John M. Thorp Jr., MD

The developed world is in the midst of an unprecedented increase in human body mass. This increase can be attributed to widespread access to large amounts of inexpensive calories—particularly carbohydrates—and diminishing physical exertion. We have “evolved” from creatures struggling to get enough food to survive to vertebrates drowning in an ocean of calories and ease.

Although obesity clearly lies on the causal pathway for diseases such as diabetes and endometrial cancer, it also is associated with many other unhealthy behaviors and exposures. For example, obese women tend to earn less money, achieve less in school, smoke, and live farther away from markets and playgrounds—and the list of confounders goes on and on. We can measure height and weight with ease and precision, but we can’t assess and quantify most of these other confounders.

Related Article: Should you start prescribing lorcaserin or orlistat to your overweight or obese patients? Robert L. Barbieri, MD (Editorial, October 2013)

Cnattingius and colleagues give us another “obesity is bad” paper, this time with the outcome of preterm delivery. They found not only an association between obesity and preterm delivery but also a “mass response effect”—that is, the association increased along with maternal BMI.

The magnitude of the associations was small (odds ratios <3.0 for preterm delivery among overweight and obese women, compared with women of normal weight), and despite valiant efforts by the investigators to control for confounding, the imprecision I mentioned above limits their findings.

I declared a personal moratorium on reading “obesity is bad” papers a few years back. Even if obesity is a real risk factor for poor perinatal outcomes and not a proxy for residual confounding, we still have no idea, short of invasive surgery, how to modify that risk. Real progress will require effective lifestyle intervention—and we know so little about how to get people to lead healthy lives. It is difficult enough to modify our own behavior (recall your New Year’s resolutions), even harder to motivate our patients to lose weight and exercise.

What this evidence means for practice
Obesity is at best a weak risk factor for preterm delivery. Unless you are more successful than I have been at getting women to modify their diet and exercise, I would not make heavy mothers feel any worse.
John M. Thorp Jr., MD

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue.
Send your letter to: obg@frontlinemedcom.com Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

The developed world is in the midst of an unprecedented increase in human body mass. This increase can be attributed to widespread access to large amounts of inexpensive calories—particularly carbohydrates—and diminishing physical exertion. We have “evolved” from creatures struggling to get enough food to survive to vertebrates drowning in an ocean of calories and ease.

Although obesity clearly lies on the causal pathway for diseases such as diabetes and endometrial cancer, it also is associated with many other unhealthy behaviors and exposures. For example, obese women tend to earn less money, achieve less in school, smoke, and live farther away from markets and playgrounds—and the list of confounders goes on and on. We can measure height and weight with ease and precision, but we can’t assess and quantify most of these other confounders.

Related Article: Should you start prescribing lorcaserin or orlistat to your overweight or obese patients? Robert L. Barbieri, MD (Editorial, October 2013)

Cnattingius and colleagues give us another “obesity is bad” paper, this time with the outcome of preterm delivery. They found not only an association between obesity and preterm delivery but also a “mass response effect”—that is, the association increased along with maternal BMI.

The magnitude of the associations was small (odds ratios <3.0 for preterm delivery among overweight and obese women, compared with women of normal weight), and despite valiant efforts by the investigators to control for confounding, the imprecision I mentioned above limits their findings.

I declared a personal moratorium on reading “obesity is bad” papers a few years back. Even if obesity is a real risk factor for poor perinatal outcomes and not a proxy for residual confounding, we still have no idea, short of invasive surgery, how to modify that risk. Real progress will require effective lifestyle intervention—and we know so little about how to get people to lead healthy lives. It is difficult enough to modify our own behavior (recall your New Year’s resolutions), even harder to motivate our patients to lose weight and exercise.

What this evidence means for practice
Obesity is at best a weak risk factor for preterm delivery. Unless you are more successful than I have been at getting women to modify their diet and exercise, I would not make heavy mothers feel any worse.
John M. Thorp Jr., MD

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue.
Send your letter to: obg@frontlinemedcom.com Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

The developed world is in the midst of an unprecedented increase in human body mass. This increase can be attributed to widespread access to large amounts of inexpensive calories—particularly carbohydrates—and diminishing physical exertion. We have “evolved” from creatures struggling to get enough food to survive to vertebrates drowning in an ocean of calories and ease.

