Obstetrics

RIVIERA MAYA, MEXICO — Women whose ejection fraction remains less than 50% after a diagnosis of peripartum cardiomyopathy face a significantly increased risk of cardiac deterioration and death with any subsequent pregnancies, Dr. Bernard Gonik said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“We know that the patient whose echocardiogram has not normalized within 6 months has a very poor prognosis in terms of future pregnancy,” said Dr. Gonik, the Fann Srere Endowed Chair in Perinatal Medicine at Wayne State University, Detroit.

“Of these women, 50% will have symptoms during a subsequent pregnancy, 33% will experience deterioration of cardiac function, 42% will have persistent cardiomyopathy, and 25% will die.”

These numbers are based on a 2001 review published in the New England Journal of Medicine. That article discussed outcomes in 92 women with the disorder who had a subsequent pregnancy. The article also identified the very poor prognosis for the 20% of women whose cardiac function does not normalize within a period of 6 months postpartum (N. Engl. J. Med. 2001;344:1567–71).

“The prognosis for these women is really bad, with up to 85% dying by 5 years,” Dr. Gonik said at the meeting, sponsored by Boston University. “Almost half of these deaths will occur within the first 6 months post partum.”

Conversely, among women with ejection fractions of more than 50%, only 6% had symptoms with a subsequent pregnancy, 17% deteriorated, 9% had persistent cardiomyopathy, and none died.

Peripartum cardiomyopathy is defined as the development of heart failure during the last month of pregnancy or within 3 months of delivery, in the absence of preexisting heart disease and with no other known cause, Dr. Gonik said.

The condition occurs in about 1 in 5,000 pregnancies. The etiology is unknown.

Risk factors include multiparity, advanced maternal age, twins, preeclampsia, hypertension, and black race.

RIVIERA MAYA, MEXICO — Women whose ejection fraction remains less than 50% after a diagnosis of peripartum cardiomyopathy face a significantly increased risk of cardiac deterioration and death with any subsequent pregnancies, Dr. Bernard Gonik said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“We know that the patient whose echocardiogram has not normalized within 6 months has a very poor prognosis in terms of future pregnancy,” said Dr. Gonik, the Fann Srere Endowed Chair in Perinatal Medicine at Wayne State University, Detroit.

“Of these women, 50% will have symptoms during a subsequent pregnancy, 33% will experience deterioration of cardiac function, 42% will have persistent cardiomyopathy, and 25% will die.”

These numbers are based on a 2001 review published in the New England Journal of Medicine. That article discussed outcomes in 92 women with the disorder who had a subsequent pregnancy. The article also identified the very poor prognosis for the 20% of women whose cardiac function does not normalize within a period of 6 months postpartum (N. Engl. J. Med. 2001;344:1567–71).

“The prognosis for these women is really bad, with up to 85% dying by 5 years,” Dr. Gonik said at the meeting, sponsored by Boston University. “Almost half of these deaths will occur within the first 6 months post partum.”

Conversely, among women with ejection fractions of more than 50%, only 6% had symptoms with a subsequent pregnancy, 17% deteriorated, 9% had persistent cardiomyopathy, and none died.

Peripartum cardiomyopathy is defined as the development of heart failure during the last month of pregnancy or within 3 months of delivery, in the absence of preexisting heart disease and with no other known cause, Dr. Gonik said.

The condition occurs in about 1 in 5,000 pregnancies. The etiology is unknown.

Risk factors include multiparity, advanced maternal age, twins, preeclampsia, hypertension, and black race.

RIVIERA MAYA, MEXICO — Women whose ejection fraction remains less than 50% after a diagnosis of peripartum cardiomyopathy face a significantly increased risk of cardiac deterioration and death with any subsequent pregnancies, Dr. Bernard Gonik said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“We know that the patient whose echocardiogram has not normalized within 6 months has a very poor prognosis in terms of future pregnancy,” said Dr. Gonik, the Fann Srere Endowed Chair in Perinatal Medicine at Wayne State University, Detroit.

“Of these women, 50% will have symptoms during a subsequent pregnancy, 33% will experience deterioration of cardiac function, 42% will have persistent cardiomyopathy, and 25% will die.”

These numbers are based on a 2001 review published in the New England Journal of Medicine. That article discussed outcomes in 92 women with the disorder who had a subsequent pregnancy. The article also identified the very poor prognosis for the 20% of women whose cardiac function does not normalize within a period of 6 months postpartum (N. Engl. J. Med. 2001;344:1567–71).

“The prognosis for these women is really bad, with up to 85% dying by 5 years,” Dr. Gonik said at the meeting, sponsored by Boston University. “Almost half of these deaths will occur within the first 6 months post partum.”

Conversely, among women with ejection fractions of more than 50%, only 6% had symptoms with a subsequent pregnancy, 17% deteriorated, 9% had persistent cardiomyopathy, and none died.

Peripartum cardiomyopathy is defined as the development of heart failure during the last month of pregnancy or within 3 months of delivery, in the absence of preexisting heart disease and with no other known cause, Dr. Gonik said.

The condition occurs in about 1 in 5,000 pregnancies. The etiology is unknown.

Risk factors include multiparity, advanced maternal age, twins, preeclampsia, hypertension, and black race.

SAN FRANCISCO— Prepregnancy body mass index and gestational weight gain are more predictive of fetal macrosomia than homeostasis model assessment and glucose load, a study has shown.

Because both of these are modifiable risk factors, “they should be emphasized in order to minimize the risk of macrosomia and associated adverse outcomes,” reported Dr. Chloe A. Zera in a poster presentation at the annual meeting of the Society for Maternal-Fetal Medicine.

In a prospective study designed to investigate whether either early or late gestational insulin resistance predicts infant birth weight and risk of macrosomia-related cesarean delivery, Dr. Zera of Boston's Brigham and Women's Hospital and colleagues collected data from 439 pregnant women enrolled in the Massachusetts General Hospital Obstetrical Maternal Study.

The information included homeostasis model assessment (HOMA) data, glucose load test (GLT) results, and clinical information including prepregnant body mass index (BMI), gestational weight gain, maternal age, delivery information, and infant birth weight.

All of the women had fasting blood samples drawn at 16–18 weeks gestation and all had GLT performed as part of routine care. Prepregnancy BMI was based on weight at first prenatal visit.

The investigators used multivariate analysis to predict infant birth weight as a function of the baseline characteristics of the study population and logistic regression to predict the odds of macrosomia and cesarean section, said Dr. Zera.

An analysis of the study population showed that 37% of the women in the study were overweight or obese prior to pregnancy, 17% of the infants in the cohort were macrosomic (more than 4,000 g), 27% of the deliveries were by cesarean section, and 30% of the cesarean deliveries were for macrosomia or failure to progress, Dr. Zera reported.

In the multivariate linear regression analysis, total gestational weight gain, prepregnancy BMI, and maternal age were significant predictors of birth weight, Dr. Zera said, noting that neither HOMA nor GLT were predictive. Both total weight gain and maternal BMI were significantly associated with risk of macrosomia in the logistical regression model, and maternal BMI alone was significantly associated with risk of cesarean section for macrosomia, she said.

Whereas glucose intolerance during pregnancy is thought to be a risk factor for macrosomia, the findings of this study suggest that “both maternal BMI and gestational weight gain may play more of a role than glucose intolerance in determining infant birth weight and subsequent risk of macrosomia and macrosomia-related cesarean delivery,” according to Dr. Zera.

Given these results, it is conceivable that reducing prepregnancy BMI and decreasing gestational weight gain may reduce the risk of macrosomia and subsequent cesarean delivery, Dr. Zera noted. As such, both should be emphasized clinically in women at risk, she said.

SAN FRANCISCO— Prepregnancy body mass index and gestational weight gain are more predictive of fetal macrosomia than homeostasis model assessment and glucose load, a study has shown.

Because both of these are modifiable risk factors, “they should be emphasized in order to minimize the risk of macrosomia and associated adverse outcomes,” reported Dr. Chloe A. Zera in a poster presentation at the annual meeting of the Society for Maternal-Fetal Medicine.

In a prospective study designed to investigate whether either early or late gestational insulin resistance predicts infant birth weight and risk of macrosomia-related cesarean delivery, Dr. Zera of Boston's Brigham and Women's Hospital and colleagues collected data from 439 pregnant women enrolled in the Massachusetts General Hospital Obstetrical Maternal Study.

The information included homeostasis model assessment (HOMA) data, glucose load test (GLT) results, and clinical information including prepregnant body mass index (BMI), gestational weight gain, maternal age, delivery information, and infant birth weight.

All of the women had fasting blood samples drawn at 16–18 weeks gestation and all had GLT performed as part of routine care. Prepregnancy BMI was based on weight at first prenatal visit.

The investigators used multivariate analysis to predict infant birth weight as a function of the baseline characteristics of the study population and logistic regression to predict the odds of macrosomia and cesarean section, said Dr. Zera.

An analysis of the study population showed that 37% of the women in the study were overweight or obese prior to pregnancy, 17% of the infants in the cohort were macrosomic (more than 4,000 g), 27% of the deliveries were by cesarean section, and 30% of the cesarean deliveries were for macrosomia or failure to progress, Dr. Zera reported.

In the multivariate linear regression analysis, total gestational weight gain, prepregnancy BMI, and maternal age were significant predictors of birth weight, Dr. Zera said, noting that neither HOMA nor GLT were predictive. Both total weight gain and maternal BMI were significantly associated with risk of macrosomia in the logistical regression model, and maternal BMI alone was significantly associated with risk of cesarean section for macrosomia, she said.

Whereas glucose intolerance during pregnancy is thought to be a risk factor for macrosomia, the findings of this study suggest that “both maternal BMI and gestational weight gain may play more of a role than glucose intolerance in determining infant birth weight and subsequent risk of macrosomia and macrosomia-related cesarean delivery,” according to Dr. Zera.

Given these results, it is conceivable that reducing prepregnancy BMI and decreasing gestational weight gain may reduce the risk of macrosomia and subsequent cesarean delivery, Dr. Zera noted. As such, both should be emphasized clinically in women at risk, she said.

SAN FRANCISCO— Prepregnancy body mass index and gestational weight gain are more predictive of fetal macrosomia than homeostasis model assessment and glucose load, a study has shown.

Because both of these are modifiable risk factors, “they should be emphasized in order to minimize the risk of macrosomia and associated adverse outcomes,” reported Dr. Chloe A. Zera in a poster presentation at the annual meeting of the Society for Maternal-Fetal Medicine.

In a prospective study designed to investigate whether either early or late gestational insulin resistance predicts infant birth weight and risk of macrosomia-related cesarean delivery, Dr. Zera of Boston's Brigham and Women's Hospital and colleagues collected data from 439 pregnant women enrolled in the Massachusetts General Hospital Obstetrical Maternal Study.

The information included homeostasis model assessment (HOMA) data, glucose load test (GLT) results, and clinical information including prepregnant body mass index (BMI), gestational weight gain, maternal age, delivery information, and infant birth weight.

All of the women had fasting blood samples drawn at 16–18 weeks gestation and all had GLT performed as part of routine care. Prepregnancy BMI was based on weight at first prenatal visit.

The investigators used multivariate analysis to predict infant birth weight as a function of the baseline characteristics of the study population and logistic regression to predict the odds of macrosomia and cesarean section, said Dr. Zera.

