Ok ladies, let’s talk about endometriosis. First of all, what is it and why should we care? For those of you lucky ones who don’t know. Endometriosis is a disease where implants of endometrial tissue set up shop all over the body, especially the pelvis and cause pain and painful and heavy periods. For most of us, while most of that endometrial lining sheds out our vaginas during our periods, some of it backwashes up through the fallopian tubes into the pelvis, where nothing happens and it just shrivels up and disappears. In the right unfortunate person, those implants set up shop wherever they want and the havoc ensues. Did you know, that endometriosis behaves almost like a cancer? It can travel through the bloodstream and end up anywhere? We don’t call it cancer because it does not kill you, but it is just as awful. I have even seen endometriosis in brains and lungs! What the hell?!!!
So, how common is it? At first glance, the stats say that it can affect one in ten women. It doesn’t sound like much at first, but when you elevate that to a global level and take into account every country and continent, that amounts to about 190 million reproductive age women who are affected at any one time! Ok, that is a crap ton.
How do you diagnose endometriosis? I have people coming in to see me all the time saying that they know that they have endometriosis and that their doctor told them. I then ask them how they know and what tests that they have had. Most of the time, they haven’t had any or they had one usn and were told that endometriosis was seen on that. AAAAANGH. I am pressing the no buzzer on that one. Besides the instance when you have some gigantic ovarian tumor cluster of endometriosis, you cannot see anything on an ultrasound so that is just not true. The only absolute way to diagnosis endometriosis would be to have a positive biopsy of a lesion or the peritoneum. The other way is to visualize lesions on a laparoscopy. The other possible way is to get a really expensive mri of the pelvis that could possibly see possible lesions that could possibly be endometriosis…or something else. On top of that, sometimes when you do get a biopsy of what appears to be normal appearing peritoneum, 20 percent of the time it could be endometriosis hiding underneath. It is a really sneaky bugger. The realy key is a tissue diagnosis but if I see a bunch of visible classic lesions on laparoscopy, I am going to go for it and treat it.
So, what can we do about it? The ultimate goal in treating endometriosis is removing its hormone food source. That’s right you guessed it ladies. The ovaries themselves provide its main food source. This means that the ultimate permanent treatment for endometriosis is to remove everything: the uterus, cervix, the tubes, and the ovaries. You can also ablate lesions individually or resect them. But, it is practically impossible to remove them completely forever. This usually means a significant surgery with a significant scar and significant down time. On top of that, you are thrown into instant surgical menopause overnight instead of the 6 months to 2 years that it normally takes. Bring on the hot flashes, night sweats, increased farting and bone loss…overnight! Yikes! But at least then it is gone for good, usually about at 6 months after surgery when the last of the hormones have washed out of the system and the microscopic implants that you could not see have resolved.
Now, we have some medical options as well. The old standard was Lupron, an injectable, every month to every three months GnRH analog that shuts down hormone production and puts the patient into medically induced menopause. It can be used for a maximum of 6 to 12 months and maybe can be repeated later if symptoms reoccur. It is expensive and the side effects are kind of awful. We now have more modern oral meds like Orilissa(elagolix) and Myfembree(relugolix). Orilissa is a GnRH antagonist like an oral version of lupron. It also has a bunch of side effects and is not recommend to use beyond 2 years. Myfembree is also an oral med which has some estradiol and norethindrone in it so the menopause side effects are less while still being able to control the endometriosis. It can also be used up to 24 months. It was originally invented to treat fibroids but I have found that it is pretty successful for endometriosis too. Both are costly and you have to jump through multiple hoops and hurdles to get them covered. But, when they work, they can be a real bonus for the patient.
Bottom line is, endometriosis completely sucks, but now there is more than one option out there. Make sure you seek out a physician who is willing to put the time in to help improve your quality of life and help treat the endometriosis in the best way possible and treat you like an individual and be mindful of your particular goals. If you can’t find one near you, come see me. I got ya covered.
So, what the heck is primary dysmenorrhea? Primary dysmenorrhea is defined as significant pain during your menstrual cycle without a specific or identifiable cause. To me, this is a bit misleading because there is a cause for the pain, and we will explain that in a bit. I think it should say without a specific anatomical or additional pathologic cause outside of the normal biochemical reactions in our bodies.
