PAIN IS NEVER NORMAL
MENSTRUAL CRAMPS ARE NEVER NORMAL
(THEY MAY BE COMMON BUT THEY ARE NEVER NORMAL)
PELVIC PAIN IS NEVER NORMAL
PAINFUL INTERCOURSE IS NEVER NORMAL
PELVIC PAIN IS NEVER “IN YOUR HEAD”
(ALTHOUGH MANY WOMEN ARE TOLD IT IS)
HOWEVER, EMOTIONAL STRESS WILL WORSEN PAIN
MANY WOMEN ERRONEOUSLY BELIEVE THAT A DIAGNOSIS OF ENDOMETRIOSIS MEANS THEY WILL NEVER BE ABLE TO HAVE CHILDREN
THIS IS NOT TRUE
IF A WOMAN WHO HAS HAD A CHILD CONTINUES TO HAVE PAINFUL PERIODS OR PELVIC PAIN, SHE PROBABLY HAS ENDOMETRIOSIS
WOMEN CAN HAVE ENDOMETRIOSIS AND NOT HAVE PAIN
FOR THEM, INFERTILITY IS THEIR MAIN “SYMPTOM”
ON AVERAGE, A WOMAN HAS TO WAIT 7 YEARS FROM THE TIME SHE STARTS TO SEEK HELP FOR HER PAIN UNTIL HER ENDOMETRIOSIS IS DIAGNOSED!
IT IS CRITICALLY IMPORTANT TO UNDERSTAND THAT ENDOMETRIOSIS IS A CHRONIC ILLNESS AND REQUIRES LONG TERM THERAPY. IT IS NOT A DISEASE YOU CAN TREAT ONCE AND THEN IGNORE.
WHAT IS EVEN MORE SAD IS THE LARGE NUMBER OF WOMEN I SEE WHO HAVE BEEN SUFFERING FOR YEARS WITH SEVERE PELVIC PAIN BUT WHO STOPPED COMPLAINING BECAUSE THEY COULD NOT GET A PHYSICIAN TO TAKE THEIR COMPLAINTS SERIOUSLY
Please understand that this pamphlet was initially written many years ago. I have updated it as often as necessary to keep the information current. As a result, things that are mentioned later in the pamphlet may conflict with earlier statements. Therefore, some of the things I discuss may be confusing but I wanted you to understand why. It is much easier to simply add an addendum to the pamphlet rather than go through it and edit everything which would be a very burdensome task.
It is a sad commentary that over the years, a large number of women have come to my office believing that to suffer is normal. They have been told and they believe that painful periods are normal. They have been told and they believe that painful intercourse is normal. They have been told and they believe that to lose several days from work or school each month is normal. They have been told and they believe (maybe) that the pain they are experiencing is “all in their head”.
When these women have sought medical help for their complaints, they have been told that their pain is normal or that there is nothing wrong with them because nothing can be felt on pelvic exam. Many women stop complaining because they cannot get anyone to take their symptoms seriously. One common phrase heard in my office are words that “I have always had cramps with my period but they are just normal cramps”. One woman said that she thought intercourse was always supposed to be painful. For her, it had never been anything but! How tragic.
There is a bias that runs throughout the medical profession. This bias holds that women are neurotic — men are not. A study published in the New England Journal of Medicine many years ago showed that if men and women went to a physician with identical complaints, the woman was more likely to be given a prescription for Valium whereas the man would be taken more seriously and “worked up” for some illness. Several other studies have shown similar results. There is a great deal of organic disease masquerading as psychosomatic problems.
There is a common belief that pelvic pain in women is mainly “all in their head”. Experience has shown me that little if any pelvic pain is purely psychosomatic. This is not to suggest that emotional factors do not play a role in a person’s perception of pain — they do. Any emotional problem or significant stress will significantly worsen pain, regardless of cause. However, it is rare to see a woman with purely psychosomatic pelvic pain.
Perhaps the most extreme example involves a young woman, the wife of a sophomore medical student, who came to me in the early 1980’s, supposedly for a routine problem. As part of my usual history, she was asked whether her periods were painful. She was asked whether or not intercourse was painful. To each of these questions, she responded no. I was, therefore, very surprised to discover that on pelvic examination, she was extremely tender.
This was discussed with her. It would be several years before she was in a position to begin a family. Despite her negative history, her pelvic examination was the classic tenderness seen with Endometriosis. A laparoscopy was therefore recommended which did indeed confirm the diagnosis of Endometriosis.
When she came back to the office after her surgery to discuss the findings and recommendations for therapy, she amazed us with the following comment. “Dr. Birnbaum,” she said, “I lied to you when I first came to the office. My periods are so painful I sometimes can’t stand it. Intercourse is sometimes so painful that we have to stop in the middle.” I asked her why she had not shared this information with me when I first questioned her and her reply was quite astounding. She said, “I’ve been to 2 other physicians with the same complaints. They both told me it was all in my head. I was afraid that you too were going to call me a nut.” Here was a woman who had lied and concealed the severity of her symptoms rather than risk being told again that it was imaginary or that there was nothing wrong with her.
I had hoped that these attitudes and beliefs had disappeared by the time we reached the 21st century. How sad and tragic that I received an email in 2006 with the following comments:
“I have also been told that all the pain that I’m having is all psychological and that I’m embellishing the pain. I have been to a few doctors through the years and a lot of them told me because, I was so young it was impossible for me to have endometriosis. That it was known as a sexually active persons disease, mind you I was told this when I was 12yrs old.”
All I could do is apologize for my “colleagues” and I made arrangements for her to come to see me.
The “endometrium” is the normal tissue which lines the uterus. Its name is derived from 2 words - “endo” meaning inside and “metros” which is the Greek word for uterus.
Endometriosis is the implantation and growth of the endometrium anywhere in the body except, of course, the inside the uterus where it belongs.
The most common site of Endometriosis is the pelvis but I have seen women with Endometriosis involving the intestinal tract, navel, skin, lung, and even the eye! It is not cancer although it does share one characteristic of a malignancy — namely, the ability to spread to the other parts of the body.
Because Endometriosis is such a variable disease and because it is often misdiagnosed and under diagnosed, the true incidence is not known. Based on a number of studies, it is estimated that 45% of women have endometriosis! It is the third leading cause of hospitalization in women during their childbearing years. A study from the Mayo Clinic many years ago found that, in women undergoing open pelvic surgery regardless of indication, Endometriosis was found in 50%. Recent data suggests that at least 50% of women over 35 have Endometriosis. Regardless of which number you believe, it is definitely a more common problem than is usually appreciated.
Depending on how patients are selected, the incidence will vary greatly. For instance, 50% of infertile women without pelvic pain have Endometriosis either as their main problem or as a significant complicating factor. On the other hand, if an infertile woman has pain, her chance of having Endometriosis increases to 80%. In women with chronic pelvic pain (defined as constant pain of at least 3 months duration or intermittent pain of 6 months duration), where fertility is not an issue, the incidence is about 70%. Always keep in mind that just because a woman is diagnosed with Endometriosis, it is not mean that is the cause of her pain.
The more Endometriosis is studied, the more it is found. Every new report claims a higher and higher incidence. It is now becoming apparent that most, if not all women probably develop the condition Endometriosis at some time in their life but that only a small percentage exhibit the clinical disease we call Endometriosis with its associated pain or infertility. Supporting this theory is a recent report in which very careful laparoscopic examination of women with no pelvic symptoms found that 50% had peritoneal implants consistent with Endometriosis. It has therefore been suggested that at least in some women, Endometriosis is not truly a disease but perhaps an exaggeration of a normal process in which the endometrial cells shed into the abdominal cavity implant but fail to proliferate or create any significant pain, scar tissue, or interfere with fertility.
Baboons are one of the few animals in nature that will develop Endometriosis spontaneously. Studies have been done in which the baboons underwent repeated laparoscopies at regular intervals. What was quickly noted was the fact that these animals would develop early superficial peritoneal Endometriosis that would frequently disappear by the time of the next laparoscopy. Furthermore, animals that were noted to be free of all visible disease were often noted to have developed Endometriosis at the time of a subsequent laparoscopy.
There is similar data in humans that is now becoming apparent — that for many women Endometriosis is not a disease in the strict sense of the word, but a transient physiologic phenomenon. There is evidence to suggest that most if not all women will develop “temporary” Endometriosis at some during their life and whether or not you make the diagnosis is more a matter of when you happen to laparoscope them rather than whether they actually have the “disease” or not. The diagnosis of early peritoneal Endometriosis may therefore sometimes be more a matter of fortuitous luck than anything else.
However, it must be always kept in mind that except for those rare instances where the woman is undergoing a laparoscopy as part of a research project, all women who are having a laparoscopy are doing so because they either are in pain, are infertile, or have some other organic pelvic problem. The only exception to this is women undergoing elective sterilization. In these women, the incidence of Endometriosis is very low (2-3%), but it increases as the interval from that woman’s last pregnancy increases. Nonetheless, we are now beginning to accumulate enough data to try to distinguish between Endometriosis, the “condition”, and Endometriosis, the “disease”.
Even if the theory is true that Endometriosis is a transient phenomenon for many women, this does not explain the fact that these women are frequently in pain (that’s the reason they are having a laparoscopy) and it does not adequately explain why suppressing their Endometriosis relieves their pelvic symptoms. I believe therefore that even “transient” Endometriosis is capable of creating considerable problems, certainly pain. Furthermore, even though there is most likely not a cause and effect relationship between early Endometriosis and infertility, we have certainly known for many years that women with early Endometriosis have impaired fertility. Whether it is an association or truly “a cause and effect” situation, the woman is still unable to have a baby.
This then raises the question of how bad does the Endometriosis have to be and what kind of symptoms or problems is it causing to cross the line between a temporary, serendipitous phenomenon and a true disease.
Of course, the next question is: “What is it that eliminates the Endometriosis in most women, but it allows it to become a progressive disease in others?” Why does the Endometriosis remain relative minimal in some women and yet become an aggressive disease in others. The answer most like lies with the immune system.
How often Endometriosis is diagnosed also depends on who is doing the diagnostic laparoscopy. A Reproductive Endocrinologist will diagnose Endometriosis more often than a general gynecologist because of our increased awareness of all the varied and often subtle appearance of the disease.
At one time, Endometriosis was believed to be primarily a disease of women in their 30’s and 40’s. It is now recognized that Endometriosis is not rare in teenage girls. A study from Boston found that 70% of teenage girls with chronic pelvic pain that did not respond to birth control pills had Endometriosis proven by laparoscopy! Think of how many teens have suffered needlessly over the years because they were led to believe that painful menstrual periods were “normal” and had to be endured or that their periods were painful because they did not exercise enough or some other well-intentioned but erroneous explanation. They suffered because the belief was that teenage girls did not get Endometriosis.
THE CAUSE OF ENDOMETRIOSIS
When something is poorly understood, in medicine as in other pursuits, numerous theories arise to explain the unexplainable. As a result, over the years, many different mechanisms have been proposed to try to explain how endometriosis develops. These have included retrograde menstruation, embryonic rest cells (cells leftover from the time that you were an embryo - such cells have the ability to develop into almost anything), and what is termed “coelomic metaplasia” - the transformation of cells that line the abdominal and pelvic cavity into endometriosis cells. All of these theories had their proponents and their detractors. None of them really seemed to explain exactly how endometriosis develops.
With advances in medicine and a better understanding of what is occurring, we now have a mechanism that seems to fit the known and observed facts. If it is not the correct theory, it will probably be the best we have until something substantially better comes along.
It has been known for many many years that virtually all women have retrograde menstruation. During the menstrual period, almost all of the blood flows out through the cervix and into the vagina. However, a tiny portion does flow back through the fallopian tubes into the pelvic cavity. It is this backward flow that we term “retrograde menstruation”.
Studies have been done looking at the fallopian tubes in women who were actively menstruating at the time of hysterectomy. Virtually all women have menstrual blood in their fallopian tubes at that time.
It has also been known for many many years that women who have any congenital anomaly or any acquired abnormality of the uterus, cervix or vagina, that either partially or completely obstructs the normal flow of menstrual blood into the vagina, are at greater risk to develop endometriosis. The theory holds that these women are more likely to have retrograde menstruation or that the retrograde menstruation which they are experiencing would be significantly greater than that which occurs in women who are not obstructed in some fashion.
The retrograde menstruation theory is the one that has been most popular and is believed by most physicians to be the precipitating cause of endometriosis. However, this does not fully resolve the matter. Since all women experience retrograde menstruation, why do only a certain percentage ever goes on to develop endometriosis?
Personally, I am not convinced that it is retrograde menstruation that causes endometriosis or at least sets the stage for its development. My belief is based upon the fact that the cells that are being shed during your menstrual flow are cells that are dying and are not very capable of implanting and growing in your pelvic cavity. However, women are constantly shedding cells from their endometrium throughout the menstrual cycle. It has been shown that you can recover these cells from the early stages of the menstrual cycle from the pelvic fluid. These are normal, healthy cells and they can even be grown in tissue culture. If indeed it is the retrograde migration of these cells (which is in a sense a variant of retrograde menstruation), the question still remains - why only some women when the phenomenon itself is virtually universal?
The answer is most likely to be found in your immune system. The primary purpose of your immune system is to get rid of anything that shouldn’t be there. This applies to infectious agents such as viruses and bacteria. It also applies to cells that are dead or dying. When a cell is in the process of dying, it has a mechanism by which it alerts the immune system that it is no longer a normal, healthy cell. The immune system attacks it and gets rid of it. Your body also gets rid of cancer cells the same way. It is believed that we are all constantly forming cells that could become cancer. Again, the immune system has the ability to recognize these cells as being abnormal and it destroys them.
Using this same line of reasoning, endometrial cells in the pelvic cavity may be normal but they are found in an abnormal location. Again, the immune system recognizes this and destroys them.
There are cells throughout your body that we call macrophages. These are your immune system’s scavengers. They are the cells that literally gobble up abnormal cells, viruses, bacteria, etc. There is increasing evidence that the macrophages in the pelvic cavity of women with endometriosis do not function properly and, therefore, they have an impaired ability to destroy the endometrial cells that are deposited there in the early stages of the menstrual cycle.
There is also evidence that these macrophages function abnormally insofar as they produce excess amounts of various hormones and other tissue factors that promote the growth of the endometrial cells and allow them to survive and proliferate. Many of these tissue factors also play a major role in inflammation and pain, which may also contribute to the symptoms the Endometriosis is causing.
This theory also explains why it is believed that virtually all women will develop “temporary endometriosis”. By this it is meant that endometrial cells will begin to grow in the pelvis but, within three to six months, the body will destroy them. Studies have been done looking at women who appear to have this condition. In such women, if the endometriosis is left untreated for six months and they undergo a repeat laparoscopy, a substantial percentage of these women will no longer have detectable endometriosis. These women cannot, therefore, really be classified as having the “disease” endometriosis. This condition suggests that their immune system is not working completely normally but it is not as defective as it would be in those women who actually go on to develop the clinical disease that we term endometriosis.
This, however, also does not fully answer the question as to why these women were having a laparoscopy in the first place since that is the only way you can diagnose this condition. The only women who would be undergoing a laparoscopy completely electively are those women who are having a tubal sterilization. Otherwise, women who are having laparoscopies are doing so because they are either infertile or having pain. Nonetheless, the evidence does indicate that an abnormality in the immune system is the most likely and most logical explanation to explain the development of endometriosis. It also goes a long way in explaining why women with endometriosis and their close relatives have an increased incidence of other diseases that we either know or suspect involve abnormalities in the immune system.
OTHER FACTORS IN ASSOCIATION WITH ENDOMETRIOSIS
Over the years, many theories have been advanced to explain Endometriosis. They are discussed in this section for your information in case you should come across them in your reading. A great deal of information has also been accumulated. Some of this is also included to help you better understand the problems often associated with Endometriosis.
In order to understand how Endometriosis gets started, it is necessary to understand what happens during a normal menstrual cycle. In a normally ovulating woman, each month an egg begins to grow and develop within a structure called the follicle. The follicle is comprised of the egg and the surrounding ovarian cells that are necessary for the growth and development of the egg. The cells of the follicle also serve as the source of estrogen which is produced during the menstrual cycle.
As the follicle develops, fluid begins to collect inside it and at the time of ovulation when the follicle is fully developed, the follicle is approximately 1 inch in diameter and contains about 1/2 teaspoon of fluid. The follicle is, by strict definition, a small cyst. Because of the fluid which the follicle contains, it is possible to visualize it on ultrasound and this, of course, is very important in tracking an infertile woman during her menstrual cycle.
Once the follicle has reached full maturity, the follicle wall ruptures and the egg is expelled. This is the process of ovulation. After the egg is released from the follicle, it is picked up by the fallopian tube. Following ovulation, fluid begins to accumulate in the deep pelvis where it can be seen on ultrasound. This is one of the indicators that ovulation has occurred.
After ovulation takes place, the follicular cells undergo a transformation and the structure that was once the follicle now becomes the corpus luteum. Prior to ovulation, the follicle produces estrogen; after ovulation, the corpus luteum produces estrogen and progesterone.
