T. Y. Khong

Value of the perinatal autopsy: Critique

In consenting to a perinatal autopsy, the primary motive of parents may be to find the exact cause of death. A critical review on the value of perinatal autopsies was performed to see whether parents could be counseled regarding their main motive. A literature search was performed in MEDLINE, EXCERPTA MEDICA, and the Cochrane library. We evaluated the value of the autopsy by comparing the clinical and autopsy diagnoses in stillbirths, neonatal deaths, and therapeutic terminations. Clinicopathologic concordance was divided into four categories: (1) change in diagnosis, (2) additional findings, (3) complete confirmation, and (4) inconclusive. We sought information on factors that may influence the value of perinatal autopsies: the type and definitions of perinatal loss; autopsy rate; level of hospital; expertise of pathologists; autopsy protocol used; whether patients were inborn or referred; and antenatal diagnosis. From the 27 articles that met our review criteria, the autopsy revealed a change in diagnosis or additional findings in 22% to 76% of cases. If confirmation of clinical findings is included, then the value of the perinatal autopsy was as high as up to 100%. Factors that could influence this rate were reported variably by investigators. When centers report their experience of the value of the perinatal autopsy, information on the factors that may influence their reports should be provided as well. Clinicians can confidently advise parents of the usefulness of the perinatal autopsy in ascertaining the cause of death or for counseling their future pregnancies.

The placenta in maternal hyperhomocysteinaemia

It is becoming increasingly apparent that mild or moderate hyperhomocysteinaemia may be associated with adverse perinatal complications and outcomes. The placental pathology in 14 pregnancies from 11 women diagnosed retrospectively to have hyperhomocysteinaemia, following a recent history of intrauterine fetal growth restriction, abruption or of thromboembolic disease, were reviewed. Most of the placental findings indicated abnormal placentation but these were not specific to maternal hyperhomocysteinaemia nor found in every placenta. Features observed included absence of trophoblast‐induced physiological vascular changes, acute atherosis, intraluminal endovascular trophoblast in the third trimester, infarction, retroplacental haematoma formation and accelerated villous maturity. Uteroplacental vascular thrombosis was also seen. Three of the women had a subsequent pregnancy where they were treated empirically with folic acid, and these resulted in improved perinatal outcomes. The finding of placental pathology warrants investigation of the woman for hyper‐ homocysteinaemia. Further randomised controlled trials of folic acid supplementation in preventing pregnancy complications associated with hyperhomocysteinaemia should be conducted.

A difficult conversation? The views and experiences of parents and professionals on the consent process for perinatal postmortem after stillbirth

Please cite this paper as: Heazell A, McLaughlin M, Schmidt E, Cox P, Flenady V, Khong T, Downe S. A difficult conversation? The views and experiences of parents and professionals on the consent process for perinatal postmortem after stillbirth. BJOG 2012;119:987–997.

Expression of endothelin-1 in amniotic fluid embolism and possible pathophysiological mechanism.

Since endothelin is a potent vasoconstrictor and bronchoconstrictor, endothelin‐1 expression in the lung was investigated using immunohistological techniques in two cases of amniotic fluid embolism. Intense expression of endothelin‐1 was observed in amniotic squames while weaker staining was seen in alveolar epithelium, bronchiolar epithelium and intraalveolar macrophages and focally in vascular endothelium. Endothelin‐1 may play a role in the early and transient haemodynamic alteration of pulmonary hypertension in amniotic fluid embolism.

Is endomyometrial injury during termination of pregnancy or curettage following miscarriage the precursor to placenta accreta

Aims: To determine the frequency with which myometrium is removed during vacuum terminations of pregnancy or dilatation and curettage after miscarriage, and to relate these findings to subsequent placenta accreta or its proxies. Methods: Archival tissues from vacuum termination of pregnancy or dilatation and blunt curettage after miscarriage were examined for the presence of myometrium. The subsequent obstetric histories were scrutinised for manual removal of placenta, postpartum haemorrhage, or retained placenta. A retrospective study comparing the frequency of miscarriage and termination in women who had or did not have a manual removal was also performed. Results: Myometrium was seen in the products of conception in 44% and 35% of termination and miscarriage tissues, respectively. One of nine women with myometrium at miscarriage had a postpartum haemorrhage in a subsequent pregnancy whereas, of the 21 women without myometrium at miscarriage, three required manual removal and seven had a postpartum haemorrhage afterwards. A past history of termination and/or miscarriage was more frequent in multigravid women who had a manual removal than those who did not. Conclusions: Endomyometrial injury is frequent at termination or dilatation and curettage after miscarriage, but the relation to subsequent placenta accreta remains unclear. Women requiring a manual removal of the placenta were likely to have had a past history of termination and/or miscarriage.

