Progesterone, 4 years later

The IUI went as planned on Saturday, and today I went in for a blood progesterone test. It came back at 15.1 ng/mL, not as high as my highest value back in April 2013, but well within the normal range. Yay!

I wrote about progesterone back then, so I won’t go into detail about it here. However, I did notice a significant packaging change since last time:

I like that the new packaging allows me to pack just the 6 suppositories I need for tomorrow’s trip to Park City. Now if I can just figure out how to keep it on the DL while sharing a fridge with all C’s residency buddies and their kids… (Not that I’m embarrassed about infertility; I just think it might be a tad awkward to explain that the bullet-shaped things next to their kids’ string cheese are going to go up my hoo-ha…)

Oh, and another fun fact: I recently learned that my trans friend takes progesterone as part of her hormone therapy. In each 28-day cycle, she takes 200 mg of oral progesterone on cycle days 14-23 (along with an injection of estradiol every two weeks). Yet another unexpected human connection, brought to me courtesy of infertility!

A bit of good news

Seven months after we lost Jane, it appears that my cycles have normalized somewhat, and we are on track for our first properly-timed natural cycle IUI. (Second IUI overall since Jane.)

Here’s a TMI TTC timeline:

Cycle start Notes Positive OPK Cycle length Ovulation?
July 24 Delivered Jane n/a 11 weeks ?
October  7 1st period postpartum CD8 and CD16 (!) 26 days In Europe, tried ourselves
November 2   CD24 35 days In Texas, tried ourselves
December 7   CD35 46 days IUI after positive OPK
January 22 CD15 26 days C out of town; office closed for holiday
February 17 Trigger Friday (CD15) ? This Saturday?


Our plan was to do as many natural cycle IUIs as Kaiser would let us get away with, but our travel plans got in the way twice, and my cycles got progressively longer and more difficult to anticipate (leading me to wonder if this is what perimenopause looks like…)

After a couple of disappointing mid-cycle ultrasounds, the nurse practitioner at Kaiser volunteered that I could call as soon as I got a ‘high’ or ‘peak’ reading on my advanced OPK, and she would squeeze me in to take a look. That’s how the IUI went down in early January (the day after an ‘oops’ positive OPK and same-day sonogram showing a mature follicle). And then Presidents’ Day went and mucked up the February cycle…


All that to say that this cycle things appear to be on-track:

  • On Sunday (CD10), I got a ‘high’ reading on my OPK.
  • I called Monday and got an appointment for a mid-cycle ultrasound today (CD13).
  • On ultrasound today, I had not one, but two nice-looking 16 mm follicles (one on each side).
  • My uterine lining looked “great” (9-10 mm?).

Since the clinic isn’t open Sunday, we scheduled an IUI for Saturday morning, with plans to trigger on Friday.

Wish me luck!

There Is No Good Card for This

This morning on my drive to work, I heard an interview with Emily McDowell on NPR. If you haven’t heard of her amazing Empathy Cards, stop reading right now and go check them out!

Seriously, I’ll wait.


After I lost Jane, a coworker sent me this card:


I went straight to and ordered 20 cards the same day.


I didn’t even realize until this morning that she has an infertility card too! (Although many of her other designs would also be perfect for infertility, pregnancy loss, or a whole bunch of other shitty things…)


Anyway, the reason for the interview was that she just coauthored a book, titled – wait for it – “There Is No Good Card for This: What to Do When Life is Scary, Awful, and Unfair to the People You Love.”


I live with my foot permanently wedged in my mouth, and have lamented the fact that I have been/would be pretty worthless at comforting a friend in the way my amazing friends (including several who read this blog) did for me.


I just added this book to my Amazon cart. Can’t wait!

Staying the course…for now

My period arrived last Sunday. I emailed Dr. Y to double check our course of action.

In particular, I wanted to see whether he thought we should start using stims (like Clomid or Menopur) to stimulate regular ovulation. Since losing Jane in July, I’ve had exactly three cycles, which were 26, 35, and 46 days long. (This trend is not particularly reassuring…) We also did a progesterone test this last cycle at 7 dpo, which came back at only 5.7 ng/mL. (I’m pretty sure it’s supposed to be higher – say, 10 ng/mL or more. Previous values from when I was trying to conceive C. Samuel and Jane were 24.5 and 9.6 ng/mL.)

