Commentary

The management of bipolar disorder during pregnancy is a critical clinical situation demanding great attention to issues such as reproductive safety of psychiatric medications used by women with bipolar disorder to maintain emotional well-being, compared with the established risk of relapse if patients stopped those medications.

Antonio_Diaz/Thinkstock

Treatment of bipolar disorder frequently includes mainstay treatment with mood stabilizers such as sodium valproate, lithium, lamotrigine, and second-generation atypical antipsychotics. While we have robust information regarding the reproductive safety of sodium valproate, it is a teratogen with a very high risk for neural tube defects. In contrast, data over the 15 years have been very supportive of the reproductive safety of lamotrigine. The last decade has seen growing use of second-generation antipsychotics, so-called atypical antipsychotics. There has been growing interest in the reproductive safety of these medicines given their use both for acute mania and for prophylaxis of bipolar disorder; they also are used as an adjunct to treat patients with major depression. Atypical antipsychotics are widely used off-label to treat obsessive compulsive disorder, other anxiety disorders, and a spectrum of psychiatric illness.

Until relatively recently, data on the reproductive safety of second-generation atypical antipsychotics has been relatively sparse, with the small number of prospective studies yielding a small total number of patients. Over the same period of time, the National Pregnancy Registry for Atypical Antipsychotics (NPRAA) at Massachusetts General Hospital (MGH) was established, modeled after the North American Antiepileptic Drug Registry as a prospective registry of women with histories of first trimester exposure to atypical antipsychotics.

Over the last several years, the MGH NPRAA has accumulated very rigorous, prospectively ascertained data on outcomes following first trimester exposure to the atypical antipsychotics. Given the high prevalence of the use of this class of medications in reproductive-age women, data on the reproductive safety of atypical antipsychotics has been anxiously awaited and also has been relatively reassuring based on sources such as the NPRAA and also analyses of data from large administrative databases. For example, a recent paper published in JAMA Psychiatry by KF Huybrechts and her colleagues of 1,360,101 pregnant women who were enrolled in the Medicaid Analytic Extract database found an adjusted relative risk of 1.05 for congenital malformations in births for patients exposed to atypical antipsychotics (2016;73[9]:938-46).

Patients most often present with questions not about the reproductive safety of a class of medications, but about the safety of a particular medicine. A recent paper from our own group published in the American Journal of Psychiatry using data from the MGH NPRAA–described outcome of fetal exposure to quetiapine with a total of 152 women exposed to quetiapine and 205 unexposed patients. These patients were prospectively followed and compared with controls not exposed to the atypical antipsychotic but having a history of psychiatric morbidity. There was a 1.29% risk of major malformations in women exposed to quetiapine vs. 1.43% in the unexposed population (2018 Aug 16. doi: 10.1176/appi.ajp.2018.18010098).

The positive features of the MGH NPRAA include the careful rigorous assessments of patients over time as well as review of their obstetric, neonatal, and pediatric records up to 6 months, with blinded adjudication of outcome. The limitation of the small sample size remains with findings including relatively wide confidence intervals. With that being said, included in the paper in the discussion section is a pooled analysis of prospective data regarding quetiapine from the world’s literature that supports the findings of even this small prospective study in our registry, namely flat risk or absence of data suggesting that quetiapine is a major teratogen (pooled risk ratio, 1.03; 95% confidence interval, 0.89-1.19).

The delineation of risk for atypical antipsychotics is an extremely important area of research from a clinical point of view because it may help inform choices made by women with bipolar disorder who are well and maintained on these medicines as they wrestle with risk of relapse when agents are discontinued on one hand and reproductive safety concerns on the other.

Although not as widely used as perhaps a decade ago, data on the reproductive safety of lithium only continue to grow and become more refined. Use of lithium, a known teratogen with studies dating back to the 1970s, has an increased risk for cardiovascular malformations with the classic reference being to the small heightened risk of Ebstein’s anomaly (0.05%-0.1%). More recent studies from large administrative databases have been published with new data regarding risk of fetal exposure to lithium.

Two recent studies on lithium help to clarify some lingering questions about lithium use during pregnancy and risk for cardiovascular malformations. In one study published in the New England Journal of Medicine, researchers have demonstrated a small increased risk for cardiac malformations associated with using lithium during the first trimester (2017;376:2245-54). After researchers controlled for potential confounding factors, the adjusted risk ratio for cardiac malformations among infants exposed to lithium was 1.65 (95% CI, 1.02-2.68), compared with nonexposed infants. In a second study published in Lancet Psychiatry (2018 Aug;5[8]:644-52), a primary data meta-analysis of pregnant women and their children from six international cohorts in Denmark, Sweden, and Canada, there was no significant difference in major cardiac malformations between the lithium-exposed group, 2.1% (0.5%-3.7%), and the reference group, 1.6% (1.0%-2.1%).

Women with particularly brittle bipolar disorder or with histories of response to lithium may, in consultation with their doctors, consider use of lithium during pregnancy given the almost 50-year history of data accumulation on its reproductive safety, compared with some of the other mood stabilizers for which there is either confirmed teratogenicity (sodium valproate) or still incomplete data. Moreover, given the high risk for postpartum relapse of mood disorder in women who suffer from bipolar disorder, it is important to remember that the most robust data on prophylactic benefit of mood stabilizer during the peripartum period are with lithium.

Reproductive age women with bipolar disorder have for decades been caught between a teratologic rock and a clinical hard place. More recent data that have emerged from rigorously conducted registries and carefully analyzed administrative databases allow for more effective collaboration between patient and doctor as together they make personal decisions that match individual clinical situations with personal wishes.

Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications. Email him at [email protected].

The management of bipolar disorder during pregnancy is a critical clinical situation demanding great attention to issues such as reproductive safety of psychiatric medications used by women with bipolar disorder to maintain emotional well-being, compared with the established risk of relapse if patients stopped those medications.

Antonio_Diaz/Thinkstock

Treatment of bipolar disorder frequently includes mainstay treatment with mood stabilizers such as sodium valproate, lithium, lamotrigine, and second-generation atypical antipsychotics. While we have robust information regarding the reproductive safety of sodium valproate, it is a teratogen with a very high risk for neural tube defects. In contrast, data over the 15 years have been very supportive of the reproductive safety of lamotrigine. The last decade has seen growing use of second-generation antipsychotics, so-called atypical antipsychotics. There has been growing interest in the reproductive safety of these medicines given their use both for acute mania and for prophylaxis of bipolar disorder; they also are used as an adjunct to treat patients with major depression. Atypical antipsychotics are widely used off-label to treat obsessive compulsive disorder, other anxiety disorders, and a spectrum of psychiatric illness.

Until relatively recently, data on the reproductive safety of second-generation atypical antipsychotics has been relatively sparse, with the small number of prospective studies yielding a small total number of patients. Over the same period of time, the National Pregnancy Registry for Atypical Antipsychotics (NPRAA) at Massachusetts General Hospital (MGH) was established, modeled after the North American Antiepileptic Drug Registry as a prospective registry of women with histories of first trimester exposure to atypical antipsychotics.

Over the last several years, the MGH NPRAA has accumulated very rigorous, prospectively ascertained data on outcomes following first trimester exposure to the atypical antipsychotics. Given the high prevalence of the use of this class of medications in reproductive-age women, data on the reproductive safety of atypical antipsychotics has been anxiously awaited and also has been relatively reassuring based on sources such as the NPRAA and also analyses of data from large administrative databases. For example, a recent paper published in JAMA Psychiatry by KF Huybrechts and her colleagues of 1,360,101 pregnant women who were enrolled in the Medicaid Analytic Extract database found an adjusted relative risk of 1.05 for congenital malformations in births for patients exposed to atypical antipsychotics (2016;73[9]:938-46).

Patients most often present with questions not about the reproductive safety of a class of medications, but about the safety of a particular medicine. A recent paper from our own group published in the American Journal of Psychiatry using data from the MGH NPRAA–described outcome of fetal exposure to quetiapine with a total of 152 women exposed to quetiapine and 205 unexposed patients. These patients were prospectively followed and compared with controls not exposed to the atypical antipsychotic but having a history of psychiatric morbidity. There was a 1.29% risk of major malformations in women exposed to quetiapine vs. 1.43% in the unexposed population (2018 Aug 16. doi: 10.1176/appi.ajp.2018.18010098).

The positive features of the MGH NPRAA include the careful rigorous assessments of patients over time as well as review of their obstetric, neonatal, and pediatric records up to 6 months, with blinded adjudication of outcome. The limitation of the small sample size remains with findings including relatively wide confidence intervals. With that being said, included in the paper in the discussion section is a pooled analysis of prospective data regarding quetiapine from the world’s literature that supports the findings of even this small prospective study in our registry, namely flat risk or absence of data suggesting that quetiapine is a major teratogen (pooled risk ratio, 1.03; 95% confidence interval, 0.89-1.19).

The delineation of risk for atypical antipsychotics is an extremely important area of research from a clinical point of view because it may help inform choices made by women with bipolar disorder who are well and maintained on these medicines as they wrestle with risk of relapse when agents are discontinued on one hand and reproductive safety concerns on the other.

Although not as widely used as perhaps a decade ago, data on the reproductive safety of lithium only continue to grow and become more refined. Use of lithium, a known teratogen with studies dating back to the 1970s, has an increased risk for cardiovascular malformations with the classic reference being to the small heightened risk of Ebstein’s anomaly (0.05%-0.1%). More recent studies from large administrative databases have been published with new data regarding risk of fetal exposure to lithium.

Two recent studies on lithium help to clarify some lingering questions about lithium use during pregnancy and risk for cardiovascular malformations. In one study published in the New England Journal of Medicine, researchers have demonstrated a small increased risk for cardiac malformations associated with using lithium during the first trimester (2017;376:2245-54). After researchers controlled for potential confounding factors, the adjusted risk ratio for cardiac malformations among infants exposed to lithium was 1.65 (95% CI, 1.02-2.68), compared with nonexposed infants. In a second study published in Lancet Psychiatry (2018 Aug;5[8]:644-52), a primary data meta-analysis of pregnant women and their children from six international cohorts in Denmark, Sweden, and Canada, there was no significant difference in major cardiac malformations between the lithium-exposed group, 2.1% (0.5%-3.7%), and the reference group, 1.6% (1.0%-2.1%).

Women with particularly brittle bipolar disorder or with histories of response to lithium may, in consultation with their doctors, consider use of lithium during pregnancy given the almost 50-year history of data accumulation on its reproductive safety, compared with some of the other mood stabilizers for which there is either confirmed teratogenicity (sodium valproate) or still incomplete data. Moreover, given the high risk for postpartum relapse of mood disorder in women who suffer from bipolar disorder, it is important to remember that the most robust data on prophylactic benefit of mood stabilizer during the peripartum period are with lithium.

Reproductive age women with bipolar disorder have for decades been caught between a teratologic rock and a clinical hard place. More recent data that have emerged from rigorously conducted registries and carefully analyzed administrative databases allow for more effective collaboration between patient and doctor as together they make personal decisions that match individual clinical situations with personal wishes.

Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications. Email him at [email protected].

The management of bipolar disorder during pregnancy is a critical clinical situation demanding great attention to issues such as reproductive safety of psychiatric medications used by women with bipolar disorder to maintain emotional well-being, compared with the established risk of relapse if patients stopped those medications.

Antonio_Diaz/Thinkstock

Treatment of bipolar disorder frequently includes mainstay treatment with mood stabilizers such as sodium valproate, lithium, lamotrigine, and second-generation atypical antipsychotics. While we have robust information regarding the reproductive safety of sodium valproate, it is a teratogen with a very high risk for neural tube defects. In contrast, data over the 15 years have been very supportive of the reproductive safety of lamotrigine. The last decade has seen growing use of second-generation antipsychotics, so-called atypical antipsychotics. There has been growing interest in the reproductive safety of these medicines given their use both for acute mania and for prophylaxis of bipolar disorder; they also are used as an adjunct to treat patients with major depression. Atypical antipsychotics are widely used off-label to treat obsessive compulsive disorder, other anxiety disorders, and a spectrum of psychiatric illness.

Until relatively recently, data on the reproductive safety of second-generation atypical antipsychotics has been relatively sparse, with the small number of prospective studies yielding a small total number of patients. Over the same period of time, the National Pregnancy Registry for Atypical Antipsychotics (NPRAA) at Massachusetts General Hospital (MGH) was established, modeled after the North American Antiepileptic Drug Registry as a prospective registry of women with histories of first trimester exposure to atypical antipsychotics.

Over the last several years, the MGH NPRAA has accumulated very rigorous, prospectively ascertained data on outcomes following first trimester exposure to the atypical antipsychotics. Given the high prevalence of the use of this class of medications in reproductive-age women, data on the reproductive safety of atypical antipsychotics has been anxiously awaited and also has been relatively reassuring based on sources such as the NPRAA and also analyses of data from large administrative databases. For example, a recent paper published in JAMA Psychiatry by KF Huybrechts and her colleagues of 1,360,101 pregnant women who were enrolled in the Medicaid Analytic Extract database found an adjusted relative risk of 1.05 for congenital malformations in births for patients exposed to atypical antipsychotics (2016;73[9]:938-46).

Patients most often present with questions not about the reproductive safety of a class of medications, but about the safety of a particular medicine. A recent paper from our own group published in the American Journal of Psychiatry using data from the MGH NPRAA–described outcome of fetal exposure to quetiapine with a total of 152 women exposed to quetiapine and 205 unexposed patients. These patients were prospectively followed and compared with controls not exposed to the atypical antipsychotic but having a history of psychiatric morbidity. There was a 1.29% risk of major malformations in women exposed to quetiapine vs. 1.43% in the unexposed population (2018 Aug 16. doi: 10.1176/appi.ajp.2018.18010098).

The positive features of the MGH NPRAA include the careful rigorous assessments of patients over time as well as review of their obstetric, neonatal, and pediatric records up to 6 months, with blinded adjudication of outcome. The limitation of the small sample size remains with findings including relatively wide confidence intervals. With that being said, included in the paper in the discussion section is a pooled analysis of prospective data regarding quetiapine from the world’s literature that supports the findings of even this small prospective study in our registry, namely flat risk or absence of data suggesting that quetiapine is a major teratogen (pooled risk ratio, 1.03; 95% confidence interval, 0.89-1.19).

The delineation of risk for atypical antipsychotics is an extremely important area of research from a clinical point of view because it may help inform choices made by women with bipolar disorder who are well and maintained on these medicines as they wrestle with risk of relapse when agents are discontinued on one hand and reproductive safety concerns on the other.

Although not as widely used as perhaps a decade ago, data on the reproductive safety of lithium only continue to grow and become more refined. Use of lithium, a known teratogen with studies dating back to the 1970s, has an increased risk for cardiovascular malformations with the classic reference being to the small heightened risk of Ebstein’s anomaly (0.05%-0.1%). More recent studies from large administrative databases have been published with new data regarding risk of fetal exposure to lithium.

Two recent studies on lithium help to clarify some lingering questions about lithium use during pregnancy and risk for cardiovascular malformations. In one study published in the New England Journal of Medicine, researchers have demonstrated a small increased risk for cardiac malformations associated with using lithium during the first trimester (2017;376:2245-54). After researchers controlled for potential confounding factors, the adjusted risk ratio for cardiac malformations among infants exposed to lithium was 1.65 (95% CI, 1.02-2.68), compared with nonexposed infants. In a second study published in Lancet Psychiatry (2018 Aug;5[8]:644-52), a primary data meta-analysis of pregnant women and their children from six international cohorts in Denmark, Sweden, and Canada, there was no significant difference in major cardiac malformations between the lithium-exposed group, 2.1% (0.5%-3.7%), and the reference group, 1.6% (1.0%-2.1%).

