In my first year out of residency I practiced in Honolulu, HI. One day in my outlying clinic in Kapolei, on the west side of Oahu, I entered an exam room to find a woman crying in pain. She said she had pain in her belly wall that had been present for years and no doctor could help her or tell what was wrong with it. She said that several months after her last cesarean delivery she started to feel this hard lump on the side of her belly. Every month right before her menstrual cycle, this lump would become exceedingly painful, both at rest and even more so with any kind of pressure.
She was absolutely distraught, and was really in my office to ask for some narcotic pain medications to treat the severe pain. So many doctors had failed to make a diagnosis on this issue that she thought it was something she would have to live with for the rest of her life.
But, that day was different, because her doctor that day had been fortunate enough to be exposed to this condition in his training. The woman had abdominal wall endometriosis that had been ignored or missed for years. I scheduled her for surgery that afternoon and by that evening she was completely cured of the problem. I asked her as she woke up whether it still hurt, and she said that she felt some pain from the surgery, but the pain from that mass was gone. It felt good to help her, and I was thankful that I had gotten training in the diagnosis and management of this condition in my residency, something that is lacking in the training of most gynecologists in this country.
Since that time, I have been fortunate to be able to help a lot of women with this condition. The first few came randomly, and to my disappointment each one had been missed by at least a few doctors before I saw them. Eventually I became known as a competent manager of this condition, along with my general expertise in endometriosis, and at that point I started to see a lot of referrals and do a significant number of surgical repairs for this problem.
Abdominal wall endometriosis is a predominantly iatrogenic condition, meaning that it is the result of something that we are doing – and that something is cesarean delivery. The vast majority of these cases are subsequent to cesarean delivery, presumably via seeding of the abdominal incision with endometrial tissue at some point during the case. We do not know exactly what are the risk factors in cesarean delivery that cause this condition, but we do know from animal models that if you take a little piece of endometrium and stick it in the fascia when you close it after surgery, abdominal wall endometriosis will result – so presumably that is what is happening.
There are a few things I think we can do to reduce the incidence of this cesarean related endometriosis. Thorough irrigation of the wound prior to closure is likely to reduce or eliminate flecks of endometrium that might implant in the abdominal wall. I also believe, based on my experience but lacking data, that closure of the parietal peritoneum will reduce the incidence of this disease. I say this because of multiple experiences where uteri are adherent to the abdominal wall contiguous with masses of abdominal wall endometriosis. In one of these cases a hysterectomy was required to entirely remove the disease.
Interestingly, people with cesarean related abdominal wall endometriosis do not necessarily have typical peritoneal endometriosis, as it is caused by direct deposit of endometrium into the abdominal wall during a surgery. However, women that have abdominal wall endometriosis who did not have prior surgery most likely do have peritoneal disease, and it is probably severe. Papers suggest that only 50% of these cases are post-surgical, but in my experience cases without prior surgery are very rare.
Abdominal wall endometriosis is a disease that is easy to diagnose if you know what the condition is and how it presents, and impossible to diagnose if you don’t. This is called availability heuristic – it is impossible to make a correct diagnosis if the disease state doesn’t exist in your brain’s medical knowledge banks.
In almost every case I have diagnosed, the patient came right out and told me they had it. Not literally of course, but rather they said the words that made the diagnosis certain. The disease presents with a hard mass that is painful at all times, but become larger and dramatically more painful prior to and during the menses. It is exquisitely tender to the touch, particularly during the most painful part of the month. With those symptoms, the diagnosis is almost certain. I can tell you that I have heard this story over and over and over, and I come right out and tell the patient what is wrong before I even look at their abdomen, and in each case it is there to be found on abdominal exam, just missed by well-intentioned people who didn’t know what to look for.
Imaging studies are useful in confirming the disease, though in my experience it is useful only to for surgical planning, as history is enough to make the diagnosis. The proper imaging should be an axial cut CT or MRI. MRI is better at showing the depth of invasion into the fascia and muscle, but either modality is adequate. If cost were an issue one could certainly get away without imaging. Some people (mostly general surgeons) will do a fine needle biopsy to confirm that it isn’t a malignant tumor, though I don’t think that is necessary and it drives up costs.
There are three things one can do with abdominal wall endometriosis, only one of which clearly leads to lasting cure of the problem.
As AWE is endometrial tissue, it will respond to high dose progestin therapy or continuous birth control pills. It will also respond to Depot-Lupron (leuprolide), and perhaps to aromatase inhibitors (eg letrozole). The upside is that these agents do work. The downside is that the patient is stuck taking them forever, or at least until menopause, and that they are not really treating the problem.
There are some recent trials that suggest efficacy in ultrasound guided injection of phenol directly into the endometrial tissue. These injections destroy whatever tissue they go into, so properly guided this probably does work. It is however something that is still in a research stage and only supported by a few recent papers (in international press.)