Although obesity clearly lies on the causal pathway for diseases such as diabetes and endometrial cancer, it also is associated with many other unhealthy behaviors and exposures. For example, obese women tend to earn less money, achieve less in school, smoke, and live farther away from markets and playgrounds—and the list of confounders goes on and on. We can measure height and weight with ease and precision, but we can’t assess and quantify most of these other confounders.

Related Article: Should you start prescribing lorcaserin or orlistat to your overweight or obese patients? Robert L. Barbieri, MD (Editorial, October 2013)

Cnattingius and colleagues give us another “obesity is bad” paper, this time with the outcome of preterm delivery. They found not only an association between obesity and preterm delivery but also a “mass response effect”—that is, the association increased along with maternal BMI.

The magnitude of the associations was small (odds ratios <3.0 for preterm delivery among overweight and obese women, compared with women of normal weight), and despite valiant efforts by the investigators to control for confounding, the imprecision I mentioned above limits their findings.

I declared a personal moratorium on reading “obesity is bad” papers a few years back. Even if obesity is a real risk factor for poor perinatal outcomes and not a proxy for residual confounding, we still have no idea, short of invasive surgery, how to modify that risk. Real progress will require effective lifestyle intervention—and we know so little about how to get people to lead healthy lives. It is difficult enough to modify our own behavior (recall your New Year’s resolutions), even harder to motivate our patients to lose weight and exercise.

What this evidence means for practice
Obesity is at best a weak risk factor for preterm delivery. Unless you are more successful than I have been at getting women to modify their diet and exercise, I would not make heavy mothers feel any worse.
John M. Thorp Jr., MD

TELL US WHAT YOU THINK!
Share your thoughts on this article or on any topic relevant to ObGyns and women’s health practitioners. Tell us which topics you’d like to see covered in future issues, and what challenges you face in daily practice. We will consider publishing your letter and in a future issue.
Send your letter to: obg@frontlinemedcom.com Please include the city and state in which you practice.
Stay in touch! Your feedback is important to us!

In contemporary obstetrics, electronic fetal monitoring (EFM) is used almost universally, and magnesium sulfate often is administered for seizure prophylaxis, tocolysis, or preterm neuroprotection. Given that magnesium crosses the placenta and is known to have both neurologic and cardiac effects and toxicities, it has been speculated that magnesium sulfate may change various characteristics of the fetal heart rate (FHR). Previous studies in small animals have failed to answer this common clinical question.

Details of the study

In this retrospective study from Washington University in St. Louis, Duffy and colleagues analyzed FHR tracings from 248 women who were exposed to magnesium sulfate, focusing on the 30 minutes just prior to delivery. These tracings were compared with those of 5,139 women who were not exposed to magnesium at all during the study.

All women in the study reached the second stage of labor, had at least 10 minutes of EFM recorded in the 30 minutes preceding delivery, and delivered at or beyond 37 weeks’ gestation. The groups were similar in regard to maternal race, mode of delivery, and tobacco and alcohol use. However, women exposed to magnesium were younger, had a higher body mass index and lower gravidity, and were more likely to be nulliparous and to have pregestational diabetes or gestational diabetes. In addition, women exposed to magnesium had a lower gestational age at delivery (38.4 [SD, 1.2] weeks vs 39.0 [SD, 1.2]weeks; P<.01), although no infants were born before 37 weeks.

Magnesium was given in accordance with the institution’s treatment guidelines for severe preeclampsia: a 6-g loading dose followed by a maintenance infusion of 2 g/hr, with monitoring for signs and symptoms of magnesium toxicity. (Magnesium was not given to women with mild preeclampsia.)