An analysis of the study population showed that 37% of the women in the study were overweight or obese prior to pregnancy, 17% of the infants in the cohort were macrosomic (more than 4,000 g), 27% of the deliveries were by cesarean section, and 30% of the cesarean deliveries were for macrosomia or failure to progress, Dr. Zera reported.

In the multivariate linear regression analysis, total gestational weight gain, prepregnancy BMI, and maternal age were significant predictors of birth weight, Dr. Zera said, noting that neither HOMA nor GLT were predictive. Both total weight gain and maternal BMI were significantly associated with risk of macrosomia in the logistical regression model, and maternal BMI alone was significantly associated with risk of cesarean section for macrosomia, she said.

Whereas glucose intolerance during pregnancy is thought to be a risk factor for macrosomia, the findings of this study suggest that “both maternal BMI and gestational weight gain may play more of a role than glucose intolerance in determining infant birth weight and subsequent risk of macrosomia and macrosomia-related cesarean delivery,” according to Dr. Zera.

Given these results, it is conceivable that reducing prepregnancy BMI and decreasing gestational weight gain may reduce the risk of macrosomia and subsequent cesarean delivery, Dr. Zera noted. As such, both should be emphasized clinically in women at risk, she said.

In a population of mothers with type 1 diabetes and their singleton infants, third-trimester glycemic measures were more predictive of bearing a large-for-gestational-age infant than were earlier parameters, and third-trimester episodic hyperglycemia was most predictive of all.

Dr. Lucrecia Herranz and colleagues at the University Hospital of La Paz in Madrid recruited from the hospital 73 mothers, who had given birth to 37 large-for-gestational-age (LGA) infants and 36 appropriate-for-gestational-age (AGA) infants. The investigators reported their findings in Diabetes Research and Clinical Practice (2007;75:42–6).

After researchers controlled for tobacco smoking and history of microsomia, mothers of LGA infants had significantly higher mean overall glucose levels in all trimesters than did mothers of AGA infants. But the difference was most pronounced in the third trimester, when LGA infants' mothers registered a mean glucose level of 7.4 mmol/L, vs. 6.9 mmol/L for mothers of AGA infants. Mean postprandial glucose in the third trimester was 8.4 mmol/L for mothers of LGA babies and 7.9 mmol/L for AGA neonates' mothers. Moreover, the portion of glucose values higher than the goal was 42% for LGA mothers and 35% for AGA mothers. HbA_1c levels were significantly higher in the LGA group than in the AGA group only in the third trimester (6.2 vs. 5.9).

Logistic regression of all third-trimester glycemic measures showed that the percentage of third-trimester glucose values above the target value posed an increased likelihood of bearing an LGA infant (OR 1.09; 95% CI 1.02–1.15). AGA infants had a mean birth weight of 3,139 g, vs. 3,830 g for the LGA infants.

Notably, the two groups of mothers, all of whom had been managed at the hospital before conception, had no preconception differences in glycemic parameters.

Dr. Herranz and colleagues noted that their study supports the findings of prior studies that have posited an effect of intermittent maternal hyperglycemia on fetal growth. “Interestingly, our data show that of all third-trimester glycemic parameters, the percentage of glucose values above glycemic target is the most powerful predictor of LGA infants,” they wrote.

In a population of mothers with type 1 diabetes and their singleton infants, third-trimester glycemic measures were more predictive of bearing a large-for-gestational-age infant than were earlier parameters, and third-trimester episodic hyperglycemia was most predictive of all.

Dr. Lucrecia Herranz and colleagues at the University Hospital of La Paz in Madrid recruited from the hospital 73 mothers, who had given birth to 37 large-for-gestational-age (LGA) infants and 36 appropriate-for-gestational-age (AGA) infants. The investigators reported their findings in Diabetes Research and Clinical Practice (2007;75:42–6).

After researchers controlled for tobacco smoking and history of microsomia, mothers of LGA infants had significantly higher mean overall glucose levels in all trimesters than did mothers of AGA infants. But the difference was most pronounced in the third trimester, when LGA infants' mothers registered a mean glucose level of 7.4 mmol/L, vs. 6.9 mmol/L for mothers of AGA infants. Mean postprandial glucose in the third trimester was 8.4 mmol/L for mothers of LGA babies and 7.9 mmol/L for AGA neonates' mothers. Moreover, the portion of glucose values higher than the goal was 42% for LGA mothers and 35% for AGA mothers. HbA_1c levels were significantly higher in the LGA group than in the AGA group only in the third trimester (6.2 vs. 5.9).

Logistic regression of all third-trimester glycemic measures showed that the percentage of third-trimester glucose values above the target value posed an increased likelihood of bearing an LGA infant (OR 1.09; 95% CI 1.02–1.15). AGA infants had a mean birth weight of 3,139 g, vs. 3,830 g for the LGA infants.

Notably, the two groups of mothers, all of whom had been managed at the hospital before conception, had no preconception differences in glycemic parameters.

Dr. Herranz and colleagues noted that their study supports the findings of prior studies that have posited an effect of intermittent maternal hyperglycemia on fetal growth. “Interestingly, our data show that of all third-trimester glycemic parameters, the percentage of glucose values above glycemic target is the most powerful predictor of LGA infants,” they wrote.

In a population of mothers with type 1 diabetes and their singleton infants, third-trimester glycemic measures were more predictive of bearing a large-for-gestational-age infant than were earlier parameters, and third-trimester episodic hyperglycemia was most predictive of all.

Dr. Lucrecia Herranz and colleagues at the University Hospital of La Paz in Madrid recruited from the hospital 73 mothers, who had given birth to 37 large-for-gestational-age (LGA) infants and 36 appropriate-for-gestational-age (AGA) infants. The investigators reported their findings in Diabetes Research and Clinical Practice (2007;75:42–6).

After researchers controlled for tobacco smoking and history of microsomia, mothers of LGA infants had significantly higher mean overall glucose levels in all trimesters than did mothers of AGA infants. But the difference was most pronounced in the third trimester, when LGA infants' mothers registered a mean glucose level of 7.4 mmol/L, vs. 6.9 mmol/L for mothers of AGA infants. Mean postprandial glucose in the third trimester was 8.4 mmol/L for mothers of LGA babies and 7.9 mmol/L for AGA neonates' mothers. Moreover, the portion of glucose values higher than the goal was 42% for LGA mothers and 35% for AGA mothers. HbA_1c levels were significantly higher in the LGA group than in the AGA group only in the third trimester (6.2 vs. 5.9).

Logistic regression of all third-trimester glycemic measures showed that the percentage of third-trimester glucose values above the target value posed an increased likelihood of bearing an LGA infant (OR 1.09; 95% CI 1.02–1.15). AGA infants had a mean birth weight of 3,139 g, vs. 3,830 g for the LGA infants.

Notably, the two groups of mothers, all of whom had been managed at the hospital before conception, had no preconception differences in glycemic parameters.

Dr. Herranz and colleagues noted that their study supports the findings of prior studies that have posited an effect of intermittent maternal hyperglycemia on fetal growth. “Interestingly, our data show that of all third-trimester glycemic parameters, the percentage of glucose values above glycemic target is the most powerful predictor of LGA infants,” they wrote.

HOT SPRINGS, VA. — Placental growth factor, an angiogenic factor normally elevated in early pregnancy, may be a valuable biomarker for detecting pregnancies destined to become preeclamptic, Dr. Ramsey Unal said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

Vascular growth factors are essential in creating and maintaining the placenta, said Dr. Unal, a resident at the Medical University of South Carolina, Charleston. Both placental growth factor (PIGF) and vascular endothelial growth factor (VEGF) are higher in early pregnancy and decrease as delivery approaches. Another factor, soluble FMS-like tyrosine kinase 1 (sFlt1), increases later in pregnancy and binds both PIGF and VEGF, decreasing their bioavailability as the pregnancy nears term.

“Normal pregnancy is a balancing act in angiogenesis,” Dr. Unal said. “At the beginning, during placentation, you have a proangiogenic state and toward the end, in preparation for delivery; you shift to an antiangiogenic state. In preeclampsia, we think the shift happens too early and is too exaggerated.”

Dr. Unal investigated the utility of using second-trimester PIGF and sFLT1 levels as predictors of preeclampsia. If the levels were already abnormal in the second trimester, she reasoned, they could easily be included in the quad screen to flag women at risk for preeclampsia.

Her retrospective study included 64 women: 21 of them developed preeclampsia and were delivered for that reason, 34 were healthy women with uncomplicated term deliveries, and 9 had chronic, prepregnancy hypertension. All the women had singleton pregnancies. Dr. Unal performed enzyme-linked immunosorbent assay testing for PIGF and sFLT1 on stored quad screen serum samples obtained from these women at 16–24 weeks' gestation.

PIGF was significantly lower in the group that went on to develop preeclampsia than it was in the normal control group, she said (mean 85.3 pg/mL vs. 133 pg/mL). There were no significant differences in sFLT1 levels between the groups. However, women with chronic hypertension had slightly, though not significantly, lower sFLT1 levels than did normal controls—an interesting relationship, Dr. Unal said. “Preeclampsia is a disease of the placenta, and hypertension can also cause placenta problems.”

PIGF levels could easily be drawn from quad screen sera, adding yet another valuable biomarker to the routine screen. “But we need a large, prospective trial before any recommendations can be made,” she said.

HOT SPRINGS, VA. — Placental growth factor, an angiogenic factor normally elevated in early pregnancy, may be a valuable biomarker for detecting pregnancies destined to become preeclamptic, Dr. Ramsey Unal said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

Vascular growth factors are essential in creating and maintaining the placenta, said Dr. Unal, a resident at the Medical University of South Carolina, Charleston. Both placental growth factor (PIGF) and vascular endothelial growth factor (VEGF) are higher in early pregnancy and decrease as delivery approaches. Another factor, soluble FMS-like tyrosine kinase 1 (sFlt1), increases later in pregnancy and binds both PIGF and VEGF, decreasing their bioavailability as the pregnancy nears term.

“Normal pregnancy is a balancing act in angiogenesis,” Dr. Unal said. “At the beginning, during placentation, you have a proangiogenic state and toward the end, in preparation for delivery; you shift to an antiangiogenic state. In preeclampsia, we think the shift happens too early and is too exaggerated.”

Dr. Unal investigated the utility of using second-trimester PIGF and sFLT1 levels as predictors of preeclampsia. If the levels were already abnormal in the second trimester, she reasoned, they could easily be included in the quad screen to flag women at risk for preeclampsia.

Her retrospective study included 64 women: 21 of them developed preeclampsia and were delivered for that reason, 34 were healthy women with uncomplicated term deliveries, and 9 had chronic, prepregnancy hypertension. All the women had singleton pregnancies. Dr. Unal performed enzyme-linked immunosorbent assay testing for PIGF and sFLT1 on stored quad screen serum samples obtained from these women at 16–24 weeks' gestation.

PIGF was significantly lower in the group that went on to develop preeclampsia than it was in the normal control group, she said (mean 85.3 pg/mL vs. 133 pg/mL). There were no significant differences in sFLT1 levels between the groups. However, women with chronic hypertension had slightly, though not significantly, lower sFLT1 levels than did normal controls—an interesting relationship, Dr. Unal said. “Preeclampsia is a disease of the placenta, and hypertension can also cause placenta problems.”

