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…
FINAL PATHOGENIC DIAGNOSIS
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)
COMMENT
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.]