The disservice of publishing preliminary results based on a premature hypothesis – Semmelweis’ ordeal revisited

TL;DR

This paper re-examines Semmelweis' scientific ordeal, arguing that premature publication of his hypothesis and results led to resistance from the medical community.

Contribution

The paper offers a new interpretation of the resistance to Semmelweis' work, emphasizing the role of premature publication and eminence-based medicine.

Findings

Semmelweis may have intentionally withheld his hypothesis and results until they were better accepted.

The resistance to Semmelweis' work was largely due to premature publication and eminence-based medicine.

A Kuhnian framework better explains the resistance than a Popperian one.

Abstract

In an interesting article, Dr Zuzana Parusniková claimed: (i) that Semmelweis’ colleagues did not recognise the importance of his animal experiments, (ii) that the resistance to Semmelweis’ hypothesis and results was due mainly to applying mono-causality and (iii) Semmelweis inability to communicate, (iv) that the New Vienna Medical School applied evidence-based medicine, and (v) that the philosophy of Karl Popper is the best interpretation of Semmelweis’ scientific approach. Here, we present some factual aspects of Semmelweis’ text from 1861 and discuss Dr Parusniková’s claims against this backdrop. We conclude that Semmelweis might intentionally have abstained from communicating his hypothesis and results between 1847 and 1849 – including the results from his animal experiments – as he thought that they would eventually be understood and accepted. Semmelweis’ hypothesis was that cadaveric matters and decaying particles were the cause of childbed fever and increased maternal mortality. This hypothesis might have been controversial, but we claim that the major reason for the resistance was eminence-based and induced by the publication of preliminary and suboptimal results, based on a premature version of his hypothesis. If the New Vienna Medical School had been influenced by evidence-based medicine, we believe that Semmelweis’ empirical results would have been accepted - as they were based on an almost randomised controlled trial - and if the results had not been associated with his hypothesis but instead had focused on a black box procedure. We agree that the philosophy of Popper might be appropriate when analysing Semmelweis’ scientific approach when abandoning low-level theories. However, to understand the resistance against Semmelweis’ hypothesis and results, it is not sufficient to refer to a Pickwickian discussion; a Kuhnian framework is more adequate.