Our bodies are composed of cells and we are always creating new cells as older ones die. Some cells are shed. You are always losing cells from your skin, your intestinal tract, etc. Similarly, women constantly shed cells from the endometrium and some of these cells work their way back through the fallopian tube out into the abdomen, then down into the deep pelvis. If a laparoscopy is carried out on a woman, it is almost always possible to find endometrial cells in the deep pelvis in the small amount of fluid that naturally collects there. These endometrial cells that have been sloughed off throughout the menstrual cycle are living cells that can be made to grow under appropriate laboratory conditions.
You may have heard that Endometriosis is caused by retrograde menstruation. By this, it is meant that menstrual blood and cells flow back through the fallopian tube out into the abdomen at the time of the menstrual period. While retrograde menstruation certainly does take place, the cells that are being shed at the time of the menstrual period are in the process of dying and, therefore, are probably not the cause of Endometriosis. I believe it is the healthy, actively growing cells which are shed early in the menstrual cycle that give rise to Endometriosis.
Other theories, such as the transformation of the lining cells of the abdomen (the peritoneum) into Endometriosis have been recently shown not to be the cause of Endometriosis.
Since it is evident that nearly all women have endometrial cells in their deep pelvis, the natural question would be — why don’t all women develop Endometriosis? What is it that allows those cells to implant and grow in some women but not in others? In those women who develop early stage Endometriosis, what allows the endometrial tissue to persist (and perhaps progress) in some and causes it to be eliminated in others?
For many years, those of us in the field of Reproductive Endocrinology have recognized that women with Endometriosis are less fertile than women who do not have Endometriosis. It was believed that in these women, the Endometriosis caused the infertility. Certainly when a woman has severe Endometriosis with considerable scar tissue around the tubes and ovaries, there is no question that the Endometriosis is causing the infertility.
However, there are many women in whom laparoscopy demonstrates only the presence of minimal or mild Endometriosis. By this it is meant that there is surface disease or some scar tissue but the Endometriosis has not progressed to the point where there is significant scar tissue or large ovarian Endometriosis cysts. I have long held the belief that at least for some of these women, they were infertile for some other reason and that other reason permitted the Endometriosis to develop. The problem is that we never had a good explanation for “that other reason”. Now we may.
I and other Reproductive Endocrinologists have long recognized that women with Endometriosis very often have evidence of other hormonal disorders. It is very common for me to see women with Endometriosis who have evidence of increased male hormone production such as facial hirsutism and/or acne. I see many women with Endometriosis who also have Poly-Cystic Ovary Syndrome. We also have recognized for many years that other types of abnormalities in the endocrine system, particularly as it affects ovulation, occur more frequently in women with Endometriosis. It was once believed that these abnormalities in ovulation were the result of the Endometriosis. It is now becoming apparent that these ovulatory abnormalities may play a major role in the development of Endometriosis.
Three principal types of ovulatory abnormalities are commonly seen in women with Endometriosis. One problem — easy to diagnose — is the failure of ovulation to occur at all. The second ovulatory abnormality is also fairly common and also fairly easy to diagnose. This is a “luteal phase defect” in which there is inadequate or insufficient amounts of progesterone produced by the corpus luteum after ovulation has occurred.
There probably truly is an entity we call the luteal phase defect. It would take a pamphlet as long as this one to explain everything about it. It is a highly controversial situation in Reproductive Endocrinology. Most women who are told they have it are not diagnosed properly. The true significance of this condition is debatable. Further confusing the whole matter is newer evidence that the real problem for most women is not inadequate progesterone production but the inability of the endometrium to respond to the progesterone. None-the-less, there are well documented cases of women who have it and it probably does play a role in Endometriosis but I am not fully certain what that role is.
The third principal ovulatory abnormality is a problem that has been recognized for many years but was thought to be a medical curiosity. It is now becoming increasingly apparent that this abnormality is quite common in women with Endometriosis. This third abnormality to which I refer is the so-called “Luteinized Unruptured Follicle Syndrome”.
In the Luteinized Unruptured Follicle (LUF) Syndrome, the egg develops within the follicle quite normally and then, after mid cycle, the follicle turns into the corpus luteum. All the hormones are made in reasonably normal amounts. It is important to remember that when a woman is being assessed for ovulation, we are not determining whether ovulation, the actual release of the egg from the ovary, has taken place. Rather, we are measuring the biological effects of the hormones that are being produced during the menstrual cycle. We make the assumption that if the hormones are being produced in proper amounts, then ovulation is presumed to be normal.
New evidence suggests that, particularly in women with Endometriosis, this is no longer a valid assumption. What happens in the Unruptured Follicle Syndrome is that even though all hormonal changes take place reasonably normally, the follicle never ruptures and the egg is never expelled from the ovary. However, since the hormones are being produced, the basal body temperature chart will show a rise; measurement of blood hormone levels will be “normal”; and if an endometrial biopsy is done, it will show that “ovulation” has taken place. However, the follicle will not collapse and there will not be any significant increase in fluid in the pelvis when an ultrasound is done.
The next question is then — how do these various abnormalities in ovulation lead to Endometriosis. The answer is found when one looks at the fluid that normally accumulates in the pelvis throughout the menstrual cycle and analyzes this fluid for its hormone content. In normally ovulating women, after ovulation has taken place, the concentration of estrogen and progesterone in the pelvic fluid rises dramatically and achieves a level much higher than the hormone concentration found in the blood. Keep in mind that estrogen is produced throughout the menstrual cycle whereas progesterone is produced only after ovulation. Keep in mind also, as was pointed out earlier, the endometrial cells are also found in this pelvic fluid. It now appears that the progesterone that accumulates in this pelvic fluid after ovulation kills the endometrial cells that have accumulated there. If there is a defect in ovulation, the progesterone accumulation either does not occur or is below normal. This then permits those endometrial cells to live and eventually implant and grow. Thus, Endometriosis is allowed to develop.
In women who do not ovulate at all, it is obvious that no progesterone is produced. In women with a luteal phase defect, inadequate progesterone is produced. The puzzle was what was going on in women with the Unruptured follicle syndrome. For reasons that are not yet apparent, in order for the progesterone level to rise in the pelvic fluid, actual ovulation must have taken place. If the follicle does not rupture and the egg is not expelled, the progesterone level in the pelvic fluid does not rise. This then serves to explain why women with the Unruptured follicle syndrome develop Endometriosis and indeed, recent evidence suggests that whereas in the general population, the Unruptured follicle syndrome is fairly rare, it occurs with significant frequency in women with Endometriosis and probably serves as one of the main causative factors. The definitive diagnosis of the Unruptured follicle syndrome is made by laparoscopy but it can be strongly suspected and sometimes even diagnosed by the use of ultrasound examinations.
Abnormalities of ovulation such as the ones that I have just described are usually fairly easy to diagnose. They are simple straightforward concepts and the diagnostic criteria for each of them is now fairly well established. However, there are a substantial number of women who do not appear to have any obvious defect in ovulation. How then can these women be explained and still preserve the integrity of the theory?
Several studies from England revealed some very interesting data concerning not only the cause of Endometriosis but also its effects on a woman’s fertility. What these studies looked at was couples who were presented in the infertility clinic and put them through a standard fertility work-up. When they reached the point in the evaluation that laparoscopy was indicated, they combined the laparoscopy with an attempt at in-vitro fertilization. They then analyzed their data in the following way. They did not consider the overall pregnancy rate from the attempt at IVF because that was too low(at that time) to draw any meaningful conclusions. Instead, they looked at the percentage of eggs that were fertilized in relationship to the cause of that couple’s infertility after they had examined all of the data.
What they found was very interesting and very enlightening. The results showed that if the couple’s main reason for infertility was tubal damage, the fertilization rate for the eggs obtained from these women was 90%. A similar figure was obtained for those couples with “unexplained infertility”. However, for those women who had early untreated Endometriosis, the fertilization rate was only 60%. This study has been expanded and the additional data confirms the original findings that the eggs from infertile women with early stage Endometriosis do not fertilize as often as those from women with other causes of infertility.
This data indicates that there may be an inherent defect in the egg of those women who develop Endometriosis. This further supports the theory that a defect in ovulation is probably a major cause of Endometriosis. This is true because the egg, in ways we do not fully understand, plays a major role in controlling its destiny during a given menstrual cycle. If there is a problem with the egg itself, then it would follow that normal ovulation could not occur.
More recently, by carefully monitoring the menstrual cycle using frequent vaginal ultrasound examinations combined with the measurement of serum hormone levels, we have been able to discover that most women with Endometriosis have subtle but definite abnormalities of ovulation that can not be detected by other means. These abnormalities do not fall into any one given pattern so they are lumped under the overall heading of “ovulatory dysfunction”. I have found that many women with Endometriosis have one or more abnormalities of ovulation when the time is spent to search for them.
The other question that must be answered is whether the ovulatory abnormalities are a cause of Endometriosis or simply an associated phenomenon.
Endometriosis is often called the “career woman’s disease”. It is a common belief that the longer a woman goes without having had a baby, the more likely she is to develop Endometriosis. In point of fact, while this is true, it is not true in the way most people think of it. The age at which a woman has her first baby may alter the time course of the Endometriosis in terms of when the symptoms may initially appear but does not affect her chances of ultimately developing the disease. In other words, if a woman has her children at a younger age, she will develop her symptoms later, but she will still develop them. Nonetheless, I assume that a woman over the age of 30 who has never had a baby has Endometriosis until proven otherwise. Perhaps we simply look for Endometriosis more diligently in an older women who is infertile because her age becomes a factor.
The question is, does simply delaying childbearing predispose a woman to Endometriosis? Maybe! Probably. In a very real sense, Endometriosis is a “career woman’s disease”. Calculations have been made looking at women who were in their reproductive years 50 to 100 years ago and compared them to women today. Once upon a time, women graduated from high school and their formal education ceased. They got married and had children. In the absence of good contraception, women would have a large number of children and breast feeding was more common than it is today. Life expectancies were much shorter.
It has been calculated that women from our grandmother’s generation and before would ovulate perhaps 50 times in their entire lives. The rest of the time they would be pregnant or breast feeding.
Today women are marrying later and having fewer children. Breast feeding, although making a come-back, is still not as common as it once was. It is estimated that currently, women will ovulate 450 times in their life.
A study from Italy showed a correlation between the chances of a woman developing Endometriosis and the total number of ovulations she experienced. One part of this theory holds that it is the repeated insult to the peritoneal cavity during retrograde menstruation that may disrupt the normal protective mechanisms in the abdominal cavity and allow the Endometriosis to occur.
The time interval since a woman’s last baby also plays a major role in whether or not she develops Endometriosis. The longer the time from a woman’s last pregnancy, the more likely Endometriosis will be identified if that woman undergoes a laparoscopy. This is true even if the woman has had several children. This was shown in a study which looked at the incidence of Endometriosis diagnosed in women undergoing laparoscopy for the purpose of having a tubal sterilization. The longer the time since the woman’s last baby, the more likely Endometriosis would be found. This most likely explains why women who have their children early show up with Endometriosis in their 30’s and 40’s.
A newborn baby girl has approximately one million eggs in her ovaries and at the time she becomes a teenager and goes through puberty, the number of eggs has dwindled to approximately 400,000. Menopause occurs when the ovary literally runs out of eggs. It is important to understand that even though, under normal circumstances, only one mature egg is produced during each menstrual cycle, many eggs begin to develop each day but never go on to maturity. It is also known that pregnancy, at least temporarily, suppresses Endometriosis. It was this observation that formed the basis for much of our hormonal therapy of Endometriosis.
In order for an egg to develop, it must be stimulated by two pituitary hormones — FSH and LH. It is known that as a woman reaches her late thirties or early forties, the level of FSH begins to rise. Although the increase is not dramatic, it is definitely detectable. From what we do know about the physiology of the ovary and ovulation, this rise in FSH is the result of the aging process in the ovary and reflects a decreased sensitivity of the eggs to respond to the pituitary hormones. The body must therefore produce more of the stimulating hormones. Putting all these facts together, it becomes apparent that the ovary uses up its “better” eggs earlier in life and the eggs that remain in the woman’s ovaries in her late thirties and early forties are not her best eggs. Therefore, as a woman ages, she begins to ovulate eggs that are not as good as the eggs she produced in her teens and her twenties.
This is all consistent with the known facts that a woman does not conceive as readily over the age of 30 as she did in her twenties and that a woman who does become pregnant over the age of 35 has a greater chance of having a baby with a genetic abnormality. Therefore, if a woman does not have a baby at all, she has never had the protective effect of a pregnancy against her developing Endometriosis. As she begins to ovulate from her poorer eggs, she is therefore more prone to have a defect in ovulation. This entire combination of factors probably accounts for the (possible) increase in Endometriosis just on the basis of age alone.
It seems that every month, a new article appears in the infertility literature describing a new abnormality of ovulation in association with Endometriosis. For instance, under normal circumstances, the corpus luteum “dies” just prior to menstruation and the serum levels of estrogen and progesterone decline rather quickly. It has recently been discovered in women with early Endometriosis, the corpus luteum continues to produce progesterone into the early days of the next menstrual cycle. In fact, the authors of this article coined a new term and talk about what they call the “Minimal Endometriosis Infertility Syndrome”, referring to all the women with a multitude of ovulatory defects in association with early Endometriosis.
Another article recently published from England tracked women through their menstrual cycles with frequent ultrasound examinations and hormone levels. They found that up to 60% of women who were infertile had ovulatory defects, even when at first glance, they appeared to ovulate normally.
For years, it was traditionally taught that Endometriosis causes infertility. In fact, it makes much more sense and provides much better answers to turn that phrase around. Infertility should be thought of as a cause of Endometriosis — not its result. In other words, women who develop Endometriosis do so because they have a basic underlying infertility ( i.e. reproductive) problem. This also applies to women who are not actively trying to conceive. It means that women who develop Endometriosis do so because they have a basic defect in their reproductive physiology irrespective of whether or not they are trying to conceive at that time.
There is now strong evidence that Endometriosis is, at least in part, an “auto-immune” disease. In such a situation, the body forms antibodies against its own tissues. There are many common illnesses that are auto-immune including Type I Diabetes, Psoriasis, Rheumatic Fever, Lupus, Hyperthyroidism, Hashimoto’s Thyroiditis (a very common cause of enlarged thyroid glands and hypothyroidism), and Rheumatoid Arthritis. It has been shown that women with Endometriosis have a much higher incidence of auto-immune diseases than the general population. Women generally tend to have a higher incidence of auto-immune diseases than do men, particularly the “collagen-vascular” diseases such as Lupus. Preliminary studies that have been done indicate that women with Endometriosis have abnormalities in the functioning of the cells within the abdominal cavity that are the initiators of the immune response. Women with Endometriosis often have detectable antibodies against their own endometrial tissue. Abnormalities in the immune system would go a long way in helping to explain the significant discrepancy between the severity of the Endometriosis and the severity of the symptoms that exists in many women with this disease. It would also explain why, at least in my experience, severe Endometriosis seems to behave in a different biological fashion than does the earlier stages of the disease. Some of the worst cases of Endometriosis I have seen have occurred in young women - often teenagers.
Again, recognizing that all women “spill” endometrial cells into the pelvic cavity, a defect in the immune system would allow these cells to persist and survive. In woman with an normally functioning immune system, these cells would be destroyed.
Please understand that having an auto-immune disease or a problem with your immune system does not mean that you have AIDS. One has absolutely nothing to do with the other.
Alterations in immune function would also explain why, for many women, Endometriosis is not a rapidly progressive disease. If it were, minimal disease would be seen primarily in teenagers, mild disease in women in their 20’s, moderate disease in the 30’s, and severe disease would only be seen in women in their 40’s. In fact, such is not the case. For many women, their disease tends to remain relatively stable over long periods of time.
On the other hand, abnormalities in the immune system would also explain why, at least in my experience, the worst cases of Endometriosis often occur in young women in their late teens or early twenties. It would also explain why for some women, Endometriosis is a progressive disease that keeps coming back as bad as ever, despite whatever therapy is given.
Endometriosis affects much more than a woman’s ability to become pregnant — it affects her overall ability to have a baby. Statistically, women with Endometriosis have fewer children than women who do not have Endometriosis. Women with Endometriosis take longer to become pregnant and they have a lesser chance of conceiving in any one given month than do women who do not have Endometriosis.
Although there have been no major breakthroughs recently, our understanding of Endometriosis does go forward, sometimes in fits and starts. Every new bit of information does bring about a better understanding as to what is going on.
Our bodies are collections of cells. These cells are held together by special “sticky” molecules calls Integrins. In studying infertile women for whom no obvious reason could be found, it was discovered that many of them do not produce Integrins in the endometrium. This lack of endometrial Integrins prevents the embryo from literally sticking to the lining of the uterus and subsequently implanting.
Additional research has shown that many women with early Endometriosis lack endometrial Integrins. Whether this is a cause and effect or simply a coincidence is not yet known. However, there is some preliminary data to suggest that if a woman has early Endometriosis, destroying that Endometriosis at laparoscopy somehow restores normal endometrial Integrins and therefore might allow that woman to become pregnant. To be sure, this is contrary to most data that suggests treating early Endometriosis does not improve a woman’s chances of getting pregnant. However, the group of women with deficient Integrins may represent a different category that might indeed benefit from an operative laparoscopy.
