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“Sampson’s Theory” - have you ever wondered what Dr. John Sampson actually wrote regarding Retrograde Menstruation as the origin of Endometriosis? Its not what you thought!

Given that endometriosis is increasingly considered a “disease treated by excision”, it is perhaps worthwhile to review the endometriosis origin paradigm of retrograde menstruation that would argue the disease is both chronic and untreatable.

The Authors Conclusions are Not Supported by the Data Provided: a critical review of John Sampson's 1927 landmark study on the origin of endometriosis.

 Perhaps Dr. John Sampson can be considered the grandfather of endometriosis treatment; his concept of retrograde menstruation is central to endometriosis management and treatment effectively unchanged over the century since 1927. For the most part unchallenged, Dr. Sampson's theory of the origin of endometriosis has enjoyed an unusual amplification and elevation to being "the most popular - if not flawed - of theories".1

I believed and based my early practice of ObGyn on Sampson's theory because it is a pathophysiology of welcome simplicity that conveniently informs a surgical treatment that is right up my Gynecologist alley - hysterectomy and bilateral salpingo-oopherectomy; it fits perfectly. But after 20 years of completely excising endometriosis, I have found that women long-suffering from the disease actually achieve durable relief, actually get better. What an elegant concept: if I get rid of all the disease that is causing symptoms, then all the symptoms arising from the disease will resolve.

But this is not what Sampson's retrograde menstruation theory would have us understand. For me, this past 20 years of clinical outcomes from endometriosis excision has been in absolute contradistinction to what retrograde menstruation had suggested: that it is an incurable disease.

I am convinced that our flawed endometriosis treatment paradigms are based on a flawed origin paradigm.

 And so, with a more critical eye,  I reread Dr. John Sampson's 1927 landmark article describing "menstrual dissemination" as the source of endometriosis.  I wanted to evaluate his often cited first public argument for the origin paradigm of retrograde menstruation that still fully informs the treatment paradigms employed a century after. On its own terms from its own century, how strong is the original proof that Dr. Sampson provided indicating that the origin of endometriosis is indeed retrograde menstruation?

 Cited here is the original article, "borrowed" by Harvard University Widener Library  from the "lender" University of Hong Kong Libraries:

John A Sampson, MD. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. American Journal of Obstetrics and Gynecology. 1927:14(4). pp 422-469.

Reviewers Comments:

Its a tough read: circular, repetitious with an overwhelming number of barely visible histologic photomicrographs and lots of very small-font footnotes (if you think pathology slides for an hour at a Grand Rounds is tough, try the article). All of the difficulty of actually reading the paper aside, he provides summary conclusions - here provided in his own words:

To his first summary point, his histologic finding of "embolic" menstrual tissue in uterine venous sinuses following hysterectomy and “venous injections” is the sole evidence provided for menstrual dissemination of endometrial tissue. Curiously, actual retrograde menstruation is not demonstrated nor discussed in his histologic study.

To his second point that menstrual blood contains menstrual tissue, he provides only histologic evidence of menstrual tissue within endometriomas and as above, as emboli in uterine venous spaces. He does not identify in his landmark paper that menstrual tissue is found in retrograde trans-tubal dissemination.

To his third point, that the endometrial tissue is found to be viable and that it "grows if transferred to situations favorable to its existence", he provides the following: "If endometrial tissue disseminated by menstruation is "thrown off to die" and is either actually "dead or dying," as has been so emphatically stated by Novak, (4) that phase of the implantation theory is likewise just as dead. If endometrial tissue disseminated by menstruation is sometimes alive and capable of growing, if transferred to suitable situations, we might expect to find embolic lesions of this tissue in the vessels of the uterine wall and even outside of that organ." 

Setting this presence of embolic lesions as the standard of proof of both the sustained viability of menstrual tissue and its capacity for implantation growth, Sampson reports on two patients on whom he performed hysterectomy on their second menstrual day wherein "An embolic or metastatic growth of endometrial tissue was found in a venous sinus of one uterus and many such lesions in the other uterus." Two patients with findings of either an embolic or metastatic phenomenon in the vessels of the uterine specimen - that was his proof of the viability of the menstrual tissue and proof of its capacity for implantation. The representative logic statement he makes is as follows: if one assumes A gives rise to B then finding B proves A gives rise to B.  It is a false logic, gross assumption without proof.

To his fourth point that peritoneum and ovary are suited to the growth of endometrial tissue, he provides a most flawed argument. He uses his clinical finding of endometriosis on "the appendix, cecum and loops of the small intestine, and their mesenteries" as proof that those peritoneal surfaces are suitable for implantation by far errant menstrual tissue. He also identifies capacity for cancers to grow on the peritoneum and on the ovary as proof that the "visceral and parietal peritoneum is suited to the growth of endometrial tissue."  It is an assumption with no proof.

To his fifth point that "the lesions of peritoneal endometriosis often occur in locations and under conditions indicating (or at least suggesting) their origin from menstrual blood escaping from the above mentioned sources" (again into venous spaces and emanating from endometrioma rupture), he again makes assumption without any proof.

 And finally, to his sixth and final point, that the peritoneal reaction to the menses-displaced endometrial tissue looks, on histologic sections, like the peritoneal reaction found in carcinomatosis is certainly not proof of the retrograde menstrual endometrium finding "surfaces suited to growth."

In review of the landmark paper published a century ago that established retrograde menstruation as the origin of endometriosis, critical peer review would certainly have generated the following Reviewer Response: "The Authors conclusions are not supported by the data provided."

To use Dr. Sampson’s own words, “the implantation theory is quite dead.”

Malcolm Mackenzie, MD

Next: “A flawed origin paradigm begets a flawed treatment paradigm: an argument for excision”

An excellent monograph on endometriosis published by APGO (American Professors of Gynecology and Obstetrics) is a must read.

Click the link below..