Relationship of Isolated Single Umbilical Artery to Fetal Growth, Aneuploidy, and Perinatal Mortality

2014 ◽  
Vol 69 (4) ◽  
pp. 193-195
Author(s):  
B.J. Voskamp ◽  
H. Fleurke-Rozema ◽  
K. Oude-Rengerink ◽  
R.J.M. Snijders ◽  
C.M. Bilardo ◽  
...  
Keyword(s):  
Perinatal Mortality ◽  
Fetal Growth ◽  
Umbilical Artery ◽  
Single Umbilical Artery ◽  
Relationship Of

Relationship of isolated single umbilical artery to fetal growth, aneuploidy and perinatal mortality: systematic review and meta-analysis

2013 ◽  
Vol 42 (6) ◽  
pp. 622-628 ◽  
Author(s):  
B. J. Voskamp ◽  
H. Fleurke-Rozema ◽  
K. Oude-Rengerink ◽  
R. J. M. Snijders ◽  
C. M. Bilardo ◽  
...  
Keyword(s):  
Systematic Review ◽  
Perinatal Mortality ◽  
Fetal Growth ◽  
Umbilical Artery ◽  
Meta Analysis ◽  
Single Umbilical Artery ◽  
Relationship Of

Explanation of Perinatal Mortality Rate in Collaborative Study

PEDIATRICS ◽  
1973 ◽  
Vol 52 (6) ◽  
pp. 891-891
Author(s):  
Arnold S. Goldstein ◽  
Henry H. Mangurten
Keyword(s):  
Mortality Rate ◽  
Perinatal Mortality ◽  
Umbilical Artery ◽  
Collaborative Study ◽  
The United States ◽  
Mortality Rates ◽  
Single Umbilical Artery ◽  
Neonatal Deaths ◽  
General Mortality ◽  
Future Management

The article by Froehlich and Fujikura1 on the prognosis of single umbilical artery is a much needed and highly informative addition to the literature. It presents a great deal of information and some important implications as to future management. We question the mortality rates quoted. They are given as percentages, and include stillbirths and neonatal deaths, i.e., perinatal mortality. The figure given as the general mortality rate is 3.8% or 38 per 1,000 births. Previous figures cited for perinatal mortality in the United States have varied from approximately 19 per 1,000 to approximately 26 per 1,000.2-4 We wonder how the figure of 38 per 1,000 was determined.

Is single umbilical artery an independent risk factor for perinatal mortality?

2009 ◽  
Vol 283 (2) ◽  
pp. 191-194 ◽  
Author(s):  
Shimon Burshtein ◽  
Amalia Levy ◽  
Gershon Holcberg ◽  
Alexander Zlotnik ◽  
Eyal Sheiner
Keyword(s):  
Risk Factor ◽  
Perinatal Mortality ◽  
Independent Risk Factor ◽  
Umbilical Artery ◽  
Single Umbilical Artery

Fetal Growth Assessment and Neonatal Birth Weight in Fetuses With an Isolated Single Umbilical Artery

2005 ◽  
Vol 105 (5, Part 1) ◽  
pp. 1093-1097 ◽  
Author(s):  
Mladen Predanic ◽  
Sriram C. Perni ◽  
Alexander Friedman ◽  
Frank A. Chervenak ◽  
Stephen T. Chasen
Keyword(s):  
Birth Weight ◽  
Fetal Growth ◽  
Umbilical Artery ◽  
Single Umbilical Artery ◽  
Neonatal Birth Weight ◽  
Growth Assessment

Single umbilical artery ligation-induced fetal growth retardation: effect on postnatal adaptation

1992 ◽  
Vol 263 (3) ◽  
pp. E575-E583 ◽  
Author(s):  
K. Oyama ◽  
J. Padbury ◽  
B. Chappell ◽  
A. Martinez ◽  
H. Stein ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Umbilical Artery ◽  
Physiological Stress ◽  
Fetal Growth Retardation ◽  
Signal Transduction System ◽  
Single Umbilical Artery ◽  
Artery Ligation ◽  
Beta Adrenergic

To assess whether prolonged intrauterine stress and resultant fetal growth retardation result in depletion of adrenal catecholamines and alter the adrenergic signal transduction system, we studied newborn sheep after single umbilical artery ligation (SUAL)-induced growth retardation. The animals were delivered at term, and postnatal cardiovascular, pulmonary, endocrine, and metabolic responses were measured. We also evaluated the status of myocardial and pulmonary beta-adrenergic receptor number and function. SUAL caused significant growth retardation but relative preservation of brain and adrenal gland weight and adrenal catecholamine content. Blood pressure, plasma free fatty acid, and glucose responses at birth were blunted in SUAL animals. The plasma epinephrine (Epi) and norepinephrine levels were comparable in both groups for the first 2 h of age. By 4 h, both plasma concentration and plasma appearance rate of Epi were reduced to 40% of control in SUAL animals (P less than 0.05). Neither beta-receptor density, affinity, nor adenylate cyclase activity were altered by SUAL in either cardiac or pulmonary membranes. These results suggest that, rather than overt depletion, there is relative sparing of initial adrenal medullary function that later waned. This response and preservation of the beta-adrenergic signal transduction system may represent partial compensation for the physiological stress induced by SUAL.

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