Endometriosis is also an environmental disease. In fact, environmental factors may be one of the more important causes of endometriosis. The incidence of Endometriosis is increasing throughout the world. Is it because we are more aware of it? Is it because it is far easier to recommend a laparoscopy than open surgery, thereby facilitating the diagnosis. Both of these are no doubt true. But what is also true is that we live in an environmental cesspool and I do not believe we fully understand the degree to which our environment has been polluted by the “advances” in our modern civilization over the past 50-75 years.
The Endometriosis Association recently took over a monkey research colony in Oregon that the original “owners” could no longer support. Except for baboons, Endometriosis does not occur naturally in any other animal species but the human female. Now, for the first time, Endometriosis could be created experimentally in animals.
To be sure, you can also create Endometriosis by sewing up the cervix of an animal and forcing retrograde menstruation in such a large amount that Endometriosis will occur. However, this is probably not true Endometriosis since the “disease” regresses if the animal’s cervix is opened. A similar situation occurs in women. Women with congenital anomalies of the reproductive system which create any outflow obstruction will create “Endometriosis” although again, this may be a different disease than the Endometriosis which arises in women without obstruction.
Getting back to the monkey colony, researchers were studying the effect of dioxin, PCB’s, and related chemicals on these animals. It was soon recognized that these monkeys developed Endometriosis! Similar “experiments” are occurring in nature. Underdeveloped countries such as Indonesia which previously had very low rates of Endometriosis are now experiencing an epidemic. Because many Western manufacturing companies are building plants in Indonesia, it has become a very polluted country. The rising rate of Endometriosis is probably not coincidental.
Evidence is rapidly accumulating that many diseases are the result of environmental pollution — breast cancer and male infertility are two of the most important.
Endometriosis is a variable disease and it has been well known for many years that there is no relationship between the severity of its symptoms and the actual extent of the Endometriosis. Women with minimal Endometriosis may have incapacitating pelvic pain whereas women with severe Endometriosis may present with infertility as the only indication as to its presence. Again, abnormalities in immune function undoubtedly explain some of this discrepancy.
For those women who do have symptoms, 3 major pain patterns are recognized. Women with Endometriosis commonly have significant pain with their periods. It is not the severity of the pain per se that provides the clue to Endometriosis but rather the pattern. Women with Endometriosis may show the same pattern of their dysmenorrhea (painful menstruation) as do women with other problems, but when certain patterns are present, they are very distinctive and very strongly suggestive of Endometriosis.
Women with Endometriosis commonly indicate that their dysmenorrhea begins as long as 2 weeks before the onset of their menstrual period (i.e., at the time of ovulation). Many women with Endometriosis have significant mid-cycle pain. Women with Endometriosis commonly indicate that their dysmenorrhea is progressively worsening. If a woman did not have dysmenorrhea as a teenager but developed it in her twenties or later, that is another important clue to Endometriosis.
In addition to the pain beginning more than a day or so before the flow, women with Endometriosis frequently report that the pain, instead of disappearing after the first day or two of the flow, will persist throughout the entire length of the period and will often persist after the flow has ended. These patterns of pain are, in my experience, seen only in women with Endometriosis.
Another common symptom of Endometriosis is deep pain with intercourse (dyspareunia). Pain on intercourse associated with deep penetration is, without exception, a symptom of organic pelvic disease. Women with Endometriosis note that intercourse is often more painful when they are premenstrual. They also often complain that not only is intercourse itself painful but that the discomfort may persist after intercourse.
Many women have said to me they were told that intercourse was painful because their uterus was tipped backward. A tipped back uterus is a normal anatomical variation and almost never, if ever, produces symptoms. Women who have tipped a back uterus with significant pelvic symptoms have some pelvic disease as the cause of their symptoms. Most women with a tipped back uterus don’t even know it unless told by a physician.
The third major symptom of Endometriosis is deep pelvic tenderness, particularly on rectal examination. Even though I am well aware that people do not like rectal examinations, they are nonetheless an essential and integral part of the pelvic examination.
The deep pelvis behind the uterus (called the “cul-de-sac”) is the most common site for Endometriosis, simply because gravity pulls the endometrial cells down where they implant and grow. In my experience, tenderness in the deep central pelvis on rectal examination is almost as diagnostic of Endometriosis as a laparoscopy.
Keep in mind that the symptoms I have just described are only general guidelines. Women with Endometriosis show amazing variability as to the amount, severity and pattern of their symptoms.
The only other major cause of chronic pelvic pain that could be confused with Endometriosis is the presence of significant pelvic adhesions and scar tissue from either a previous infection or pervious pelvic surgery. In some instances, it is impossible on the basis of the woman’s symptoms and pelvic exam to make a distinction.
MYTH - RUPTURED OVARIAN CYSTS ARE A CAUSE OF PELVIC PAIN
A large part of my practice involves the treatment of women with pelvic pain. I commonly see women who are having pain who have been told that their symptoms are due to an ovarian cyst that burst.
The usual scenario runs something like this. A woman is experiencing pelvic pain and she goes to her gynecologist or to an Emergency Room. A pelvic examination does not reveal any evidence of a cyst or other obvious abnormalities. An ultrasound examination is then ordered which shows fluid in the deep pelvis. The woman is then told that the fluid represents a cyst that ruptured or burst and that was the cause of her pain.
It sounds very good; it sounds very plausible; it sounds very reasonable. It just doesn’t happen to be true.
Most ovarian cysts do not cause pain, particularly smaller ones. Even those that do cause pain usually cause only mild discomfort or perhaps a vague awareness that there is something there. Severe pain is only rarely due to an ovarian cyst.
The ovary forms a “cyst” every month. The follicle in which the egg is developing is, by definition, an ovarian cyst. Any process that disrupts the normal functioning of the ovary may cause the follicle to accumulate excess fluid. Usually, after one or two menstrual cycles, these cysts will disappear on their own and they rarely cause symptoms.
Following ovulation, the follicle becomes the corpus luteum. During the process of formation, a small amount of bleeding occurs into the follicle immediately after ovulation as the corpus luteum is just developing. Again, if a woman has a problem that is disrupting the normal changes that occur in the ovary during each menstrual cycle, excess amounts of bleeding will occur into the corpus luteum or it may accumulate excessive amounts of other fluid later in the menstrual cycle.
Those cysts that develop from an abnormal follicle we call “follicular cysts.” Those cysts that develop from an abnormal corpus luteum we call “luteal cysts.”
Since these cysts develop because of an abnormality in the normal functioning of the ovary, we group them under the overall heading of “functional cysts.” This is to distinguish them from cystic tumors of the ovary.
The most common cause of chronic pelvic pain in women is endometriosis. Women with endometriosis often have larger amounts of fluid in their pelvis than women who do not have endometriosis. Therefore, it would be quite normal for a woman who is experiencing pain to demonstrate fluid in her pelvis on ultrasound. It was not a ruptured cyst that was producing that fluid, it was in fact her undiagnosed endometriosis.
Functional cysts that disappear on their own do not, as a rule, create excess amounts of fluid in the pelvis. However, women with endometriosis frequently have ovulatory abnormalities that predispose them to develop functional cysts.
If a woman is having pain that is due to a cyst, the cyst will be usually felt on pelvic exam and will always be seen on ultrasound. You cannot blame pain on a “ruptured” cyst if you are basing that assumption on the presence of fluid seen on ultrasound.
Just about every woman I see with Endometriosis has been told at one time or another that she has an “Irritable Bowel Syndrome” (IBS) or a “spastic colon” or one of a dozen other terms often used to describe GI symptoms for which there was no obvious diagnosis. Women with endometriosis frequently have gastrointestinal symptoms and, until relatively recently, these symptoms were attributed to either an irritable bowel syndrome, a spastic colon, or, to those of us knowledgeable about endometriosis, to actual intestinal involvement from the disease itself.
It has become increasingly apparent over the past few years that many women with Endometriosis have intestinal involvement. In other words, there are actual implants of Endometriosis either on or in the bowel wall. The medical literature reports an incidence of intestinal involvement ranging from 3 to 34 percent, the average being about 12%. Based on all the figures, a report in the New England Journal of Medicine estimates that 5% of all women have intestinal Endometriosis.
Pelvic Endometriosis is usually (but not always) limited to pre-menopausal women — those with functioning ovaries. Intestinal Endometriosis is different. It is not rare in post-menopausal women. In fact, when a post-menopausal woman develops Endometriosis, it almost always presents with intestinal involvement. Because 70% of intestinal Endometriosis involves the sigmoid colon or rectum, these women are initially believed to have colon or rectal cancer.
The other intestinal sites ( in decreasing order of frequency ) are: appendix, cecum ( the initial portion of the colon), ileum ( the last portion of the small intestine), and lastly, the transverse colon. I suspect that this sequence is due mainly to how far the individual organs are from the pelvis and, therefore, how likely the endometrial cells are to implant on them.
Women with intestinal Endometriosis very often have symptoms but, in most cases, the correct diagnosis is not made. In order to diagnose intestinal Endometriosis, it is necessary to ask the right questions. When the proper questions are asked, the diagnosis is easy. The diagnosis is usually made by history, because x-rays of the intestines do not show it and other studies such as colonoscopy do not show it either. Laparoscopy may or may not demonstrate implants on the bowel wall but you have to know where to look for them. Endometriosis implants in the bowel wall may not be detectable except at the time of open abdominal surgery.
Diagnosing intestinal Endometriosis is relatively easy. A woman with intestinal Endometriosis will tell me that she has significant GI symptoms that vary with her menstrual cycle. The symptoms may be present only at the time of the menstrual period or they may be present all month long and worsen at the time of the period. The most common symptoms include loss of appetite, nausea (but vomiting is rare), diarrhea, increased gas, significant bloating, crampy abdominal pain, painful bowel movements, and sharp stabbing rectal pain. Many women also complain of constipation that seems to vary with the menstrual cycle. Unexplained iron-deficiency anemia may also be a clue to the presence of intestinal Endometriosis. Menstrually associated rectal bleeding is diagnostic of intestinal Endometriosis.
In many instances, it is obvious that the woman has intestinal Endometriosis. Either she has menstrually associated rectal bleeding or she has visible implants of Endometriosis on the intestine (either to the large intestine or the small intestine) at the time of laparoscopy. However, there is a sizable group of women who have all of these symptoms but who do not have rectal bleeding and whose intestinal surfaces appear normal at the time of laparoscopy. I was always willing to attribute the symptoms to either microscopic implants of Endometriosis in the bowel wall or perhaps larger implants that were also presumed to be hidden. Keep in the mind that it is the exception, not the rule, to find a woman who has a large mass of endometriosis in the bowel wall.
Recent studies have now shown that rather than attributing the gastrointestinal symptoms to hidden Endometriosis, there is in fact an associated intestinal abnormality that is seen in women with Endometriosis - abnormalities that are not found in women without this disease.
Researchers from Baylor University in Houston looked at a group of women with documented Endometriosis to study their intestinal function. They noted that women with Endometriosis frequently complain of chronic abdominal pain (not necessarily confined to the pelvis), nausea, vomiting, early satiety, bloating, distention and altered bowel habits. The study used some rather sophisticated tests but what it showed is that women with Endometriosis have significant alteration in the muscular action of their bowel wall. These types of abnormalities, often with increased frequency of contractions of the muscles of the intestinal wall, were never seen in normal women.
Interestingly, they also showed that the women with Endometriosis had reactive hypoglycemia during a glucose tolerance test.. The blood sugars dropped to an abnormally low level despite having normal insulin levels. This would indicate that women with Endometriosis may be inordinately sensitive to the actions of insulin such that they end up with lower blood sugar levels for a given amount of insulin. One mechanism that has been proposed is that the nerves that help regulate the function of the intestines overreact to the amount of insulin present..
We have known for many years that progesterone has a profound effect on the gastrointestinal tract.. This explains why pregnant women are constipated. The high levels of progesterone seen in pregnancy slow the motility of the intestines.
There is now good evidence that other hormones involved in the reproductive tract such as FSH and LH, and perhaps even HCG, are also antagonistic to intestinal motility and could also explain additionally why various functional disorders of the GI tract such as Irritable Bowel Syndrome seem to have a predilection for women. This would also explain why women with true IBS have a premenstrual worsening of their symptoms. Because these various reproductive hormones affect gastrointestinal motility, drugs such as Lupron may have a beneficial role to play in treating severe cases of IBS even when not associated with endometriosis.
In women with documented endometriosis who have symptoms of IBS that we think are mainly related to her endometriosis and the associated intestinal abnormalities, recent studies indicate that dietary changes may have a beneficial effect on the symptoms. These dietary changes would include reduction or elimination of what we call glycemic carbohydrates. These are the carbohydrates that your body will easily convert into absorbable sugar and include such things as refined flour, refined sugar, white potatoes, corn, white rice, and related foods.
Eliminating caffeine and tyramine (mainly found in red wine) may be a benefit. Adding omega 3 fatty acids (fish oil derivatives) has also been shown to have a beneficial effect.
How this will all play out is uncertain at this time. However, it does clearly indicate that women with Endometriosis have intestinal symptoms which do not appear to be related to actual intestinal involvement from Endometriosis but rather an associated intrinsic abnormality in the intestinal wall. This immediately opens the door to the concept that women who develop Endometriosis have underlying endocrine and metabolic abnormalities that differ significantly from women who do not have Endometriosis leading to the conclusion that Endometriosis is a far more complex disease than simply the implants of endometrium where they do not belong.
Many of the symptoms I have just listed are also those of the irritable bowel syndrome so it is easy to see why this label is often put on women. Furthermore, many women with chronic pelvic pain develop what is called a “Complex Chronic Pelvic Pain Syndrome” of which irritable bowel syndrome is a common feature. Additionally, any problem a woman has, especially pain, will often wax and wane with her menstrual cycle. Therefore, it is often very difficult to sort out which problem is causing which symptoms. Many women probably have both, just to confuse the issue even more.
For many years it has been recognized that Endometriosis is a major factor in infertility. There is no doubt that there is a strong association between Endometriosis and infertility. That is not to say there is a direct cause and effect, especially with the earlier stages of the disease. At one time, it was believed that Endometriosis caused infertility. However, it is now becoming increasingly apparent that there are basic physiologic abnormalities in women that not only make them infertile but also then predispose them to develop Endometriosis. In some women, the Endometriosis progresses to the point where it becomes their major problem whereas in other women, Endometriosis remains minimal and thereby serves as a clue as to what other factors may be present.
Everyone is aware of the fact that many women with Endometriosis are less likely to conceive. The term “fecundity” refers to a woman’s ability to become pregnant. In normal, fertile couples, the monthly fecundity rate is 20-25%. Turned around, it means a normal woman will be pregnant in 4-6 months of active trying.
Spontaneous (untreated) monthly fecundity rates in women with Endometriosis are on 4-6%! Some studies have reported even lower rates. This means that without therapy, it will take a woman with Endometriosis (even early stage disease) at least 5 times as long to achieve a pregnancy.
Treating early stage Endometriosis itself, either with surgery or medical regimens only increases the monthly fecundity rate to somewhere between 5-7%. However, (and this is in keeping with the well documented high frequency of ovulatory abnormalities seen in women with Endometriosis), adding a regimen of ovulatory stimulation with drugs such as Clomid, Pergonal, Gonal-F, or similar drugs in combination with Intra-Uterine Insemination will increase the monthly fecundity rate to somewhere between 10-15t%.
What many people also do not recognize is that Endometriosis profoundly affects a woman’s overall fertility — not just her ability to become pregnant but also her ability to remain pregnant. Women with Endometriosis have far worse obstetrical histories than women who do not have Endometriosis.
Although the data has been challenged, several studies have indicated that women with untreated Endometriosis have a spontaneous abortion rate of approximately 40-50% contrasted to the 10-15% abortion rate in the general population. Treating the Endometriosis reduces the abortion rate to “normal”. Interestingly, women with the earlier stages of Endometriosis seem to have a higher abortion rate than women with more advanced Endometriosis, perhaps because their disease may be diagnosed later.
Women with Endometriosis statistically have fewer children than women who do not have Endometriosis. When looking at the obstetrical history of women before their Endometriosis is definitively diagnosed, within the 5 years prior to the diagnosis of their Endometriosis, these women are much more likely to have had not only a spontaneous abortion (one or more) but also tubal pregnancies, premature labors and stillborns. Why Endometriosis should affect a woman’s reproductive capabilities in this fashion is unknown at this time. Abnormalities in the immune system may be the answer but the data is still preliminary. It is for this reason that it is necessary to establish a diagnosis of Endometriosis in women with the appropriate symptoms even though they have been pregnant before. This is a fact that many people do not understand.
Endometriosis is very commonly associated (?cause) with “one child infertility”. Many women who had absolutely no trouble conceiving the first time and then who find it impossible to have a second child are found to have Endometriosis at the time of laparoscopy.
The most important thing in medicine is to make the right diagnosis. A basic principle of medicine is that treatment follows diagnosis. It is improper medicine to treat someone without a proper diagnosis. The only way a definite diagnosis of Endometriosis can be made, with rare exceptions, is by laparoscopy.
