A study of endometriosis, endosalpingiosis, endocervicosis, and peritoneo-ovarian sclerosis : a clinical and pathologic study / by James Robert Goodall.

  • Goodall, James Robert, 1877-1947.
Date:
1943
Catalogue details

Licence: In copyright

Credit: A study of endometriosis, endosalpingiosis, endocervicosis, and peritoneo-ovarian sclerosis : a clinical and pathologic study / by James Robert Goodall. Source: Wellcome Collection.

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    with a degree of permanency proportionate to the stationary state of a minor hormonal imbalance. It is not possible to determine why some growths proliferate outwardly along the line of least resistance, while others invade the underlying tissues, even though they may be dense and resistant. In connection with the hypertrophy of normal tissues which accom¬ panies any form of acute endometriosis, a very interesting case recently came under observation, that of a married woman aged 42 years. She had had menorrhagia and metrorrhagia for the past three months. On bimanual examination the cervix, bilaterally torn, was greatly hyper¬ trophied and soft. The uterus was the size of a three-months’ pregnancy, symmetrical and soft - uncommonly like a pregnancy. The Aschheim- Zondek was negative. At operation the right ovary contained several cysts, the largest the size of an English walnut. Its walls were sclerosed and rigid. The smaller cysts were similarly, though less, affected. The left ovary was small and atrophic. The uterus, the size of a three-months’ pregnancy, was so like a pregnant uterus that I was in grave doubt about removing it. Trusting, however, on the accuracy of the test, I did a total hysterectomy. Upon opening the uterus there was a most beautiful specimen of diffuse endo¬ metrial endometriosis. There were nine polypi—some small, others large and broadly sessile—upon an endometrium fully one-half inch thick throughout. One of the polypi was hemorrhagic, and was the source of the uterine bleeding. But the most interesting feature was the tremendous muscular hypertrophy of the uterus. The walls were two inches thick, soft, succulent, exactly like the hypertrophy of pregnancy, and of a consistency indistinguishable from that of pregnancy. The ovarian cysts were follicular, and the largest had a thin sickle of internal-capsule-lutein cells covering about one-quarter of the circumference of the sclerosed cyst wall. My assistant pithily said, “A beautiful case of endocrine imbalance ovarian in origin. There is everything here that you would find in a pregnancy—except a fetus and a corpus luteum. The fetus in pregnancy does not directly cause the uterus to grow, it just changes the endocrine functions of the ovary, and it is the endocrines of this organ which cause the hypertrophy.” His statement was true. Microscopically the uterine wall was indistinguishable from the hypertrophy of pregnancy. This softness of the uterus in acute endometriosis is in sharp contrast to the hardness of the hypertrophied uterus in chronic endometriotic states.