D'Aloja et al. [Citation1] address a medico-legal approach to a hypoxic-ischaemic event in the perinatal period, offering a brief and highly selective survey of the literature. They then state that ‘a severe metabolic acidosis at the time of birth or shortly after it, in the absence of other demonstrable cause of brain lesion, is going to be accepted as the reliable proof of a foetal distress during the labour or the first few hours supporting the hypothesis of a medical malpractice.’ The authors indicate that in these circumstances there may well be a judgment for the plaintiff.
We write to stress that it is neither legitimate to conclude on the basis of severe acidosis that there has been medical mismanagement, nor even that acute intrapartum hypoxic events have occurred. Locatelli et al. [Citation2] reported that in term singletons with low Apgar scores and pH <7, chronic placental vascular pathology was much more common than in infants with low Apgar scores but no severe acidosis. These investigators stressed that ‘detection of acidemia at delivery in a neonate with low Apgar score should not be simplistically attributed to clinical mismanagement of labour; rather it should suggest the possibility of an intrauterine vascular disease (a chronic process antedating labour) as the underlying causative mechanism.’
At Children's National Medical Center, we too have recently observed that chronic placental pathology is common in placentas of severely acidotic term and late preterm infants with neonatal encephalopathy referred for therapeutic hypothermia. According to a distinguished expert in placental pathology, ‘In-labour catastrophes are rare, and when present are rarely either diagnosable or intervenable. Most cases of unexpected bad outcomes have chronic insults in the placenta’ [Citation3]. Obstetric and neonatal caregivers may find that examination of the placentas of severely depressed infants can give information valuable to the understanding of what went wrong when an infant is born depressed and acidotic.
References
- d'Aloja E, Muller M, Paribello F, Demontis R, Faa A. Neonatal asphyxia and forensic medicine. J Matern Fetal Neonatal Med 2009;22(Suppl 3):54–56.
- Locatelli A, Incerti M, Ghidini A, Greco M, Villa E, Paterlini G. Factors associated with umbilical artery academia in term infants with low Apgar scores at 5 minutes. Eur J Obstet Gynecol Reprod Biol 2008;139:146–150.
- Roberts DJ. Placental pathology, a survival guide. Arch Pathol Lab Med 2008;132:641–651.
Author's reply
Ernesto d'Aloja, Mima Müller, Francesco Paribello, Roberto Demontis & Armando Faa
Forensic Science Department, Cagliari University,Monserrato, CA, USA
Correspondence: Ernesto d'Aloja, Forensic Science Department, Cagliari University, SS 554 bivio Sestu, 09142, Monserrato, CA, USA. Tel:+1-39-070-6754731. E-mail: [email protected]
Dear Sir
Nelson et al. [Citation1] in their letter criticise our conclusions, assuming that ‘it is neither legitimate to conclude on the basis of severe acidosis that there has been medical mismanagement, nor even that acute intrapartum hypoxic events have occurred’.
We may partially agree to their point, even if our attempt was to consider the cerebral palsy issue from a juridical point of view.
As reported in the article, we are fully conscious that several papers (see for all Graham et al. [Citation2]) dealing with the predictive value of a pH<7 concluded that only a minor percentage of infants with an acid pH at birth will develop a cerebral palsy.
But our point was different. We tried to stress the importance for gynaecologists and paediatricians to fully investigate in each case of neonatal hypoxic events the ‘biological’ causes of it. Considering these catastrophic events ‘avoidable’ – even if in the forementioned minority of cases – physicians may have all the tools to demonstrate that the damage is not to be considered as the result of a ‘medical mismanagement’.
On the basis of our daily experience in the Italian Courts of Justice, we are well aware that in most cases of cerebral palsy litigation, the fundamental clinical and pathological data (such as umbilical pH values or an in-depth placental examination) may miss. If so, it's a very hard task for the obstetric and neonatal caregivers to confute the plaintiff assumption of a negligent behaviour as the causative episode responsible of the dreadful neurological damage.
As a final remark, we may agree with the warning proposed by Nelson to a more cautious medico-legal approach to the cerebral palsy issue, but at the same time we'd like to invite all the gynaecologists and paediatricians to a more complete peripartum analysis of all the biological causes other than a ‘medical mismanagement’. Even if this procedure may sometimes lead to an ‘acknowledgement of personal guilt’.
References
- Nelson KB et al Severe acidosis need not to be the result of caregiver mismanagement. J Matern Fetal Neonatal Med 2010.
- Graham EM, Ruis KA, Hartman AL, Northington FJ, Fox HE. A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathy. AJOG 2008;199:587–595.