Laparoscopy is necessary even if there is little doubt as to the diagnosis. In such instances, the laparoscopy serves to do 2 things. First, it definitely establishes the diagnosis because, as I have already pointed out, a woman’s pelvic pain could be due to other causes. Secondly, it allows the physician to determine the actual amount of Endometriosis that is present. This is critically important because therapy for the infertile woman is dependent on the actual amount of Endometriosis present, not the severity of her symptoms. In a woman not desirous of pregnancy, the severity of her symptoms often plays a greater role in determining the choice of treatment although obviously both are important.
A blood test — the CA-125 level — has been developed which some have claimed may permit the diagnosis of Endometriosis to be made without laparoscopy. It is true that this test may raise the suspicion of Endometriosis when it might not have otherwise been suspected. However, this blood test will not eliminate the need for laparoscopy, at least for the foreseeable future. There are several reasons for this. First, it is not yet proven that the blood test is that reliable. Second, the treatment of Endometriosis is based mainly on the extent of the disease which can only be determined by direct visualization. The blood test is still too uncertain to replace traditional diagnostic treating.
Most importantly, many other pelvic problems besides Endometriosis frequently give a elevated result. Many other common, benign conditions such as fibroids will elevate the CA-125 level in premenopausal women. Pelvic infection, the condition most commonly confused with Endometriosis, will elevate the CA-125 level. The principal value of this test may be to alert the physician to the presence of Endometriosis in the woman who has no symptoms.
There is also some evidence that changes in the CA-125 levels correlate well with persistence of the disease and decrease in pain. If the level drops, the likelihood is that the therapy is working. Lastly, some insurance companies, most notably Blue Cross, refuse to pay for a CA-125 level unless the woman has ovarian cancer. Thus, women with these types of insurance are being denied the best care possible because their insurance company wants to save money.
Another place where the CA-125 level is important is the evaluation of a woman with pelvic pain. If a woman is examined during the first few days of her menstrual period (something which many women understandably do not like); if she has tender nodularity in the deep pelvis; and if she has an elevated CA-125 level, then there is a strong probability that she has invasive Endometriosis. Invasive Endometriosis must be treated differently. Indeed, a laparoscopy may not even demonstrate the extent of the disease and unless appropriate preparations are made, the maximum benefit from the surgery will not be possible.
The therapy of Endometriosis has undergone a great deal of evolution over the past 10-20 years which reflects not only better therapeutic modalities but also a better understanding of Endometriosis. It is important to recognize that Endometriosis is principally (but not totally) a hormonally dependent disease. As long as there is ovarian hormone production, there will be the continued presence of Endometriosis.
It is also important to understand that women have a considerable amount of Endometriosis that is “invisible”. By this, I mean that the Endometriosis is either not visible at the time of laparoscopy because it is buried underneath other tissues (as is the case with invasive disease) or, just as importantly, the implants may be microscopic. It is these two facts that forms the basis of much of the therapy of Endometriosis and also explains the failures.
As part of any discussion of the treatment of Endometriosis, it is critically important to understand the following. There are 3 objectives in treating Endometriosis — controlling pain, controlling the disease itself, and enhancing fertility. You can always treat 1 of the 3 at any one given time; you can sometimes treat 2 of the 3; you can never treat all 3 at the same time.
Prior to the 1950’s, Endometriosis was a purely surgical disease. Women with severe pelvic symptoms but with normal pelvic exams were ignored but those with obvious abnormalities on pelvic exam underwent open surgery. Those in the latter group were then told to go home, get into bed, and stay there until they conceived.
In the 1950’s, the late Dr. Robert Kistner from Boston recognized the beneficial effect of pregnancy on Endometriosis. He was also one of the physicians doing research on the hormones that were destined to become birth control pills. He therefore reasoned that if pregnancy helped Endometriosis, creating a “pseudo-pregnancy” state using hormonal therapy would also help. This formed the basis for the first non-surgical treatment for Endometriosis. High dose, continuous oral contraceptives were used to stop a woman’s period for 6-9 months. Unfortunately, side effects were common and many women could not complete the entire course of therapy. Furthermore, the initial claims that this treatment improved a woman’s chances of conceiving were later shown not to be valid.
Nonetheless, some women were helped, and even today, I use a modified “pseudo-pregnancy” regimen, placing a woman on continuous BCP for 3-4 months at a time. This often relieves the symptoms of Endometriosis while minimizing the side effects of the pill.
The observations of Dr. Kistner formed the basis of the hormonal therapies so commonly used today. However, there may be a basic flaw that explains why hormone therapy is often ineffective. Dr. Kistner and others assumed that it was the continuous exposure of the Endometriosis to the high levels of hormones produced during pregnancy that was responsible for the remission of the disease.
Although the data is still limited, we now know that significant changes are occurring in a woman’s immune system during pregnancy. Keep in mind the fetus is a genetically unique being, different from its mother. One question for which we would love to have an answer: Why does not the mother reject her fetus as a foreign body just as she would a transplanted kidney (if immune suppressant drugs were not administered)? What allows the fetus to exist in an immunologically protected state?
Knowing what we now do concerning the relationship between the immune system and Endometriosis, I can make as good an argument that it is the alteration in the mother’s immune system that accounts for the remission of Endometriosis during pregnancy — not the hormonal changes. It would not be difficult to mimic to a certain degree the hormonal alterations seen in pregnancy. This might yield better clinical results than using high dose birth control pills. Undoubtedly, it is the immune system that explains why Endometriosis can arise for the first time in women long past menopause or why Endometriosis can persist even though a woman has undergone a surgical menopause.
Unfortunately, the drugs currently available to suppress the immune system create problems far worse than Endometriosis. To use them would violate the basic principle of medical care, “First, do no harm”. Thus, we are left with only surgery and/or hormones to treat this disease. There is some data relating the hormone Prolactin to the immune system but it is very preliminary.
There are two approaches to the treatment of Endometriosis — it can either be treated or it can be “cured“. I use the term “cured” very cautiously. Some people feel that Endometriosis can never be cured, only controlled. I do not completely share this opinion but it does have some validity. Even hysterectomy does not always cure Endometriosis . The choice of therapy obviously depends upon a great many factors.
To “cure” Endometriosis, all ovarian function must be permanently eliminated. This involves hysterectomy with removal of the tubes and ovaries. By completely eliminating ovarian function in this fashion, the vast majority of women will experience almost complete relief of their pelvic symptoms. Unfortunately, I (at least) am seeing an ever increasing number of women for whom hysterectomy has been a less than satisfactory solution. These women continue to have significant pelvic pain despite their surgery. (See my pamphlet on Chronic Pelvic Pain.)
In some of these cases where the woman has persistent symptoms after “complete” removal of the reproductive organs, it is often found that a small piece of ovary was left behind at the time of her initial surgery. This is called the “ovarian remnant syndrome”. Surgery to remove the retained piece of ovary is much more difficult than a hysterectomy and often has a higher rate of complications. Unfortunately, these women usually continue to have pain because of the severe adhesions which result from the numerous surgeries they must undergo.
There is a commonly held myth that hysterectomy alone is an adequate cure for Endometriosis. In fact, 40-50% of women who undergo hysterectomy alone with retention of their ovaries (one or both) will be back in the operating room within five years to have the ovaries removed. Some studies (and my own personal experience) would indicate that the number is much higher and the interval to the second surgery is much shorter. A newsletter from the Endometriosis Association supports these facts.
There is a countering belief however which holds that the ovaries should be retained and that you should take your chances as to whether or not subsequent removal will be necessary. European gynecologists are the chief proponents of this. To be sure, with modern techniques, removing ovaries by laparoscopy is usually not difficult, but it can be. This not only subjects the woman to the increased risk of multiple surgeries, it also increases the chance of her developing an “ovarian remnant syndrome”, which is usually a major problem.
In younger women (under age 40), conserving the ovaries is an option that should be seriously considered. There is now a strong movement to conserve ovaries in all women who are not at high risk for ovarian cancer. The ovaries do not cease hormone production after menopause — they only stop producing estrogen. Ovarian androgen production (male hormone) continues and we are finally waking up to the fact that perhaps Mother Nature has a reason for this and the ovaries should be left in place. However, this is still not fully resolved and more information is necessary.
There is another myth which is quite prevalent. This myth states that after hysterectomy for Endometriosis, estrogen therapy will maintain and perpetuate the disease. Because of this myth, many women are reluctant to undergo hysterectomy because they think their problem will not be solved. Like many myths, there are instances when this is true but for the majority of women, estrogen therapy after hysterectomy does not have any effect on the disease and it regresses. Furthermore, women who undergo hysterectomy with removal of the ovaries at a relatively young age for Endometriosis will require estrogen therapy for the prevention of osteoporosis, heart disease, and other complications of menopause.
After complete removal of the uterus, tubes and ovaries, most women can be successfully treated with the drug Megace. This will suppress the hot flashes and allow the Endometriosis to regress. Estrogen therapy can then be started 4-6 months later with less chance that the Endometriosis will be activated. However, some studies have shown than women who start Estrogen immediately following a hysterectomy do not suffer any greater or more frequent recurrence of the Endometriosis than women who delay Estrogen therapy for 6 months or more.
There are several organizations whose sole reason for existing is to talk women out of hysterectomy as a treatment for anything, with the possible exception of cancer (and even then, they seem to believe that hysterectomy is unnecessary). Recently, books have been published and “800” numbers are appearing all telling women not to have hysterectomies. Unfortunately, they promote a very biased and distorted view. When you read their literature, it readily becomes apparent that while they decry the use of hysterectomy, they have no viable alternatives or solutions for the woman with severe, often incapacitating symptoms. Their basic theme seems to be, don’t have a hysterectomy — suffer!
To be sure, there are women who continue to have symptoms such as pain following hysterectomy. Other women may complain of sexual dysfunction, weight gain, depression, etc. It is this group that serves as the basis for all horror stories in various magazine and newspaper articles, TV talk shows, etc. Keep in mind that a basic principle of journalism states that “airplanes landing safely never make headlines”. I am firmly convinced that, with proper selection, 99% of women who undergo hysterectomy for Endometriosis never regret their decision and never have any problems later. What is the most common complaint I hear following hysterectomy? — “Dr. Birnbaum, I wish I had done this a long time ago.”
There are several criteria that must be satisfied before hysterectomy is entertained as a definitive treatment for Endometriosis. First, the Endometriosis must be producing symptoms that are no longer tolerable. In addition, the woman must also have reached the conclusion that she wishes no further children. Lastly, the woman should have undergone at least one attempt at more conservative management — particularly operative laparoscopy. If these criteria are satisfied, the woman is a candidate for hysterectomy.
Another reason for the failure of hysterectomy to eliminate the woman’s pain is the simple fact that her Endometriosis was not the reason for her pain. I have established the “Delaware Valley Center for Chronic Pelvic Pain”, similar to other pain centers which exist in other parts of the country. It is now becoming increasingly evident that just because a woman has Endometriosis and has pelvic pain, it is incorrect to automatically assume that the former is causing the latter. Directing therapy solely towards the Endometriosis causes many women to go through useless and ineffective treatments that ultimately cause more harm than good.
One common concern that women share who are contemplating hysterectomy is whether or not the surgery will be successful. If they undergo the surgery, will they be pain-free afterwards?
There is now a way to determine this with some degree of certainty. The drugs now available to treat Endometriosis — Lupron or Synarel — simulate the effects of hysterectomy by pharmacologically eliminating ovarian function. If a woman takes one of these drugs and her pain disappears, she can be reasonably sure that hysterectomy will also eliminate her pain. If however, her pain persists, she ought to be concerned that surgery may not work. It means there is some other cause for her pain in addition to the Endometriosis that needs to be evaluated prior to committing to hysterectomy.
The effectiveness of GnRH suppression in relieving the symptoms of Endometriosis is so high that I am becoming more and more convinced that a woman who has Endometriosis, goes on GnRH suppression, and fails to achieve relief of her symptoms is most likely in pain for some other reason. This would explain why hysterectomy often does not relieve their pain either.
I have women in my practice with deeply invasive cul-de-sac Endometriosis who have large masses of Endometriosis in their deep pelvis. Most of these women have been rendered pain free by the use of GnRH suppression. Therefore, even in those women who have the types of Endometriosis that we know are most commonly associated with pelvic pain, if their pain is due to their Endometriosis, GnRH suppression will be effective.
There are obvious exceptions to this as there is with anything in medicine. Some women will require hysterectomy for Endometriosis even though they do not have significant pelvic symptoms because the Endometriosis is creating damage and injury to other organs that could affect the woman’s life and health even though it is not producing much in the way of pain. The most common problem in this category is obstruction of the urinary tract. There are also women who undergo hysterectomy even though they would like to have children some day. In such instances, the Endometriosis is interfering with their ability to live a normal life and all other attempts at more conservative therapy have been tried and failed.
These last two categories I have mentioned are fairly uncommon. The vast majority of women who undergo hysterectomy for Endometriosis have had a least one child and the indication for their hysterectomy is unrelenting pelvic pain.
For most women with significant Endometriosis, hysterectomy will remain a valuable option. However, because of the problems which I have already mentioned, besides the often significant psychological ramifications of hysterectomy, I am also of the firm belief that hysterectomy should only be considered when all other reasonable approaches to therapy have been tried and failed.
There is another down-side to hysterectomy that I am encountering more frequently and this has to do with a woman’s age. I cannot give any proof for these statements but I am convinced that the younger a woman is when she has her ovaries removed, the less well she tolerates it. At one time, I and most other physicians believed that hormone replacement therapy following surgery was an adequate substitute for what the woman’s ovaries had been producing. I am no longer convinced this is true. It may true for the woman age 45 and over, but maybe not and as I mentioned above, perhaps all women should have their ovaries left in at the time of hysterectomy. However, women under the age of 40 will almost always do much better if their ovaries are left in — especially in terms of sex drive and sexual function. However, as discussed above, the woman must recognized the risk of having to undergo additional surgery if her pain or other symptoms have not been relieved.
The other approach to Endometriosis is treatment. By treatment, I mean therapy directed at controlling the symptoms and/or pelvic damage created by the Endometriosis in an attempt to relieve pain and/or enhance the woman’s fertility. Such therapies are “conservative” because they conserve the woman’s ability to have a child. As in many things in medicine, the choice of therapy is tailored to the woman’s needs as much as possible.
There are a few basic guidelines to which I try to adhere as much as possible. However, with the disease that is as variable as Endometriosis, the rules are broken as often as they are followed.
Open abdominal surgery should be avoided unless there is absolutely no other choice. The most common reason for open surgery would be the presence of severe bowel involvement or very severe adhesions and scar tissue not safely treatable by laparoscopic techniques.
Just as an aside, women should avoid open abdominal surgery for pelvic disease whenever possible. The currently available laparoscopic techniques are such that many pelvic problems, particularly in younger women, can be treated in this way. The most common reason for pelvic adhesions is previous pelvic surgery. Much of my practice deals not with treating pelvic disease per se but rather the damage created by previous open pelvic surgery.
There is a surgical approach that combines the best of both worlds — it permits the therapy to be carried out mainly by laparoscopy but still permits an open procedure when necessary. This technique is called “Minimal Access Surgery” or “Minimally Invasive Surgery”. A laparoscopy is carried out first and all that can be accomplished by laparoscopic surgery is done. Then, a small incision is made and the remaining surgery is carried out. For instance, a fallopian tube or ovary can be removed from the body, repaired, and then returned to its normal location. I have done a number of myomectomies this way. General surgeons are now using this technique for people requiring bowel surgery. I have used it quite successfully in treating tubal disease or very severe Endometriosis. Since the incision is small, the hospital stay is shorter and the recovery time is lessened.
It is critically important to keep in mind that the various medical therapies for Endometriosis do not cure it nor does “conservative” surgery cure Endometriosis. Because of the known presence of Endometriosis in other areas of the pelvis that are not visible at the time of surgery, it is fairly common to see the Endometriosis begin to recur after therapy has stopped. It is impossible, of course, to predict those women in whom the Endometriosis will recur to any significant degree and also, the rate at which the Endometriosis will recur can not be predicted. Two facts must always be kept in mind. First, operative laparoscopy may or may not relieve pain. Second, unless you are trying to become pregnant, operative laparoscopy must be followed by hormonal suppression or you will have gone through the surgery for nothing.
The approach to therapy that I am going to outline in the next few paragraphs is based upon all the evidence that is currently available in the medical literature combined with my own personal experience with treating this crazy disease. As newer information becomes available, my approach will be modified. Therefore, there is a good chance that this pamphlet will even be out of date by the time you read it.
There are several factors which have dramatically altered our approach to Endometriosis and which have also significantly improved the results we obtain. These factors include a better understanding as to the origins of the disease, the factors which maintain the disease, the widespread nature of the disease even when visual inspection of the pelvis does not indicate this, the development of effective drugs to help control the disease and lastly, the development of operative laparoscopy and related techniques of pelviscopic surgery. By combining all of these factors, effective therapy for Endometriosis is now possible for most women.
