Perinatal and postneonatal mortality among Indigenous and non-Indigenous infants born in Western Australia, 1980-1998.

OBJECTIVE: To describe cause-specific perinatal and postneonatal mortality for Indigenous and non-Indigenous infants using a new classification system. DESIGN: Total population retrospective cohort study. PARTICIPANTS AND SETTING: All registered births in Western Australia of birthweight greater than 399 g from 1980 to 1998, inclusive. MAIN OUTCOME MEASURES: Rates and time trends for all births 1980-1998, and cause-specific rates for births 1980-1993 of fetal, neonatal and postneonatal mortality among Indigenous and non-indigenous infants, using a classification system designed for use in perinatal, postneonatal and childhood deaths. RESULTS: For Indigenous infants born 1980-1998, the mortality rate before the first birthday was 2.7 times (95% CI, 2.5-2.9 times) that for non-Indigenous infants. Indigenous infants born 1980-1993 had a higher mortality rate in all cause-of-death categories. The highest relative risk was for deaths attributable to infection (8.1; 95% CI, 6.5-10.0) which occurred primarily in the postneonatal period; the source of the infection was less likely to be identified in Indigenous deaths. From 1980-1998, the rate of neonatal deaths decreased at a greater rate for Indigenous than for non-Indigenous infants. However, while stillbirth and sudden infant death syndrome rates for non-Indigenous births fell, they remained static for Indigenous births. CONCLUSIONS: The new classification system, which considers the underlying rather than immediate cause of death, enables investigation of the causes of all deaths, from stillbirths to childhood. This system has highlighted the comparative importance of infection as a cause of death for Indigenous infants, particularly in the postneonatal period.

Cumulative mortality in children aged 1 to 6 years born in Western Australia from 1980-89.

PURPOSE: To investigate cumulative mortality for children aged 1-6 years born in Western Australia from 1980 to 1989. STUDY DESIGN: Births and deaths were ascertained from a linked total population database supplemented by information from postmortem records. Deaths were classified according to the underlying cause, and mortality rates, including factor specific rates, were calculated. Trends were investigated and comparisons were made using relative risks with 95% confidence intervals. RESULTS: Cumulative mortality was 2.2/1000 infant survivors, with a significant decrease during the years studied. Mortality was almost four times higher for Indigenous children, with no decrease. Accidents comprised 45.6% of all deaths, birth defects 17.3%, cancer and leukaemias 12.5%, and infections 11.0%. Low birth weight, preterm birth, and young maternal age significantly increased the risk of death in both Indigenous and non-Indigenous children; single marital status was also a significant risk factor for non-Indigenous children. CONCLUSION: High quality data and appropriate classification systems are essential to enable effective monitoring of childhood deaths and the planning of preventive programmes. Further decreases in mortality rates might be dependent on ensuring that resources are directed towards improving social and economic conditions for Indigenous and other disadvantaged families.

Antepartum risk factors for newborn encephalopathy: the Western Australian case-control study.

OBJECTIVE: To ascertain antepartum predictors of newborn encephalopathy in term infants. DESIGN: Population based, unmatched case-control study. SETTING: Metropolitan area of Western Australia, June 1993 to September 1995. SUBJECTS: All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls. MAIN OUTCOME MEASURES: Adjusted odds ratio estimates. RESULTS: The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. The risk of newborn encephalopathy increased with increasing maternal age and decreased with increasing parity. There was an increased risk associated with having a mother who was unemployed (odds ratio 3.60), an unskilled manual worker (3.84), or a housewife (2.48). Other risk factors from before conception were not having private health insurance (3.46), a family history of seizures (2.55), a family history of neurological disease (2.73), and infertility treatment (4.43). Risk factors during pregnancy were maternal thyroid disease (9.7), severe pre-eclampsia (6.30), moderate or severe bleeding (3.57), a clinically diagnosed viral illness (2.97), not having drunk alcohol (2.91); and placenta described at delivery as abnormal (2.07). Factors related to the baby were birth weight adjusted for gestational age between the third and ninth centile (4.37) or below the third centile (38.23). The risk relation with gestational age was J shaped with 38 and 39 weeks having the lowest risk. CONCLUSIONS: The causes of newborn encephalopathy are heterogeneous and many of the causal pathways start before birth.

Intrapartum risk factors for newborn encephalopathy: the Western Australian case-control study.