Women with particularly brittle bipolar disorder or with histories of response to lithium may, in consultation with their doctors, consider use of lithium during pregnancy given the almost 50-year history of data accumulation on its reproductive safety, compared with some of the other mood stabilizers for which there is either confirmed teratogenicity (sodium valproate) or still incomplete data. Moreover, given the high risk for postpartum relapse of mood disorder in women who suffer from bipolar disorder, it is important to remember that the most robust data on prophylactic benefit of mood stabilizer during the peripartum period are with lithium.

Reproductive age women with bipolar disorder have for decades been caught between a teratologic rock and a clinical hard place. More recent data that have emerged from rigorously conducted registries and carefully analyzed administrative databases allow for more effective collaboration between patient and doctor as together they make personal decisions that match individual clinical situations with personal wishes.

Dr. Cohen is the director of the Ammon-Pinizzotto Center for Women’s Mental Health at Massachusetts General Hospital in Boston, which provides information resources and conducts clinical care and research in reproductive mental health. He has been a consultant to manufacturers of psychiatric medications. Email him at [email protected].

Question: Which of the following statements regarding the law on evidence is incorrect?

A. Expert testimony is always needed to establish the applicable standard of care in a negligence lawsuit.

B. According to the Federal Rules of Evidence, a witness may be qualified as an expert based on knowledge, skill, experience, training, or education.

C. It is the judge, not the jury, who determines whether a witness is admissible as an expert.

D. Expert testimony is a requirement in medical malpractice lawsuits, unless a plaintiff can successfully invoke the res ipsa loquitur doctrine.

E. Only a few states have enacted statutes specifying that an expert must be in the same specialty as the defendant, and in some cases, a nonphysician such as a nurse or pharmacist may be allowed to testify.

Answer: A. Under the tort of negligence, a defendant’s conduct is measured by what is expected of the reasonable person – the man on the street. The jury can usually decide on its own, without the aid of an expert, what that level of care ought to be. However, in medical malpractice lawsuits, the law requires an expert to testify to the requisite standard of care, as this determination is believed to be beyond the scope of the layperson.

An exception, rarely invoked, is the res ipsa loquitur doctrine, where “the thing speaks for itself.” There, an expert is not necessary because of common knowledge, e.g., when a surgeon inadvertently leaves a sponge or instrument inside a body cavity.

Whether one is admitted as an expert is within the sole discretion of the judge, who is guided by the Federal Rules of Evidence. Typically, an expert is in the same medical specialty, but there are instances of professionals of unlike specialties qualifying as experts. Examples include a nephrologist testifying against a urologist, an infectious disease specialist offering an expert opinion in a stroke case, a pharmacist testifying on the issue of a medication side effect, and a nurse on bedsores.

We had previously reviewed the law governing expert medical testimony in these columns.¹ However, three recent cases awaiting final adjudication caught our attention, as they raise important and serious legal issues.

The first frontally suggests that jury members may rely on their own notion of what constitutes an appropriate standard of care. Although it is established law in Maryland that expert testimony is required to set that standard in medical malpractice litigation, the recent Maryland case of Armacost v. Davis appeared to modify this principle, leading to a plaintiff verdict.²

The facts involved a neurosurgeon’s anterior cervical discectomy and fusion surgery, which was complicated by a pinpoint opening at the end of the incision. This eventually developed into a MRSA abscess. In his lawsuit, the plaintiff alleged that surgery was neither medically necessary nor appropriate, that there was no proper informed consent, and that the diagnosis of his postoperative infection was delayed.

A pivotal part of the trial centered on a Baltimore county judge’s instructions to the jury that it could consider what a layperson would deem reasonable standard of care. Moreover, the judge refused to modify the jury instructions when the doctor-defendant objected and asked that the standard of care be measured by the expectations for a neurosurgeon. The jury returned a verdict in favor of the plaintiff in the amount of $329,000.

Upon appeal, the Court of Special Appeals of Maryland ruled that the jury instructions were improper and therefore ordered a new trial. It held: “Medical malpractice claims are not general negligence claims, and so jury instructions on general negligence, although correct statements of Maryland law, are not supported by the facts of a case centered on the allegedly negligent conduct of a physician. Accordingly, we hold that the trial court erred in giving general negligence instructions in a medical malpractice case.”

The case is now before Maryland’s highest court, the Court of Appeals of Maryland, which is expected to uphold this decision and reject the reasonable person (instead of reasonable doctor) standard used by the lower court.

The second case deals with whether a jury in a medical liability trial may be prejudiced if they hear four medical experts testify for the physician and just one expert testify for the plaintiff. In Shallow v. Follwell, the defendant doctor performed a laparoscopic hernia repair, which was complicated by bowel perforation, atrial fibrillation, sepsis, and death.³

At trial, plaintiffs produced one expert witness, whereas Dr. Follwell had four, with expertise in cardiology, critical care, vascular surgery, and colorectal surgery. The trial court judge instructed the jury not to give weight to the number of experts on either side, and based on the testimony, the jury found that Dr. Follwell did not cause the perforated bowel or the patient’s death.

However, on appeal, the Missouri Court of Appeals overturned the verdict after finding that the trial court erred in allowing “unfairly cumulative and prejudicial repetition of certain expert opinions.” The Missouri Supreme Court is currently being asked to render a final opinion on the matter. In its supporting brief, the American Medical Association’s Litigation Center is urging the high court to “ensure that Missouri trial judges are empowered to safeguard the use of sound science in their courtrooms,” and that “given the highly specialized nature of medicine today, multiple experts may be required to ensure a jury has a proper understanding of the relevant medical science.”⁴

The third case addresses whether trial judges can suppress expert witness testimony attesting that a known complication of a medical procedure can occur absent any negligence.

The case involved a laparoscopic hysterectomy performed by a gynecologist. The patient’s bowel was perforated during the procedure.⁵ Expert witnesses from both sides testified about bowel perforation and professional standards, and the trial court allowed the defendant’s expert to state that such an injury was a commonplace risk even if surgery was performed properly.

The plaintiff objected to this testimony; but the trial judge overruled the plaintiff’s objection, and the jury found in favor of the gynecologist. Upon appeal, the Pennsylvania Superior Court reversed, concluding that the defendant’s expert testimony was irrelevant and misleading, and immaterial to the issue of whether the defendant’s treatment met the standard of care. It held that the evidence was inadmissible and ordered a new trial. The case is now before the Pennsylvania Supreme Court.

The foregoing three cases are yet to be finally adjudicated, but controversies in these and similar issues can be expected to continue. Expert testimony is dispositive at trial, and both sides rely heavily on it. Little wonder malpractice litigation is frequently framed as a “battle of the experts.”
 

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at [email protected].

References

1. Internal Medicine News, “Expert medical testimony,” Sept. 9, 2010; “Qualifying as an expert,” Jan. 2, 2015; “Dispensing with expert testimony,” April 19, 2016.

2. Armacost v. Davis, 175 A.3d 150 (Ct. App. Md, 2017).

3. Shallow v. Follwell, (No. ED103811, Mo. App., Eastern Dist., Div. 4, 2017).

4. Henry TA, “Is it OK to have 4-to-1 expert ratio in medical liability case?” AMA Wire, June 22, 2018.

5. Mitchell v. Shikora, 161 A.3d 970 (Pa. Super. 2017).

Question: Which of the following statements regarding the law on evidence is incorrect?

A. Expert testimony is always needed to establish the applicable standard of care in a negligence lawsuit.

B. According to the Federal Rules of Evidence, a witness may be qualified as an expert based on knowledge, skill, experience, training, or education.

C. It is the judge, not the jury, who determines whether a witness is admissible as an expert.

D. Expert testimony is a requirement in medical malpractice lawsuits, unless a plaintiff can successfully invoke the res ipsa loquitur doctrine.

E. Only a few states have enacted statutes specifying that an expert must be in the same specialty as the defendant, and in some cases, a nonphysician such as a nurse or pharmacist may be allowed to testify.

Answer: A. Under the tort of negligence, a defendant’s conduct is measured by what is expected of the reasonable person – the man on the street. The jury can usually decide on its own, without the aid of an expert, what that level of care ought to be. However, in medical malpractice lawsuits, the law requires an expert to testify to the requisite standard of care, as this determination is believed to be beyond the scope of the layperson.

An exception, rarely invoked, is the res ipsa loquitur doctrine, where “the thing speaks for itself.” There, an expert is not necessary because of common knowledge, e.g., when a surgeon inadvertently leaves a sponge or instrument inside a body cavity.

Whether one is admitted as an expert is within the sole discretion of the judge, who is guided by the Federal Rules of Evidence. Typically, an expert is in the same medical specialty, but there are instances of professionals of unlike specialties qualifying as experts. Examples include a nephrologist testifying against a urologist, an infectious disease specialist offering an expert opinion in a stroke case, a pharmacist testifying on the issue of a medication side effect, and a nurse on bedsores.

We had previously reviewed the law governing expert medical testimony in these columns.¹ However, three recent cases awaiting final adjudication caught our attention, as they raise important and serious legal issues.

The first frontally suggests that jury members may rely on their own notion of what constitutes an appropriate standard of care. Although it is established law in Maryland that expert testimony is required to set that standard in medical malpractice litigation, the recent Maryland case of Armacost v. Davis appeared to modify this principle, leading to a plaintiff verdict.²

The facts involved a neurosurgeon’s anterior cervical discectomy and fusion surgery, which was complicated by a pinpoint opening at the end of the incision. This eventually developed into a MRSA abscess. In his lawsuit, the plaintiff alleged that surgery was neither medically necessary nor appropriate, that there was no proper informed consent, and that the diagnosis of his postoperative infection was delayed.

A pivotal part of the trial centered on a Baltimore county judge’s instructions to the jury that it could consider what a layperson would deem reasonable standard of care. Moreover, the judge refused to modify the jury instructions when the doctor-defendant objected and asked that the standard of care be measured by the expectations for a neurosurgeon. The jury returned a verdict in favor of the plaintiff in the amount of $329,000.

Upon appeal, the Court of Special Appeals of Maryland ruled that the jury instructions were improper and therefore ordered a new trial. It held: “Medical malpractice claims are not general negligence claims, and so jury instructions on general negligence, although correct statements of Maryland law, are not supported by the facts of a case centered on the allegedly negligent conduct of a physician. Accordingly, we hold that the trial court erred in giving general negligence instructions in a medical malpractice case.”

The case is now before Maryland’s highest court, the Court of Appeals of Maryland, which is expected to uphold this decision and reject the reasonable person (instead of reasonable doctor) standard used by the lower court.

The second case deals with whether a jury in a medical liability trial may be prejudiced if they hear four medical experts testify for the physician and just one expert testify for the plaintiff. In Shallow v. Follwell, the defendant doctor performed a laparoscopic hernia repair, which was complicated by bowel perforation, atrial fibrillation, sepsis, and death.³

At trial, plaintiffs produced one expert witness, whereas Dr. Follwell had four, with expertise in cardiology, critical care, vascular surgery, and colorectal surgery. The trial court judge instructed the jury not to give weight to the number of experts on either side, and based on the testimony, the jury found that Dr. Follwell did not cause the perforated bowel or the patient’s death.

However, on appeal, the Missouri Court of Appeals overturned the verdict after finding that the trial court erred in allowing “unfairly cumulative and prejudicial repetition of certain expert opinions.” The Missouri Supreme Court is currently being asked to render a final opinion on the matter. In its supporting brief, the American Medical Association’s Litigation Center is urging the high court to “ensure that Missouri trial judges are empowered to safeguard the use of sound science in their courtrooms,” and that “given the highly specialized nature of medicine today, multiple experts may be required to ensure a jury has a proper understanding of the relevant medical science.”⁴

The third case addresses whether trial judges can suppress expert witness testimony attesting that a known complication of a medical procedure can occur absent any negligence.

The case involved a laparoscopic hysterectomy performed by a gynecologist. The patient’s bowel was perforated during the procedure.⁵ Expert witnesses from both sides testified about bowel perforation and professional standards, and the trial court allowed the defendant’s expert to state that such an injury was a commonplace risk even if surgery was performed properly.

The plaintiff objected to this testimony; but the trial judge overruled the plaintiff’s objection, and the jury found in favor of the gynecologist. Upon appeal, the Pennsylvania Superior Court reversed, concluding that the defendant’s expert testimony was irrelevant and misleading, and immaterial to the issue of whether the defendant’s treatment met the standard of care. It held that the evidence was inadmissible and ordered a new trial. The case is now before the Pennsylvania Supreme Court.

The foregoing three cases are yet to be finally adjudicated, but controversies in these and similar issues can be expected to continue. Expert testimony is dispositive at trial, and both sides rely heavily on it. Little wonder malpractice litigation is frequently framed as a “battle of the experts.”
 

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at [email protected].

References

1. Internal Medicine News, “Expert medical testimony,” Sept. 9, 2010; “Qualifying as an expert,” Jan. 2, 2015; “Dispensing with expert testimony,” April 19, 2016.

2. Armacost v. Davis, 175 A.3d 150 (Ct. App. Md, 2017).

3. Shallow v. Follwell, (No. ED103811, Mo. App., Eastern Dist., Div. 4, 2017).

4. Henry TA, “Is it OK to have 4-to-1 expert ratio in medical liability case?” AMA Wire, June 22, 2018.

5. Mitchell v. Shikora, 161 A.3d 970 (Pa. Super. 2017).

Question: Which of the following statements regarding the law on evidence is incorrect?

A. Expert testimony is always needed to establish the applicable standard of care in a negligence lawsuit.

B. According to the Federal Rules of Evidence, a witness may be qualified as an expert based on knowledge, skill, experience, training, or education.

C. It is the judge, not the jury, who determines whether a witness is admissible as an expert.

D. Expert testimony is a requirement in medical malpractice lawsuits, unless a plaintiff can successfully invoke the res ipsa loquitur doctrine.

E. Only a few states have enacted statutes specifying that an expert must be in the same specialty as the defendant, and in some cases, a nonphysician such as a nurse or pharmacist may be allowed to testify.

Answer: A. Under the tort of negligence, a defendant’s conduct is measured by what is expected of the reasonable person – the man on the street. The jury can usually decide on its own, without the aid of an expert, what that level of care ought to be. However, in medical malpractice lawsuits, the law requires an expert to testify to the requisite standard of care, as this determination is believed to be beyond the scope of the layperson.

An exception, rarely invoked, is the res ipsa loquitur doctrine, where “the thing speaks for itself.” There, an expert is not necessary because of common knowledge, e.g., when a surgeon inadvertently leaves a sponge or instrument inside a body cavity.

Whether one is admitted as an expert is within the sole discretion of the judge, who is guided by the Federal Rules of Evidence. Typically, an expert is in the same medical specialty, but there are instances of professionals of unlike specialties qualifying as experts. Examples include a nephrologist testifying against a urologist, an infectious disease specialist offering an expert opinion in a stroke case, a pharmacist testifying on the issue of a medication side effect, and a nurse on bedsores.

We had previously reviewed the law governing expert medical testimony in these columns.¹ However, three recent cases awaiting final adjudication caught our attention, as they raise important and serious legal issues.