As important as our improved knowledge may be in helping to choose the best therapy for a woman with Endometriosis, it is equally important in helping to decide whom not to treat. For many women, Endometriosis may be a coincidental diagnosis and not the primary cause of their problem. Learning to make this distinction is critically important. I have many women in my practice who are in chronic pain from surgery for pelvic problems such as simple ovarian cysts that were best left untreated. They were operated on because the cyst was found during a laparoscopy at which Endometriosis was also diagnosed. The conclusion was reached that if the woman was in pain, if she had Endometriosis, and she also had a small cyst, then somehow they were all related and surgery was opted for. Once they got onto that “slippery slope”, the first surgery created more problems such as scar tissue and adhesions that inevitably led to pain and then to additional therapies such as repeated surgeries.
This problem often results from one of the most common myths in Gynecology, namely that ruptured ovarian cysts are a cause of pelvic pain. A large part of my practice involves the treatment of women with pelvic pain. I commonly see women who are having pain who have been told that their symptoms are due to an ovarian cyst that burst.
The usual scenario runs something like this. A woman is experiencing pelvic pain and she goes to her gynecologist. A pelvic examination does not reveal any evidence of a cyst or other obvious abnormalities. An ultrasound examination is then ordered which shows fluid in the deep pelvis. The woman is then told that the fluid represents a cyst that ruptured or burst and that was the cause of her pain.
It sounds very good; it sounds very plausible; it sounds very reasonable. It just doesn’t happen to be true. Most ovarian cysts do not cause pain, particularly smaller ones. Even those that do cause pain usually cause only mild discomfort or perhaps a vague awareness that there is something there. Severe pain is only rarely due to an ovarian cyst. One thing is certain — endometriosis cysts almost never cause pain unless they rupture.
Keep in mind that in normally ovulating women, an ovarian cyst ruptures every month. The follicle in which the egg develops is a cyst. The process of ovulation involves the rupture of the follicle wall followed by the expulsion of the egg. This does not cause pain. The pain that women experience at the time of ovulation is due to the rapid growth of the follicle with stretching of the follicle wall just prior to ovulation. Ovulation with collapse of the follicle actually relieves the pain.
The most common cause of chronic pelvic pain in women is endometriosis. Women with endometriosis often have larger amounts of fluid in their pelvis than women who do not have endometriosis. Therefore, it would be quite normal for a woman who is experiencing pain to demonstrate fluid in her pelvis on ultrasound. It was not a ruptured cyst that was producing that fluid, it was in fact her undiagnosed endometriosis.
If a woman is having pain that is due to a cyst, the cyst will be usually felt on pelvic exam and will always be seen on ultrasound. You cannot blame pain on a “ruptured” cyst if you are basing that assumption on the presence of fluid seen on ultrasound.
One of the most important initial decisions that must be made in treating Endometriosis is whether or not the woman is interested in having a baby at the time she is initially seen for therapy. That is a whole topic in itself and will be discussed later.
If a woman with Endometriosis is not interested in conceiving immediately , but will wish to have a child someday, hormonal suppression is principal mode of therapy.
Obviously, the woman will have undergone a diagnostic laparoscopy to establish the diagnosis of Endometriosis. At the time of the laparoscopy, an attempt will be made to treat the Endometriosis that is visible and also carry out other procedures that will attempt to relieve pelvic pain. Operative laparoscopy, when carried out in this way, can have a significant ameliorative effect on the Endometriosis. However, following this hormonal suppression is mandatory to keep the Endometriosis from recurring or to slow down the rate of recurrence. For some women, such hormonal therapy is initially carried out by the use of a low dose oral contraceptive. Other types of hormonal therapy such as Provera are occasionally employed.
Danazol (Danocrine) therapy may be used to initially suppress the Endometriosis. However, because of the side effects and potential risks of Danazol, long term suppressive therapy is usually not desirable. However, it is important to keep in mind that Danazol is still a valuable drug for the treatment of Endometriosis because it has the unique property of being an immune suppressant. Since Endometriosis is, in part, an immune disease, this fact makes it an effective drug when others have failed.
There are now available for the treatment of Endometriosis drugs which represent the best hormonal therapy possible at this time. These drugs are analogs (first cousins) of Gonadotropin Releasing Hormone — (GnRH) — the hormone produced in the brain which controls the Reproductive Endocrine system and ultimately ovulation. By the use of the GnRH analogs, it is possible to completely suppress the pituitary gland and thereby completely suppress the ovary. This produces a pharmacologically induced menopause which then causes significant regression of the Endometriosis. However, this menopausal state, with very low estrogen levels, creates all the problems associated with menopause. Annoying side effects such as hot flashes, mood swings, insomnia, vaginal dryness, etc. are not uncommon. Hot flashes are almost universal.
Menopause is also associated with potentially serious problems such as loss of bone mass leading to osteoporosis and changes in cholesterol which may lead to an increased risk of heart disease. Women who are taking one of the GnRH analogs alone will often develop a measurable bone loss after 6 months of therapy.
When a woman undergoes a natural menopause at age 50 or so, or undergoes a surgical menopause with removal of the ovaries, she will usually be put on Hormone Replacement Therapy (HRT). Properly administered HRT will eliminate the hot flashes; maintain adequate vaginal lubrication; prevent osteoporosis; reduce the risk of heart attack; reduce the risk of uterine cancer; reduce the risk of colon cancer; and allow that woman to live a healthier life compared to women who do not take HRT.
It occurred to me and others that combining HRT with GnRH therapy allows us to eliminate or substantially reduce the problems associated with GnRH therapy alone. Since I give HRT to women following natural or surgical menopause, why not give it to women with a drug-induced menopause?
Although this approach is still officially “off label” (i.e. not FDA approved), there is good data available to indicate that it is safe and effective. Recent studies have shown that bone mass is preserved and osteoporosis does not develop. We have known for a long time that HRT helps prevent changes in cholesterol. I have had women on GnRH/HRT therapy for 5 years or more and they have done extremely well.
The reason for this discussion is that GnRH/HRT therapy is currently the best long term treatment available for Endometriosis. Many women experience complete (or near-complete) relief of symptoms with this regimen when nothing else had worked. I am not aware of any long term risks associated with GnRH itself. The risks of GnRH are those created by the low estrogen levels. Since we maintain post-menopausal women on HRT for many, many years, there is no reason why we should not be able to do the same for women on GnRH. Women undertaking this therapy for an extended time must understand that it is officially experimental, but there is no reason to believe it is not safe. It will remain “experimental” because no drug company will invest the many millions of dollars necessary to prove its effectiveness since so many people are already using it.
What is the biggest obstacle to a woman being treated in this manner? — her insurance company’s refusal to pay for it. I had a young woman in my practice who had previously undergone a laparoscopy. She was told she had a normal pelvis. Shortly thereafter, she came to me with classic symptoms of Endometriosis. I had to carry out a repeat laparoscopy where obvious Endometriosis was seen.
Because other therapies had been tried and failed, I started this woman on GnRH with HRT and in a fairly short period of time, she was pain free.
This woman’s employer then switched her insurance to a large local HMO. I was called by a physician employed by this HMO and I was told that since the GnRH therapy had exceeded the 6 months approved by the FDA, they (the HMO) would no longer pay for it. I asked how I was supposed to treat my patient and no answer was given. I was told that if this woman’s pain returned, they would reconsider allowing her to go back on the GnRH! I wonder how much of a role the fact that these drugs cost approximately $1000 per month played in the HMO’s decision?
When her pain came back, as it usually does, GnRH was restarted. Unfortunately, as is often the case, the degree of pain relief was not as good the second time around as it had initially been. Had the HMO cared more about her welfare than their bottom line, this woman would have been kept pain free.
Unfortunately, I see this as the future of medicine under the health care “reforms” being put in place by the insurance companies. As bad as the “health care reforms” proposed by President Clinton in his first term were, their defeat sent a very clear message to the insurance industry. The HMO’s and other managed care organizations recognized that they could screw the American public anyway they wanted and Congress would not get in their way. We are now paying a heavy price for this. The law mandating 48 hours of hospital care following delivery is a direct result of this. Babies were literally dying and it became such a scandal, Congress could no longer ignore it. Now, by law, women are allowed to stay for 48 hours. Stay tuned for the next chapter.
Therapy of the woman who is trying to conceive is a totally different matter. Part of the problem in treating Endometriosis in the infertile woman is the fact that we really don’t understand how, particularly in the earlier stages of Endometriosis, the disease affects a woman’s fertility. There is a great deal of data that does address this but to include it in this pamphlet would overwhelm you with so much information that I fear the major message would be lost. As I have already pointed out, it makes much more sense and provides a much better understanding if the woman’s Endometriosis is considered to be the result of or coincidental to her infertility and not the cause. This is true in the case of early stage Endometriosis but not more advanced disease.
For reasons that are completely unknown, some women’s Endometriosis progresses to a more advanced stage in which case it is obviously affecting her fertility by the scar tissue that it produces around the tubes and ovaries or the large ovarian Endometriosis cysts seen in the more advanced stages of the disease. In many of these cases, hereditary factors play a role. Endometriosis definitely runs in families and when it does so, it tends to occur earlier and become more severe more quickly than when it pops up randomly.
For those women who develop progressive Endometriosis, it is also now becoming apparent that they can be divided into two categories. Those with “upper pelvic disease” - tubes and ovaries - and those with “lower pelvic disease” - those women who develop deeply invasive Endometriosis in the cul-de-sac.
Upper pelvic disease is associated with ovarian Endometriosis, adhesions and infertility.
Lower pelvic disease is associated with pelvic pain and dyspareunia. However, these women tend not to have as much tubal and ovarian adhesions and it is less associated with infertility.
This concept fits nicely into the observed fact concerning the association of Endometriosis with infertility. It is obvious when a woman has large ovarian endometriomas or severe tubal and ovarian adhesions as to why she is not conceiving.
These facts provide us with a simple explanation as to the relationship between early superficial Endometriosis and infertility, namely that there is no “cause and effect” relationship although there is unquestionably an association. This is why women with early Endometriosis are classified in the same way as women with “unexplained” infertility. The presence of early Endometriosis does not explain their infertility.
Endometriosis is “staged” or classified as being either minimal, mild, moderate or severe. This classification scheme is based strictly on the amount of Endometriosis present and the damage it has produced — not the symptoms. Further more, the classification is designed to help treat the infertile woman — it is not a classification for pain and it really doesn’t do that good a job for the actual amount of Endometriosis present. A woman with a painless, solitary large endometrioma (Endometriosis cyst) in an ovary will be classified as “moderate” while a woman with extensive amounts of superficial peritoneal disease causing severe pain will be classified as “minimal”. It has been well known for many years that there is no correlation between the amount of Endometriosis that a woman might have and the physical symptoms it is producing. It is not rare to see a woman with minimal Endometriosis to have severe pain and yet women with severe Endometriosis may have no pain at all!
It is important to always remember that many studies have shown that treating minimal and most mild Endometriosis has no benefit for an infertile woman. If infertile women with minimal Endometriosis are divided into two groups, all other infertility factors corrected to the greatest degree possible, and then women in one group have their Endometriosis treated directly whereas the Endometriosis in the other group is not treated at all, at the end of two years, the pregnancy rates in the two groups are the same. However, it is important to remember that the pregnancy rate will still be less than the general population. Therefore, there is no reason to treat minimal or mild Endometriosis with long term hormonal suppression. However, it is important to keep in mind that there is a therapeutic effect from a diagnostic laparoscopy itself which the woman will undoubtedly have undergone.
The advent of the operative laparoscope has changed this. If a woman undergoes diagnostic laparoscopy and minimal or mild Endometriosis is found, most physicians are now treating the Endometriosis they see with operative laparoscopy. Whether this will prove to enhance these women’s fertility will take several years to determine. Some preliminary studies show an increased pregnancy rate following operative ablation of minimal Endometriosis — other studies show no difference.
One study from Montreal did show that in infertile couples where the wife’s minimal Endometriosis was the only detectable abnormality, treating the Endometriosis by operative laparoscopy did shorten the interval it took to achieve a pregnancy. However, the overall rate of conception was not increased.
Newer studies have also shown that for the infertile woman, surgical therapy of her Endometriosis is the only treatment (of the disease itself) that will improve her chances of become pregnant. Hormonal suppression of her disease (no matter which drug is used) does not increase her chances of conception. Keep in mind that other therapies will usually be necessary.
The operative laparoscope has also revolutionized the treatment of moderate Endometriosis. Formerly, women with moderate Endometriosis were deemed to have sufficiently severe pathology to justify major open surgery. However, the overwhelming majority of women with moderate Endometriosis can have it effectively treated by operative laparoscopy and these women should benefit greatly from this approach in that they will be spared the need to undergo major open surgery or other therapies.
At one time it was proposed that Danazol therapy alone was sufficient therapy for Endometriosis in the infertile woman. The statistics now quite clearly show that Danazol therapy is only adjunctive and the vast majority of reproductive surgeons, including myself, feel quite strongly that Endometriosis is primarily a surgical disease. It is all very nice when medical therapy helps. However, surgery remains the most important therapy. More importantly, statistics that have been reported following treatment of early Endometriosis with operative laparoscopy indicate pregnancy rates that are as good, if not better, than those formerly achieved by either Danazol or major open surgery. Furthermore, operative surgery is a “one-shot” thing and the overall time necessary to treat the Endometriosis is significantly lessened.
There is no justification to put an infertile woman with early stage (Minimal or Mild) Endometriosis on hormonal suppression. It wastes time and does not improve her chances of conceiving.
The use of the operative laparoscope and related pelviscopic surgical procedures was heralded with great optimism. There is no question that operative laparoscopy has permitted many women to avoid open surgery.
The advent of operative laparoscopy and related surgical techniques is revolutionizing surgery, not only GYN surgery but general surgery as well. Appendectomies, gall bladder surgery, hernia repairs, etc. are all being done by laparoscopy. As a result, patients are able to spend less time in the hospital and the recovery time is less.
Newer techniques in GYN surgery such as a Total Laparoscopic Hysterectomy (TLH), Laparoscopically Assisted Vaginal Hysterectomy (LAVH), a Laparoscopic Supracervical Hysterectomy (LSH), or a Laparoscopically Assisted Supracervical Hysterectomy (LASH) also allow women to undergo surgical procedures with less time in the hospital and shorter recuperation times. Newer techniques also permit the treatment of problems such as tubal pregnancies and ovarian cysts by much less invasive routes with overall benefit to the patient.
Therefore, as this pamphlet is being revised (March, 2011) the best therapy for Endometriosis for the infertile woman is as follows. If the woman’s Endometriosis is minimal, operative laparoscopy will be carried out. This may relieve symptoms and hopefully will enhance the woman’s fertility.
For mild Endometriosis, operative laparoscopy will also be sufficient therapy. In almost all instances, the Endometriosis can be treated “completely” by the operative laparoscope. For the infertile woman, no other therapy for her Endometriosis is needed.
For most cases of moderate and occasional cases of severe Endometriosis, operative laparoscopy is also effective and sufficient therapy. However, the operative laparoscope is not a magic cure-all. There will still be some women whose Endometriosis is not completely treatable by a single operative laparoscopy. In these women, GnRH suppression followed by open surgery will be necessary.
In some instances, operative laparoscopy, followed by hormonal suppression, followed by repeat operative laparoscopy is a better alternative for the more advanced stages of Endometriosis. Having two laparoscopies several months apart is actually less burdensome and better tolerated than one open abdominal surgery. The pregnancy rates with operative laparoscopy are as good if not better than with open surgery.
Open surgery should be reserved for those women with severe disease and severe pain that cannot be treated by less invasive surgery. Women with severe bowel involvement will also require open surgery. Some are claiming that they can do bowel surgery through the laparoscope. They can, but it takes them 7 hours to do it. Subjecting a woman to a 7 hour surgical procedure (we call them “foreveroscopies”) when the same result could be obtained in a much shorter period of time by other means does not serve the best interests of the patient. It also results in much more adhesion formation.
Adhesion formation is also less with laparoscopic surgery than with open surgery. However, contrary to popular belief, adhesions are not totally eliminated by the use of operative laparoscopy. In fact, adhesions are more related to whether the surgery is done “open” or by laparoscopy. Open surgery results in far more adhesion formation than if the same procedure is done through the laparoscope. However, even laparoscopy will result in adhesions.
Reformation of adhesions is a problem after any surgery, whether or not a LASER is used, whether or not Interceed is used, etc. The more severe the adhesions at the time of the initial surgery, the more severe will be the reformation of the adhesions. For this reason, any woman undergoing any type of Endometriosis, infertility, or related surgery by open abdominal surgery should have a “second-look laparoscopy” performed 6-8 weeks after the initial operation. More recent data and my own personal experience also indicates that women undergoing operative laparoscopy who are found to have significant adhesions from whatever cause should also undergo a second-look laparoscopy. This would include women with either moderate or severe Endometriosis. Minimal or mild cases of Endometriosis do not usually require second look surgery.
