Kristin Patzkowsky, MD
Endometriomas and fertility
Patient Awareness Day
The Lifecycle of Endometriosis: From Diagnosis to Coping with Disease
Sunday April 17, 2016
Lenox Hill Hospital, Einhorn Auditorium
Thank you, thank you for having me. I am Kristin Patzkowsky and until a year ago I was in New York so it is always nice to come back for any occasion and this is a wonderful event that Dr. Seckin is hosting here today, I am pleased to be a part.
Today I am going to speak about endometriomas and fertility. Before we can get too much into fertility we have to actually talk about what an endometrioma is. An endometrioma is an endometriosis cyst of the ovary, also known as a chocolate cyst. These occur in 20 to 40 percent of patients with endometriosis. It is called a chocolate cyst because when they rupture the fluid within is old blood. It can be thin, it can be thick but it looks like chocolate. We often see them bilaterally on the right and the left. On the picture on the lower right here when they occur bilaterally they are usually referred to as kissing ovaries. They tend to scar to the back wall of the uterus and they kiss – meet in the center.
Endometriomas, unless they are incredibly small and only on one side, typically are pretty advanced endometriosis, stage three or four endometriosis. As Dr. Shin referred to earlier we have a scoring system for endometriosis which refers to the extent of disease. What is important to recognize is that the symptoms do not always correlate to the extent or severity of disease. It is not uncommon that I am in the OR doing surgery for fibroids and surprise someone has stage four endometriosis. It is always I find amazing but the symptoms do not correlate to the extent of disease.
The symptoms of endometriomas are similar to the regular old symptoms of endometriosis; pain with periods, pain outside of periods, pain with sex, infertility and no symptoms.
If you have been given a diagnosis of endometriomas does that mean you are never going to have children? No. Endometriosis does not equal infertility. Endometriosis is certainly associated with subfertility but it does not mean infertility. Thirty to 50 percent of patients with endometriosis will have difficulty getting pregnant.
What are the causes of subfertility in the population with endometriosis? We do not totally know. We think we have some ideas but it is still a little bit of a mystery as to why the two are associated. In general we know endometriosis occurs in about 10 percent of reproductive age women and 30 percent of infertility population, so we definitely see it more commonly in an infertility population. We are going to talk about these three causes.
One of the causes that we think is related to infertility is that endometriosis essentially can produce a toxic environment. These implants in the pelvis or implants on the ovaries they are active when your ovaries are working and you are having cycles these implants are producing estrogen, aromatase, cytokines, interleukins and all sorts of inflammatory substances and we think those inflammatory substances can impact the embryo, the ability of an embryo to implant, the receptivity of the endometrium, and especially with endometriomas themselves. An endometrioma is, again, a cyst within the ovary. If you have that sitting in the ovary itself then that can have a negative impact upon the ovarian cortex.
I actually think this is Dr. Seckin’s picture, I just googled it. Endometriosis can cause – this one makes a lot of sense to a lot of people – but can cause infertility because of distorted anatomy. In order to appreciate distorted anatomy this is distorted anatomy I assure you, you have to know what normal anatomy looks like. A normal uterus, this actually has a fibroid, but, a normal uterus looks like the picture on the left, moves around, you can clearly see the ovaries, you can see the fallopian tubes draped over top. In pregnancy an egg is released from the ovary. It travels down the fallopian tube and makes it way to the uterine cavity. If you have a pelvis that looks like this, it makes sense that when the fallopian tube is not even identifiable and not near the ovary any longer and everything is stuck in cement, it makes sense that an egg would have difficulty travelling along the course of the fallopian tube.
Another hot topic these days is endometriosis and its impact on the ovarian reserve. We are going to talk more about ovarian reserve and it is a little bit technical but you are going to hear that a lot if you see an infertility doctor, if you see a doctor who specializes in endometriosis, especially when we are talking about endometriomas. But ovarian reserve essentially refers to your ability to produce quality eggs.
You have your maximum number of eggs before you are even born. Midway through your mother’s pregnancy you have about six to seven million eggs. Once you are born that drops to about a million and then about puberty 300 to 500,000, once you hit menopause, about 1,000. Fertility starts to really decline in the mid-30s as a consequence of diminishing ovarian reserve. There are a lot of tests that we use to measure ovarian reserve, sort of the alphabet soup of testing. A lot of times we throw out these terms, FSH, AMH and AFC. What are they? I think it is important for you to recognize what they are because we do use them a lot, especially when we are talking about ovarian reserve.
