OBG Management

CASE 34-year-old woman with lipid panel results from 1 year ago

A woman with no chronic medical conditions was seen by her gynecologist for a routine well-woman examination. She does not see another primary care provider. She is age 34 years and has a levonorgestrel intrauterine device that was placed after the birth of her second child 2 years prior. She does not take any other medications. She has never smoked and drinks a glass of wine with dinner a couple of times each week. She finds it challenging with her full-time job and her parental responsibilities with 2 young children to get regular exercise but otherwise is active. She does not have a family history of premature cardiovascular disease. Last year, during her prior well-woman examination, she had a fasting lipid panel: her low-density lipoprotein (LDL) was 102 mg/dL (reference range, ≤160 mg/dL), high-density lipoprotein (HDL) 52 mg/dL (reference range, ≥40 mg/dL), triglycerides 140 mg/dL (reference range, <160 mg/dL), and total cholesterol 182 mg/dL (reference range, <200 mg/dL).

During this visit, the patient’s vitals are normal (blood pressure 116/58) and her physical examination is unremarkable. Her physician orders routine labs to be checked, including a fasting lipid panel. She has to figure out when she will be able to get these labs drawn, as she needs to coordinate with her work and childcare schedules. A week later, she leaves work at 4:00 PM and picks up her young children (aged 2 and 4 years) from childcare, bringing them to the laboratory to have her blood drawn. Not only are her children cranky in the waiting room, but she is feeling tired as she hasn’t eaten all day because her physician told her she is supposed to be fasting. She has to pay for parking at the lot for the laboratory since it is connected to the medical center.

Was this lipid panel high value?

When and how often should we be checking lipid panels?

Do patients need to fast for these tests?
 

The potential benefits and costs of routine lipid panel screening

Hyperlipidemia is relatively prevalent, usually asymptomatic, and has been linked to cardiovascular outcomes. Thus, screening for lipid abnormalities is recommended to identify patients that would benefit from various interventions aimed at reducing cardiovascular disease risk, including lipid-lowering therapy.¹ High levels of LDL cholesterol and low levels of HDL cholesterol are important risk factors for coronary heart disease.

Lipid panels are widely available blood tests with modest monetary costs, generally ranging from about $10 to $100 in the outpatient setting. Of note, a 2014 study examining inpatient charges for this common laboratory test found that hospital charges in California ranged from about $10 to $10,000 for a lipid panel.² Despite the relatively low cost of each individual lipid panel, the aggregate costs to the health system of these frequently and widely performed tests are large. In fact, low-cost, high-volume health services, such as repeat cholesterol testing, account for the majority of unnecessary health spending in the United States, contributing nearly twice as much unnecessary cost as high-priced low-value services.³

To the patient, the cost is not only monetary. Some patients will need to take an additional hour or two off work as well as consider childcare, transportation, parking, and other mundane logistics to sit in a laboratory waiting room—a cost that may not be considered modest at all by the patient.^4,5

Therefore, like most services in health care, the answer to whether or not a lipid panel is high-value care is: it depends.⁵ In the correct circumstances, the test generally is regarded as high value due to well-documented potential benefits and low monetary costs. However, when performed unnecessarily—either in patient groups that are unlikely to benefit or at intervals that are too soon to add helpful information—then all that is left are the financial and psychosocial costs, which make this a low-value test in these scenarios. For this patient, this test contributed to inconvenience and mild hardships with essentially no benefit, thus would be considered low-value care.

Continue to: When should we perform lipid screening in low-risk women?

When should we perform lipid screening in low-risk women?

There are conflicting guidelines and opinions about at what age lipid screening should be routinely performed in adults. The United States Preventive Services Task Force (USPSTF) 2016 guidelines found “insufficient evidence that screening for dyslipidemia before age 40 years has an effect on either short- or longer-term cardiovascular outcomes.”⁶ Therefore, the USPSTF “recommends neither for nor against screening for dyslipidemia in this age group,” and instead encourages “clinicians to use their clinical judgment for [these] patients.”⁶

A common practice is to obtain a baseline lipid profile at the time of initiation of care with an adult primary care practitioner, if the patient was not previously screened, and to then determine subsequent testing based on these results and the patient’s risk factors for cardiovascular disease. For patients with normal lipid screening results and lower cardiovascular risk factors (no hypertension, diabetes mellitus, cigarette smoking, family history of premature coronary heart disease), experts suggest follow-up lipid screening be performed in men at age 35 and in women at age 45.⁷ Therefore, for this patient who had essentially a normal lipid panel a year prior, she should not have required repeat lipid testing until she is age 45.

As for how frequently subsequent lipid testing should be performed, the Centers for Disease Control and Prevention states, “most healthy adults should have their cholesterol checked every 4 to 6 years.”⁸ Those taking lipid-lowering medications or those with risk factors such as heart disease, diabetes, or concerning family history should have their cholesterol checked more frequently. If patients are near a threshold for treatment, some experts suggest repeating measurements every 3 years, but even in these settings, annual testing would be considered excessive.⁷

A standard lipid panel screen includes total cholesterol, LDL, HDL, and triglycerides. While a variety of assays have been developed that subfractionate lipoprotein particles based on size, density, or charge, these tests do not add value for low-risk patient screening and should only be used on an individualized basis for selected intermediate to high-risk patients. The American Society for Clinical Pathology released a Choosing Wisely recommendation that advises, “Do not routinely order expanded lipid panels (particle sizing, nuclear magnetic resonance) as screening tests for cardiovascular disease.”⁹

Do lipid panels need to be fasting?

For adults who are not taking lipid-lowering therapy, measurement of either a fasting or a nonfasting plasma lipid profile is effective for documenting baseline LDL and estimating cardiovascular risk.¹ In other words, nonfasting lipid testing is appropriate for most low-risk screening. Nonfasting testing generally is more convenient for patients; however, nonfasting lipid panels could result in elevated triglyceride levels. If an initial nonfasting lipid profile reveals a triglyceride level of 400 mg/dL or higher, then a repeat lipid profile in the fasting state should be performed for assessment of fasting triglyceride levels and baseline LDL.¹ Some patients may prefer to simply get a fasting lipid panel initially so that they do not run the risk of having to return for a second test, especially if they are at increased risk for high triglyceride levels (ie, if they are obese, have diabetes, or are taking medications such as steroids, which can increase triglyceride levels).

The bottom line

Some patients receive primary care directly from their gynecologist, and thus it is important for women’s health clinicians to be aware of appropriate cholesterol screening practices. While lipid panels may commonly be ordered routinely as part of annual health check-ups, the evidence suggests that this is an unnecessary practice that contributes to wasteful health spending at both individual and system levels; it also is an avoidable inconvenience for patients. It is unclear when lipid screening should be initiated for adult patients, but it seems reasonable to check baseline levels for a new patient who has not previously been screened. In low-risk patients with normal lipid panel levels, experts recommend initiating retesting at age 45 for women and obtaining repeat lipid levels no more than every 4 to 6 years. For most patients, nonfasting lipid levels will suffice for screening. Avoiding common unnecessary testing is an effective way to improve value for patients. ●

CASE 34-year-old woman with lipid panel results from 1 year ago

A woman with no chronic medical conditions was seen by her gynecologist for a routine well-woman examination. She does not see another primary care provider. She is age 34 years and has a levonorgestrel intrauterine device that was placed after the birth of her second child 2 years prior. She does not take any other medications. She has never smoked and drinks a glass of wine with dinner a couple of times each week. She finds it challenging with her full-time job and her parental responsibilities with 2 young children to get regular exercise but otherwise is active. She does not have a family history of premature cardiovascular disease. Last year, during her prior well-woman examination, she had a fasting lipid panel: her low-density lipoprotein (LDL) was 102 mg/dL (reference range, ≤160 mg/dL), high-density lipoprotein (HDL) 52 mg/dL (reference range, ≥40 mg/dL), triglycerides 140 mg/dL (reference range, <160 mg/dL), and total cholesterol 182 mg/dL (reference range, <200 mg/dL).

During this visit, the patient’s vitals are normal (blood pressure 116/58) and her physical examination is unremarkable. Her physician orders routine labs to be checked, including a fasting lipid panel. She has to figure out when she will be able to get these labs drawn, as she needs to coordinate with her work and childcare schedules. A week later, she leaves work at 4:00 PM and picks up her young children (aged 2 and 4 years) from childcare, bringing them to the laboratory to have her blood drawn. Not only are her children cranky in the waiting room, but she is feeling tired as she hasn’t eaten all day because her physician told her she is supposed to be fasting. She has to pay for parking at the lot for the laboratory since it is connected to the medical center.

Was this lipid panel high value?

When and how often should we be checking lipid panels?

Do patients need to fast for these tests?
 

The potential benefits and costs of routine lipid panel screening

Hyperlipidemia is relatively prevalent, usually asymptomatic, and has been linked to cardiovascular outcomes. Thus, screening for lipid abnormalities is recommended to identify patients that would benefit from various interventions aimed at reducing cardiovascular disease risk, including lipid-lowering therapy.¹ High levels of LDL cholesterol and low levels of HDL cholesterol are important risk factors for coronary heart disease.

Lipid panels are widely available blood tests with modest monetary costs, generally ranging from about $10 to $100 in the outpatient setting. Of note, a 2014 study examining inpatient charges for this common laboratory test found that hospital charges in California ranged from about $10 to $10,000 for a lipid panel.² Despite the relatively low cost of each individual lipid panel, the aggregate costs to the health system of these frequently and widely performed tests are large. In fact, low-cost, high-volume health services, such as repeat cholesterol testing, account for the majority of unnecessary health spending in the United States, contributing nearly twice as much unnecessary cost as high-priced low-value services.³

To the patient, the cost is not only monetary. Some patients will need to take an additional hour or two off work as well as consider childcare, transportation, parking, and other mundane logistics to sit in a laboratory waiting room—a cost that may not be considered modest at all by the patient.^4,5

Therefore, like most services in health care, the answer to whether or not a lipid panel is high-value care is: it depends.⁵ In the correct circumstances, the test generally is regarded as high value due to well-documented potential benefits and low monetary costs. However, when performed unnecessarily—either in patient groups that are unlikely to benefit or at intervals that are too soon to add helpful information—then all that is left are the financial and psychosocial costs, which make this a low-value test in these scenarios. For this patient, this test contributed to inconvenience and mild hardships with essentially no benefit, thus would be considered low-value care.

Continue to: When should we perform lipid screening in low-risk women?

When should we perform lipid screening in low-risk women?

There are conflicting guidelines and opinions about at what age lipid screening should be routinely performed in adults. The United States Preventive Services Task Force (USPSTF) 2016 guidelines found “insufficient evidence that screening for dyslipidemia before age 40 years has an effect on either short- or longer-term cardiovascular outcomes.”⁶ Therefore, the USPSTF “recommends neither for nor against screening for dyslipidemia in this age group,” and instead encourages “clinicians to use their clinical judgment for [these] patients.”⁶

A common practice is to obtain a baseline lipid profile at the time of initiation of care with an adult primary care practitioner, if the patient was not previously screened, and to then determine subsequent testing based on these results and the patient’s risk factors for cardiovascular disease. For patients with normal lipid screening results and lower cardiovascular risk factors (no hypertension, diabetes mellitus, cigarette smoking, family history of premature coronary heart disease), experts suggest follow-up lipid screening be performed in men at age 35 and in women at age 45.⁷ Therefore, for this patient who had essentially a normal lipid panel a year prior, she should not have required repeat lipid testing until she is age 45.

As for how frequently subsequent lipid testing should be performed, the Centers for Disease Control and Prevention states, “most healthy adults should have their cholesterol checked every 4 to 6 years.”⁸ Those taking lipid-lowering medications or those with risk factors such as heart disease, diabetes, or concerning family history should have their cholesterol checked more frequently. If patients are near a threshold for treatment, some experts suggest repeating measurements every 3 years, but even in these settings, annual testing would be considered excessive.⁷

A standard lipid panel screen includes total cholesterol, LDL, HDL, and triglycerides. While a variety of assays have been developed that subfractionate lipoprotein particles based on size, density, or charge, these tests do not add value for low-risk patient screening and should only be used on an individualized basis for selected intermediate to high-risk patients. The American Society for Clinical Pathology released a Choosing Wisely recommendation that advises, “Do not routinely order expanded lipid panels (particle sizing, nuclear magnetic resonance) as screening tests for cardiovascular disease.”⁹

Do lipid panels need to be fasting?

For adults who are not taking lipid-lowering therapy, measurement of either a fasting or a nonfasting plasma lipid profile is effective for documenting baseline LDL and estimating cardiovascular risk.¹ In other words, nonfasting lipid testing is appropriate for most low-risk screening. Nonfasting testing generally is more convenient for patients; however, nonfasting lipid panels could result in elevated triglyceride levels. If an initial nonfasting lipid profile reveals a triglyceride level of 400 mg/dL or higher, then a repeat lipid profile in the fasting state should be performed for assessment of fasting triglyceride levels and baseline LDL.¹ Some patients may prefer to simply get a fasting lipid panel initially so that they do not run the risk of having to return for a second test, especially if they are at increased risk for high triglyceride levels (ie, if they are obese, have diabetes, or are taking medications such as steroids, which can increase triglyceride levels).

