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ORIGINAL RESEARCH |
From the Yale University School of Medicine, Department of Obstetrics and Gynecology, New Haven, Connecticut; and Unversity of British Columbia, Department of Pediatrics, B.C. Children’s Hospital, Vancouver, British Columbia, Canada.
Address reprint requests to: Keith P. Williams, Yale University School of Medicine, Department of Obstetrics and Gynecology, 333 Cedar Street, PO Box 208063, New Haven, CT 06520-8063; E-mail: keith.williams{at}yale.edu.
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ABSTRACT |
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7.1). METHODS: We reviewed the maternal and neonatal charts of 238 patients at a gestational age of 32 weeks or more with cord gases done at delivery and an umbilical artery pH of 7.1 or less. All infants transferred to the neonatal intensive care unit were studied, and those with neonatal seizures secondary to hypoxic ischemic encephalopathy were identified. We used the perinatal outcome of early neonatal seizures secondary to hypoxic ischemic encephalopathy to divide the patients into two groups. The relationship between the umbilical artery parameters of pH, base deficit, partial oxygen pressure (pO2), partial carbon dioxide pressure (pCO2), and the neonatal outcome of seizures were determined with Student t tests and multiple logistic regression analysis.
RESULTS: Umbilical artery base deficit, pO2, and pCO2 were significantly elevated in newborns who had seizures, whereas cord pH was decreased. Using multiple regression analysis the variable neonatal seizure was predicted only by low umbilical artery pH. A pH of less than 7 was more sensitive (73.8%) than a base excess of -16 (52.5%) in predicting the development of neonatal seizures.
CONCLUSION: Our data suggest that severe fetal acidemia identified by a pH less than 7.0 was the most important umbilical blood gas variable for predicting early onset of neonatal seizures.
Various clinical and blood gas variables have been used to predict the development of poor neonatal outcome as defined by hypoxic ischemic encephalopathy.1–4 Previous studies used pH less than 7 as indicative of severe metabolic acidosis, with a 30% sensitivity to predict a poor outcome.5,6 Low et al7 found that the metabolic acidotic component of the umbilical artery gas parameter as defined by a base deficit over -16 is a more effective factor to predict the development of hypoxic ischemic encephalopathy than purely respiratory acidemia.
Various scoring systems used to define hypoxic ischemic encephalopathy in neonates include factors such as hypertonia, depression, coma, and depressed respiration.1,8 The most clearly defined factor in hypoxic ischemic encephalopathy is the development of seizures that place the infant in a category of moderate to severe hypoxic ischemic encephalopathy.1,2 Other umbilical artery blood gas parameters, including partial oxygen pressure (pO2), partial carbon dioxide pressure (pCO2), and oxygen saturation have been used in previous studies but not as frequently to aid in the prediction of neonatal morbidity. We correlated the association of umbilical artery blood gas variables collected at birth with early-onset neonatal seizures related to hypoxic ischemic encephalopathy.
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METHODS |
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Data are presented as mean ± standard deviation for continuous variables. Statistical analysis was done with Student t tests to detect significant differences between the seizure group and the nonseizure group. After testing for skewness of the data with the Kolmogorov-Smirnov test we then utilized a multiple logistic regression technique that included only the umbilical artery blood gas parameters that were found on univariate analysis to be significantly associated with the development of seizures. A P value less than .05 was considered statistically significant. Sensitivity, specificity, and positive and negative likelihood ratios were then developed with the umbilical artery blood gas predictors of pH, base deficit, and pCO2 on the primary outcome of neonatal seizures. Likelihood ratios were used because they are less affected by the prevalence of the condition.9
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RESULTS |
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. Infants with seizures showed significantly reduced umbilical artery pH, decreased base deficit, elevated pO2, and elevated pCO2. The oxygen saturation was not significantly different between the two groups. Because pO2, pCO2, pH, and base deficit were significantly associated with seizures in the univariate analysis, multiple logistic regression models were used to analyze independent contributions of these specific blood gas variables with seizures. Variables were entered into the model by forward stepwise selection. Using this multiple regression technique, the outcome of neonatal seizure was predicted only by low umbilical artery pH (odds ratio 5.73; 95% confidence interval 2.43, 9.54; P < 001). Before this, cord pH and cord base excess were correlated (correlation coefficient .727), and a multiple logistic regression model was constructed to predict seizures without pH in the model. The base deficit did not significantly predict seizures (odds ratio 1; 95% confidence interval 0.98, 1; P < 055).
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). The variables of pO2 and pCO2 were not helpful in predicting the development of seizures.
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DISCUSSION |
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Low et al7 identified the duration of acidemia with the accumulation of fixed acids, as reflected by cord base deficit, as a better predictor than pH of acidemic asphyxial insult at birth. However, other studies of asphyxial complications at birth have established a pH of less than 7.0 as being most predictive of the development of neonatal complications.5,10 Although the statistically significant pH cutoff for seizures with hypoxic ischemic encephalopathy has been determined to be 7.0, Goldaber et al5 determined that only 67% of newborns with unexplained seizures had an umbilical pH of 7.00 or less, and they defined a sensitivity and specificity of pH less than 7.00 and mixed acidemia were 88% and 41%, respectively, to predict the development of seizures. We utilized a pH cutoff of 7.1 because that was the highest pH at which a neonatal seizure secondary to hypoxic ischemic encephalopathy occurred. We found that 12.5% of seizures occurred with a pH between 7.0 and 7.05 and a further 12.5% of seizures occurred with a pH between 7.05 and 7.1.