Absence of Innervation of the Uteroplacental Arteries in Normal and Abnormal Human Pregnancies

The spiral arteries of the human uterus are considerably remodeled structurally during pregnancy to facilitate an increase in blood flow. An immunohistochemical study was undertaken to determine whether the spiral arteries were innervated and, if so, whether they were denervated in the process of the physiologic vascular changes of normal pregnancy or, conversely, remained innervated in the absence of physiologic changes in abnormal pregnancy. Uterine tissues from nonpregnant nulliparous women, from normal early pregnancy, from normal late pregnancy, from abnormal early pregnancy (i.e. spontaneous abortions), and from abnormal late pregnancy (i.e. preeclampsia and intrauterine growth retardation) were subjected to immunohistochemistry using a panel of neuron-associated antibodies (neurofilament, neuron-specific enolase, S100 protein, protein gene product 9.5). All sections of the nonpregnant uterus showed an abundance of nerves deep in the myometrium, some of which were associated with radial and arcuate arteries. Very few nerves were demonstrated at the endomyometrial junction and no nerves were seen accompanying the intramyometrial spiral arteries. In both normal and abnormal pregnancy, nerves were not detected in the decidua or accompanying intradecidual spiral arteries, whether they were physiologically altered or not. Nerves were seen in the myometrium in 7 of 10 normal and in 1 of the 8 third-trimester abnormal placental beds, but none were seen accompanying intramyometrial spiral arteries, whether showing physiological changes or not. The lack of innervation of the spiral arteries in the nonpregnant state as well as in normal and abnormal pregnancy suggests that nonneurogenic mechanisms control blood flow at the spiral-arterial level.

Evidence-based pathology: umbilical cord coiling

&NA; The generation of a pathology test result must be based on criteria that are proven to be acceptably reproducible and clinically relevant to be evidence‐based. This review de‐constructs the umbilical cord coiling index to illustrate how it can stray from being evidence‐based. Publications related to umbilical cord coiling were retrieved and analysed with regard to how the umbilical coiling index was calculated, abnormal coiling was defined and reference ranges were constructed. Errors and other influences that can occur with the measurement of the length of the umbilical cord or of the number of coils can compromise the generation of the coiling index. Definitions of abnormal coiling are not consistent in the literature. Reference ranges defining hypocoiling or hypercoiling have not taken those potential errors or the possible effect of gestational age into account. Even the way numerical test results in anatomical pathology are generated, as illustrated by the umbilical coiling index, warrants a critical analysis into its evidence base to ensure that they are reproducible or free from errors.

Placental fetal vascular thrombosis lesions and maternal thrombophilia

Aims: Following intrauterine fetal death (IUFD), the placental fetal vessels undergo regressive changes. These changes are virtually indistinguishable from lesions that are the result of fetal vascular thrombosis (FVT). This study investigated the relation between these lesions and maternal thrombophilia. Methods: Placenta slides of 65 IUFDs with known maternal thrombophilia test results (compound MTHFR C677T and A1298C heterozygosity, n = 10; MTHFR 677TT homozygosity, n = 3; protein S deficiency, n = 0; factor V Leiden mutation, n = 2; prothrombin gene mutation G20210A, n = 1; lupus anticoagulant, n = 2; antiphospholipid syndrome, n = 1; MTHFR C677T heterozygosity, n = 5; MTHFR A1298C heterozygosity, n = 4; and MTHFR 1298CC homozygosity, n = 2) and of 30 livebirths with positive maternal thrombophilia test results (n = 5, 2, 0, 9, 2, 0, 2, 7, 2 and 1, respectively, for those thrombophilias) were microscopically examined for septation, fetal vessel thrombosis, intimal fibrin cushions, avascular villi, haemorrhagic endovasculitis and fibromuscular sclerosis. Results: Thirty of the 65 IUFDs had a positive maternal thrombophilia test; 22 of these 30 had FVT lesions. Thirty two of the 35 IUFDs with a negative maternal thrombophilia test had FVT lesions. Septation, defined as multiple lumens or ‘recanalisation’ in a placental vessel, was the lesion seen most often in IUFD (n = 41) whether by itself (n = 13) or in combination with other FVT lesions. Five of the 30 livebirths had FVT lesions but septation was not seen in any of the placentas from the 30 livebirths. FVT lesions did not have a significant relation with maternal thrombophilia. Conclusions: The finding of fetal vascular thrombosis lesions in stillbirths does not imply thrombophilia as the cause of the fetal death. Factors other than thrombophilia may play a role in the cause of FVT lesions.

Decision influences and aftermath: parents, stillbirth and autopsy

Background  Stillbirth, among the most distressing experiences an adult may face, is also a time when parents must decide whether an autopsy or other post‐mortem examinations will be performed on their infant. Autopsies can reveal information that might help explain stillbirth, yet little is known about how people make this difficult decision.

Making stillbirths visible: a systematic review of globally reported causes of stillbirth

Stillbirth is a global health problem. The World Health Organization (WHO) application of the International Classification of Diseases for perinatal mortality (ICD‐PM) aims to improve data on stillbirth to enable prevention.