Dr. Y said we can try Clomid if I want, but he doesn’t think it will be any more effective than natural cycle IUI. He does however recommend supplementing with those awful progesterone suppositories. Given my ever-changing ovulation date, he said we could try waiting to schedule my next ultrasound until my advanced OPK gives a ‘high’ reading. So we’re staying the course for now.

On Monday, I spoke to students and faculty from the Biology and Chemistry departments about losing Jane Margaret (sharing what happened and what I did to cope during my leave). The talk forced me to organize my thoughts about several things, which should eventually find their way into this blog.

Tuesday was the 6-month anniversary of losing Jane.

Back in the stirrups

Nearly six months after losing Jane, life has returned to some version of normal. I started back at work teaching on Tuesday, and on Wednesday we were finally able to accomplish our first natural cycle IUI since the loss.

So here I am in another two-week wait. It’s a strangely comfortable place to be.


Jane’s headstone at Christmas

Well, fuck!

That’s what I said when I read my most recent email from Dr. Y’s nurse:


Yes, she writes her emails all in caps like that, as if I needed any more reason to feel alarmed.

My AMH is less than 0.03. I didn’t know the test measured amounts that low.

In what feels like another lifetime, I once wrote a long post about what AMH (and FSH and estradiol) mean for fertility.

Here’s a summary of my results the four times I’ve taken these tests. Prior to yesterday, 0.17 ng/mL was the lowest AMH of anyone I know in real life (including my Resolve support group).

  1/26/13 5/4/13 4/24/15 10/8/16
estradiol (E2) 24.6 pg/mL 27.2 pg/mL 23 pg/mL 20 pg/mL
follicle stimulating hormone (FSH) 13.7 mIU/mL 13.5 mIU/mL 9.7 mIU/mL 17.7 mIU/mL
anti-Mullerian hormone (AMH) 0.17 ng/mL 0.22 ng/mL 0.31 ng/mL <0.03 ng/mL


I’m feeling pretty hopeless at the moment.

At least I get to go to Rome on Sunday.

When to try again

And now we arrive at the last of our unpleasant decisions following Jane’s passing:

Decision 10: When to try again.

By way of background for those of you who are new to my blog: three years ago, after an early miscarriage followed by 6 months of unsuccessful trying on our own, I was diagnosed with diminished ovarian reserve. I’m a non-responder to stims, having produced only a single egg during medicated IUI, and IVF cycles. Miraculously, we conceived our first rainbow baby C. Samuel spontaneously in between IVF cycles. After C. Samuel was born, we decided to try for #2 via natural cycle IUI. On the sixth month of this, we conceived Jane Margaret.

Some conclusions from our adventures in infertility:

  • I have precious few good eggs left. (One of my doctors predicted that I would go through menopause before age 40…I’ll be 38 next month.)
  • I consistently ovulate one (and only one) egg per month, with or without stims.
  • When we’ve been lucky enough to have one of C’s supersperm catch a good egg, the babies that result are beautiful and perfect (though I can’t say the same for the resulting placentas).  😦

Contrast that with the following advice re: trying again after stillbirth:

  • The American Pregnancy Association recommends waiting several months up to a year to try again after a stillbirth.
  • Dr. R recommended waiting 3-6 months before trying again.
  • Dr. R mentioned a study suggesting that shorter time between pregnancies may be correlated with shorter umbilical cords (part of Jane’s perfect storm), though she acknowledged that the study wasn’t especially compelling.

Having discussed all of these considerations and more, C and I quickly agreed on a decision:

We want to try again as soon as possible! 

We both find the egg scarcity argument more compelling than the emotional self-care concerns. What if I ovulate my last good egg on one of the months that we’re “waiting to try”?!

As it happens, my own body forced a bit of a compromise, since it took 11 weeks for my period to come back after Jane’s passing. My bitchy Aunt Flo showed up on Friday, and on Saturday I got my blood drawn to repeat my CD3 (in this case CD2) bloodwork. Unlike last time, my FSH went in the wrong direction (up to 17.7 mIU/mL). :/


At least C. Samuel is optimistic. He busted this song out during a recent visit to Ong Ba’s (Grandma & Grandpa’s) house. Neither C nor I had ever heard it before.


The Rainbow Song lyrics:

Red orange yellow green blue purple,

red orange yellow green blue purple,

red orange yellow green blue purple,

makes the rainbow bright bright bright!