The bottom line

Some patients receive primary care directly from their gynecologist, and thus it is important for women’s health clinicians to be aware of appropriate cholesterol screening practices. While lipid panels may commonly be ordered routinely as part of annual health check-ups, the evidence suggests that this is an unnecessary practice that contributes to wasteful health spending at both individual and system levels; it also is an avoidable inconvenience for patients. It is unclear when lipid screening should be initiated for adult patients, but it seems reasonable to check baseline levels for a new patient who has not previously been screened. In low-risk patients with normal lipid panel levels, experts recommend initiating retesting at age 45 for women and obtaining repeat lipid levels no more than every 4 to 6 years. For most patients, nonfasting lipid levels will suffice for screening. Avoiding common unnecessary testing is an effective way to improve value for patients. ●

CASE 34-year-old woman with lipid panel results from 1 year ago

A woman with no chronic medical conditions was seen by her gynecologist for a routine well-woman examination. She does not see another primary care provider. She is age 34 years and has a levonorgestrel intrauterine device that was placed after the birth of her second child 2 years prior. She does not take any other medications. She has never smoked and drinks a glass of wine with dinner a couple of times each week. She finds it challenging with her full-time job and her parental responsibilities with 2 young children to get regular exercise but otherwise is active. She does not have a family history of premature cardiovascular disease. Last year, during her prior well-woman examination, she had a fasting lipid panel: her low-density lipoprotein (LDL) was 102 mg/dL (reference range, ≤160 mg/dL), high-density lipoprotein (HDL) 52 mg/dL (reference range, ≥40 mg/dL), triglycerides 140 mg/dL (reference range, <160 mg/dL), and total cholesterol 182 mg/dL (reference range, <200 mg/dL).

During this visit, the patient’s vitals are normal (blood pressure 116/58) and her physical examination is unremarkable. Her physician orders routine labs to be checked, including a fasting lipid panel. She has to figure out when she will be able to get these labs drawn, as she needs to coordinate with her work and childcare schedules. A week later, she leaves work at 4:00 PM and picks up her young children (aged 2 and 4 years) from childcare, bringing them to the laboratory to have her blood drawn. Not only are her children cranky in the waiting room, but she is feeling tired as she hasn’t eaten all day because her physician told her she is supposed to be fasting. She has to pay for parking at the lot for the laboratory since it is connected to the medical center.

Was this lipid panel high value?

When and how often should we be checking lipid panels?

Do patients need to fast for these tests?
 

The potential benefits and costs of routine lipid panel screening

Hyperlipidemia is relatively prevalent, usually asymptomatic, and has been linked to cardiovascular outcomes. Thus, screening for lipid abnormalities is recommended to identify patients that would benefit from various interventions aimed at reducing cardiovascular disease risk, including lipid-lowering therapy.¹ High levels of LDL cholesterol and low levels of HDL cholesterol are important risk factors for coronary heart disease.

Lipid panels are widely available blood tests with modest monetary costs, generally ranging from about $10 to $100 in the outpatient setting. Of note, a 2014 study examining inpatient charges for this common laboratory test found that hospital charges in California ranged from about $10 to $10,000 for a lipid panel.² Despite the relatively low cost of each individual lipid panel, the aggregate costs to the health system of these frequently and widely performed tests are large. In fact, low-cost, high-volume health services, such as repeat cholesterol testing, account for the majority of unnecessary health spending in the United States, contributing nearly twice as much unnecessary cost as high-priced low-value services.³

To the patient, the cost is not only monetary. Some patients will need to take an additional hour or two off work as well as consider childcare, transportation, parking, and other mundane logistics to sit in a laboratory waiting room—a cost that may not be considered modest at all by the patient.^4,5

Therefore, like most services in health care, the answer to whether or not a lipid panel is high-value care is: it depends.⁵ In the correct circumstances, the test generally is regarded as high value due to well-documented potential benefits and low monetary costs. However, when performed unnecessarily—either in patient groups that are unlikely to benefit or at intervals that are too soon to add helpful information—then all that is left are the financial and psychosocial costs, which make this a low-value test in these scenarios. For this patient, this test contributed to inconvenience and mild hardships with essentially no benefit, thus would be considered low-value care.

Continue to: When should we perform lipid screening in low-risk women?

When should we perform lipid screening in low-risk women?

There are conflicting guidelines and opinions about at what age lipid screening should be routinely performed in adults. The United States Preventive Services Task Force (USPSTF) 2016 guidelines found “insufficient evidence that screening for dyslipidemia before age 40 years has an effect on either short- or longer-term cardiovascular outcomes.”⁶ Therefore, the USPSTF “recommends neither for nor against screening for dyslipidemia in this age group,” and instead encourages “clinicians to use their clinical judgment for [these] patients.”⁶

A common practice is to obtain a baseline lipid profile at the time of initiation of care with an adult primary care practitioner, if the patient was not previously screened, and to then determine subsequent testing based on these results and the patient’s risk factors for cardiovascular disease. For patients with normal lipid screening results and lower cardiovascular risk factors (no hypertension, diabetes mellitus, cigarette smoking, family history of premature coronary heart disease), experts suggest follow-up lipid screening be performed in men at age 35 and in women at age 45.⁷ Therefore, for this patient who had essentially a normal lipid panel a year prior, she should not have required repeat lipid testing until she is age 45.

As for how frequently subsequent lipid testing should be performed, the Centers for Disease Control and Prevention states, “most healthy adults should have their cholesterol checked every 4 to 6 years.”⁸ Those taking lipid-lowering medications or those with risk factors such as heart disease, diabetes, or concerning family history should have their cholesterol checked more frequently. If patients are near a threshold for treatment, some experts suggest repeating measurements every 3 years, but even in these settings, annual testing would be considered excessive.⁷

A standard lipid panel screen includes total cholesterol, LDL, HDL, and triglycerides. While a variety of assays have been developed that subfractionate lipoprotein particles based on size, density, or charge, these tests do not add value for low-risk patient screening and should only be used on an individualized basis for selected intermediate to high-risk patients. The American Society for Clinical Pathology released a Choosing Wisely recommendation that advises, “Do not routinely order expanded lipid panels (particle sizing, nuclear magnetic resonance) as screening tests for cardiovascular disease.”⁹

Do lipid panels need to be fasting?

For adults who are not taking lipid-lowering therapy, measurement of either a fasting or a nonfasting plasma lipid profile is effective for documenting baseline LDL and estimating cardiovascular risk.¹ In other words, nonfasting lipid testing is appropriate for most low-risk screening. Nonfasting testing generally is more convenient for patients; however, nonfasting lipid panels could result in elevated triglyceride levels. If an initial nonfasting lipid profile reveals a triglyceride level of 400 mg/dL or higher, then a repeat lipid profile in the fasting state should be performed for assessment of fasting triglyceride levels and baseline LDL.¹ Some patients may prefer to simply get a fasting lipid panel initially so that they do not run the risk of having to return for a second test, especially if they are at increased risk for high triglyceride levels (ie, if they are obese, have diabetes, or are taking medications such as steroids, which can increase triglyceride levels).

The bottom line

Some patients receive primary care directly from their gynecologist, and thus it is important for women’s health clinicians to be aware of appropriate cholesterol screening practices. While lipid panels may commonly be ordered routinely as part of annual health check-ups, the evidence suggests that this is an unnecessary practice that contributes to wasteful health spending at both individual and system levels; it also is an avoidable inconvenience for patients. It is unclear when lipid screening should be initiated for adult patients, but it seems reasonable to check baseline levels for a new patient who has not previously been screened. In low-risk patients with normal lipid panel levels, experts recommend initiating retesting at age 45 for women and obtaining repeat lipid levels no more than every 4 to 6 years. For most patients, nonfasting lipid levels will suffice for screening. Avoiding common unnecessary testing is an effective way to improve value for patients. ●

Gray KJ, Bordt EA, Atyeo C, et al. COVID-19 vaccine response in pregnant and lactating women: a cohort study. Am J Obstet Gynecol. 2021;S0002-9378(21)00187-3. doi: 10.1016/j.ajog.2021.03.023

EXPERT COMMENTARY

Pregnant women are among those at highest risk for severe disease and death from SARS-CoV-2 infection. However, exclusion of pregnant and lactating women from the initial COVID-19 vaccine trials has made counseling these patients challenging due to both the novelty of the vaccines themselves and the general lack of data in this vulnerable population. Data for the efficacy and risks of vaccination are needed to inform shared decision making between clinician and patient.

Details of the study

Gray and colleagues conducted a prospective cohort study of 84 pregnant, 31 lactating, and 16 nonpregnant women who received 1 of the 2 COVID-19 mRNA vaccines approved by the US Food and Drug Administration for emergency use authorization (BNT162b2 Pfizer/BioNTech or mRNA-1273 Moderna). The study’s primary objective was to evaluate the humoral immune response (antibody quantification) and adverse effects of these vaccines in the pregnant and lactating women compared with both nonpregnant women and a cohort of 37 women who had natural COVID-19 infection during pregnancy.

Antibody quantification from blood and breast milk was performed at 4 time points: V0, the first vaccine dose; V1, the second vaccine dose; V2, 2 to 6 weeks after the second vaccine dose; and at delivery. Umbilical cord blood also was collected from the subset of delivered patients (n = 13).

Results. The ultimately IgG-dominated antibody response to the vaccine in pregnant and lactating women was comparable to that in nonpregnant women, and all vaccine antibody responses were significantly higher than that in response to natural SARS-CoV-2 infection. IgG antibodies also were found in umbilical cord blood and breast milk, supporting the transfer of immunity to both the fetus and infant. There were no significant differences in adverse effects between pregnant and nonpregnant women.

Study strengths and limitations

This study’s main strength is that it demonstrated a similar increase in humoral immune response to the COVID-19 mRNA vaccines in a previously unstudied population of pregnant and lactating women, supporting the potential efficacy of the vaccines in this group at high risk for complications from SARS-CoV-2. Other data to support this include the increased vaccine antibody response compared with the antibody response after SARS-CoV-2 infection in pregnant women as well as the presence of maternal-infant transfer of antibodies via cord blood and breast milk. All of these are important data to inform patients and practitioners who are trying to make shared, informed decisions about a novel vaccine during a global pandemic.

The main limitation of this study is a limited patient population of mostly White, non-Hispanic, health care workers with few comorbidities and only 13 delivered vaccinated patients within the study period. Long-term immunity, immune responses other than antibody titers, and potential fetal effects also were not explored in this study. ●

Gray KJ, Bordt EA, Atyeo C, et al. COVID-19 vaccine response in pregnant and lactating women: a cohort study. Am J Obstet Gynecol. 2021;S0002-9378(21)00187-3. doi: 10.1016/j.ajog.2021.03.023

EXPERT COMMENTARY

Pregnant women are among those at highest risk for severe disease and death from SARS-CoV-2 infection. However, exclusion of pregnant and lactating women from the initial COVID-19 vaccine trials has made counseling these patients challenging due to both the novelty of the vaccines themselves and the general lack of data in this vulnerable population. Data for the efficacy and risks of vaccination are needed to inform shared decision making between clinician and patient.

Details of the study

Gray and colleagues conducted a prospective cohort study of 84 pregnant, 31 lactating, and 16 nonpregnant women who received 1 of the 2 COVID-19 mRNA vaccines approved by the US Food and Drug Administration for emergency use authorization (BNT162b2 Pfizer/BioNTech or mRNA-1273 Moderna). The study’s primary objective was to evaluate the humoral immune response (antibody quantification) and adverse effects of these vaccines in the pregnant and lactating women compared with both nonpregnant women and a cohort of 37 women who had natural COVID-19 infection during pregnancy.

Antibody quantification from blood and breast milk was performed at 4 time points: V0, the first vaccine dose; V1, the second vaccine dose; V2, 2 to 6 weeks after the second vaccine dose; and at delivery. Umbilical cord blood also was collected from the subset of delivered patients (n = 13).

Results. The ultimately IgG-dominated antibody response to the vaccine in pregnant and lactating women was comparable to that in nonpregnant women, and all vaccine antibody responses were significantly higher than that in response to natural SARS-CoV-2 infection. IgG antibodies also were found in umbilical cord blood and breast milk, supporting the transfer of immunity to both the fetus and infant. There were no significant differences in adverse effects between pregnant and nonpregnant women.

Study strengths and limitations

This study’s main strength is that it demonstrated a similar increase in humoral immune response to the COVID-19 mRNA vaccines in a previously unstudied population of pregnant and lactating women, supporting the potential efficacy of the vaccines in this group at high risk for complications from SARS-CoV-2. Other data to support this include the increased vaccine antibody response compared with the antibody response after SARS-CoV-2 infection in pregnant women as well as the presence of maternal-infant transfer of antibodies via cord blood and breast milk. All of these are important data to inform patients and practitioners who are trying to make shared, informed decisions about a novel vaccine during a global pandemic.

The main limitation of this study is a limited patient population of mostly White, non-Hispanic, health care workers with few comorbidities and only 13 delivered vaccinated patients within the study period. Long-term immunity, immune responses other than antibody titers, and potential fetal effects also were not explored in this study. ●

Gray KJ, Bordt EA, Atyeo C, et al. COVID-19 vaccine response in pregnant and lactating women: a cohort study. Am J Obstet Gynecol. 2021;S0002-9378(21)00187-3. doi: 10.1016/j.ajog.2021.03.023

EXPERT COMMENTARY

Pregnant women are among those at highest risk for severe disease and death from SARS-CoV-2 infection. However, exclusion of pregnant and lactating women from the initial COVID-19 vaccine trials has made counseling these patients challenging due to both the novelty of the vaccines themselves and the general lack of data in this vulnerable population. Data for the efficacy and risks of vaccination are needed to inform shared decision making between clinician and patient.

Details of the study

Gray and colleagues conducted a prospective cohort study of 84 pregnant, 31 lactating, and 16 nonpregnant women who received 1 of the 2 COVID-19 mRNA vaccines approved by the US Food and Drug Administration for emergency use authorization (BNT162b2 Pfizer/BioNTech or mRNA-1273 Moderna). The study’s primary objective was to evaluate the humoral immune response (antibody quantification) and adverse effects of these vaccines in the pregnant and lactating women compared with both nonpregnant women and a cohort of 37 women who had natural COVID-19 infection during pregnancy.

Antibody quantification from blood and breast milk was performed at 4 time points: V0, the first vaccine dose; V1, the second vaccine dose; V2, 2 to 6 weeks after the second vaccine dose; and at delivery. Umbilical cord blood also was collected from the subset of delivered patients (n = 13).

Results. The ultimately IgG-dominated antibody response to the vaccine in pregnant and lactating women was comparable to that in nonpregnant women, and all vaccine antibody responses were significantly higher than that in response to natural SARS-CoV-2 infection. IgG antibodies also were found in umbilical cord blood and breast milk, supporting the transfer of immunity to both the fetus and infant. There were no significant differences in adverse effects between pregnant and nonpregnant women.

