BACKGROUND: In contrast to other high-resource countries, the United States has experienced increases in the rates of severe maternal morbidity. In addition, the United States has pronounced racial and ethnic disparities in severe maternal morbidity, especially for non-Hispanic Black people, who have twice the rate as non-Hispanic White people.OBJECTIVE: This study aimed to examine whether the racial and eth-nic disparities in severe maternal morbidity extended beyond the rates of these complications to include disparities in maternal costs and lengths of stay, which could indicate differences in the case severity.STUDY DESIGN: This study used California's linkage of birth certifi-cates to inpatient maternal and infant discharge data for 2009 to 2011. Of the 1.5 million linked records, 250,000 were excluded because of incomplete data, for a final sample of 1,262,862. Cost-to-charge ratios were used to estimate costs from charges (including readmissions) after adjusting for inflation to December 2017. Mean diagnosis-related group-specific reimbursement was used to estimate physician payments. We used the Centers for Disease Control and Pre-vention definition of severe maternal morbidity, including readmissions up to 42 days after delivery. Adjusted Poisson regression models esti-mated the differential risk of severe maternal morbidity for each racial or ethnic group, compared with the non-Hispanic White group. General-ized linear models estimated the associations of race and ethnicity with costs and length of stay.RESULTS: Asian or Pacific Islander, Non-Hispanic Black, Hispanic, and other race or ethnicity patients all had higher rates of severe maternal morbidity than non-Hispanic White patients. The largest disparity was between non-Hispanic White and non-Hispanic Black patients, with unad-justed overall rates of severe maternal morbidity of 1.34% and 2.62%, respectively (adjusted risk ratio, 1.61; P<.001). Among patients with severe maternal morbidity, the adjusted regression estimates showed that non-Hispanic Black patients had 23% (P<.001) higher costs (marginal effect of $5023) and 24% (P<.001) longer hospital stays (marginal effect of 1.4 days) than non-Hispanic White patients. These effects changed when cases, such as cases where a blood transfusion was the only indica-tion of severe maternal morbidity, were excluded, with 29% higher costs (P<.001) and 15% longer length of stay (P<.001). For other racial and ethnic groups, the increases in costs and length of stay were smaller than those observed for non-Hispanic Black patients, and many were not signif-icantly different from non-Hispanic White patients. Hispanic patients had higher rates of severe maternal morbidity than non-Hispanic White patients; however, Hispanic patients had significantly lower costs and length of stay than non-Hispanic White patients.CONCLUSION: There were racial and ethnic differences in the costs and length of stay among patients with severe maternal morbidity across the groupings that we examined. The differences were especially large for non-Hispanic Black patients compared with non-Hispanic White patients. Non-Hispanic Black patients experienced twice the rate of severe maternal morbidity; in addition, the higher relative costs and longer lengths of stay for non-Hispanic Black patients with severe maternal morbidity support greater case severity in that population. These findings suggest that efforts to address racial and ethnic inequities in maternal health need to consider differences in case severity in addition to the differences in the rates of severe maternal morbidity and that these differences in case severity merit additional investigation.
Over the last 15 years, the United States has experienced major increases in the rates of severe maternal morbidity (SMM) or maternal “near misses.” Initial estimates of the costs of SMM have used delivery hospitalization data, which exclude physician costs and hospital readmissions from the estimates. The objective of this study was to expand existing estimates of the costs of SMM to include readmissions and physician costs and to examine whether SMM had an effect on infant costs.Secondary data analysis. We used the CDC definition of SMM, including readmissions up to 42 days postpartum. GLM models with a gamma distribution and a log link were used to estimate the effect of SMM on costs, controlling for race/ethnicity, cesarean delivery, type of insurance, parity, maternal age and BMI, multiple births, and an obstetric severity index. The infant models also controlled for gestational age, infant gender, and serious congenital anomalies. Models were estimated with and without hospital fixed‐effects.California linked birth certificate‐patient discharge data for mothers and infants for 2009‐2011. About 200 000 were excluded for missing charge data (almost all insured by Kaiser Permanante). Cost‐to‐charge ratios were used to estimate costs from charges (including readmissions) and adjust for inflation to December 2017 dollars. Mean DRG‐specific reimbursement was used to estimate physician payments. The final sample was 1 262 862.A case of SMM increases delivery costs to a mean of about three times those of a normal, uncomplicated delivery, $7014 vs $20 756. The added costs were $10 396 for vaginal deliveries and $15 838 for c‐sections. Physician costs were over 20% of total SMM costs, $2290 (vaginal) and $3521 (cesarean), respectively. Including readmissions increased the SMM rate by 14.5%; these cases had a mean cost of $19 500, of which $4500 were MD costs. Mean infant costs were $23 318 with SMM and $6135 without, but this difference was much smaller for term deliveries ($5394 vs $2685). The risk‐adjusted estimate was that SMM increased maternal costs by 72% and 71% and infant costs by 27% and 32%, with and without hospital fixed‐effects, respectively.The per case maternal costs of SMM are triple those of a normal delivery. Further, readmissions and physician costs are important and previously unreported factors that add about $5000/case to the estimated maternal costs of SMM, increase the prevalence of SMM by 14.5%, and explain much of why our estimates are higher than previous reports ($6100‐8600). SMM is also associated with modest increases in infant costs. Projecting our costs to the entire United States results in $825 million in addition maternal costs; adjusting for California’s higher costs still results in over $500 m in additional costs due to SMM.The costs of SMM extend well beyond those of the added costs of the delivery hospitalization. Failure to account for SMM‐associated readmissions or physician costs result in a meaningful under‐estimate of the costs of SMM. The additional infant costs associated with SMM need further investigation.National Institutes of Health.