PIGF levels could easily be drawn from quad screen sera, adding yet another valuable biomarker to the routine screen. “But we need a large, prospective trial before any recommendations can be made,” she said.

HOT SPRINGS, VA. — Placental growth factor, an angiogenic factor normally elevated in early pregnancy, may be a valuable biomarker for detecting pregnancies destined to become preeclamptic, Dr. Ramsey Unal said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

Vascular growth factors are essential in creating and maintaining the placenta, said Dr. Unal, a resident at the Medical University of South Carolina, Charleston. Both placental growth factor (PIGF) and vascular endothelial growth factor (VEGF) are higher in early pregnancy and decrease as delivery approaches. Another factor, soluble FMS-like tyrosine kinase 1 (sFlt1), increases later in pregnancy and binds both PIGF and VEGF, decreasing their bioavailability as the pregnancy nears term.

“Normal pregnancy is a balancing act in angiogenesis,” Dr. Unal said. “At the beginning, during placentation, you have a proangiogenic state and toward the end, in preparation for delivery; you shift to an antiangiogenic state. In preeclampsia, we think the shift happens too early and is too exaggerated.”

Dr. Unal investigated the utility of using second-trimester PIGF and sFLT1 levels as predictors of preeclampsia. If the levels were already abnormal in the second trimester, she reasoned, they could easily be included in the quad screen to flag women at risk for preeclampsia.

Her retrospective study included 64 women: 21 of them developed preeclampsia and were delivered for that reason, 34 were healthy women with uncomplicated term deliveries, and 9 had chronic, prepregnancy hypertension. All the women had singleton pregnancies. Dr. Unal performed enzyme-linked immunosorbent assay testing for PIGF and sFLT1 on stored quad screen serum samples obtained from these women at 16–24 weeks' gestation.

PIGF was significantly lower in the group that went on to develop preeclampsia than it was in the normal control group, she said (mean 85.3 pg/mL vs. 133 pg/mL). There were no significant differences in sFLT1 levels between the groups. However, women with chronic hypertension had slightly, though not significantly, lower sFLT1 levels than did normal controls—an interesting relationship, Dr. Unal said. “Preeclampsia is a disease of the placenta, and hypertension can also cause placenta problems.”

PIGF levels could easily be drawn from quad screen sera, adding yet another valuable biomarker to the routine screen. “But we need a large, prospective trial before any recommendations can be made,” she said.

RIVIERA MAYA, MEXICO — A perimortem cesarean delivery should be performed within 5 minutes of maternal cardiac arrest to maximize survival chances for both the fetus and its mother, presenters said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“I've done it a dozen times in 28 years, and it's probably the most frightening thing you will ever encounter,” said Dr. John Marx, chair of emergency medicine at the Carolinas Medical Center, Charlotte, N.C. “It is the fastest, hardest decision making you will ever do.”

Only about 300 cases of perimortem cesarean section have been reported in the literature, and many of these were confounded by inadequate reporting of time from maternal injury, drawing into question whether the fetus had any chance of survival.

A 2005 review identified 38 cases since 1986 in which the procedure was appropriately documented, and supported it for two reasons: to save the life of a viable fetus and/or to maximize maternal response to resuscitation (AJOG 2005;192:1916–21).

The indication for maternal salvage is a rather new thought, said Dr. Bernard Gonik, the Fann S. Srer Chair of Perinatal Medicine at Wayne State University, Detroit. “There are data indicating that the procedure can dramatically improve maternal cardiac output by emptying the uterus so that it's not pressing on the vena cava and inhibiting return. This can improve cardiac output by 25%.”

The pregnant uterus consumes a large amount of maternal blood, causing gravid women to become anoxic much more quickly during a crisis. “That's another reason to add C-section to your resuscitation efforts,” Dr. Gonik said.

The 2005 review included resuscitation information for 22 women; 12 of them showed profoundly increased response after the procedure. Of 20 potentially salvageable mothers, 13 were discharged from the hospital in good condition.

Time is the most critical factor when a pregnant woman with a gestationally viable fetus arrests, both physicians said. “The earlier you deliver, the more likely you are to have a neurologically intact baby,” Dr. Gonik said, noting that the review indicated that 98% of babies born within 5 minutes of maternal arrest were neurologically intact.

Dr. Marx agreed. “If you get the fetus out within 5 minutes you have a good chance not only for it to survive but to have good neurologic outcome. If you wait 15 minutes, the chance of survival and good neurologic outcome is dim. I'm not sure which is worse from a legal perspective: to wind up with a baby who will never, ever be OK, or to wind up with a dead fetus.”

Difficult decisions abound in this kind of situation, both men said. The patient will not be physically or mentally able to give informed consent, and very often, no kin are available to help in that regard. Opinions differ on the importance of accurately assessing gestational age, which is best done via ultrasound. Dr. Marx advised against performing the procedure to try and save a fetus of less than 24 weeks. But some audience members commented that fetal age is irrelevant, since the primary indication should be to maximize maternal outcome.

A similar discussion arose around fetal heart rate: Whereas a good rate is a deciding factor for some physicians, others proceed with the delivery regardless of the rate, in the hopes of saving the mother's life.

“My counterpoint would be this,” Dr. Marx said. “Turning the mother onto her left side 50 to 30 degrees should help considerably in maximizing maternal response [by decreasing pressure on the inferior vena cava]. Secondly, if we think the fetus has no chance of survival, we may end up doing a thoracotomy on the mother, cross-clamping to eliminate any blood lost to the uterus. We want to be very, very cautious about delivering a fetus that is only semi-viable. That's the conundrum.”

The procedure demands a team effort by the most experienced people available. “You call obstetrics, you call surgery, and you call people who have expert ultrasound capabilities if you don't have them,” Dr. Marx said. “And this is not a procedure for a third-year medical student. You want the most competent person in the room, whether it's the obstetrician or the emergency physician.”

The delivery is a midline crash vertical incision “from stem to stern” through all tissue levels of the anterior uterus. “If the placenta is in the way, either push it aside or cut through it,” Dr. Marx said.

Despite concerns about informed consent and the ethics of delivering a nonviable or impaired fetus, physicians who perform a perimortem C-section for the correct indication probably aren't in legal danger, Dr. Gonik said. “No physician in the U.S. has ever been found liable in one of these cases. They typically do not go to court or get the physician or hospital in trouble because they were attempting to save the baby.”

However, he strongly cautioned, “Never perform this in anticipation of the mother arresting. If the patient is unstable and you proceed, you could push her into needing resuscitation.”

RIVIERA MAYA, MEXICO — A perimortem cesarean delivery should be performed within 5 minutes of maternal cardiac arrest to maximize survival chances for both the fetus and its mother, presenters said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“I've done it a dozen times in 28 years, and it's probably the most frightening thing you will ever encounter,” said Dr. John Marx, chair of emergency medicine at the Carolinas Medical Center, Charlotte, N.C. “It is the fastest, hardest decision making you will ever do.”

Only about 300 cases of perimortem cesarean section have been reported in the literature, and many of these were confounded by inadequate reporting of time from maternal injury, drawing into question whether the fetus had any chance of survival.

A 2005 review identified 38 cases since 1986 in which the procedure was appropriately documented, and supported it for two reasons: to save the life of a viable fetus and/or to maximize maternal response to resuscitation (AJOG 2005;192:1916–21).

The indication for maternal salvage is a rather new thought, said Dr. Bernard Gonik, the Fann S. Srer Chair of Perinatal Medicine at Wayne State University, Detroit. “There are data indicating that the procedure can dramatically improve maternal cardiac output by emptying the uterus so that it's not pressing on the vena cava and inhibiting return. This can improve cardiac output by 25%.”

The pregnant uterus consumes a large amount of maternal blood, causing gravid women to become anoxic much more quickly during a crisis. “That's another reason to add C-section to your resuscitation efforts,” Dr. Gonik said.

The 2005 review included resuscitation information for 22 women; 12 of them showed profoundly increased response after the procedure. Of 20 potentially salvageable mothers, 13 were discharged from the hospital in good condition.

Time is the most critical factor when a pregnant woman with a gestationally viable fetus arrests, both physicians said. “The earlier you deliver, the more likely you are to have a neurologically intact baby,” Dr. Gonik said, noting that the review indicated that 98% of babies born within 5 minutes of maternal arrest were neurologically intact.

Dr. Marx agreed. “If you get the fetus out within 5 minutes you have a good chance not only for it to survive but to have good neurologic outcome. If you wait 15 minutes, the chance of survival and good neurologic outcome is dim. I'm not sure which is worse from a legal perspective: to wind up with a baby who will never, ever be OK, or to wind up with a dead fetus.”

Difficult decisions abound in this kind of situation, both men said. The patient will not be physically or mentally able to give informed consent, and very often, no kin are available to help in that regard. Opinions differ on the importance of accurately assessing gestational age, which is best done via ultrasound. Dr. Marx advised against performing the procedure to try and save a fetus of less than 24 weeks. But some audience members commented that fetal age is irrelevant, since the primary indication should be to maximize maternal outcome.

A similar discussion arose around fetal heart rate: Whereas a good rate is a deciding factor for some physicians, others proceed with the delivery regardless of the rate, in the hopes of saving the mother's life.

“My counterpoint would be this,” Dr. Marx said. “Turning the mother onto her left side 50 to 30 degrees should help considerably in maximizing maternal response [by decreasing pressure on the inferior vena cava]. Secondly, if we think the fetus has no chance of survival, we may end up doing a thoracotomy on the mother, cross-clamping to eliminate any blood lost to the uterus. We want to be very, very cautious about delivering a fetus that is only semi-viable. That's the conundrum.”

The procedure demands a team effort by the most experienced people available. “You call obstetrics, you call surgery, and you call people who have expert ultrasound capabilities if you don't have them,” Dr. Marx said. “And this is not a procedure for a third-year medical student. You want the most competent person in the room, whether it's the obstetrician or the emergency physician.”

The delivery is a midline crash vertical incision “from stem to stern” through all tissue levels of the anterior uterus. “If the placenta is in the way, either push it aside or cut through it,” Dr. Marx said.

Despite concerns about informed consent and the ethics of delivering a nonviable or impaired fetus, physicians who perform a perimortem C-section for the correct indication probably aren't in legal danger, Dr. Gonik said. “No physician in the U.S. has ever been found liable in one of these cases. They typically do not go to court or get the physician or hospital in trouble because they were attempting to save the baby.”

However, he strongly cautioned, “Never perform this in anticipation of the mother arresting. If the patient is unstable and you proceed, you could push her into needing resuscitation.”

RIVIERA MAYA, MEXICO — A perimortem cesarean delivery should be performed within 5 minutes of maternal cardiac arrest to maximize survival chances for both the fetus and its mother, presenters said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“I've done it a dozen times in 28 years, and it's probably the most frightening thing you will ever encounter,” said Dr. John Marx, chair of emergency medicine at the Carolinas Medical Center, Charlotte, N.C. “It is the fastest, hardest decision making you will ever do.”

Only about 300 cases of perimortem cesarean section have been reported in the literature, and many of these were confounded by inadequate reporting of time from maternal injury, drawing into question whether the fetus had any chance of survival.

A 2005 review identified 38 cases since 1986 in which the procedure was appropriately documented, and supported it for two reasons: to save the life of a viable fetus and/or to maximize maternal response to resuscitation (AJOG 2005;192:1916–21).