OBJECTIVE: To identify intrapartum predictors of newborn encephalopathy in term infants. DESIGN: Population based, unmatched case-control study. SETTING: Metropolitan area of Western Australia, June 1993 to September 1995. SUBJECTS: All 164 term infants with moderate or severe newborn encephalopathy; 400 randomly selected controls. MAIN OUTCOME MEASURES: Adjusted odds ratio estimates. RESULTS: The birth prevalence of moderate or severe newborn encephalopathy was 3.8/1000 term live births. The neonatal fatality was 9.1%. Maternal pyrexia (odds ratio 3.82), a persistent occipitoposterior position (4.29), and an acute intrapartum event (4.44) were all risk factors for newborn encephalopathy. More case infants than control infants were induced (41.5% and 30.5%, respectively) and fewer case infants were delivered by caesarean section without labour (3.7% and 14.5%, respectively). Operative vaginal delivery (2.34) and emergency caesarean section (2.17) were both associated with an increased risk. There was an inverse relation between elective caesarean section (0.17) and newborn encephalopathy. After application of a set of consensus criteria for elective caesarean section only three (7%) eligible case mothers compared with 33 (65%) eligible control mothers were sectioned electively. Of all the case infants, 113 (69%) had only antepartum risk factors for newborn encephalopathy identified; 39 (24%) had antepartum and intrapartum factors; eight (5%) had only intrapartum factors; and four (2%) had no recognised antepartum or intrapartum factors. CONCLUSIONS: The causes of newborn encephalopathy are heterogeneous and many relate to the antepartum period. Elective caesarean section has an inverse association with newborn encephalopathy. Intrapartum hypoxia alone accounts for only a small proportion of newborn encephalopathy. These results question the view that most risk factors for newborn encephalopathy lie in the intrapartum period.

An analysis of sudden infant death syndrome in aboriginal infants.

The purpose of this case-control study was to identify antenatal and perinatal risk factors for sudden infant death syndrome (SIDS) in Aboriginal infants in Western Australia (WA). Cases were all Aboriginal infants born in WA from 1980 to 1990 inclusive and classified as dying from SIDS in WA. Controls consisted of a matched group and a random group both selected from liveborn Aboriginal infants born from 1980 to 1990. Multivariate modelling showed that SIDS in Aboriginal infants was strongly related to young maternal age (< 20 years, odds ratio (OR) = 2.89), high parity (parity > 3, OR = 4.40) and being small-for-gestational age (OR = 3.36) but was not associated with single marital status (OR = 0.95) or male sex (OR = 0.97). Although the study was based on routinely collected data, results do highlight some important groups for SIDS prevention. To gain further knowledge in terms of SIDS in Aboriginal infants, there is an urgent need to collect information concerning infant care practices in the Aboriginal community.

Sudden infant death syndrome in Australian aboriginal and non-aboriginal infants: an analytical comparison.

Our previous research has shown that the sudden infant death syndrome (SIDS) rate for Aboriginal infants in Western Australia (WA) is markedly higher than that for non-Aboriginal infants. The aim of this study was to identify factors that may be important in explaining this disparity. A case-control study was conducted based on routinely collected data for the population of WA singleton births from 1980 to 1990 inclusive. Cases were infants born and classified as dying from SIDS in WA (Aboriginal n = 88, non-Aboriginal n = 409). Controls were infants born in WA and not classified as dying from SIDS; 2% samples of both Aboriginal and non-Aboriginal infants were included. The risk of dying from SIDS in Aboriginal infants was 3.86 times [95% confidence interval (CI) = 2.98 to 5.02] that in non-Aboriginal infants. Statistically significant univariable risk factors for SIDS in Aboriginal infants were preterm birth, low birthweight and small-for-gestational-age; for non-Aboriginal infants they included these factors as well as single marital status, young maternal age, parity of one or greater and male sex. Comparing Aboriginal with non-Aboriginal controls, most of the risk factors were more common in the Aboriginal population. Multiple logistic regression analysis indicated that Aboriginal infants were 1.43 times [95% CI = 1.04 to 1.95] more likely to die from SIDS than non-Aboriginal infants. Differences in the risk factor profile for Aboriginal and non-Aboriginal infants were sought using interaction terms. The only important differences were that the risk of SIDS in Aboriginal infants, unlike that in non-Aboriginal infants, appeared not to be strongly related to male sex or to single marital status. Thus, the results show that the disparity between the incidence of SIDS in the Aboriginal and non-Aboriginal populations can be explained largely, although not totally, by the high prevalence of routinely recorded risk factors in the Aboriginal population. A limitation of this study is that data on the postnatal risk factors of prone sleeping, maternal smoking and non-breastfeeding were unavailable. The residual excess risk for Aboriginal infants may be a result of these recognised postnatal risk factors and/or other infant care practices that are not routinely recorded in our data base, or to underlying social and economic conditions. Further study of all these potential risk factors is warranted.