One other factor must also be mentioned when discussing the treatment of Endometriosis in the infertile woman and that is the duration of her infertility. The success rate in terms of that woman conceiving depends perhaps more than anything else on how long she has been trying to conceive before her Endometriosis was diagnosed. If she has been trying to conceive for more than 3 years, her ultimate chance of becoming pregnant will be significantly reduced regardless of how severe (or how mild) her Endometriosis is. It is for this reason that I am very aggressive in diagnosing and treating Endometriosis.
The age of the infertile woman also must be considered. In women with Endometriosis as with other infertility problems, the older she is, the less likely she will be to conceive.
Another important factor in assessing the infertile couple in whom the wife has proven Endometriosis is the status of her husband (or partner). Regardless of what else is done, if a woman with Endometriosis is infertile and her husband’s semen quality is “subfertile”, the overall success in terms of achieving a pregnancy is half the rate of those couples where the husband’s “fertility” is normal.
In summary, it is my current opinion that the following plan of treatment represents the best approach to the woman with known or suspected Endometriosis. It takes into consideration all that is now known and that which is believed to be true about Endometriosis and Endometriosis-related infertility. It is also based on the fact that women who are infertile and who are found to have the earlier stages of Endometriosis will usually have long standing infertility.
As an initial step, a diagnostic laparoscopy is carried out. This establishes the diagnosis definitively and permits proper staging of the disease. It also permits me to determine if any other significant pelvic problems are present. Women with Endometriosis frequently have other associated pelvic pathology.
Endometriosis is currently classified by the American Society for Reproductive Medicine as being either “minimal”, “mild”, “moderate” or “severe”. For a woman with minimal and mild disease, satisfactory treatment of the Endometriosis by operative laparoscopy is almost always possible. For the woman who is trying to conceive, no further therapy of her Endometriosis is necessary.
For the woman with moderate disease, in some instances, operative laparoscopy will treat the disease effectively and no other therapy would be necessary, depending on the severity of the adhesions and other factors. Some women with moderate Endometriosis are in that stage because of a large ovarian Endometriosis cyst with little or no adhesions. For these women, a second look laparoscopy probably would not be necessary, depending on what follow-up ultrasounds show. For women with significant adhesion formation, a repeat laparoscopy would be indicated.
For the woman with severe Endometriosis ( or more advanced moderate Endometriosis), a single operative laparoscopy will not be able to treat all her disease adequately and effectively. In such situations, hormonal suppression followed by repeat operative laparoscopy is necessary. Open abdominal surgery is occasionally required for the most severe cases, particularly if there is significant bowel involvement.
For the woman who has had a previous open abdominal operation for Endometriosis or some other problem, it may not be possible to treat her pelvic disease by operative laparoscopy. Again, as in the case of severe Endometriosis, open abdominal surgery may be required, particularly if a second look laparoscopy cannot adequately treat the problem.
Once the woman has gone through whatever surgical procedures are required to treat her disease to the greatest degree possible, Controlled Ovarian Hyperstimulation combined with Intra-Uterine Insemination (COH / IUI) would then be instituted.
The rationale for this approach is as follows. Based on all the available evidence and experience of Reproductive Endocrinologists, treating early Endometriosis does increase a woman’s chances of conceiving. I do feel that women with early Endometriosis fall into the same category as couples with “unexplained infertility” or “Minimal Abnormality Infertility”. In such couples, COH / IUI has been definitely shown to significantly improve pregnancy rates.
In women with more advanced Endometriosis, there is no sense wasting time to see if she could conceive on her own. She will be most “fertile” immediately after she has completed her surgical therapy. Instituting COH / IUI immediately will maximize that woman’s chances of conceiving as quickly as possible.
Once a woman has completed whatever surgical therapies are appropriate followed by 6-9 good cycles of COH / IUI and has not conceived, then she has gone through all infertility therapy except for the Assisted Reproductive Technologies such as In-Vitro Fertilization (IVF) or GIFT. This approach thus allows the maximum gain in the shortest period of time without wasting a lot of effort and money on diagnostic work-ups or treatment programs of dubious value and efficacy.
The current American Society for Reproductive Medicine (ASRM) classification of Endometriosis (see attached sheet) has 4 stages for the disease — minimal, mild, moderate, and severe. You will sometimes see it classified as Stages I, II, III, and IV. There is good evidence that severe Endometriosis with a point score over 70 is a different disease, particularly in terms of infertility. Women going through IVF with early stage Endometriosis have as good a chance of become pregnant as women with other types of infertility. However, women with severe Endometriosis seem to have a lower pregnancy rate, even with IVF.
There is also evidence now that Minimal Endometriosis may be different than the more advanced stages. Genetic studies have shown that there appears to be a difference in the earliest form of the disease compared to the more advanced disease. This is in keeping with my observation that women with Minimal disease usually do not get worse as determined by laparoscopy. However, many women with the more advanced stages frequently do progress with time.
Preliminary data does suggest a way around this. A study from England showed that in women with severe Endometriosis, 6 months of GnRH suppression significantly improved the success rates with IVF. I have also had several women with severe Endometriosis conceive after prolonged GnRH therapy (without IVF). They were initially put on the drug because they were not interested in becoming pregnant when they were first treated. However, to be complete, other studies have not confirmed this.
This suggests that women with severe Endometriosis who are interested in becoming pregnant ought to consider prolonged GnRH therapy after surgical treatment has been completed. While this does extend the period of time during which the woman will not be able to conceive, the increased chance of becoming pregnant may be a worthwhile tradeoff.
There is some data that women with the most severe cases of Endometriosis (ASRM score over 70) have a much lower pregnancy rate than women with severe Endometriosis whose score is between 40 and 70. As a result, some physicians believe that women with the most severe cases should not even waste their time trying to conceive in the usual manner. These women should go directly into IVF.
In that best of all possible worlds, this is probably true though I have had a number of women conceive even with very severe disease. Unfortunately, we do not live in a perfect world and it is getting less perfect. More and more insurance companies are cutting back on infertility benefits — more and more infertile women will not get the care they should have.
Pennsylvania Blue Cross Blue Shield has eliminated coverage for all Assisted Reproductive Technologies, including Intra-Uterine Insemination. To be fair, a few (only a few) Personal Choice plans cover IVF. People living in New Jersey are lucky. The State of New Jersey now requires that all people covered by a plan with more than 50 members must have all infertility care paid for, even IVF.
In fact, according to the information I have seen, every state that borders Pennsylvania requires insurance companies to pay for infertility care! Why not us?
As the insurance companies are “reforming” health care, it is getting worse. Infertility care is becoming like plastic surgery. Those who can afford it will be able to get it but it will be cash up front in the same manner as IVF. Many women, such as those with the most severe cases of Endometriosis, would be better served by IVF but are denied such care by constraints imposed by the insurance companies. I therefore urge you to write your Senators and Members of Congress and insist that whatever health care reforms are initiated include full benefits for infertility.
Even if a national health care reform program is still several years away, the insurance companies are instituting “reforms” on their own now which effectively prevent the infertile couple from receiving any care whatsoever! In fact, despite what President Obama says, the insurance companies are already coming up with schemes to keep you from getting the care you require. They have tons of money to lobby Congress and other legislatures. Politicians listen to money - first, last, and always.
In summary, it is now well established that women who have had open major pelvic surgery for any reason or operative laparoscopy for significant pelvic disease, the likelihood of adhesion formation is very high. Second-look laparoscopy is recommended to reduce the adhesion formation, reduce pain, and hopefully, enhance fertility. There is, however, no evidence that a third laparoscopy (usually) has any beneficial effect. This approach to therapy is presented here as a general guideline. Every woman is different and I individualize therapy based upon the needs of the particular woman and her particular situation.
There is one critically important fact concerning Endometriosis that must always be kept in mind — namely that so long as a woman has at least one functioning ovary, she will continue to have Endometriosis. It may not bother her much, depending upon the therapy that she has gone through, but she cannot ever consider herself to be “cured” until all ovarian function has ceased. Even then, in a small minority of women, the Endometriosis will continue to be a problem. In rare instances, Endometriosis appears for the first time in post-menopausal women. In such circumstances, the Endometriosis is usually located in the bowel.
Endometriosis cannot be thought of as you would think of the common cold or flu, etc. It is not something that can be treated once and then ignored. It is a chronic illness that you will have for many years and decisions concerning therapy must take into consideration not only the immediate problem to be solved but the long term management as well. Even though Endometriosis is a benign disease, it shares many features of a malignancy. It persists despite therapy. It can spread to other parts of the body. It can invade normal tissues, etc. I have seen many women in my office who were told that after six months of Danazol or some other therapy their Endometriosis was cured. It is critically important that you always remember that this is not the case.
Specific thoughts and comments about LASER laparoscopy are also necessary. When LASER laparoscopy first came into common use in the late 1980’s, many GYN’s started doing it. Very quickly the debate started as to what was the proper technique for treating Endometriosis by LASER laparoscopy. Opinions ran from those who advocated lasering the entire pelvis (even “normal” tissues) to those who said that a LASER should never be used.
What is true is that I am seeing more and more women whose pelvic pain is not due to the Endometriosis they once had but to severe scar tissue in the pelvis created by repeated operative laparoscopies. The rule has usually been that if a woman undergoes a laparoscopy for Endometriosis and a LASER is available in the operating room, it will be used. More importantly, if a woman has documented Endometriosis and has recurrent or persistent symptoms, she will probably undergo repeated operative laparoscopies — especially if she has changed physicians in her pursuit of relief from pain.
However, repeated operative laparoscopies for early Endometriosis is definitely counterproductive. A woman who is in pain after repeated operative laparoscopies is probably in pain more as a result of scar tissue created by the surgery than the Endometriosis itself.
I am now convinced that these repeated operative laparoscopies, particularly if only superficial, “freckle” disease is present, cause more harm than good. This is particularly true if the physician performing the laparoscopy is too timid and only “brushes” the implants with the laser beam. This superficial lasering does not treat the disease adequately and ultimately causes more harm than good. If Endometriosis is to be treated through the laparoscope, it must be completely treated — not partially.
We also know that the natural history of Endometriosis is that it worsens by invading the deep pelvic tissues and causes dense scar tissue. Repeated lasering does the same thing. I have now seen a number women in severe pain with dense scar tissue in the pelvis but virtually no visible Endometriosis. Because of the dense scar, hysterectomy does not always relieve their pain.
One last comment about LASER laparoscopy. If you search the Internet, you will find a number of websites devoted to Endometriosis and Pelvic Pain. Keep in mind that much of what you find is incorrect and often very self-serving. It has been estimated that half of the medical information on the web is incorrect. What you will quickly find is that there is a considerable divergence of opinion as to the proper surgical technique to be used in treating Endometriosis. The important lesson to be learned is that there is no one technique that fits everyone. Furthermore, while some physicians may claim that Endometriosis should only be excised (cut out), others can show that equally good results can be obtained with either a laser or electric cautery. No one has proven that any technique is better than any other. It is more a function of the surgeon, not the instrument.
I personally feel it is incorrect to lock yourself into a position from which you cannot retreat. As has been said, if your only tool is a hammer, every problem becomes a nail. There are many patients in whom I use a combination of techniques — laser, cautery, or excision. In many instances, Endometriosis in certain locations is better treated by one technique as opposed to another. I do not believe you do your patient a favor by being so locked into one philosophy or technique that you are precluded from doing what is best for that patient rather than what your reputation “demands” what you do.
Adenomyosis is a common problem that usually affects women in their thirties and forties, particularly if they have had children. It is a variant of Endometriosis. Both are diseases in which the endometrium (the tissue that lines the uterus) implants and grows in locations outside its normal location inside the uterus. Many women with Adenomyosis will have Endometriosis as well.
Both Endometriosis and Adenomyosis involve the growth of the endometrium - the lining of the uterus - outside the uterine cavity. In the case of Endometriosis, the endometrium is growing completely outside the uterus, involving other pelvic tissues and organs.
In the case of Adenomyosis, the endometrium actually invades the muscle wall of the uterus. However, it still remains confined within the uterus itself.
The symptoms of Adenomyosis include periods that are very heavy and/or very painful. It does not, as a rule, produce pelvic pain between periods and it usually does not produce painful intercourse — but it may.
Pelvic examination will often reveal a uterus that is enlarged and sometimes quite tender, particularly if the woman is examined at or near the time of her menstrual period.
Vaginal ultrasound will demonstrate the uterus to be diffusely enlarged and the echo pattern of the muscle wall of the uterus (using vaginal ultrasound) will often be altered. Many times the woman is thought to have fibroids because of the enlarged uterus but ultrasound will not demonstrate them to be present.
There are other clues you can get from an ultrasound that will make the diagnosis of Adenomyosis. First, please understand that under normal circumstances, the front and back walls of the uterus will be of approximately equal thickness. In Adenomyosis, there is often a significant discrepancy.
Occasionally, ultrasound will show small cysts within the myometrium (the official name for the muscle wall of the uterus).
Performing a simple office ultrasound call a “sonohysterogram” very often will also help make the diagnosis. A sonohysterogram is an ultrasound in which a very thin catheter is inserted into the uterus and saline is then injected. This allows visualization of the inside the uterus — something not possible with a standard ultrasound.
Normally, a sonohysterogram is a painless procedure. However, in women with Adenomyosis, either insertion of the catheter or instillation of the saline will provoke uterine cramping and sometimes pain. Very often, the sonohysterogram actually reproduces the pain the woman has been experiencing. When this occurs, it almost certainly makes the diagnosis and very often helps identify the cause of pelvic pain for which an answer was not always apparent.
I see this often in women who have pain that is mainly on one side or the other. The uterus is a “midline” organ and therefore (theoretically) should produce midline pain. However, I have seen many women who, during a sonohysterogram feel pain on one side or the other — the side where they were feeling the pain. In these instances, it is obvious that the source of the pain is the uterus even though the woman’s symptoms suggested some other cause.
Definitive diagnosis can sometimes be made by laparoscopy at which time a needle biopsy of the uterine wall is performed. Because Adenomyosis is a diffuse process, the needle biopsy may obtain tissue from affected areas. However, having done this numerous times, my experience is that a biopsy actually showing the Adenomyosis is rare. As a result, I no longer do them. If the uterine biopsies are not definitive, MRI of the pelvis will often show the disease.
Because Adenomyosis usually occurs in women in their late thirties and forties who have already had children, future pregnancy is often not a consideration. For these women, hysterectomy is the treatment of choice.
If the woman is not interested in undergoing hysterectomy, long term GnRH suppression with Estrogen Replacement Therapy is the next best therapy.
The Progesterone containing IUD (the Mirena) is often very effective in relieving the symptoms of Adenomyosis. The IUD is good for 5 years before it has to be changed.
Most of the evidence currently available indicates that women who have Adenomyosis are infertile. Because of the diffuse invasion of the myometrium (the muscle wall of the uterus) by the endometrial tissue, conservative surgical removal is impossible.
There are now a few reports in the medical literature of women who have successfully conceived with Adenomyosis following six months of GnRH suppression, similar to the treatment of women with severe Endometriosis. It is at least an option that should be offered rather than immediately proceeding to hysterectomy which previously was the only therapy available.
There are also reports that Uterine Artery Embolization is effective for the treatment of Adenomyosis. However, most insurances will consider this to be experimental and therefore will not cover it, even though it is a simpler procedure than hysterectomy.
In the case of Adenomyosis, removal of the uterus alone is sufficient. Removal of the ovaries is not as important as it might be with Endometriosis. However, many women with Adenomyosis also have Endometriosis in which case removal of the ovaries is something that needs to be considered.
LAPAROSCOPY OR NO
When I see someone in the office complaining of pelvic pain, I can tell with a high degree of accuracy, based upon the woman’s symptoms, physical examination, ultrasound, etc., whether or not I think she has endometriosis. However, just knowing whether someone has endometriosis is only the beginning. Therefore, it is almost always that I will recommend a laparoscopy even if you have had such surgeries in the past. The reasons are as follows:
First, even though I am usually correct when I tell someone they have endometriosis, no one is perfect and establishing an accurate diagnosis is of paramount importance.
Not only is knowing whether someone has endometriosis important, we must also determine the severity of the endometriosis. This cannot be determined by any means other than direct visualization by laparoscopy. Since there is no correlation between the amount of pain that a woman may experience and the amount of endometriosis that she has, laparoscopy must be done. This is of importance in helping to manage chronic pelvic pain in general - it is essential for the woman who is trying to become pregnant.
If a woman is coming to me for infertility and we believe she has endometriosis, “staging” the endometriosis is a very important part of her management.
This becomes a “Catch 22”. If I knew in advance that the woman had early stage endometriosis (minimal or mild), then a laparoscopy is of lesser importance. Although it has been shown that surgical treatment of early stage endometriosis does improve a woman’s chances of conceiving, the benefit to be gained from the surgical procedure is really not all that much. A compelling argument could be made to avoid the surgery.
However, if the woman has late stage endometriosis (moderate or severe), then surgical correction of her disease will significantly improve her chances of conception and, therefore, it needs to be done. Since we can’t tell in advance how bad the endometriosis is, the laparoscopy becomes necessary.