The indication for maternal salvage is a rather new thought, said Dr. Bernard Gonik, the Fann S. Srer Chair of Perinatal Medicine at Wayne State University, Detroit. “There are data indicating that the procedure can dramatically improve maternal cardiac output by emptying the uterus so that it's not pressing on the vena cava and inhibiting return. This can improve cardiac output by 25%.”

The pregnant uterus consumes a large amount of maternal blood, causing gravid women to become anoxic much more quickly during a crisis. “That's another reason to add C-section to your resuscitation efforts,” Dr. Gonik said.

The 2005 review included resuscitation information for 22 women; 12 of them showed profoundly increased response after the procedure. Of 20 potentially salvageable mothers, 13 were discharged from the hospital in good condition.

Time is the most critical factor when a pregnant woman with a gestationally viable fetus arrests, both physicians said. “The earlier you deliver, the more likely you are to have a neurologically intact baby,” Dr. Gonik said, noting that the review indicated that 98% of babies born within 5 minutes of maternal arrest were neurologically intact.

Dr. Marx agreed. “If you get the fetus out within 5 minutes you have a good chance not only for it to survive but to have good neurologic outcome. If you wait 15 minutes, the chance of survival and good neurologic outcome is dim. I'm not sure which is worse from a legal perspective: to wind up with a baby who will never, ever be OK, or to wind up with a dead fetus.”

Difficult decisions abound in this kind of situation, both men said. The patient will not be physically or mentally able to give informed consent, and very often, no kin are available to help in that regard. Opinions differ on the importance of accurately assessing gestational age, which is best done via ultrasound. Dr. Marx advised against performing the procedure to try and save a fetus of less than 24 weeks. But some audience members commented that fetal age is irrelevant, since the primary indication should be to maximize maternal outcome.

A similar discussion arose around fetal heart rate: Whereas a good rate is a deciding factor for some physicians, others proceed with the delivery regardless of the rate, in the hopes of saving the mother's life.

“My counterpoint would be this,” Dr. Marx said. “Turning the mother onto her left side 50 to 30 degrees should help considerably in maximizing maternal response [by decreasing pressure on the inferior vena cava]. Secondly, if we think the fetus has no chance of survival, we may end up doing a thoracotomy on the mother, cross-clamping to eliminate any blood lost to the uterus. We want to be very, very cautious about delivering a fetus that is only semi-viable. That's the conundrum.”

The procedure demands a team effort by the most experienced people available. “You call obstetrics, you call surgery, and you call people who have expert ultrasound capabilities if you don't have them,” Dr. Marx said. “And this is not a procedure for a third-year medical student. You want the most competent person in the room, whether it's the obstetrician or the emergency physician.”

The delivery is a midline crash vertical incision “from stem to stern” through all tissue levels of the anterior uterus. “If the placenta is in the way, either push it aside or cut through it,” Dr. Marx said.

Despite concerns about informed consent and the ethics of delivering a nonviable or impaired fetus, physicians who perform a perimortem C-section for the correct indication probably aren't in legal danger, Dr. Gonik said. “No physician in the U.S. has ever been found liable in one of these cases. They typically do not go to court or get the physician or hospital in trouble because they were attempting to save the baby.”

However, he strongly cautioned, “Never perform this in anticipation of the mother arresting. If the patient is unstable and you proceed, you could push her into needing resuscitation.”

SAN FRANCISCO — Maternal peripartum cardiomyopathy, seen in 1 in 3,000 live births, generally carries a good prognosis, Dr. Michael Crawford said at a meeting sponsored by the California chapter of the American College of Cardiology.

Diagnosis of peripartum cardiomyopathy—or of other heart diseases during pregnancy—often is delayed because the symptoms of pregnancy can mimic the heart disease symptoms, said Dr. Crawford, professor of medicine at the University of California, San Francisco,

A majority of women with peripartum cardiomyopathy recover after delivery, but 10%–20% require heart transplantation and 1%–2% die, data suggest. The patient's ejection fraction 2 months after diagnosis appears to be the best prognostic factor, he said at the meeting, also sponsored by the university.

Treatment for cardiomyopathy differs for pregnant women compared with nonpregnant patients because some drugs shouldn't be used until after delivery.

ACE inhibitors and warfarin are teratogenic, and β-blockers can lead to fetal bradycardia.

“You get by with diuretics, digoxin, and hydralazine during pregnancy” for peripartum cardiomyopathy, Dr. Crawford said.

In a recent study at a large medical center, ejection fractions improved at least 15% in 62% of women with peripartum cardiomyopathy, remained unchanged in 25%, and declined in 13% (Am. Heart J. 2006;152:509–13).

Ejection fractions returned to normal in 45%. Ten percent of patients required transplantation. No patients died during an average 43-month follow-up. “That's encouraging,” he noted.

The initial echocardiogram, obtained between 1 month prepartum and 5 months post partum, did not predict which patients required transplantation, nor which had final ejection fractions below or above 50%. “Don't get discouraged with the first echo,” Dr. Crawford said. Echocardiograms 2 months later predicted outcomes in that study.

Patients with ejection fractions below 20% probably are headed for transplant. Those with ejection fractions between 20% and 50% should see some improvement but are unlikely to return to normal. If the 2-month ejection fraction is above 40%, the patient is likely to recover fully (defined as an ejection fraction greater than 50%), he said.

Shortness of breath and decreased exercise capacity, which are symptoms of cardiomyopathy, also are symptoms of a normal pregnancy. Fatigue, orthopnea, and dizziness or syncope, which might be symptoms of other heart disease, also are normal symptoms of pregnancy.

Electrocardiograms in normal pregnancies often detect sinus tachycardia, and may show nonspecific ST-T changes. As the pregnancy advances, the heart's axis shifts more to the left.

Physical findings in normal pregnancies may include jugular venous distension, an enlarged left ventricle apex, right ventricle heave, a palpable pulmonary artery pulse, third heart sounds, systolic ejection murmurs, venous hums, or a mammary souffle noise if you listen over the breast.

“It can be confusing,” Dr. Crawford said.

The most common peripartum cardiovascular problem is venous thromboembolism, which is the leading cause of death in pregnancy, he added.

Consider prophylactic medication in women with risk factors (thrombophilia, history of thrombosis, antiphospholipid syndrome, lupus erythematosus, sickle cell anemia, or any kind of heart disease that would lead to thrombus formation).

Coronary artery disease during pregnancy is more common than one might think, perhaps because more women are having children later in life, he added.

Maternal MI occurs in 6 out of 100,000 deliveries, three to four times more common than is expected in age-matched nonpregnant women.

SAN FRANCISCO — Maternal peripartum cardiomyopathy, seen in 1 in 3,000 live births, generally carries a good prognosis, Dr. Michael Crawford said at a meeting sponsored by the California chapter of the American College of Cardiology.

Diagnosis of peripartum cardiomyopathy—or of other heart diseases during pregnancy—often is delayed because the symptoms of pregnancy can mimic the heart disease symptoms, said Dr. Crawford, professor of medicine at the University of California, San Francisco,

A majority of women with peripartum cardiomyopathy recover after delivery, but 10%–20% require heart transplantation and 1%–2% die, data suggest. The patient's ejection fraction 2 months after diagnosis appears to be the best prognostic factor, he said at the meeting, also sponsored by the university.

Treatment for cardiomyopathy differs for pregnant women compared with nonpregnant patients because some drugs shouldn't be used until after delivery.

ACE inhibitors and warfarin are teratogenic, and β-blockers can lead to fetal bradycardia.

“You get by with diuretics, digoxin, and hydralazine during pregnancy” for peripartum cardiomyopathy, Dr. Crawford said.

In a recent study at a large medical center, ejection fractions improved at least 15% in 62% of women with peripartum cardiomyopathy, remained unchanged in 25%, and declined in 13% (Am. Heart J. 2006;152:509–13).

Ejection fractions returned to normal in 45%. Ten percent of patients required transplantation. No patients died during an average 43-month follow-up. “That's encouraging,” he noted.

The initial echocardiogram, obtained between 1 month prepartum and 5 months post partum, did not predict which patients required transplantation, nor which had final ejection fractions below or above 50%. “Don't get discouraged with the first echo,” Dr. Crawford said. Echocardiograms 2 months later predicted outcomes in that study.

Patients with ejection fractions below 20% probably are headed for transplant. Those with ejection fractions between 20% and 50% should see some improvement but are unlikely to return to normal. If the 2-month ejection fraction is above 40%, the patient is likely to recover fully (defined as an ejection fraction greater than 50%), he said.

Shortness of breath and decreased exercise capacity, which are symptoms of cardiomyopathy, also are symptoms of a normal pregnancy. Fatigue, orthopnea, and dizziness or syncope, which might be symptoms of other heart disease, also are normal symptoms of pregnancy.

Electrocardiograms in normal pregnancies often detect sinus tachycardia, and may show nonspecific ST-T changes. As the pregnancy advances, the heart's axis shifts more to the left.

Physical findings in normal pregnancies may include jugular venous distension, an enlarged left ventricle apex, right ventricle heave, a palpable pulmonary artery pulse, third heart sounds, systolic ejection murmurs, venous hums, or a mammary souffle noise if you listen over the breast.

“It can be confusing,” Dr. Crawford said.

The most common peripartum cardiovascular problem is venous thromboembolism, which is the leading cause of death in pregnancy, he added.

Consider prophylactic medication in women with risk factors (thrombophilia, history of thrombosis, antiphospholipid syndrome, lupus erythematosus, sickle cell anemia, or any kind of heart disease that would lead to thrombus formation).

Coronary artery disease during pregnancy is more common than one might think, perhaps because more women are having children later in life, he added.

Maternal MI occurs in 6 out of 100,000 deliveries, three to four times more common than is expected in age-matched nonpregnant women.

SAN FRANCISCO — Maternal peripartum cardiomyopathy, seen in 1 in 3,000 live births, generally carries a good prognosis, Dr. Michael Crawford said at a meeting sponsored by the California chapter of the American College of Cardiology.

Diagnosis of peripartum cardiomyopathy—or of other heart diseases during pregnancy—often is delayed because the symptoms of pregnancy can mimic the heart disease symptoms, said Dr. Crawford, professor of medicine at the University of California, San Francisco,

A majority of women with peripartum cardiomyopathy recover after delivery, but 10%–20% require heart transplantation and 1%–2% die, data suggest. The patient's ejection fraction 2 months after diagnosis appears to be the best prognostic factor, he said at the meeting, also sponsored by the university.

Treatment for cardiomyopathy differs for pregnant women compared with nonpregnant patients because some drugs shouldn't be used until after delivery.

ACE inhibitors and warfarin are teratogenic, and β-blockers can lead to fetal bradycardia.

“You get by with diuretics, digoxin, and hydralazine during pregnancy” for peripartum cardiomyopathy, Dr. Crawford said.

In a recent study at a large medical center, ejection fractions improved at least 15% in 62% of women with peripartum cardiomyopathy, remained unchanged in 25%, and declined in 13% (Am. Heart J. 2006;152:509–13).

Ejection fractions returned to normal in 45%. Ten percent of patients required transplantation. No patients died during an average 43-month follow-up. “That's encouraging,” he noted.