Study strengths and limitations

This study’s main strength is that it demonstrated a similar increase in humoral immune response to the COVID-19 mRNA vaccines in a previously unstudied population of pregnant and lactating women, supporting the potential efficacy of the vaccines in this group at high risk for complications from SARS-CoV-2. Other data to support this include the increased vaccine antibody response compared with the antibody response after SARS-CoV-2 infection in pregnant women as well as the presence of maternal-infant transfer of antibodies via cord blood and breast milk. All of these are important data to inform patients and practitioners who are trying to make shared, informed decisions about a novel vaccine during a global pandemic.

The main limitation of this study is a limited patient population of mostly White, non-Hispanic, health care workers with few comorbidities and only 13 delivered vaccinated patients within the study period. Long-term immunity, immune responses other than antibody titers, and potential fetal effects also were not explored in this study. ●

The rate of obstetric anal sphincter injury (OASIS) is approximately 4.4% of vaginal deliveries, with 3.3% 3rd-degree tears and 1.1% 4th-degree tears.¹ In the United States in 2019 there were 3,745,540 births—a 31.7% rate of cesarean delivery (CD) and a 68.3% rate of vaginal delivery—resulting in approximately 112,600 births with OASIS.² A meta-analysis reported that, among 716,031 vaginal births, the risk factors for OASIS included: forceps delivery (relative risk [RR], 3.15), midline episiotomy (RR, 2.88), occiput posterior fetal position (RR, 2.73), vacuum delivery (RR, 2.60), Asian race (RR, 1.87), primiparity (RR, 1.59), mediolateral episiotomy (RR, 1.55), augmentation of labor (RR, 1.46), and epidural anesthesia (RR, 1.21).³ OASIS is associated with an increased risk for developing postpartum perineal pain, anal incontinence, dyspareunia, and wound breakdown.⁴ Complications following OASIS repair can trigger many follow-up appointments to assess wound healing and provide physical therapy.

This editorial review focuses on evolving recommendations for preventing and repairing OASIS.

The optimal cutting angle for a mediolateral episiotomy is 60 degrees from the midline

For spontaneous vaginal delivery, a policy of restricted episiotomy reduces the risk of OASIS by approximately 30%.⁵ With an operative vaginal delivery, especially forceps delivery of a large fetus in the occiput posterior position, a mediolateral episiotomy may help to reduce the risk of OASIS, although there are minimal data from clinical trials to support this practice. In one clinical trial, 407 women were randomly assigned to either a mediolateral or midline episiotomy.⁶ Approximately 25% of the births in both groups were operative deliveries. The mediolateral episiotomy began in the posterior midline of the vaginal introitus and was carried to the right side of the anal sphincter for 3 cm to 4 cm. The midline episiotomy began in the posterior midline of the vagina and was carried 2 cm to 3 cm into the midline perineal tissue. In the women having a midline or mediolateral episiotomy, a 4th-degree tear occurred in 5.5% and 0.4% of births, respectively. For the midline or mediolateral episiotomy, a third-degree tear occurred in 18.4% and 8.6%, respectively. In a prospective cohort study of 1,302 women with an episiotomy and vaginal birth, the rate of OASIS associated with midline or mediolateral episiotomy was 14.8% and 7%, respectively (P<.05).⁷ In this study, the operative vaginal delivery rate was 11.6% and 15.2% for the women in the midline and mediolateral groups, respectively.

The angle of the mediolateral episiotomy may influence the rate of OASIS and persistent postpartum perineal pain. In one study, 330 nulliparous women who were assessed to need a mediolateral episiotomy at delivery were randomized to an incision with a 40- or 60-degree angle from the midline.⁸ Prior to incision, a line was drawn on the skin to mark the course of the incision and then infiltrated with 10 mL of lignocaine. The fetal head was delivered with a Ritgen maneuver. The length of the episiotomy averaged 4 cm in both groups. After delivery, the angle of the episiotomy incision was reassessed. The episiotomy incision cut 60 degrees from the midline was measured on average to be 44 degrees from the midline after delivery of the newborn. Similarly, the incision cut at a 40-degree angle was measured to be 24 degrees from the midline after delivery. The rates of OASIS in the women who had a 40- and 60-degree angle incision were 5.5% and 2.4%, respectively (P = .16).

Continue to: Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair...

Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair

Many experts recommend one dose of a prophylactic antibiotic prior to, or during, OASIS repair in order to reduce the risk of wound complications. In a trial 147 women with OASIS were randomly assigned to receive one dose of a second-generation cephalosporin (cefotetan or cefoxitin) with extended anaerobic coverage or a placebo just before repair of the laceration.⁹ At 2 weeks postpartum, perineal wound complications were significantly lower in women receiving one dose of prophylactic antibiotic with extended anaerobe coverage compared with placebo—8.2% and 24.1%, respectively (P = .037). Additionally, at 2 weeks postpartum, purulent wound discharge was significantly lower in women receiving antibiotic versus placebo, 4% and 17%, respectively (P = .036). Experts writing for the Society of Obstetricians and Gynaecologists of Canada also recommend one dose of cefotetan or cefoxitin.¹⁰ Extended anaerobic coverage also can be achieved by administering a single dose of BOTH cefazolin 2 g by intravenous (IV) infusion PLUS metronidazole 500 mg by IV infusion or oral medication.¹¹ For women with severe penicillin allergy, a recommended regimen is gentamicin 5 mg/kg plus clindamycin 900 mg by IV infusion.¹¹ There is evidence that for colorectal or hysterectomy surgery, expanding prophylactic antibiotic coverage of anaerobes with cefazolin PLUS metronidazole significantly reduces postoperative surgical site infection.^12,13 Following an OASIS repair, wound breakdown is a catastrophic problem that may take many months to resolve. Administration of a prophylactic antibiotic with extended coverage of anaerobes may help to prevent wound breakdown.

Prioritize identifying and separately repairing the internal anal sphincter

The internal anal sphincter is a smooth muscle that runs along the outside of the rectal wall and thickens into a sphincter toward the anal canal. The internal anal sphincter is thin and grey-white in appearance, like a veil. By contrast, the external anal sphincter is a thick band of red striated muscle tissue. In one study of 3,333 primiparous women with OASIS, an internal anal sphincter injury was detected in 33% of cases.¹⁴ In this large cohort, the rate of internal anal sphincter injury with a 3A tear, a 3B tear, a complete tear of the external sphincter and a 4th-degree perineal tear was 22%, 23%, 42%, and 71%, respectively. The internal anal sphincter is important for maintaining rectal continence and is estimated to contribute 50% to 85% of resting anal tone.¹⁵ If injury to the internal anal sphincter is detected at a birth with an OASIS, it is important to separately repair the internal anal sphincter to reduce the risk of postpartum rectal incontinence.¹⁶

Polyglactin 910 vs Polydioxanone (PDS) Suture—Is PDS the winner?

Polyglactin 910 (Vicryl) is a braided suture that is absorbed within 56 to 70 days. Polydioxanone suture is a long-lasting monofilament suture that is absorbed within 200 days. Many colorectal surgeons and urogynecologists prefer PDS suture for the repair of both the internal and external anal sphincters.¹⁶ Authors of one randomized trial of OASIS repair with Vicryl or PDS suture did not report significant differences in most clinical outcomes.¹⁷ However, in this study, anal endosonographic imaging of the internal and external anal sphincter demonstrated more internal sphincter defects but not external sphincter defects when the repair was performed with Vicryl rather than PDS. The investigators concluded that comprehensive training of the surgeon, not choice of suture, is probably the most important factor in achieving a good OASIS repair. However, because many subspecialists favor PDS suture for sphincter repair, specialists in obstetrics and gynecology should consider this option.

Continue to: Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

The breakdown of an OASIS repair is an obstetric catastrophe with complications that can last many months and sometimes stretch into years. The best approach to a perineal laceration wound breakdown remains controversial. It is optimal if all patients with a wound breakdown can be offered an early secondary repair or healing by secondary intention, permitting the patient to select the best approach for their specific situation.

As noted by the pioneers of early repair of episiotomy dehiscence, Drs. Hankins, Haugh, Gilstrap, Ramin, and others,^18-20 conventional doctrine is that an episiotomy repair dehiscence should be managed expectantly, allowing healing by secondary intention and delaying repair of the sphincters for a minimum of 3 to 4 months.²¹ However, many small case-series report that early secondary repair of a perineal laceration wound breakdown is possible following multiple days of wound preparation prior to the repair, good surgical technique and diligent postoperative follow-up care. One large case series reported on 72 women with complete perineal wound dehiscence who had early secondary repair.²² The median time to complete wound healing following early repair was 28 days. About 36% of the patients had one or more complications, including skin dehiscence, granuloma formation, perineal pain, and sinus formation. A pilot randomized trial reported that, compared with expectant management of a wound breakdown, early repair resulted in a shorter time to wound healing.²³

Early repair of perineal wound dehiscence often involves a course of care that extends over multiple weeks. As an example, following a vaginal birth with OASIS and immediate repair, the patient is often discharged from the hospital to home on postpartum day 3. The wound breakdown often is detected between postpartum days 6 to 10. If early secondary repair is selected as the best treatment, 1 to 6 days of daily debridement of the wound is needed to prepare the wound for early secondary repair. The daily debridement required to prepare the wound for early repair is often performed in the hospital, potentially disrupting early mother-newborn bonding. Following the repair, the patient is observed in the hospital for 1 to 3 days and then discharged home with daily wound care and multiple follow-up visits to monitor wound healing. Pelvic floor physical therapy may be initiated when the wound is healed. The prolonged process required for early secondary repair may be best undertaken by a subspecialty practice.²⁴

The surgical repair and postpartum care of OASIS continues to evolve. In your practice you should consider:

• performing a mediolateral episiotomy at a 60-degree angle to reduce the risk of OASIS in situations where there is a high risk of anal sphincter injury, such as in forceps delivery
• using one dose of a prophylactic antibiotic with extended anaerobic coverage, such as cefotetan or cefoxitin
• focus on identifying and separately repairing an internal anal sphincter injury
• using a long-lasting absorbable suture, such as PDS, to repair the internal and external anal sphincters
• ensuring that the patient with a dehiscence following an episiotomy or anal sphincter injury has access to early secondary repair. Standardizing your approach to the prevention and repair of anal sphincter injury will benefit the approximately 112,600 US women who experience OASIS each year. ●

The rate of obstetric anal sphincter injury (OASIS) is approximately 4.4% of vaginal deliveries, with 3.3% 3rd-degree tears and 1.1% 4th-degree tears.¹ In the United States in 2019 there were 3,745,540 births—a 31.7% rate of cesarean delivery (CD) and a 68.3% rate of vaginal delivery—resulting in approximately 112,600 births with OASIS.² A meta-analysis reported that, among 716,031 vaginal births, the risk factors for OASIS included: forceps delivery (relative risk [RR], 3.15), midline episiotomy (RR, 2.88), occiput posterior fetal position (RR, 2.73), vacuum delivery (RR, 2.60), Asian race (RR, 1.87), primiparity (RR, 1.59), mediolateral episiotomy (RR, 1.55), augmentation of labor (RR, 1.46), and epidural anesthesia (RR, 1.21).³ OASIS is associated with an increased risk for developing postpartum perineal pain, anal incontinence, dyspareunia, and wound breakdown.⁴ Complications following OASIS repair can trigger many follow-up appointments to assess wound healing and provide physical therapy.

This editorial review focuses on evolving recommendations for preventing and repairing OASIS.

The optimal cutting angle for a mediolateral episiotomy is 60 degrees from the midline

For spontaneous vaginal delivery, a policy of restricted episiotomy reduces the risk of OASIS by approximately 30%.⁵ With an operative vaginal delivery, especially forceps delivery of a large fetus in the occiput posterior position, a mediolateral episiotomy may help to reduce the risk of OASIS, although there are minimal data from clinical trials to support this practice. In one clinical trial, 407 women were randomly assigned to either a mediolateral or midline episiotomy.⁶ Approximately 25% of the births in both groups were operative deliveries. The mediolateral episiotomy began in the posterior midline of the vaginal introitus and was carried to the right side of the anal sphincter for 3 cm to 4 cm. The midline episiotomy began in the posterior midline of the vagina and was carried 2 cm to 3 cm into the midline perineal tissue. In the women having a midline or mediolateral episiotomy, a 4th-degree tear occurred in 5.5% and 0.4% of births, respectively. For the midline or mediolateral episiotomy, a third-degree tear occurred in 18.4% and 8.6%, respectively. In a prospective cohort study of 1,302 women with an episiotomy and vaginal birth, the rate of OASIS associated with midline or mediolateral episiotomy was 14.8% and 7%, respectively (P<.05).⁷ In this study, the operative vaginal delivery rate was 11.6% and 15.2% for the women in the midline and mediolateral groups, respectively.

The angle of the mediolateral episiotomy may influence the rate of OASIS and persistent postpartum perineal pain. In one study, 330 nulliparous women who were assessed to need a mediolateral episiotomy at delivery were randomized to an incision with a 40- or 60-degree angle from the midline.⁸ Prior to incision, a line was drawn on the skin to mark the course of the incision and then infiltrated with 10 mL of lignocaine. The fetal head was delivered with a Ritgen maneuver. The length of the episiotomy averaged 4 cm in both groups. After delivery, the angle of the episiotomy incision was reassessed. The episiotomy incision cut 60 degrees from the midline was measured on average to be 44 degrees from the midline after delivery of the newborn. Similarly, the incision cut at a 40-degree angle was measured to be 24 degrees from the midline after delivery. The rates of OASIS in the women who had a 40- and 60-degree angle incision were 5.5% and 2.4%, respectively (P = .16).

Continue to: Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair...

Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair

Many experts recommend one dose of a prophylactic antibiotic prior to, or during, OASIS repair in order to reduce the risk of wound complications. In a trial 147 women with OASIS were randomly assigned to receive one dose of a second-generation cephalosporin (cefotetan or cefoxitin) with extended anaerobic coverage or a placebo just before repair of the laceration.⁹ At 2 weeks postpartum, perineal wound complications were significantly lower in women receiving one dose of prophylactic antibiotic with extended anaerobe coverage compared with placebo—8.2% and 24.1%, respectively (P = .037). Additionally, at 2 weeks postpartum, purulent wound discharge was significantly lower in women receiving antibiotic versus placebo, 4% and 17%, respectively (P = .036). Experts writing for the Society of Obstetricians and Gynaecologists of Canada also recommend one dose of cefotetan or cefoxitin.¹⁰ Extended anaerobic coverage also can be achieved by administering a single dose of BOTH cefazolin 2 g by intravenous (IV) infusion PLUS metronidazole 500 mg by IV infusion or oral medication.¹¹ For women with severe penicillin allergy, a recommended regimen is gentamicin 5 mg/kg plus clindamycin 900 mg by IV infusion.¹¹ There is evidence that for colorectal or hysterectomy surgery, expanding prophylactic antibiotic coverage of anaerobes with cefazolin PLUS metronidazole significantly reduces postoperative surgical site infection.^12,13 Following an OASIS repair, wound breakdown is a catastrophic problem that may take many months to resolve. Administration of a prophylactic antibiotic with extended coverage of anaerobes may help to prevent wound breakdown.

Prioritize identifying and separately repairing the internal anal sphincter

The internal anal sphincter is a smooth muscle that runs along the outside of the rectal wall and thickens into a sphincter toward the anal canal. The internal anal sphincter is thin and grey-white in appearance, like a veil. By contrast, the external anal sphincter is a thick band of red striated muscle tissue. In one study of 3,333 primiparous women with OASIS, an internal anal sphincter injury was detected in 33% of cases.¹⁴ In this large cohort, the rate of internal anal sphincter injury with a 3A tear, a 3B tear, a complete tear of the external sphincter and a 4th-degree perineal tear was 22%, 23%, 42%, and 71%, respectively. The internal anal sphincter is important for maintaining rectal continence and is estimated to contribute 50% to 85% of resting anal tone.¹⁵ If injury to the internal anal sphincter is detected at a birth with an OASIS, it is important to separately repair the internal anal sphincter to reduce the risk of postpartum rectal incontinence.¹⁶

Polyglactin 910 vs Polydioxanone (PDS) Suture—Is PDS the winner?

Polyglactin 910 (Vicryl) is a braided suture that is absorbed within 56 to 70 days. Polydioxanone suture is a long-lasting monofilament suture that is absorbed within 200 days. Many colorectal surgeons and urogynecologists prefer PDS suture for the repair of both the internal and external anal sphincters.¹⁶ Authors of one randomized trial of OASIS repair with Vicryl or PDS suture did not report significant differences in most clinical outcomes.¹⁷ However, in this study, anal endosonographic imaging of the internal and external anal sphincter demonstrated more internal sphincter defects but not external sphincter defects when the repair was performed with Vicryl rather than PDS. The investigators concluded that comprehensive training of the surgeon, not choice of suture, is probably the most important factor in achieving a good OASIS repair. However, because many subspecialists favor PDS suture for sphincter repair, specialists in obstetrics and gynecology should consider this option.

Continue to: Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

The breakdown of an OASIS repair is an obstetric catastrophe with complications that can last many months and sometimes stretch into years. The best approach to a perineal laceration wound breakdown remains controversial. It is optimal if all patients with a wound breakdown can be offered an early secondary repair or healing by secondary intention, permitting the patient to select the best approach for their specific situation.

As noted by the pioneers of early repair of episiotomy dehiscence, Drs. Hankins, Haugh, Gilstrap, Ramin, and others,^18-20 conventional doctrine is that an episiotomy repair dehiscence should be managed expectantly, allowing healing by secondary intention and delaying repair of the sphincters for a minimum of 3 to 4 months.²¹ However, many small case-series report that early secondary repair of a perineal laceration wound breakdown is possible following multiple days of wound preparation prior to the repair, good surgical technique and diligent postoperative follow-up care. One large case series reported on 72 women with complete perineal wound dehiscence who had early secondary repair.²² The median time to complete wound healing following early repair was 28 days. About 36% of the patients had one or more complications, including skin dehiscence, granuloma formation, perineal pain, and sinus formation. A pilot randomized trial reported that, compared with expectant management of a wound breakdown, early repair resulted in a shorter time to wound healing.²³

Early repair of perineal wound dehiscence often involves a course of care that extends over multiple weeks. As an example, following a vaginal birth with OASIS and immediate repair, the patient is often discharged from the hospital to home on postpartum day 3. The wound breakdown often is detected between postpartum days 6 to 10. If early secondary repair is selected as the best treatment, 1 to 6 days of daily debridement of the wound is needed to prepare the wound for early secondary repair. The daily debridement required to prepare the wound for early repair is often performed in the hospital, potentially disrupting early mother-newborn bonding. Following the repair, the patient is observed in the hospital for 1 to 3 days and then discharged home with daily wound care and multiple follow-up visits to monitor wound healing. Pelvic floor physical therapy may be initiated when the wound is healed. The prolonged process required for early secondary repair may be best undertaken by a subspecialty practice.²⁴

The surgical repair and postpartum care of OASIS continues to evolve. In your practice you should consider:

• performing a mediolateral episiotomy at a 60-degree angle to reduce the risk of OASIS in situations where there is a high risk of anal sphincter injury, such as in forceps delivery
• using one dose of a prophylactic antibiotic with extended anaerobic coverage, such as cefotetan or cefoxitin
• focus on identifying and separately repairing an internal anal sphincter injury
• using a long-lasting absorbable suture, such as PDS, to repair the internal and external anal sphincters
• ensuring that the patient with a dehiscence following an episiotomy or anal sphincter injury has access to early secondary repair. Standardizing your approach to the prevention and repair of anal sphincter injury will benefit the approximately 112,600 US women who experience OASIS each year. ●

The rate of obstetric anal sphincter injury (OASIS) is approximately 4.4% of vaginal deliveries, with 3.3% 3rd-degree tears and 1.1% 4th-degree tears.¹ In the United States in 2019 there were 3,745,540 births—a 31.7% rate of cesarean delivery (CD) and a 68.3% rate of vaginal delivery—resulting in approximately 112,600 births with OASIS.² A meta-analysis reported that, among 716,031 vaginal births, the risk factors for OASIS included: forceps delivery (relative risk [RR], 3.15), midline episiotomy (RR, 2.88), occiput posterior fetal position (RR, 2.73), vacuum delivery (RR, 2.60), Asian race (RR, 1.87), primiparity (RR, 1.59), mediolateral episiotomy (RR, 1.55), augmentation of labor (RR, 1.46), and epidural anesthesia (RR, 1.21).³ OASIS is associated with an increased risk for developing postpartum perineal pain, anal incontinence, dyspareunia, and wound breakdown.⁴ Complications following OASIS repair can trigger many follow-up appointments to assess wound healing and provide physical therapy.

This editorial review focuses on evolving recommendations for preventing and repairing OASIS.

The optimal cutting angle for a mediolateral episiotomy is 60 degrees from the midline

For spontaneous vaginal delivery, a policy of restricted episiotomy reduces the risk of OASIS by approximately 30%.⁵ With an operative vaginal delivery, especially forceps delivery of a large fetus in the occiput posterior position, a mediolateral episiotomy may help to reduce the risk of OASIS, although there are minimal data from clinical trials to support this practice. In one clinical trial, 407 women were randomly assigned to either a mediolateral or midline episiotomy.⁶ Approximately 25% of the births in both groups were operative deliveries. The mediolateral episiotomy began in the posterior midline of the vaginal introitus and was carried to the right side of the anal sphincter for 3 cm to 4 cm. The midline episiotomy began in the posterior midline of the vagina and was carried 2 cm to 3 cm into the midline perineal tissue. In the women having a midline or mediolateral episiotomy, a 4th-degree tear occurred in 5.5% and 0.4% of births, respectively. For the midline or mediolateral episiotomy, a third-degree tear occurred in 18.4% and 8.6%, respectively. In a prospective cohort study of 1,302 women with an episiotomy and vaginal birth, the rate of OASIS associated with midline or mediolateral episiotomy was 14.8% and 7%, respectively (P<.05).⁷ In this study, the operative vaginal delivery rate was 11.6% and 15.2% for the women in the midline and mediolateral groups, respectively.

The angle of the mediolateral episiotomy may influence the rate of OASIS and persistent postpartum perineal pain. In one study, 330 nulliparous women who were assessed to need a mediolateral episiotomy at delivery were randomized to an incision with a 40- or 60-degree angle from the midline.⁸ Prior to incision, a line was drawn on the skin to mark the course of the incision and then infiltrated with 10 mL of lignocaine. The fetal head was delivered with a Ritgen maneuver. The length of the episiotomy averaged 4 cm in both groups. After delivery, the angle of the episiotomy incision was reassessed. The episiotomy incision cut 60 degrees from the midline was measured on average to be 44 degrees from the midline after delivery of the newborn. Similarly, the incision cut at a 40-degree angle was measured to be 24 degrees from the midline after delivery. The rates of OASIS in the women who had a 40- and 60-degree angle incision were 5.5% and 2.4%, respectively (P = .16).

Continue to: Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair...

Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair

Many experts recommend one dose of a prophylactic antibiotic prior to, or during, OASIS repair in order to reduce the risk of wound complications. In a trial 147 women with OASIS were randomly assigned to receive one dose of a second-generation cephalosporin (cefotetan or cefoxitin) with extended anaerobic coverage or a placebo just before repair of the laceration.⁹ At 2 weeks postpartum, perineal wound complications were significantly lower in women receiving one dose of prophylactic antibiotic with extended anaerobe coverage compared with placebo—8.2% and 24.1%, respectively (P = .037). Additionally, at 2 weeks postpartum, purulent wound discharge was significantly lower in women receiving antibiotic versus placebo, 4% and 17%, respectively (P = .036). Experts writing for the Society of Obstetricians and Gynaecologists of Canada also recommend one dose of cefotetan or cefoxitin.¹⁰ Extended anaerobic coverage also can be achieved by administering a single dose of BOTH cefazolin 2 g by intravenous (IV) infusion PLUS metronidazole 500 mg by IV infusion or oral medication.¹¹ For women with severe penicillin allergy, a recommended regimen is gentamicin 5 mg/kg plus clindamycin 900 mg by IV infusion.¹¹ There is evidence that for colorectal or hysterectomy surgery, expanding prophylactic antibiotic coverage of anaerobes with cefazolin PLUS metronidazole significantly reduces postoperative surgical site infection.^12,13 Following an OASIS repair, wound breakdown is a catastrophic problem that may take many months to resolve. Administration of a prophylactic antibiotic with extended coverage of anaerobes may help to prevent wound breakdown.

Prioritize identifying and separately repairing the internal anal sphincter

The internal anal sphincter is a smooth muscle that runs along the outside of the rectal wall and thickens into a sphincter toward the anal canal. The internal anal sphincter is thin and grey-white in appearance, like a veil. By contrast, the external anal sphincter is a thick band of red striated muscle tissue. In one study of 3,333 primiparous women with OASIS, an internal anal sphincter injury was detected in 33% of cases.¹⁴ In this large cohort, the rate of internal anal sphincter injury with a 3A tear, a 3B tear, a complete tear of the external sphincter and a 4th-degree perineal tear was 22%, 23%, 42%, and 71%, respectively. The internal anal sphincter is important for maintaining rectal continence and is estimated to contribute 50% to 85% of resting anal tone.¹⁵ If injury to the internal anal sphincter is detected at a birth with an OASIS, it is important to separately repair the internal anal sphincter to reduce the risk of postpartum rectal incontinence.¹⁶

Polyglactin 910 vs Polydioxanone (PDS) Suture—Is PDS the winner?

Polyglactin 910 (Vicryl) is a braided suture that is absorbed within 56 to 70 days. Polydioxanone suture is a long-lasting monofilament suture that is absorbed within 200 days. Many colorectal surgeons and urogynecologists prefer PDS suture for the repair of both the internal and external anal sphincters.¹⁶ Authors of one randomized trial of OASIS repair with Vicryl or PDS suture did not report significant differences in most clinical outcomes.¹⁷ However, in this study, anal endosonographic imaging of the internal and external anal sphincter demonstrated more internal sphincter defects but not external sphincter defects when the repair was performed with Vicryl rather than PDS. The investigators concluded that comprehensive training of the surgeon, not choice of suture, is probably the most important factor in achieving a good OASIS repair. However, because many subspecialists favor PDS suture for sphincter repair, specialists in obstetrics and gynecology should consider this option.

Continue to: Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

The breakdown of an OASIS repair is an obstetric catastrophe with complications that can last many months and sometimes stretch into years. The best approach to a perineal laceration wound breakdown remains controversial. It is optimal if all patients with a wound breakdown can be offered an early secondary repair or healing by secondary intention, permitting the patient to select the best approach for their specific situation.

