Cause Of Fetal Death Research Articles

Foetal autopsy-categories and causes of death.

Intrauterine death(IUD)/ Stillbirth forms a major part of perinatal mortality which thereby is a good indicator of pregnancy wastage as well as quality of healthcare available. The key objectives of autopsy examination are to know the cause(s) of death, elucidation of pathogenic mechanism and quality control of clinical management. The aim of this study was to identify the prevalent causes of IUD, thereby taking appropriate measures to prevent them and decrease the perinatal mortality rate. The study included 14 cases of IUD received for autopsy in the Department of Pathology over a period of five years. Autopsies were performed as per standard protocol and included full anthropometric profile, external examination, gross and microscopic evaluation of different organs and placenta. Total number of 14 fetal autopsies were performed over a period of 5 years. The causes were broadly classified as fetal, maternal and placental. Placental causes were seen in majority of cases (48.57%) followed by fetal (35.72%) and then maternal (21.42). Most prevalent cause of death was congenital anomalies (28.6%) followed by placental insufficiency (21.4%) and chorioamnionitis (14.2%). Determination of causes of fetal death would prove beneficial to the clinicians and parents for better management and care in future pregnancies as well as in genetic counseling.

Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome

Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF-α, and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF-α, respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF-α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF-α. Body weight correlated negatively with IL-6 and positively with CRP and TNF-α. Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers.

79 UTERINE AND PLACENTAL INTERACTIONS DURING NECROTIC TIP DEVELOPMENT IN THE PIG FROM DAY 22 TO 42 OF GESTATION

Placental development is important for fetal development and nutrient and waste transport. The pig, a litter bearing animal, has an epitheliochorial placenta that forms a noninvasive attachment with the uterine endometrium. Insufficient placental development is one of the primary causes of fetal death and reduced fetal growth after 35 days of gestation. Necrotic tips develop at the distal ends of each allantochorion between Day 22 and 42 of gestation. During this same period, placenta attaches to the uterine endometrium and establish fetal blood supplies and nutrient exchange. The attached placenta is composed of a central highly vascular placental (HVP) region adjacent to the fetus and less vascular placental (LVP) regions on either side to the fetus, the paraplacenta and necrotic tips, which form after 27 days of gestation. The objective of this study was to comprehensively evaluate uterine–placental interactions and necrotic tip development from 22 to 42 days of gestation in the gilt. Gilts (n = 25) were bred by AI at first detection of oestrus (Day 0) and harvested at 22, 27, 32, 37, or 42 days of gestation. Each conceptus was counted and weighed to identify the large, medium, and small fetus in each litter. From these fetuses, HVP and LVP sections of tissue and necrotic tip (no placental attachment) were collected. Intact attached uterus and placenta were collected for histology and preserved in paraformaldehyde. Placentas were then stripped from the endometrium and individually weighed. Hematoxylin and eosin staining of uterine : placental sections was used to identify uterine fold development in the HVP, LVP, and uterine endometrial morphology in the necrotic tip regions. Three folds were measured for depth, width, and area using BQ Nova Prime software (Bioquant Image Analysis, Nashville, TN, USA). Data were analysed using PROC MIXED in SAS (SAS Institute Inc., Cary, NC, USA). Litter size, 12.1 ± 3.4, was similar (P = 0.86) for all days of gestation. Fetal and placental weight increased (P < 0.05) as day of gestation increased. Average fetal weight was similar (P = 0.30) for Day 27 and 32 with a tendency (P = 0.09) to increase by Day 37 before a significant increase at Day 42 (P = 0.002). The placenta increased (P = 0.02) in weight throughout this period of gestation, with the greatest increase in weight between 37 and 42 days of gestation. The LVP zones had no measureable fold formation until Day 32 from most conceptuses, and all LVP zones displayed microfold formation by Day 37. Necrotic tips became apparent after 27 days of gestation. Necrotic tip areas of the uterus had observable modifications from Day 32 to 42 of gestation, developing folds with dramatic changes in endometrial cell size and morphology. This work demonstrated fundamental time points in placental development that correspond to fetal growth and microfold formation. Gestation Day 27 through 32 show limited changes in either fetal growth or increased placental weight; however, significant morphological changes occur throughout the placenta, and even necrotic tips demonstrating the dynamic architecture of the establishing porcine placenta during early gestation.