Optimizing our pediatric emergency care system requires all hospitals to stabilize and triage severely ill or injured children and then transport to an appropriate care location in a timely fashion. However, prior research found wide variation in the readiness of hospitals to care for children in the emergency department setting. The pediatric readiness of hospitals treating severely ill or injured children is unknown. Our objective was to determine the percentage of children with severe illness or injury who initially receive care at a low pediatric readiness hospital, and identify patient and hospital factors associated with receipt of care at such institutions.
Background Variation in readmission rates may assess the quality of a provider through the quality of inpatient care or transitions from inpatient to outpatient providers. The aim of this project was to validate readmission rates as a measure of NICU quality. Methods Using birth certificates linked to maternal and infant hospital discharge records, a cohort was constructed of 23–34 week gestation infants who survived to hospital discharge at a California hospital discharging over 50 such infants per year between 1995–2009 (N = 296,509 at 141 hospitals). Unadjusted variations in hospital readmission rates within 7, 14, 30, 90, and 365 days after discharge were compared to rates adjusted for hospital casemix, including patient gestational age, insurance status, race/ethnicity, and maternal education, and BPD, IVH, NEC, and ROP as measures of chronic health conditions. Results Unadjusted readmission rates varied significantly between hospitals and across geographic regions, ranging from 2.2–28.4% 7–14 days after discharge to 2.7–34.4% 365 days after discharge. Some of this variation was explained by hospital casemix. However, after risk adjustment, there remained a 7.9–11.5 fold difference in readmission rates between hospitals with the lowest and highest rates across the five time frames that did not change when complications of preterm birth were included in the risk-adjustment model. Conclusions There is substantial variation in readmission rates of premature infants that is only partially explained by gestational age and social factors. Readmission rates may provide a measure of the quality of NICU care and the integration of services within a geographic area.
OBJECTIVES We sought to determine the importance of socioeconomic factors, maternal comorbid conditions, antepartum and intrapartum complications of pregnancy, and fetal factors in mediating racial disparities in fetal deaths. METHODS. We undertook a mediation analysis on a retrospective cohort study of hospital-based deliveries with a gestational age between 23 and 44 weeks in California, Missouri, and Pennsylvania from 1993 to 2005 (n = 7,104,674). RESULTS Among non-Hispanic Black women and Hispanic women, the fetal death rate was higher than among non-Hispanic White women (5.9 and 3.6 per 1000 deliveries, respectively, vs 2.6 per 1000 deliveries; P < .01). For Black women, fetal factors mediated the largest percentage (49.6%; 95% confidence interval [CI] = 42.7, 54.7) of the disparity in fetal deaths, whereas antepartum and intrapartum factors mediated some of the difference in fetal deaths for both Black and Asian women. Among Hispanic women, socioeconomic factors mediated 35.8% of the disparity in fetal deaths (95% CI = 25.8%, 46.2%). CONCLUSIONS The factors that mediate racial/ethnic disparities in fetal death differ depending on the racial/ethnic group. Interventions targeting mediating factors specific to racial/ethnic groups, such as improved access to care, may help reduce US fetal death disparities.
