Focus on the Primary Prevention of Intrauterine Adhesions: Current Concept and Vision

Wen-Ling Lee, Chia-Hao Liu, Min Cheng, Wen-Hsun Chang, Wei-Min Liu, Peng-Hui Wang, Wen-Ling Lee, Chia-Hao Liu, Min Cheng, Wen-Hsun Chang, Wei-Min Liu, Peng-Hui Wang

Abstract

Intrauterine adhesion (IUA), and its severe form Asherman syndrome (Asherman's syndrome), is a mysterious disease, often accompanied with severe clinical problems contributing to a significant impairment of reproductive function, such as menstrual disturbance (amenorrhea), infertility or recurrent pregnancy loss. Among these, its correlated infertility may be one of the most challenging problems. Although there are many etiologies for the development of IUA, uterine instrumentation is the main cause of IUA. Additionally, more complicated intrauterine surgeries can be performed by advanced technology, further increasing the risk of IUA. Strategies attempting to minimize the risk and reducing its severity are urgently needed. The current review will expand the level of our knowledge required to face the troublesome disease of IUA. It is separated into six sections, addressing the introduction of the normal cyclic endometrial repairing process and its abruption causing the formation of IUA; the etiology and prevalence of IUA; the diagnosis of IUA; the classification of IUA; the pathophysiology of IUA; and the primary prevention of IUA, including (1) delicate surgical techniques, such as the use of surgical instruments, energy systems, and pre-hysteroscopic management, (2) barrier methods, such as gels, intrauterine devices, intrauterine balloons, as well as membrane structures containing hyaluronate-carboxymethylcellulose or polyethylene oxide-sodium carboxymethylcellulose as anti-adhesive barrier.

Keywords: endometrium; hysteroscopic surgery; intrauterine adhesion; pathophysiology; prevention.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Three proposed key components of endometrial biology are present to maintain normal uterine physiology.
Figure 2
Figure 2
The pathophysiology of change in intrauterine adhesion.
Figure 3
Figure 3
The recent development of agents available for the primary prevention of intrauterine adhesions after uterine surgery.

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