Pathology review of sudden and unexpected death in aboriginal and non-aboriginal infants.

Previous research showed that the sudden infant death syndrome (SIDS) rate for Aboriginal infants significantly increased during the 1980s in Western Australia (WA) and raised the possibility of a diagnostic transfer of Aboriginal infant deaths from other causes to SIDS over this period. Here, therefore we review the pathology of SIDS and other sudden and unexpected deaths in infancy (SUDI) for Aboriginal and non-Aboriginal infants in WA between 1980 and 1988. The aim was to investigate whether there had been differences in the diagnosis and/or classification of SIDS according to whether the infants were Aboriginal or non-Aboriginal. The study population comprised: (1) all Aboriginal cases of SIDS and other SUDI between 1980 and 1988, and (2) corresponding random samples of non-Aboriginal cases. A two-stage process was employed for the review. First, histology slides were reviewed for each case where the aboriginality of the infant was Aboriginal and the original cause of death were unknown to the pathologists. Second, all paper records (i.e. death scene investigations, laboratory tests and medical reports) except for the original cause of death information were reviewed by the pathologists. The results showed that there was excellent agreement between the final review diagnosis and the original diagnosis for both Aboriginal and non-Aboriginal SUDI. Thus, there was no evidence for a diagnostic shift among Aboriginal infant deaths and the review supported the observed increase in the SIDS rate for Aboriginal infants.

Predictors of neonatal encephalopathy in full-term infants.

OBJECTIVE: Preliminary investigation of the contribution of adverse antepartum and intrapartum factors to neonatal encephalopathy in singleton neonates born full term. DESIGN: Matched case-control study based on incidence density sampling of controls. SETTING: Two major teaching hospitals (one paediatric and one obstetric) and three peripheral maternity hospitals in Perth, Western Australia (population 1.2 million). SUBJECTS: 89 cases, all the full term singleton neonates born during an eight month period in 1992 who fulfilled one or more of six criteria during the first week of life (seizures, abnormal conscious state, persistent hypertonia or hypotonia, and feeding or respiratory difficulties of central origin). One full term control infant without neonatal encephalopathy was matched to each case by sex, hospital of delivery, time of day and day of the week of birth, and maternal health insurance status. MAIN OUTCOME MEASURES: Odds ratio estimates of relative risk of neonatal encephalopathy associated with antepartum and intrapartum factors. RESULTS: Estimated incidence of moderate or severe encephalopathy in first week of life was 3.75 per 1000 full term live births. Thirteen cases and no controls had evidence suggestive of important intrapartum hypoxia, and in only five of these cases was the neurological condition at birth attributed to events during the intrapartum period. Univariate conditional logistic regression analysis identified significant differences between cases and controls for maternal vaginal bleeding in pregnancy, maternal thyroxine treatment, congenital abnormalities, induction of labour, interval from membrane rupture to delivery, maternal pyrexia in labour, augmentation of labour, abnormal intrapartum cardiotocograms, and meconium in labour. Family history of convulsions also approached significance. CONCLUSIONS: Our preliminary results suggest that intrapartum hypoxia, according to currently used criteria, was not the cause of neonatal encephalopathy in most cases in this population. Our findings suggest that many aetiologies of neonatal encephalopathy originate in the antepartum period.

Sudden infant death syndrome in aboriginal and non-aboriginal infants.

This study, based on routinely recorded data, was designed to compare the epidemiology of sudden infant death syndrome (SIDS) in Aboriginal and non-Aboriginal infants in Western Australia (WA). All cases of SIDS occurring in infants born in WA from 1980 to 1988 were included in the study. There were 66 Aboriginal (6.1 per 1000 live births) and 337 non-Aboriginal (1.7 per 1000 live births) infants who died from SIDS. It was found that there was a significant linear increase in the Aboriginal SIDS rate over the study period while the non-Aboriginal rate remained relatively constant. For non-Aboriginal infants, there was an elevated risk of SIDS for young maternal age, single marital status and male gender but this was not found for Aboriginal infants. There was a significant difference in the age at death distribution for the two populations. Low birthweight and preterm birth were risk factors for both Aboriginal and non-Aboriginal infants. There may be differences in the aetiology and/or classification of SIDS between the two populations.

