This month I started a fellowship that predominantly involves taking care of women with cancer. Through surgery, chemotherapy, and other medications we do our best to cure or hold back malignancies of many kinds. In these past weeks, I have taken care of several patients who are Jehovah Witnesses, an experience that has been quite interesting.
In most cases, what religion a person subscribes to has little to no impact on their clinical outcome. We have an exception, however, when it comes to a Jehovah’s Witness with cancer. JHW patients to a rule will not accept blood products of any kind, which greatly limits their ability to be effectively treated for cancer. In some cases they cannot have surgery the surgery they need is unsafe without the possibility of blood transfusion. In some cases they cannot take chemotherapy because blood transfusion is required to survive the associated myelosuppression. As surgery and chemotherapy are our two best treatment, they are at a major disadvantage.
When I was a resident, I had a pretty hard opinion about this. I heard a lot of different view on the topic, but the position of one of my attendings resonated best with me. He felt that his job as a physician was to protect the health of his patients, and that if a JHW was dying in front of him he was going to transfuse them whether they liked it or not. He was quite clear about this upfront, and told JHW patients that if they were not happy about this they should find another doctor. He even arranged for attending coverage for emergent issues if need be. He felt that the preventable death of a patient was an emotional trauma he didn’t want to be exposed to, almost as if the patient, through refusal of blood, was exposing him to unnecessary emotional violence. While this was a very hard line, I respected the boldness of it, and that he was being true to his internal values. I held a similar feeling for the first few years of my attendinghood, though I never had to test it until my third year out of residency.
In a few posts I have mentioned Reciever Operator Curves (ROC), and a few folks have asked what I mean, so I want to explain it. This is an extremely important concept in medicine, and in decision making in general. Unfortunately, it is also quite complex. So complex in fact, that it is possible to explain an ROC in very high end mathematical speaking, such that few would understand (and yes, it can get over my head as well.) To see this kind of explanation, check out the Wikipedia entry on the ROC. But I want to try to make it a little simpler.
Tranexamic acid was recently approved by the FDA for treatment of fibroid related mennoraghia, under the trade name Lysteda. Being ignorant of this drug, I wanted to do a little research. Being a blogger, I want to share this research.
Apparently, this drug has been available in Europe for quite a long time, and there is substantial evidence of its efficacy and safety for treatment of a wide variety of bleeding issues, both gynecologic and otherwise. Tranexamic acid (Wiki, WA) is in class of drugs called antifibrinolytics. It is related to the drug Amicar (ε-aminocaproic acid) which is used in the US most notably after dental procedures as a mouthwash in patients with bleeding disorders. These drugs function by blockade of lysine binding sites on plasminogen, thus blocking degradation of plasminogen into plasmin (sort of an anti-tPA). Through this mechanism it stabilizes clots and prevents clot breakdown, thus augmenting the clotting system and decreasing bleeding.
When I was an intern in Charleston, SC, I quickly learned the importance of the labor curve. When checking out with my chief, I was often asked the question “Is she on the curve?” Quickly I learned the idea that women that “fall off the curve” were in a dysfunctional labor pattern, and were more likely to require a cesarean delivery. I dutifully listened to all this, and did many a cesarean for active phase arrest. As a junior level I did the cesareans, and as chief I called them. But at the same time, I had doubts about all of this.
Academic OB/GYN isn’t just about me blathering on about current literature and interviewing folks – its about YOU too! If there is any way I can help you, I want to know. Send research questions, and I’ll try to answer them. Need a video of some kind of surgery, I’ll try to make it. Want a place to publish your ideas about our field, the blog’s all yours. Wanna get some ideas from your colleagues that read the blog? We can do it.
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Throughout my career heard so many reasons why the fern slide didn’t fern in the apparently ruptured patient.
“She’s only 19 weeks, they don’t fern this early.”
“There’s blood in the sample, that makes it not fern.”
“She has chorio, that makes it not fern.”
Over the years, this has driven me a bit crazy, because the real reason that the slide is not ferned is not any of these reasons. The reason there is no fern on the slide is because the fluid on the slide is not amniotic fluid.
I was recently on call and we had 2 patients on our board having second trimester inductions, one for ruptured membranes at 17 weeks and another for fetal anomaly. Both patients were being treated with what seemed like a strange regimen of misoprostol, 400 mcg miso vaginally _and_ 400 mcg orally, every 4 hours. I had never heard of this regimen, and was wondering where it came from. None of the residents seemed to know, only that it had been passed down through some route to them.
It struck me as odd that people are using misoprostol in all kinds of different ways, despite the large amount of available evidence in the literature. In fact, it may be one of the most thoroughly studied topics in obstetrics, having been the subject of many randomized trials, a standard of research rarely achieved in our field. Studies have included both pharmacokinetic and clinical data. For better or for worse, abortion is the single most common procedure performed for women worldwide, and the patient population tends to be appreciative and willing to participate in research. Sadly, the mammoth amount of data available seems overlooked by the majority of practicing obstetricians, given the wide variation in practice I have observed. As such, I want to review a few of the major articles here.
Ok folks – I gotta a braintwister for us all.
I was on call this morning and the nurse was letting me know that a patient with an IUPC had a baseline pressure of 40 mm Hg, and anything above 30 mm Hg was considered abnormal. I didn’t know what to say to that, because the whole idea of baseline pressure never made sense to me.
First, the IUPC is zeroed theroetically to the air, so the baseline pressure should be relative to air. But, we have no idea what intraabdominal pressure is! When we do urodynamics we need to subtract intraabdominal pressure from the bladder pressure to really understand how hard the detrusor is contracting. It seems to me that we would need the same information to say anything meaningful about the intrauterine pressure in an absolute sense. Otherwise, the baseline pressure could be influenced by things like patient position and position of the baby (making a different amount of direct pressure on the IUPC.) The whole concept seems sort of flawed to me.
Certainly if baseline uterine tone were really increasing, that might have some meaning. But are we really measuring what we think we are measuring?
So what did I tell the nurse? I said “don’t worry about it. the whole concept makes no sense.”
What would you have told her?