Even if a woman has had a previous laparoscopy at which time endometriosis was definitively diagnosed, I still will need to do another laparoscopy and the reasons are as follows:
The majority of women with pelvic pain have more than one reason for that pain. (Please refer to my pamphlet devoted to pelvic pain). It, therefore, becomes critically important to identify every pain generator in the pelvis. Unfortunately, General OB/GYN’s are not taught about this problem during their residency and, unless they have a specific interest in chronic pain, they simply were never taught how to identify many of the causes of pelvic pain such as inguinal hernias, Spigelian hernias, sciatic hernias, pelvic congestion syndrome, uterine anomalies, etc. I have seen many many patients in my office over the years who had had previous laparoscopies where endometriosis was diagnosed but many of their other problems were missed.
Although I fully understand a patient’s reluctance to go through a surgical procedure, if pelvic pain is a significant issue for you, the only way to really begin to identify and treat all the possible causes of your pain is to do a laparoscopy.
ARE YOU TOO YOUNG TO HAVE A LAPAROSCOPY?
As I have already mentioned, at one time it was believed that teen-age girls and young women did not get Endometriosis. Since the advent of laparoscopy, we now recognize that Endometriosis frequently occurs in teenage girls. It is by no means rare in young women of this age.
Despite this, I have seen a number of women who, over the years, have suffered needlessly because, when they were teenagers, that they were “too young” to have a laparoscopy. As a result, these women had severe pain with their periods and were often disabled with severe pain between periods. They suffered for years and years because the proper diagnosis was never established and appropriate therapy was never implemented.
If a person has symptoms of a disease that are significant, that person deserves appropriate diagnostic testing, regardless of age. If you had symptoms of appendicitis, you would not be too young for surgery. Why should Endometriosis be any different?
Since we now know that 70% of teenage girls with chronic pelvic pain have Endometriosis, the idea that a teenage girl is too young to have a laparoscopy is nonsense. Teenage girls with severe pelvic pain are just as deserving of a proper diagnostic evaluation and treatment as are women in their 20’s or 30’s.
ENDOMETRIOSIS AND CANCER
One question frequently asked by women with endometriosis concerns the possible relationship between their endometriosis and the development of some form of cancer. There has not been much data developed concerning this issue but there has been some recent publications offering some new information.
There are several issues that need discussion. First, is whether or not endometriosis itself becomes malignant.
I treat as much if not more endometriosis than anyone else in the metropolitan Philadelphia area. In over twenty-five years of practice, I have only seen one case of endometriosis itself become malignant. Therefore, such a transformation must be exceedingly rare.
This becomes a relevant issue when women with a history of endometriosis either undergo a hysterectomy or go through natural menopause. In the discussions that I have with these women, I am frequently asked whether the estrogen therapy will stimulate the endometriosis (it might) and whether that stimulation will cause it to become malignant (we don’t know). It is certainly well established that if a woman still has her uterus and is given estrogen alone (without progesterone) there is a small but measurable increase in the risk of developing uterine (endometrial) cancer.
Since endometriosis implants are in fact endometrium, it would seem reasonable to conclude that they too are capable of undergoing the same sort of malignant transformation as the normal endometrium inside the uterus. However, I have never seen this happen. The one case of endometrioid cancer arising in endometriosis that I have seen occurred in a premenopausal woman who had not been taking any Hormone Replacement Therapy.
It must be kept in mind that the endometrium in the endometriosis implants is not normal endometrial tissue. Studies have been done that show this tissue does not always respond to hormones the same way the normal tissue inside the uterus responds. This may serve as a protective mechanism.
Another issue is the fact that it has only been relatively recently that large numbers of postmenopausal women with a history of endometriosis have been given Hormone Replacement Therapy. It will take another five to ten years to determine whether there is cause for concern.
If a woman undergoes a hysterectomy with removal of her tubes and ovaries (the only “cure” for Endometriosis), she should take estrogen afterwards. No one really knows whether she should take progesterone as well. It is something that needs to be fully discussed with any woman in this situation.
The other major issue is whether women who have endometriosis are at increased risk to develop other forms of cancer. A recent study from Sweden suggests that women with a history of endometriosis are more likely to develop breast cancer, thyroid cancer and non-Hodgkin’s Lymphoma. These cancers were noted to be more common in women with non-ovarian endometriosis and adenomyosis.
An increased risk of ovarian cancer was noted in women with ovarian endometriosis.
This is the first report that I have seen suggesting an increased risk of these cancers in women with endometriosis. The fact that this report came from Sweden may been significant. I have seen other epidemiological studies reported from Sweden where the statistics were faulty. Many of these studies looked at small groups of patients and then tried to project those numbers onto a larger population. These kinds of statistical analyses may suggest a relationship but do not prove it definitely.
The question naturally arises - why do women with endometriosis develop these cancers more frequently? It is less likely that having endometriosis itself somehow predisposes women to develop these cancers. It is much more likely that women with endometriosis develop these cancers because they share common causes.
As I have indicated elsewhere in this pamphlet, there is now overwhelming evidence that environmental pollution plays a major role in the development of endometriosis. Endometriosis can be induced experimentally in monkeys by giving them PCB’s and dioxin. We know that our environment is heavily polluted with both of these substances.
There is also very strong evidence suggesting that breast cancer is related to PCB and dioxin. The chemical industry does not want you to know this because they are afraid of the lawsuits that will be generated. Nonetheless, there is good data to suggest a strong link. Since both endometriosis and breast cancer are linked to dioxin, this may be the common denominator.
There is also evidence linking non-Hodgkin’s Lymphoma to environmental pollution as well.
It is not so easy to develop a common link between ovarian endometriosis and ovarian cancer. If there were such a link, one would expect that endometriosis of the ovary would lead to endometrioid cancer of the ovary but this is a very rare form of ovarian cancer.
A more likely explanation is that endometriosis is associated with reduced fertility. Women who have never had children are at greater risk to develop ovarian cancer. Each baby reduces a woman’s risk of ovarian cancer by twenty percent.
It also must be mentioned here that those women who have undergone hormone treatment for the correction of infertility are NOT at increased risk to develop ovarian cancer. There were a few published papers several years ago suggesting an increased risk in women who took either Clomiphene or Pergonal (or similar drugs). A recent publication clearly showed that there is no increased risk.
It is important that you understand that this is only preliminary data but it is important to keep it in mind - particularly for those women who are contemplating hysterectomy. The decision to remove or conserve at least one ovary must be balanced against the possible increased risk of ovarian cancer. As I have already noted, there is the unknown risk of developing cancer in the endometriosis implants themselves although I believe that time will prove this to be a very rare complication.
ENDOMETRIOSIS AND OVARIAN CANCER UPDATE-2012
In early 2012, a paper was published that for the first time (at least to my knowledge) showed that women with endometriosis are at increased risk to develop ovarian cancer. However, the malignancies they did develop tended to be less aggressive tumors than the common garden-variety ovarian cancer that is already wide spread by the time it is diagnosed in most women.
This, if nothing else, provides a compelling argument for removal of the ovaries at the time of hysterectomy for women who have chosen that therapy to treat the disease.
For the woman with endometriosis does not require hysterectomy, she needs to be aware that her ovaries need careful monitoring to make sure that nothing develops.
ENDOMETRIOSIS TREATMENT SUMMARY
The following is an overall summary of the treatment best suited for a woman with endometriosis, taking into consideration all of the various factors involved. Obviously, with a disease as variable and unpredictable as Endometriosis, there will always be an exception. What I have tried to state in this section are general principles to give you basic guidelines to help you decide which therapy is best for you.
It is also important to keep in mind that Endometriosis is still fundamentally a surgical disease even though hormonal therapies help to control it.
The first question to be answered is whether or not the woman wants to become pregnant now, whether she would like to become pregnant at some time in the future, or whether she is not interested in ever becoming pregnant.
SECTION I - PREGNANCY NOW
1. Evaluate male fertility with a semen analysis and postcoital tests.
2. Evaluate menstrual cycle to determine whether ovulation is occurring normally.
3. Carry out a laparoscopy.
If the endometriosis is minimal or mild (based on the ASRM* classification), there is no significant ovulatory abnormality, there is no male factor, the duration of the infertility is less than a year or two, and the woman is under 30 years of age, waiting 3-6 months to see if a spontaneous conception will occur is an option. However, more aggressive therapy using Super-Ovulation combined with IUI will significantly increase the woman’s chances of becoming pregnant..
If the endometriosis is minimal or mild and the duration of the infertility is more than two years, the treatment of choice is Superovulation with Intra-Uterine Insemination. Gonadotropin therapy is the best treatment unless you are covered by an HMO or other insurance which does not pay for these drugs. In such instances, Clomiphene must be used. The results are not as good as with Gonadotropin therapy, but better than no therapy at all.
If the endometriosis is low in the moderate range, a surgical laparoscopy followed by the institution of Superovulation therapy with IUI, is the treatment of choice.
If the endometriosis is high in the moderate range (according to the ASRM classification), a surgical laparoscopy followed by 6 months of GnRH followed by Superovulation with IUI is the best approach.
If the endometriosis is severe, a operative laparoscopy will be performed. Following this several months of GnRH (Lupron or Synarel) suppression is instituted followed by a second look laparoscopy. After the second look laparoscopy, the GnRH suppression is maintained until the woman has been on the drug for a total of six months. Following this, Superovulation with IUI is instituted. However, I have had many women conceive without additional therapy following this treatment regimen,
If the Endometriosis is very severe (ASRM score > 70), the disease is frequently too extensive to safely and (more importantly) appropriately treat by laparoscopy. In such instances, after the initial laparoscopy which assesses the severity of the disease, the woman should go on GnRH suppression for 2-3 months, followed by open surgery, followed by a second look laparoscopy. The GnRH is maintained for a total of 6 months.
I realize this a lot to ask a woman to undergo. However, you must understand that if the ASRM score is that high, you are dealing with very very severe disease that must be aggressively treated if a successful outcome is to be achieved.
The therapies mentioned are only a broad outline and are obviously subject to modification. The most critical factor in determining which therapy will be chosen is often the couples’ insurance coverage and what it will or will not pay for – not what is necessarily best for that couple.
SECTION II - PREGNANCY SOMETIME IN THE FUTURE
If a woman with endometriosis is desirous of becoming pregnant at some time in the future but not when she initially presents for treatment, a operative laparoscopy should be carried out. Following this, GnRH suppression with Estrogen Replacement Therapy is the treatment of choice. This therapy can be maintained almost indefinitely until the woman is interested in conceiving. Other types of hormonal suppression can also be used, depending on numerous factors too variable to be discussed here. It is important to understand that GnRH therapy is the best but a satisfactory result can be obtained with other drugs as well.
If a woman undergoes a laparoscopy for endometriosis and is not interested in becoming pregnant at that time or in the immediate future, she must be put on some sort of hormonal therapy following the surgery. Otherwise, the benefits gained from the surgery will be lost and you are almost guaranteeing that woman will need additional surgery.
Just as important, without hormonal suppression after the surgery, the odds are overwhelming that the endometriosis symptoms will recur.
My experience over the years has been back to most women who have been put on hormonal suppression therapy after their surgery are treated with birth control pills. My experience is that birth control pills are the least effective therapy for endometriosis although they do work for some women.
Another problem which I frequently see deals with women who have been put on the pill and they do not work. More often than not, her birth control pill then is switched to another brand, often multiple times. It is important to understand that despite the drug companies advertising hype, all birth control pills are the same. If one birth control pill does not work, changing to another pill won’t work either.
SECTION III - FUTURE PREGNANCY IS NOT A CONSIDERATION
If a woman is not interested in preserving or enhancing her future fertility, a laparoscopy must still be carried out to establish a definitive diagnosis and “stage” the disease. It is also extremely important to make sure there are no other problems causing or contributing to the woman’s pain. Decisions as to future therapy can then be made based upon all the information available, especially whether or not other causes of the woman’s pelvic pain were found at the time of laparoscopy. The following therapies should then be offered.
Following the laparoscopy, the woman should go on GnRH suppression for a period of three to six months. This is done because the GnRH suppression mimics the effect of a hysterectomy. Hysterectomy is the definitive treatment for most women with significantly symptomatic endometriosis.
For reasons that I cannot fully explain, it has become increasingly apparent that women under 40 do not seem to tolerate hysterectomy as well as women older than forty. This is particularly true if the ovaries are going to be removed which is an integral part of endometriosis therapy. Therefore, the following approach is recommended to take all of these factors into consideration. There is no one therapy that is best. Each therapy is tailored to the needs of the woman. It may take several months of trial and error to determine which is best for a given person.
If Endometriosis is found and felt to be the main cause of the woman’s pain, GnRH suppression for 3-6 months is one option. The GnRH suppression can then be stopped to determine whether there is any carry-over effect. Some women will experience a temporary remission of their endometriosis symptoms following discontinuance of the GnRH. Unfortunately, this is usually not a permanent solution and the pain usually comes back.
Some women will elect to maintain the GnRH indefinitely as alternative to hysterectomy. Estrogen Replacement Therapy must be added to control menopausal symptoms and prevent or reduce the deleterious effects of the low estrogen levels created by the GnRH.
If the endometriosis symptoms recur, then hysterectomy with retention of the ovaries should be carried out. Laparoscopic removal of the ovaries would then be offered if the endometriosis symptoms recurred.
The decision to keep or remove the ovaries is often complicated and will be discussed in the next section.
If GnRH suppression does not relieve the endometriosis symptoms, depending upon the nature of the disease, the nature of the symptoms, the location of the pain, etc., a full evaluation must be undertaken to determine whether other causes of pelvic pain may be present. Failure of the GnRH to relieve the pain may mean that hysterectomy will not either.
One of the biggest arguments and problems surrounding hysterectomy in general and especially hysterectomy for Endometriosis, is whether or not the ovaries should be removed. As I have already pointed in other pamphlets, there are certain clinical situations which demand bilateral oophorectomy. These include a hysterectomy that has been performed for uterine cancer or ovarian cancer.
If the hysterectomy has been performed for endometriosis or other problems, the arguments are less clear. There is still a debate and the issue may never be completely resolved. I would like to give you at this time my personal opinion and the reasons why I believe what I do. However, it is still a matter of choice for the woman in most instances. Newer advances in medicine have also forced a reappraisal and the issue is far from settled.
The ovary has 2 principal functions — the making of eggs and the making of estrogen. Obviously, both are necessary for the woman to have children. Once the uterus has been removed, the reproductive capability of that woman is usually no longer a consideration and therefore, only the ovary’s hormone production is of significance. I am not aware of any scientific evidence that the estrogen produced by the woman’s ovaries, if they are left in place, is any better for her than the estrogen she would take by mouth if the ovaries were removed.
However, the ovaries produce other hormones beside estrogen. The other main hormone produced by the ovary is androgen - male hormone. In fact, the ovary continues to produce significant amounts of androgen after menopause, even though estrogen production decreases.
Admittedly, for years we minimized or ignored the significance of the ovarian androgen production. Now, however, evidence is that the androgens are beneficial and that women will do better if their ovaries are left in place. Certainly, in some women, a normal sex drive is dependent on ovarian androgen production.
This is not to say that there a compelling reasons to remove the ovaries in some women. Each woman must be assessed individually and the best decision for her made.
First of all, it is actually technically easier to remove the ovaries that it is to leave them in place, notwithstanding a common myth to the contrary. While this is not a major factor, it is nonetheless true. Furthermore, an ovary left in place may become adherent to the side of the pelvis or to the top of the vagina. In such instances, it can produce considerable pain.
3-5 % of women who undergo hysterectomy in which the ovaries are left will subsequently undergo surgery to remove those ovaries. While this is certainly not a large number, if you are in that group, it means a second operation for you.
If a woman has a hysterectomy for endometriosis and the ovaries are left, she has a 50% chance of requiring another surgery within 5 years. Women who undergo a hysterectomy for Endometriosis and have the ovaries removed have a 90% chance that their pain will be substantially better. If the ovaries are left in, only 60% will get relief. Each woman needs to make up her mind based on these facts. Nonetheless, if that woman is young, it may be better to leave at least one ovary and take a chance.
If a woman undergoes removal of her ovaries before the age of 35, her chances of subsequently developing breast cancer are reduced. One out of 9 women in this country will develop breast cancer over her lifetime. If a woman has her ovaries removed at a young age, this will reduce her risk. If the woman has a strong family history of breast cancer, I personally believe that if she has a reason for hysterectomy, removal of the ovaries should be strongly considered.
The most common cancer of the female reproductive tract is cervical cancer and the second most common cancer is uterine cancer. Cancer of the ovary is number three. However, we have good diagnostic and therapeutic measures for cervical and uterine cancer. Therefore, our ability to cure women of these two malignancies is good.
On the other hand, we do not have a good early warning system for ovarian cancer and, therefore, although ovarian cancer is number three in frequency, ovarian cancer is the leading cause of death from pelvic malignancy. Removal of the ovaries at the time of hysterectomy at least insures that women that she need never worry about ovarian cancer.
What about arguments in favor of leaving the ovaries, when possible? One is the fact that the woman will not have to take any hormones until she goes through natural menopause at approximately age 50.