The first frontally suggests that jury members may rely on their own notion of what constitutes an appropriate standard of care. Although it is established law in Maryland that expert testimony is required to set that standard in medical malpractice litigation, the recent Maryland case of Armacost v. Davis appeared to modify this principle, leading to a plaintiff verdict.²

The facts involved a neurosurgeon’s anterior cervical discectomy and fusion surgery, which was complicated by a pinpoint opening at the end of the incision. This eventually developed into a MRSA abscess. In his lawsuit, the plaintiff alleged that surgery was neither medically necessary nor appropriate, that there was no proper informed consent, and that the diagnosis of his postoperative infection was delayed.

A pivotal part of the trial centered on a Baltimore county judge’s instructions to the jury that it could consider what a layperson would deem reasonable standard of care. Moreover, the judge refused to modify the jury instructions when the doctor-defendant objected and asked that the standard of care be measured by the expectations for a neurosurgeon. The jury returned a verdict in favor of the plaintiff in the amount of $329,000.

Upon appeal, the Court of Special Appeals of Maryland ruled that the jury instructions were improper and therefore ordered a new trial. It held: “Medical malpractice claims are not general negligence claims, and so jury instructions on general negligence, although correct statements of Maryland law, are not supported by the facts of a case centered on the allegedly negligent conduct of a physician. Accordingly, we hold that the trial court erred in giving general negligence instructions in a medical malpractice case.”

The case is now before Maryland’s highest court, the Court of Appeals of Maryland, which is expected to uphold this decision and reject the reasonable person (instead of reasonable doctor) standard used by the lower court.

The second case deals with whether a jury in a medical liability trial may be prejudiced if they hear four medical experts testify for the physician and just one expert testify for the plaintiff. In Shallow v. Follwell, the defendant doctor performed a laparoscopic hernia repair, which was complicated by bowel perforation, atrial fibrillation, sepsis, and death.³

At trial, plaintiffs produced one expert witness, whereas Dr. Follwell had four, with expertise in cardiology, critical care, vascular surgery, and colorectal surgery. The trial court judge instructed the jury not to give weight to the number of experts on either side, and based on the testimony, the jury found that Dr. Follwell did not cause the perforated bowel or the patient’s death.

However, on appeal, the Missouri Court of Appeals overturned the verdict after finding that the trial court erred in allowing “unfairly cumulative and prejudicial repetition of certain expert opinions.” The Missouri Supreme Court is currently being asked to render a final opinion on the matter. In its supporting brief, the American Medical Association’s Litigation Center is urging the high court to “ensure that Missouri trial judges are empowered to safeguard the use of sound science in their courtrooms,” and that “given the highly specialized nature of medicine today, multiple experts may be required to ensure a jury has a proper understanding of the relevant medical science.”⁴

The third case addresses whether trial judges can suppress expert witness testimony attesting that a known complication of a medical procedure can occur absent any negligence.

The case involved a laparoscopic hysterectomy performed by a gynecologist. The patient’s bowel was perforated during the procedure.⁵ Expert witnesses from both sides testified about bowel perforation and professional standards, and the trial court allowed the defendant’s expert to state that such an injury was a commonplace risk even if surgery was performed properly.

The plaintiff objected to this testimony; but the trial judge overruled the plaintiff’s objection, and the jury found in favor of the gynecologist. Upon appeal, the Pennsylvania Superior Court reversed, concluding that the defendant’s expert testimony was irrelevant and misleading, and immaterial to the issue of whether the defendant’s treatment met the standard of care. It held that the evidence was inadmissible and ordered a new trial. The case is now before the Pennsylvania Supreme Court.

The foregoing three cases are yet to be finally adjudicated, but controversies in these and similar issues can be expected to continue. Expert testimony is dispositive at trial, and both sides rely heavily on it. Little wonder malpractice litigation is frequently framed as a “battle of the experts.”
 

Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. For additional information, readers may contact the author at [email protected].

References

1. Internal Medicine News, “Expert medical testimony,” Sept. 9, 2010; “Qualifying as an expert,” Jan. 2, 2015; “Dispensing with expert testimony,” April 19, 2016.

2. Armacost v. Davis, 175 A.3d 150 (Ct. App. Md, 2017).

3. Shallow v. Follwell, (No. ED103811, Mo. App., Eastern Dist., Div. 4, 2017).

4. Henry TA, “Is it OK to have 4-to-1 expert ratio in medical liability case?” AMA Wire, June 22, 2018.

5. Mitchell v. Shikora, 161 A.3d 970 (Pa. Super. 2017).

Over the past several months, I’ve found myself increasingly reflective on the intersection of culture, relationships, and my professional work with those who have an autism spectrum disorder. Last winter, an adolescent boy treated by myself and other providers died by suicide. Adam (name changed) had been diagnosed with autism as a toddler and had struggled with anxiety and depression for several years; in the office, as he grew into an athletic teenager, Adam spoke more frequently about “not fitting in” with his peers and therapeutic focus was placed on building Adam’s sense of himself and fostering his self-confidence and perceived self-competence. His unexpected death was a tremendous shock, and his loved ones – including the clinical team – desperately searched for answers that could help add some understanding to the heartbreaking event.

Rawpixel/Thinkstock

As I attempted to search for answers and reconcile national news with my clinical and teaching experiences, I was struck by something that Andrew Solomon eloquently captured in his June 2018 New Yorker article that again touches upon the theme of connection.⁶ Mr. Solomon writes “modernity is alienating” and about how he receives correspondence from those who struggle with depression. “What is most striking to me is how alone many of them are ... these people are so alone that they are effectively invisible to the rest of us ... many of them describe suicidal feelings,” he noted.

The power of connection in our day-to-day work is undeniable. The influence of human interaction and appreciating one’s unique narrative is a bedrock of clinical care and can unquestionably allow us to better understand individual suffering, deliver optimal care, and combat shame as Hannah Gadsby boldly shared in her recent Netflix comedy special “Nanette.” This shame can drive one to experience earth-shattering depressive episodes and influence thoughts of suicide. “We simply cannot make it on our own,” Ms. Gadsby explains, “we’re humans. We’re to be connected.” Humans are indeed hardwired for connection; isolation and disconnection can lead to significant health problems and are linked with mental health concerns. The former U.S. Surgeon General Vivek H. Murthy, MD, has referred to loneliness as an epidemic, and those with autism may be at increased risk for feeling lonely and isolated.^7,8

Synthesizing thoughts about relationships, suicide, loneliness, love, well-being, and autism produces a complicated web of, well, connections. Suicide in the autism population hasn’t been well researched, but one 2016 study revealed sobering numbers about suicide being a leading cause of premature death in people with autism.⁹ How do these numbers associate with feelings of isolation, wanting to fit in, and troubles talking about emotions – all of which can characterize those with ASD? Data, not surprisingly, support the role of loneliness as a risk factor for the development of depression and suicidal ideation in those with ASD.¹⁰ In addition, social-communication challenges, even in the absence of an autism diagnosis, are related to depression and suicidality.¹¹ Another recent study showed a relationship between autistic traits and depression symptoms, an association seemingly linked to being bullied.¹² We cannot continue to hold onto the myth that individuals with autism don’t desire relationships and love because it’s these desires and not being able to fulfill them, limited opportunities to engage in meaningful experiences, and feeling different that can lead to negative outcomes.

Dr. Dickerson, a child and adolescent psychiatrist, is assistant professor of psychiatry at the University of Vermont, Burlington, where he is director of the autism diagnostic clinic. Email him at [email protected].

References

1. Harv Rev Psychiatry. 2018 Jul/Aug;26(4):201-15.

2. MMWR Morb Mortal Wkly Rep. 2018 Jun 8;67(22):617-24.

3. www.healthvermont.gov/YRBS

4. MMWR Surveill Summ. 2017 Oct;66(18):1-16.

5. JAMA Pediatr. 2015 May;169(5):466-73.

6. “Anthony Bourdain, Kate Spade, and the Preventable Tragedies of Suicide,” By Anthony Solomon, The New Yorker. Jun 8, 2018.

7. “Work and the Loneliness Epidemic,” By Vivek H. Murthy, Harvard Business Review. Sep 28, 2017.

8. Child Dev. 2000 Mar-Apr;71(2):447-56.

9. Br J Psychiatry. 2016 Mar;208(3):232-8.

10. Depress Anxiety. 2018 Jul;35(7):648-57.

11. J Am Acad Child Adolesc Psychiatry. 2018 May;57(5):313-20.

12. JAMA Psychiatry. 2018 Aug 1;75(8):835-43.

13. The Lancet Psychiatry. 2017 Jun;4(6):e11.

14. “Promoting Individual, Family, and Community Connectedness to Prevent Suicidal Behavior,” Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, www.cdc.gov/injury.

15. JAMA Psychiatry. 2018 Jul 11. doi: 10.1001/jamapsychiatry.2018.1776.

Over the past several months, I’ve found myself increasingly reflective on the intersection of culture, relationships, and my professional work with those who have an autism spectrum disorder. Last winter, an adolescent boy treated by myself and other providers died by suicide. Adam (name changed) had been diagnosed with autism as a toddler and had struggled with anxiety and depression for several years; in the office, as he grew into an athletic teenager, Adam spoke more frequently about “not fitting in” with his peers and therapeutic focus was placed on building Adam’s sense of himself and fostering his self-confidence and perceived self-competence. His unexpected death was a tremendous shock, and his loved ones – including the clinical team – desperately searched for answers that could help add some understanding to the heartbreaking event.

Rawpixel/Thinkstock

As I attempted to search for answers and reconcile national news with my clinical and teaching experiences, I was struck by something that Andrew Solomon eloquently captured in his June 2018 New Yorker article that again touches upon the theme of connection.⁶ Mr. Solomon writes “modernity is alienating” and about how he receives correspondence from those who struggle with depression. “What is most striking to me is how alone many of them are ... these people are so alone that they are effectively invisible to the rest of us ... many of them describe suicidal feelings,” he noted.

The power of connection in our day-to-day work is undeniable. The influence of human interaction and appreciating one’s unique narrative is a bedrock of clinical care and can unquestionably allow us to better understand individual suffering, deliver optimal care, and combat shame as Hannah Gadsby boldly shared in her recent Netflix comedy special “Nanette.” This shame can drive one to experience earth-shattering depressive episodes and influence thoughts of suicide. “We simply cannot make it on our own,” Ms. Gadsby explains, “we’re humans. We’re to be connected.” Humans are indeed hardwired for connection; isolation and disconnection can lead to significant health problems and are linked with mental health concerns. The former U.S. Surgeon General Vivek H. Murthy, MD, has referred to loneliness as an epidemic, and those with autism may be at increased risk for feeling lonely and isolated.^7,8

Synthesizing thoughts about relationships, suicide, loneliness, love, well-being, and autism produces a complicated web of, well, connections. Suicide in the autism population hasn’t been well researched, but one 2016 study revealed sobering numbers about suicide being a leading cause of premature death in people with autism.⁹ How do these numbers associate with feelings of isolation, wanting to fit in, and troubles talking about emotions – all of which can characterize those with ASD? Data, not surprisingly, support the role of loneliness as a risk factor for the development of depression and suicidal ideation in those with ASD.¹⁰ In addition, social-communication challenges, even in the absence of an autism diagnosis, are related to depression and suicidality.¹¹ Another recent study showed a relationship between autistic traits and depression symptoms, an association seemingly linked to being bullied.¹² We cannot continue to hold onto the myth that individuals with autism don’t desire relationships and love because it’s these desires and not being able to fulfill them, limited opportunities to engage in meaningful experiences, and feeling different that can lead to negative outcomes.

Dr. Dickerson, a child and adolescent psychiatrist, is assistant professor of psychiatry at the University of Vermont, Burlington, where he is director of the autism diagnostic clinic. Email him at [email protected].

References

1. Harv Rev Psychiatry. 2018 Jul/Aug;26(4):201-15.

2. MMWR Morb Mortal Wkly Rep. 2018 Jun 8;67(22):617-24.

3. www.healthvermont.gov/YRBS

4. MMWR Surveill Summ. 2017 Oct;66(18):1-16.

5. JAMA Pediatr. 2015 May;169(5):466-73.

6. “Anthony Bourdain, Kate Spade, and the Preventable Tragedies of Suicide,” By Anthony Solomon, The New Yorker. Jun 8, 2018.

7. “Work and the Loneliness Epidemic,” By Vivek H. Murthy, Harvard Business Review. Sep 28, 2017.

8. Child Dev. 2000 Mar-Apr;71(2):447-56.

9. Br J Psychiatry. 2016 Mar;208(3):232-8.

10. Depress Anxiety. 2018 Jul;35(7):648-57.

11. J Am Acad Child Adolesc Psychiatry. 2018 May;57(5):313-20.

12. JAMA Psychiatry. 2018 Aug 1;75(8):835-43.

13. The Lancet Psychiatry. 2017 Jun;4(6):e11.

14. “Promoting Individual, Family, and Community Connectedness to Prevent Suicidal Behavior,” Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, www.cdc.gov/injury.

15. JAMA Psychiatry. 2018 Jul 11. doi: 10.1001/jamapsychiatry.2018.1776.

Over the past several months, I’ve found myself increasingly reflective on the intersection of culture, relationships, and my professional work with those who have an autism spectrum disorder. Last winter, an adolescent boy treated by myself and other providers died by suicide. Adam (name changed) had been diagnosed with autism as a toddler and had struggled with anxiety and depression for several years; in the office, as he grew into an athletic teenager, Adam spoke more frequently about “not fitting in” with his peers and therapeutic focus was placed on building Adam’s sense of himself and fostering his self-confidence and perceived self-competence. His unexpected death was a tremendous shock, and his loved ones – including the clinical team – desperately searched for answers that could help add some understanding to the heartbreaking event.

Rawpixel/Thinkstock

As I attempted to search for answers and reconcile national news with my clinical and teaching experiences, I was struck by something that Andrew Solomon eloquently captured in his June 2018 New Yorker article that again touches upon the theme of connection.⁶ Mr. Solomon writes “modernity is alienating” and about how he receives correspondence from those who struggle with depression. “What is most striking to me is how alone many of them are ... these people are so alone that they are effectively invisible to the rest of us ... many of them describe suicidal feelings,” he noted.

The power of connection in our day-to-day work is undeniable. The influence of human interaction and appreciating one’s unique narrative is a bedrock of clinical care and can unquestionably allow us to better understand individual suffering, deliver optimal care, and combat shame as Hannah Gadsby boldly shared in her recent Netflix comedy special “Nanette.” This shame can drive one to experience earth-shattering depressive episodes and influence thoughts of suicide. “We simply cannot make it on our own,” Ms. Gadsby explains, “we’re humans. We’re to be connected.” Humans are indeed hardwired for connection; isolation and disconnection can lead to significant health problems and are linked with mental health concerns. The former U.S. Surgeon General Vivek H. Murthy, MD, has referred to loneliness as an epidemic, and those with autism may be at increased risk for feeling lonely and isolated.^7,8

Synthesizing thoughts about relationships, suicide, loneliness, love, well-being, and autism produces a complicated web of, well, connections. Suicide in the autism population hasn’t been well researched, but one 2016 study revealed sobering numbers about suicide being a leading cause of premature death in people with autism.⁹ How do these numbers associate with feelings of isolation, wanting to fit in, and troubles talking about emotions – all of which can characterize those with ASD? Data, not surprisingly, support the role of loneliness as a risk factor for the development of depression and suicidal ideation in those with ASD.¹⁰ In addition, social-communication challenges, even in the absence of an autism diagnosis, are related to depression and suicidality.¹¹ Another recent study showed a relationship between autistic traits and depression symptoms, an association seemingly linked to being bullied.¹² We cannot continue to hold onto the myth that individuals with autism don’t desire relationships and love because it’s these desires and not being able to fulfill them, limited opportunities to engage in meaningful experiences, and feeling different that can lead to negative outcomes.