Low et al7 reviewed the role of type of acidosis to determine the incidence of newborn complications and defined metabolic acidosis as a base deficit of more than -16 and respiratory acidosis as pCO2 over 75 mm Hg but without an umbilical artery base deficit of -16 or less. They suggested that base deficit was a more appropriate mechanism to assess the risk of newborn complications. Moderate or severe intrapartum complications occurred with base deficit of -12 to -16 mmol/L in 10% of cases, whereas complications occurred in 40% of neonates with umbilical artery base deficit greater than -16 mmol/L at birth. They determined that metabolic acidosis base deficit greater than -16 had an incidence of complications of 78% compared with 23% in infants with respiratory acidosis. Our study used neonatal seizures within the first 24 or 48 hours of birth in neonates with hypoxic ischemic encephalopathy as the primary outcome because it is a neonatal outcome that most reports agree places the neonate in a moderate or severe hypoxic ischemic encephalopathy category and might be the neonatal outcome that best prognosticates the future well-being of the infant.11–14
Few studies have addressed other umbilical artery components, ie, pO2, pCO2, and oxygen saturation, as significant predictors of neonatal morbidity. Andres et al15 attempted to correlate various blood gas variables, including pH of less than 7.0, with neonatal outcome. They found that pH less than 7.0 was the most significant variable for predicting morbidity. The only shortcoming of their study was that it had only two infants with seizures, so their ability to use those data to predict this outcome was limited. Our study had 40 infants with seizures. Sehdev et al16 also looked at predictive models for neonatal morbidity using pH and base deficit but did not include other factors, such as pO2, pCO2, and oxygen saturation in their model. Socol et al17 showed that lower umbilical pH and higher base deficit correlated with neonates who had a complicated newborn course. Multiple logistic regression analysis in that study determined that both umbilical artery pH and base deficit were independently related to a complicated newborn course.
We found that pH was a more sensitive indicator of newborn seizures than base deficit. Previous reports, however, indicated that the base deficit, because it reflects a buildup of fixed acids, is more reflective of the development of newborn encephalopathy. Our study differs in that we assessed infants with a pH of 7.1 or less, whereas most studies used a pH of less than 7.18–21 In addition, our study attempted to predict seizures only and not newborn encephalopathy. With a sensitivity of 73% and a positive predictive value of 40%, it is obvious that factors other than pH, which were not assessed in our study, are important in predicting neonatal seizures. A continued search for other factors that could be identified at birth, including nucleated red blood cells,22 could aid in the determination of fetuses at highest risk of seizures and subsequent poor neurologic outcome.
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Footnotes |
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Received February 6, 2002. Received in revised form April 2, 2002. Accepted April 18, 2002.
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REFERENCES |
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2. Low JA, Galbraith RS, Muir DW, Killen HL, Pater EA, Karchmar EJ. Motor and cognitive deficits after intrapartum fetal asphyxia in the mature infant. Am J Obstet Gynecol 1988;158:356–61.[Medline]
3. Low JA, Galbraith RS, Muir DW, Killen HL, Pater EA, Karchmar EJ. Mortality and morbidity after intrapartum asphyxia in the preterm fetus. Obstet Gynecol 1992;80: 57–61.
4. Pelowski A, Finer NN. Birth asphyxia in the term infant. In: Sinclair J, Lucey J, eds. Effective care of the newborn infant. Oxford: Oxford University Press, 1992:263–6.
5. Goldaber KG, Gilstrap LG, Leveno KJ, Dax JS, McIntire DD. Pathologic fetal acidemia. Obstet Gynecol 1991;78: 1103–7.
6. American College of Obstetricians and Gynecologists. Operative vaginal delivery. Technical bulletin no. 152. Washington, DC: American College of Obstetricians and Gynecologists, 1991.
7. Low JA, Lindsay BG, Derrick EJ. Threshold of metabolic acidosis associated with newborn complications. Am J Obstet Gynecol 1997;177:1391–4.[Medline]
8. Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. Arch Neurol 1976;33:696–705.[Abstract]
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16. Sehdev HM, Stamilio DM, Macones GA, Graham E, Morgan MA. Predictive factors for neonatal morbidity in neonates with an umbilical arterial cord pH less than 7.00. Am J Obstet Gynecol 1997;177:1030–4.[Medline]
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18. Van Den Berg PP, Nelen WLDM, Jongsma HW, Nijland R, Kolee LAA, Nijhuis HW, et al. Neonatal complications in newborns with an umbilical artery pH ht7.00. Am J Obstet Gynecol 1996;175:1152–7.[Medline]
19. Goodwin TM, Belai I, Hernandez P, Durand M, Paul RH. Asphyxial complications in the term newborn with severe umbilical acidemia. Am J Obstet Gynecol 1992;162: 1506–12.
20. Thorp JA, Sampson JE, Parisi VM, Creasy RK. Routine umbilical cord blood gas determinations. Am J Obstet Gynecol 1989;161:600–5.
21. Winkler CL, Hauth JC, Tucker JM, Owen J, Brumfield CG. Neonatal complications at term as related to the degree of umbilical artery acidemia. Am J Obstet Gynecol 1991;164:637–41.[Medline]
22. Korst L, Phelan JP, Ahn MO. Nucleated red blood cells: An update on the marker for fetal asphyxia? Am J Obstet Gynecol 1996:175;843.[Medline]
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