The initial echocardiogram, obtained between 1 month prepartum and 5 months post partum, did not predict which patients required transplantation, nor which had final ejection fractions below or above 50%. “Don't get discouraged with the first echo,” Dr. Crawford said. Echocardiograms 2 months later predicted outcomes in that study.

Patients with ejection fractions below 20% probably are headed for transplant. Those with ejection fractions between 20% and 50% should see some improvement but are unlikely to return to normal. If the 2-month ejection fraction is above 40%, the patient is likely to recover fully (defined as an ejection fraction greater than 50%), he said.

Shortness of breath and decreased exercise capacity, which are symptoms of cardiomyopathy, also are symptoms of a normal pregnancy. Fatigue, orthopnea, and dizziness or syncope, which might be symptoms of other heart disease, also are normal symptoms of pregnancy.

Electrocardiograms in normal pregnancies often detect sinus tachycardia, and may show nonspecific ST-T changes. As the pregnancy advances, the heart's axis shifts more to the left.

Physical findings in normal pregnancies may include jugular venous distension, an enlarged left ventricle apex, right ventricle heave, a palpable pulmonary artery pulse, third heart sounds, systolic ejection murmurs, venous hums, or a mammary souffle noise if you listen over the breast.

“It can be confusing,” Dr. Crawford said.

The most common peripartum cardiovascular problem is venous thromboembolism, which is the leading cause of death in pregnancy, he added.

Consider prophylactic medication in women with risk factors (thrombophilia, history of thrombosis, antiphospholipid syndrome, lupus erythematosus, sickle cell anemia, or any kind of heart disease that would lead to thrombus formation).

Coronary artery disease during pregnancy is more common than one might think, perhaps because more women are having children later in life, he added.

Maternal MI occurs in 6 out of 100,000 deliveries, three to four times more common than is expected in age-matched nonpregnant women.

SAN FRANCISCO — Consider not only the risks of antidepressant drugs but also the risks of not treating depression during pregnancy, Dr. Andrea J. Singer recommended.

Approximately 1 in 10 women become depressed at some point during pregnancy. In addition to nonpharmacologic therapies such as increased social support, cognitive-behavioral therapy, or counseling as first-line treatments, many depressed women need supplemental antidepressant medication, she said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

“How we treat depends on the severity of depression. There are clear data that a significantly depressed mother is at more risk than a mother on antidepressant medication,” Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington, said at the meeting.

Because the effectiveness of antidepressant medications generally is comparable between classes and within classes of drugs, the choice of pharmacotherapy—and which medication—rests on questions of safety and tolerability for both the mother and fetus, patient preference, cost, and the quantity and quality of data available on the drug.

If depression is not adequately treated, the woman will have a higher risk for suicide, poor maternal and fetal nutrition, adverse neonatal outcomes, continued depression into the postpartum period, and impaired mother-child bonding, said Dr. Singer.

Depression during pregnancy is associated with an increased likelihood of using drugs, alcohol, or nicotine and a decreased likelihood of getting early prenatal care.

Depressed pregnant women often don't report depression but more often complain of physical health problems, compared with nondepressed pregnant women, she added.

The incidence of premature births is higher in depressed than in nondepressed women. Compared with term deliveries, children born prematurely tend to perform less well in school, are less likely to graduate from high school, and have higher rates of neurosensory impairments, bipolar disorder, and subnormal height.

Antidepressants probably are the best-studied class of drugs used during pregnancy, though the amount of data from controlled clinical trials still is small, said Dr. Singer. She is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Two studies in the past decade encompassing a total of 1,089 women found no causal relationship between use of tricyclic and noncyclic antidepressants and adverse pregnancy outcomes, Dr. Singer said.

In general, no increase in teratogenic risk has been found with use of the SSRIs fluvoxamine or sertraline, which are the antidepressants most commonly prescribed for pregnant women.

One recent study suggests that paroxetine use during the first trimester might be associated with an increased risk of cardiovascular birth defects, particularly ventricular septal defects, she said.

In addition, there have been several reports of possible withdrawal symptoms in babies who were exposed to SSRIs during or at the end of the third trimester. The reports describe neonatal jitteriness, irritability, or respiratory difficulties.

Physicians may want to consider temporarily halting maternal SSRI therapy near the end of the third trimester in some patients who can tolerate an interruption in therapy and restarting the medication in the postpartum period, Dr. Singer suggested. Watch neonates born to women who took SSRIs late in pregnancy for potential withdrawal signs, she added.

The women at greatest risk for developing depression during pregnancy are those with a history of depression before pregnancy. “That's a red flag to follow the patient closely during pregnancy,” she said.

Other risk factors for depression during pregnancy include a history of premenstrual dysphoric disorder, younger maternal age, living alone or with limited social support, ambivalence about the pregnancy, conflict with her spouse or significant other, and having multiple other children.

SAN FRANCISCO — Consider not only the risks of antidepressant drugs but also the risks of not treating depression during pregnancy, Dr. Andrea J. Singer recommended.

Approximately 1 in 10 women become depressed at some point during pregnancy. In addition to nonpharmacologic therapies such as increased social support, cognitive-behavioral therapy, or counseling as first-line treatments, many depressed women need supplemental antidepressant medication, she said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

“How we treat depends on the severity of depression. There are clear data that a significantly depressed mother is at more risk than a mother on antidepressant medication,” Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington, said at the meeting.

Because the effectiveness of antidepressant medications generally is comparable between classes and within classes of drugs, the choice of pharmacotherapy—and which medication—rests on questions of safety and tolerability for both the mother and fetus, patient preference, cost, and the quantity and quality of data available on the drug.

If depression is not adequately treated, the woman will have a higher risk for suicide, poor maternal and fetal nutrition, adverse neonatal outcomes, continued depression into the postpartum period, and impaired mother-child bonding, said Dr. Singer.

Depression during pregnancy is associated with an increased likelihood of using drugs, alcohol, or nicotine and a decreased likelihood of getting early prenatal care.

Depressed pregnant women often don't report depression but more often complain of physical health problems, compared with nondepressed pregnant women, she added.

The incidence of premature births is higher in depressed than in nondepressed women. Compared with term deliveries, children born prematurely tend to perform less well in school, are less likely to graduate from high school, and have higher rates of neurosensory impairments, bipolar disorder, and subnormal height.

Antidepressants probably are the best-studied class of drugs used during pregnancy, though the amount of data from controlled clinical trials still is small, said Dr. Singer. She is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Two studies in the past decade encompassing a total of 1,089 women found no causal relationship between use of tricyclic and noncyclic antidepressants and adverse pregnancy outcomes, Dr. Singer said.

In general, no increase in teratogenic risk has been found with use of the SSRIs fluvoxamine or sertraline, which are the antidepressants most commonly prescribed for pregnant women.

One recent study suggests that paroxetine use during the first trimester might be associated with an increased risk of cardiovascular birth defects, particularly ventricular septal defects, she said.

In addition, there have been several reports of possible withdrawal symptoms in babies who were exposed to SSRIs during or at the end of the third trimester. The reports describe neonatal jitteriness, irritability, or respiratory difficulties.

Physicians may want to consider temporarily halting maternal SSRI therapy near the end of the third trimester in some patients who can tolerate an interruption in therapy and restarting the medication in the postpartum period, Dr. Singer suggested. Watch neonates born to women who took SSRIs late in pregnancy for potential withdrawal signs, she added.

The women at greatest risk for developing depression during pregnancy are those with a history of depression before pregnancy. “That's a red flag to follow the patient closely during pregnancy,” she said.

Other risk factors for depression during pregnancy include a history of premenstrual dysphoric disorder, younger maternal age, living alone or with limited social support, ambivalence about the pregnancy, conflict with her spouse or significant other, and having multiple other children.

SAN FRANCISCO — Consider not only the risks of antidepressant drugs but also the risks of not treating depression during pregnancy, Dr. Andrea J. Singer recommended.

Approximately 1 in 10 women become depressed at some point during pregnancy. In addition to nonpharmacologic therapies such as increased social support, cognitive-behavioral therapy, or counseling as first-line treatments, many depressed women need supplemental antidepressant medication, she said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

“How we treat depends on the severity of depression. There are clear data that a significantly depressed mother is at more risk than a mother on antidepressant medication,” Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington, said at the meeting.

Because the effectiveness of antidepressant medications generally is comparable between classes and within classes of drugs, the choice of pharmacotherapy—and which medication—rests on questions of safety and tolerability for both the mother and fetus, patient preference, cost, and the quantity and quality of data available on the drug.

If depression is not adequately treated, the woman will have a higher risk for suicide, poor maternal and fetal nutrition, adverse neonatal outcomes, continued depression into the postpartum period, and impaired mother-child bonding, said Dr. Singer.

Depression during pregnancy is associated with an increased likelihood of using drugs, alcohol, or nicotine and a decreased likelihood of getting early prenatal care.

Depressed pregnant women often don't report depression but more often complain of physical health problems, compared with nondepressed pregnant women, she added.

The incidence of premature births is higher in depressed than in nondepressed women. Compared with term deliveries, children born prematurely tend to perform less well in school, are less likely to graduate from high school, and have higher rates of neurosensory impairments, bipolar disorder, and subnormal height.

Antidepressants probably are the best-studied class of drugs used during pregnancy, though the amount of data from controlled clinical trials still is small, said Dr. Singer. She is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Two studies in the past decade encompassing a total of 1,089 women found no causal relationship between use of tricyclic and noncyclic antidepressants and adverse pregnancy outcomes, Dr. Singer said.

In general, no increase in teratogenic risk has been found with use of the SSRIs fluvoxamine or sertraline, which are the antidepressants most commonly prescribed for pregnant women.

One recent study suggests that paroxetine use during the first trimester might be associated with an increased risk of cardiovascular birth defects, particularly ventricular septal defects, she said.

In addition, there have been several reports of possible withdrawal symptoms in babies who were exposed to SSRIs during or at the end of the third trimester. The reports describe neonatal jitteriness, irritability, or respiratory difficulties.

Physicians may want to consider temporarily halting maternal SSRI therapy near the end of the third trimester in some patients who can tolerate an interruption in therapy and restarting the medication in the postpartum period, Dr. Singer suggested. Watch neonates born to women who took SSRIs late in pregnancy for potential withdrawal signs, she added.

The women at greatest risk for developing depression during pregnancy are those with a history of depression before pregnancy. “That's a red flag to follow the patient closely during pregnancy,” she said.

Other risk factors for depression during pregnancy include a history of premenstrual dysphoric disorder, younger maternal age, living alone or with limited social support, ambivalence about the pregnancy, conflict with her spouse or significant other, and having multiple other children.

SAN FRANCISCO — Fecal incontinence after childbirth is a common, sometimes severe, and underrecognized problem that could be reduced with greater efforts to prevent anal sphincter ruptures, Dr. Michael P. Aronson told attendees at a conference sponsored by the Society of Gynecologic Surgeons.

Attempts to fix the damage after delivery do not work well, according to Dr. Aronson, director of women's health services at the University of Massachusetts, Worcester. Even when surgical repairs of lacerations are deemed successful, many women remain incontinent and some develop new defecatory dysfunction.

“It really matters what happens at the delivery,” he said. “If you can prevent that sphincter rupture, you can prevent a whole field of woes down the line for that patient.”