Two research nurses blinded to all exposure and outcome data used National Institute of Child Health and Human Development (NICHD) nomenclature to categorize FHR tracings. Magnesium exposure was associated with:

• a mean 3-beat difference in baseline FHR
• an increased likelihood of baseline FHR below 120 bpm
• greater likelihood that FHR variability was reduced or diminished.

The presence or number of accelerations or decelerations did not differ significantly between groups, but magnesium exposure was associated with fewer prolonged decelerations. These associations remained after excluding women who had adverse neonatal outcomes.

Fetal tachycardia was strongly associated with fetal acidemia and adverse neonatal outcomes in both groups. And prolonged decelerations were associated with an increased risk of fetal acidemia in women not exposed to magnesium and were present in all cases of fetal acidemia in exposed women.

The authors concluded that magnesium may mask signs of fetal distress.

Findings have little clinical utility

Despite the large numbers of women in this study and the rigorous methods utilized, the findings will be of little help to clinicians interpreting EFM tracings from fetuses whose mothers are receiving magnesium. The differences between groups were small, and the overwhelming majority of changes fell within the normal range.

More important than FHR changes is actual newborn condition. In a secondary analysis from the Beneficial Effects of Antenatal Magnesium trial from the Maternal-Fetal Medicine Units Network, Johnson and colleagues demonstrated that cord-blood magnesium levels did not predict the need for delivery room resuscitation.¹ In this trial, pediatricians were blinded as to whether the mother was receiving magnesium or placebo. These results cast real doubt on the hypothesis that maternal magnesium exposure alters the condition of the fetus or newborn in a clinically meaningful way.

We want to hear from you! Tell us what you think.

In contemporary obstetrics, electronic fetal monitoring (EFM) is used almost universally, and magnesium sulfate often is administered for seizure prophylaxis, tocolysis, or preterm neuroprotection. Given that magnesium crosses the placenta and is known to have both neurologic and cardiac effects and toxicities, it has been speculated that magnesium sulfate may change various characteristics of the fetal heart rate (FHR). Previous studies in small animals have failed to answer this common clinical question.

Details of the study

In this retrospective study from Washington University in St. Louis, Duffy and colleagues analyzed FHR tracings from 248 women who were exposed to magnesium sulfate, focusing on the 30 minutes just prior to delivery. These tracings were compared with those of 5,139 women who were not exposed to magnesium at all during the study.

All women in the study reached the second stage of labor, had at least 10 minutes of EFM recorded in the 30 minutes preceding delivery, and delivered at or beyond 37 weeks’ gestation. The groups were similar in regard to maternal race, mode of delivery, and tobacco and alcohol use. However, women exposed to magnesium were younger, had a higher body mass index and lower gravidity, and were more likely to be nulliparous and to have pregestational diabetes or gestational diabetes. In addition, women exposed to magnesium had a lower gestational age at delivery (38.4 [SD, 1.2] weeks vs 39.0 [SD, 1.2]weeks; P<.01), although no infants were born before 37 weeks.

Magnesium was given in accordance with the institution’s treatment guidelines for severe preeclampsia: a 6-g loading dose followed by a maintenance infusion of 2 g/hr, with monitoring for signs and symptoms of magnesium toxicity. (Magnesium was not given to women with mild preeclampsia.)

Two research nurses blinded to all exposure and outcome data used National Institute of Child Health and Human Development (NICHD) nomenclature to categorize FHR tracings. Magnesium exposure was associated with:

• a mean 3-beat difference in baseline FHR
• an increased likelihood of baseline FHR below 120 bpm
• greater likelihood that FHR variability was reduced or diminished.

The presence or number of accelerations or decelerations did not differ significantly between groups, but magnesium exposure was associated with fewer prolonged decelerations. These associations remained after excluding women who had adverse neonatal outcomes.

Fetal tachycardia was strongly associated with fetal acidemia and adverse neonatal outcomes in both groups. And prolonged decelerations were associated with an increased risk of fetal acidemia in women not exposed to magnesium and were present in all cases of fetal acidemia in exposed women.

The authors concluded that magnesium may mask signs of fetal distress.