The final intervention, which is both curative and reliable, is surgical resection of the abdominal wall disease. In my experience, complete resection of the indurated tissue in the subcutaneous space, including resection of underlying fascia if necessary, is curative of the problem. I have had only one patient who did not experience complete relief, and subsequent imaging showed that she had a satellite area of disease that was not resected in the first surgery. She was cured in a subsequent surgery to remove this additional disease.
This procedure is performed under anesthesia by opening up the old cesarean scar, identifying the endometrial implants, and resecting them. In some cases the implant is superficial enough that removal does not require entry in the rectus fascia. In other cases the disease is invasive into the fascia or even the underlying recurs muscle, requiring resecting a portion of the abdominal fascia. Small fascial defects can be closed primarily, while larger ones can require mesh reconstruction of the fascia prior to closure.
I have removed quite a number of these, and in my experience about half require some level of mesh reconstruction. There are some studies that show a much lower likelihood than that, though I suspect they had a population with less severe disease than I have seen. My criteria for mesh reconstruction is a lack of ability to reapproximate the fascia without significant tension. I have predominantly used a biologic mesh (either Strattice (porcine dermis) or Veritas (bovine pericardium)) which is reabsorbed and replaced with fibrosis over time. Some operators use a permanent mesh. Permanent mesh is likely superior for large defects, though it comes with a chance of infection requiring removal. Porcine or bovine mesh will not get infected easily (if placed in a sterile field), but there is greater risk of subsequent hernia formation. We lack any randomized trials to direct us on exactly what type of mesh we should use in this diseases state, other than the general surgery literature on general abdominal wall reconstruction.
Placement of mesh is does by a simple inlay technique. I use 2-0 PDS suture to secure the mesh. Very large defects may require underlay or component separation techniques, in which case I will involve a general surgeon in the closure.
With the placement of any biologic mesh, drainage is imperative as seroma formation is quite common without it. Drains are left in place until drainage is minimal (10-20 cc a day), which can be as long as a month. My experience with inadvertent (gets pulled out accidentally) or impatient (resident pulls it out thinking that 50cc a day was little enough) has been consistently negative, with seroma reformation being common. While patients dislike drains, they can be managed, and they are preferable to a wound that is draining clear fluid for a period of time.
If you are a physician seeing a patient with the symptoms I mention, please think about this diseases state. If you make the diagnosis you will be doing better than 90+% of people out there.
If you are a patient with these symptoms, tell your physician your own diagnosis. If they are not able to help you with it, consider visiting beautiful Portland, OR and I would be honored to help you.
Dr Fogelson practices gynecologic surgery with a specialty in pelvic pain and endometriosis at Pearl Women’s Center in Portland, OR, where he sees patients from Oregon, the northwest region, and the nation.
For more information contact us at email@example.com, or call (503) 771-1883
Today I sat in the infection control committee at Grady Memorial hospital and listened to two sales pitches for products meant to decrease surgical site infection. I am a tough sell at these meetings. Some might even say that I am the asshole in the room. But really the issue is that I say what everyone else is thinking but are too polite to say.
The first pitch was from Ethicon, who was marketing their antimicrobial impregnated suture. The presentation shows convincing evidence that the suture, placed in a petri dish surrounded by bacteria, does in fact inhibit bacterial growth. There were many claims made that it also decreased the rates of wound infections in comparison to using typical suture. When I questioned what data there were to suggest this, I was told that the data was all in my handouts.
I looked down at my handouts and found no data whatsoever. I found a bibliography of about thirty articles that investigated the product. I pointed out that there is no data, just a list of articles. I was reassured that these data support everything that they are saying.
At this point I was kind of pissed.
A warning to all – this post is really for the docs out there. If you are not in the medical profession, you might find this humorous, or you might find it completely unintelligible – so read on with that warning.
When I was a medical student and resident, we routinely presented obstetrical patients in a common format:
Age – Gravity (how many times pregnant) – Parity (how many children delivered) – gestational age extra information.
For example, this patient is a 24 year old (age) G2 (gravity) P1 (Parity) at 29 6/7 weeks with a history of a preterm delivery in her first pregnancy (extra information).
To me, this format makes sense and when I am listening to a presentation it is easy to hear and process.
Unfortunately, things have changed. We seem to have adopted a new system that incorporates all the extra information into a numerical abbreviation system. Now we do this:
Age – Gravity – Parity Full Term – Parity Preterm – Miscarriages/Abortions – Live Children – gestational age – extra information ( which may not be required any more)
For example, the previous presentation would be “this is a 24 year old G2P0101 at 29 6/7 weeks”.
For some reason, this just doesn’t work for me. Inevitably what happens is that the resident quickly says all of these numbers and my brain freezes. I now have to spend the next 3 or 4 seconds of my attention processing these numbers into some actual meaning that I can interpret. During those 3 or 4 seconds the resident has continued their presentation, but I have not heard what they said because I was trying to figure out what they said before meant.
The problem here is over-abreviation. Abreviation is good when it improves efficiency, but there can be too much of a good thing, and I think we have that right here.