Objective: Test the hypothesis that very low birth-weight (VLBW) infants fed every 2 h (q2) are able to reach full enteral feedings more quickly than infants fed every 3 h (q3). Study Design: We performed a retrospective cohort study comparing q2 infants ( n =103) with q3 infants ( n =251). The primary outcome was days from start of a feeding advance to full feedings (120 ml per kg per day). Multivariable regression models were used to control for maternal and perinatal factors that preceded the initiation of the feeding advance. Result: Infants fed q2 reached full feedings 2.7 days sooner than q3 infants (95% confidence interval (CI) 1.5, 3.9). After adjustment for confounders, q2 infants reached full feedings 3.7 (95% CI 1.6, 5.9) days more quickly. Infants fed q3 were more likely to receive >28 days of parenteral nutrition (odds ratio (OR) 4.7; 95% CI 1.5, 14.4), and were more likely to have feeds held for ⩾7 days (OR 4.7, 95% CI 1.9, 11.7). Conclusion: VLBW infants demonstrate improved feeding tolerance when fed more frequently.
OBJECTIVE: We have sought to utilize a large general practice database to track maternal exposure to infertility treatments or medications and childhood behavioral disorders. DESIGN: Retrospective Cohort Study. MATERIALS AND METHODS: A 10 percent sample of The Health Improvement Network (THIN), a general practice database from the United Kingdom was used for this study which would reflect approximately 1% of identifiable pregnancies as both mother and child had a probability of 0.1 of being in our dataset. A cohort of pregnant women and their offspring was isolated by identifying pregnancy delivery events. Maternal records were searched for exposure as defined by diagnostic codes for "In Vitro Fertilization" or "Infertility" as well as for prescriptions for infertility medications including clomid and injectable gonadotropins. Child records were identified by examining individuals with the same household code whose birthday corresponded to delivery. These records were searched for the outcome of a composite of childhood behavioral diagnoses including autism, attention deficit disorder, mental retardation and developmental delay. Statistical analysis was performed using Chi Squared tests of proportions. RESULTS: 5,169 mother-child pairs were identified. 93 of these children were identified as having a diagnosis of a childhood behavioral disorder. 495 children were born to women with an infertility diagnosis, treatment or medication code. The incidence of childhood behavioral diagnosis was 0.019 in offspring of women with no infertility diagnosis versus 0.008 in offspring of women with infertility. The relative risk of childhood behavioral diagnosis in offspring of women with infertility was 0.42 (0.16, 1.15), which was not significant (p=0.08).Table 1Childhood Behavioral Disorders in THINChildhood Behavioral Disorder Diagnosis(+)(-)TotalRiskRelative Risk(+) Infertility Diagnosis or Treatment44914950.008(-) Infertility Diagnosis or Treatment89458511890.0190.42Total5169(0.16, 1.15)p=0.08 Open table in a new tab p=0.08 CONCLUSIONS: Utilizing a large general practice database, we were able to identify a cohort of pregnant women and their offspring. Utilizing a small sample of this database, infertility diagnosis did not seem to be a risk factor for increased childhood behavioral disorders. This is a novel approach for evaluating maternal exposure to assisted reproduction technology and childhood outcomes. The findings will be replicated in the full cohort.
We have observed that oxidative phosphorylation (OXPHOS) by isolated mitochondria (MITO) increases at birth in liver and kidney (Ped. Res. 37,214), but not heart (this meeting), and that newborn hypoxia prevents increased OXPHOS. To determine whether initiation of MITO biogenesis is also regulated by oxygen availability pre-term rabbit pups (30-31 days gestation, term=32 days) delivered by C-section were either sacrificed at birth (time zero) or maintained under normoxic (21% O2, NOX) or hypoxic(10% O2, HYPOX) conditions for 4 hours at 35° C. MITO were isolated and in-vitro protein synthesis (PS) determined by measuring 35S methionine incorporation. PS was greater in heart MITO from NOX vs HYPOX or time zero pups (113 ± 18 vs 55.2 ± 20 or 60.0 ± 13 CPM/ mg Prot / 30 min respectively, n=6, p < 0.05) while PS rate was similar for liver (48 ± 13 vs 47 ± 10 or 51.3 ± 11) and kidney (44.1± 15 vs 37.5 ± 20 or 39.5 ± 13) MITO. Nucleotide regulation of PS in NOX and HYPOX pups was also evaluated. PS was reduced by 40-50% (p < 0.05) when isolated MITO from heart, liver and kidney were incubated with 5 mM ATP + 1 mM GTP. Inhibition was similar in MITO from NOX and HYPOX pups. In summary, MITO biogenesis at birth is modulated by nucleotides in all organs and oxygen availability in heart, but not liver or kidney. Taken together these data demonstrate that metabolic adaptation at birth involve increased MITO OXPHOS or biogenesis, changes which are modulated by oxygenation in an organ specific manner.