Sudden infant death syndrome and infant mortality in aboriginal and non-aboriginal infants.

The aim of this study was to investigate sudden infant death syndrome (SIDS) in the context of total infant mortality for Aboriginal and non-Aboriginal infants. Deaths for infants born in Western Australia from 1980 to 1988 inclusive were ascertained from a total population data base. Infant mortality rates and rates by period and cause of death were calculated for both populations. Aboriginal infants had a mortality rate three times that for non-Aboriginal infants (23.6 cf. 7.9 per 1000 live births) and both populations showed a similar rate of decline in mortality over the study period. There were differences in the proportion of deaths occurring neonatally and postneonatally in the two populations. In terms of SIDS, 21% of the deaths in Aboriginal infants occurred neonatally compared with 7% for non-Aboriginal infants. The overall cause of infant death distribution differed significantly between the two populations (P < 0.001). During the study period, Aboriginal infants showed a significant increase in deaths due to SIDS and a significant decrease in those due to birth defects and low birthweight. These results suggest it would be useful to review the pathology and diagnosis of sudden unexplained death in infancy.

A case-control study of unexplained antepartum stillbirths.

OBJECTIVE: To ascertain factors that will identify women who are at increased risk of unexplained antepartum stillbirth. DESIGN: Matched case-control study. The cases and controls were initially analysed as a whole group and again after dichotomizing into those of low birthweight (< 2500 g) and those of normal birthweight (> or = 2500 g). SETTING: Western Australia 1980-1983. SUBJECTS: Unexplained antepartum stillbirths of > or = 1000 g birthweight (cases) and liveborn infants individually matched for year of birth, plurality, sex and birthweight of infant and race of mother (controls). RESULTS: The case pregnancies had more polyhydramnios (OR 10.83, 95% CI 2.41-48.69) and cord problems (OR 6.57 95% CI 1.36-31.75) than the controls but, paradoxically, other obstetric and medical complications were less common in the cases. The association with polyhydramnios persisted when the analysis was confined to those with low birthweight. With normal birthweight fetal distress was more frequent in the cases (OR 3.65 95% CI 1.36-9.80) but there were few other differences. CONCLUSIONS: The clinical and diagnostic systems currently in use are unable to identify many fetuses at risk of death. Decreases in the rate of unexplained antepartum stillbirths await the discovery of new preventable causes, or of innovations in clinical or laboratory aspects of obstetric care.

A case-control study of intrapartum stillbirths.

OBJECTIVE: To determine antenatal and intrapartum risk factors for intrapartum stillbirths in a total population. DESIGN: Matched case-control study. SETTING: Western Australia 1980-1983. SUBJECTS: Intrapartum stillbirths of > or = 1000 g birthweight (cases) and liveborn infants (controls) individually matched for year of birth, plurality, sex and birthweight of infant and race of mother. RESULTS: Intrapartum stillbirths were more likely than controls to have had placental abruption (OR = 9.55, CI = 2.09-43.69), fetal distress (OR = 4.64, CI = 1.92-11.19), cord prolapse (OR = 10.00, CI = 1.17-85.60) and unhealthy placentas (OR = 2.26, CI = 1.13-4.52), and more likely to have been born by vaginal breech manoeuvre (OR = 3.51, CI = 1.40-8.80) and emergency caesarean section (OR = 2.15, CI = 1.13-4.10); mothers of intrapartum stillbirths were less likely to have had no labour (OR = 0.14, CI = 0.04-0.55) and to have been delivered normally (OR = 0.20, CI = 0.10-0.40). Mothers of cases born by emergency caesarean section had longer labours than mothers of controls born by this method. All intrapartum stillbirths with breech presentation were born by vaginal breech manoeuvre compared with only 53% of the controls; the remainder of the controls were born by caesarean section. CONCLUSIONS: Results indicate that little could have been done early in pregnancy to prevent the intrapartum stillbirths as no antenatal risk factors predicted these deaths. Most of the risk factors identified related to labour and delivery problems. Considering cases born by emergency caesarean section, delivery of the mother earlier in labour may have prevented some of the deaths.

The epidemiological characteristics of unexplained antepartum stillbirths.