Dysmenorrhea can interfere with our quality of life and our daily activities and performance. You know what I mean. We all know women who have to miss work or school because of their severe cramps, pain and bleeding. Dysmenorrhea is the most common gynecologic condition affecting women. The percent is reported anywhere from 17% to 90% depending on what you read. Sometimes the pain is minimal but sometimes it literally stops the woman from being able to function. Current statistics state that up to 15% of women that have dysmenorrhea actually miss work or school or functioning in general with regularity. Even for those women that do not miss work or school, the pain is often enough to reduce focus and productivity. In the United States, it is estimated that there are about 600 million hours of productivity lost to dysmenorrhea. This translates to about 2 billion dollars annually. I think that deserves our attention. Just keep it in mind the next time a work or school colleague has to stay home because they are in pain with their period. This stuff is real folks!
So, what causes this pain? What is primary dysmenorrhea? Primary dysmenorrhea is pain with menses that has no underlying pathology. Dysmenorrhea is called secondary if it caused by another condition like endometriosis, fibroids, pelvic inflammatory disease, or interstitial cystitis. For the purposes of this blog, we are going to focus on primary dysmenorrhea.
Primary dysmenorrhea usually starts at the onset of ovulatory menstrual cycles. Usually women do not ovulate for about 6 to 12 months after menarche( the onset of menses for the first time). Sometimes ovulation does not start for up to 2 years. The pain is usually crampy, comes and goes, and increases in intensity. It starts just before the bleeding starts and lasts up to 72 hours. There can also be nausea, bloating, diarrhea and vomiting.
Who is at risk for primary dysmenorrhea? There are multiple factors: 1) body mass index less than 20, 2) smoking, 3) longer menstrual cycles, 4) irregular or heavy flow, 5) history of sexual assault, 6) menarche younger than 12, 7) age younger than 30, and a family history of dysmenorrhea. Usually it gets better with age and after child bearing
Here is the pathophysiology of primary dysmenorrhea. The pain is probably due to the increased prostanoid secretion. So, what the heck is a prostanoid? Prostanoids are prostaglandins, thoromboxanes, and prostacyclins. And what are those things? Basically, all we need to know is that these are chemicals that cause cramps. So, the process goes something like this. When we ovulate, our progesterone stabilizes something called lysosomes, which are like storage containers full of inflammatory chemicals. At the end of the luteal phase of our cycle, our progesterone levels go down and the lysosomes break down and release something called phopholipase A2. Well this phopholipase starts the cyclooxygenase pathway, which then causes production of the prostanoids that I mentioned before. Then voila! Cramps! The main prostanoids that concern us in dysmenorrhea are the prostaglandins. They are the compounds that cause uterine contractions that restrict blood flow in the uterus. Because blood flow is restricted, there is less oxygen. Because there is less oxygen, metabolites are produced that stimulate pain receptors. In addition to that, some of the prostaglandins lower pain threshold because they actually sensitize the nerve receptors. And, if that weren’t enough, the prostaglandins are also responsible for all the gi symptoms we know and hate. There are other compunds that are involved in this process as well but since the prostaglandins are the main culprit, we are going to focus on those for the purposes of this blog.
As if the prostaglandins weren’t enough of an issue, it has also been documented that women who suffer from primary dysmenorrhea actually have an altered pain sensitivity in the first place. Altered pain perception in dysmenorrhea has been studied all the way back to the 1940s. This altered perception is part of central sensitization syndromes. These syndromes are all associated with pain hypersensitivity without documented tissue injury, inflammation or an actual nervous system lesion. This include several disorders such as low back pain, tension headaches and irritable bowel syndrome. All of these conditions lead to amplified sensory input. These result in the patient having more pain with less stimuli.
I think we have now effectively established that primary dysmenorrhea sucks. So, what can we do about it? There are multiple options. Right now we are going to focus on the non-surgical ones. The goal of each option is to interfere with the prostaglandin production, decrease muscle tone in the uterus, or inhibit pain perception with analgesia. Before we go into these options, it is important to remember that the real key to success and compliance with any regimen is SHARED DECISION MAKING between the patient and the doctor. Have the patient be an active part of deciding on treatment, after discussing side-effects, efficacy, etc and this will help greatly. If the patient is invested in the option, it is much more likely to be helpful.
The first category of options is hormonal. Combined( both estrogen and progesterone) birth control pills are number one in this category. They are effective in about 70-80% of patients. They inhibit ovulation and prevent multiplying of endometrial cells, which decreases prostaglandins, progesterone and vasopressin. This applies to the pill, ring and the patch. Extended use( skipping the placebos) seems to be the most affective. There is a possible risk of blood clots with this method, although this risk is very small in low risk, non-smoking patients.