As noted by the pioneers of early repair of episiotomy dehiscence, Drs. Hankins, Haugh, Gilstrap, Ramin, and others,^18-20 conventional doctrine is that an episiotomy repair dehiscence should be managed expectantly, allowing healing by secondary intention and delaying repair of the sphincters for a minimum of 3 to 4 months.²¹ However, many small case-series report that early secondary repair of a perineal laceration wound breakdown is possible following multiple days of wound preparation prior to the repair, good surgical technique and diligent postoperative follow-up care. One large case series reported on 72 women with complete perineal wound dehiscence who had early secondary repair.²² The median time to complete wound healing following early repair was 28 days. About 36% of the patients had one or more complications, including skin dehiscence, granuloma formation, perineal pain, and sinus formation. A pilot randomized trial reported that, compared with expectant management of a wound breakdown, early repair resulted in a shorter time to wound healing.²³

Early repair of perineal wound dehiscence often involves a course of care that extends over multiple weeks. As an example, following a vaginal birth with OASIS and immediate repair, the patient is often discharged from the hospital to home on postpartum day 3. The wound breakdown often is detected between postpartum days 6 to 10. If early secondary repair is selected as the best treatment, 1 to 6 days of daily debridement of the wound is needed to prepare the wound for early secondary repair. The daily debridement required to prepare the wound for early repair is often performed in the hospital, potentially disrupting early mother-newborn bonding. Following the repair, the patient is observed in the hospital for 1 to 3 days and then discharged home with daily wound care and multiple follow-up visits to monitor wound healing. Pelvic floor physical therapy may be initiated when the wound is healed. The prolonged process required for early secondary repair may be best undertaken by a subspecialty practice.²⁴

The surgical repair and postpartum care of OASIS continues to evolve. In your practice you should consider:

• performing a mediolateral episiotomy at a 60-degree angle to reduce the risk of OASIS in situations where there is a high risk of anal sphincter injury, such as in forceps delivery
• using one dose of a prophylactic antibiotic with extended anaerobic coverage, such as cefotetan or cefoxitin
• focus on identifying and separately repairing an internal anal sphincter injury
• using a long-lasting absorbable suture, such as PDS, to repair the internal and external anal sphincters
• ensuring that the patient with a dehiscence following an episiotomy or anal sphincter injury has access to early secondary repair. Standardizing your approach to the prevention and repair of anal sphincter injury will benefit the approximately 112,600 US women who experience OASIS each year. ●

Cerebral palsy (CP) is the most common cause of severe neurodisability in children, and it occurs in about 2 to 3 per 1,000 births worldwide.¹ This nonprogressive disorder is characterized by symptoms that include spasticity, dystonia, choreoathetosis, and/or ataxia that are evident in the first few years of life. While many perinatal variables have been associated with CP, in most cases a specific cause is not identified.

Other neurodevelopmental disorders, such as intellectual disability, epilepsy, and autism spectrum disorder, are often associated with CP.² These other neurodevelopmental disorders are often genetic, and this has raised the question as to whether CP also might have a substantial genetic component, although this has not been investigated in any significant way until recently. This topic is of great interest to the obstetric community, given that CP often is attributed to obstetric events, including mismanagement of labor and delivery.

Emerging evidence of a genetic-CP association

In an article published recently in JAMA, Moreno-De-Luca and colleagues sought to determine the diagnostic yield of exome sequencing for CP.³ This large cross-sectional study included results of exome sequencing performed in 2 settings. The first setting was a commercial laboratory in which samples were sent for analysis due to a diagnosis of CP, primarily in children (n = 1,345) with a median age of 8.8 years. A second cohort, recruited from a neurodevelopmental disorders clinic at Geisinger, included primarily adults (n = 181) with a median age of 41.9 years.

As is standard in exome sequencing, results were considered likely causative if they were classified as pathogenic or likely pathogenic based on criteria of the American College of Genetics and Genomics. In the laboratory group, 32.7% (440 of 1,345) had a genetic cause of the CP identified, while in the clinic group, 10.5% (19 of 181) had a genetic etiology found. Although most of the identified genetic variants were de novo (that is, they arose in the affected individual and were not clearly inherited), some were inherited from carrier parents.³

A number of other recent studies also have investigated genetic causes of CP and similarly have reported that a substantial number of cases are genetic. Several studies that performed chromosomal microarray analysis in individuals with CP found deleterious copy number variants in 10% to 31% of cases.^4-6 Genomic variants detectable by exome sequencing have been reported in 15% to 20% of cases.³ In a recent study in Nature Genetics, researchers performed exome sequencing on 250 parent-child “trios” in which the child had CP, and they found that 14% of cases had an associated genetic variant that was thought to be causative.⁴ These studies all provide consistent evidence that a substantial proportion of CP cases are due to genetic causes.

Contributors to CP risk

Historically, CP was considered to occur largely as a result of perinatal anoxia. In 1862, the British orthopedic surgeon William John Little first reported an association between prematurity, asphyxia, difficult delivery, and CP in a paper presented to the Obstetrical Society of London.⁷ Subsequently, much effort has gone into the prevention of perinatal asphyxia and birth injury, although our ability to monitor fetal well-being remains limited. Nonreassuring fetal heart rate patterns are nonspecific and can occur for many reasons other than fetal asphyxia. Studies of electronic fetal monitoring have found that continuous monitoring primarily leads to an increase in cesarean delivery with no decrease in CP or infant mortality.⁸

While some have attributed this to failure to accurately interpret the fetal heart rate tracing, it also may be because a substantial number of CP cases are due to genetic and other causes, and that very few in fact result from preventable intrapartum injury.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics agree that knowledge gaps preclude definitive determination that a given case of neonatal encephalopathy is attributable to an acute intrapartum event, and they provide criteria that must be fulfilled to establish a reasonable causal link between an intrapartum event and subsequent long-term neurologic disability.⁹ However, there continues to be a belief in the medical, scientific, and lay communities that birth asphyxia, secondary to adverse intrapartum events, is the leading cause of CP. A “brain-damaged infant” remains one of the most common malpractice claims, and birth injury one of the highest paid claims. Such claims generally allege that intrapartum asphyxia has caused long-term neurologic sequelae, including CP.

While it is true that prematurity, infection, hypoxia-ischemia, and pre- and perinatal stroke all have been implicated as contributing to CP risk, large population-based studies have shown that birth asphyxia accounts for less than 12% of CP cases.¹⁰ Specifically, recent data indicate that acute intrapartum hypoxia-ischemia occurs only in about 6% of CP cases. In other words, it does occur and may contribute to some cases, but this is likely a smaller percent than previously thought, and genetic factors now appear to be far more significant contributors.¹¹

Continue to: Exploring a genetic etiology...

In considering the etiologies of CP, it is important to note that 21% to 40% of individuals with CP have an associated congenital anomaly, suggesting a genetic origin in at least some individuals. Moreover, a 40% heritability has been estimated in CP, which is comparable to the heritability rate for autism spectrum disorders.¹²

In the recent study by Moreno-De-Luca and colleagues, some of the gene variants detected were previously associated with other forms of neurodevelopmental disability, such as epilepsy and autism spectrum disorder.³ Many individuals in the study cohort were found to have multiple neurologic comorbidities, for example, CP as well as epilepsy, autism spectrum disorder, and/or intellectual disability. The presence of these additional comorbidities increased the likelihood of finding a genetic cause; the authors found that the diagnostic yield ranged from 11.2% with isolated CP to 32.9% with all 3 comorbidities. The yield was highest with CP and intellectual disability and CP with all 3 comorbidities. A few genes were particularly common, and some were reported previously in association with CP and/or other neurodevelopmental disorders. In some patients, variants were found in genes or gene regions associated with disorders that do not frequently include CP, such as Rett syndrome.³

Implications for ObGyns

The data from the study by Moreno-De-Luca and colleagues are interesting and relevant to pediatricians, neurologists, and geneticists, as well as obstetricians. Understanding the cause of any disease or disorder improves care, including counseling regarding the cause, the appropriate interventions or therapy, and in some families, the recurrence risk in another pregnancy. The treatment for CP has not changed significantly in many years. Increasingly, detection of an underlying genetic cause can guide precision treatments; thus, the detection of specific gene variants allows a targeted approach to therapy.

Identification of a genetic cause also can significantly impact recurrence risk counseling and prenatal diagnosis options in another pregnancy. In general, the empiric recurrence risk of CP is quoted as 1% to 2%,¹³ and with de novo variants this does not change. However, with inherited variants the recurrence risk in future children is substantially higher. While 72% of the genetic variants associated with CP in the Moreno-De-Luca study were de novo with a low recurrence risk, in the other 28% the mode of inheritance indicated a substantial risk of recurrence (25%–50%) in another pregnancy.³ Detecting such causative variant(s) allows not only accurate counseling about recurrence risk but also preimplantation genetic testing or prenatal diagnosis when recurrence risk is high.

In the field of obstetrics, the debate about the etiology of CP is important largely due to the medicolegal implications. Patient-oriented information on the internet often states that CP is caused by damage to the child’s brain just before, during, or soon after birth, supporting potential blame of those providing care during those times. Patient-oriented websites regarding CP do not list genetic disorders among the causes but rather include primarily environmental factors, such as prematurity, low birth weight, in utero infections, anoxia or other brain injury, or perinatal stroke. Even the Centers for Disease Control and Prevention website lists brain damage as the primary etiology of CP.¹⁴ Hopefully, these new data will increase a broader understanding of this condition.

Exome sequencing is now recommended as a first-tier test for individuals with many neurodevelopmental disorders, including epilepsy, intellectual disability, and autism spectrum disorder.¹⁵ However, comprehensive genetic testing is not typically recommended or performed in cases of CP. Based on recent data, including the report by Moreno-De-Luca and colleagues, it would seem that CP should be added to the list of disorders for which exome sequencing is ordered, given the similar prevalence and diagnostic yield. ●

Cerebral palsy (CP) is the most common cause of severe neurodisability in children, and it occurs in about 2 to 3 per 1,000 births worldwide.¹ This nonprogressive disorder is characterized by symptoms that include spasticity, dystonia, choreoathetosis, and/or ataxia that are evident in the first few years of life. While many perinatal variables have been associated with CP, in most cases a specific cause is not identified.

Other neurodevelopmental disorders, such as intellectual disability, epilepsy, and autism spectrum disorder, are often associated with CP.² These other neurodevelopmental disorders are often genetic, and this has raised the question as to whether CP also might have a substantial genetic component, although this has not been investigated in any significant way until recently. This topic is of great interest to the obstetric community, given that CP often is attributed to obstetric events, including mismanagement of labor and delivery.

Emerging evidence of a genetic-CP association

In an article published recently in JAMA, Moreno-De-Luca and colleagues sought to determine the diagnostic yield of exome sequencing for CP.³ This large cross-sectional study included results of exome sequencing performed in 2 settings. The first setting was a commercial laboratory in which samples were sent for analysis due to a diagnosis of CP, primarily in children (n = 1,345) with a median age of 8.8 years. A second cohort, recruited from a neurodevelopmental disorders clinic at Geisinger, included primarily adults (n = 181) with a median age of 41.9 years.

As is standard in exome sequencing, results were considered likely causative if they were classified as pathogenic or likely pathogenic based on criteria of the American College of Genetics and Genomics. In the laboratory group, 32.7% (440 of 1,345) had a genetic cause of the CP identified, while in the clinic group, 10.5% (19 of 181) had a genetic etiology found. Although most of the identified genetic variants were de novo (that is, they arose in the affected individual and were not clearly inherited), some were inherited from carrier parents.³

A number of other recent studies also have investigated genetic causes of CP and similarly have reported that a substantial number of cases are genetic. Several studies that performed chromosomal microarray analysis in individuals with CP found deleterious copy number variants in 10% to 31% of cases.^4-6 Genomic variants detectable by exome sequencing have been reported in 15% to 20% of cases.³ In a recent study in Nature Genetics, researchers performed exome sequencing on 250 parent-child “trios” in which the child had CP, and they found that 14% of cases had an associated genetic variant that was thought to be causative.⁴ These studies all provide consistent evidence that a substantial proportion of CP cases are due to genetic causes.

Contributors to CP risk

Historically, CP was considered to occur largely as a result of perinatal anoxia. In 1862, the British orthopedic surgeon William John Little first reported an association between prematurity, asphyxia, difficult delivery, and CP in a paper presented to the Obstetrical Society of London.⁷ Subsequently, much effort has gone into the prevention of perinatal asphyxia and birth injury, although our ability to monitor fetal well-being remains limited. Nonreassuring fetal heart rate patterns are nonspecific and can occur for many reasons other than fetal asphyxia. Studies of electronic fetal monitoring have found that continuous monitoring primarily leads to an increase in cesarean delivery with no decrease in CP or infant mortality.⁸

While some have attributed this to failure to accurately interpret the fetal heart rate tracing, it also may be because a substantial number of CP cases are due to genetic and other causes, and that very few in fact result from preventable intrapartum injury.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics agree that knowledge gaps preclude definitive determination that a given case of neonatal encephalopathy is attributable to an acute intrapartum event, and they provide criteria that must be fulfilled to establish a reasonable causal link between an intrapartum event and subsequent long-term neurologic disability.⁹ However, there continues to be a belief in the medical, scientific, and lay communities that birth asphyxia, secondary to adverse intrapartum events, is the leading cause of CP. A “brain-damaged infant” remains one of the most common malpractice claims, and birth injury one of the highest paid claims. Such claims generally allege that intrapartum asphyxia has caused long-term neurologic sequelae, including CP.

While it is true that prematurity, infection, hypoxia-ischemia, and pre- and perinatal stroke all have been implicated as contributing to CP risk, large population-based studies have shown that birth asphyxia accounts for less than 12% of CP cases.¹⁰ Specifically, recent data indicate that acute intrapartum hypoxia-ischemia occurs only in about 6% of CP cases. In other words, it does occur and may contribute to some cases, but this is likely a smaller percent than previously thought, and genetic factors now appear to be far more significant contributors.¹¹

Continue to: Exploring a genetic etiology...

In considering the etiologies of CP, it is important to note that 21% to 40% of individuals with CP have an associated congenital anomaly, suggesting a genetic origin in at least some individuals. Moreover, a 40% heritability has been estimated in CP, which is comparable to the heritability rate for autism spectrum disorders.¹²

In the recent study by Moreno-De-Luca and colleagues, some of the gene variants detected were previously associated with other forms of neurodevelopmental disability, such as epilepsy and autism spectrum disorder.³ Many individuals in the study cohort were found to have multiple neurologic comorbidities, for example, CP as well as epilepsy, autism spectrum disorder, and/or intellectual disability. The presence of these additional comorbidities increased the likelihood of finding a genetic cause; the authors found that the diagnostic yield ranged from 11.2% with isolated CP to 32.9% with all 3 comorbidities. The yield was highest with CP and intellectual disability and CP with all 3 comorbidities. A few genes were particularly common, and some were reported previously in association with CP and/or other neurodevelopmental disorders. In some patients, variants were found in genes or gene regions associated with disorders that do not frequently include CP, such as Rett syndrome.³

Implications for ObGyns

The data from the study by Moreno-De-Luca and colleagues are interesting and relevant to pediatricians, neurologists, and geneticists, as well as obstetricians. Understanding the cause of any disease or disorder improves care, including counseling regarding the cause, the appropriate interventions or therapy, and in some families, the recurrence risk in another pregnancy. The treatment for CP has not changed significantly in many years. Increasingly, detection of an underlying genetic cause can guide precision treatments; thus, the detection of specific gene variants allows a targeted approach to therapy.