Findings have little clinical utility

Despite the large numbers of women in this study and the rigorous methods utilized, the findings will be of little help to clinicians interpreting EFM tracings from fetuses whose mothers are receiving magnesium. The differences between groups were small, and the overwhelming majority of changes fell within the normal range.

More important than FHR changes is actual newborn condition. In a secondary analysis from the Beneficial Effects of Antenatal Magnesium trial from the Maternal-Fetal Medicine Units Network, Johnson and colleagues demonstrated that cord-blood magnesium levels did not predict the need for delivery room resuscitation.¹ In this trial, pediatricians were blinded as to whether the mother was receiving magnesium or placebo. These results cast real doubt on the hypothesis that maternal magnesium exposure alters the condition of the fetus or newborn in a clinically meaningful way.

We want to hear from you! Tell us what you think.

In contemporary obstetrics, electronic fetal monitoring (EFM) is used almost universally, and magnesium sulfate often is administered for seizure prophylaxis, tocolysis, or preterm neuroprotection. Given that magnesium crosses the placenta and is known to have both neurologic and cardiac effects and toxicities, it has been speculated that magnesium sulfate may change various characteristics of the fetal heart rate (FHR). Previous studies in small animals have failed to answer this common clinical question.

Details of the study

In this retrospective study from Washington University in St. Louis, Duffy and colleagues analyzed FHR tracings from 248 women who were exposed to magnesium sulfate, focusing on the 30 minutes just prior to delivery. These tracings were compared with those of 5,139 women who were not exposed to magnesium at all during the study.

All women in the study reached the second stage of labor, had at least 10 minutes of EFM recorded in the 30 minutes preceding delivery, and delivered at or beyond 37 weeks’ gestation. The groups were similar in regard to maternal race, mode of delivery, and tobacco and alcohol use. However, women exposed to magnesium were younger, had a higher body mass index and lower gravidity, and were more likely to be nulliparous and to have pregestational diabetes or gestational diabetes. In addition, women exposed to magnesium had a lower gestational age at delivery (38.4 [SD, 1.2] weeks vs 39.0 [SD, 1.2]weeks; P<.01), although no infants were born before 37 weeks.

Magnesium was given in accordance with the institution’s treatment guidelines for severe preeclampsia: a 6-g loading dose followed by a maintenance infusion of 2 g/hr, with monitoring for signs and symptoms of magnesium toxicity. (Magnesium was not given to women with mild preeclampsia.)

Two research nurses blinded to all exposure and outcome data used National Institute of Child Health and Human Development (NICHD) nomenclature to categorize FHR tracings. Magnesium exposure was associated with:

• a mean 3-beat difference in baseline FHR
• an increased likelihood of baseline FHR below 120 bpm
• greater likelihood that FHR variability was reduced or diminished.

The presence or number of accelerations or decelerations did not differ significantly between groups, but magnesium exposure was associated with fewer prolonged decelerations. These associations remained after excluding women who had adverse neonatal outcomes.

Fetal tachycardia was strongly associated with fetal acidemia and adverse neonatal outcomes in both groups. And prolonged decelerations were associated with an increased risk of fetal acidemia in women not exposed to magnesium and were present in all cases of fetal acidemia in exposed women.

The authors concluded that magnesium may mask signs of fetal distress.

Findings have little clinical utility

Despite the large numbers of women in this study and the rigorous methods utilized, the findings will be of little help to clinicians interpreting EFM tracings from fetuses whose mothers are receiving magnesium. The differences between groups were small, and the overwhelming majority of changes fell within the normal range.

More important than FHR changes is actual newborn condition. In a secondary analysis from the Beneficial Effects of Antenatal Magnesium trial from the Maternal-Fetal Medicine Units Network, Johnson and colleagues demonstrated that cord-blood magnesium levels did not predict the need for delivery room resuscitation.¹ In this trial, pediatricians were blinded as to whether the mother was receiving magnesium or placebo. These results cast real doubt on the hypothesis that maternal magnesium exposure alters the condition of the fetus or newborn in a clinically meaningful way.

We want to hear from you! Tell us what you think.