Dr. Dickerson, a child and adolescent psychiatrist, is assistant professor of psychiatry at the University of Vermont, Burlington, where he is director of the autism diagnostic clinic. Email him at [email protected].

References

1. Harv Rev Psychiatry. 2018 Jul/Aug;26(4):201-15.

2. MMWR Morb Mortal Wkly Rep. 2018 Jun 8;67(22):617-24.

3. www.healthvermont.gov/YRBS

4. MMWR Surveill Summ. 2017 Oct;66(18):1-16.

5. JAMA Pediatr. 2015 May;169(5):466-73.

6. “Anthony Bourdain, Kate Spade, and the Preventable Tragedies of Suicide,” By Anthony Solomon, The New Yorker. Jun 8, 2018.

7. “Work and the Loneliness Epidemic,” By Vivek H. Murthy, Harvard Business Review. Sep 28, 2017.

8. Child Dev. 2000 Mar-Apr;71(2):447-56.

9. Br J Psychiatry. 2016 Mar;208(3):232-8.

10. Depress Anxiety. 2018 Jul;35(7):648-57.

11. J Am Acad Child Adolesc Psychiatry. 2018 May;57(5):313-20.

12. JAMA Psychiatry. 2018 Aug 1;75(8):835-43.

13. The Lancet Psychiatry. 2017 Jun;4(6):e11.

14. “Promoting Individual, Family, and Community Connectedness to Prevent Suicidal Behavior,” Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, www.cdc.gov/injury.

15. JAMA Psychiatry. 2018 Jul 11. doi: 10.1001/jamapsychiatry.2018.1776.

The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.¹ The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.² Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.¹ Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.^3,4

Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. Tinea can be complicated by kerion development, which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.^3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.

While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.¹ The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.^6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.

It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.¹T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.⁸ Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.⁸ Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.¹ Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.

Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.⁵ Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.⁹

Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.

References

1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).

2. Pediatr Dermatol. 2018 May;35(3):323-8

3. Arch Dis Child. 2016 May;101(5):503.

4. IDCases. 2018 Jun 28;14:e00418.

5. Int J Dermatol. 2018 Jan;57(1):3-9.

6. Pediatr Rev. 2007 May;28(5):164-74.

7. Clin Cosmet Investig Dermatol. 2010;3:89-98.

8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.

9. Med Mycol. 1999 Apr;37(2):97-9.

The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.¹ The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.² Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.¹ Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.^3,4

Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. Tinea can be complicated by kerion development, which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.^3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.

While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.¹ The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.^6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.

It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.¹T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.⁸ Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.⁸ Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.¹ Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.

Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.⁵ Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.⁹

Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.

References

1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).

2. Pediatr Dermatol. 2018 May;35(3):323-8

3. Arch Dis Child. 2016 May;101(5):503.

4. IDCases. 2018 Jun 28;14:e00418.

5. Int J Dermatol. 2018 Jan;57(1):3-9.

6. Pediatr Rev. 2007 May;28(5):164-74.

7. Clin Cosmet Investig Dermatol. 2010;3:89-98.

8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.

9. Med Mycol. 1999 Apr;37(2):97-9.

The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.¹ The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.² Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.¹ Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.^3,4

Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. Tinea can be complicated by kerion development, which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.^3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.

While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.¹ The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.^6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.

It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.¹T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.⁸ Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.⁸ Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.¹ Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.

Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.⁵ Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.⁹

Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.

References

1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).

2. Pediatr Dermatol. 2018 May;35(3):323-8

3. Arch Dis Child. 2016 May;101(5):503.

4. IDCases. 2018 Jun 28;14:e00418.

5. Int J Dermatol. 2018 Jan;57(1):3-9.

6. Pediatr Rev. 2007 May;28(5):164-74.

7. Clin Cosmet Investig Dermatol. 2010;3:89-98.

8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.

9. Med Mycol. 1999 Apr;37(2):97-9.

“We’ll have one strawberry sugar cone, two chocolate swirls, and a mocha almond.”

iStock

“Dr. Wilkoff, I haven’t seen you in ... must be 5 years. You look great! How’s retirement going?”

“You look great too, Kim. The neighborhood has needed an ice cream parlor like yours for a long time. How’s the family?”

Alerted by the commotion of our catching up, Kim’s husband came outside to see what was going on. Looking at my wife, he said, “You know he saved our daughter’s life?”

Well, not exactly. A timely referral to a psychologist I knew was good with eating disorders had started the slow process of returning their anorectic daughter to health. I thanked him and tried to put a more historically correct spin on his story.

Most of my encounters with former patients and their parents aren’t as dramatic as this one at Kim’s Ice Cream Shack, but they always leave me with a warm, positive feeling that stays with me all day. Every now and then they include a compliment or a thank you, but most of the time the conversations are dominated by questions about how the other are doing and what our families are up to.

One of the perks of living in the town where you practice is that your patients also are your neighbors. Not every physician views this proximity as a positive, but for me, it was a gift that has kept on giving after I retired.

Our house phone number was always listed in the phone book, and I can count on the fingers of two hands how many times in 40 years that I received what I would consider an inappropriate or invasive call. Our office offered evening and weekend hours and a generous schedule of phone-in call times. But I’m convinced that it was the neighbor-to-neighbor relationship that kept the work/home balance intact. Even though I may have helped a plumber and his wife with their sick children, that professional arrangement didn’t include a free pass to call him after hours if I knew my leaking faucet could wait until the weekend was over.

By the same token, when a patient or a customer is also your neighbor there is an unspoken ethic that the service you provide must be your best effort. That’s not an admission that I was in the habit of offering substandard care to “folks from away,” but there is special motivation when your work is being scrutinized by people you’re likely to see next week at the grocery store checkout.

Office visits with neighbors often tended to take longer because there was a tendency to drift off topic and ask about a sibling’s baseball game I had read about in the paper or how the lobster catch was running that season. On the other hand, I must admit that I did my share of reporting (really it was bragging) on my own children’s accomplishments.

But now I’m reaping the benefits of those extra minutes invested in the office, because I suspect former patients and their families are more likely to want to reminisce when we meet in a restaurant or at the farmers’ market.

If you are a young physician and worrying about finding a good work/life balance, I urge you to consider living and working and then staying on in a place in which your patients also will be your neighbors. It will enrich your work experience and repay you many times over when it’s time to retire.

If you can’t find that place, at least treat your patients as though they were your neighbors.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

“We’ll have one strawberry sugar cone, two chocolate swirls, and a mocha almond.”

iStock

“Dr. Wilkoff, I haven’t seen you in ... must be 5 years. You look great! How’s retirement going?”

“You look great too, Kim. The neighborhood has needed an ice cream parlor like yours for a long time. How’s the family?”

Alerted by the commotion of our catching up, Kim’s husband came outside to see what was going on. Looking at my wife, he said, “You know he saved our daughter’s life?”

Well, not exactly. A timely referral to a psychologist I knew was good with eating disorders had started the slow process of returning their anorectic daughter to health. I thanked him and tried to put a more historically correct spin on his story.

Most of my encounters with former patients and their parents aren’t as dramatic as this one at Kim’s Ice Cream Shack, but they always leave me with a warm, positive feeling that stays with me all day. Every now and then they include a compliment or a thank you, but most of the time the conversations are dominated by questions about how the other are doing and what our families are up to.

One of the perks of living in the town where you practice is that your patients also are your neighbors. Not every physician views this proximity as a positive, but for me, it was a gift that has kept on giving after I retired.

Our house phone number was always listed in the phone book, and I can count on the fingers of two hands how many times in 40 years that I received what I would consider an inappropriate or invasive call. Our office offered evening and weekend hours and a generous schedule of phone-in call times. But I’m convinced that it was the neighbor-to-neighbor relationship that kept the work/home balance intact. Even though I may have helped a plumber and his wife with their sick children, that professional arrangement didn’t include a free pass to call him after hours if I knew my leaking faucet could wait until the weekend was over.

By the same token, when a patient or a customer is also your neighbor there is an unspoken ethic that the service you provide must be your best effort. That’s not an admission that I was in the habit of offering substandard care to “folks from away,” but there is special motivation when your work is being scrutinized by people you’re likely to see next week at the grocery store checkout.

Office visits with neighbors often tended to take longer because there was a tendency to drift off topic and ask about a sibling’s baseball game I had read about in the paper or how the lobster catch was running that season. On the other hand, I must admit that I did my share of reporting (really it was bragging) on my own children’s accomplishments.

But now I’m reaping the benefits of those extra minutes invested in the office, because I suspect former patients and their families are more likely to want to reminisce when we meet in a restaurant or at the farmers’ market.

If you are a young physician and worrying about finding a good work/life balance, I urge you to consider living and working and then staying on in a place in which your patients also will be your neighbors. It will enrich your work experience and repay you many times over when it’s time to retire.

If you can’t find that place, at least treat your patients as though they were your neighbors.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

“We’ll have one strawberry sugar cone, two chocolate swirls, and a mocha almond.”

iStock

“Dr. Wilkoff, I haven’t seen you in ... must be 5 years. You look great! How’s retirement going?”

“You look great too, Kim. The neighborhood has needed an ice cream parlor like yours for a long time. How’s the family?”

Alerted by the commotion of our catching up, Kim’s husband came outside to see what was going on. Looking at my wife, he said, “You know he saved our daughter’s life?”

Well, not exactly. A timely referral to a psychologist I knew was good with eating disorders had started the slow process of returning their anorectic daughter to health. I thanked him and tried to put a more historically correct spin on his story.

Most of my encounters with former patients and their parents aren’t as dramatic as this one at Kim’s Ice Cream Shack, but they always leave me with a warm, positive feeling that stays with me all day. Every now and then they include a compliment or a thank you, but most of the time the conversations are dominated by questions about how the other are doing and what our families are up to.

One of the perks of living in the town where you practice is that your patients also are your neighbors. Not every physician views this proximity as a positive, but for me, it was a gift that has kept on giving after I retired.

Our house phone number was always listed in the phone book, and I can count on the fingers of two hands how many times in 40 years that I received what I would consider an inappropriate or invasive call. Our office offered evening and weekend hours and a generous schedule of phone-in call times. But I’m convinced that it was the neighbor-to-neighbor relationship that kept the work/home balance intact. Even though I may have helped a plumber and his wife with their sick children, that professional arrangement didn’t include a free pass to call him after hours if I knew my leaking faucet could wait until the weekend was over.

By the same token, when a patient or a customer is also your neighbor there is an unspoken ethic that the service you provide must be your best effort. That’s not an admission that I was in the habit of offering substandard care to “folks from away,” but there is special motivation when your work is being scrutinized by people you’re likely to see next week at the grocery store checkout.

Office visits with neighbors often tended to take longer because there was a tendency to drift off topic and ask about a sibling’s baseball game I had read about in the paper or how the lobster catch was running that season. On the other hand, I must admit that I did my share of reporting (really it was bragging) on my own children’s accomplishments.

But now I’m reaping the benefits of those extra minutes invested in the office, because I suspect former patients and their families are more likely to want to reminisce when we meet in a restaurant or at the farmers’ market.

If you are a young physician and worrying about finding a good work/life balance, I urge you to consider living and working and then staying on in a place in which your patients also will be your neighbors. It will enrich your work experience and repay you many times over when it’s time to retire.

If you can’t find that place, at least treat your patients as though they were your neighbors.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

Low-dose aspirin for the prevention of preeclampsia has been studied for more than 25 years, often with contradictory and confusing results. Studies have enrolled patients with varying levels of risk, assessed risk differently, and used different definitions of preeclampsia as well as a variety of aspirin dosages and treatment-initiation dates. Undoubtedly, this heterogeneity has made interpretation and comparisons difficult and frustrating.

Recently, systematic reviews and meta-analyses have improved our understanding of the role of low-dose aspirin, providing solid evidence that low-dose aspirin started after the first-trimester reduces the occurrence of preeclampsia in high-risk women. Data also suggest that low-dose aspirin reduces the incidence of fetal growth restriction and preterm birth in these women.

There is reasonable evidence, moreover, that low-dose aspirin provides similar benefit in women with modest levels of risk and that it’s best to begin aspirin use at 12-14 weeks’ gestation rather than later in the second trimester. Finally, there’s also good evidence that 81 mg of aspirin is a minimum dose for effectiveness and that higher doses – as much as 150 mg – are probably more effective.

Despite this evidence and current recommendations for low-dose aspirin use by the U.S. Preventive Services Task Force and the American College of Obstetricians and Gynecologists, its use in practice is varied. Obstetricians and other obstetrics providers are not consistently making the recommendation, and pharmacists are not consistently supporting it.

Without more consistent initiation of low-dose aspirin prophylaxis and more consistent adherence, we are losing an opportunity to reduce serious maternal morbidity and mortality. We also are underutilizing an important tool for the reduction of racial and other health disparities relating to preterm birth, maternal death, and other complications of preeclampsia.


 

Dr. Lockwood: Epidemiology, etiology, and clinical value of aspirin

The use of low-dose aspirin can have a high impact, considering that preeclampsia complicates 3.4% of pregnancies nationally and accounts for at least 9% of maternal deaths (BMJ. 2013 Nov;347:f6564).

Preeclampsia also has been shown in multiple long-term epidemiologic studies to be a strong risk factor for future cardiovascular disease and metabolic disorders in women – especially when it occurs in multiple pregnancies or develops preterm. Moreover, it is associated with stillbirth, intrauterine growth restriction (IUGR), and oligohydramnios in the fetus (BMJ. 2013 Nov;347:f6564).

It is important to remember that criteria for a diagnosis of preeclampsia changed in 2013 such that the detection of proteinuria is no longer required. Preeclampsia is defined today as the new onset of hypertension and proteinuria, or hypertension and end-organ dysfunction with or without proteinuria, after 20 weeks in a previously normotensive woman, according to the ACOG Task Force on Hypertension in Pregnancy.

The leading risk factor appears to be previous preeclampsia. In a systematic review and meta-analysis of 92 cohort studies that looked at the pooled relative risk of developing preeclampsia in the presence or absence of 14 commonly reported and accepted risk factors, prior preeclampsia topped the list, putting patients at an eightfold increased risk (relative risk 8.4) (BMJ. 2016 Apr 19;353:i1753).

Nulliparity (relative risk, 2.1) and multiple gestation (RR, 2.9) presented lesser risks but still were significant, and preexisting medical conditions increased risk as well. Notably, both chronic hypertension and a body mass index (BMI) greater than 30 had a fivefold increased risk (RR, 5.1), and preexisting diabetes presented more than a threefold increased risk (RR, 3.7). The review covered more than 25 million pregnancies in 27 countries.

