Article

Prevention of cerebral palsy during labour: Role of foetal lactate

Department of Obstetrics & Gynaecology and Genetic Biology, University of Verona, Verona, Italy.
Archives of Gynecology and Obstetrics (Impact Factor: 1.28). 08/2008; 278(1):17-22. DOI: 10.1007/s00404-007-0531-1
Source: PubMed

ABSTRACT Intrapartum foetal monitoring goal is to prevent foetal asphyxia and its most severe consequence: cerebral palsy (CP). In this paper we describe the detection methods and the criteria needed to assess asphyxia during labour for preventing CP. Foetal cerebral damage assessment is considered from the medical-legal point of view. CP represents the most frequent pathology of childhood related to pregnancy and childbirth with an incidence of 0.2% in children born alive. It is clinically regarded as the result of a spectrum of diseases due to damage or to faded development of the nervous system which generally appears at the time of the first stage of intra-uterine growth or depends on problems arising at birth. The goal of our analysis is to recall the various moments in which this event can take place and, if possible, the moment and the degree of the event of asphyxia and its effect on foetal conditions, in order to control and treat it.
One hundred and eighty-eight fetuses were evaluated by means of Apgar score, intrapartum cardiotocography, observation of the presence of meconium stained amniotic fluid, and clinical features of distress at birth. Lactate concentrations were measured during labour and at delivery in blood samples obtained from the foetal presenting part (foetal scalp) and from the umbilical cord with the use of a rapid electrochemical technique.
Evidence of clinical foetal distress was not related to the severity of asphyxia. An increased lactate level was found in asphyctic infants and a clear correlation between lactic acidosis and foetal distress was documented. Low Apgar scores were observed in infants with moderate or severe asphyxia at delivery. Scalp lactate correlated significantly with umbilical artery lactate (P = 0.49, 0.01), but with neither Apgar score at 1 min (R = -0.21, ns) nor at 5 min (R = -0.11, ns). Lactate concentration was higher in case of instrumental delivery compared to spontaneous delivery (P = 0.0001). No perfect correlation was found between lactate level and neonatal outcome, but there were not a significant number of neonates with immediate complications. The rate of instrumental delivery in the distress group was significantly higher than in that of the healthy fetuses (P < 0.01), so spontaneous labour was less frequently associated with foetal distress than instrumental delivery (P < 0.01). In the distress group, severe variable decelerations were generally recorded in the second stage of labour. The incidence of neonatal Apgar score </=7 in neonates with abnormal baseline foetal heart rate (FHR) was higher than in those with severe variable decelerations, mild variable decelerations, and transient tachycardia (P < 0.05). The duration of the active second stage of labour correlated significantly with the presence of foetal lactate (P < 0.001) at the time of crowning of foetal head, and the presence of lactate in umbilical cord blood at delivery (P < 0.001). Expulsion time >/=45 min, compared with a shorter active second stage, and acidaemia at birth implied larger arterial-venous lactate differences (P < 0.001). The presence of foetal lactate at crowning was also significantly associated with the level of umbilical arterial-venous lactate difference (P = 0.03).
Analysis of the fetus should start with the assessment of lactates and acid-base balance. The method which revolutionized the techniques of foetal monitoring is undoubtedly represented by cardiotocography. However, likely most of neurological outcomes are not correlated with a perinatal event or with peripartum asphyxia. Approximately 10% of cases of CP would actually be due to perinatal asphyxia, and this percentage approaches approximately to 15% if we consider only newborns at term. This again confirms the weak association of a causal relationship between asphyxia and CP. In addition, available foetal suffering markers are vague and allow to identify only less than half of the effective cases of newborns which will develop CP.

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