[Deep breath] Here we go again.

Can we possibly have enough luck left over for another miracle?

How to memorialize Jane

In the first few days after we lost Jane, we were inundated with more beautiful flowers than we knew what to do with. So when I started drafting a Facebook post about what happened, my mom wisely recommended that we select a charity for people to donate to in lieu of sending flowers. C and I talked briefly about a children’s dental charity or organization that supports parents of stillborn babies (either locally or nationally), but we couldn’t agree.

Then C had the idea of starting a fund for a permanent memorial to Jane. He investigated fundraising sites and selected (since it charges lower fees than the more popular We set up the site with a goal of $2,000 (to cover the cost of a park bench at a nearby city), and shared the sad news about Jane on Facebook. And the money, along with incredible messages of love and support, rolled in…

To date, 149 people, including family and friends and colleagues (and some complete strangers!) have given almost $12,000 in support of Jane’s memorial fund.

We were blown away by everyone’s generosity.

Which brought us to Decision 9: How should we memorialize Jane?

We felt a solemn responsibility to Jane – and to all the people who donated – to choose a meaningful and (semi-)permanent memorial. We investigated several options:

1) A memorial bench. C contacted our city’s department of Parks & Recreation and learned that they “don’t do benches anymore”. It seems the cost to maintain the benches exceeded the income from the benches. (Why not just raise the price of the benches? I guess there’s not a lot of incentive to raise money for park improvements…)

In any case, we moved on to the next city north of here. They have a memorial bench program, at a current cost of about $1600 for a bench. The catch: there are no benches (or spots for benches) currently available. They put us on the waitlist (#32 on the list), and said they’d call us when they get to our name, probably in a few years.

The next city north had benches immediately available, including one “beach site”. The price was about the same: $1650. But we weren’t exactly excited about the idea of driving 40 minutes to sit on Jane’s bench…

Major Research University, where C went for undergrad and I did my postdoc, is only 3 miles away, in the same direction we have to travel to get to the freeway. A handsome and well-dressed young man in the development office was happy to show us what they had available: 9 benches with ocean views available for naming, each at a price of $15,000, plus any required maintenance or repair costs. C and I, along with my mom and sister and our friend R visited each bench and liked several. Our favorite was this one:


Our favorite option for a memorial bench for Jane

I also investigated memorial bench options at the Small Christian University where I work. They proved to be more flexible and economical with their bench options than Major Research University. Basically, we could pick any spot on campus (including ocean views) and select the style of bench we want, for about $6,000. The downside was that the campus is 11 miles from our house in a part of town where C rarely visits.

One thing we learned is that none of the memorial benches (or indeed any of the memorials) are truly permanent. Naming rights on benches at Major Research University are guaranteed for 8-10 years, with the possibility of longer. At Small Christian University, they didn’t give a promised timeline, but pointed out that other benches have been around for 20+ years. In both cases, when the bench needed to be replaced, we would have ‘first dibs’ to repeat our donation and get a new one.

2) Our local aquarium. C. Samuel LOVES the aquarium, which is 3 miles from our house (adjacent to, and affiliated with, Major Research University) so that was the next place we investigated. They also had benches available (with the same pricing as the university ones), in addition to a number of other options ranging from a ‘permanent’ sea star plaque ($1500) to a plaque on any of the tanks (prices varied from around $1,000-15,000…per year), to naming the soon-to-be remodeled “aquarium nursery” (the tanks where they display the baby fish; I think she estimated $15,000 for this; I didn’t clarify how long the naming rights would last).


The current aquarium nursery. We have the option of dedicating the new nursery in memory of Jane.

The (large) downside to the aquarium is that friends and family members who donated to Jane’s memorial fund would not be able to see her memorial without purchasing a ticket. We moved on to other options.

3) The library. At this point, C decided we could use some help. He messaged our friend M, who works in philanthropy for the public library. She is AWESOME and replied that she would come meet with us the next day with some ideas. Naturally, she first mentioned our local library, which had a variety of naming opportunities, ranging from a reading nook (for $15,000) to the new high tech public laboratory (which includes a walk-up molecular biology lab and 3D printer; for about $100,000).