Incidence and Pattern of Congenital Malformations in Gorgan-north of Iran

Congenital malformations are emerged as a common cause of fetal death and one of the most important causes of prenatal mortality and morbidity. This study was done to determine the incidence and pattern of congenital malformations in a referral hospital in Gorgan, North of Iran. This cross-sectional study was done on 6204 live birth in Dezyani hospital in Gorgan, North of Iran during a 12-month period from January 1st to December 31st of 2007. Gender, type of congenital malformations according to International Classification of Diseases (ICD-10) and maternal ethnicity were recorded. Data for each newborn was filled in a questionnaire. Data analyzed by using SPSS software version 16 and I�2 test. The overall incidence of congenital malformations among newborns was 17.7 per 1000 live births. The incidence of congenital malformations was 22.4 per 1000 in males (RR = 1.68 Q95%: 1.14-2.48) and 13.06 per 1000 in females. Anomalies of the central nervous system had the highest incidence (7.3 per 1000) followed by congenital heart defects (5.2 per 1000) and musculoskeletal system (3.7 per 1000) births. According to ethnicity the incidence rate of congenital malformations was 16.5,17.2 and 20 per 1000 live births in native Fars, Turkman (RR = 1.04 CI95%:65-1.67) and Sistani (RR = 1.2 CI95%: 0.78-1.85) groups, respectively. This study showed that the incidence rate of congenital malformations is increased from 10.1 -17.7 per 1000 live birth in Northern Iran during an 8 years period.

Approach to Trauma During Pregnancy

Approach to Trauma During Pregnancy

Successful Management of a Case of Pregnancy Failure in a Degu (Octodon degus)

A 3-month-old female degu (Octodon degus) was presented because blood was noticed in its cage. On physical examination, firm masses were palpable within the caudal abdomen and traces of blood appeared to be coming from the patient’s vaginal opening. Radiographic images showed areas of ill-defined mineralization within the uterus, consistent with fetus formation. Three fetuses could be identified. Ultrasound examination of the degu failed to confirm viable fetal heartbeats. Pregnancy failure with fetal death was suspected. Overnight 1 fetus was passed, but medical therapy with oxytocin failed to induce delivery of the 2 remaining fetuses by the following morning. The degu was therefore anesthetized, an ovariohysterectomy was performed, and the patient made an uncomplicated recovery. Histopathological examination of the fetuses failed to identify any abnormalities. In the uterus, histology confirmed a minimal to mild diffuse, chronic active endometritis. The definitive cause of fetal death was not identified.

Gastroschisis is a defect of the Umbilical ring: Evidence from Morphological evaluation of stillborn fetuses

Gastroschisis (GS) is usually described as an abdominal wall defect, to the right of a normally inserted umbilical cord, without membraneous covering of the extruded organs. However, precise anatomical descriptions are lacking in the literature. Our aims were to provide evidence that allows reconsideration of its current definition, as well as an explanation for prenatal death, based on detailed observation of stillborn fetuses with GS and a review of the literature. Prenatal studies, clinical examinations, and histological findings of five stillborn fetuses with isolated GS are described and photographic evidence is provided. In all five cases, the umbilical cord was only attached to the left side of the umbilical ring, while the right side remained uncovered, allowing evisceration of abdominal organs. Histological evidence of mucoid-like tissue at the free border of the ring suggests that at that site the cord was initially inserted and later detached. Characteristics of the umbilical ring, bowel dilatation, and autopsy findings of acute asphyxia strongly support compression of umbilical vessels as the cause of fetal death. Based on these findings, on the lack of evidence in the literature demonstrating full-thickness abdominal wall separating the defect from the umbilical cord, and on a critical review of the proposed mechanisms favoring the hypothesis of a defect separate from the umbilical ring, we propose that GS represents a failure in the normal attachment between umbilical cord and umbilical ring. The consistent clinical course of fetuses with prenatal demise suggests careful targeted monitoring during late gestation.