Dr. Aronson, a professor of obstetrics and gynecology, held up his own institution, a major tertiary care center, as an example of how shining a spotlight on the issue can reduce third- and fourth-degree anal sphincter lacerations.

Officials recognized that they had a problem in the summer of 2003, when the laceration rate was 8%. A year later, the rate was 6%, a reduction Dr. Aronson attributed mostly to better definitions and entering of data. Meanwhile, he noted, an education program also focused attention on the problem.

As of the spring of 2006, he reported, the rate had declined to 2.8%—better than the national standard of 3%. Defining and measuring was crucial, Dr. Aronson said, adding that “the improvement is sustainable.”

He estimated that nationwide, sphincter disruption occurs during 0.5% of vaginal births, a rate that he translated into 150,000 cases each year. If 25% of these new mothers has incontinence as a sequela, he calculated, 37,500 women are affected each year—or one new case every 14 minutes. Moreover, when incontinence occurs after sphincter rupture, he warned, symptoms increase over time.

(Anal sphincter lacerations are not the only cause of fecal incontinence, Dr. Aronson noted. Stretching the pudendal nerve during delivery can also be a contributing factor. In one study, about a third of women without a tear suffered from incontinence 5 years after giving birth.)

Dr. Aronson advocated avoiding midline episiotomy as a way of preventing anal sphincter ruptures. Numerous studies have shown it to be associated with incontinence and sphincter ruptures in up to one-fourth of patients, he said. “Midline episiotomy should be avoided if at all possible.”

Operative delivery is also significantly associated with sphincter ruptures, Dr. Aronson added. He quoted odds ratios ranging from 6.7 with forceps delivery to 2.3 with vacuum delivery.

Moreover, a history of sphincter rupture should be a serious consideration when deciding how to deliver a woman's subsequent children, according to Dr. Aronson. He warned that women who have had a third- or fourth-degree laceration are at higher risk of a new laceration in subsequent births.

Although one large cohort study of 19,000 women reported no increase with a prior history of laceration, he said, other cohort studies and a 24-year review of the Swedish Birth Registry supported increased risk. The relative risk in these studies ranged from 2.5 to 6.5.

Standard surgical repairs of anal sphincter lacerations do not heal well, Dr. Aronson continued. Ultrasound examinations have shown defect rates ranging from 79% after 3 months to 90% after the 1st week in cases that appeared to be on the mend.

“This is a tough repair,” he said. “We all know as surgeons that tension is the enemy of healing. There's tension on this right off the bat.”

When all else fails, turning the patient over to a urogynecologist or colorectal surgeon is not likely to fix the problem, Dr. Aronson added. He cited one study of successful overlapping sphincteroplasty in which 51 patients needed no further surgeries. Yet not one patient was totally continent and 14 developed new defecatory dysfunction over the next 5 years.

“Fecal incontinence is a terrible problem, much more prevalent than you know,” he said. “Our tools to fix it are not good. It is better to prevent it.”

SAN FRANCISCO — Fecal incontinence after childbirth is a common, sometimes severe, and underrecognized problem that could be reduced with greater efforts to prevent anal sphincter ruptures, Dr. Michael P. Aronson told attendees at a conference sponsored by the Society of Gynecologic Surgeons.

Attempts to fix the damage after delivery do not work well, according to Dr. Aronson, director of women's health services at the University of Massachusetts, Worcester. Even when surgical repairs of lacerations are deemed successful, many women remain incontinent and some develop new defecatory dysfunction.

“It really matters what happens at the delivery,” he said. “If you can prevent that sphincter rupture, you can prevent a whole field of woes down the line for that patient.”

Dr. Aronson, a professor of obstetrics and gynecology, held up his own institution, a major tertiary care center, as an example of how shining a spotlight on the issue can reduce third- and fourth-degree anal sphincter lacerations.

Officials recognized that they had a problem in the summer of 2003, when the laceration rate was 8%. A year later, the rate was 6%, a reduction Dr. Aronson attributed mostly to better definitions and entering of data. Meanwhile, he noted, an education program also focused attention on the problem.

As of the spring of 2006, he reported, the rate had declined to 2.8%—better than the national standard of 3%. Defining and measuring was crucial, Dr. Aronson said, adding that “the improvement is sustainable.”

He estimated that nationwide, sphincter disruption occurs during 0.5% of vaginal births, a rate that he translated into 150,000 cases each year. If 25% of these new mothers has incontinence as a sequela, he calculated, 37,500 women are affected each year—or one new case every 14 minutes. Moreover, when incontinence occurs after sphincter rupture, he warned, symptoms increase over time.

(Anal sphincter lacerations are not the only cause of fecal incontinence, Dr. Aronson noted. Stretching the pudendal nerve during delivery can also be a contributing factor. In one study, about a third of women without a tear suffered from incontinence 5 years after giving birth.)

Dr. Aronson advocated avoiding midline episiotomy as a way of preventing anal sphincter ruptures. Numerous studies have shown it to be associated with incontinence and sphincter ruptures in up to one-fourth of patients, he said. “Midline episiotomy should be avoided if at all possible.”

Operative delivery is also significantly associated with sphincter ruptures, Dr. Aronson added. He quoted odds ratios ranging from 6.7 with forceps delivery to 2.3 with vacuum delivery.

Moreover, a history of sphincter rupture should be a serious consideration when deciding how to deliver a woman's subsequent children, according to Dr. Aronson. He warned that women who have had a third- or fourth-degree laceration are at higher risk of a new laceration in subsequent births.

Although one large cohort study of 19,000 women reported no increase with a prior history of laceration, he said, other cohort studies and a 24-year review of the Swedish Birth Registry supported increased risk. The relative risk in these studies ranged from 2.5 to 6.5.

Standard surgical repairs of anal sphincter lacerations do not heal well, Dr. Aronson continued. Ultrasound examinations have shown defect rates ranging from 79% after 3 months to 90% after the 1st week in cases that appeared to be on the mend.

“This is a tough repair,” he said. “We all know as surgeons that tension is the enemy of healing. There's tension on this right off the bat.”

When all else fails, turning the patient over to a urogynecologist or colorectal surgeon is not likely to fix the problem, Dr. Aronson added. He cited one study of successful overlapping sphincteroplasty in which 51 patients needed no further surgeries. Yet not one patient was totally continent and 14 developed new defecatory dysfunction over the next 5 years.

“Fecal incontinence is a terrible problem, much more prevalent than you know,” he said. “Our tools to fix it are not good. It is better to prevent it.”

SAN FRANCISCO — Fecal incontinence after childbirth is a common, sometimes severe, and underrecognized problem that could be reduced with greater efforts to prevent anal sphincter ruptures, Dr. Michael P. Aronson told attendees at a conference sponsored by the Society of Gynecologic Surgeons.

Attempts to fix the damage after delivery do not work well, according to Dr. Aronson, director of women's health services at the University of Massachusetts, Worcester. Even when surgical repairs of lacerations are deemed successful, many women remain incontinent and some develop new defecatory dysfunction.

“It really matters what happens at the delivery,” he said. “If you can prevent that sphincter rupture, you can prevent a whole field of woes down the line for that patient.”

Dr. Aronson, a professor of obstetrics and gynecology, held up his own institution, a major tertiary care center, as an example of how shining a spotlight on the issue can reduce third- and fourth-degree anal sphincter lacerations.

Officials recognized that they had a problem in the summer of 2003, when the laceration rate was 8%. A year later, the rate was 6%, a reduction Dr. Aronson attributed mostly to better definitions and entering of data. Meanwhile, he noted, an education program also focused attention on the problem.

As of the spring of 2006, he reported, the rate had declined to 2.8%—better than the national standard of 3%. Defining and measuring was crucial, Dr. Aronson said, adding that “the improvement is sustainable.”

He estimated that nationwide, sphincter disruption occurs during 0.5% of vaginal births, a rate that he translated into 150,000 cases each year. If 25% of these new mothers has incontinence as a sequela, he calculated, 37,500 women are affected each year—or one new case every 14 minutes. Moreover, when incontinence occurs after sphincter rupture, he warned, symptoms increase over time.

(Anal sphincter lacerations are not the only cause of fecal incontinence, Dr. Aronson noted. Stretching the pudendal nerve during delivery can also be a contributing factor. In one study, about a third of women without a tear suffered from incontinence 5 years after giving birth.)

Dr. Aronson advocated avoiding midline episiotomy as a way of preventing anal sphincter ruptures. Numerous studies have shown it to be associated with incontinence and sphincter ruptures in up to one-fourth of patients, he said. “Midline episiotomy should be avoided if at all possible.”

Operative delivery is also significantly associated with sphincter ruptures, Dr. Aronson added. He quoted odds ratios ranging from 6.7 with forceps delivery to 2.3 with vacuum delivery.

Moreover, a history of sphincter rupture should be a serious consideration when deciding how to deliver a woman's subsequent children, according to Dr. Aronson. He warned that women who have had a third- or fourth-degree laceration are at higher risk of a new laceration in subsequent births.

Although one large cohort study of 19,000 women reported no increase with a prior history of laceration, he said, other cohort studies and a 24-year review of the Swedish Birth Registry supported increased risk. The relative risk in these studies ranged from 2.5 to 6.5.

Standard surgical repairs of anal sphincter lacerations do not heal well, Dr. Aronson continued. Ultrasound examinations have shown defect rates ranging from 79% after 3 months to 90% after the 1st week in cases that appeared to be on the mend.

“This is a tough repair,” he said. “We all know as surgeons that tension is the enemy of healing. There's tension on this right off the bat.”

When all else fails, turning the patient over to a urogynecologist or colorectal surgeon is not likely to fix the problem, Dr. Aronson added. He cited one study of successful overlapping sphincteroplasty in which 51 patients needed no further surgeries. Yet not one patient was totally continent and 14 developed new defecatory dysfunction over the next 5 years.

“Fecal incontinence is a terrible problem, much more prevalent than you know,” he said. “Our tools to fix it are not good. It is better to prevent it.”

RIVIERA MAYA, MEXICO — Prenatal exposure to intrauterine infection is emerging as a possible cause of many cases of cerebral palsy previously classified as idiopathic, Dr. Errol Norwitz said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“Recent data suggest that it is the fetus's inflammatory response which causes problems both in terms of preterm labor and neuronal injury,” said Dr. Norwitz, director of maternal-fetal medicine at Yale-New Haven Hospital, Conn. “Even in the absence of a positive amniotic fluid culture in women with chorioamnionitis, we see proinflammatory cytokines, prostaglandins, and other markers of infection.”

Animal studies have demonstrated direct brain injury from such infections. Fetal rabbits exposed to intrauterine Escherichia coli infections develop white matter injuries, while fetal rhesus monkeys demonstrated brain injuries associated with chronic group B streptococcus intrauterine infections.

In human fetuses, epidemiologic evidence points to a similar association, with infection and brain injury leading to cerebral palsy, Dr. Norwitz said. “In normal- and low-birth-weight infants, we see an association between periventricular leukomalacia and both group B strep sepsis and histologic chorioamnionitis.”

The premature labor associated with intrauterine infection may be triggered by the fetus's inflammatory response, so as to escape the contaminated intrauterine environment. “What we are suggesting here is that the infectious agent gets into the baby by the ascending route or, rarely, across the placenta, and the baby's inflammatory response leads independently to preterm birth,” Dr. Norwitz said. “It's a protective mechanism, because if the baby didn't do this, it would probably die in utero due to overwhelming sepsis.”