4) County Parks & Recreation. She also had printed out a 24-page booklet of naming opportunities for the county Parks & Recreation Department. These included baseball fields, playgrounds, hiking trails, sports arenas/courts, amphitheaters, skate parks, splash parks, swimming pools, and community gardens, at prices ranging from $2,000 – $200,000. Awesome and extensive as the options were, they were all 30 minutes or more from our home, in residential areas in unincorporated parts of the county, which we are unlikely to visit regularly.

5) A play structure. M also asked about our local park. We told her how C had called the city already about the bench, and found them pretty unreceptive to memorial gifts. M suggested that she might have better luck, given her position at the library, and asked if we knew what we might want. We told her that we would love to plant a tree at our local park, and/or to replace a play structure. There is a little fire truck play structure that C. Samuel especially loves, and that has seen better days… She said she would try to get through to the right person to see what our options are.


C. Samuel, in the fire truck at our local park. Notice the peeling paint and chipped wood.

A few days later, M called us. She had found the ‘right’ person – Tyler at Parks & Rec, and had discussed several options with him. He had told M that the play structures at our local park could use a good paint job, and that if we wanted we could purchase supplies and organize a team to come and sand and paint the structures. C and I were both less than enthused about that idea! Fortunately, he also offered that C. Samuel’s favorite fire truck play structure could stand to be replaced. We also could plant a tree, not in our first choice location (the playground), but in another lovely part of the park. The catch was that our city Parks & Rec does not allow memorial plaques, and would not be open to names or even initials on the new structure or tree. Tyler offered a possible compromise: we could have imprints of Jane’s hand- and footprints embedded in the new play structure.

We loved the idea!

The company that makes the play structures (Kompan) is located in Denmark and gave an initial rough estimate of about $12,000, possibly a bit more. Manufacturing will take a couple months, then they’ll ship the parts here, and Parks & Rec staff will put it together on site. Tyler estimated that it will be put in place in early 2017. To plant the tree, we just need to get approval from the city arborist, and pay the cost of the tree and labor to plant it. Since they don’t do memorial gifts, we will have to purchase the structure directly from the company, rather than making a tax-deductible donation to our city Parks & Rec. They also won’t guarantee a length of time that the play structure will remain in place, but Tyler pointed out that the current structure has been in place since 1996, and that while the current structure is painted wood, the new one will be made of a special composite plastic that should last much longer. He imagines that the structure won’t move until the entire park is remodeled, which there are no plans to do, and several obstacles in the way of (including ADA compliance issues and a very strong local resistance to change).

So, that’s the plan! Here’s the rendering we just got from Kompan showing what the fire truck should look like. We can’t wait!


A perfect storm

Last Wednesday, I ran into a mom of one of C. Samuel’s classmates for the first time since we lost Jane. Reflexively, she asked, “So, what happened exactly?” then immediately seemed to regret it, saying “You probably don’t want to talk about it.” I suspect this is the thought process most people go through when they hear our daughter was stillborn.

For the record, I don’t at all mind talking about it.

At the time of Jane’s birth, we knew extremely little. Dr. R suspected a placental abruption: I had no risk factors for stillbirth aside from maternal age; even with the close monitoring that came with going past term, I showed no indicators of an underlying cause; and my labor progressed extremely quickly (a classic sign of abruption). Moreover, Jane came out looking perfect, with no signs of cord injury (the other likely cause for demise of an otherwise healthy pregnancy).

Six weeks after my due date, we went to our follow-up appointment with Dr. R. By then, the results had come back from the dozens of tests performed on me…

The verdict?

Dr. R said that to the best of her knowledge, Jane’s death was the result of “a perfect storm.” I Googled the expression, and found it defined as “A situation where a calamity is caused by the convergence and amplifying interaction of a number of factors”. Sounds about right.

What were the factors converging to result in Jane’s demise?

Dr. R said there were three contributors that we know of, namely:

  • We know that Jane had a small, insufficient placenta, although we don’t know why. Risk factors for this include drug use, high blood pressure, pre-eclampsia, gestational diabetes, advanced maternal age, and infertility. Dr. R said she had looked into the infertility link further, and found that it has only been demonstrated for pregnancies achieved through IVF…so not Jane. The only known risk factor I had was advanced maternal age.
  • Jane had a shorter-than-normal umbilical cord. I’ve learned that the normal range is 35-80 cm, and that Jane’s was 30 cm after being cut. Dr. R freely acknowledged that some may have been lost in the cutting. So definitely on the short side, but not far outside the normal range. She said that a short cord increases the risk of a cord injury.
  • The main vessel of Jane’s placenta contained some “old, organized clots”. Dr. R suggested this may be due to an event that pinched the cord. (More on this in my placental pathology report, reproduced in part here.)