Barth syndrome

First described in 1983, Barth syndrome (BTHS) is widely regarded as a rare X-linked genetic disease characterised by cardiomyopathy (CM), skeletal myopathy, growth delay, neutropenia and increased urinary excretion of 3-methylglutaconic acid (3-MGCA). Fewer than 200 living males are known worldwide, but evidence is accumulating that the disorder is substantially under-diagnosed. Clinical features include variable combinations of the following wide spectrum: dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), endocardial fibroelastosis (EFE), left ventricular non-compaction (LVNC), ventricular arrhythmia, sudden cardiac death, prolonged QTc interval, delayed motor milestones, proximal myopathy, lethargy and fatigue, neutropenia (absent to severe; persistent, intermittent or perfectly cyclical), compensatory monocytosis, recurrent bacterial infection, hypoglycaemia, lactic acidosis, growth and pubertal delay, feeding problems, failure to thrive, episodic diarrhoea, characteristic facies, and X-linked family history. Historically regarded as a cardiac disease, BTHS is now considered a multi-system disorder which may be first seen by many different specialists or generalists. Phenotypic breadth and variability present a major challenge to the diagnostician: some children with BTHS have never been neutropenic, whereas others lack increased 3-MGCA and a minority has occult or absent CM. Furthermore, BTHS was first described in 2010 as an unrecognised cause of fetal death. Disabling mutations or deletions of the tafazzin (TAZ) gene, located at Xq28, cause the disorder by reducing remodeling of cardiolipin, a principal phospholipid of the inner mitochondrial membrane. A definitive biochemical test, based on detecting abnormal ratios of different cardiolipin species, was first described in 2008. Key areas of differential diagnosis include metabolic and viral cardiomyopathies, mitochondrial diseases, and many causes of neutropenia and recurrent male miscarriage and stillbirth. Cardiolipin testing and TAZ sequencing now provide relatively rapid diagnostic testing, both prospectively and retrospectively, from a range of fresh or stored tissues, blood or neonatal bloodspots. TAZ sequencing also allows female carrier detection and antenatal screening. Management of BTHS includes medical therapy of CM, cardiac transplantation (in 14% of patients), antibiotic prophylaxis and granulocyte colony-stimulating factor (G-CSF) therapy. Multidisciplinary teams/clinics are essential for minimising hospital attendances and allowing many more individuals with BTHS to live into adulthood.

English

INTRODUCTION: The cord disposition and length of umbilical cord in the amniotic cavity remain unrecognised till the birth of the baby.Cord complications remain one of the major causes of foetal death. OBJECTIVES: To study

Dificuldades para a identificação da causa do óbito fetal: como resolver?

To identify the causes of fetal death in the studied population and to measure their contribution in identifying the cause of this outcome. To propose the use of the system Relevant Condition of Death (ReCoDe) in elucidating the causes of fetal death to minimize the number of unknown causes. Cross-sectional study related to fetal deaths seen at a specialized academic hospital in the South of Brazil, from January 2000 to December 2009. The data were collected in the death certificates, maternal medical records and the reports of study of fetuses and attachments, and the findings were compared. Data analysis was performed using SPSS version 17.0. Were included 111 fetuses and their respective mothers in this study. The comparison between the diagnostic causes in the pathology and clinical evaluation showed 74 (66.7%) and 73 (65.8%), respectively. Together, they found a potential cause in 48.7% of cases, while 16.2% remained unknown. When analyzing both together with the ReCoDe system, only 9.9% of stillbirths remained as "unclassified." The proportion of diagnoses in the cause of death among the pathological and clinical evaluation showed no significant difference. When comparing the results of the cause of death suggested by the clinic/pathology with the use of the ReCoDe system, it appears that this tool has helped to clarify the cause by reducing the amount of those that remained without a possible etiology.

