Incidence, risk factors, and temporal trends in severe postpartum hemorrhage.

OBJECTIVE: Because the diagnosis of postpartum hemorrhage (PPH) depends on the accoucheur's subjective estimate of blood loss and varies according to mode of delivery, we examined temporal trends in severe PPH, defined as PPH plus receipt of a blood transfusion, hysterectomy, and/or surgical repair of the uterus. STUDY DESIGN: We analyzed 8.5 million hospital deliveries in the US Nationwide Inpatient Sample from 1999 to 2008 for temporal trends in, and risk factors for, severe PPH, based on International Classification of Diseases, 9th revision, clinical modification diagnosis and procedure codes. Sequential logistic regression models that account for the stratified random sampling design were used to assess the extent to which changes in risk factors explain the trend in severe PPH. RESULTS: Of the total 8,571,209 deliveries, 25,906 (3.0 per 1000) were complicated by severe PPH. The rate rose from 1.9 to 4.2 per 1000 from 1999 to 2008 (P for yearly trend < .0001), with increases in severe atonic and nonatonic PPH, due especially to PPH with transfusion, but also PPH with hysterectomy. Significant risk factors included maternal age ≥35 years (adjusted odds ratio [aOR], 1.5; 95% confidence interval [CI], 1.5-1.6), multiple pregnancy (aOR, 2.8; 95% CI, 2.6-3.0), fibroids (aOR, 2.0; 95% CI, 1.8-2.2), preeclampsia (aOR, 3.1; 95% CI, 2.9-3.3), amnionitis (aOR, 2.9; 95% CI, 2.5-3.4), placenta previa or abruption (aOR, 7.0; 95% CI, 6.6-7.3), cervical laceration (aOR, 94.0; 95% CI, 87.3-101.2), uterine rupture (aOR, 11.6; 95% CI, 9.7-13.8), instrumental vaginal delivery (aOR, 1.5; 95% CI, 1.4-1.6), and cesarean delivery (aOR, 1.4; 95% CI, 1.3-1.5). Changes in risk factors, however, accounted for only 5.6% of the increase in severe PPH. CONCLUSION: A doubling in incidence of severe PPH over 10 years was not explained by contemporaneous changes in studied risk factors.

Anophthalmia and microphthalmia in the Alberta Congenital Anomalies Surveillance System.

BACKGROUND: A higher than expected rate of anophthalmia/microphthalmia (A/M) for 1999 was noted in both the Alberta Congenital Anomalies Surveillance System (ACASS) and the Canadian Congenital Anomalies Surveillance System (CCASS). Since this increase was at variance with the previous 19 years, we performed a review to determine whether the increase was true and, if so, the possible explanation. METHODS: We reviewed the records of the cases of A/M in the ACASS together with the accompanying attachments (e.g., consultant, autopsy and chromosome reports) for 1991-2001. In addition, we contacted all 91 registered ophthalmologists in Alberta. Letters were also written to the Edmonton and Calgary offices of the Canadian National Institute for the Blind (CNIB). RESULTS: Sixty cases of A/M were ascertained over the study period. Of the 88 active ophthalmologists in the province, 21 (24%) replied, but no new cases were ascertained from this source. No replies were received from the CNIB. We constructed five categories of clinical phenotypes for the 60 cases: 20 had a chromosomal etiology, 13 had a recognized syndrome or association, 16 had extraocular malformations, 5 had other eye anomalies, and 6 had A/M only. Pregnancy terminations were not included. The higher rate in 1999 was mainly due to cases with a chromosomal etiology or a recognized syndrome or association. There was no indication that a teratogen was causing a cluster of A/M cases, as our annual rates were comparable to those for other jurisdictions not only in Canada but also in other countries. INTERPRETATION: Our review confirmed that the rate of A/M in Alberta in 1999 was high but that the increase was mainly due to five cases of trisomy 13 together with one case associated with a syndrome (Meckel-Gruber). Our findings provide reassurance that there was no environmental cause of clustering of anophthalmia or microphthalmia. This review demonstrates the importance of ongoing population-based surveillance in providing baseline birth prevalence rates for evaluating trends and clusters.

Incidence of neural tube defects in Ontario, 1986-1999.

BACKGROUND: Prenatal screening and the promotion of folic acid intake could affect the incidence of neural tube defects (NTDs). We examined trends in the total NTD incidence, as detected in live births, stillbirths and therapeutic abortions, from 1986 to 1999 in Ontario. METHODS: To capture cases of NTDs we used data from the Canadian Congenital Anomalies Surveillance System and hospital data on therapeutic abortions. We calculated the total incidence of NTDs by combining the numbers of NTDs occurring in live births, stillbirths and therapeutic abortions. RESULTS: The total NTD incidence rate increased from 11.7 per 10,000 pregnancies in 1986 to 16.2 per 10,000 in 1995, and it subsequently decreased to 8.6 per 10,000 by 1999. The NTD birth rate (live births and stillbirths) decreased from 10.6 per 10,000 births in 1986 to 5.3 per 10,000 in 1999. The rate of therapeutic abortions with an NTD or hydrocephalus rose from 17.5 per 10,000 abortions in 1986 to 50.7 per 10,000 in 1995 and fell to 28.7 per 10,000 abortions in 1999. INTERPRETATION: The total NTD incidence rate increased from 1986 to 1995, probably because of increased prenatal screening and better detection of NTDs. The decline from 1995 to 1999 may have been due to increased folic acid intake among women at the time of conception.