The etiology of preeclampsia still is not completely understood. There is evidence that underlying decidual inflammation, including increased activated macrophages and decreased uterine natural killer cells (uNK), promotes shallow placentation leading to incomplete uterine spiral artery remodeling, relative placental hypoxia, and progressive release of placental antiangiogenic substances such as soluble fms-like tyrosine kinase 1 (sFlt1) and endoglin (Am J Pathol. 2013 Sep;183[3]:841-56; Reprod Sci. 2015 Nov;22[11]:1461-7). The latter result in systemic endothelial cell damage, reduced endothelial prostacyclin (PGI2), and increased platelet thromboxane A2, triggering vasospasm and increased platelet turnover that ultimately lead to the typical signs and symptoms of preeclampsia.

The research focus traditionally has been on the placenta, but more recently the uterine decidual contribution has received more attention. A recent study published in the Proceedings of the National Academy of Sciences offers evidence that affected women have defective decidualization during and after severe preeclampsia, suggesting that the defect could be detected prior to conception.

Investigators isolated endometrial cells from women at the end of a pregnancy complicated by preeclampsia and found a transcriptional signature that persisted for years. They then linked the defect to impaired cytotrophoblast invasion (Proc Natl Acad Sci. 2017;114[40]:E8468-77). This elegant and provocative study suggests that it might be possible in the future to evaluate the endometrium and try to enhance stromal cell decidualization before pregnancy.

Currently, the rationale for using aspirin to prevent preeclampsia lies with its ability to inhibit platelet production of thromboxane and block NF-kB, a protein complex that plays a role in systemic and/or decidual inflammation. There likely are numerous mechanisms of action, however, including some that improve placentation.

Among the most recent studies on timing and dosage is a systematic review and meta-analysis of 45 randomized controlled trials with 20,909 women randomized to 50-150 mg aspirin daily or to placebo or no treatment. The investigators stratified the results by gestational age at the time of aspirin initiation and found that timing matters. Women who began aspirin at or before 16 weeks had the most significant reductions in preeclampsia (RR, 0.57) and severe preeclampsia (RR, 0.47), as well as fetal growth restriction (RR, 0.56), with a dose-response effect up to 150 mg.

When aspirin was initiated after 16 weeks, there was a much smaller reduction of preeclampsia (RR, 0.81) and no effects for severe preeclampsia or IUGR. Nor was there any dose-response effect (Am J Obstet Gynecol. 2017; 216[2]:110-20.e6).

In contrast, another recent meta-analysis of individual participant data on 32,217 women recruited in 31 randomized controlled trials found no significant difference among women who were randomized before 16 weeks versus those who were randomized at 16 weeks or later (Am J Obstet Gynecol. 2017 Feb;216[2]:121-8.e2). It’s important to note that this analysis covered other antiplatelet agents as well and that it stratified outcomes by gestational age with a slightly later cutoff point.

What do official guidelines say? The USPSTF’s recommendation, issued in 2014, calls for low-dose aspirin at 81 mg/day after 12 weeks’ gestation in women who have one or more high-risk factors, and consideration of such treatment in patients with “several” moderate-risk factors (Ann Intern Med. 2014 Dec 2;161[11]:819-26). In July 2018, ACOG reaffirmed its earlier support for low-dose aspirin in a committee opinion that recommends 81 mg/day beginning at 12-28 weeks’ gestation, optimally before 16 weeks’, for women who have one or more high-risk factors or more than one moderate-risk factor (Obstet Gynecol. 2018 Jul;132[1]:e44-e52).

My own take, based on published literature, including my own research, is that low-dose aspirin reduces the frequency of preeclampsia, particularly cases occurring preterm, as well as related IUGR, by approximately 10%-20% in moderate- and high-risk women. Regarding dose and gestational age for initiation, I have split the difference of what’s reflected in the literature and in guidelines. I advise 122 mg (a tablet-and-a-half) a day, starting at 12-14 weeks’, for patients at high and moderate levels of risk. For patients who are not seen until later, low-dose aspirin can be started up to 28 weeks’ gestation.
 

Dr. Abbott: Messaging and education to reduce disparities

Black women are not only more likely to develop preeclampsia, but they’re also more likely to have more severe complications and worse outcomes. In one analysis, black women with preeclampsia experienced an almost threefold higher risk of maternal mortality and intrauterine fetal death than did white women with the disorder (Hypertens Pregnancy. 2015 Nov;34[4]:506-15).

At Boston Medical Center, 30% of pregnant women have a diagnosis of preeclampsia or hypertension at term. In addition to 68% identifying as Hispanic/black or black, half of the families we care for have incomes less than $20,000, and 30% are non–English speaking. Low-dose prenatal aspirin is therefore an important tool for reducing racial health disparities as well as disparities created by health literacy, economic status, and language and cultural barriers. At BMC, New England’s largest safety-net hospital, we’ve found that the factors driving health disparities often overlap.

To increase the use of low-dose aspirin for women at moderate to high risk, we marry education about aspirin’s effectiveness and safety with education about the potential severity of hypertension and preeclampsia. We counsel patients who are hospitalized at delivery with gestational or chronic hypertension, or fetal growth restriction, about how preeclampsia can be very serious – contrary to what they’ve experienced or what friends or family may have shared. We also counsel them about signs and symptoms of severe preeclampsia that warrant consulting their provider. And overall, we deliberately use the term “prenatal aspirin” so that, over time and in the broader community, it will become associated with good prenatal care and risk reduction.

To counter perceived risks and dangers that we identified through focus groups and interviews, our patient education materials state that low-dose aspirin in pregnancy will not cause increased bleeding, does not reach the baby’s blood, does not increase the risk of miscarriage, and has not been shown to have negative effects on the baby’s initial development (www.prenatalaspirin.com/education-materials). We try to engage family members whenever possible, and we recognize that the black population has historical reasons to be concerned or suspicious that aspirin might not be safe for them.

Especially for underserved patients who receive prescriptions for low-dose aspirin, we must ensure that pharmacists will dispense the medication. A national survey of pharmacists (not yet published) found that over two-thirds were unaware of the USPSTF guidelines, and that only a minority would feel comfortable dispensing low-dose aspirin during pregnancy. In our community, some pharmacists have told patients to return to their physician and inquire more. Until recently, one of the major pharmacy chains placed a warning label on aspirin bottles being dispensed to women who also had an active prescription for prenatal vitamins.

We are working both with pharmacies and with pharmacy schools to impact the education of current and future pharmacists on guidelines and recommendations for low-dose aspirin prophylaxis. In addition, when I write a prescription for prenatal aspirin, starting at 12 weeks’ whenever possible, I include the message “for the purpose of trying to reduce pregnancy complications.”

Dr. Lockwood is senior vice president at University of South Florida Health and dean of Morsani College of Medicine at the University of South Florida, Tampa. He said he had no relevant financial disclosures or conflicts of interest. Dr. Abbot is a specialist in maternal-fetal medicine, the director of obstetrics and gynecology, and assistant dean for patient safety and quality improvement education at Boston Medical Center. She also is an associate professor of obstetrics and gynecology at Boston University. She disclosed a grant from the March of Dimes. Email them at [email protected].

Low-dose aspirin for the prevention of preeclampsia has been studied for more than 25 years, often with contradictory and confusing results. Studies have enrolled patients with varying levels of risk, assessed risk differently, and used different definitions of preeclampsia as well as a variety of aspirin dosages and treatment-initiation dates. Undoubtedly, this heterogeneity has made interpretation and comparisons difficult and frustrating.

Recently, systematic reviews and meta-analyses have improved our understanding of the role of low-dose aspirin, providing solid evidence that low-dose aspirin started after the first-trimester reduces the occurrence of preeclampsia in high-risk women. Data also suggest that low-dose aspirin reduces the incidence of fetal growth restriction and preterm birth in these women.

There is reasonable evidence, moreover, that low-dose aspirin provides similar benefit in women with modest levels of risk and that it’s best to begin aspirin use at 12-14 weeks’ gestation rather than later in the second trimester. Finally, there’s also good evidence that 81 mg of aspirin is a minimum dose for effectiveness and that higher doses – as much as 150 mg – are probably more effective.

Despite this evidence and current recommendations for low-dose aspirin use by the U.S. Preventive Services Task Force and the American College of Obstetricians and Gynecologists, its use in practice is varied. Obstetricians and other obstetrics providers are not consistently making the recommendation, and pharmacists are not consistently supporting it.

Without more consistent initiation of low-dose aspirin prophylaxis and more consistent adherence, we are losing an opportunity to reduce serious maternal morbidity and mortality. We also are underutilizing an important tool for the reduction of racial and other health disparities relating to preterm birth, maternal death, and other complications of preeclampsia.


 

Dr. Lockwood: Epidemiology, etiology, and clinical value of aspirin

The use of low-dose aspirin can have a high impact, considering that preeclampsia complicates 3.4% of pregnancies nationally and accounts for at least 9% of maternal deaths (BMJ. 2013 Nov;347:f6564).

Preeclampsia also has been shown in multiple long-term epidemiologic studies to be a strong risk factor for future cardiovascular disease and metabolic disorders in women – especially when it occurs in multiple pregnancies or develops preterm. Moreover, it is associated with stillbirth, intrauterine growth restriction (IUGR), and oligohydramnios in the fetus (BMJ. 2013 Nov;347:f6564).

It is important to remember that criteria for a diagnosis of preeclampsia changed in 2013 such that the detection of proteinuria is no longer required. Preeclampsia is defined today as the new onset of hypertension and proteinuria, or hypertension and end-organ dysfunction with or without proteinuria, after 20 weeks in a previously normotensive woman, according to the ACOG Task Force on Hypertension in Pregnancy.

The leading risk factor appears to be previous preeclampsia. In a systematic review and meta-analysis of 92 cohort studies that looked at the pooled relative risk of developing preeclampsia in the presence or absence of 14 commonly reported and accepted risk factors, prior preeclampsia topped the list, putting patients at an eightfold increased risk (relative risk 8.4) (BMJ. 2016 Apr 19;353:i1753).

Nulliparity (relative risk, 2.1) and multiple gestation (RR, 2.9) presented lesser risks but still were significant, and preexisting medical conditions increased risk as well. Notably, both chronic hypertension and a body mass index (BMI) greater than 30 had a fivefold increased risk (RR, 5.1), and preexisting diabetes presented more than a threefold increased risk (RR, 3.7). The review covered more than 25 million pregnancies in 27 countries.

The etiology of preeclampsia still is not completely understood. There is evidence that underlying decidual inflammation, including increased activated macrophages and decreased uterine natural killer cells (uNK), promotes shallow placentation leading to incomplete uterine spiral artery remodeling, relative placental hypoxia, and progressive release of placental antiangiogenic substances such as soluble fms-like tyrosine kinase 1 (sFlt1) and endoglin (Am J Pathol. 2013 Sep;183[3]:841-56; Reprod Sci. 2015 Nov;22[11]:1461-7). The latter result in systemic endothelial cell damage, reduced endothelial prostacyclin (PGI2), and increased platelet thromboxane A2, triggering vasospasm and increased platelet turnover that ultimately lead to the typical signs and symptoms of preeclampsia.

The research focus traditionally has been on the placenta, but more recently the uterine decidual contribution has received more attention. A recent study published in the Proceedings of the National Academy of Sciences offers evidence that affected women have defective decidualization during and after severe preeclampsia, suggesting that the defect could be detected prior to conception.

Investigators isolated endometrial cells from women at the end of a pregnancy complicated by preeclampsia and found a transcriptional signature that persisted for years. They then linked the defect to impaired cytotrophoblast invasion (Proc Natl Acad Sci. 2017;114[40]:E8468-77). This elegant and provocative study suggests that it might be possible in the future to evaluate the endometrium and try to enhance stromal cell decidualization before pregnancy.

Currently, the rationale for using aspirin to prevent preeclampsia lies with its ability to inhibit platelet production of thromboxane and block NF-kB, a protein complex that plays a role in systemic and/or decidual inflammation. There likely are numerous mechanisms of action, however, including some that improve placentation.

Among the most recent studies on timing and dosage is a systematic review and meta-analysis of 45 randomized controlled trials with 20,909 women randomized to 50-150 mg aspirin daily or to placebo or no treatment. The investigators stratified the results by gestational age at the time of aspirin initiation and found that timing matters. Women who began aspirin at or before 16 weeks had the most significant reductions in preeclampsia (RR, 0.57) and severe preeclampsia (RR, 0.47), as well as fetal growth restriction (RR, 0.56), with a dose-response effect up to 150 mg.

When aspirin was initiated after 16 weeks, there was a much smaller reduction of preeclampsia (RR, 0.81) and no effects for severe preeclampsia or IUGR. Nor was there any dose-response effect (Am J Obstet Gynecol. 2017; 216[2]:110-20.e6).

In contrast, another recent meta-analysis of individual participant data on 32,217 women recruited in 31 randomized controlled trials found no significant difference among women who were randomized before 16 weeks versus those who were randomized at 16 weeks or later (Am J Obstet Gynecol. 2017 Feb;216[2]:121-8.e2). It’s important to note that this analysis covered other antiplatelet agents as well and that it stratified outcomes by gestational age with a slightly later cutoff point.

What do official guidelines say? The USPSTF’s recommendation, issued in 2014, calls for low-dose aspirin at 81 mg/day after 12 weeks’ gestation in women who have one or more high-risk factors, and consideration of such treatment in patients with “several” moderate-risk factors (Ann Intern Med. 2014 Dec 2;161[11]:819-26). In July 2018, ACOG reaffirmed its earlier support for low-dose aspirin in a committee opinion that recommends 81 mg/day beginning at 12-28 weeks’ gestation, optimally before 16 weeks’, for women who have one or more high-risk factors or more than one moderate-risk factor (Obstet Gynecol. 2018 Jul;132[1]:e44-e52).

My own take, based on published literature, including my own research, is that low-dose aspirin reduces the frequency of preeclampsia, particularly cases occurring preterm, as well as related IUGR, by approximately 10%-20% in moderate- and high-risk women. Regarding dose and gestational age for initiation, I have split the difference of what’s reflected in the literature and in guidelines. I advise 122 mg (a tablet-and-a-half) a day, starting at 12-14 weeks’, for patients at high and moderate levels of risk. For patients who are not seen until later, low-dose aspirin can be started up to 28 weeks’ gestation.
 

Dr. Abbott: Messaging and education to reduce disparities

Black women are not only more likely to develop preeclampsia, but they’re also more likely to have more severe complications and worse outcomes. In one analysis, black women with preeclampsia experienced an almost threefold higher risk of maternal mortality and intrauterine fetal death than did white women with the disorder (Hypertens Pregnancy. 2015 Nov;34[4]:506-15).

At Boston Medical Center, 30% of pregnant women have a diagnosis of preeclampsia or hypertension at term. In addition to 68% identifying as Hispanic/black or black, half of the families we care for have incomes less than $20,000, and 30% are non–English speaking. Low-dose prenatal aspirin is therefore an important tool for reducing racial health disparities as well as disparities created by health literacy, economic status, and language and cultural barriers. At BMC, New England’s largest safety-net hospital, we’ve found that the factors driving health disparities often overlap.

To increase the use of low-dose aspirin for women at moderate to high risk, we marry education about aspirin’s effectiveness and safety with education about the potential severity of hypertension and preeclampsia. We counsel patients who are hospitalized at delivery with gestational or chronic hypertension, or fetal growth restriction, about how preeclampsia can be very serious – contrary to what they’ve experienced or what friends or family may have shared. We also counsel them about signs and symptoms of severe preeclampsia that warrant consulting their provider. And overall, we deliberately use the term “prenatal aspirin” so that, over time and in the broader community, it will become associated with good prenatal care and risk reduction.