AutochthonousLeishmania siamensisin Horse, Florida, USA

Autochthonous<i>Leishmania siamensis</i>in Horse, Florida, USA

The role of DNA microarrays in the evaluation of fetal death

Fetal death occurs in 15% of clinically recognized pregnancies. Cytogenetic abnormalities are present in 50% of spontaneous abortions (fetal deaths < 20 weeks) whereas the rate is 6% to 13% for stillbirths (fetal deaths ≥ 20 weeks). Microarray has been demonstrated to increase the diagnosis of genetic abnormalities by providing coverage of the entire genome at a higher density, detecting as small as 50 to 100 kb deletions or duplications, known as copy number changes. Microarray is particularly suited for evaluation of fetal death because DNA can still be analyzed in macerated fetuses and nonviable tissue, two situations where culturing and karyotyping is known to have low yield. Microarray has already proven successful in providing additional genetic information beyond karyotype in spontaneous abortion. The few studies on the use of microarray in stillbirth evaluation have been promising, demonstrating an increase in the diagnosis of clinically relevant genetic abnormalities when compared with karyotype. As the cost and technology improve, microarray may ultimately become the first line screen for genetic abnormalities in stillbirth. The accurate diagnosis of a genetic abnormality as the cause for fetal death may provide closure for families, prevent unnecessary treatments, and enable clinicians to more accurately counsel and manage subsequent pregnancies.

Maternal Education and Stillbirth

Associations between risk factors and perinatal outcomes may be biased at preterm gestational ages, if preterm delivery behaves as an effect modifier due to other unmeasured factors in the causal pathway. We evaluated whether fetuses-at-risk denominators could be used in regression models instead of conventional denominators to obtain less biased estimates of the association between maternal education and stillbirth at preterm gestational intervals. Data included 2,143,134 live-born and 8946 stillborn singletons from 1981 through 2006 in Québec, Canada. Odds ratios and 95% confidence intervals were estimated for the relationship between education and stillbirth according to cause of fetal death, adjusting for maternal age, marital status, home language, parity, and period. We examined associations for 4 gestational intervals (<28, 28-31, 32-36, and ≥37 completed weeks), using both conventional denominators (ie, preterm live births) and fetuses-at-risk denominators. Stillbirth rates were greater for mothers with fewer years of education at all gestational intervals. Using conventional denominators, low education (relative to high education) was more strongly associated with term than preterm stillbirth and was apparently protective at <28 weeks. Using fetuses-at-risk denominators, low education was more strongly associated with preterm stillbirth than term stillbirth, even at <28 weeks. Low education was most strongly associated with diabetic-related stillbirth at ≥28 weeks (odds ratio = 5.04) relative to high education. Low education is associated with stillbirth throughout gestation, especially diabetic-related stillbirth. Use of fetuses-at-risk denominators in regression models can avoid potentially biased estimates obtained with conventional denominators at preterm gestational ages.