Also, in addition to estrogen, the ovary makes male hormone (androgen) which we know is the hormone responsible for your sex drive. I have seen women who suffered a noticeable loss of sexual desire and sexual response following hysterectomy with removal of the ovaries at a younger age (under 40). Occasionally, even older women will notice a decrease in libido when their ovaries are removed. Furthermore, most of these were women undergoing hysterectomy for endometriosis so that 1) removal of the ovaries was advisable and 2) they had no regrets concerning their surgery since their pelvic pain and other symptoms were relieved.
It is possible to give these women male hormone and this is usually successful in correcting their sexual problem. Unfortunately, the levels of male hormone necessary to improve sex often result in hair growth on the chin, acne, and other symptoms of increased androgen. However, these women, when offered a choice, would usually rather pluck than lose their sexual response.
I am trying to be fair and present a complete picture. The number of women whose sexual desire suffers following removal of the ovaries is small. Furthermore, I have many women in my practice who, in their 30’3 and 40’s, have no sexual desire at all despite having normal ovarian function. Sexual desire in women is far more complex than just hormones.
I have also reached the conclusion that younger women do not seem to “tolerate” hysterectomy as well as older women. Age 40 seems to be the cutoff. I cannot tell you why and there is no known scientiﬁc reason why this should be so. I doubt it is something that could be proven scientiﬁcally. Nonetheless, I do feel that a younger woman who would signiﬁcantly beneﬁt from hysterectomy and yet her life and/or health would not be compromised if it were not done should seek alternatives such as a myomectomy, operative laparoscopy, operative hysteroscopy, endometrial ablation, or GnRH suppression in an attempt to avoid hysterectomy.
I have seen many women in my office for a second opinion for hysterectomy where the initial recommendation did not offer any alternatives. The feeling was — either have the hysterectomy or suffer. The fact that there are other therapies was not mentioned.
The arguments pro and con concerning estrogen therapy are covered in another of my pamphlets in much greater detail but I would like to at least summarize them here as part of this discussion. It is my firm conviction that all women after menopause, be it natural or surgical, should be on estrogen therapy for the rest of their lives.
There is no significant risk to taking estrogen after menopause despite all that you might read or see on TV. There is without question a significant decreased risk of osteoporosis, major fractures, and heart disease in women who receive estrogen therapy following menopause. There is increasing evidence that estrogen reduces the risk of colon cancer and Alzheimer’s disease. Estrogen therapy probably reduces the risk of developing cataracts. Women who take estrogen live longer, healthier lives.
Many women are confused about hysterectomy because of the many myths that abound. The situation is further complicated by several groups of “true believers”, organizations who are vehemently anti-hysterectomy. To the members of these groups, hysterectomy is tantamount to abuse. I have read their literature and it is based on myth and half-truths. They take the one woman who may have had a problem following hysterectomy and try to make others think that she is the rule — not the exception. Furthermore, although they are against hysterectomy, they have no alternative solutions for the woman with serious pelvic problems except to live with them. Their attitude is “Don’t have a hysterectomy — SUFFER”! Most women with significant pelvic disease find that to be an unacceptable option.
The more recent feeling (as of 2011) is that at least one ovary should be left in unless there are compelling reasons to remove both. If a woman loses both ovaries at a young age and does not take estrogen, she has a significant increased risk of heart disease.
I have only tried to give you some of the highlights of the discussion as to whether or not the ovaries should be removed or left. Obviously, you and I will have a long discussion before any final decision is made.
In summary, I am more and more leaning toward ovarian conservation, especially in younger women. Yes, it is a calculated risk, especially if the hysterectomy is done for Endometriosis. There is the risk of needing additional surgery. Nonetheless, the problems associated with a significant decrease in libido can be as devastating as the possibility of another operation. Each woman must decide for herself.
ENDOMETRIOSIS and HEREDITY
IF YOU OR A CLOSE FAMILY MEMBER HAS ENDOMETRIOSIS, IT IS VITALLY IMPORTANT THAT YOU READ THIS.
Endometriosis is a hereditary disease. It is not as simple as the color of your hair or the color of your eyes. Although the genetics is far more complex, we do know that Endometriosis occurs seven times more frequently when there is a family history of the disease than if there were not.
A large study recently completed by The Endometriosis Association has provided strong evidence about something which we had long suspected but did not have sufficient data. This study showed that not only does Endometriosis have a hereditary and familial tendency, certain other diseases are also more likely to occur in women and relatives of women with Endometriosis.
The Endometriosis Association study showed that there is an increased risk of breast cancer, ovarian cancer, and melanoma in women and in the relatives of women who have Endometriosis. Some of this is not new information - there have been studies in the past that have suggested this - but the data was never strong enough to come to any firm conclusions. This most recent study surveyed over 20,000 women.
If you or a close family member has Endometriosis, it is critically important that you be screened periodically for breast cancer (simply good medicine anyway) and ovarian cancer. Screening for breast cancer involves a yearly mammography beginning at age 40. If, however, you have a first degree relative (mother, sister, or daughter) who developed breast cancer younger than age 45, mammography should be started five years before the age at which that woman was diagnosed with her breast cancer.
We do not, as yet, have as good a screening technique for ovarian cancer as we do for other diseases such as breast cancer and cervical cancer. Nonetheless, a recent study published in the British journal “The Lancet” did show that yearly vaginal ultrasound exams were of benefit in increasing the likelihood of early diagnosis.
The association between melanoma (the deadliest form of skin cancer) and Endometriosis is less obvious. Nonetheless, there has been evidence over the years to suggest that women with Endometriosis have a higher incidence of melanoma and certain pre-malignant skin conditions.. This most recent study now indicates that their close relatives have an increased risk as well.
The best screening for melanoma is to be evaluated periodically by a Dermatologist. I would, therefore, suggest that you, if you have Endometriosis, or any close relatives of a woman with Endometriosis, see a Dermatologist for an initial screen. Follow-up exams would then be scheduled based upon the Dermatologist’s recommendation. You may have to educate the Dermatologist — many are not aware of this association.
The studies have also shown that the families of women with Endometriosis have a higher risk of non-Hodgkin’s lymphoma.
Several other important findings from this study include the following: the incidence of diabetes in the general population is approximately 6%. However, in the families of women with Endometriosis, the incidence is 42%!
Women with Endometriosis have a higher incidence of thyroid disease including an underactive thyroid (Hypothyroidism), an overactive thyroid (Hyperthyroidism or Graves’ Disease), and Hashimoto’s Thyroiditis (an autoimmune disease that is very common in women).
In addition, other autoimmune diseases that are seen somewhat more frequently in women with Endometriosis and in their immediate families include Rheumatoid Arthritis, Lupus, Multiple Sclerosis, and Meniere’s disease.
DISEASES IN WOMEN WITH ENDO OR THEIR FAMILIES
DISEASE WOMEN WITH ENDO THEIR FAMILIES GEN POPULATION
HYPOTHYROIDISM 7% 15% 2%
HYPERTHYROIDISM 1.5% 6% 1%
HASHIMOTO’S 2% 2% 0.01%
RHEUMATOID ARTHRITIS 2% 17% 0.8%
LUPUS 0.8% 6% 0.05%
MULTIPLE SCLEROSIS 0.6% 6% 0.1%
MENIERE’S DISEASE 0.9% 3% 0.2%
These findings are not surprising. There has been a large body of evidence accumulated over the last 10 to 15 years that Endometriosis is, in large part, an autoimmune disease. Many of the diseases that are found more frequently in women with Endometriosis and their immediate families are also autoimmune. Most thyroid disease is autoimmune in origin. Juvenile or Type 1 diabetes is definitely autoimmune. Some instances of what we believe to be so-called adult onset diabetes - Type 2 - may actually be another variant of an autoimmune disease as well.
What these studies are now beginning to address is the issue that Endometriosis frequently occurs in young women. By identifying such women and monitoring them carefully we may be able to prevent them from developing more serious problems later in life. The various cancers mentioned in this study - especially ovarian cancer and breast cancer - were diagnosed at a younger age in women with Endometriosis than in women who are not affected.
Please understand that this newer information is the result of a large study conducted by The Endometriosis Association. If you have Endometriosis, please join. If you know of someone with Endometriosis, please ask them to join. It is only with our continued support that important studies like this will be able to provide us with the important information we all need. You may contact The Endometriosis Association at 1-800-992-3636.
They may also be contacted on the internet at www.endometriosisassn.org.
In summary then, you can appreciate that Endometriosis is a very common and very complex disease. It varies significantly in its severity, in the severity of the symptoms it produces, and its effect on the woman’s health and fertility. Because of the tremendous variability of the disease, each woman or couple must be treated in an individualized fashion selecting those therapies that appear to have the best chance of success. I hope that this discussion has given you better understanding of the disease and a better understanding of what it is I am trying to do.
HOW TO SUSPECT YOU MIGHT HAVE ENDOMETRIOSIS
If you have been given my endometriosis pamphlet, it is because, as a result of our office discussions, I am suspicious that you may have this disease (unless you have been previously diagnosed with it).
One question that immediately comes to mind for many people are – why did I suspect that you might have this disease? I wanted to share with you some of the signs, symptoms and other criteria that I use in determining whether or not I think a woman has endometriosis or not.
1. PELVIC PAIN
We have known for many, many years that endometriosis is the most common disease associated with chronic pelvic pain. This does not mean that every woman with chronic pelvic pain has endometriosis. Just as important, it does not mean that just because you have endometriosis that it is the cause of your pain. Nonetheless, if you are suffering from a chronic pelvic pain syndrome, endometriosis has to be high on the list of possibilities.
The three main symptoms of endometriosis are pain, pain and pain. Women with endometriosis will have painful periods, pain in between their periods, and pain with intercourse. Some will have only one – some may have all three.
Sometimes, it is not the severity of the pain but the pattern of the pain that raises a red flag.
Even though I firmly believe that painful periods are never normal, many women have cramps with their periods that are mild and occur only on the first day or two of the flow. While these women certainly might have endometriosis, in the overall scheme of things, it is not very likely. However, if a woman tells me that her menstrual pain begins several days or longer before the flow actually starts, if that woman tells me that her menstrual pain lasts throughout the entire flow, or if that woman tells me that the pain actually will persist after the flow has ended, these are big red flags for endometriosis.
Many teenage girls have menstrual cramps. They usually disappear by the time she get to her early 20’s. If a woman continues to have cramps in her mid-late 20’s or 30’s, endometriosis has to be strongly considered.
As I have said elsewhere and have no doubt told you in the office, deep pain with intercourse is never normal and in my experience, is always an indicator of some organic pelvic disease. I have seen one or two exceptions to this over the years but they are very, very rare. Even in those instances, it could be argued that there is a pelvic abnormality that was creating the pain.
Entry pain with intercourse is usually a symptom of some organic pelvic disease but there are some exceptions.
Intermenstrual pelvic pain (pain felt at a time other than when you are having your period) is, again, in my experience, almost always a symptom of some organic pelvic disease.
We have known for many years that at least 50% of all infertile women have endometriosis and therefore I immediately begin to suspect it in someone who comes to me with an infertility problem. It does not necessarily mean that the endometriosis is the cause of the infertility, but it may often be a contributory factor.
3. AUTO IMMUNE DISEASE
We have known for a long time that endometriosis is very often associated with autoimmune diseases of various types. If therefore during my history, I learn that either a woman or someone in her family has an autoimmune disease, this is another red flag that a woman herself may have endometriosis.
4. HISTORY OF A “RUPTURED OVARIAN CYST”
As I have discussed earlier in this pamphlet, one of the most common indicators of endometriosis is a woman who comes to me and tells me that she went to the emergency room with severe pain, they did an ultrasound and told her that she had an ovarian cyst that ruptured. When I hear this story, I can almost guarantee you the woman has endometriosis.
5. FAMILY HISTORY
As I mentioned earlier in this pamphlet, endometriosis is a hereditary disease, at least in part. If I learn that a woman has a 1st degree relative (mother, sister, or daughter) with endometriosis, the likelihood of her having endometriosis increases 7 times compared to the general population.
6. PHYSICAL SIGNS
In addition to some of the red flags that I have just discussed, there are things that I look for on physical exam that also make me suspicious that you may have endometriosis.
The uterus is a mid line organ. Under normal circumstances the uterus sits directly in the middle of your pelvis.
One of the signs of endometriosis is when the uterus is pulled to one side or the other. I am not talking about a uterus that is retroflexed (tipped back). That is a common normal variant and although it may be seen with endometriosis, it is extremely common in women who don’t have endometriosis.
However, when I encounter a patient whose uterus is pulled far off the midline, either to the left or to the right, that is a red flag.
The other major red flag is pelvic tenderness. No one likes a pelvic exam. However, a normal pelvic exam should be annoying. You should feel pressure. You should never feel pain. Nothing on a normal pelvic exam should make you should say “ouch”.
Tenderness in specific parts of the pelvis are another red flag adds to the presence of endometriosis. The two most common areas are tenderness in the posterior fornix of the vagina and tenderness in the cul-de-sac. The posterior fornix is the area in the upper vagina behind the cervix.
The other area that raises a red flag is tenderness in the posterior pelvis – either the cul-de-sac or the uterosacral ligaments – when felt on rectal exam.
I know that no one likes a rectal exam. However, I am still surprised at how many women I see, women who have had numerous pelvic examinations, tell me that they never had a rectal exam before I did one. If you don’t do a rectal exam, you cannot evaluate the posterior part of the pelvis properly. Many times, as I described earlier in the pamphlet, significant tenderness in the posterior pelvis is one of the most important clues that I get as to the presence of endometriosis.
Based upon my many years of experience dealing with this disease, I very often suspect it in women who come to me for various reasons, even though the fact that they may have endometriosis is not a high priority item.
Just because I suspect that you may have endometriosis does not always mean that we have to do anything about it. The only way to diagnosis endometriosis is by laparoscopy. Not every woman requires a laparoscopy. It depends upon what your main problems are and it depends on whether or not diagnosing endometriosis is an important part of trying to solve your problems.
7. MENSTRUALLY ASSOCIATED UNUSUAL SYMPTOMS
There are a number of scenarios, that although uncommon, when present are almost always an indication of endometriosis. I have seen all of these and when present there is no doubt in my mind that the woman has endometriosis.
For each of these situations, I will, when appropriate give you the medical term and then explain it.
One problem I have seen on several occasions is “catamenial hematochezia”. The term catamenial means anything related to the menstrual cycle. Hematochezia simply means “blood in the stool”.
I have seen several women over the years that have told me that they experience rectal bleeding only when they have their period. This is virtually diagnostic of colon endometriosis. Nothing else I can think of would produce that symptom.
Many years ago I saw a woman who, every time she got her period, literally went into respiratory failure. Her lungs were slowly deteriorating and her pulmonary specialist told her that she would probably die.
When she came to me, she also had classic symptoms of pelvic endometriosis. I proved that she had it by laparoscopy and when I treated her endometriosis, her pulmonary symptoms completely disappeared. She was relatively young, recently married and had a somewhat difficult choice to make (although not really that difficult). She had to decide whether she wanted to have children or whether she wanted to live. She chose the latter and when I did a hysterectomy on her, her pulmonary symptoms completely disappeared and never returned.
I could never explain exactly what was going on with this woman. I spoke to numerous colleagues around the country and even called several people at NIH. My best guess is that she had pulmonary endometriosis and experienced some sort of bizarre allergic or immune reaction to the menstrual blood.
I have seen several patients with “catamenial hemoptysis”. Hemoptysis is the medical term for coughing up blood. Again, although very uncommon when this happens, pulmonary endometriosis almost always has to be the cause.
I have also seen several women over the years with “catamenial pneumothorax”. Pneumothorax is the medical term for literally air in the chest. It can happen to people for a variety of reasons. It simply means that air has gotten into the space between your lung and chest wall. This causes the lungs to collapse.
A pneumothorax is not rare in people who have had an injury to their chest. A broken rib can cause it on occasion. Some people are born with a congenital abnormality where they have tiny blisters on the surface of the lung and if one of these blisters should burst, air can get into the space between the lungs and chest wall.
However, if a woman develops a pneumothorax only when she gets her period, this almost always has to be endometriosis involving the surface of the lung.
It is important to keep in mind that no matter what underlying medical disorder a woman might have, it will always wax and wane with her menstrual cycle. However, the scenarios that I have just depicted involve women who have no other obvious associated medical conditions but who develop very bizarre symptoms in association with their menstrual period. In these cases, endometriosis is almost always the culprit.
8. MELANOMA OR “PRE-MELANOMA
Women with endometriosis have an increased incidence of melanoma. If I see a woman who has a history of melanoma or who has had a mole removed that was considered to be on its way to becoming a melanoma, that is another “red flag” for endometriosis.
INFLAMMATORY BOWEL DISEASE.
A study published in 2012 showed that women with endometriosis are at increased risk to develop inflammatory bowel disease such as ulcerative colitis and Crohn’s disease. Although the reason for this is not known, there is a theory that these two diseases may in fact, be autoimmune, although it has never truly been proven.
The study showed that sometimes the bowel disease may not show up for many, many years after the endometriosis has been diagnosed. Therefore, if you have endometriosis, you need to be aware of this because if you start to have significant intestinal symptoms, you need to be fully evaluated.
* ASRM - American Society for Reproductive Medicine, formerly the American Fertility Society
© Michael D. Birnbaum, M.D. 2013