Critical Imperative for the Reform of British Interpretation of Fetal Heart Rate Decelerations: Analysis of FIGO and NICE Guidelines, Post-Truth Foundations, Cognitive Fallacies, Myths and Occam’s Razor

Abstract

Cardiotocography (CTG) has disappointingly failed to show good predictability for fetal acidemia or neonatal outcomes in several large studies. A complete rethink of CTG interpretation will not be out of place. Fetal heart rate (FHR) decelerations are the most common deviations, benign as well as manifestation of impending fetal hypoxemia/acidemia, much more commonly than FHR baseline or variability. Their specific nomenclature is important (center-stage) because it provides the basic concepts and framework on which the complex “pattern recognition” of CTG interpretation by clinicians depends. Unfortunately, the discrimination of FHR decelerations seems to be muddled since the British obstetrics adopted the concept of vast majority of FHR decelerations being “variable” (cord-compression). With proliferation of confusing waveform criteria, “atypical variables” became the commonest cause of suspicious/pathological CTG. However, National Institute for Health and Care Excellence (NICE) (2014) had to disband the “typical” and “atypical” terminology because of flawed classifying criteria. This analytical review makes a strong case that there are major and fundamental framing and confirmation fallacies (not just biases) in interpretation of FHR decelerations by NICE (2014) and International Federation of Gynecology and Obstetrics (FIGO) (2015), probably the biggest in modern medicine. This “post-truth” approach is incompatible with scientific practice. Moreover, it amounts to setting oneself for failure. The inertia to change could be best described as “backfire effect”. There is abundant evidence that head-compression (and other non-hypoxic mediators) causes rapid rather than shallow/gradual decelerations. Currently, the vast majority of decelerations are attributed to unproven cord compression underpinned by flawed disproven pathophysiological hypotheses. Their further discrimination based on abstract, random, trial and error criteria remains unresolved suggesting a false premise to begin with. This is not surprising considering that the commonest pathophysiology of intrapartum hypoxemia is contraction-induced reduction in uteroplacental perfusion (sometimes already compromised) and not cord compression at all. This distorted categorization causes confusion, false-alarm fatigue and difficulty in focusing on real pathological decelerations making CTG interpretation dysfunctional ultimately compromising patient safety. Obstetricians/midwives should demand reverting to the previous more scientific British categorization of decelerations based solely on time relationship to contractions as advocated by the pioneers like Hon and Caldeyro-Barcia, rather than accepting the current “post-truth” scenario.

Is the hypothesis that the commonest fetal heart rate decelerations are caused by peripheral chemoreflex due to fetal hypoxaemia correct?

“…But both twins would be equally susceptible to hypoxaemia due to cord compression (with membranes intact) or reduction in uteroplacental perfusion. Hence, this observation strongly suggests that head compression makes a modest contribution to these early decelerations as a part of a multifactorial aetiology (Sholapurkar, ). The above observation was originally described by Hon, who in addition noticed early decelerations to be much rarer in breech labour where the head is subjected to much less compression (Hon, ).…”

“…The commonest FHR decelerations in labour look rapid (or descent time <30 s) on CTG with a paper speed of 1 cm min −1 and their trough roughly corresponds to the peak of contractions. Figures and demonstrate that these most common decelerations simply cannot be explained by ‘hypoxaemia’ but by non‐hypoxaemic mechanisms only (Sholapurkar, ). Figure shows that hypoxaemia (whether due to decreased uteroplacental perfusion or cord compression) builds up during the contraction phase and starts a deceleration.…”

“…Chemoreflex‐induced FHR deceleration will start recovering at point F and recovery will extend beyond the end of contraction. Thus, hypoxaemic trigger is very likely to produce a classical ‘late deceleration’ (Sholapurkar, ). Shaded area: level of IUP where fetal will continue to drop.…”

“…The recovery of FHR deceleration at the peak of contraction cannot be explained by chemoreflex due to fetal hypoxaemia or cerebral anoxia, which will continue to worsen up to point F . These most common decelerations can be explained by non‐hypoxaemic vagal reflex – with head compression not complete explanation but playing a part (Sholapurkar, ). This is not disproven by selective animal study showing partial recovery of FHR decelerations in the middle of complete cord‐occlusion non‐representative of labour.…”

“…It has been proposed that during most uterine contractions in labour there is transient fetal 'asphyxia' (but not always enough to produce FHR deceleration) and hence, when FHR decelerations do occur, they must all be because of asphyxia (Lear et al 2016 (Sholapurkar, 2017). Figure 3 shows that hypoxaemia (whether due to decreased uteroplacental perfusion or cord compression) builds up during the contraction phase and starts a deceleration.…”