Pregnancies complicated by maternal syphilis and fetal death

To describe the characteristics of pregnancies complicated by maternal syphilis and fetal death. Retrospective descriptive study performed by reviewing the medical records of 48 pregnant women with maternal syphilis and fetal death outcome admitted to Hospital Geral de Nova Iguaçu, Baixada Fluminense, State of Rio de Janeiro, during the period from 2005 to 2008. Birth weight >500 g and fetal death documented by Death Certificate were the inclusion criteria. The following aspects were analyzed: sociodemographic factors, reproductive history, aspects of the current pregnancy, prenatal care, Venereal Disease Research Laboratory (VDRL) testing, and other gestational conditions, in addition to syphilis. The fetal deaths were classified as maternal, placental or fetal. Percentage, mean, standard deviation (SD), maximum and minimum values were reported. The mean maternal age was 22.7 years (SD=0.9 years), and at least 50% of the patients had low educational level. At hospital admission, 68.8% of the subjects were in the third trimester, with a mean gestational age of 29.2 weeks (SD=0.5), and more than 50% were in labor. The vast majority of fetal deaths (93%) occurred before maternal hospitalization. Among the patients who received prenatal care (54.2%), 30.8% had no VDRL test, 30.8 and 15.4% had a reactive and non-reactive result, respectively, and none had more than one prenatal VDRL test. At the time of childbirth, most of the mothers (95.8%) carried out VDRL testing. Overall, the VDRL titers varied from 1:1 to 1:512, with predominant values >1:4 (91.7%). In 23% of cases other clinical conditions related to fetal death, in addition to syphilis, were found. The infection was the main clinically identified cause of fetal death in this patient series. Fetal death occurred during the preterm period and in the presence of high titers of maternal infection, suggesting recent syphilis infection.

Case report: lethal fetal head injury and placental abruption in a pregnant trauma patient

Fetal trauma in blunt abdominal trauma is uncommon, but traumatic fetal head injury is almost universally fatal to the fetus. Placental abruption is the most common injury to the gravid uterus in trauma, and when the mother survives, it is the most common cause of fetal death. The imaging diagnosis of these conditions may be difficult since there are only three cases reported in the literature of intrauterine skull fractures on plain films [3, 8, 10], ultrasound is in sensitive in the diagnosis of placental abruption [24], and the most sensitive test to diagnose placental abruption is external fetal monitoring with devices that measure uterine tone and contractility and fetal heart rate [23]. The diagnosis of fetal trauma and placental abruption may be made on contrast enhanced CT performed through the abdomen and pelvis of pregnant trauma patients. For these reasons, it is useful for the radiologist interpreting the CT scan to recognize fetal head injuries and placental abruption in pregnant trauma patients.Fig. 7 Axial scans through the bony pelvis demonstrate an unstable pelvic fracture with posterior pelvic ring disruption.There is a zone 2 fracture of the left sacrum and a fracture of the left obturator ring (arrowheads)

Gestational alloimmune liver disease: a cause of fetal death in utero

Recent evidence suggests that neonatal haemochromatosis is caused by gestational alloimmune liver disease (GALD), and is an underdiagnosed entity, especially in cases of unexplained stillbirth or premature birth. 1 We present an autopsy case of a 35-year-old mother, G4P3, who was diagnosed with fetal death in utero (FDIU) at 32 weeks gestation. She had a previous child born with severe liver damage of unknown cause but suspected to be alloimmune. Her subsequent pregnancy was treated with immu-noglobulin and she delivered a normal child. This pregnancy immunoglobulin was not administered due to side-effects. At 32 weeks she noticed reduced fetal movements and FDIU was diagnosed. A full autopsy was performed which found features of terminal hypoxia, advanced liver autolysis, but no morphological abnormalities and negative Perls stain. Due to high clinical suspicion of neonatal haemochromatosis, liver autopsy samples and liver biopsy of child with severe hepatitis were sent to Children’s Memorial Research Centre, Chicago, for further analysis. Slides were stained with C5b-9 complex and were unequivocally positive in both liver biopsies. This is strong evidence that FDIU and severe hepatitis was due to GALD. Pathologists and clinicians need to be aware of GALD as a cause of FDIU.