All antepartum stillbirths weighing 1000 g or more born in Western Australia from 1980 to 1983 were categorised as 'unexplained' or 'explained' based on information from Perinatal Death Certificates. Using data from hospital and doctors' antenatal records a number of variables in each stillbirth category were compared by unconditional logistic regression. Significant differences were observed between the two groups in medical disorders and abnormalities of pregnancy, thus confirming our classification system. Compared with mothers of 'explained' antepartum stillbirths, mothers of unexplained antepartum stillbirths tended to have younger ages at delivery and had associated lower parity, more antenatal visits to the medical practitioner, fewer hospital admissions, a greater chance of having received care by a general practitioner than by a specialist obstetrician and were of more advanced gestation at the time of diagnosis. The results of this study indicate that the epidemiological characteristics of pregnancies resulting in unexplained antepartum stillbirths differ from those resulting in explained antepartum stillbirths. This suggests that unexplained antepartum stillbirths are not merely the result of inadequate obstetrical management but consist of a series of fetal disease states which are not currently amenable to detection.

Stillbirths in Western Australia 1980-1983: influence of race, residence and place of birth.

All stillbirths in Western Australia from 1980-83 weighing 1,000 g and over were identified from perinatal death certificates, and their causes and demographic correlates described. The stillbirth rate was 4.91 per 1,000 total births; nearly 65% were antepartum, 25% intrapartum and in 10% the time of death was unknown. The cause of death of most stillbirths was unknown (52%) or associated with lethal congenital malformations (13%), antepartum haemorrhage (12%) or maternal hypertension (8%). Whilst Aboriginal women had much higher stillbirth rates (10.80) than non-Aboriginal women (4.57), their patterns of time and causes of death were similar. Both antepartum and intrapartum stillbirth rates were much higher at low birth-weights and low gestational ages in both racial groups. Women living in rural areas who delivered in the metropolitan area had much higher antepartum (11.02) and intrapartum (3.31) stillbirth rates than either rural women delivering in rural areas (1.89 and 1.34) or metropolitan women delivering in the metropolitan area (2.72, 0.98). This reflects the transfer of rural high risk pregnant women or those with fetal death in utero, for delivery in metropolitan specialist hospitals.

Assessment of precancerous lesions of the uterine cervix for evidence of human papillomavirus infection: a histological and immunohistochemical study.

Cervical biopsies obtained by colposcopic direction from 358 women were histologically examined for squamous dysplasia (cervical intra-epithelial neoplasia; CIN) and human papillomavirus (HPV) infection. Of the 358 biopsies, 136 were stained by an immunoperoxidase method using an antiserum against genus-specific (common) antigen of bovine papillomavirus. HPV antigens were detected in 40% of biopsies showing definite histological evidence of HPV effect, and in 7.9% and 2.6% of those with possible or no HPV effect, respectively. HPV effect was commonly seen in association with CIN. The frequency of histological evidence of HPV effect and positive immunoperoxidase staining decreased with increasing grades of CIN. HPV antigen was found in 57% of areas of HPV change with minor atypia, 34% of zones of CIN I and in only 8% of zones of CIN II. No antigenic staining or definite histological evidence of HPV effect was observed within areas of CIN III. Antigen was generally confined to the nuclei of superficial koilocytes, cells with lesser degrees of perinuclear clearing and parakeratotic cells. These results how a strong association between HPV infection and precancerous lesions of the uterine cervix and are consistent with the hypothesis that production of the HPV structural antigen requires a high degree of squamous cell maturation. The immunoperoxidase findings and the histopathological observations support the view that HPV change and dysplasia are part of a morphological continuum in which the cytopathic effect of HPV is expressed mainly in lower grades of dysplasia.

Comparison of peroxidase-antiperoxidase and avidin-biotin complex methods for the detection of papillomavirus in histological sections of the cervix uteri.

A study was undertaken to determine the relative sensitivities of the peroxidase-antiperoxidase (PAP) and avidin-biotin complex (ABC) methods for the detection of human papillomavirus (HPV) antigens in acetic acid-ethanol fixed paraffin-embedded cervical tissue. Tissue sections prepared from 14 women suspected to have HPV infections with either atypia or dysplasia were stained immunohistochemically using an antiserum against genus-specific (common) antigen of bovine papillomavirus. Detection of HPV antigen was approximately twice as frequent by the ABC method as by the PAP method. Of the 14 cases studied, 43% were found to be HPV positive by the PAP method whereas 79% were HPV positive by the ABC method. In addition, the number of cells found to be HPV positive by the ABC method was approximately double the number by the PAP method.