And so to all you med students, residents, and docs, I encourage you to set an example by extinguishing this extended numerology from your obstetrical presentations. Just say it in plain English. We will all understand you better.
Last night I had the pleasure to watch an HBO special documenting a masterclass given by singer Josh Groban to three young music students. Over the course the show, Groban coached the students through composition of an original song, and it culminated with their performance of a song that had not existed a week previously at his concert in Chicago. It was a great show that I quite enjoyed, and if you like Groban or music, you should check it out.
The show also made me think quite a bit about how my job teaching residents is quite a bit different than the job most teachers have.
Medicine is a strange career, in comparison to most, in that a doctor does not go on their first true job interview until they are nearly 30 years old. Prior to that, its really just trying to get into college, then trying to get into medical school, then trying to get into the right residency…. but never really interviewing for a job, per se. My first job interview was with Dr Kenneth Ward, then the chair of the University of Hawai’i department of obstetrics and gynecology. I was interviewing for an academic position, and the interview seemed to be going pretty well. We both liked technology, and were both Apple fans, so there was a fair bit to talk about other than just the job. Overall, we seemed to hit it off. Then he asked me a serious question. “So Nick, what was your greatest accomplishment in residency?” Read more…
This is an edited video of a robotic hysterectomy and salpingoopherectomy in a patient with stage IV endometriosis, with bilateral endometrioma, cul de sac obliteration, and severe retroperitoneal fibrosis. The video demonstrates ureterolysis, dissection of ovarian vessels from the ureter, and management of colpotomy in the setting of dense adhesions.
For clinical consultation with Dr Fogelson, call Pearl Women’s Center in Portland, OR at (503) 771-1883 or send email to firstname.lastname@example.org
This week in the news there have been a number of articles about a new technology that has allowed the creation of an embryo from three parents, and boy it is creating controversy.
Three parents you say?
Yes. Of a sort.
The case in point regards a woman who unfortunately had a child with a deadly mitochondrial disease. Mitochondria are organelles (“small organs”) inside each of our cells where ATP, our primary energy source, is made. Mitochondria are special in that unlike other organelles, they carry their own DNA. In the case of this woman’s tragically afflicted baby, defective DNA that could not support much life.
Geneticists have developed technology to create an healthy embryo without the defective mitochondria by placing a nuclei from the woman’s mitochondrially defective egg into a donor egg, after removing that egg’s nuclei. They then fertilized the new proto-egg with the husband’s sperm to create a new embryo. In essence, the egg had three parents – two in the nuclei, and a third one in the mitochondria.
And the world shuddered.
From all corners were cries of “we’re playing GOD!!!”. “We are altering the human race!!” “We’re no better than Mengele!!”
Most of this comes from a bright line we have put around genetics research that says we will not genetically engineer human beings. Legitimate bioethicists have felt that this is something we should not do, because of a ‘slippery slope’ towards eugenics. Religious radicals are just uncomfortable with advancement in science in any kind. They say it is because it is against God, but I think it is because a true understanding of how the universe works deprecates the validity of their religion, and thus sparks a crisis of faith.
But either way, most people think that manipulating human DNA is unethical.
I, for some reason, don’t see it this way. In fact, I couldn’t be happier that we have made this leap, and hope we keep leaping. We are coming to understand how we are put together, and in such we are coming to understand how to manipulate that process. That is exciting, not concerning.
We are not “Playing God”. For us to be “Playing God”, a “God” would have to have been the reason we came to be on this earth. And unequivocally, it is not. The evidence for evolution is so unbreakably strong that to claim that we are here because of “God” is purely ignorant. Humans are on this earth because our genes were selected for over millions of years, not because somebody put us here. If you believe in God, fine. But please don’t hold humanity back from our future by claiming that we are breaking your religious rules.
Even worse is the claim that to genetically engineer a human is akin to Nazi experiments. True, Hitler wanted to manipulate the future of humanity. But he didn’t want to do it by changing the genetic information of the future. He did it by murdering the people who were already here. To claim these are the same thing is an affront to geneticists, and is too good for Hitler.
In truth, I am absolutely head over heels excited to hear that we were able to eliminate a deadly genetic disease from a family through genetic means. What this means to me is that we are actually CURING disease, not just treating the symptoms that it produces.
Evolution is something that is terribly misunderstood. Its detractors really don’t get how it works. People who don’t understand it think it is about the selection of individuals over others, and thus don’t believe it could ever have ended up in us, but that is not really how it works. It is the selection of GENES that drives evolution, not the selection of individuals.
The problem in this case is that mitochondrial genes do not reproduce sexually, but are rather copied directly from their parent mitochondira, and as such they do not evolve. As such, problems in the mitochondria are passed on forever, never changing except by random mutation.
But now, for the first time, mitochondrial DNA is evolving. Perhaps not by natural selection, but it is evolving nonetheless. And that is exciting.
Don’t take this to believe that I am ignorant of the potential problems. But they are technical, not ethical. Obviously we can not open the doors to unlimited human experimentation, but this is a first step, and it is a good one.