Dr. R suspects one additional contributor to Jane’s death:

  • Dr. R still believes I had a placental abruption. She said she can’t prove it (for example, my test for maternal fetal hemorrhage was negative), but supporting evidence includes my crazy, tumultuous labor (from 1 – 10 cm in less than 2 hours), old brown blood in my amniotic fluid (which was visible upon dilation), and “port wine-colored” blood delivered with Jane in my amniotic fluid.

Would Jane have been okay otherwise?

There’s no way to know if Jane would have suffered from my crappy placenta and blood clots if she had been delivered earlier. She looked perfect at delivery, so…perhaps not.

Was Jane “growth restricted”?

Dr. R said we can’t tell if Jane fit the definition for intrauterine growth restriction (IUGR) or if she was just small for gestational age (SGA).

Was there an underlying cause?

Kaiser did tons of tests on me. All came back essentially normal. I do not have a clotting disorder. I did not appear to have any relevant infection during my pregnancy with Jane. Dr. R promised to send me my test results by mail. (She did, and I summarized them here.)

How could we prevent this from happening in a future pregnancy (assuming we can get pregnant again)?

For any future pregnancy, Dr. R would recommend that I take low-dose aspirin through 36 weeks to prevent clots. (I actually took the low-dose aspirin through the first trimester with both Jane and C. Samuel, on the advice of Dr. Y. Given my test results, she does not currently recommend heparin.) We would do monthly growth ultrasounds, along with additional Doppler scans to check the baby’s blood flow (specifically the cord flow and “mid-cerebral artery flow”). We would do “intense testing,” including a repeat of my blood clotting tests. If anything looked bad once the baby reached viability, we “will act” (that is, deliver him or her early). Dr. R also recommends a scheduled C-section, rather than taking the risk of fetal distress or an accident during labor.

When should we try again?

Dr. R gave me the all-okay physically. She mentioned that some studies suggest that a shorter break between pregnancies correlates with shorter umbilical cords, but she didn’t think the quality of evidence was good. She indicated a desire to talk to Dr. Y more about this.

I’d like to write a longer post on the subject of trying again. Suffice it to say that neither C nor I want to wait long.

Are you going to retire?

Dr. R answered confidently, “Oh I’m going to see this through!” She also shared (perhaps unprofessionally, although I hardly fault her for it!) that she had a dream that we had another, healthy child. I hope her dream proves to be prophetic!

On our way out the door, I handed Dr. R a Thank You card, in which I shared our feelings of gratitude to her, along with a photo of us with Jane:


When I got home, there was an email from Dr. R in my Kaiser inbox:

Hi, K and C! I rushed out to catch you but you were too fast and got away. The card was so touching and beautiful! Thank you so very much for the picture. It means so much to me, more than any words can express. I am here for you in any way that I can help. Please feel free to reach out at any time. In peace, Dr R


After learning of Jane’s passing, I was subjected to a large number of blood and urine tests, and my placenta was sent to be examined by a pathologist. Most of the samples were collected in the hospital (while I was still in labor with Jane, or shortly after). A few more blood tests were added roughly a month later, after I shared some information about my family history (re: blood clots) with Dr. R.

I’m not a physician and haven’t spent a lot of time looking into these tests and what they mean. But on this 2 month anniversary of Jane’s birth and death, I’m parking them here for posterity, and also as an easy way to share them with my physician friends (or anyone else who cares to take a look). I’ll wait to summarize the key takeaways as they pertain to Jane’s death and to any future pregnancies in a future post about our follow-up appointment with Dr. R.

