Abstract
Objectives
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.
Study design
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.
Results
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).
Conclusions
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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References
Aly H (2005) Mechanical ventilation and cerebral palsy. Pediatrics 115:1765–1767
Ancel PY, Livinec F, Larroque B, Marret S, Arnaud C, Pierrat V, Dehan M, N’Guyen S, Escande B, Burguet A, Thiriez G, Picaud JC, André M, Bréart G, Kaminski M, EPIPAGE Study Group (2006) Cerebral palsy among very preterm children in relation to gestational age and neonatal ultrasound abnormalities: the EPIPAGE cohort study. Pediatrics 117:828–835
Arpino C, D’Argenzio L, Ticconi C, Di Paolo A, Stellin V, Lopez L, Curatolo P (2005) Brain damage in preterm infants: etiological pathways. Ann Ist Sup Sanita 41:229–237
Bashiri A, Burstein E, Mazor M (2006) Cerebral palsy and fetal inflammatory response syndrome: a review. J Perinat Med 34:5–12
Blair E, Stanley F (2001) Obstetrical responsability for abnormal fetal outcome. In: Chamberlain G, Steer P (eds) Turnbull’s obstetrics. Churchill Livingstone, London
Bonellie SR, Currie D, Chalmers J (2005) Comparison of risk factors for cerebral palsy in twins and singletons. Dev Med Child Neurol 47:587–591
Borruto F, Comparetto C, Wegher E, Treisser A (2005) Un nuovo metodo di screening della sofferenza fetale in sala parto: il lattato. Atti 81° Congresso Nazionale SIGO, Bologna, Settembre 20–24
Borruto F, Zacutti A (1989) Nuevos parametros en cinetica fetal. Progr Diag Prenat 1:90–92
Damman O (2004) Perinatal lung/brain damage and long term outcome in preterm newborns. In: Proceedings of the pediatrics and obstetrics Hannover medicine school, Germany
Fanaroff JM, Wilson-Costello DE, Newman NS, Montpetite MM, Fanaroff AA (2006) Treated hypotension is associated with neonatal morbidity and hearing loss in extremely low birth weight infants. Pediatrics 117:1131–1135
Folkerth RD (2005) Neuropathologic substrate of cerebral palsy. J Child Neurol 20:940–949
Gibson CS, MacLennan AH, Goldwater PN, Haan EA, Priest K, Dekker GA, South Australian Cerebral Palsy Research Group (2006) Neurotropic viruses and cerebral palsy: population based case-control study. BMJ 332:76–80
Gibson CS, MacLennan AH, Goldwater PN, Haan EA, Priest K, Dekker GA, South Australian Cerebral Palsy Research Group (2006) The association between inherited cytokine polymorphisms and cerebral palsy. Am J Obstet Gynecol 194:1–11
Gluckman PD, Gunn AJ, Wyatt JS (2006) Hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med 354:1643–1645
Goffinet F (2003) Anoxie per-partum et handicaps de l’enfant: aspects epidemiologiques. J Gynécol Obstét 32:1s111–1s113
Golomb MR, Garg BP, Williams LS (2006) Outcomes of children with infantile spasms after perinatal stroke. Pediatr Neurol 34:291–295
Hoon AH Jr (2005) Neuroimaging in cerebral palsy: patterns of brain dysgenesis and injury. J Child Neurol 20:936–939
Hutton JL, Pharoah PO (2006) Life expectancy in severe cerebral palsy. Arch Dis Child 91:254–258
Inder T, Neil J, Yoder B, Rees S (2005) Patterns of cerebral injury in a primate model of preterm birth and neonatal intensive care. J Child Neurol 20:965–967
Jacobson B (2004) Antenatal risk factors for cerebral palsy. Best Pract Res Clin Obstet Gynaecol 18:425–436
Johnston MV, Ferriero DM, Vannucci SJ, Hagberg H (2005) Models of cerebral palsy: which ones are best? J Child Neurol 20:984–987
Keinan D, Smith P, Zilberman U (2006) Microstructure and chemical composition of primary teeth in children with Down syndrome and cerebral palsy. Arch Oral Biol 51:836–843
Kirton A, Deveber G (2006) Cerebral palsy secondary to perinatal ischemic stroke. Clin Perinatol 33:367–386
Morgan MA, Hankins GD, Zinberg S, Schulkin J (2005) Neonatal encephalopathy and cerebral palsy revisited: the current state of knowledge and the impact of American college of obstetricians and gynecologists task force report. J Perinatol 25:519–525
Nordstrom L (2004) Fetal scalp and cord blood lactate. Best Pract Res Clin Obstet Gynaecol 18:467–476
Odding E, Roebroeck ME, Stam HJ (2006) The epidemiology of cerebral palsy: incidence, impairments and risk factors. Disabil Rehabil 28:183–191
Perlman JM (2006a) Hyperthermia in the delivery: potential impact on neonatal mortality and morbidity. Clin Perinatol 33:55–63
Perlman JM (2006b) Intrapartum asphyxia and cerebral palsy: is there a link? Clin Perinatol 33:335–353
Perlman JM (2006c) Summary proceedings from the neurology group on hypoxic-ischemic encephalopathy. Pediatrics 117:S28–S33
Pierre F (2003) Aspect médico-légaux: l’obstétricien en accusation et en expert. J Gynécol Obstét 32:1s114–1s118
Rosenbaum P (2006) Classification of abnormal neurological outcome. Early Hum Dev 82:167–171
Sankar C, Mundkur N (2005) Cerebral palsy—definition, classification, etiology, and early diagnosis. Indian J Pediatr 72:865–868
Strijbis EM, Oudman I, van Essen P, MacLennan AH (2006) Cerebral palsy and the application of the international criteria for acute intrapartum hypoxia. Obstet Gynecol 107:1357–1365
van der Heide JC, Fock JM, Otten B, Stremmelaar E, Hadders-Algra M (2005) Kinematic characteristics of postural control during reaching in preterm children with cerebral palsy. Pediatr Res 58:586–593
William B (2004) Cardiotocography and medico-legal issues. Best Pract Res Clin Obstet Gynaecol 18:457–466
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Borruto, F., Comparetto, C. & Treisser, A. Prevention of cerebral palsy during labour: role of foetal lactate. Arch Gynecol Obstet 278, 17–22 (2008). https://doi.org/10.1007/s00404-007-0531-1
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DOI: https://doi.org/10.1007/s00404-007-0531-1