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7/18/2017 Evaluation of Fetal Death: Definition of Fetal Death, Frequency of Fetal Death, Diagnosis of Fetal Death

Evaluation of Fetal Death


Updated: Mar 13, 2016
Author: Patricia J Mattingly, MD; Chief Editor: Carl V Smith, MD more...

Definition of Fetal Death


The loss of a fetus at any stage is a fetal demise. According to the 2003 revision of the Procedures for
Coding Cause of Fetal Death Under ICD-10, the National Center for Health Statistics defines fetal
death as "death prior to the complete expulsion or extraction from its mother of a product of human
conception, irrespective of the duration of pregnancy and which is not an induced termination of
pregnancy. The death is indicated by the fact that after such expulsion or extraction, the fetus does
not breathe or show any other evidence of life, such as beating of the heart, pulsation of the umbilical
cord, or definite movement of voluntary muscles. Heartbeats are to be distinguished from transient
cardiac contractions; respirations are to be distinguished from fleeting respiratory efforts or gasps."

In the United States, the term stillbirth or fetal demise does not have a standard definition.

For statistical purposes, fetal losses are classified according to gestational age. A death that occurs
prior to 20 weeks' gestation is usually classified as a spontaneous abortion; those occurring after 20
weeks constitute a fetal demise or stillbirth. Many states use a fetal weight of 350 g or more to define
a fetal demise.

Although this definition of fetal death is the most frequently used in medical literature, it is by no
means the only definition in use. Even within the United States, the differences in the definitions used
are substantial.

In addition, not all states interpret the weeks of gestation in the same manner. In California, 20 weeks'
gestation is worded "twenty utero gestational weeks" and has therefore been interpreted to be 23
weeks from the last menstrual period. (Implantation in the uterus does not occur until 1 wk after
fertilization.) Physicians must check the reporting requirements for the state(s) in which they practice.

Frequency of Fetal Death


In 2006, data from the National Vital Statistics Report showed a US national average stillbirth rate of
6.05 per 1000 births, 3% lower than in 2005. [1] Worldwide, this rate varies considerably depending on
the quality of medical care available in the country in question and the definitions used for classifying
fetal deaths. Underreporting in developing nations is common, which makes comparisons even more
difficult.

In 2009, the estimated global number of stillbirths was 2.64 million (uncertainty range, 2.14-3.82
million). [2] The worldwide stillbirth rate declined by 14.5% from 22.1 stillbirths per 1000 births in 1995
to 18.9 stillbirths per 1000 births in 2009.

Diagnosis of Fetal Death

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History and physical examination are of limited value in the diagnosis of fetal death. In most patients,
the only symptom is decreased fetal movement. An inability to obtain fetal heart tones upon
examination suggests fetal demise; however, this is not diagnostic and death must be confirmed by
ultrasonographic examination.

Fetal demise is diagnosed by visualization of the fetal heart and the absence of cardiac activity.

Management of Fetal Death


Once the diagnosis of fetal demise has been confirmed, the patient should be informed of her
condition. Often, allowing the mother to see the lack of cardiac activity helps her to accept the
diagnosis.

Termination of pregnancy should be offered after diagnosis. Patient responses vary in regard to this
recommendation; some wish to begin induction immediately, while others wish to delay induction for a
period of hours or days until they are emotionally prepared.

When a dead fetus has been in utero for 3-4 weeks, fibrinogen levels may drop, leading to a
coagulopathy. [3] This is rarely a problem because of earlier recognition and induction. In some cases
of twin pregnancies, induction after the death of a twin may be delayed to allow the viable twin to
mature.

Induction may be accomplished with preinduction cervical ripening followed by intravenous oxytocin
(see Cervical Ripening). Patients with a history of a prior cesarean delivery should be treated
cautiously because of the risk of uterine rupture, just as in any birth following cesarean delivery (see
Vaginal Birth After Cesarean Delivery). The risk of uterine rupture during induction for fetal demise in
the late second and early third trimester is unknown. [4]

Early fetal demise may be managed with laminaria insertion followed by dilatation and evacuation. In
women with fetal death before 28 weeks' gestation, induction may be accomplished using
prostaglandin E2 vaginal suppositories (10-20 mg q4-6h), misoprostol (ie, prostaglandin E1) vaginally
or orally (400 mcg q4-6h), and/or oxytocin (preferred in women with prior uterine surgery).

Mifepristone 200 mg orally followed by misoprostol 400 mcg every 4-6 hours orally or vaginally
appears to be the most efficacious and results in the shortest time to delivery. [5] In settings in which
mifepristone is unavailable, misoprostol alone is also highly effective. For women with a prior
cesarean delivery after 28 weeks gestation, mechanical ripening can be performed with a Foley
catheter, and induction can be continued with oxytocin.