Without further ado, here are all my test results. Results outside the normal range are highlighted in orange. (UPDATE: It looks like the tabulated data doesn’t display on smartphones; I recommend viewing on a computer if you want to see my numbers and/or the standard ranges for each of these tests…)


Complete Blood Count

This is a routine test “used to evaluate…overall health and detect a wide range of disorders, including anemia, infection and leukemia” Source

23-Jul 19-Aug Standard Range
HCT 40.6 40.9 37.0-47.0 %
HGB 14.3 13.8 12.0-16.0 g/dL
MCH 32.5 31.6 27.0-35.0 pg/cell
MCHC 35.1 33.7 32.0-37.0 g/dL
MCV 92.4 93.7 81.0-99.0 fL
Platelets, Automated Count 167 188 130-400 x1000/mcL
RBC, Auto 4.39 4.36 4.20-5.40 Mill/mcL
RDW, Blood 13.2 12.4 11.5-14.5 %
WBC’s Auto 14.8 6 4.0-11.0  x1000/mcL


Clotting-related tests

One of the risk factors for fetal demise is maternal blood clotting, either due to an inherited thrombophilia, or an autoimmune disease that can lead to a “hypercoagulable state” like Lupus or antiphospholipid syndrome. From what I can gather, the following tests are all related to my tendency to form blood clots.

  • Activated partial thromboplastin time “(aPTT or APTT) is a medical test [used for] detecting abnormalities in blood clotting” Source
  • Fibrinogen is a “glycoprotein in vertebrates that helps in the formation of blood clots…[It is typically] elevated in pregnancy…Low levels of fibrinogen can indicate a systemic activation of the clotting system.” Source
  • Lupus, antiphospholipid syndrome, the prothrombin G20210A gene mutation, and factor V Leiden thrombophilia are all conditions that might predispose me to clotting problems.
  • Cardiolipin antibodies and beta-2 glycoprotein antibodies are commonly tested along with the Lupus anticoagulant screen. According to my Kaiser lab results, “Clinical associations [for cardiolipin antibodies test] include SLE (25-50%), Arterial or Venous Thrombosis, Recurrent Fetal Loss, Thrombocytopenia, Valvular Heart Disease.”
  • Homocysteine is an amino acid. “Abnormally high levels of homocysteine in the serum, above 15 µmol/L, are a medical condition called hyperhomocysteinemia. This has been claimed to be a significant risk factor for the development of a wide range of diseases, including thrombosis” Source
  • Protein C “plays an important role in regulating anticoagulation, inflammation, cell death, and maintaining the permeability of blood vessel walls in humans and other animals.” Source
  • Protein S has a “role in the anti coagulation pathway, where it functions as a cofactor to Protein C in the inactivation of Factors Va and VIIIa.” Source
  • Antithrombin III is a “small protein molecule that inactivates several enzymes of the coagulation system” Source
23-July 19-Aug Standard Range Notes
activated partial thromboplastin time (APTT) 26 25-37 sec
fibrinogen 554 218-441 mg/dL
thrombophilia, 20210G-A, F2 mutation analysis negative negative
APTT 35 23-38 sec All part of the Lupus anticoagulant screen
dilute Russell viper venom induced 36 29-43 sec
Lupus anticoagulant negative negative
cardiolipin IGG, EIA 2.5 <=14.9 GPL units
cardiolipin IGM, EIA 7.4 <=12.4 MPL units
beta 2 glycoprotein 1 IGG 1 <=20 SGU
beta 2 glycoprotein 1 IGM 4 <=20 SMU
beta 2 glycoprotein 1 IGA 3 <=20 SAU
thrombophilia, 20210G-A, F2 mutation analysis negative negative
factor V Leiden thrombophilia negative negative
homocysteine, subst conc, SERP 6 5-15 mcmol/L
activated protein C resistance ratio 1.9 >= 1.9 Factor V Leiden expected to cause APC resistance ratio below 1.9
protein-C activity (actual/normal) 116 95-172 % Factor VIII levels greater than 250% may lead to under-estimation of protein C level
protein-S – functional, plasma, QN 106 50-118 % Factor VIII levels greater than 250% may lower protein S measurements.
antithrombin III activity 109 80-120 %


Liver-related tests

I’m guessing liver function is of interest for detecting intrahepatic cholestasis of pregnancy, preeclampsia, HELLP syndrome, or acute fatty liver of pregnancy? Or maybe hepatitis?

  • Alanine transaminase (ALT) and aspartate transaminase (AST) are liver enzymes. “Serum AST level, serum ALT (alanine transaminase) level, and their ratio (AST/ALT ratio) are commonly measured clinically as biomarkers for liver health.” Source
  • Bile acids (including cholic acid, deoxycholic acid, and chenodeoxycholic acid) are “steroid acids found predominantly in the bile of mammals and other vertebrates…synthesized in the liver…[and] aid in the diagnosis of a number of conditions, including … intrahepatic cholestasis of pregnancy.” Source
  23-July Standard Range
ALT 8 <=54 U/L
AST 29 <=30 U/L
cholic acid: 3.7 <= 1.8 umol/L
deoxycholic acid: 1.5 <= 2.4 umol/L
chenodeoxycholic acid: <0.5 <= 3.1 umol/L
total bile acids: 5.2 <= 6.8 umol/L


Kidney-related tests

Poorly controlled diabetes is another maternal cause of fetal demise. The following tests evaluated my kidney function and blood glucose levels.