Identification of a genetic cause also can significantly impact recurrence risk counseling and prenatal diagnosis options in another pregnancy. In general, the empiric recurrence risk of CP is quoted as 1% to 2%,¹³ and with de novo variants this does not change. However, with inherited variants the recurrence risk in future children is substantially higher. While 72% of the genetic variants associated with CP in the Moreno-De-Luca study were de novo with a low recurrence risk, in the other 28% the mode of inheritance indicated a substantial risk of recurrence (25%–50%) in another pregnancy.³ Detecting such causative variant(s) allows not only accurate counseling about recurrence risk but also preimplantation genetic testing or prenatal diagnosis when recurrence risk is high.

In the field of obstetrics, the debate about the etiology of CP is important largely due to the medicolegal implications. Patient-oriented information on the internet often states that CP is caused by damage to the child’s brain just before, during, or soon after birth, supporting potential blame of those providing care during those times. Patient-oriented websites regarding CP do not list genetic disorders among the causes but rather include primarily environmental factors, such as prematurity, low birth weight, in utero infections, anoxia or other brain injury, or perinatal stroke. Even the Centers for Disease Control and Prevention website lists brain damage as the primary etiology of CP.¹⁴ Hopefully, these new data will increase a broader understanding of this condition.

Exome sequencing is now recommended as a first-tier test for individuals with many neurodevelopmental disorders, including epilepsy, intellectual disability, and autism spectrum disorder.¹⁵ However, comprehensive genetic testing is not typically recommended or performed in cases of CP. Based on recent data, including the report by Moreno-De-Luca and colleagues, it would seem that CP should be added to the list of disorders for which exome sequencing is ordered, given the similar prevalence and diagnostic yield. ●

Cerebral palsy (CP) is the most common cause of severe neurodisability in children, and it occurs in about 2 to 3 per 1,000 births worldwide.¹ This nonprogressive disorder is characterized by symptoms that include spasticity, dystonia, choreoathetosis, and/or ataxia that are evident in the first few years of life. While many perinatal variables have been associated with CP, in most cases a specific cause is not identified.

Other neurodevelopmental disorders, such as intellectual disability, epilepsy, and autism spectrum disorder, are often associated with CP.² These other neurodevelopmental disorders are often genetic, and this has raised the question as to whether CP also might have a substantial genetic component, although this has not been investigated in any significant way until recently. This topic is of great interest to the obstetric community, given that CP often is attributed to obstetric events, including mismanagement of labor and delivery.

Emerging evidence of a genetic-CP association

In an article published recently in JAMA, Moreno-De-Luca and colleagues sought to determine the diagnostic yield of exome sequencing for CP.³ This large cross-sectional study included results of exome sequencing performed in 2 settings. The first setting was a commercial laboratory in which samples were sent for analysis due to a diagnosis of CP, primarily in children (n = 1,345) with a median age of 8.8 years. A second cohort, recruited from a neurodevelopmental disorders clinic at Geisinger, included primarily adults (n = 181) with a median age of 41.9 years.

As is standard in exome sequencing, results were considered likely causative if they were classified as pathogenic or likely pathogenic based on criteria of the American College of Genetics and Genomics. In the laboratory group, 32.7% (440 of 1,345) had a genetic cause of the CP identified, while in the clinic group, 10.5% (19 of 181) had a genetic etiology found. Although most of the identified genetic variants were de novo (that is, they arose in the affected individual and were not clearly inherited), some were inherited from carrier parents.³

A number of other recent studies also have investigated genetic causes of CP and similarly have reported that a substantial number of cases are genetic. Several studies that performed chromosomal microarray analysis in individuals with CP found deleterious copy number variants in 10% to 31% of cases.^4-6 Genomic variants detectable by exome sequencing have been reported in 15% to 20% of cases.³ In a recent study in Nature Genetics, researchers performed exome sequencing on 250 parent-child “trios” in which the child had CP, and they found that 14% of cases had an associated genetic variant that was thought to be causative.⁴ These studies all provide consistent evidence that a substantial proportion of CP cases are due to genetic causes.

Contributors to CP risk

Historically, CP was considered to occur largely as a result of perinatal anoxia. In 1862, the British orthopedic surgeon William John Little first reported an association between prematurity, asphyxia, difficult delivery, and CP in a paper presented to the Obstetrical Society of London.⁷ Subsequently, much effort has gone into the prevention of perinatal asphyxia and birth injury, although our ability to monitor fetal well-being remains limited. Nonreassuring fetal heart rate patterns are nonspecific and can occur for many reasons other than fetal asphyxia. Studies of electronic fetal monitoring have found that continuous monitoring primarily leads to an increase in cesarean delivery with no decrease in CP or infant mortality.⁸

While some have attributed this to failure to accurately interpret the fetal heart rate tracing, it also may be because a substantial number of CP cases are due to genetic and other causes, and that very few in fact result from preventable intrapartum injury.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics agree that knowledge gaps preclude definitive determination that a given case of neonatal encephalopathy is attributable to an acute intrapartum event, and they provide criteria that must be fulfilled to establish a reasonable causal link between an intrapartum event and subsequent long-term neurologic disability.⁹ However, there continues to be a belief in the medical, scientific, and lay communities that birth asphyxia, secondary to adverse intrapartum events, is the leading cause of CP. A “brain-damaged infant” remains one of the most common malpractice claims, and birth injury one of the highest paid claims. Such claims generally allege that intrapartum asphyxia has caused long-term neurologic sequelae, including CP.

While it is true that prematurity, infection, hypoxia-ischemia, and pre- and perinatal stroke all have been implicated as contributing to CP risk, large population-based studies have shown that birth asphyxia accounts for less than 12% of CP cases.¹⁰ Specifically, recent data indicate that acute intrapartum hypoxia-ischemia occurs only in about 6% of CP cases. In other words, it does occur and may contribute to some cases, but this is likely a smaller percent than previously thought, and genetic factors now appear to be far more significant contributors.¹¹

Continue to: Exploring a genetic etiology...

In considering the etiologies of CP, it is important to note that 21% to 40% of individuals with CP have an associated congenital anomaly, suggesting a genetic origin in at least some individuals. Moreover, a 40% heritability has been estimated in CP, which is comparable to the heritability rate for autism spectrum disorders.¹²

In the recent study by Moreno-De-Luca and colleagues, some of the gene variants detected were previously associated with other forms of neurodevelopmental disability, such as epilepsy and autism spectrum disorder.³ Many individuals in the study cohort were found to have multiple neurologic comorbidities, for example, CP as well as epilepsy, autism spectrum disorder, and/or intellectual disability. The presence of these additional comorbidities increased the likelihood of finding a genetic cause; the authors found that the diagnostic yield ranged from 11.2% with isolated CP to 32.9% with all 3 comorbidities. The yield was highest with CP and intellectual disability and CP with all 3 comorbidities. A few genes were particularly common, and some were reported previously in association with CP and/or other neurodevelopmental disorders. In some patients, variants were found in genes or gene regions associated with disorders that do not frequently include CP, such as Rett syndrome.³

Implications for ObGyns

The data from the study by Moreno-De-Luca and colleagues are interesting and relevant to pediatricians, neurologists, and geneticists, as well as obstetricians. Understanding the cause of any disease or disorder improves care, including counseling regarding the cause, the appropriate interventions or therapy, and in some families, the recurrence risk in another pregnancy. The treatment for CP has not changed significantly in many years. Increasingly, detection of an underlying genetic cause can guide precision treatments; thus, the detection of specific gene variants allows a targeted approach to therapy.

Identification of a genetic cause also can significantly impact recurrence risk counseling and prenatal diagnosis options in another pregnancy. In general, the empiric recurrence risk of CP is quoted as 1% to 2%,¹³ and with de novo variants this does not change. However, with inherited variants the recurrence risk in future children is substantially higher. While 72% of the genetic variants associated with CP in the Moreno-De-Luca study were de novo with a low recurrence risk, in the other 28% the mode of inheritance indicated a substantial risk of recurrence (25%–50%) in another pregnancy.³ Detecting such causative variant(s) allows not only accurate counseling about recurrence risk but also preimplantation genetic testing or prenatal diagnosis when recurrence risk is high.

In the field of obstetrics, the debate about the etiology of CP is important largely due to the medicolegal implications. Patient-oriented information on the internet often states that CP is caused by damage to the child’s brain just before, during, or soon after birth, supporting potential blame of those providing care during those times. Patient-oriented websites regarding CP do not list genetic disorders among the causes but rather include primarily environmental factors, such as prematurity, low birth weight, in utero infections, anoxia or other brain injury, or perinatal stroke. Even the Centers for Disease Control and Prevention website lists brain damage as the primary etiology of CP.¹⁴ Hopefully, these new data will increase a broader understanding of this condition.

Exome sequencing is now recommended as a first-tier test for individuals with many neurodevelopmental disorders, including epilepsy, intellectual disability, and autism spectrum disorder.¹⁵ However, comprehensive genetic testing is not typically recommended or performed in cases of CP. Based on recent data, including the report by Moreno-De-Luca and colleagues, it would seem that CP should be added to the list of disorders for which exome sequencing is ordered, given the similar prevalence and diagnostic yield. ●

Obesity affects approximately 30% of American women, and while it is easy to diagnose, it is often difficult to address with our patients. Healthy eating and regular physical activity are the time-tested ways to achieve and maintain an appropriate weight.

For women with moderate obesity, leveraging technology is a great way to help them sensibly achieve weight loss. To evaluate the quality of a mobile app targeted to address obesity, it is particularly important to consider an app’s usefulness, functionality, and design. Clinicians can evaluate these elements with the use of the ACOG-recommended rubric, which provides criteria for judging usefulness, accuracy, authority, objectivity, timeliness, functionality, design, security, and value.

Obesity app considerations

A particularly valuable app feature that rates high on the usefulness measure is the capability for real-time motivational guidance that encourages the user to meet her daily goals. The ability to quickly and accurately scan and upload food items to an app and quantify portions using common comparative illustrations for measurement would give an app a high score on functionality. Coveted design features to enhance the user’s experience, such as syncing real time with wearable devices and catering to both visual and text learners, increase the value of an app.

In addition, an app with the combined features of a personal dietitian and a fitness trainer can employ techniques to encourage healthy eating and physical activity to self-monitor food intake and exercise. Features that calculate the user’s calorie level based on age, sex, height, and activity and offer a personalized dashboard to track carbohydrates, proteins, and fat breakdown (including nutrients and water intake) also can increase effectiveness. These features engage users to become more motivated toward an active lifestyle to balance food intake.

By incorporating apps that combine behavioral strategies with individualization, community presence, and feedback, we can successfully partner with our patients to address obesity. ●

Obesity affects approximately 30% of American women, and while it is easy to diagnose, it is often difficult to address with our patients. Healthy eating and regular physical activity are the time-tested ways to achieve and maintain an appropriate weight.

For women with moderate obesity, leveraging technology is a great way to help them sensibly achieve weight loss. To evaluate the quality of a mobile app targeted to address obesity, it is particularly important to consider an app’s usefulness, functionality, and design. Clinicians can evaluate these elements with the use of the ACOG-recommended rubric, which provides criteria for judging usefulness, accuracy, authority, objectivity, timeliness, functionality, design, security, and value.

Obesity app considerations

A particularly valuable app feature that rates high on the usefulness measure is the capability for real-time motivational guidance that encourages the user to meet her daily goals. The ability to quickly and accurately scan and upload food items to an app and quantify portions using common comparative illustrations for measurement would give an app a high score on functionality. Coveted design features to enhance the user’s experience, such as syncing real time with wearable devices and catering to both visual and text learners, increase the value of an app.

In addition, an app with the combined features of a personal dietitian and a fitness trainer can employ techniques to encourage healthy eating and physical activity to self-monitor food intake and exercise. Features that calculate the user’s calorie level based on age, sex, height, and activity and offer a personalized dashboard to track carbohydrates, proteins, and fat breakdown (including nutrients and water intake) also can increase effectiveness. These features engage users to become more motivated toward an active lifestyle to balance food intake.

By incorporating apps that combine behavioral strategies with individualization, community presence, and feedback, we can successfully partner with our patients to address obesity. ●

Obesity affects approximately 30% of American women, and while it is easy to diagnose, it is often difficult to address with our patients. Healthy eating and regular physical activity are the time-tested ways to achieve and maintain an appropriate weight.

For women with moderate obesity, leveraging technology is a great way to help them sensibly achieve weight loss. To evaluate the quality of a mobile app targeted to address obesity, it is particularly important to consider an app’s usefulness, functionality, and design. Clinicians can evaluate these elements with the use of the ACOG-recommended rubric, which provides criteria for judging usefulness, accuracy, authority, objectivity, timeliness, functionality, design, security, and value.

Obesity app considerations

A particularly valuable app feature that rates high on the usefulness measure is the capability for real-time motivational guidance that encourages the user to meet her daily goals. The ability to quickly and accurately scan and upload food items to an app and quantify portions using common comparative illustrations for measurement would give an app a high score on functionality. Coveted design features to enhance the user’s experience, such as syncing real time with wearable devices and catering to both visual and text learners, increase the value of an app.