The exact mechanism of neuronal damage remains unknown, he said. “There appears to be a fetal vasculitis with activation of leukocytes. This causes a huge surge in proinflammatory cytokines, with an imbalance between the proinflammatory and the anti-inflammatory cytokines. Some of the activated cells appear to cross the blood-brain barrier and cause damage to the brain.” In fact, he said, some studies have shown that elevated proinflammatory cytokines are common in the brains of patients with cerebral palsy and periventricular leukomalacia. A 1997 study found tumor necrosis factor-α, interleukin-1 β, or interleukin-6 in 88% of cases with the lesions, but only 18% of cases without them (Am. J. Obstet. Gynecol. 1997;177:406–11). Another study of neonatal brains with and without the lesions concluded that an immune-mediated inflammatory process might play a role in the development of such lesions, with TNF-α perhaps playing the major role (Neurology 2001;56:1278–84).

Interestingly, higher levels have also been noted in the serum and amniotic fluid of neonates who later developed cerebral palsy (Ann. Neuro. 1999;44:665–75; Am. J. Obstet. Gynecol. 1997;117:19–26).

Given these findings, questions arise about a possible protective effect of immediate cesarean delivery in mothers with intrauterine infection, Dr. Norwitz said. “Right now, intrauterine infection is an absolute indication for delivery, but in some cases, it can take 18–36 hours to get these babies delivered. Are these kids, sitting in this infected environment for all that time, at increased risk? Once we make the diagnosis, should we be getting that baby out immediately by cesarean? Currently there is no indication for this, but I wouldn't be surprised if this changes in 5–10 years, as our understanding of this area develops.”

Estimates are that only 10% of cerebral palsy cases are due to an identifiable intrapartum event, he said. But this statistic and the evolving understanding of the possible role of infection don't ease the difficulty of defending such cases in court, cautioned John Scully, a defendant's lawyer from Dallas. The conference was sponsored by Boston University.

RIVIERA MAYA, MEXICO — Prenatal exposure to intrauterine infection is emerging as a possible cause of many cases of cerebral palsy previously classified as idiopathic, Dr. Errol Norwitz said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“Recent data suggest that it is the fetus's inflammatory response which causes problems both in terms of preterm labor and neuronal injury,” said Dr. Norwitz, director of maternal-fetal medicine at Yale-New Haven Hospital, Conn. “Even in the absence of a positive amniotic fluid culture in women with chorioamnionitis, we see proinflammatory cytokines, prostaglandins, and other markers of infection.”

Animal studies have demonstrated direct brain injury from such infections. Fetal rabbits exposed to intrauterine Escherichia coli infections develop white matter injuries, while fetal rhesus monkeys demonstrated brain injuries associated with chronic group B streptococcus intrauterine infections.

In human fetuses, epidemiologic evidence points to a similar association, with infection and brain injury leading to cerebral palsy, Dr. Norwitz said. “In normal- and low-birth-weight infants, we see an association between periventricular leukomalacia and both group B strep sepsis and histologic chorioamnionitis.”

The premature labor associated with intrauterine infection may be triggered by the fetus's inflammatory response, so as to escape the contaminated intrauterine environment. “What we are suggesting here is that the infectious agent gets into the baby by the ascending route or, rarely, across the placenta, and the baby's inflammatory response leads independently to preterm birth,” Dr. Norwitz said. “It's a protective mechanism, because if the baby didn't do this, it would probably die in utero due to overwhelming sepsis.”

The exact mechanism of neuronal damage remains unknown, he said. “There appears to be a fetal vasculitis with activation of leukocytes. This causes a huge surge in proinflammatory cytokines, with an imbalance between the proinflammatory and the anti-inflammatory cytokines. Some of the activated cells appear to cross the blood-brain barrier and cause damage to the brain.” In fact, he said, some studies have shown that elevated proinflammatory cytokines are common in the brains of patients with cerebral palsy and periventricular leukomalacia. A 1997 study found tumor necrosis factor-α, interleukin-1 β, or interleukin-6 in 88% of cases with the lesions, but only 18% of cases without them (Am. J. Obstet. Gynecol. 1997;177:406–11). Another study of neonatal brains with and without the lesions concluded that an immune-mediated inflammatory process might play a role in the development of such lesions, with TNF-α perhaps playing the major role (Neurology 2001;56:1278–84).

Interestingly, higher levels have also been noted in the serum and amniotic fluid of neonates who later developed cerebral palsy (Ann. Neuro. 1999;44:665–75; Am. J. Obstet. Gynecol. 1997;117:19–26).

Given these findings, questions arise about a possible protective effect of immediate cesarean delivery in mothers with intrauterine infection, Dr. Norwitz said. “Right now, intrauterine infection is an absolute indication for delivery, but in some cases, it can take 18–36 hours to get these babies delivered. Are these kids, sitting in this infected environment for all that time, at increased risk? Once we make the diagnosis, should we be getting that baby out immediately by cesarean? Currently there is no indication for this, but I wouldn't be surprised if this changes in 5–10 years, as our understanding of this area develops.”

Estimates are that only 10% of cerebral palsy cases are due to an identifiable intrapartum event, he said. But this statistic and the evolving understanding of the possible role of infection don't ease the difficulty of defending such cases in court, cautioned John Scully, a defendant's lawyer from Dallas. The conference was sponsored by Boston University.

RIVIERA MAYA, MEXICO — Prenatal exposure to intrauterine infection is emerging as a possible cause of many cases of cerebral palsy previously classified as idiopathic, Dr. Errol Norwitz said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“Recent data suggest that it is the fetus's inflammatory response which causes problems both in terms of preterm labor and neuronal injury,” said Dr. Norwitz, director of maternal-fetal medicine at Yale-New Haven Hospital, Conn. “Even in the absence of a positive amniotic fluid culture in women with chorioamnionitis, we see proinflammatory cytokines, prostaglandins, and other markers of infection.”

Animal studies have demonstrated direct brain injury from such infections. Fetal rabbits exposed to intrauterine Escherichia coli infections develop white matter injuries, while fetal rhesus monkeys demonstrated brain injuries associated with chronic group B streptococcus intrauterine infections.

In human fetuses, epidemiologic evidence points to a similar association, with infection and brain injury leading to cerebral palsy, Dr. Norwitz said. “In normal- and low-birth-weight infants, we see an association between periventricular leukomalacia and both group B strep sepsis and histologic chorioamnionitis.”

The premature labor associated with intrauterine infection may be triggered by the fetus's inflammatory response, so as to escape the contaminated intrauterine environment. “What we are suggesting here is that the infectious agent gets into the baby by the ascending route or, rarely, across the placenta, and the baby's inflammatory response leads independently to preterm birth,” Dr. Norwitz said. “It's a protective mechanism, because if the baby didn't do this, it would probably die in utero due to overwhelming sepsis.”

The exact mechanism of neuronal damage remains unknown, he said. “There appears to be a fetal vasculitis with activation of leukocytes. This causes a huge surge in proinflammatory cytokines, with an imbalance between the proinflammatory and the anti-inflammatory cytokines. Some of the activated cells appear to cross the blood-brain barrier and cause damage to the brain.” In fact, he said, some studies have shown that elevated proinflammatory cytokines are common in the brains of patients with cerebral palsy and periventricular leukomalacia. A 1997 study found tumor necrosis factor-α, interleukin-1 β, or interleukin-6 in 88% of cases with the lesions, but only 18% of cases without them (Am. J. Obstet. Gynecol. 1997;177:406–11). Another study of neonatal brains with and without the lesions concluded that an immune-mediated inflammatory process might play a role in the development of such lesions, with TNF-α perhaps playing the major role (Neurology 2001;56:1278–84).

Interestingly, higher levels have also been noted in the serum and amniotic fluid of neonates who later developed cerebral palsy (Ann. Neuro. 1999;44:665–75; Am. J. Obstet. Gynecol. 1997;117:19–26).

Given these findings, questions arise about a possible protective effect of immediate cesarean delivery in mothers with intrauterine infection, Dr. Norwitz said. “Right now, intrauterine infection is an absolute indication for delivery, but in some cases, it can take 18–36 hours to get these babies delivered. Are these kids, sitting in this infected environment for all that time, at increased risk? Once we make the diagnosis, should we be getting that baby out immediately by cesarean? Currently there is no indication for this, but I wouldn't be surprised if this changes in 5–10 years, as our understanding of this area develops.”

Estimates are that only 10% of cerebral palsy cases are due to an identifiable intrapartum event, he said. But this statistic and the evolving understanding of the possible role of infection don't ease the difficulty of defending such cases in court, cautioned John Scully, a defendant's lawyer from Dallas. The conference was sponsored by Boston University.

ROME — Under many circumstances, it's just not possible to anticipate postpartum hemorrhage. However, the invasive placenta is a notable exception, Dr. Anne C. Roberts said at the annual meeting of the Cardiovascular and Radiological Interventional Society of Europe.

The most important message regarding patients with invasive placenta is to plan ahead for the possibility of severe postpartum hemorrhage, said Dr. Roberts, executive vice-chair of radiology at the University of California, San Diego.

Invasive placenta is the leading cause of emergency hysterectomy in the United States. Placenta accreta and increta are typically readily managed by the obstetrician. It's percreta that causes the most serious bleeding problems, even though it accounts for only about 5% of all cases of invasive placenta. Indeed, percreta carries a 7% maternal mortality.

“[Percreta] acts like a tumor,” Dr. Roberts observed. “It's a serious problem because these patients lose an enormous amount of blood, particularly if they're not diagnosed predelivery.”

“You want to treat these patients [as if] they are pelvic bleeders from trauma. We know that if you get to patients with pelvic bleeding from trauma early you don't have them going into DIC [disseminated intravascular coagulation] or needing a lot of blood transfusions. These [patients] are [similar to] trauma patients, and we need to get them in and treat them right away,” Dr. Roberts said.

Percreta appears to be on the increase and parallels rising cesarean section rates. The reported incidence in the 1950s was 1 in 30,000 deliveries. By the 1990s, that figure had risen to as high as 1 in 2,500 deliveries. Although C-section is the No. 1 risk factor, D&C, myomectomy, or any other form of uterine surgery also increases the risk.

Virtually all women with invasive placenta have a placenta previa on ultrasound. If that placenta doesn't move out of the way as the patient is followed through pregnancy—and particularly if she has a history of prior C-section—MRI can be used to determine whether she has percreta.

When asked by obstetric colleagues to help manage a patient with percreta prior to delivery, Dr. Roberts' approach is to prophylactically place occlusive balloon catheters in the internal iliac arteries, leaving the balloons deflated and the guidewires in place.

Although she and her colleagues formerly arranged to have blood donated ahead of time, this measure has become unnecessary as surgeons have gained greater expertise in these cases. However, large-bore catheters are put in place beforehand for rapid infusion of fluids should this be necessary during delivery.

“We don't inflate the balloons unless the obstetricians say, 'We're getting into trouble with bleeding,'”Dr. Roberts explained. “We started out inflating them as soon as the baby was delivered but found patients very quickly develop collateral flow causing bleeding, probably from the posterior division as well as from branches of the profunda [femoris] arteries.”

The balloons are deflated once the invasive placenta is removed and the bleeding sites are repaired.