Pain management in patients undergoing induction of labor for fetal demise is an important part of
patient care. Often, a morphine or hydromorphone patient-controlled analgesia device is sufficient for
successful pain control. Should a patient desire superior pain control to intravenous narcotics,
epidural anesthesia should be offered.

Causes of Fetal Death


The etiology of fetal demise is unknown in 25-60% of all cases. In cases where a cause is clearly
identified, the cause of fetal death can be attributable to fetal, maternal, or placental pathology. One
prospective study attributed 64.9% of fetal death to placental pathology overall. The same study noted
higher rates of fetal demise secondary to placental pathology at late gestational age. [6]

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A meta-analysis of 96 population-based studies found that maternal overweight and obesity was the
highest-ranking modifiable risk factor for stillbirth. [7, 8, 9] Advanced maternal age (>35 y) and maternal
smoking were also significant. Small size for gestational age and abruption were the highest-ranking
pregnancy disorder risk factors for stillbirth. Obstetric conditions and placental abnormalities were the
most common causes of stillbirth in one population-based study, with a higher number of stillbirths
associated with obstetric complications occurring in non-Hispanic black women. [10] Preexisting
diabetes and hypertension are also important contributors to stillbirth. [11]

Maternal
See the list below:

Prolonged pregnancy (>42 wk)


Diabetes (poorly controlled)
Systemic lupus erythematosus
Antiphospholipid syndrome
Infection
Hypertension
Preeclampsia
Eclampsia
Hemoglobinopathy
Advanced maternal age
Rh disease
Uterine rupture
Maternal trauma or death
Inherited thrombophilias

Fetal

See the list below:

Multiple gestations
Intrauterine growth restriction
Congenital abnormality
Genetic abnormality
Infection (ie, parvovirus B19, CMV, Listeria)
Hydrops

Placental
See the list below:

Cord accident
Abruption
Premature rupture of membranes
Vasa previa
Fetomaternal hemorrhage
Placental insufficiency

Risk factors (weak predictive value)

See the list below:

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African American race


Advanced maternal age
History of fetal demise
Maternal infertility
History of small for gestational age infant
Small for gestational age infant
Obesity
Paternal age

Evaluation of Fetal Demise


The time following a fetal death is extremely difficult for both the family and the health care providers.
In this stressful time it is important to ensure that the emotional needs of the family are met.

A useful resource is a grief packet that can be given to the parents following the demise. This usually
includes referrals for counseling, support groups, and other resources. A container or folder can be
included so that the family can preserve keepsakes such as photos, footprints, or a lock of hair.
Spiritual support is an important resource during such difficult times and should always be offered to
patients and their families.

Currently, which tests are most effective in evaluating a fetal demise have not been agreed upon.
Therefore, authorities vary in their recommendations. Most of the testing recommendations in the past
have been based on expert opinion rather than scientific studies. The Stillbirth Collaborative Research
Network currently has ongoing studies, which will hopefully define the optimal diagnostic evaluation
for this difficult clinical problem. In an effort to better understand the underlying pathophysiology that
leads to fetal demise and thereby create appropriate interventions, experts proposed a uniform
international classification system and recommended a complete stillbirth workup for every case of
fetal demise. [12]

Up to 60% of stillbirths have no identifiable etiology. Attempting to determine the cause of fetal death
remains important because it may influence estimates of recurrence and future preconceptional
counseling, pregnancy management, prenatal diagnostic procedures, and neonatal management.

Many institutions use a selective workup based on clinical findings. For example, when clinical
findings strongly suggest a cause for the fetal demise at Santa Clara Valley Medical Center, either no
further testing or limited testing is performed. Causes deemed fairly obvious include cord accident (ie,
prolapse, entanglement, true knot, tight nuchal cord), anencephaly, or previously known lethal
karyotype. In such cases, no further workup is necessary.

If severe clinical abruption is present, testing can be limited to toxicology screening and possibly a
thrombophilia workup.

The most important part of the workup of a fetal demise is the autopsy of the fetus. The decision to
proceed with an autopsy must be made by the parents and informed consent is necessary. With
parents who are resistant to the idea of a complete autopsy, a limited fetal evaluation should be
discussed with the family. Although uncommon, postmortem MRIs can provide valuable information in
the evaluation of a fetus when an autopsy cannot be performed.

The placenta and the membranes should be carefully examined, including cultures. Again, an
algorithm or checklist is helpful to avoid omissions (see image below). This inspection is even more
important if the family declines an autopsy.