  • Creatinine is “an easily measured byproduct of muscle metabolism that is excreted unchanged by the kidneys”, so creatinine levels in blood rise if kidneys aren’t doing a good job of removing it. Glomerular Filtration Rate (GFR) is the “volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman’s capsule per unit time.” Both are measures of renal function.
  • Blood glucose is the level of sugar in my blood. An abnormally high value might be indicative of diabetes.
  • Hemoglobin A1C (HGBA1C) screening measures hemoglobin (the oxygen-carrying protein in blood) that has been modified with a glucose molecule. In the presence of continually high blood glucose levels, HGBA1C builds up slowly over time, so its value gives you an idea of how well blood glucose has been controlled over the past three-months.
  23-July Standard Range Notes
Creatinine 0.46 <=1.10 mg/dL
Glomerular Filtration Rate >89 >89 mL/min/BSA
Glucose, Random 91 70-140 mg/dL
HGBA1C% 4.9 4.8-5.6% >6.5% is diagnostic of diabetes. 5.7-6.4% indicates increased risk for future diabetes


Tests for infections

  • Syphilis is a sexually-transmitted bacterial infection. Untreated in the mother, it can pass to a fetus and cause a variety of horrible outcomes including stillbirth. Source
  • Parvovirus B19 (aka fifth disease) is a mild viral disease that may, in rare cases, cause anemia and/or miscarriage. (Interestingly, I found the same said of Coxsackie virus, for example here, which I did get while pregnant with Jane… I’ll have to ask Dr. R about it…)
  • Cytomegalovirus is a virus in the herpes family that typically causes no or mild symptoms. It’s not clear to me whether a causal relationship has been established, but at least a few articles seem to point to a correlation with stillbirth (for example, see this source).
  • Toxoplasmosis is a parasitic infection caused by Toxoplasma gondii, commonly transmitted by eating undercooked foods (like rare steak), or coming in contact with cat poop (for example, when changing the litter box, or gardening). Toxoplasmosis usually causes mild or no symptoms in non-immunocompromised adults, but when it passes from a pregnant mom to a fetus, it can cause a variety of terrible outcomes, including stillbirth. Source

The latter three tests include tests for two different types of antibodies: IgG and IgM. The IgG antibodies are the long-term antibodies that are present if I have ever been infected with the pathogen; these antibodies confer immunity to future infections by the same pathogen. The IgM antibodies are part of the short-term response to an active or recent infection. Their presence in my blood at the time of Jane’s death would indicate an infection that happened during my pregnancy (i.e. one that could have impacted Jane). For more, see this.

As you can see below, it appears I have been infected by parvovirus B19 and cytomegalovirus at some point, but not a recent infection that might explain what happened to Jane. This is somewhat good news, since it means I am now immune to getting these infections in a future pregnancy. Unfortunately, I have not been infected by Toxoplasmosis… which means I’ll be stuck eating my steaks well done in any future pregnancy…

  23-July Standard Range Notes
Treponema pallidum AB, EIA (Syphilis screen) nonreactive nonreactive
Parvovirus B19 Ab IgG: 4.9 <0.9 IgG persists for years and provides life-long immunity
Parvovirus B19 Ab IgM: 0.2 <0.9 probably no current or recent infection
Cytomegalovirus IGG, SER, QN 5.4 <= 0.8 AI IgG antibody to CMV detected which may indicate exposure to CMV infection
Cytomegalovirus IGM, EIA < 8.0 <=29.9 AU/mL A positive test may indicate a current or recent infection.
Toxoplasma gondii IGG, SER, QN < 3 <9 IU/mL
Toxoplasma gondii IGM 0.06 <= 0.549 RFV No serologic evidence of infection with Toxoplasma gondii


