.

For monitoring, I did a bunch of genetic testing at around 11 weeks (through which we learned the gender), the first growth scan at 18 weeks, and an ultrasound every 3 weeks thereafter until about 24 weeks, at which point I switched to biweekly scans. At 28 weeks we began monitoring blood flow to the baby by measuring Dopplers, and we also began biophysical profiles. All of the scans are done at the MFM’s office, since they have much more powerful machines than my regular OB’s. At 32 weeks I also started weekly nonstress tests at my doctor’s. At 34 weeks the BPPs will increase to twice a week.

I started regular kick counts at 24-25 weeks, earlier than what is medically recommended, but what I needed to do for my own sanity. I’ll write more about that in future posts—I have a lot to say on the matter. Since 28 weeks I have been to the labor and delivery unit at the hospital five times for concerns over possible decrease in fetal movement. So far, each time, we’ve passed the NST and BPP with no problems and checked out within two hours.

Although the baby’s growth, Dopplers, NSTs, and BPPs have all come out looking great at every scan, we still have no way of knowing whether the placenta will start to fail in the last few weeks. We have a lot of information on this pregnancy, but we don’t have the information from Luke’s pregnancy to compare it with, since he was on the routine monitoring for “low-risk” pregnancies, which included a mere two ultrasounds and regular measurements of fundal height and heart rate. Luke’s last ultrasound was at 32 weeks and everything appeared fine, and while we can never be sure whether his condition was present from the very beginning of his pregnancy and may have been detected with more intense monitoring, we do know something went catastrophically wrong between 32 and 37 weeks.

Consequently, at the advice of my MFM, just before 33 weeks, I had two doses of steroids (betamethasone, AKA CElestone) to aid in the baby’s lung maturity should I need to deliver before 37 weeks. Unfortunately, one of the possible side effects is decreased fetal movement, which I did indeed experience, triggering a hefty amount of PTSD and sending me on a late-night trip to L&D within eight hours of receiving the second shot. He performed beautifully on his NST and BPP and I was sent home to monitor movements and see if they picked back up, which thankfully they did.

To sum up, my treatment plan consists of:

• Baby aspirin, 81 mg daily, taken at night (stopping at 36 weeks)
• Self-administered injection of enoxaparin, 60 mg/ml, once daily (stopping 24 hours prior to delivery and resuming 24 hours after delivery, for one month)
• Vitamed MD (prenatal with folate)
• Metanx (extra folate), 1 pill twice daily
• Other supplements (DHA, Vitamin D, probiotics)
• 2 rounds of steroid (betamethasone/Celestone) administered 24 hours apart to aid in lung maturity in case of delivery before 37 weeks
• Regular growth scans, increasing to twice weekly at 24 weeks (at my insistence)
• Biweekly Doppler measurements and BPPs at 28 weeks (in addition to growth scans)
• Weekly NSTs at 32 weeks
• Twice-weekly BPPs and Doppler measurements at 34 weeks
• Intense monitoring of fetal movement (AKA kick counts all day, every day)
• Acupuncture and psychotherapy

I wish I could say something sarcastic or witty or wry at some point here, but the truth is that all of this has been as overwhelming and daunting as it sounds, and I’m basically spent at this point. Which is why, when people ask me how I am feeling, I wish they would ask me how I am doing, because, while it seems trivial, that phrasing acknowledges an understanding on the part of the questioner that this is no normal pregnancy in which physical discomfort is the biggest complaint, and that crippling fear and anxiety are the main beasts, to be wrestled daily. So there you have it.