Short Communication Journal of Pregnancy and Reproduction J Pregnancy Reprod , 2018 doi: 10.15761/JPR.1000127 Volume 1(5): 1-3 ISSN: 2515-1665 Re-visiting the role of intra-partum cardio-tocography (I-P CTG) in cerebral palsy jurisprudence: Time to take cognizance George Gregory Buttigieg 1 * and Kirill Micallef Stafrace 2 1 University of Malta, Msida MSD 2080, Malta 2 University of Malta, Msida MSD 2080, Malta Abstract Both clinical obstetrics as well the relevant medico-legal litigation was severely let down by false scientifc conclusions emanating from the USA in the 1960’s. Te false assumptions considered birth asphyxia as the predominant cause of new-born Cerebral Palsy and proclaimed the just introduced fetal cardio-tocography (CTG), as the great saviour from CP through the detection of intra-partum hypoxia. Although today, ffty odd years later, science admits that neither conclusion is correct, CTG has retained its misplaced strength in CP litigation. Not only does it still hold much pre-eminence in both UK and US jurisprudence, but sometimes, it constitutes the sole basis of discussion. Te only scientifcally valid and practical way of correction is the recognition that CP due to intra-partum hypoxia has the underlying hallmark pathology of Hypoxic Ischaemic Encephalopathy (HIE). Tis constitutes no more than 20% of CP. Other aspects of obstetric care, including in the antenatal period may have a basis for alleging negligence, but CP due to peri-partum hypoxia must be accompanied by HIE. Te 2003/2014 criteria for diagnosing HIE were established by the American College of Obstetricians in liaison with the American Academy of Paediatricians. Tis provides a reliable guide to the diagnosis by integrating clinical obstetrics/ neonatology/midwifery observations, fetal/ newborn biochemical data, newborn cerebral MRI/ MRI spectroscopy imaging, and evidence of fetal multisystem organ failure. Tese must be the new parameters on which CP jurisprudence should be justly and scientifcally based. Correspondence to: George Gregory Buttigieg, University of Malta, Msida MSD 2080, Malta, E-mail: George.g.buttigieg@um.edu.mt Received: December 05, 2017; Accepted: December 20, 2017; Published: January 04, 2018 Introduction In cases alleging medical negligence as a cause of Cerebral Palsy, it is still the general rule that Cardio-tocographic (CTG) analysis is the brunt of evidence brought forward by the plaintif, in both UK and USA. Furthermore, it is not unusual for intra-partum CTG (I-P CTG) analysis, with or without fetal acid-base confrmation of fetal distress, to be the sole evidence, on which the defendant’s fate is determined. While accepting that intra-partum CTG evidence is essentially the only parameter of assessing fetal response to the stress of labour, the extrapolation of this investigation as the sole medico-legal evidence of negligence as causative of Cerebral Palsy, is no longer tenable [1]. Although not directly relevant to the validity of this statement, one should also bear in mind that Cerebral Palsy constitutes 60–70% of the total yearly malpractice sum paid by the UK NHS Litigation Authority [2]. Hypoxic ischaemic encephalopathy I-P CTG, by itself, cannot establish a diagnosis of fetal hypoxia and acidosis. Even in a bad case scenario, an abnormal I-P CTG tracing, the incidence of fetal hypoxaemia and acidosis can be confrmed in only 50– 60% of cases [3]. Here, we shall not dwell on the myriad pitfalls of I-P CTG interpretation such as intra- and inter-observational errors, CTG nomenclature limitations, CTG’s high specifcity and low sensitivity… leading to the “shifing sands phenomenon” of this ubiquitously used investigation. However, an abnormal I-P CTG tracing is an indication for confrming or negating intra-uterine hypoxia such as by Fetal Blood Sampling (FBS), with or without one of the more modern methods such as STAN. Te crucial question is whether the fetal hypoxia and subsequent acid-base disturbance was severe enough to cause Hypoxic Ischaemic Encephalopathy (HIE), the underlying cerebral lesion contributing to the estimated 20% of Cerebral Palsy caused at birth (70% are due to prenatal causes and about 10% by post-natal causes). Although liability through negligence may also operate antenatally e.g. a mismanaged chorio-amnionitis, the discussion at hand, centres on alleged negligence in labour with resultant fetal hypoxia. In fact, one may surmise that the vacuum caused by the diminution of alleged labour mismanagement as based on unjustifed I-PCTG analysis, will eventually shif onto justifable ante-natal management scrutiny. However, sticking with the facts here, any intra-partum hypoxia proved to be present by acid-base/ STAN confrmation of I-P CTG tracing abnormality must be shown to have induced HIE. Tis should be the crux of the basis medico-legal argumentation alleging negligence. And how does one show this, clinically and in a practical way for the Courts to analyse and refect upon? Te ACOG as light bearer It was in the 1960’s, that the cause of Cerebral Palsy in general was wrongly honed on labour and on the fact that oxygen deprivation was the cause. We now know that this is the cause of the great minority of cases, but the damage was done and is still operative today. Pre-1970 related malpractice claims were few [4], but by 1985, they comprised