In addition, an app with the combined features of a personal dietitian and a fitness trainer can employ techniques to encourage healthy eating and physical activity to self-monitor food intake and exercise. Features that calculate the user’s calorie level based on age, sex, height, and activity and offer a personalized dashboard to track carbohydrates, proteins, and fat breakdown (including nutrients and water intake) also can increase effectiveness. These features engage users to become more motivated toward an active lifestyle to balance food intake.

By incorporating apps that combine behavioral strategies with individualization, community presence, and feedback, we can successfully partner with our patients to address obesity. ●

FDA guidance for power morcellation

“The FDA has granted marketing authorization for one containment system and continues to encourage innovation in this area” said the report. Olympus’ Pneumoliner is the only FDA cleared containment device to provide a laparoscopic option for appropriately identified patients undergoing myomectomy and hysterectomy. The containment system is sold with Olympus’ PK Morcellator, but the company says that it has made the Pneumoliner available to physicians choosing an alternate to the PK Morcellator, provided that there is device compatibility. The Pneumoliner “reduces the spread of benign tissue into the abdominal cavity, in which pathologies, like fibroids, may regrow when tissue or cells are inadvertently left behind,” according to Olympus.

For more information, visit : https://medical.olympusamerica.com/products/contained-tissue-extraction-system

Vaginal odor elimination gel

The gel is sold in 7 single-day applications, with a single tube used per day at bedtime to eliminate unwanted odor. To maintain freshness and comfort, a single tube of Relactagel can be used for 2 to 3 days after a woman’s menstrual cycle, says Kora Healthcare. The company warns that mild irritation can occur with product use during fungal infections or when small tears are present in the vaginal tissue and that use should be discontinued if irritation occurs. In addition, if trying to become pregnant Relatagel should not be used, advises Kora Healthcare, although the gel is not a contraceptive.

For more information, visit: https://www.relactagel.com/.

Intrauterine electrosurgery system

For more information, visit: https://medical.olympusamerica.com/

FDA guidance for power morcellation

“The FDA has granted marketing authorization for one containment system and continues to encourage innovation in this area” said the report. Olympus’ Pneumoliner is the only FDA cleared containment device to provide a laparoscopic option for appropriately identified patients undergoing myomectomy and hysterectomy. The containment system is sold with Olympus’ PK Morcellator, but the company says that it has made the Pneumoliner available to physicians choosing an alternate to the PK Morcellator, provided that there is device compatibility. The Pneumoliner “reduces the spread of benign tissue into the abdominal cavity, in which pathologies, like fibroids, may regrow when tissue or cells are inadvertently left behind,” according to Olympus.

For more information, visit : https://medical.olympusamerica.com/products/contained-tissue-extraction-system

Vaginal odor elimination gel

The gel is sold in 7 single-day applications, with a single tube used per day at bedtime to eliminate unwanted odor. To maintain freshness and comfort, a single tube of Relactagel can be used for 2 to 3 days after a woman’s menstrual cycle, says Kora Healthcare. The company warns that mild irritation can occur with product use during fungal infections or when small tears are present in the vaginal tissue and that use should be discontinued if irritation occurs. In addition, if trying to become pregnant Relatagel should not be used, advises Kora Healthcare, although the gel is not a contraceptive.

For more information, visit: https://www.relactagel.com/.

Intrauterine electrosurgery system

For more information, visit: https://medical.olympusamerica.com/

FDA guidance for power morcellation

“The FDA has granted marketing authorization for one containment system and continues to encourage innovation in this area” said the report. Olympus’ Pneumoliner is the only FDA cleared containment device to provide a laparoscopic option for appropriately identified patients undergoing myomectomy and hysterectomy. The containment system is sold with Olympus’ PK Morcellator, but the company says that it has made the Pneumoliner available to physicians choosing an alternate to the PK Morcellator, provided that there is device compatibility. The Pneumoliner “reduces the spread of benign tissue into the abdominal cavity, in which pathologies, like fibroids, may regrow when tissue or cells are inadvertently left behind,” according to Olympus.

For more information, visit : https://medical.olympusamerica.com/products/contained-tissue-extraction-system

Vaginal odor elimination gel

The gel is sold in 7 single-day applications, with a single tube used per day at bedtime to eliminate unwanted odor. To maintain freshness and comfort, a single tube of Relactagel can be used for 2 to 3 days after a woman’s menstrual cycle, says Kora Healthcare. The company warns that mild irritation can occur with product use during fungal infections or when small tears are present in the vaginal tissue and that use should be discontinued if irritation occurs. In addition, if trying to become pregnant Relatagel should not be used, advises Kora Healthcare, although the gel is not a contraceptive.

For more information, visit: https://www.relactagel.com/.

Intrauterine electrosurgery system

For more information, visit: https://medical.olympusamerica.com/

Female genital cutting (FGC), also known as female circumcision or female genital mutilation, is defined by the World Health Organization (WHO) as “the partial or total removal of the external female genitalia, or other injury to the female genital organs for non-medical reasons.”¹ It is a culturally determined practice that is mainly concentrated in certain parts of Africa, the Middle East, and Asia and now is observed worldwide among migrants from those areas.¹ Approximately 200 million women and girls alive today have undergone FGC in 31 countries, although encouragingly the practice’s prevalence seems to be declining, especially among younger women.²

Too often, FGC goes unrecognized in women who present for medical care, even in cases where a genitourinary exam is performed and documented.^3,4 As a result, patients face delays in diagnosis and management of associated complications and symptoms. Female genital cutting is usually excluded from medical school or residency training curricula,⁵ and physicians often lack familiarity with the necessary clinical or surgical management of patients who have had the procedure.⁶ It is crucial, however, that ObGyns feel comfortable recognizing FGC and clinically caring for pregnant and nonpregnant patients who have undergone the procedure. The obstetric-gynecologic setting should be the clinical space in which FGC is correctly diagnosed and from where patients with complications can be referred for appropriate care.

FGC: Through the lens of inequity

Providing culturally competent and sensitive care to women who have undergone FGC is paramount to reducing health care inequities for these patients. Beyond the medical recommendations we review below, we suggest the following considerations when approaching care for these patients.

Acknowledge our biases. It is paramount for us, as providers, to acknowledge our own biases and how these might affect our relationship with the patient and how our care is received. This starts with our language and terminology: The term female genital mutilation can be judgmental or offensive to our patients, many of whom do not consider themselves to have been mutilated. This is why we prefer to use the term female genital cutting, or whichever word the patient uses, so as not to alienate a patient who might already face many other barriers and microaggressions in seeking health care.

Control our responses. Another way we must check our bias is by controlling our reactions during history taking or examining patients who have undergone FGC. Understandably, providers might be shocked to hear patients recount their childhood experiences of FGC or by examining an infibulated scar, but patients report noticing and experiencing hurt, distress, and shame when providers display judgment, horror, or disgust.⁷ Patients have reported that they are acutely aware that they might be viewed as “backward” and “primitive” in US health care settings.⁸ These kinds of feelings and experiences can further exacerbate patients’ distrust and avoidance of the health care system altogether. Therefore, providers should acknowledge their own biases regarding the issue as well as those of their staff and work to mitigate them.

Avoid stigmatization. While FGC can have long-term effects (discussed below), it is important to remember that many women who have undergone FGC do not experience symptoms that are bothersome or feel that FGC is central to their lives or lived experiences. While we must be thorough in our history taking to explore possible urinary, gynecologic, and sexual symptoms of concern and bother to the patient, we must avoid stigmatizing our patients by assuming that all who have undergone FGC are “sexually disabled,” which may lead a provider to recommend medically unindicated intervention, such as clitoral reconstruction.⁹

Continue to: Classifying FGC types...

Classifying FGC types

The WHO has classified FGC into 4 different types¹:

• type 1, partial or total removal of the clitoris or prepuce
• type 2, partial or total removal of part of the clitoris and labia minora
• type 3 (also known as infibulation), the narrowing of the vaginal orifice by cutting, removing, and/or repositioning the labia, and
• type 4, all other procedures to the female genitalia for nonmedical reasons.

Long-term complications

Female genital cutting, especially types 2 and 3, can lead to long-term obstetric and gynecologic complications that the ObGyn should be able to diagnose and manage (TABLE).

The most common long-term complications of FGC are dysmenorrhea, dyspareunia, recurrent vaginal and urinary tract infections, and sexual dysfunction/dissatisfaction.¹⁰ One recent cross-sectional study that used validated questionnaires on pelvic floor and psychosexual symptoms found that women with FGC had higher distress scores than women who had not undergone FGC, indicating various pelvic floor symptoms responsible for impact on their daily lives.¹¹

Infertility can result from a combination of physical barriers (vaginal stenosis and an infibulated scar) and psychologic barriers secondary to dyspareunia, for example.¹² Labor and delivery also presents a challenge to both patients and providers, especially in cases of infibulation. Studies show that patients who have undergone FGC are at increased risk of adverse obstetric outcomes, including postpartum hemorrhage, episiotomy, cesarean delivery, and extended hospital stay.¹³ Neonatal complications, including infant resuscitation and perinatal death, are more commonly reported in studies outside the United States.¹³

Clinical management recommendations

It is important to be aware of the WHO FCG classifications and be able to recognize evidence of the procedure on examination. The ObGyn should perform a detailed physical exam of the external genitalia as well as a pelvic floor exam of every patient. If the patient does not disclose a history of FGC but it is suspected based on the examination, the clinician should inquire sensitively if the patient is aware of having undergone any genital procedures.

Especially when a history of FGC has been confirmed, clinicians should ask patients sensitively about their urinary and sexual function and satisfaction. Validated tools, such as the Female Sexual Function Index, the Female Sexual Distress Scale, and the Pelvic Floor Disability Index, may be helpful in gathering an objective and detailed assessment of the patient’s symptoms and level of distress.¹⁴ Clinicians also should ask about the patient’s detailed obstetric history, particularly regarding the second stage, delivery, and postpartum complications. The clinician also should specifically inquire about a history of defibulation or additional genital procedures.

Patients with urethral strictures or stenosis may require an exam under anesthesia, cystoscopy, urethral dilation, or urethroplasty.¹² Those with chronic urinary tract or vaginal infections may require chronic oral suppressive therapy or defibulation (described below). Defibulation also may be considered for relief of severe dysmenorrhea and menorrhagia that may be resulting from hematocolpos. The ObGyn also should make certain to evaluate for other common causes of these symptoms that may be unrelated to FGC, such as endometriosis.

Many women who have undergone FGC do not report dyspareunia or sexual dissatisfaction; however, infibulation especially has been associated with higher rates of these sequelae.¹² In addition to defibulation, pelvic floor physical therapy with an experienced therapist may be helpful for patients with pelvic floor dysfunction, vaginismus, and/or dyspareunia.

The defibulation procedure

Defibulation (or deinfibulation) is a surgical reconstructive procedure that opens the infibulated scar of patients who have undergone type 3 FGC (infibulation), thus exposing the urethra and introitus, and in almost half of cases an intact clitoris.¹⁵ Defibulation may be specifically requested by a patient or it may be recommended by the ObGyn either for reducing complications of pregnancy or to address the patient’s gynecologic, sexual, or urogynecologic symptoms by allowing penetrative intercourse, urinary flow, physiologic delivery, and menstruation.¹⁶

Defibulation should be performed under regional or general anesthesia and can be performed during pregnancy (or even in labor). An anterior incision is made on the infibulated scar, creating a new labia major, and the edges are sutured separately. Postoperatively, patients should be instructed to perform sitz baths and to expect a change in their urinary voiding stream.¹² The few studies that have evaluated defibulation have shown high rates of success in addressing preoperative symptoms; the complication rates of defibulation are low and the satisfaction rates are high.¹⁶

The ethical conundrum of reinfibulation

Reinfibulation is defined as the restitching or reapproximation of scar tissue or the labia after delivery or a gynecologic procedure, and it is often performed routinely after every delivery in patients’ countries of origin.¹⁷

Postpartum reinfibulation on patient request raises legal and ethical issues for the ObGyn. In the United Kingdom, reinfibulation is illegal, and some international organizations, including the International Federation of Gynecology and Obstetrics and the WHO, have recommended against the practice. In the United States, reinfibulation of an adult is legal, as it falls under the umbrella of elective female genital cosmetic surgery.^18,19

The procedure could create or exacerbate long-term complications and should generally be discouraged. However, if despite extensive counseling (preferably in the prenatal period) a patient insists on having the procedure, the ObGyn may need to elevate the principle of patient autonomy and either comply or find a practitioner who is comfortable performing it. One retrospective review in Switzerland suggested that specific care and informative counseling prenatally with the inclusion of a patient’s partner in the discussion can improve the acceptability of defibulation without reinfibulation.²⁰

Conclusion

It is important for ObGyns to be familiar with the practice of FGC and to be trained in its recognition on examination and care for the long-term complications that can result from the practice. At the same time, ObGyns should be especially conscious of their biases in order to provide culturally competent care and reduce health care stigmatization and inequities for these patients.

Female genital cutting (FGC), also known as female circumcision or female genital mutilation, is defined by the World Health Organization (WHO) as “the partial or total removal of the external female genitalia, or other injury to the female genital organs for non-medical reasons.”¹ It is a culturally determined practice that is mainly concentrated in certain parts of Africa, the Middle East, and Asia and now is observed worldwide among migrants from those areas.¹ Approximately 200 million women and girls alive today have undergone FGC in 31 countries, although encouragingly the practice’s prevalence seems to be declining, especially among younger women.²

Too often, FGC goes unrecognized in women who present for medical care, even in cases where a genitourinary exam is performed and documented.^3,4 As a result, patients face delays in diagnosis and management of associated complications and symptoms. Female genital cutting is usually excluded from medical school or residency training curricula,⁵ and physicians often lack familiarity with the necessary clinical or surgical management of patients who have had the procedure.⁶ It is crucial, however, that ObGyns feel comfortable recognizing FGC and clinically caring for pregnant and nonpregnant patients who have undergone the procedure. The obstetric-gynecologic setting should be the clinical space in which FGC is correctly diagnosed and from where patients with complications can be referred for appropriate care.