Progesterone only contraception like Depo Provera or the Mirena Iud. They also inhibit ovulation and eliminate menstrual cycles. Sometimes these methods can cause irregular bleeding. Since this bleeding is still anovulatory, it is not associated with dysmenorrhea. The risk of blood clots is lower with this method. Sometimes there is weight gain reported, but this can usually be avoided with proper nutrition monitoring. Depo Provera itself has been associated with decreased bone density, which seems to be completely reversible after stopping it. While this sounds concerning, it has not been deemed enough of a reason to discourage patient from using it.
There are non hormonal options as well for primary dysmenorrhea. NSAIDS( non steroidal anti inflammatory drugs) are a first line treatment and are effective for the vast majority of patients. They work by inhibiting the cyclooxygenase enzyme we were talking about earlier, which then suppresses prostaglandin production. It’s like stopping the cramps before they can even be created! They also have a direct analgesic effect at the central nervous system level. There is not a lot of evidence to say that one is better than the others. Usually medications like Motrin, ibuprofen, Alleve, and Anaprox are among the first choice options. More expensive medications like Celebrex are reserved for second options. Ideally, these are taken as needed only. One suggested regimen is to start the medication 2 days prior to the onset of menses and continue for the first 72 hours of the menstrua cycle. The key is not to wait until the pain has already gotten started and try to catch up to it, but to act proactively.
Another possible non hormonal option is Magnesium. Magnesium appears to reduce the amount of prostaglandins in menstrual fluid. It is also a muscle relaxant and causes blood vessel dilation. This sounds logical but there is not a lot of data just yet.
Calcium channel blockers like Nifedipine can cause muscle relaxation and decrease prostaglandin production and possibly reduce uterine contractions. More data is needed here as well. I personally would feel hesitant to prescribe a blood pressure medicine for cramping.
Vitamin E, in some small studies has been shown to reduce dysmenorrhea. It has been shown to increase oxygen delivery to uterine cells, decrease prostaglandins production, and inhibit cyclooxygenase. This should result in reduction in pain and cramping. Unfortunately, so far the majority of this data is in the mice population.
Ginger also inhibits cyclooxygenase activity and decreases menstrual pain. The added bonus to ginger is that it is also an antiemetic( anti nausea) so it may help with the gi effects as well. Thus far the doses studied have ranged from 750 to 2000 mg a day with the same efficacy as NSAIDS. Go Ginger!
There are some other proposed non hormonal options for dysmenorrhea as well. All of these require further study but they are interesting prospects. The first is transcutaneous electrical nerve stimulation(TENS). This is hypothesized to work in three ways. 1) it sends electrical impulses to the nerve root, elevates the pain threshold, and the pain sensation is not felt. 2) It stimulates the release of endorphins which reduce pain. 3) It increases dilation of blood vessels in the uterine muscle and reduces hypoxia which also reduces pain.
Acupuncture( needles) and acupressure( firm pressure) stimulate designated locations to relieve pain. There are specific sites on the body on the auricle of the ear, the medial calf muscle, and near the medial malleolus of the ankle that have been identified as possible beneficial treatment areas for dysmenorrhea. There are no specific regimens that have been backed up by studies to recommend with confidence at this point. So far, the range varies from a once a menstrual cycle treatment to daily for 7 days during the menstrual cycle. More to follow later here.
Let’s not forget the good old heating pad applied directly to the suprapubic region. Local heat improves tissue oxygenation, dilutes the levels of prostaglandins and increases blood flow. All of these effects can lead to decreased pain as well. A lot more evidence is needed, but it makes sense.
Apparently exercise and yoga play a role here as well by increasing endorphin release, lowering stress and anxiety, and increasing blood flow. I am here to tell you that as good as that sounds, the thought of jumping on the exercise bike or doing some aerobics in the middle of a crazy period sounds a little daunting to me. I get that there is some moderate quality evidence that this helps over the long term, plus the other health benefits of exercise, but I still think I would have a hard time putting it into practice. I am going to opt to continue to follow how that plays out.
There are a number of herbal and complimentary remedies that have been suggested as well. Rose tea, fish oil, krill oil, sweet fennel seed, low fat vegetarian diet and decreased dairy intake. So far, there is no high quality evidence for any specific dietary supplement. Still, the side effects are minimal so they may be worth trying.
The bottom line is, dysmenorrhea is a real thing that affects millions of women and costs billions of dollars in lost productivity. Beyond that, it can really affect quality of life and daily function both mentally and physically. It deserves our careful attention with a thoughtful plan tailored to the patient’s specific needs and risk factors.
