More than two decades ago (while I was practicing obstetrics), I was sued. To this day, I am upset; moreover, I remember the details of the case as if it happened yesterday: A patient was in spontaneous labor at term and the baby was head down (vertex), however, instead of the head presenting in a flexed position so that the chin was “tucked under” it was a face presentation and the head was extended. I waited for labor to progress and ruptured the membranes in the hope that as usual the baby’s head would flex. It didn’t, and since this position would not permit a simple vaginal delivery, I performed a cesarean section and delivered a vibrant, lustily crying baby girl. Mother and baby went home in the usual time without any complications. Two years later, the mother reported that her daughter was deaf. A diagnosis of congenital deafness was made and I was subsequently sued… with the claim that had I performed the C section earlier, the baby’s hearing would not have been affected. That’s the story. But, it’s not the end.

The attorney for the plaintiff stated that the injury was so significant that he would get more money from a jury than the amount for which I, at that time, had coverage. Moreover, the insurance company did not want to go through the expense of a trial, especially with that particular attorney. (He lectured at conferences for personal injury attorneys that the cause of an injury was not the major issue for pursuing cases, the degree of injury was the major ‘let’s sue’ imperative.) My malpractice insurance company pressured me to settle on what it felt was a nominal amount. I reluctantly agreed but felt depressed and humiliated. I almost stopped practicing obstetrics. The joy of following women through their pregnancies and deliveries was now tempered with a concern that no matter what I did right, their obstetrical outcome could be perceived as wrong. Oh, and my premiums went up for several years.

This confession of litigious dismay is one I have never shared. But when I saw the article in the August 18th issue of The New England Journal of Medicine titled, “Malpractice Risk According to Physician Specialty”, I had a medical management flashback.

The authors analyzed malpractice data from 1991 through 2005 for all physicians who were covered by a large professional liability insurer with a nationwide client base of 40,916 physicians and 233,738 physicians’ years of coverage. They reported the proportion of physicians who had malpractice claims in a year, the claims leading to payment for the plaintiffs and the size of these payments. This data was used to estimate the risk of ever being sued among physicians in high and low-risk specialties.

As expected, the highest-risk specialty for malpractice suits was neurosurgery. Next came thoracic-cardiovascular surgery, then general surgery, plastic surgery, gastroenterology (probably as a result of perforations during procedures) and following that… obstetrics and gynecology. (We were 5th.) However, once a physician stops delivering babies and practices gynecology only, the risk goes down and becomes 12th on the list. (Reassuring for me in my present practice). The specialty that had the least suits was psychiatry. (So seeking professional advice on my previous angst would not put said professional at risk!).
Across specialties, 7.4% of physicians annually faced a malpractice claim and 1.6% made an indemnity payment. Again this varied according to specialty from 19.1% in neurosurgery, 18.9% in thoracic-cardiovascular surgery, 12% in obstetrics and gynecology and 2.5% in psychiatry. Across all the specialties the mean indemnity payment was $274,887, but the highest payment for awards went to pathologists (for what I assume was the wrong diagnosis).

Now to cumulative risk for those of us who continue to practice into our 40′s (which barely takes us past our specialty training): Roughly 55% of physicians in internal medicine and its subspecialties were projected to face a malpractice claim by the age of 45 years and 89% by the age of 65. This number rose to 80% of physicians in surgical specialties and 74% of obstetricians and gynecologists by the age of 45. (I guess I shouldn’t have felt singled out.)

The authors projected that the proportion of physicians facing a malpractice claim by the age of 65 was 99% for those in high-risk specialties (basically the surgical specialties) and 75% of physicians in low-risk specialties..

The career risk of making an indemnity payment (i.e. the plaintiff wins and is awarded damages) was however less: roughly 5% for physicians in low-risk specialties and 33% for high-risk specialists by the age of 45. This rose to 19% and 71% respectively by the age of 65.

The authors then went on to make a statement that I feel applies to my experience and that of so many of my colleagues. “Physicians can insure against indemnity payments through malpractice insurance, but they cannot insure against the indirect cost of litigation, such as time, stress, added work, and reputational damage.” These numbers certainly explain why so many physicians practice defensive medicine. Obviously, this is not cost effective for our society, our national and personal budgets. The authors of this well researched article made no recommendations. Frankly, neither can I… except to say that we should keep as up-to-date as possible on evidenced based practices.

