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  • Title: [Can subpartal fetal acidosis be avoided? Investigations on the complex causes of intrauterine asphyxia].
    Author: Roemer VM, Mähling B.
    Journal: Z Geburtshilfe Neonatol; 2002; 206(5):172-81. PubMed ID: 12395290.
    Abstract:
    OBJECTIVE: The extent to which faulty medical treatment and defective apparatus are concomitant causes for the development of subpartal acidosis was investigated in a retrospective study. At the same time, the incidence of acidosis in the Lippe-Detmold Hospital, Department of Gynaecology and Obstetrics, its morbidity and mortality were analysed. METHODS: Data from all case histories of neonates with acidosis (pH in the umbilical artery < 7.100) who were born between 1 st January 1992 and 31 st December 1998 at the Department of Gynecology and Obstetrics at the Lippe-Detmold Hospital were evaluated electronically. Analytical measurements of blood gases (pH, pCO 2 and pO 2 ) in umbilical artery and venous blood were available from all cases. The base excess was corrected by computations according to Siggaard-Andersen and R. Zander for the actual oxygen saturation. The delivery cardiotocograms (CTG) were appraised qualitatively. Equipment defects, mistakes on the part of doctors and/or midwives (including the head of the department) were recorded after critical analysis of each individual case and documented in accordance with a key. The neonatal data were taken from the files of the paediatric division of the hospital (head of the department Dr. K. Wesseler). RESULTS: In seven years under report, 9.876 babies were born, 156 (1.58 %) of whom showed a pH of less than 7.100 in the umbilical arterial blood. The mean actual pH value was 7.047 +/- 0.058, and the oxygen-corrected base excess was - 16.3 +/- 3.2 mmol/l. Correction of the base excess resulted in a numerical lowering by about 2.0 mmol/l. The rate of premature births was 17.4 %. One newborn baby died of hypoxic shock (0.67 %). 94 % of these neonates could be discharged in a healthy condition. 4.6 % still showed symptoms on discharge. Disorders of respiratory adaptation were the most prominent feature in morbidity from acidosis (about 18 %). Only two babies showed neonatal convulsions. Renal, cardiac and haemostaseological complications were rarely observed. Only 5 (3.9 %) of the 128 neonates with available recordings did not show any pathological changes in the CTG. 26.4 % of all acidoses had to be designated as "pure fate". In a further 35 % medical mistakes could not be discerned. Consequently, 61.4 % of the acidoses had to be designated as "unavoidable". In the remaining roughly 40 %, inadequate cardiotocographical knowledge, inattentiveness, defective equipment etc. clearly played a causal role. In the severe cases (pH in the umbilical artery < 7.000), medical mistakes were much more frequent (50 %). CONCLUSIONS: Three-fifths of all subpartal acidoses in this study have a fateful nature, i.e. they cannot be prevented even by optimal professional management in good time. About two-fifths are avoidable if appropriate equipment and trained staff are available around the clock. Use of cardiotocography alone enables the threat of asphyxia to be detected in 97 % of the cases. The short-term prognosis of subpartal acidosis is good provided very low pH values (< 6.900) can be avoided. In perinatological studies, the base excess value should be corrected by computation. "Quality control" worthy of the name should include critical single-case analysis at least in severe acidosis.
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