Stillbirth and Lessons for Pregnancy Care

STILLBIRTH—DEATH OF A FETUS IN UTERO DURING THE second half of pregnancy—has until recently been a neglected topic in perinatal medicine despite its frequent occurrence, conservatively estimated worldwide at more than 2.6 million deaths in 2008. In the United States, fetal mortality is almost as common as infant mortality, affecting 1 in every 160 pregnancies. Investigations into the causes of stillbirth and means to prevent it are receiving more attention. In 2006, the Eunice Kennedy Shriver National Institute of Child Health and Human Development funded the first multicenter prospective population-based study of adequate size of stillbirth in the United States with the hope of addressing important scientific gaps. This issue of JAMA includes 2 reports from the Stillbirth Collaborative Research Network (SCRN) that provide lessons about the causes of fetal death, opportunities to prevent stillbirth, and the implications of stillbirth research for all adverse pregnancy outcomes. In a carefully constructed study that sought to capture all stillbirths in 5 defined geographic areas, the SCRN investigators enrolled every mother and stillborn neonate and also enrolled as controls 2 mothers and their liveborn neonate(s) (614 stillbirths and 1816 live births). Based on a comprehensive review of prenatal, intrapartum, and neonatal information, the authors confirmed known associations of stillbirth risk with maternal diabetes, obesity, smoking, multifetal pregnancy, and black race, and identified increased stillbirth risk for women pregnant for the first time or living alone. Risk factors evident at the beginning of pregnancy had low positive predictive value and were associated with relatively few stillbirths, limiting the opportunities for early intervention. The level of detail enabled novel analyses that revealed 4 distinct categories of stillbirth based on gestational age, maternal race/ethnicity, and causes of death. Fetal deaths before 28 weeks’ gestation included a group of fetal deaths between 20 and 24 weeks that occurred during labor and were more common among black women, and a second group in which fetal death from placental problems and other obstetrical conditions preceded labor. After 28 weeks’ gestation, fetal deaths related to maternal hypertension predominated between 24 and 31 weeks, whereas cord abnormalities were the most common cause in the last weeks of pregnancy. Fetal death during labor before 24 weeks’ gestation is a consequence of extreme prematurity because interventions on behalf of the fetus are not indicated before viability. Black women, whose rate of preterm birth is double that of women from other racial/ethnic backgrounds, comprised a majority of this group. Stillbirth and preterm birth are often considered as separate entities, but this is strong evidence that the 2 are more closely linked than has been previously recognized. Additional evidence of common origins of stillbirth and preterm birth comes from the SCRN analyses of the risk of prior pregnancy outcomes for future stillbirth. As expected, a history of prior stillbirth was associated with increased risk (adjusted odds ratio, 5.9; 95% CI, 3.18-11.00). Increased risk of stillbirth (adjusted odds ratio, 3.13; 95% CI, 2.06-4.75) was also found in “nulliparous” women who had experienced a pregnancy loss before 20 weeks. These women are not parous in that they have not delivered a live or stillborn infant after 20 weeks’ gestation, but their increased risk of subsequent stillbirth supports the contention that the traditional 20-week boundary between “miscarriage” and “birth” is not clinically or scientifically useful and thus should be abandoned. Because pregnancy losses before and after 20 weeks’ gestation have historically been thought to result from different pathways, research and vital statistics data have been collected and analyzed within that model. Recent reviews suggest otherwise, based on reports that stillbirths are associated with adverse outcomes in future pregnancies, as are second-trimester losses before and after 20 weeks. The SCRN reports add to the increasing realization that the current obstetrical taxonomy is an obstacle to improving pregnancy outcomes. Optimal investigation of the origins, treatment, and prevention of stillbirth and preterm birth will require data collected on deliveries before and after 20 weeks, regardless of whether the fetus is alive or not at the time of presentation for care.

Death Before Birth: Fetal Health and Mortality in Historical Perspective (review)