To counter perceived risks and dangers that we identified through focus groups and interviews, our patient education materials state that low-dose aspirin in pregnancy will not cause increased bleeding, does not reach the baby’s blood, does not increase the risk of miscarriage, and has not been shown to have negative effects on the baby’s initial development (www.prenatalaspirin.com/education-materials). We try to engage family members whenever possible, and we recognize that the black population has historical reasons to be concerned or suspicious that aspirin might not be safe for them.

Especially for underserved patients who receive prescriptions for low-dose aspirin, we must ensure that pharmacists will dispense the medication. A national survey of pharmacists (not yet published) found that over two-thirds were unaware of the USPSTF guidelines, and that only a minority would feel comfortable dispensing low-dose aspirin during pregnancy. In our community, some pharmacists have told patients to return to their physician and inquire more. Until recently, one of the major pharmacy chains placed a warning label on aspirin bottles being dispensed to women who also had an active prescription for prenatal vitamins.

We are working both with pharmacies and with pharmacy schools to impact the education of current and future pharmacists on guidelines and recommendations for low-dose aspirin prophylaxis. In addition, when I write a prescription for prenatal aspirin, starting at 12 weeks’ whenever possible, I include the message “for the purpose of trying to reduce pregnancy complications.”

Dr. Lockwood is senior vice president at University of South Florida Health and dean of Morsani College of Medicine at the University of South Florida, Tampa. He said he had no relevant financial disclosures or conflicts of interest. Dr. Abbot is a specialist in maternal-fetal medicine, the director of obstetrics and gynecology, and assistant dean for patient safety and quality improvement education at Boston Medical Center. She also is an associate professor of obstetrics and gynecology at Boston University. She disclosed a grant from the March of Dimes. Email them at [email protected].

Low-dose aspirin for the prevention of preeclampsia has been studied for more than 25 years, often with contradictory and confusing results. Studies have enrolled patients with varying levels of risk, assessed risk differently, and used different definitions of preeclampsia as well as a variety of aspirin dosages and treatment-initiation dates. Undoubtedly, this heterogeneity has made interpretation and comparisons difficult and frustrating.

Recently, systematic reviews and meta-analyses have improved our understanding of the role of low-dose aspirin, providing solid evidence that low-dose aspirin started after the first-trimester reduces the occurrence of preeclampsia in high-risk women. Data also suggest that low-dose aspirin reduces the incidence of fetal growth restriction and preterm birth in these women.

There is reasonable evidence, moreover, that low-dose aspirin provides similar benefit in women with modest levels of risk and that it’s best to begin aspirin use at 12-14 weeks’ gestation rather than later in the second trimester. Finally, there’s also good evidence that 81 mg of aspirin is a minimum dose for effectiveness and that higher doses – as much as 150 mg – are probably more effective.

Despite this evidence and current recommendations for low-dose aspirin use by the U.S. Preventive Services Task Force and the American College of Obstetricians and Gynecologists, its use in practice is varied. Obstetricians and other obstetrics providers are not consistently making the recommendation, and pharmacists are not consistently supporting it.

Without more consistent initiation of low-dose aspirin prophylaxis and more consistent adherence, we are losing an opportunity to reduce serious maternal morbidity and mortality. We also are underutilizing an important tool for the reduction of racial and other health disparities relating to preterm birth, maternal death, and other complications of preeclampsia.


 

Dr. Lockwood: Epidemiology, etiology, and clinical value of aspirin

The use of low-dose aspirin can have a high impact, considering that preeclampsia complicates 3.4% of pregnancies nationally and accounts for at least 9% of maternal deaths (BMJ. 2013 Nov;347:f6564).

Preeclampsia also has been shown in multiple long-term epidemiologic studies to be a strong risk factor for future cardiovascular disease and metabolic disorders in women – especially when it occurs in multiple pregnancies or develops preterm. Moreover, it is associated with stillbirth, intrauterine growth restriction (IUGR), and oligohydramnios in the fetus (BMJ. 2013 Nov;347:f6564).

It is important to remember that criteria for a diagnosis of preeclampsia changed in 2013 such that the detection of proteinuria is no longer required. Preeclampsia is defined today as the new onset of hypertension and proteinuria, or hypertension and end-organ dysfunction with or without proteinuria, after 20 weeks in a previously normotensive woman, according to the ACOG Task Force on Hypertension in Pregnancy.

The leading risk factor appears to be previous preeclampsia. In a systematic review and meta-analysis of 92 cohort studies that looked at the pooled relative risk of developing preeclampsia in the presence or absence of 14 commonly reported and accepted risk factors, prior preeclampsia topped the list, putting patients at an eightfold increased risk (relative risk 8.4) (BMJ. 2016 Apr 19;353:i1753).

Nulliparity (relative risk, 2.1) and multiple gestation (RR, 2.9) presented lesser risks but still were significant, and preexisting medical conditions increased risk as well. Notably, both chronic hypertension and a body mass index (BMI) greater than 30 had a fivefold increased risk (RR, 5.1), and preexisting diabetes presented more than a threefold increased risk (RR, 3.7). The review covered more than 25 million pregnancies in 27 countries.

The etiology of preeclampsia still is not completely understood. There is evidence that underlying decidual inflammation, including increased activated macrophages and decreased uterine natural killer cells (uNK), promotes shallow placentation leading to incomplete uterine spiral artery remodeling, relative placental hypoxia, and progressive release of placental antiangiogenic substances such as soluble fms-like tyrosine kinase 1 (sFlt1) and endoglin (Am J Pathol. 2013 Sep;183[3]:841-56; Reprod Sci. 2015 Nov;22[11]:1461-7). The latter result in systemic endothelial cell damage, reduced endothelial prostacyclin (PGI2), and increased platelet thromboxane A2, triggering vasospasm and increased platelet turnover that ultimately lead to the typical signs and symptoms of preeclampsia.

The research focus traditionally has been on the placenta, but more recently the uterine decidual contribution has received more attention. A recent study published in the Proceedings of the National Academy of Sciences offers evidence that affected women have defective decidualization during and after severe preeclampsia, suggesting that the defect could be detected prior to conception.

Investigators isolated endometrial cells from women at the end of a pregnancy complicated by preeclampsia and found a transcriptional signature that persisted for years. They then linked the defect to impaired cytotrophoblast invasion (Proc Natl Acad Sci. 2017;114[40]:E8468-77). This elegant and provocative study suggests that it might be possible in the future to evaluate the endometrium and try to enhance stromal cell decidualization before pregnancy.

Currently, the rationale for using aspirin to prevent preeclampsia lies with its ability to inhibit platelet production of thromboxane and block NF-kB, a protein complex that plays a role in systemic and/or decidual inflammation. There likely are numerous mechanisms of action, however, including some that improve placentation.

Among the most recent studies on timing and dosage is a systematic review and meta-analysis of 45 randomized controlled trials with 20,909 women randomized to 50-150 mg aspirin daily or to placebo or no treatment. The investigators stratified the results by gestational age at the time of aspirin initiation and found that timing matters. Women who began aspirin at or before 16 weeks had the most significant reductions in preeclampsia (RR, 0.57) and severe preeclampsia (RR, 0.47), as well as fetal growth restriction (RR, 0.56), with a dose-response effect up to 150 mg.

When aspirin was initiated after 16 weeks, there was a much smaller reduction of preeclampsia (RR, 0.81) and no effects for severe preeclampsia or IUGR. Nor was there any dose-response effect (Am J Obstet Gynecol. 2017; 216[2]:110-20.e6).

In contrast, another recent meta-analysis of individual participant data on 32,217 women recruited in 31 randomized controlled trials found no significant difference among women who were randomized before 16 weeks versus those who were randomized at 16 weeks or later (Am J Obstet Gynecol. 2017 Feb;216[2]:121-8.e2). It’s important to note that this analysis covered other antiplatelet agents as well and that it stratified outcomes by gestational age with a slightly later cutoff point.

What do official guidelines say? The USPSTF’s recommendation, issued in 2014, calls for low-dose aspirin at 81 mg/day after 12 weeks’ gestation in women who have one or more high-risk factors, and consideration of such treatment in patients with “several” moderate-risk factors (Ann Intern Med. 2014 Dec 2;161[11]:819-26). In July 2018, ACOG reaffirmed its earlier support for low-dose aspirin in a committee opinion that recommends 81 mg/day beginning at 12-28 weeks’ gestation, optimally before 16 weeks’, for women who have one or more high-risk factors or more than one moderate-risk factor (Obstet Gynecol. 2018 Jul;132[1]:e44-e52).

My own take, based on published literature, including my own research, is that low-dose aspirin reduces the frequency of preeclampsia, particularly cases occurring preterm, as well as related IUGR, by approximately 10%-20% in moderate- and high-risk women. Regarding dose and gestational age for initiation, I have split the difference of what’s reflected in the literature and in guidelines. I advise 122 mg (a tablet-and-a-half) a day, starting at 12-14 weeks’, for patients at high and moderate levels of risk. For patients who are not seen until later, low-dose aspirin can be started up to 28 weeks’ gestation.
 

Dr. Abbott: Messaging and education to reduce disparities

Black women are not only more likely to develop preeclampsia, but they’re also more likely to have more severe complications and worse outcomes. In one analysis, black women with preeclampsia experienced an almost threefold higher risk of maternal mortality and intrauterine fetal death than did white women with the disorder (Hypertens Pregnancy. 2015 Nov;34[4]:506-15).

At Boston Medical Center, 30% of pregnant women have a diagnosis of preeclampsia or hypertension at term. In addition to 68% identifying as Hispanic/black or black, half of the families we care for have incomes less than $20,000, and 30% are non–English speaking. Low-dose prenatal aspirin is therefore an important tool for reducing racial health disparities as well as disparities created by health literacy, economic status, and language and cultural barriers. At BMC, New England’s largest safety-net hospital, we’ve found that the factors driving health disparities often overlap.

To increase the use of low-dose aspirin for women at moderate to high risk, we marry education about aspirin’s effectiveness and safety with education about the potential severity of hypertension and preeclampsia. We counsel patients who are hospitalized at delivery with gestational or chronic hypertension, or fetal growth restriction, about how preeclampsia can be very serious – contrary to what they’ve experienced or what friends or family may have shared. We also counsel them about signs and symptoms of severe preeclampsia that warrant consulting their provider. And overall, we deliberately use the term “prenatal aspirin” so that, over time and in the broader community, it will become associated with good prenatal care and risk reduction.

To counter perceived risks and dangers that we identified through focus groups and interviews, our patient education materials state that low-dose aspirin in pregnancy will not cause increased bleeding, does not reach the baby’s blood, does not increase the risk of miscarriage, and has not been shown to have negative effects on the baby’s initial development (www.prenatalaspirin.com/education-materials). We try to engage family members whenever possible, and we recognize that the black population has historical reasons to be concerned or suspicious that aspirin might not be safe for them.

Especially for underserved patients who receive prescriptions for low-dose aspirin, we must ensure that pharmacists will dispense the medication. A national survey of pharmacists (not yet published) found that over two-thirds were unaware of the USPSTF guidelines, and that only a minority would feel comfortable dispensing low-dose aspirin during pregnancy. In our community, some pharmacists have told patients to return to their physician and inquire more. Until recently, one of the major pharmacy chains placed a warning label on aspirin bottles being dispensed to women who also had an active prescription for prenatal vitamins.

We are working both with pharmacies and with pharmacy schools to impact the education of current and future pharmacists on guidelines and recommendations for low-dose aspirin prophylaxis. In addition, when I write a prescription for prenatal aspirin, starting at 12 weeks’ whenever possible, I include the message “for the purpose of trying to reduce pregnancy complications.”

Dr. Lockwood is senior vice president at University of South Florida Health and dean of Morsani College of Medicine at the University of South Florida, Tampa. He said he had no relevant financial disclosures or conflicts of interest. Dr. Abbot is a specialist in maternal-fetal medicine, the director of obstetrics and gynecology, and assistant dean for patient safety and quality improvement education at Boston Medical Center. She also is an associate professor of obstetrics and gynecology at Boston University. She disclosed a grant from the March of Dimes. Email them at [email protected].

Some of our readers might remember the old saying, “Take two aspirin and call me in the morning,” as advice physicians gave to patients experiencing a minor malady. Aspirin often has been called a “wonder drug” as its uses continue to expand. From its first recorded use in the Ebers papyrus as an anti-inflammatory agent, to its first use in a clinical trial showing that it induces remission of fever and joint inflammation, to the discovery that it could prevent death from heart attack, to its anticancer properties, aspirin remains one of the most researched drugs in use today. According to ClinicalTrials.gov, there are over 465 active and nearly 1,000 completed aspirin-related clinical trials around the world.

Despite its myriad benefits, aspirin has been linked to bleeding, nausea, and gastrointestinal ulcers. Additionally, more research is needed to determine the risks/benefits of daily aspirin in younger adults (under age 50 years) or older adults (over age 70 years), although the ASPREE (Aspirin in Reducing Events in the Elderly) trial, expected to be completed in 2019, is working to determine the effects of daily low-dose aspirin (100 mg) on the health of people over age 65.

It is tempting to consider aspirin one of modern medicine’s so-called silver bullets, and, for women with a history of gestational hypertension and preeclampsia, it just might be. Aspirin use, especially daily aspirin, is typically not recommended during pregnancy, and most ob.gyns. will include aspirin on the “do not take” list they give to their patients during prenatal examinations. Women at risk for developing preeclampsia are the exceptions to this general rule, and a number of clinical studies have indicated that use of low-dose aspirin can help prevent disease as well as secondary outcomes for mother (i.e., placental abruption, antepartum hemorrhage) and baby (i.e., intrauterine growth restriction, stillbirth). In addition, aspirin is an easily obtainable, low-cost preventive measure for any patient at high risk.

To discuss the value of low-dose aspirin to prevent preeclampsia and how ob.gyns. can educate their patients and other health care professionals about its benefits, we have invited Charles J. Lockwood, MD, MHCM, senior vice president of University of South Florida Health and dean of Morsani College of Medicine at the University of South Florida, Tampa, and Jodi F. Abbott, MD, MSc, MHCM, director of obstetrics and gynecology at Boston Medical Center, and associate professor of obstetrics and gynecology at Boston University, to coauthor this month’s Master Class.

Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of this column. Contact him at [email protected].

Some of our readers might remember the old saying, “Take two aspirin and call me in the morning,” as advice physicians gave to patients experiencing a minor malady. Aspirin often has been called a “wonder drug” as its uses continue to expand. From its first recorded use in the Ebers papyrus as an anti-inflammatory agent, to its first use in a clinical trial showing that it induces remission of fever and joint inflammation, to the discovery that it could prevent death from heart attack, to its anticancer properties, aspirin remains one of the most researched drugs in use today. According to ClinicalTrials.gov, there are over 465 active and nearly 1,000 completed aspirin-related clinical trials around the world.

Despite its myriad benefits, aspirin has been linked to bleeding, nausea, and gastrointestinal ulcers. Additionally, more research is needed to determine the risks/benefits of daily aspirin in younger adults (under age 50 years) or older adults (over age 70 years), although the ASPREE (Aspirin in Reducing Events in the Elderly) trial, expected to be completed in 2019, is working to determine the effects of daily low-dose aspirin (100 mg) on the health of people over age 65.

