Asherman's syndrome pathophysiology

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Editor(s)-in-Chief: Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Canan S Fornusek, Ph.D.; Associate Editor-In-Chief: Saud Khan M.D.

Overview

Pathophysiology

The cavity of the uterus is lined by the endometrium. This lining is composed of two layers, the functional layer which is shed during menstruation and an underlying basal layer which is necessary for regenerating the functional layer. Trauma to the basal layer, typically after a dilation and curettage (D&C) performed after a miscarriage, or delivery, or for elective abortion can lead to the development of intrauterine scars resulting in adhesions which can obliterate the cavity to varying degrees. In the extreme, the whole cavity has been scarred and occluded. Even with relatively few scars, the endometrium may fail to respond to estrogens and rests. Often, patients experience secondary menstrual irregularities characterized by changes in flow and duration of bleeding (amenorrhea, hypomenorrhea, or oligomenorrhea) [1] and become infertile. Menstrual anomlies are often but not always correlated with severity: adhesions restricted to only the cervix or lower uterus may block menstruation. Pain during menstruation and ovulation are also sometimes experienced, and can be attributed to blockages.

References

  1. Klein SM, Garcia C-R (1973). "Asherman's syndrome: a critique and current review". Fertility and Sterility. 24 (9): 722–735. PMID 4725610.


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