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This is an example of a checklist to be used following fetal death. Courtesy of Santa Clara Valley Medical Center.

Fetal karyotype can be obtained from a sample of amniotic fluid (preferred), fetal blood, or fetal tissue
(skin or fascia lata). Fetal karyotype should be considered in all cases. It is especially important if the
fetus is dysmorphic, has growth retardation, is hydropic, or has anomalies or other signs of
chromosomal abnormality. Chromosomal analysis should also be considered in patients with multiple
pregnancy losses, especially with a history of second- and third-trimester losses or when a parent has
a balanced translocation or mosaic chromosomal pattern. Many authorities (including the ACOG
committee on evaluation of stillbirth) recommend obtaining this test in every fetal demise. The addition
of microarray testing to traditional karyotype may be of benefit in the evaluation of these fetuses. The
ability to obtain results appears to be higher as is the detection rate for abnormalities. [13, 14]

A summary of the protocol for the fetus and placenta is as follows:

Careful inspection
Placental cultures for suspected listeria infection (To obtain placental cultures, separate the
amnion and the chorion and submit a culture specimen using Stuart media.)
Radiographs, if indicated
Autopsy
MRI, if no autopsy
Fetal karyotype

Maternal Studies
Maternal studies that should also be considered during the workup of a fetal demise include the
following:

Diabetes testing using hemoglobin A1C and a fasting blood glucose


Syphilis screening using the VDRL or rapid plasma reagent test
Thyroid function testing (ie, TSH, FT4)
Urine toxicology screening

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The above tests have traditionally been a part of an evaluation for the etiology of fetal demise. If
diabetes screening has been performed during the prenatal period, repeat testing for diabetes is
probably not necessary. Similarly, if the patient has no signs or symptoms of thyroid disease, thyroid
dysfunction is unlikely to be the cause of the demise. However, these tests are inexpensive and
normal results may be reassuring to the patient.

Additional tests that should be considered are as follows:

Antibody screening
CBC count with platelet count
Kleihauer-Betke test
Laboratory tests for antiphospholipid syndrome: See Antiphospholipid Antibody Syndrome and
Pregnancy.
Inherited thrombophilia panel
The enthusiasm for laboratory testing for inherited thrombophilias for adverse pregnancy
outcome is waning. Inherited thrombophilias are common in the general population but are
probably rare causes of fetal demise. A multicenter, prospective, observational cohort
study concluded that there was no association between prothrombin G20210A mutation
and pregnancy loss, preeclampsia, abruption, or SGA neonates in a low-risk population.
[15] The current ACOG Practice Bulletin, Management of Stillbirth, is now recommending

inherited thrombophilia testing only in selected cases. [16] In a more recent ACOG Practice
Bulletin, Inherited Thrombophilias in Pregnancy, there is no recommendation to screen for
inherited thrombophilias with pregnancy loss. [17]
While some authorities recommend maternal testing in all cases of fetal demise, a more
selective approach is to limit testing to patients who have a history of venous thrombosis,
positive family history, severe placental pathology, severe preeclampsia in the second or
early third trimester, abruption, or significant intrauterine growth retardation. The value of
thrombophilia testing in any circumstance in obstetrics has recently been questioned. [18,
19]
Infection: See Bacterial Infections and Pregnancy. Infection is a cause of fetal demise. The
frequency is higher in developing countries. Autopsy and histologic evaluation of the placenta is
probably the best way to document an infectious etiology for a fetal demise.

Authority opinions vary as to which panel of tests is appropriate. Traditionally, most authorities have
recommended obtaining TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex virus)
antibody titers. In reality, this is rarely helpful in the diagnosis. In addition, it is questionable whether
cytomegalovirus virus causes fetal demise. If no obvious cause for the demise is established or if
clinical signs or symptoms suggest infection, consider testing for (1) cytomegalovirus (acute and
chronic titers), (2) rubella virus (acute and chronic titers, if not immune), (3) parvovirus (acute and
chronic titers), and (4) Toxoplasmosis gondii (acute and chronic titers) and (5) syphilis. A more cost-
effective approach is to limit testing for cytomegalovirus, rubella virus, and T gondii to those patients in
whom clinical findings suggest the possibility of intrauterine infection (ie, those with intrauterine growth
restriction, microcephaly).

Testing for Fetal Demise


The following provides a summary of the current status of testing for fetal demise. This is adopted with
permission from the work of Dr. Robert M. Silver and the Stillbirth Collaborative Research Network.
This summary has been modified as more recent studies have become available.