It is tempting to consider aspirin one of modern medicine’s so-called silver bullets, and, for women with a history of gestational hypertension and preeclampsia, it just might be. Aspirin use, especially daily aspirin, is typically not recommended during pregnancy, and most ob.gyns. will include aspirin on the “do not take” list they give to their patients during prenatal examinations. Women at risk for developing preeclampsia are the exceptions to this general rule, and a number of clinical studies have indicated that use of low-dose aspirin can help prevent disease as well as secondary outcomes for mother (i.e., placental abruption, antepartum hemorrhage) and baby (i.e., intrauterine growth restriction, stillbirth). In addition, aspirin is an easily obtainable, low-cost preventive measure for any patient at high risk.

To discuss the value of low-dose aspirin to prevent preeclampsia and how ob.gyns. can educate their patients and other health care professionals about its benefits, we have invited Charles J. Lockwood, MD, MHCM, senior vice president of University of South Florida Health and dean of Morsani College of Medicine at the University of South Florida, Tampa, and Jodi F. Abbott, MD, MSc, MHCM, director of obstetrics and gynecology at Boston Medical Center, and associate professor of obstetrics and gynecology at Boston University, to coauthor this month’s Master Class.

Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of this column. Contact him at [email protected].

Some of our readers might remember the old saying, “Take two aspirin and call me in the morning,” as advice physicians gave to patients experiencing a minor malady. Aspirin often has been called a “wonder drug” as its uses continue to expand. From its first recorded use in the Ebers papyrus as an anti-inflammatory agent, to its first use in a clinical trial showing that it induces remission of fever and joint inflammation, to the discovery that it could prevent death from heart attack, to its anticancer properties, aspirin remains one of the most researched drugs in use today. According to ClinicalTrials.gov, there are over 465 active and nearly 1,000 completed aspirin-related clinical trials around the world.

Despite its myriad benefits, aspirin has been linked to bleeding, nausea, and gastrointestinal ulcers. Additionally, more research is needed to determine the risks/benefits of daily aspirin in younger adults (under age 50 years) or older adults (over age 70 years), although the ASPREE (Aspirin in Reducing Events in the Elderly) trial, expected to be completed in 2019, is working to determine the effects of daily low-dose aspirin (100 mg) on the health of people over age 65.

It is tempting to consider aspirin one of modern medicine’s so-called silver bullets, and, for women with a history of gestational hypertension and preeclampsia, it just might be. Aspirin use, especially daily aspirin, is typically not recommended during pregnancy, and most ob.gyns. will include aspirin on the “do not take” list they give to their patients during prenatal examinations. Women at risk for developing preeclampsia are the exceptions to this general rule, and a number of clinical studies have indicated that use of low-dose aspirin can help prevent disease as well as secondary outcomes for mother (i.e., placental abruption, antepartum hemorrhage) and baby (i.e., intrauterine growth restriction, stillbirth). In addition, aspirin is an easily obtainable, low-cost preventive measure for any patient at high risk.

To discuss the value of low-dose aspirin to prevent preeclampsia and how ob.gyns. can educate their patients and other health care professionals about its benefits, we have invited Charles J. Lockwood, MD, MHCM, senior vice president of University of South Florida Health and dean of Morsani College of Medicine at the University of South Florida, Tampa, and Jodi F. Abbott, MD, MSc, MHCM, director of obstetrics and gynecology at Boston Medical Center, and associate professor of obstetrics and gynecology at Boston University, to coauthor this month’s Master Class.

Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of this column. Contact him at [email protected].

Some of us seem completely blank, but our minds are predisposed to constantly engage in various mental activities. Our minds can problem solve, fantasize, remember past events, get preoccupied with a book or movie, pay attention to social relationships and/or pay attention to our relationship with ourselves, focus on what we are doing in the moment, and more.

©Thinkstock

Many of us understand that our minds sometime operate on more than one level, for example, I can be talking or listening to someone in the “front of my mind” and be thinking something seemingly unrelated in the “back of my mind.” Accordingly, our minds are like a cornucopia of thoughts, feelings, and memories, to name a few, making them a very complex and intricate aspect of our lives. Sometimes we try to take a break from this never-ending mental activity by going to sleep or even taking drugs to “turn our minds off.”

Another important aspect of our minds is “will.” I like to think that most of us are familiar with the concept of “will” and put ours to good use. We intentionally or unintentionally use our wills in various ways – to improve ourselves; have fun; dawdle our lives away on imaginary activities; accomplish something tangible (for example, write a paper or wash the kitchen floor); pay attention to what we are doing in the moment; be healthy; and practice cultivating a “sound mind.”

Many of us would agree that to be of sound mind means having the ability to be comfortable with ourselves; to have some regulation of our emotions and affects; not to worry too much, but just enough to stay motivated; and to apply our minds toward accomplishing a goal we have chosen for ourselves. A sound mind also involves having a good memory, being aware and awake, being able to sort things out and adapt to various difficulties life throws at us, solving problems creatively and effectively, being able to relax, and being able to have a purpose in our lives that we have some success in fulfilling.

As a psychiatrist, I often have been curious about how people use their minds and how they direct their mental activities, or, if they do not direct their mental activities at all and simply meander through their mental lives not doing much thinking about thinking (many of us do both). Further, what is even more curious to me is how we psychiatrists use our minds; after all, we are supposed to be the experts. Certainly, with the advent of psychoanalysis, cognitive-behavioral therapy and other techniques, we are teaching our patients, and, hopefully, learning ourselves about how to manage our minds and what they preoccupy themselves with thinking. Of course, there were the methods of Abraham A. Low, MD, about “will training,” which I consider the first iteration of CBT. Prior to psychoanalysis and Low’s ideas, there have always been various forms of mindfulness.

Dr. Bell is staff psychiatrist at Jackson Park Hospital Surgical-Medical/Psychiatric Inpatient Unit; clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago. He serves as chair of psychiatry at Windsor University, St. Kitts.

Some of us seem completely blank, but our minds are predisposed to constantly engage in various mental activities. Our minds can problem solve, fantasize, remember past events, get preoccupied with a book or movie, pay attention to social relationships and/or pay attention to our relationship with ourselves, focus on what we are doing in the moment, and more.

©Thinkstock

Many of us understand that our minds sometime operate on more than one level, for example, I can be talking or listening to someone in the “front of my mind” and be thinking something seemingly unrelated in the “back of my mind.” Accordingly, our minds are like a cornucopia of thoughts, feelings, and memories, to name a few, making them a very complex and intricate aspect of our lives. Sometimes we try to take a break from this never-ending mental activity by going to sleep or even taking drugs to “turn our minds off.”

Another important aspect of our minds is “will.” I like to think that most of us are familiar with the concept of “will” and put ours to good use. We intentionally or unintentionally use our wills in various ways – to improve ourselves; have fun; dawdle our lives away on imaginary activities; accomplish something tangible (for example, write a paper or wash the kitchen floor); pay attention to what we are doing in the moment; be healthy; and practice cultivating a “sound mind.”

Many of us would agree that to be of sound mind means having the ability to be comfortable with ourselves; to have some regulation of our emotions and affects; not to worry too much, but just enough to stay motivated; and to apply our minds toward accomplishing a goal we have chosen for ourselves. A sound mind also involves having a good memory, being aware and awake, being able to sort things out and adapt to various difficulties life throws at us, solving problems creatively and effectively, being able to relax, and being able to have a purpose in our lives that we have some success in fulfilling.

As a psychiatrist, I often have been curious about how people use their minds and how they direct their mental activities, or, if they do not direct their mental activities at all and simply meander through their mental lives not doing much thinking about thinking (many of us do both). Further, what is even more curious to me is how we psychiatrists use our minds; after all, we are supposed to be the experts. Certainly, with the advent of psychoanalysis, cognitive-behavioral therapy and other techniques, we are teaching our patients, and, hopefully, learning ourselves about how to manage our minds and what they preoccupy themselves with thinking. Of course, there were the methods of Abraham A. Low, MD, about “will training,” which I consider the first iteration of CBT. Prior to psychoanalysis and Low’s ideas, there have always been various forms of mindfulness.

Dr. Bell is staff psychiatrist at Jackson Park Hospital Surgical-Medical/Psychiatric Inpatient Unit; clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago. He serves as chair of psychiatry at Windsor University, St. Kitts.

Some of us seem completely blank, but our minds are predisposed to constantly engage in various mental activities. Our minds can problem solve, fantasize, remember past events, get preoccupied with a book or movie, pay attention to social relationships and/or pay attention to our relationship with ourselves, focus on what we are doing in the moment, and more.

©Thinkstock

Many of us understand that our minds sometime operate on more than one level, for example, I can be talking or listening to someone in the “front of my mind” and be thinking something seemingly unrelated in the “back of my mind.” Accordingly, our minds are like a cornucopia of thoughts, feelings, and memories, to name a few, making them a very complex and intricate aspect of our lives. Sometimes we try to take a break from this never-ending mental activity by going to sleep or even taking drugs to “turn our minds off.”

Another important aspect of our minds is “will.” I like to think that most of us are familiar with the concept of “will” and put ours to good use. We intentionally or unintentionally use our wills in various ways – to improve ourselves; have fun; dawdle our lives away on imaginary activities; accomplish something tangible (for example, write a paper or wash the kitchen floor); pay attention to what we are doing in the moment; be healthy; and practice cultivating a “sound mind.”

Many of us would agree that to be of sound mind means having the ability to be comfortable with ourselves; to have some regulation of our emotions and affects; not to worry too much, but just enough to stay motivated; and to apply our minds toward accomplishing a goal we have chosen for ourselves. A sound mind also involves having a good memory, being aware and awake, being able to sort things out and adapt to various difficulties life throws at us, solving problems creatively and effectively, being able to relax, and being able to have a purpose in our lives that we have some success in fulfilling.

As a psychiatrist, I often have been curious about how people use their minds and how they direct their mental activities, or, if they do not direct their mental activities at all and simply meander through their mental lives not doing much thinking about thinking (many of us do both). Further, what is even more curious to me is how we psychiatrists use our minds; after all, we are supposed to be the experts. Certainly, with the advent of psychoanalysis, cognitive-behavioral therapy and other techniques, we are teaching our patients, and, hopefully, learning ourselves about how to manage our minds and what they preoccupy themselves with thinking. Of course, there were the methods of Abraham A. Low, MD, about “will training,” which I consider the first iteration of CBT. Prior to psychoanalysis and Low’s ideas, there have always been various forms of mindfulness.

Dr. Bell is staff psychiatrist at Jackson Park Hospital Surgical-Medical/Psychiatric Inpatient Unit; clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago. He serves as chair of psychiatry at Windsor University, St. Kitts.

The optimist says the glass is half-full. The pessimist says it is half-empty. An engineer says the glass is twice as large as needed to contain the specified amount of fluid. To some people, that mindset makes engineers negative people. We focus on weaknesses and inefficiencies. A chain is only as strong as its weakest link. There is no partial credit when building a bridge. 98% right is still wrong.

When I worked as an engineer, critiquing ideas was a daily activity. I am used to conflicting opinions. Industry trains people to be professional and act appropriately when disagreeing with a colleague. Tact is the art of making a point without making an enemy. Engineering has a strong culture of focusing on a problem rather than on personalities. Upper management made it clear that in any turf war, both sides will lose. Academia has a different culture. Turf wars in academia are so bitter because the stakes are so small.

Pediatrics has less confrontation and competitiveness than do other subspecialties. That makes the work environment more pleasant, as long as every other group in the hospital isn’t walking all over you. Pediatricians often view themselves as dedicated to doing what is right for the children, even to the point of martyrdom. Some early pediatric hospitalist programs got into economic trouble because they adopted tasks that benefited the children but that weren’t being performed by other physicians precisely because those tasks were neither valued nor compensated. Learning to say “No” is hard but necessary.

As a clinical ethics consultant, I was consulted when conflict had developed between providers and patients/parents or between different specialties. Ethics consults are rarely about what philosophers would call ethics. They are mostly about miscommunication, empowering voices to be heard and clarifying values. Practical skills in de-escalation and mediation are more important than either law or philosophy degrees.

There are downsides to avoiding confrontation. Truth suffers. Integrity is lost. Goals become corrupted. I will give two examples. One ED had a five-level triage system. Level 1 was reserved for life-threatening situations such as gunshot wounds and resuscitations. So I was surprised to see a “bili” baby triaged at Level 1. He was a good baby with normal vitals. Admission for phototherapy was reasonable, but the urgency of a bilirubin of 19 did not match that of a gunshot wound. A colleague warned me not to even consider challenging the practice. A powerful physician at that institution had made it policy years earlier.

I witnessed a similar dynamic many times at that institution. Residents are even better than 4-year-olds at noticing hypocritical behavior. Once they perceive that the dynamic is political power and not science, they adapt quickly. A couple days later, I asked a resident if he really thought an IV was necessary for a toddler we were admitting. He replied no, but if he hadn’t put an IV in, the hospital wouldn’t get paid for the admission. To him, that was the unspoken policy. The action didn’t even cause him moral distress. I worry about that much cynicism so early in a career. Cognitive dissonance starts small and slowly creeps its way into everything.

The art of managing conflict is particularly important in pediatric hospital medicine because of its heavy investment in reducing overdiagnosis and overtreatment. Many pediatric hospitalists are located at academic institutions and more subject to its turf wars than outpatient colleagues practicing in small groups. The recent conference for pediatric hospital medicine was held in Atlanta, a few blocks from the Center for Civil and Human Rights. That museum evokes powerful images of struggles around the world. My two takeaway lessons: Silence is a form of collaboration. Tyrannical suppression of dissent magnifies suffering.

In poorly managed academic institutions, it can be harmful to one’s career to ask questions, challenge assumptions, and seek truth. A recent report found that the Department of Veterans Affairs health system also has a culture that punishes whistle-blowers. Nationally, politics has become polarized. Splitting, once considered a dysfunctional behavior, has become normalized. So I understand the reluctance to speak up. One must choose one’s battles.

Given the personal and career risks, why confront inaccurate research, wasteful practices, and unjust policies? I believe that there is a balance and a choice each person must make. Canadian engineers wear an iron ring to remind themselves of their professional responsibilities. Doctors wear white coats. Personally, I share a memory with other engineers of my generation. In January 1986, NASA engineers could not convince their managers about a risk. The space shuttle Challenger exploded. I heard about it in the medical school’s cafeteria. So for me, disputation is part of the vocation.

 

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

The optimist says the glass is half-full. The pessimist says it is half-empty. An engineer says the glass is twice as large as needed to contain the specified amount of fluid. To some people, that mindset makes engineers negative people. We focus on weaknesses and inefficiencies. A chain is only as strong as its weakest link. There is no partial credit when building a bridge. 98% right is still wrong.

When I worked as an engineer, critiquing ideas was a daily activity. I am used to conflicting opinions. Industry trains people to be professional and act appropriately when disagreeing with a colleague. Tact is the art of making a point without making an enemy. Engineering has a strong culture of focusing on a problem rather than on personalities. Upper management made it clear that in any turf war, both sides will lose. Academia has a different culture. Turf wars in academia are so bitter because the stakes are so small.

Pediatrics has less confrontation and competitiveness than do other subspecialties. That makes the work environment more pleasant, as long as every other group in the hospital isn’t walking all over you. Pediatricians often view themselves as dedicated to doing what is right for the children, even to the point of martyrdom. Some early pediatric hospitalist programs got into economic trouble because they adopted tasks that benefited the children but that weren’t being performed by other physicians precisely because those tasks were neither valued nor compensated. Learning to say “No” is hard but necessary.

