Patterns of first‐year survival among infants with selected congenital anomalies in Texas, 1995–1997

Nembhard, Wendy N.; Waller, D. Kim; Sever, Lowell E.; Canfield, Mark A.

doi:10.1002/tera.1073

Cited by 90 publications

(113 citation statements)

References 23 publications

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“…This effect of multiple congenital anomalies on survival has been described in other population-based studies of birth defects. 2,8,15,16 Racial/ethnic disparities in survival were found in the present study, as reported by others. After multivariable adjustment, NH blacks with functional single ventricle had a 41% greater risk of death compared with NH whites.…”

Section: Fixler Et Al Five-year Mortality Of Functional Single Ventriclesupporting

confidence: 90%

“…Nevertheless, patients with hypoplastic left heart syndrome (HLHS) and single ventricle did not show evidence for improvement in outcome. In 2001, Nembhard et al 8 reported first-year survival among infants with congenital anomalies in Texas born between 1995 and 1997. This population-based registry study showed that 1-year survival was lower for HLHS (20.9%) than for all other birth defects studied except anencephaly.…”

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confidence: 99%

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Mortality in First 5 Years in Infants With Functional Single Ventricle Born in Texas, 1996 to 2003

et al. 2010

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Section: Fixler Et Al Five-year Mortality Of Functional Single Ventriclesupporting

confidence: 90%

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confidence: 99%

Mortality in First 5 Years in Infants With Functional Single Ventricle Born in Texas, 1996 to 2003

et al. 2010

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“…This is due primarily to congenital heart disease, which affects half of all children with DS (Halliday et al 1995;Morris et al 1999;Nembhard et al 2001;Frid et al 2004). Despite advances in neonatal care, DS survival is only 90-95% at 1 year and between 85 and 90% at 10 years (Leonard et al 2000;Forrester and Merz 2002;Glasson et al 2002;Bell et al 2003;Frid et al 2004;Marino et al 2004).…”

Section: Own Syndrome (Ds) Is Caused By Trisomy 21 Andmentioning

confidence: 99%

Perinatal Loss of Ts65Dn Down Syndrome Mice

et al. 2006

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Ts65Dn mice inherit a marker chromosome, T(17 16 )65Dn, producing segmental trisomy for orthologs of about half of the genes on human chromosome 21. These mice display a number of phenotypes that are directly comparable to those in humans with trisomy 21 and are the most widely used animal model of Down syndrome (DS). However, the husbandry of Ts65Dn mice is complicated. Males are sterile, and only 20-40% of the offspring of Ts65Dn mothers are trisomic at weaning. The lower-than-expected frequency of trisomic offspring has been attributed to losses at meiosis, during gestation and at postnatal stages, but no systematic studies support any of these suppositions. We show that the T( 17 16 )65Dn marker chromosome is inherited at expected frequency and is fully compatible with development to midgestation. Disproportional loss of trisomic offspring occurs in late gestation and continues through birth to weaning. Different maternal H2 haplotypes are significantly associated with the frequency of trisomy at weaning in patterns different from those reported previously. The proportion of trisomic mice per litter decreases with age of the Ts65Dn mother. These results provide the first statistical and numerical evidence supporting the prenatal and perinatal pattern of loss in the Ts65Dn mouse model of DS.

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“…Patients with trisomy 18 have prenatal-onset severe growth retardation, characteristic craniofacial features, various visceral and skeletal malformations, and significant psychomotor mental retardation [Carey, 2001]. Several populationbased studies showed a remarkably reduced lifespan, with survival rates at age 1 year from 0 to 10% and with median survival time from 3 to 14.5 days [Carter et al, 1985;Young et al, 1986;Goldstein and Nielsen, 1988;Root and Carey, 1994;Embleton et al, 1996;Naguib et al, 1999;Nembhard et al, 2001;Brewer et al, 2002;Rasmussen et al, 2003]. The major causes of death were reported to be apnea and withdrawal of treatment [Embleton et al, 1996], and the presence of a congenital heart defect did not seem be associated with early death [Embleton et al, 1996;Rasmussen et al, 2003].…”

Section: Introductionmentioning

confidence: 99%

Neonatal management of trisomy 18: Clinical details of 24 patients receiving intensive treatment

Kosho

Nakamura

Kawame

et al. 2006

American J of Med Genetics Pt A

175

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Management of neonates with trisomy 18 is controversial, supposedly due to the prognosis and the lack of precise clinical information concerning efficacy of treatment. To delineate the natural history of trisomy 18 managed under intensive treatment, we reviewed detailed clinical data of 24 patients with full trisomy 18 admitted to the neonatal intensive care unit of Nagano Children's Hospital, providing intensive treatment to those with trisomy 18, from 1994 to 2003. Cesarean, resuscitation by intubation, and surgical operations were performed on 16 (67%), 15 (63%), and 10 (42%) of the patients, respectively. Mechanical ventilation was required by 21 (88%), and 6 (29%) of them were extubated. Survival rate at age 1 week, 1 month, and 1 year was 88%, 83%, and 25%, respectively. Median survival time was 152.5 days. Respiration was not stabilized in two patients with left diaphragmatic eventration and hypoplasia accompanied by lung hypoplasia, even with maximal ventilation. The common underlying factors associated with death were congenital heart defects and heart failure (96%), followed by pulmonary hypertension (78%). The common final modes of death were sudden cardiac or cardiopulmonary arrest (26%) and possible progressive pulmonary hypertension-related events (26%). These data of improved survival, through neonatal intensive treatment, are helpful for clinicians to offer the best information on treatment options to families of patients with trisomy 18. ß 2006 Wiley-Liss, Inc.

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Patterns of first‐year survival among infants with selected congenital anomalies in Texas, 1995–1997

Abstract: Overall, first-year survival for infants with congenital anomalies was high. Additional population-based studies are needed to quantify improvements in first-year survival.

Cited by 90 publications

References 23 publications

Mortality in First 5 Years in Infants With Functional Single Ventricle Born in Texas, 1996 to 2003

Mortality in First 5 Years in Infants With Functional Single Ventricle Born in Texas, 1996 to 2003

Perinatal Loss of Ts65Dn Down Syndrome Mice

Neonatal management of trisomy 18: Clinical details of 24 patients receiving intensive treatment

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