Apparently yes… but before you buy stock in Bayer or stock up on years’ worth of aspirin at Costco, let me give you the result of some pooled (meaning statistically conjoined) studies: A recent article published in the medical journal Lancet analyzed 8 aspirin trials which included a total of 25,570 patients. Most of the trials were originally conducted in order to establish the effect of aspirin on prevention of vascular events such as stroke and heart attack. The patients were randomized to daily aspirin versus no aspirin over a mean duration of treatment for 4 years or longer. The trials included 3 large United Kingdom studies in which follow-up of over 20 years was done by reviewing death certificates and data from cancer registries. During that time, a total of 674 cancer deaths occurred.

The Lancet article presented some complicated particulars with charts and tables… I’ll spare you the details. But yes, aspirin reduced the risk of certain types of cancer deaths by approximately 20%. (This refers to relative risk; those who took the aspirin for 4 years or more had 20% fewer cancer deaths than those who did not.) The lessening of relative risk for cancer death was apparent just 5 years after starting the aspirin for esophageal, pancreatic, brain and lung cancer, but was delayed for stomach, colorectal and prostate cancer. Long-term aspirin was found to reduce only certain types of lung and esophageal cancers, (adenocarcinoma, which develops from gland-forming cells). The decrease in cancer rates had no correlation to dose; 75 mg was sufficient and higher doses made no difference. This means that daily “baby aspirin” which contains 81mg is more than enough. And most importantly, there were no gender differences found in the analysis! (The studies included sufficient women to make this statement… in the past studies were done primarily on men and extrapolation from male driven studies was used when it came to giving advice to women.) Moreover, aspirin worked to diminish the relative risk of these types of cancer deaths in those who smoked. (Although we always have to remember that smokers will have more of these cancers and are more likely to die from them compared to nonsmokers; unless, of course they stop). The benefit of long-term aspirin increased with age, so that the absolute reduction in 20-year cancer risk of death was 7.08% at or beyond the age of 65.

Bottom line: According to these studies, the effect of aspirin on reducing cancer death is not immediate, but takes 5 to more than 7.5 years and requires consistent dosing of 75mg a day. The 24 million dollar (or should I say the 20-year) question is whether complications from long-term aspirin use, especially bleeding (ulcers and hemorrhagic stroke) ultimately negate its positive impact. We each have our own risk profile. Before embarking on a very long course of this medication (even if it is over-the-counter), I would urge you to discuss the risks and benefits with your doctor.


I just don’t know what to discuss this week amidst our national and global economic woes, the famine in the horn of Africa and the conflicts throughout the world all of which seem to be escalating. So I’ll escape to a review journal (Obstetric and Gynecological Survey to be exact) and discuss a new hypothesis… that a hormone secreted by our adrenal glands helps prevent death from coronary heart disease.

Dehydroepiandrosterone sulfate (DHEA-S) is the most abundant circulating sex steroid “pro-hormone” in our youth. It peaks by the time we are twenty and decreases with age. It is termed a pro-hormone because it can be converted to testosterone and estrogen. We don’t yet know the exact receptor for DHEA-S or whether it works without conversion. (This is not a religious statement.) In the past it was considered a “youth” hormone, since it peaked in our youth and diminished with age. The level of DHEA-S has also been thought to correlate with sexual response and libido. Many studies and articles looking for a fountain of youth and sexuality have, however, been unable to demonstrate that high levels of DHEA-S equate with great (or even so, so) sex and/or longevity.

A study published in the Journal of Clinical Endocrinology Metabolism in 2010 called the Women’s Ischemic Syndrome Evaluation followed 270 postmenopausal women who were referred for coronary angiography for suspected ischemia (lack of oxygen to the heart muscle). They were seen annually for 9 years. The researchers found a significant association between lower DHEA-S levels and both higher coronary heart disease mortality and all-cause death. Compared with the women in the highest DHEA-S category (they divided them into 3 groups or tertiles), those with the lowest DHEA-S tertile had a 6 year CVD mortality of 17.4% vs. 8..2% and all cause mortality of 20.6% vs. 9.7%.

In other words, lower levels of circulating DHEA-S were predictive of higher CVD and all-cause mortality in women who already had signs of ischemic heart disease. Was this a cause or simply an association (i.e. does worsening ischemic heart disease lead or go together with low levels of this pro-hormone, or do the low levels somehow lead to a worsening and ultimate death from this coronary disorder)? And if a woman has ischemic heart disease, should she be treated with DHEA-S to help her prognosis? What about the rest of us? Should we get the level of this hormone tested? If it’s low, should we worry? Should we supplement it?

Until we know exactly how this pro-hormone works and what it does, the answer remains an enigma. So why not share a study that raises all these questions and does not satisfactory supply answers in a week that seems to have no answers?