As a clinical ethics consultant, I was consulted when conflict had developed between providers and patients/parents or between different specialties. Ethics consults are rarely about what philosophers would call ethics. They are mostly about miscommunication, empowering voices to be heard and clarifying values. Practical skills in de-escalation and mediation are more important than either law or philosophy degrees.

There are downsides to avoiding confrontation. Truth suffers. Integrity is lost. Goals become corrupted. I will give two examples. One ED had a five-level triage system. Level 1 was reserved for life-threatening situations such as gunshot wounds and resuscitations. So I was surprised to see a “bili” baby triaged at Level 1. He was a good baby with normal vitals. Admission for phototherapy was reasonable, but the urgency of a bilirubin of 19 did not match that of a gunshot wound. A colleague warned me not to even consider challenging the practice. A powerful physician at that institution had made it policy years earlier.

I witnessed a similar dynamic many times at that institution. Residents are even better than 4-year-olds at noticing hypocritical behavior. Once they perceive that the dynamic is political power and not science, they adapt quickly. A couple days later, I asked a resident if he really thought an IV was necessary for a toddler we were admitting. He replied no, but if he hadn’t put an IV in, the hospital wouldn’t get paid for the admission. To him, that was the unspoken policy. The action didn’t even cause him moral distress. I worry about that much cynicism so early in a career. Cognitive dissonance starts small and slowly creeps its way into everything.

The art of managing conflict is particularly important in pediatric hospital medicine because of its heavy investment in reducing overdiagnosis and overtreatment. Many pediatric hospitalists are located at academic institutions and more subject to its turf wars than outpatient colleagues practicing in small groups. The recent conference for pediatric hospital medicine was held in Atlanta, a few blocks from the Center for Civil and Human Rights. That museum evokes powerful images of struggles around the world. My two takeaway lessons: Silence is a form of collaboration. Tyrannical suppression of dissent magnifies suffering.

In poorly managed academic institutions, it can be harmful to one’s career to ask questions, challenge assumptions, and seek truth. A recent report found that the Department of Veterans Affairs health system also has a culture that punishes whistle-blowers. Nationally, politics has become polarized. Splitting, once considered a dysfunctional behavior, has become normalized. So I understand the reluctance to speak up. One must choose one’s battles.

Given the personal and career risks, why confront inaccurate research, wasteful practices, and unjust policies? I believe that there is a balance and a choice each person must make. Canadian engineers wear an iron ring to remind themselves of their professional responsibilities. Doctors wear white coats. Personally, I share a memory with other engineers of my generation. In January 1986, NASA engineers could not convince their managers about a risk. The space shuttle Challenger exploded. I heard about it in the medical school’s cafeteria. So for me, disputation is part of the vocation.

 

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

The optimist says the glass is half-full. The pessimist says it is half-empty. An engineer says the glass is twice as large as needed to contain the specified amount of fluid. To some people, that mindset makes engineers negative people. We focus on weaknesses and inefficiencies. A chain is only as strong as its weakest link. There is no partial credit when building a bridge. 98% right is still wrong.

When I worked as an engineer, critiquing ideas was a daily activity. I am used to conflicting opinions. Industry trains people to be professional and act appropriately when disagreeing with a colleague. Tact is the art of making a point without making an enemy. Engineering has a strong culture of focusing on a problem rather than on personalities. Upper management made it clear that in any turf war, both sides will lose. Academia has a different culture. Turf wars in academia are so bitter because the stakes are so small.

Pediatrics has less confrontation and competitiveness than do other subspecialties. That makes the work environment more pleasant, as long as every other group in the hospital isn’t walking all over you. Pediatricians often view themselves as dedicated to doing what is right for the children, even to the point of martyrdom. Some early pediatric hospitalist programs got into economic trouble because they adopted tasks that benefited the children but that weren’t being performed by other physicians precisely because those tasks were neither valued nor compensated. Learning to say “No” is hard but necessary.

As a clinical ethics consultant, I was consulted when conflict had developed between providers and patients/parents or between different specialties. Ethics consults are rarely about what philosophers would call ethics. They are mostly about miscommunication, empowering voices to be heard and clarifying values. Practical skills in de-escalation and mediation are more important than either law or philosophy degrees.

There are downsides to avoiding confrontation. Truth suffers. Integrity is lost. Goals become corrupted. I will give two examples. One ED had a five-level triage system. Level 1 was reserved for life-threatening situations such as gunshot wounds and resuscitations. So I was surprised to see a “bili” baby triaged at Level 1. He was a good baby with normal vitals. Admission for phototherapy was reasonable, but the urgency of a bilirubin of 19 did not match that of a gunshot wound. A colleague warned me not to even consider challenging the practice. A powerful physician at that institution had made it policy years earlier.

I witnessed a similar dynamic many times at that institution. Residents are even better than 4-year-olds at noticing hypocritical behavior. Once they perceive that the dynamic is political power and not science, they adapt quickly. A couple days later, I asked a resident if he really thought an IV was necessary for a toddler we were admitting. He replied no, but if he hadn’t put an IV in, the hospital wouldn’t get paid for the admission. To him, that was the unspoken policy. The action didn’t even cause him moral distress. I worry about that much cynicism so early in a career. Cognitive dissonance starts small and slowly creeps its way into everything.

The art of managing conflict is particularly important in pediatric hospital medicine because of its heavy investment in reducing overdiagnosis and overtreatment. Many pediatric hospitalists are located at academic institutions and more subject to its turf wars than outpatient colleagues practicing in small groups. The recent conference for pediatric hospital medicine was held in Atlanta, a few blocks from the Center for Civil and Human Rights. That museum evokes powerful images of struggles around the world. My two takeaway lessons: Silence is a form of collaboration. Tyrannical suppression of dissent magnifies suffering.

In poorly managed academic institutions, it can be harmful to one’s career to ask questions, challenge assumptions, and seek truth. A recent report found that the Department of Veterans Affairs health system also has a culture that punishes whistle-blowers. Nationally, politics has become polarized. Splitting, once considered a dysfunctional behavior, has become normalized. So I understand the reluctance to speak up. One must choose one’s battles.

Given the personal and career risks, why confront inaccurate research, wasteful practices, and unjust policies? I believe that there is a balance and a choice each person must make. Canadian engineers wear an iron ring to remind themselves of their professional responsibilities. Doctors wear white coats. Personally, I share a memory with other engineers of my generation. In January 1986, NASA engineers could not convince their managers about a risk. The space shuttle Challenger exploded. I heard about it in the medical school’s cafeteria. So for me, disputation is part of the vocation.

 

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

Defensive medicine exists. The question is how often it happens and how large a role it plays in making medical care in the United States so costly. When Dr. Tom Price was a congressman, he was quoted as saying that defensive medicine is responsible for more than 25% of every dollar this country spends on health care. (“A Fear of Lawsuits Really Does Seem to Result in Extra Medical Tests” Margot Sanger-Katz, New York Times, July 23, 2018). Neither I nor anyone else had any data to support or refute Dr. Price’s claim in 2010, but based on 50 years of practicing and observing medicine, I don’t find his claim completely unreasonable.

iStock

Defensive medicine has been going on for so many generations of physicians that most doctors practicing today don’t realize they are doing it. A physician may order a full battery of chemistries on a patient presenting with mild anemia when only a CBC is necessary because that’s the way he was trained.

However, the evidence to support my suspicion that defensive medicine is a significant financial drain on our economy has been difficult to tease out of the tangled web of confounders that is woven into our patchwork health care system. A recent study by two economists provides a glimpse into the role of defensive medicine in the cost of health care (“Defensive Medicine: Evidence from Military Immunity” Michael D. Frakes and Jonathan Gruber, National Bureau of Economic Research, July 2018). Using the unusual combination of circumstances in which military personnel and their dependents can or cannot sue depending on where they are receiving care, the investigators found that “liability immunity reduces inpatient spending by 5% with no measurable negative effect on patient outcomes.” While that may not be as high as Dr. Price or I think it may be, 5% of three trillion dollars is serious money.

The bigger problem is that defensive medicine is ugly, artless, and intellectually unsatisfying. While the patient may not view your diagnosis of his chronic debilitating or terminal illness as a work of art, there are such things as beautiful diagnoses. One may be beautiful in its simplicity and its ability to unify a variety of previously unexplained symptoms. Another diagnosis may be the intellectually stimulating result of a carefully thought out branching decision tree to solve a puzzling array of complaints using a minimum of costly studies.

Defensive medicine decisions are made primarily to avoid mistakes and omissions. Physicians often behave as though we believe our errors will always be fatal. That may be somewhat true for surgeons, but for the rest of us errors can be an important part of learning. The unfortunate outcome of an error, particularly one of omission, can usually be avoided by following the patient closely, remaining available ... and continuing to exude an aura of caring.

With close and thoughtful follow-up, you are going to discover pretty quickly when you have missed the target. Patients understand that we aren’t going to get the correct diagnosis or prescribe the best treatment on the first try every time. What patients don’t understand and what may prompt them to sue is feeling that they are being ignored.

While practicing defensive medicine isn’t usually listed as one of the cardinal symptoms of physician burnout, it probably deserves more attention. With some introspection and a bit of courage, recasting what you do in terms of its artistry and intellectual integrity could add a new and positive dimension to how you practice medicine. How many of your decisions are being made to avoid an error? Wouldn’t it be more fun to be making beautiful diagnoses you can be proud of?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Is My Child Overtired?: The Sleep Solution for Raising Happier, Healthier Children.” Email him at [email protected].

Defensive medicine exists. The question is how often it happens and how large a role it plays in making medical care in the United States so costly. When Dr. Tom Price was a congressman, he was quoted as saying that defensive medicine is responsible for more than 25% of every dollar this country spends on health care. (“A Fear of Lawsuits Really Does Seem to Result in Extra Medical Tests” Margot Sanger-Katz, New York Times, July 23, 2018). Neither I nor anyone else had any data to support or refute Dr. Price’s claim in 2010, but based on 50 years of practicing and observing medicine, I don’t find his claim completely unreasonable.

iStock

Defensive medicine has been going on for so many generations of physicians that most doctors practicing today don’t realize they are doing it. A physician may order a full battery of chemistries on a patient presenting with mild anemia when only a CBC is necessary because that’s the way he was trained.

However, the evidence to support my suspicion that defensive medicine is a significant financial drain on our economy has been difficult to tease out of the tangled web of confounders that is woven into our patchwork health care system. A recent study by two economists provides a glimpse into the role of defensive medicine in the cost of health care (“Defensive Medicine: Evidence from Military Immunity” Michael D. Frakes and Jonathan Gruber, National Bureau of Economic Research, July 2018). Using the unusual combination of circumstances in which military personnel and their dependents can or cannot sue depending on where they are receiving care, the investigators found that “liability immunity reduces inpatient spending by 5% with no measurable negative effect on patient outcomes.” While that may not be as high as Dr. Price or I think it may be, 5% of three trillion dollars is serious money.

The bigger problem is that defensive medicine is ugly, artless, and intellectually unsatisfying. While the patient may not view your diagnosis of his chronic debilitating or terminal illness as a work of art, there are such things as beautiful diagnoses. One may be beautiful in its simplicity and its ability to unify a variety of previously unexplained symptoms. Another diagnosis may be the intellectually stimulating result of a carefully thought out branching decision tree to solve a puzzling array of complaints using a minimum of costly studies.

Defensive medicine decisions are made primarily to avoid mistakes and omissions. Physicians often behave as though we believe our errors will always be fatal. That may be somewhat true for surgeons, but for the rest of us errors can be an important part of learning. The unfortunate outcome of an error, particularly one of omission, can usually be avoided by following the patient closely, remaining available ... and continuing to exude an aura of caring.

With close and thoughtful follow-up, you are going to discover pretty quickly when you have missed the target. Patients understand that we aren’t going to get the correct diagnosis or prescribe the best treatment on the first try every time. What patients don’t understand and what may prompt them to sue is feeling that they are being ignored.

While practicing defensive medicine isn’t usually listed as one of the cardinal symptoms of physician burnout, it probably deserves more attention. With some introspection and a bit of courage, recasting what you do in terms of its artistry and intellectual integrity could add a new and positive dimension to how you practice medicine. How many of your decisions are being made to avoid an error? Wouldn’t it be more fun to be making beautiful diagnoses you can be proud of?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Is My Child Overtired?: The Sleep Solution for Raising Happier, Healthier Children.” Email him at [email protected].

Defensive medicine exists. The question is how often it happens and how large a role it plays in making medical care in the United States so costly. When Dr. Tom Price was a congressman, he was quoted as saying that defensive medicine is responsible for more than 25% of every dollar this country spends on health care. (“A Fear of Lawsuits Really Does Seem to Result in Extra Medical Tests” Margot Sanger-Katz, New York Times, July 23, 2018). Neither I nor anyone else had any data to support or refute Dr. Price’s claim in 2010, but based on 50 years of practicing and observing medicine, I don’t find his claim completely unreasonable.

iStock

Defensive medicine has been going on for so many generations of physicians that most doctors practicing today don’t realize they are doing it. A physician may order a full battery of chemistries on a patient presenting with mild anemia when only a CBC is necessary because that’s the way he was trained.

However, the evidence to support my suspicion that defensive medicine is a significant financial drain on our economy has been difficult to tease out of the tangled web of confounders that is woven into our patchwork health care system. A recent study by two economists provides a glimpse into the role of defensive medicine in the cost of health care (“Defensive Medicine: Evidence from Military Immunity” Michael D. Frakes and Jonathan Gruber, National Bureau of Economic Research, July 2018). Using the unusual combination of circumstances in which military personnel and their dependents can or cannot sue depending on where they are receiving care, the investigators found that “liability immunity reduces inpatient spending by 5% with no measurable negative effect on patient outcomes.” While that may not be as high as Dr. Price or I think it may be, 5% of three trillion dollars is serious money.

The bigger problem is that defensive medicine is ugly, artless, and intellectually unsatisfying. While the patient may not view your diagnosis of his chronic debilitating or terminal illness as a work of art, there are such things as beautiful diagnoses. One may be beautiful in its simplicity and its ability to unify a variety of previously unexplained symptoms. Another diagnosis may be the intellectually stimulating result of a carefully thought out branching decision tree to solve a puzzling array of complaints using a minimum of costly studies.

Defensive medicine decisions are made primarily to avoid mistakes and omissions. Physicians often behave as though we believe our errors will always be fatal. That may be somewhat true for surgeons, but for the rest of us errors can be an important part of learning. The unfortunate outcome of an error, particularly one of omission, can usually be avoided by following the patient closely, remaining available ... and continuing to exude an aura of caring.

With close and thoughtful follow-up, you are going to discover pretty quickly when you have missed the target. Patients understand that we aren’t going to get the correct diagnosis or prescribe the best treatment on the first try every time. What patients don’t understand and what may prompt them to sue is feeling that they are being ignored.

While practicing defensive medicine isn’t usually listed as one of the cardinal symptoms of physician burnout, it probably deserves more attention. With some introspection and a bit of courage, recasting what you do in terms of its artistry and intellectual integrity could add a new and positive dimension to how you practice medicine. How many of your decisions are being made to avoid an error? Wouldn’t it be more fun to be making beautiful diagnoses you can be proud of?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Is My Child Overtired?: The Sleep Solution for Raising Happier, Healthier Children.” Email him at [email protected].