The value of prophylactic balloon placement was highlighted in Dr. Roberts' retrospective nonrandomized study involving 40 patients with invasive placenta. The 17 patients in the occlusive balloon group had more serious disease as evidenced by the fact that 16 had percreta, including 13 with complex percreta, compared with just 5 and 1, respectively, of 23 controls. Yet the balloon group required 28% less intravenous fluids and had less estimated blood loss.

Moreover, only 3 women in the balloon group had surgical complications such as ureteral injury or bladder puncture, compared with 13 controls; this difference probably resulted from surgeons in the balloon arm feeling less rushed, she said.

Postpartum hemorrhage is sometimes treated with internal iliac artery ligation, a procedure having less than a 50% success rate.

If that fails, emergency hysterectomy is the next step. But there is a conservative option available for women interested in maintaining fertility: transcatheter embolization.

Arterial embolization is highly effective therapy for postpartum bleeding, said fellow presenter Dr. Hicham T. Abada of the University of Iowa, Iowa City.

In his experience treating 160 patients, the success rate in stopping bleeding was 94.4%. And in the few patients where rebleeding occurred, it did so an average of 6 hours post embolization. By that point, the women were well stabilized and in far better shape to undergo a second embolization procedure or hysterectomy, which six patients opted for instead of repeat embolization.

There were no deaths in this large patient series. Fifty percent of the women developed DIC, 30% developed shock, and 20% required acute massive transfusion. The mean drop in hemoglobin was 4.5 g/dL. Uterine atony was the cause of postpartum hemorrhage in 75% of cases. Thirty percent of women had a C-section.

Six subsequent pregnancies occurred in this population.

The literature quotes an 8% complication rate for arterial embolization in the setting of postpartum hemorrhage, with the bulk of adverse events consisting of contrast media reactions or relatively minor puncture site problems. Bladder or uterine necrosis has been reported infrequently; in Dr. Abada's series there were no such cases.

The arrows in each image (taken before arterial embolization) point to areas of extravasation of contrast media, which indicate postpartum bleeding. Photos courtesy Dr. Hicham T. Abada

ROME — Under many circumstances, it's just not possible to anticipate postpartum hemorrhage. However, the invasive placenta is a notable exception, Dr. Anne C. Roberts said at the annual meeting of the Cardiovascular and Radiological Interventional Society of Europe.

The most important message regarding patients with invasive placenta is to plan ahead for the possibility of severe postpartum hemorrhage, said Dr. Roberts, executive vice-chair of radiology at the University of California, San Diego.

Invasive placenta is the leading cause of emergency hysterectomy in the United States. Placenta accreta and increta are typically readily managed by the obstetrician. It's percreta that causes the most serious bleeding problems, even though it accounts for only about 5% of all cases of invasive placenta. Indeed, percreta carries a 7% maternal mortality.

“[Percreta] acts like a tumor,” Dr. Roberts observed. “It's a serious problem because these patients lose an enormous amount of blood, particularly if they're not diagnosed predelivery.”

“You want to treat these patients [as if] they are pelvic bleeders from trauma. We know that if you get to patients with pelvic bleeding from trauma early you don't have them going into DIC [disseminated intravascular coagulation] or needing a lot of blood transfusions. These [patients] are [similar to] trauma patients, and we need to get them in and treat them right away,” Dr. Roberts said.

Percreta appears to be on the increase and parallels rising cesarean section rates. The reported incidence in the 1950s was 1 in 30,000 deliveries. By the 1990s, that figure had risen to as high as 1 in 2,500 deliveries. Although C-section is the No. 1 risk factor, D&C, myomectomy, or any other form of uterine surgery also increases the risk.

Virtually all women with invasive placenta have a placenta previa on ultrasound. If that placenta doesn't move out of the way as the patient is followed through pregnancy—and particularly if she has a history of prior C-section—MRI can be used to determine whether she has percreta.

When asked by obstetric colleagues to help manage a patient with percreta prior to delivery, Dr. Roberts' approach is to prophylactically place occlusive balloon catheters in the internal iliac arteries, leaving the balloons deflated and the guidewires in place.

Although she and her colleagues formerly arranged to have blood donated ahead of time, this measure has become unnecessary as surgeons have gained greater expertise in these cases. However, large-bore catheters are put in place beforehand for rapid infusion of fluids should this be necessary during delivery.

“We don't inflate the balloons unless the obstetricians say, 'We're getting into trouble with bleeding,'”Dr. Roberts explained. “We started out inflating them as soon as the baby was delivered but found patients very quickly develop collateral flow causing bleeding, probably from the posterior division as well as from branches of the profunda [femoris] arteries.”

The balloons are deflated once the invasive placenta is removed and the bleeding sites are repaired.

The value of prophylactic balloon placement was highlighted in Dr. Roberts' retrospective nonrandomized study involving 40 patients with invasive placenta. The 17 patients in the occlusive balloon group had more serious disease as evidenced by the fact that 16 had percreta, including 13 with complex percreta, compared with just 5 and 1, respectively, of 23 controls. Yet the balloon group required 28% less intravenous fluids and had less estimated blood loss.

Moreover, only 3 women in the balloon group had surgical complications such as ureteral injury or bladder puncture, compared with 13 controls; this difference probably resulted from surgeons in the balloon arm feeling less rushed, she said.

Postpartum hemorrhage is sometimes treated with internal iliac artery ligation, a procedure having less than a 50% success rate.

If that fails, emergency hysterectomy is the next step. But there is a conservative option available for women interested in maintaining fertility: transcatheter embolization.

Arterial embolization is highly effective therapy for postpartum bleeding, said fellow presenter Dr. Hicham T. Abada of the University of Iowa, Iowa City.

In his experience treating 160 patients, the success rate in stopping bleeding was 94.4%. And in the few patients where rebleeding occurred, it did so an average of 6 hours post embolization. By that point, the women were well stabilized and in far better shape to undergo a second embolization procedure or hysterectomy, which six patients opted for instead of repeat embolization.

There were no deaths in this large patient series. Fifty percent of the women developed DIC, 30% developed shock, and 20% required acute massive transfusion. The mean drop in hemoglobin was 4.5 g/dL. Uterine atony was the cause of postpartum hemorrhage in 75% of cases. Thirty percent of women had a C-section.

Six subsequent pregnancies occurred in this population.

The literature quotes an 8% complication rate for arterial embolization in the setting of postpartum hemorrhage, with the bulk of adverse events consisting of contrast media reactions or relatively minor puncture site problems. Bladder or uterine necrosis has been reported infrequently; in Dr. Abada's series there were no such cases.

The arrows in each image (taken before arterial embolization) point to areas of extravasation of contrast media, which indicate postpartum bleeding. Photos courtesy Dr. Hicham T. Abada

ROME — Under many circumstances, it's just not possible to anticipate postpartum hemorrhage. However, the invasive placenta is a notable exception, Dr. Anne C. Roberts said at the annual meeting of the Cardiovascular and Radiological Interventional Society of Europe.

The most important message regarding patients with invasive placenta is to plan ahead for the possibility of severe postpartum hemorrhage, said Dr. Roberts, executive vice-chair of radiology at the University of California, San Diego.

Invasive placenta is the leading cause of emergency hysterectomy in the United States. Placenta accreta and increta are typically readily managed by the obstetrician. It's percreta that causes the most serious bleeding problems, even though it accounts for only about 5% of all cases of invasive placenta. Indeed, percreta carries a 7% maternal mortality.

“[Percreta] acts like a tumor,” Dr. Roberts observed. “It's a serious problem because these patients lose an enormous amount of blood, particularly if they're not diagnosed predelivery.”

“You want to treat these patients [as if] they are pelvic bleeders from trauma. We know that if you get to patients with pelvic bleeding from trauma early you don't have them going into DIC [disseminated intravascular coagulation] or needing a lot of blood transfusions. These [patients] are [similar to] trauma patients, and we need to get them in and treat them right away,” Dr. Roberts said.

Percreta appears to be on the increase and parallels rising cesarean section rates. The reported incidence in the 1950s was 1 in 30,000 deliveries. By the 1990s, that figure had risen to as high as 1 in 2,500 deliveries. Although C-section is the No. 1 risk factor, D&C, myomectomy, or any other form of uterine surgery also increases the risk.

Virtually all women with invasive placenta have a placenta previa on ultrasound. If that placenta doesn't move out of the way as the patient is followed through pregnancy—and particularly if she has a history of prior C-section—MRI can be used to determine whether she has percreta.

When asked by obstetric colleagues to help manage a patient with percreta prior to delivery, Dr. Roberts' approach is to prophylactically place occlusive balloon catheters in the internal iliac arteries, leaving the balloons deflated and the guidewires in place.

Although she and her colleagues formerly arranged to have blood donated ahead of time, this measure has become unnecessary as surgeons have gained greater expertise in these cases. However, large-bore catheters are put in place beforehand for rapid infusion of fluids should this be necessary during delivery.

“We don't inflate the balloons unless the obstetricians say, 'We're getting into trouble with bleeding,'”Dr. Roberts explained. “We started out inflating them as soon as the baby was delivered but found patients very quickly develop collateral flow causing bleeding, probably from the posterior division as well as from branches of the profunda [femoris] arteries.”

The balloons are deflated once the invasive placenta is removed and the bleeding sites are repaired.

The value of prophylactic balloon placement was highlighted in Dr. Roberts' retrospective nonrandomized study involving 40 patients with invasive placenta. The 17 patients in the occlusive balloon group had more serious disease as evidenced by the fact that 16 had percreta, including 13 with complex percreta, compared with just 5 and 1, respectively, of 23 controls. Yet the balloon group required 28% less intravenous fluids and had less estimated blood loss.

Moreover, only 3 women in the balloon group had surgical complications such as ureteral injury or bladder puncture, compared with 13 controls; this difference probably resulted from surgeons in the balloon arm feeling less rushed, she said.

Postpartum hemorrhage is sometimes treated with internal iliac artery ligation, a procedure having less than a 50% success rate.

If that fails, emergency hysterectomy is the next step. But there is a conservative option available for women interested in maintaining fertility: transcatheter embolization.

Arterial embolization is highly effective therapy for postpartum bleeding, said fellow presenter Dr. Hicham T. Abada of the University of Iowa, Iowa City.

In his experience treating 160 patients, the success rate in stopping bleeding was 94.4%. And in the few patients where rebleeding occurred, it did so an average of 6 hours post embolization. By that point, the women were well stabilized and in far better shape to undergo a second embolization procedure or hysterectomy, which six patients opted for instead of repeat embolization.

There were no deaths in this large patient series. Fifty percent of the women developed DIC, 30% developed shock, and 20% required acute massive transfusion. The mean drop in hemoglobin was 4.5 g/dL. Uterine atony was the cause of postpartum hemorrhage in 75% of cases. Thirty percent of women had a C-section.

Six subsequent pregnancies occurred in this population.

The literature quotes an 8% complication rate for arterial embolization in the setting of postpartum hemorrhage, with the bulk of adverse events consisting of contrast media reactions or relatively minor puncture site problems. Bladder or uterine necrosis has been reported infrequently; in Dr. Abada's series there were no such cases.

The arrows in each image (taken before arterial embolization) point to areas of extravasation of contrast media, which indicate postpartum bleeding. Photos courtesy Dr. Hicham T. Abada