Commonly accepted tests

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See the list below:

Thorough maternal history


Fetal autopsy
Placental evaluation
Karyotype
Indirect Coombs test
Serologic test for syphilis
Testing for fetal-maternal hemorrhage (Kleihauer-Betke or other)
Urine toxicology screen
Parvovirus serology
Lupus anticoagulant, for antiphospholipid testing
Anticardiolipin anticoagulant, for antiphospholipid testing
Anti-B 2 -glycoprotein 1 IgG or IgM antibodies

Useful in some circumstances


See the list below:

Factor V Leiden
Prothrombin mutation
Protein C, protein S, and antithrombin III deficiency
TSH
Hemoglobin A1C
TORCH titers
Placental cultures
Testing for other thrombophilias

Developing technology

See the list below:

Comparative genomic hybridization


Testing for single gene mutations
Testing for confined placental mosaicism
Nucleic acid-based testing for infection

Management of Future Pregnancy


If a particular medical problem is identified in the mother, it should be addressed prior to conception.
For example, tight control of blood glucose prior to conception can substantially reduce the risk of
congenital anomalies in the fetus. Preconceptional counseling is helpful if congenital anomalies or
genetic abnormalities are found. Genetic screening and detailed ultrasound can evaluate future
pregnancies. In some cases, such as cord occlusion, the patient can be assured that recurrence is
very unlikely.

Fetal death of unknown cause is a special problem. Because a large number of etiologies of fetal
demise exist, a provider has difficulty determining risk of stillbirth for any particular pregnancy.
Evidence-based models such as Active Management of Risk In Pregnancy At Term (AMOR-IPAT) are
being created in an effort to better estimate this risk. [20] Although recurrent fetal loss is uncommon,
patients are naturally anxious. Most patients find increased fetal surveillance with the next pregnancy
reassuring, even though such testing is not clearly beneficial. The ACOG recommends antepartum

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testing starting at 32-34 weeks' gestation in an otherwise healthy mother with history of stillbirth. [16]
Weekly biophysical profile or fetal heart rate testing can be combined with maternal kick counts in the
third trimester. For patients who have experienced earlier loss, frequent ultrasound is reassuring.

Optimal management of chronic medical conditions is important prior to the next pregnancy.

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Media Gallery

This is an example of a checklist to be used following fetal death. Courtesy of Santa Clara Valley
Medical Center.

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Contributor Information and Disclosures

Author

Patricia J Mattingly, MD Clinical Instructor, Resident Physician, Department of Obstetrics and


Gynecology, Carolinas Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Saju Joy, MD, MS Associate Director, Division Chief of Maternal-Fetal Medicine, Department of
Obstetrics and Gynecology, Carolinas Medical Center

Saju Joy, MD, MS is a member of the following medical societies: American College of Obstetricians
and Gynecologists, American Institute of Ultrasound in Medicine, Society for Maternal-Fetal Medicine,
American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical
Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Carl V Smith, MD The Distinguished Chris J and Marie A Olson Chair of Obstetrics and Gynecology,
Professor, Department of Obstetrics and Gynecology, Senior Associate Dean for Clinical Affairs,
University of Nebraska Medical Center

Carl V Smith, MD is a member of the following medical societies: American College of Obstetricians
and Gynecologists, American Institute of Ultrasound in Medicine, Association of Professors of
Gynecology and Obstetrics, Central Association of Obstetricians and Gynecologists, Society for
Maternal-Fetal Medicine, Council of University Chairs of Obstetrics and Gynecology, Nebraska
Medical Association

Disclosure: Nothing to disclose.


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Acknowledgements

Michele P Hugin, MD, FACOG Ryan Program Director, Department of Obstetrics and Gynecology,
Santa Clara Valley Medical Center; Clinical Associate Professor, Department of Obstetrics and
Gynecology, Stanford University School of Medicine

Michele P Hugin, MD, FACOG is a member of the following medical societies: Alpha Omega Alpha,
American College of Obstetricians and Gynecologists, Association of Reproductive Health
Professionals, and National Abortion Federation

Disclosure: Merck Consulting fee Speaking and teaching James L Lindsey, MD Retired Staff,
Department of Obstetrics and Gynecology, Santa Clara Valley Medical Center; Clinical Associate
Professor, Department of Obstetrics and Gynecology, Stanford University School of Medicine

James L Lindsey, MD is a member of the following medical societies: American College of


Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Sultana L Sultani, MD Resident Physician, Department of Obstetrics and Gynecology, Santa Clara
Valley Medical Center

Sultana L Sultani, MD is a member of the following medical societies: American College of


Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Ackowledgments

The authors wish to thank Dr Robert M Silver and the Stillbirth Collaborative Research Network.

http://emedicine.medscape.com/article/259165-overview#a1 12/12

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