Reviewed by: Death Before Birth: Fetal Health and Mortality in Historical Perspective Karol K. Weaver Robert Woods. Death Before Birth: Fetal Health and Mortality in Historical Perspective. Oxford: Oxford University Press, 2009. xvii + 294 pp. Ill. $110.00 (978-0-19-954275-8). Robert Woods’s Death Before Birth: Fetal Health and Mortality in Historical Perspective is an intriguing book. Its subject matter concerns fetal health and mortality with a focus on how fetal deaths declined over time. Woods clearly explains the difficulties the topic presents to researchers. Despite the issues faced, Woods deftly applies both demography and history to the subject. The resulting work is a text that will inspire others to take up the history of the fetus, fetal health, and fetal mortality. Woods notes that historians have looked at multiple actors when studying the history of pregnancy and birth. He points out that researchers have focused their investigations on pregnant women, midwives, professional medical practitioners, and infants. His book, however, concentrates on one of the most important, but overlooked, actors during pregnancy and birth—the fetus. Specifically, Woods explores the history of fetal health and mortality. He concludes that the decrease in fetal mortality was aided by the availability of antibiotics in the twentieth century, disease prevention as a result of vaccination programs, and improvements in obstetrical care. The author shows that the topic of fetal health and mortality is difficult to study. Woods explains that he faced several issues when approaching the subject matter: the language used to describe fetal health and mortality is varied, there are numerous definitions of various fetal incidents, the recording of age depends on the culture in which it takes place, the registration of fetal deaths differs depending on the purpose of the record and on who is doing the recording, and the causes of fetal death are often difficult to determine. Woods, for example, presents the varied definitions related to fetal mortality via an excellent table; table 2.1 (pp. 15–16) succinctly lays out the multiple words that can be employed to describe fetal health and mortality. Through the use of history and demography, Woods traces developments in fetal health and mortality. His historical analysis depends on several types of primary sources: parish registers, the case notes of midwives and man-midwives, and the clinical reports of obstetricians. Woods not only analyzes these sources but also includes extended passages from several primary sources for the reader. His inclusion of a selection of observations from Sarah Stone’s A Complete Practice of Midwifery allows the reader into the historical process and shows that, despite being a “neglected area” (p. 1) of study, the history of fetal health and mortality is possible. In addition to history, Woods, a professor of geography, employs demography. He complements his written demographic analysis with graphs and [End Page 653] charts. Woods summarizes his methodological approach when he states, “This study is avowedly anti-disciplinary; it does not offer a history in the normal sense, rather it wants to know how and why change occurred in the long term and it will be prepared to use whatever is available and relevant to reach that goal” (p. 9). Death Before Birth will appeal to a variety of readers. Historians will find a work that focuses on a topic that has been neglected by scholars who specialize in the history of birth and pregnancy. The volume demonstrates that the sources are there to complete further work on the medical history of the fetus and alerts researchers to some of the difficulties they might face. Students of geography also will appreciate Woods’s demographic analysis. Woods has opened a new scholarly avenue and has provided future researchers with the map to investigate further the field of fetal health and mortality. Karol K. Weaver Susquehanna University Copyright © 2011 The Johns Hopkins University Press

Evaluation of 1025 fetal deaths: proposed diagnostic workup

We sought to evaluate the contribution of different diagnostic tests for determining cause of fetal death. Our goal was to propose a workup guideline. In a multicenter prospective cohort study from 2002 through 2008, for 1025 couples with fetal death ≥20 weeks' gestation, an extensive nonselective diagnostic workup was performed. A panel classified cause and determined contribution of diagnostics for allocating cause. A Kleihauer-Betke, autopsy, placental examination, and cytogenetic analysis were abnormal in 11.9% (95% confidence interval [CI], 9.8-14.2), 51.5% (95% CI, 47.4-55.2), 89.2% (95% CI, 87.2-91.1), and 11.9% (95% CI, 8.7-15.7), respectively. The most valuable tests for determination of cause were placental examination (95.7%; 95% CI, 94.2-96.8), autopsy (72.6%; 95% CI, 69.2-75.9), and cytogenetic analysis (29.0%; 95% CI, 24.4-34.0). Autopsy, placental examination, cytogenetic analysis, and testing for fetal maternal hemorrhage are basic tests for workup after fetal death. Based on the results of these tests or on specific clinical characteristics, further sequential testing is indicated.

Triplet pregnancy complicated by two acardiac fetuses

Triplet pregnancy complicated by two acardiac fetuses