FSH is follicle stimulating hormone. It is made in the brain. It is a blood test that is performed and it is sort of an indirect measure of egg quantity. When you are young your brain sends out the FSH telling your ovaries to ovulate. You are young, your ovaries are working great and so very easily, very quickly, a woman ovulates. As you get older and your ovaries are not working as well anymore your brain really has to keep sending out that FSH ovulate, ovulate, ovulate. The pathology behind it is a little bit more complicated but that is essentially the gist. Your FSH increases with decreasing ovarian reserve.
Anti-mullerian hormone – the name anti-mullerian hormone is actually named for what the hormone does in a male fetus during development and has nothing to do with female ovaries. The name does not really make sense, anti-mullerian hormone. This also is an indirect measure of egg quantity. It is made by the little small follicles that are in your ovaries. When you are young and you have lots of great follicles in your ovaries, eggs, then you anti-mullerian hormone is high. As you age and your follicles decline then your AMH naturally goes down.
Your antral follicle count is the only one that is not a blood test. It is actually an ultrasound and literally all it is is you are doing an ultrasound and you are counting how many eggs are in the ovary. On the left that is the beautiful ovary with lots of nice eggs and on the right, what my ovary looks like, with not a lot of eggs.
The other thing that is a little bit helpful is FSH and antral follicle count have to be timed so they are usually around day two, well, FSH day two, day three the antral follicle count would also be in the early phase of your menstrual cycle. Anti-mullerian hormone can be at any point. FSH also cannot be measured if you are on birth control pills because that is not really a true measure of what you are doing on your own.
These are helpful and we like to use them as physicians, especially we like to be able to say “okay, what this number means is XYZ but the problem is, is that these numbers are predictive of how well you might respond to hormonal stimulation so if you have IVF, if you need to have medicines to help you have a baby, these are helpful and they tell us how well you respond, how many eggs you might make. But these are not predictive of your ability to conceive or of egg quality.
The problem with endometriomas and ovarian reserve by looking at women who have endometriosis and comparing them to women who do not have endometriomas we have found that in women who have endometriomas there are fewer eggs in the surrounding ovarian tissue around the endometrioma. It appears that the eggs do not mature as well and there also is a lower antral follicle count and AMH hormone. So that is terrible, we should get rid of them.
Not so much! Because the surgical treatment of endometriomas can also reduce ovarian reserve. It can worse what is already not so great to begin with. This is further increased when you have cysts of both ovaries, if they are bilateral. It also is true any time you are doing surgery especially for endometriomas they are very sticky. It can be difficult to separate the cyst wall itself from the ovary. There is a small risk of ovarian failure or menopause if in the setting of bilateral endometriomas.
This is great but what we really care about from a patient perspective is you do not care about, I mean you do, your antral follicle count and your AMH, what you really want to know is can I have a baby? And similar to FSH, AMH, antral follicle count those are numbers we know that there is a response of ovaries to having endometrioma and to having removal of endometrioma but again, it does not always correlate to your ability to have a baby.
Obviously if your AMH is not measurable and your FSH is in the menopausal range that is a different situation. But when it is sort of, it is always in the grey zone just to make life complicated, but it does not necessarily mean that you will not be able to have a child. In women with endometriomas and infertility we actually know that in the infertile population in the symptomatic endometrioma surgery can improve your chance of spontaneous conception.
When you are talking about IVF actually what we see is that you can have the similar reproductive outcome, so even though I just said that endometriomas have a negative impact and removing the endometrioma can have a negative impact and it can decrease your AMH, when we look at IVF outcomes they appear to be the same whether or not you remove the endometrioma or not. And we think that that reduced ovarian reserve might be due to the endometrioma itself rather than surgery.
You have to think very carefully about when to intervene, whether or not you should intervene and it really is based on several factors, symptoms, if you have huge endometriomas and are in debilitating pain, we have to do something. You cannot get pregnant and go through an IVF cycle if you cannot walk. The size also – there is definitely consensus we really leave small endometriomas alone but when someone has 12 cm bilateral endometriomas there are other things we have to factor in when we are talking about pregnancy, like your ability to even – if you stimulate the ovary are you going to get much? Are you going to be able to reach the follicles that are there? Is there a risk of contaminating if you go get those eggs with the endometrioma fluid? You can potentially see that endometrioma and have infected endometrioma, which is a mess. There are a lot of things that have go be taken into consideration.
Also the larger, and the more complex these endometriomas become we also have to start worrying about the potential for malignancy. While that risk is low it does exist. There are situations where you do have to intervene.
The management of endometriomas is very controversial. There are no clear guidelines. And there really has to be a very thoughtful and thorough conversation between the patient and the physicians, which often includes the infertility doctor as well as the surgeon who might be doing the surgery if not the infertility doctor, which often is not the case.
That is it. Thank you!