This calls for a 101 on ovarian function: During our reproductive lives, the ovaries provide us with our essential female hormones… estrogen and progesterone which are taken up by receptors in every cell in our body. These hormones are produced through the development of primordial eggs or oocytes within the ovaries. The ovary of the female fetus is endowed with a huge number of oocytes… 6 to 7 million to be sort of exact. But by the time we are born, that number dwindles to “just” 1 million. And by the time we hit puberty, we have a paltry 400,000. Then during our reproductive years, thousands die each month (this is termed “atresia”) while one oocyte becomes a follicle that has the potential for ovulation. This dominant follicle develops for 2 weeks, producing more and more estrogen; it then extrudes an egg that can be fertilized.

Subsequent to ovulation the follicle, now bereft of its egg, is called a corpus luteum. It produces, in addition to estrogen, progesterone and together they create a lush environment in the uterinelining for potential implantation of a fertilized egg (now called a blastocyst).

At what point does all this change? Do regular cycles mean that pregnancy will occur at the “touch” of a sperm (or thousands of them)? It turns out that reproductive menopause can occur years or even a decade before hormonal menopause. There is a national trend to delay childbearing. In my practice in LA, I practically never see women under 35 who are ready to conceive. A common question posed by my patients is “How long can I wait?” or “Is it too late?” So I thought it would be appropriate to share some of the information that was recently published in the “Postgraduate Obstetrics and Gynecology” publication that is sent to me and my colleagues biweekly for continuing education.

A woman’s fertility is definitely dependent on her age. The incidence of infertility in women 20 to 24 years old is 7%; this increases to 15% between ages 30 and 34 and then to 29% in women aged 40 to 44 years.  Not only does the quantity of oocytes dwindle, but so does their quality. The rate of spontaneous miscarriage is 10% before the age of 30; it almost doubles to 18% between ages of 35 and 39 years and then rises to 54% in those older than 45. It’s not the age of the uterus that counts, but that of the eggs. If donor eggs of younger women are used, the pregnancy and miscarriage rates are the same in women younger and older than 40.

IVF success with a woman’s own eggs is dependent on the age of her eggs. (This obviously means her own age, no matter how young she looks!) According to the Society for Assisted Reproductive Technology, women between the ages of 35 and 37 have a 37.3% live birth rate, women between 38 and 40 a 28.2% live birth rate and women between 41 and 42 a 16.7% live birth rate with their own eggs.

There are several ways to assess ovarian reserve and get some reassurance as to whether the oocytes are good enough for a successful pregnancy. (By success we mean a live birth, not whether the child can get into an Ivy League school.) Simply having regular periods is not sufficient evidence.

The first test that most doctors will run is a follicular stimulation hormone (FSH) blood test. FSH is the messenger hormone produced by the pituitary. It “commands” the ovaries’ oocytes to begin the steps towards ovulation. If the estrogen level is low (which is what happens with the onset of the period), the FSH revs up and oocytes’ development takes off. Once a dominant follicle develops and it produces its estrogen, the FSH level goes down (negative feedback). If there are not enough oocytes to pass “go” and the ovary’s reserves are low, the FSH continues to be secreted in a desperate attempt to get those oocytes to do their thing. High levels of FSH in the beginning of the cycle (we usually check around day 2 or 3 after the menstrual cycle has begun) indicate poor ovarian response. And FSH will stay up permanently once the ovaries have run out of oocytes, i.e. throughout menopause. In general, the FSH level should be between 4 and 10 mIU/mL during the early part of an “ovulatory” menstrual cycle. Levels higher than 10 to 15 are considered borderline and those higher than 16 mIU/mL are considered abnormally elevated, indicating poor reserves and predicting diminished success with fertility treatment.

There are other endocrine markers that may show low ovarian reserves. One is called antimullerian hormone or AMH. It is produced by ovarian cells from 36 weeks of gestation until menopause. With menopause it decreases to undetectable levels. AMH is not affected by pregnancy or birth control pills and may be the first ovarian reserve marker that declines. Another endocrine test that can predict potential fertility issues with age is a blood test for inhibin B, a growth factor in the ovary. It rises in the beginning of the cycle and then goes down during the second half. Low levels in the early cycle indicate diminished ovarian reserve.

Finally, ultrasound may help predict the ovaries’ reserve. The number of small “ready to go” follicles can be counted and if there are 10 or less that are seen in a scan, ovarian reserve may be compromised.

If you or a family member question whether you can wait or if it’s too late to try to conceive with your own eggs (especially if you are considering expensive and potentially invasive fertility procedures); screening for ovarian reserve should be done. The easiest test is an FSH level on day 2 of your cycle. It can be done in conjunction with these other tests, but it probably remains the simplest and least expensive method of reserve determination. The question, “How many eggs are left?”, is valid for all women who want to postpone pregnancy.