Immune-related/antibody tests

  • Rhesus disease (in which the mother’s immune system attacks her baby’s red blood cells) is also on this list of possible causes for stillbirth.
  • The Coombs test for autoimmune hemolytic anemia is looking at whether my immune system is attacking my own red blood cells (I think).
ABO and RH blood type A Pos
Crossmatch Result Compatible
Indirect Coombs test: Blood Group Antibody Screen neg


Other blood tests:

Fetomaternal hemorrhage screen, aka  Kleihauer–Betke test, is “a blood test used to measure the amount of foetal hemoglobin transferred from a foetus to its mother’s bloodstream.” “Causes of increased foetal-maternal haemorrhage are seen as a result of trauma, placental abruption or may be spontaneous with no cause found…Foetal-maternal haemorrhage is one cause of intrauterine death (IUD).” (emphasis mine) Source

23-July Notes
Adult RBC, Blood 2000 Conducted by counting 2000 red blood cells in my blood
Fetal RBC, Blood 0 None of those cells were determined to be from Jane
Fetal/Adult RBC Ratio, Blood 0
Fetal-Maternal Hemorrhage Volume 0 mL


Thyroid stimulating hormone (TSH) is a protein hormone measured to test for hypothyroidism (or hyperthyroidism, but I can’t find anything in a quick Google search about that relating to pregnancy outcomes…) From what I can tell, thyroid disorders may be correlated with fetal demise and/or low birth weight. Source

  23-July Standard Range
TSH 1.8 0.35-4.00 mcIU/mL


Drug tests

Smoking and illicit drug use are associated with an increased risk of stillbirth. Source

I should point out that Dr. R gave me two doses of IV morphine while I was waiting for my blood test (and approval for my epidural). So it didn’t come as a surprise to anyone when I came back positive for opiates generally, or morphine specifically. The tests included two sets of screening tests (in which they homed in on morphine), followed by a confirmatory test using gas chromatography-mass spectrometry (GCMS).

Drug screen (AMP, METH, BAR, BZD, COC, OPI, PCP, THC, TCA), Urine, Using test w visual read

23-July Standard Range
THC, Urine negative negative
Phenylcyclidine, Urine screen negative negative
Cocaine, UR, QL, Screening test negative negative
Methamphetamine, UR, QL, Screening test negative negative
Opiates, Urine, QL Preliminary positive. Pending confirmation. negative
Amphetamine, UR, QL, Screening test negative negative
Benzodiazepines, Urine Screen negative negative
Tricyclic antidepresseants, Urine screen negative negative
Barbiturates, UR, QL, Screening test negative negative


Opioid Screen, Pain MGMT (BUP, FEN, 6MAM, MTD, OPI, OXYCOD, HDC, TRA), Urine, Automated Analyzer w EIA

  23-July Standard Range
Buprenorphine, UR, QL negative negative
Fentanyl, UR, QL negative negative
Hydrocodone, UR, QL neg neg
Heroin metabolite (6-MAM), UR, QL negative negative
Methadone, Urine screen negative negative
Opiates, Urine, QL POSITIVE negative
Oxycodone, UR, QL, Screening test negative negative
Tramadol, UR, QL, Screening test negative negative
pH, Urine 5.4 5.0-8.0
Specific gravity, Urine 1.01 1.002-1.030
Creatinine, Urine 35.5 >=20.0 mg/dL
Specimen validity, Urine normal


Opiates, Urine, Confirmatory GC/MS

Opiates, UR, Confirm morphine detected


Surgical pathology

I found the placental pathology report to be the most interesting item in the pages from my medical record that Dr. R shared with me…


Placental, vaginal delivery

  • Term placenta (40 weeks 6 days), size extremely small (~450 g expected, 225 g actual)
  • Thrombi of mainstem fetal vessels, organizing and old
  • Normal villous features (no increased immaturity, villitis or infarction)
  • Rare hemosiderin deposits within chorion, likely clinically insignificant
  • No evidence of decidual vasculopathy for chorioamnionitis
  • Short trivascular umbilical cord (>50 cm expected, 30 cm actual)


Although the placental weight can vary with maternal constitutional size, 225 grams is truly small and may, or may not have resulted in utero placental insufficiency. The more common causes of vascular thrombi are infection, cord compression and coagulopathy. In view of the short umbilical cord (if 30 cm is the true length), it is possible that there was compromised [sic] due the cord with the onset of labor.

[The report goes on to describe the appearance of the placenta, etc.]