FGC: Through the lens of inequity

Providing culturally competent and sensitive care to women who have undergone FGC is paramount to reducing health care inequities for these patients. Beyond the medical recommendations we review below, we suggest the following considerations when approaching care for these patients.

Acknowledge our biases. It is paramount for us, as providers, to acknowledge our own biases and how these might affect our relationship with the patient and how our care is received. This starts with our language and terminology: The term female genital mutilation can be judgmental or offensive to our patients, many of whom do not consider themselves to have been mutilated. This is why we prefer to use the term female genital cutting, or whichever word the patient uses, so as not to alienate a patient who might already face many other barriers and microaggressions in seeking health care.

Control our responses. Another way we must check our bias is by controlling our reactions during history taking or examining patients who have undergone FGC. Understandably, providers might be shocked to hear patients recount their childhood experiences of FGC or by examining an infibulated scar, but patients report noticing and experiencing hurt, distress, and shame when providers display judgment, horror, or disgust.⁷ Patients have reported that they are acutely aware that they might be viewed as “backward” and “primitive” in US health care settings.⁸ These kinds of feelings and experiences can further exacerbate patients’ distrust and avoidance of the health care system altogether. Therefore, providers should acknowledge their own biases regarding the issue as well as those of their staff and work to mitigate them.

Avoid stigmatization. While FGC can have long-term effects (discussed below), it is important to remember that many women who have undergone FGC do not experience symptoms that are bothersome or feel that FGC is central to their lives or lived experiences. While we must be thorough in our history taking to explore possible urinary, gynecologic, and sexual symptoms of concern and bother to the patient, we must avoid stigmatizing our patients by assuming that all who have undergone FGC are “sexually disabled,” which may lead a provider to recommend medically unindicated intervention, such as clitoral reconstruction.⁹

Continue to: Classifying FGC types...

Classifying FGC types

The WHO has classified FGC into 4 different types¹:

• type 1, partial or total removal of the clitoris or prepuce
• type 2, partial or total removal of part of the clitoris and labia minora
• type 3 (also known as infibulation), the narrowing of the vaginal orifice by cutting, removing, and/or repositioning the labia, and
• type 4, all other procedures to the female genitalia for nonmedical reasons.

Long-term complications

Female genital cutting, especially types 2 and 3, can lead to long-term obstetric and gynecologic complications that the ObGyn should be able to diagnose and manage (TABLE).

The most common long-term complications of FGC are dysmenorrhea, dyspareunia, recurrent vaginal and urinary tract infections, and sexual dysfunction/dissatisfaction.¹⁰ One recent cross-sectional study that used validated questionnaires on pelvic floor and psychosexual symptoms found that women with FGC had higher distress scores than women who had not undergone FGC, indicating various pelvic floor symptoms responsible for impact on their daily lives.¹¹

Infertility can result from a combination of physical barriers (vaginal stenosis and an infibulated scar) and psychologic barriers secondary to dyspareunia, for example.¹² Labor and delivery also presents a challenge to both patients and providers, especially in cases of infibulation. Studies show that patients who have undergone FGC are at increased risk of adverse obstetric outcomes, including postpartum hemorrhage, episiotomy, cesarean delivery, and extended hospital stay.¹³ Neonatal complications, including infant resuscitation and perinatal death, are more commonly reported in studies outside the United States.¹³

Clinical management recommendations

It is important to be aware of the WHO FCG classifications and be able to recognize evidence of the procedure on examination. The ObGyn should perform a detailed physical exam of the external genitalia as well as a pelvic floor exam of every patient. If the patient does not disclose a history of FGC but it is suspected based on the examination, the clinician should inquire sensitively if the patient is aware of having undergone any genital procedures.

Especially when a history of FGC has been confirmed, clinicians should ask patients sensitively about their urinary and sexual function and satisfaction. Validated tools, such as the Female Sexual Function Index, the Female Sexual Distress Scale, and the Pelvic Floor Disability Index, may be helpful in gathering an objective and detailed assessment of the patient’s symptoms and level of distress.¹⁴ Clinicians also should ask about the patient’s detailed obstetric history, particularly regarding the second stage, delivery, and postpartum complications. The clinician also should specifically inquire about a history of defibulation or additional genital procedures.

Patients with urethral strictures or stenosis may require an exam under anesthesia, cystoscopy, urethral dilation, or urethroplasty.¹² Those with chronic urinary tract or vaginal infections may require chronic oral suppressive therapy or defibulation (described below). Defibulation also may be considered for relief of severe dysmenorrhea and menorrhagia that may be resulting from hematocolpos. The ObGyn also should make certain to evaluate for other common causes of these symptoms that may be unrelated to FGC, such as endometriosis.

Many women who have undergone FGC do not report dyspareunia or sexual dissatisfaction; however, infibulation especially has been associated with higher rates of these sequelae.¹² In addition to defibulation, pelvic floor physical therapy with an experienced therapist may be helpful for patients with pelvic floor dysfunction, vaginismus, and/or dyspareunia.

The defibulation procedure

Defibulation (or deinfibulation) is a surgical reconstructive procedure that opens the infibulated scar of patients who have undergone type 3 FGC (infibulation), thus exposing the urethra and introitus, and in almost half of cases an intact clitoris.¹⁵ Defibulation may be specifically requested by a patient or it may be recommended by the ObGyn either for reducing complications of pregnancy or to address the patient’s gynecologic, sexual, or urogynecologic symptoms by allowing penetrative intercourse, urinary flow, physiologic delivery, and menstruation.¹⁶

Defibulation should be performed under regional or general anesthesia and can be performed during pregnancy (or even in labor). An anterior incision is made on the infibulated scar, creating a new labia major, and the edges are sutured separately. Postoperatively, patients should be instructed to perform sitz baths and to expect a change in their urinary voiding stream.¹² The few studies that have evaluated defibulation have shown high rates of success in addressing preoperative symptoms; the complication rates of defibulation are low and the satisfaction rates are high.¹⁶

The ethical conundrum of reinfibulation

Reinfibulation is defined as the restitching or reapproximation of scar tissue or the labia after delivery or a gynecologic procedure, and it is often performed routinely after every delivery in patients’ countries of origin.¹⁷

Postpartum reinfibulation on patient request raises legal and ethical issues for the ObGyn. In the United Kingdom, reinfibulation is illegal, and some international organizations, including the International Federation of Gynecology and Obstetrics and the WHO, have recommended against the practice. In the United States, reinfibulation of an adult is legal, as it falls under the umbrella of elective female genital cosmetic surgery.^18,19

The procedure could create or exacerbate long-term complications and should generally be discouraged. However, if despite extensive counseling (preferably in the prenatal period) a patient insists on having the procedure, the ObGyn may need to elevate the principle of patient autonomy and either comply or find a practitioner who is comfortable performing it. One retrospective review in Switzerland suggested that specific care and informative counseling prenatally with the inclusion of a patient’s partner in the discussion can improve the acceptability of defibulation without reinfibulation.²⁰

Conclusion

It is important for ObGyns to be familiar with the practice of FGC and to be trained in its recognition on examination and care for the long-term complications that can result from the practice. At the same time, ObGyns should be especially conscious of their biases in order to provide culturally competent care and reduce health care stigmatization and inequities for these patients.

Female genital cutting (FGC), also known as female circumcision or female genital mutilation, is defined by the World Health Organization (WHO) as “the partial or total removal of the external female genitalia, or other injury to the female genital organs for non-medical reasons.”¹ It is a culturally determined practice that is mainly concentrated in certain parts of Africa, the Middle East, and Asia and now is observed worldwide among migrants from those areas.¹ Approximately 200 million women and girls alive today have undergone FGC in 31 countries, although encouragingly the practice’s prevalence seems to be declining, especially among younger women.²

Too often, FGC goes unrecognized in women who present for medical care, even in cases where a genitourinary exam is performed and documented.^3,4 As a result, patients face delays in diagnosis and management of associated complications and symptoms. Female genital cutting is usually excluded from medical school or residency training curricula,⁵ and physicians often lack familiarity with the necessary clinical or surgical management of patients who have had the procedure.⁶ It is crucial, however, that ObGyns feel comfortable recognizing FGC and clinically caring for pregnant and nonpregnant patients who have undergone the procedure. The obstetric-gynecologic setting should be the clinical space in which FGC is correctly diagnosed and from where patients with complications can be referred for appropriate care.

FGC: Through the lens of inequity

Providing culturally competent and sensitive care to women who have undergone FGC is paramount to reducing health care inequities for these patients. Beyond the medical recommendations we review below, we suggest the following considerations when approaching care for these patients.

Acknowledge our biases. It is paramount for us, as providers, to acknowledge our own biases and how these might affect our relationship with the patient and how our care is received. This starts with our language and terminology: The term female genital mutilation can be judgmental or offensive to our patients, many of whom do not consider themselves to have been mutilated. This is why we prefer to use the term female genital cutting, or whichever word the patient uses, so as not to alienate a patient who might already face many other barriers and microaggressions in seeking health care.

Control our responses. Another way we must check our bias is by controlling our reactions during history taking or examining patients who have undergone FGC. Understandably, providers might be shocked to hear patients recount their childhood experiences of FGC or by examining an infibulated scar, but patients report noticing and experiencing hurt, distress, and shame when providers display judgment, horror, or disgust.⁷ Patients have reported that they are acutely aware that they might be viewed as “backward” and “primitive” in US health care settings.⁸ These kinds of feelings and experiences can further exacerbate patients’ distrust and avoidance of the health care system altogether. Therefore, providers should acknowledge their own biases regarding the issue as well as those of their staff and work to mitigate them.

Avoid stigmatization. While FGC can have long-term effects (discussed below), it is important to remember that many women who have undergone FGC do not experience symptoms that are bothersome or feel that FGC is central to their lives or lived experiences. While we must be thorough in our history taking to explore possible urinary, gynecologic, and sexual symptoms of concern and bother to the patient, we must avoid stigmatizing our patients by assuming that all who have undergone FGC are “sexually disabled,” which may lead a provider to recommend medically unindicated intervention, such as clitoral reconstruction.⁹

Continue to: Classifying FGC types...

Classifying FGC types

The WHO has classified FGC into 4 different types¹:

• type 1, partial or total removal of the clitoris or prepuce
• type 2, partial or total removal of part of the clitoris and labia minora
• type 3 (also known as infibulation), the narrowing of the vaginal orifice by cutting, removing, and/or repositioning the labia, and
• type 4, all other procedures to the female genitalia for nonmedical reasons.

Long-term complications

Female genital cutting, especially types 2 and 3, can lead to long-term obstetric and gynecologic complications that the ObGyn should be able to diagnose and manage (TABLE).

The most common long-term complications of FGC are dysmenorrhea, dyspareunia, recurrent vaginal and urinary tract infections, and sexual dysfunction/dissatisfaction.¹⁰ One recent cross-sectional study that used validated questionnaires on pelvic floor and psychosexual symptoms found that women with FGC had higher distress scores than women who had not undergone FGC, indicating various pelvic floor symptoms responsible for impact on their daily lives.¹¹

Infertility can result from a combination of physical barriers (vaginal stenosis and an infibulated scar) and psychologic barriers secondary to dyspareunia, for example.¹² Labor and delivery also presents a challenge to both patients and providers, especially in cases of infibulation. Studies show that patients who have undergone FGC are at increased risk of adverse obstetric outcomes, including postpartum hemorrhage, episiotomy, cesarean delivery, and extended hospital stay.¹³ Neonatal complications, including infant resuscitation and perinatal death, are more commonly reported in studies outside the United States.¹³

Clinical management recommendations

It is important to be aware of the WHO FCG classifications and be able to recognize evidence of the procedure on examination. The ObGyn should perform a detailed physical exam of the external genitalia as well as a pelvic floor exam of every patient. If the patient does not disclose a history of FGC but it is suspected based on the examination, the clinician should inquire sensitively if the patient is aware of having undergone any genital procedures.

Especially when a history of FGC has been confirmed, clinicians should ask patients sensitively about their urinary and sexual function and satisfaction. Validated tools, such as the Female Sexual Function Index, the Female Sexual Distress Scale, and the Pelvic Floor Disability Index, may be helpful in gathering an objective and detailed assessment of the patient’s symptoms and level of distress.¹⁴ Clinicians also should ask about the patient’s detailed obstetric history, particularly regarding the second stage, delivery, and postpartum complications. The clinician also should specifically inquire about a history of defibulation or additional genital procedures.

Patients with urethral strictures or stenosis may require an exam under anesthesia, cystoscopy, urethral dilation, or urethroplasty.¹² Those with chronic urinary tract or vaginal infections may require chronic oral suppressive therapy or defibulation (described below). Defibulation also may be considered for relief of severe dysmenorrhea and menorrhagia that may be resulting from hematocolpos. The ObGyn also should make certain to evaluate for other common causes of these symptoms that may be unrelated to FGC, such as endometriosis.

Many women who have undergone FGC do not report dyspareunia or sexual dissatisfaction; however, infibulation especially has been associated with higher rates of these sequelae.¹² In addition to defibulation, pelvic floor physical therapy with an experienced therapist may be helpful for patients with pelvic floor dysfunction, vaginismus, and/or dyspareunia.

The defibulation procedure

Defibulation (or deinfibulation) is a surgical reconstructive procedure that opens the infibulated scar of patients who have undergone type 3 FGC (infibulation), thus exposing the urethra and introitus, and in almost half of cases an intact clitoris.¹⁵ Defibulation may be specifically requested by a patient or it may be recommended by the ObGyn either for reducing complications of pregnancy or to address the patient’s gynecologic, sexual, or urogynecologic symptoms by allowing penetrative intercourse, urinary flow, physiologic delivery, and menstruation.¹⁶

Defibulation should be performed under regional or general anesthesia and can be performed during pregnancy (or even in labor). An anterior incision is made on the infibulated scar, creating a new labia major, and the edges are sutured separately. Postoperatively, patients should be instructed to perform sitz baths and to expect a change in their urinary voiding stream.¹² The few studies that have evaluated defibulation have shown high rates of success in addressing preoperative symptoms; the complication rates of defibulation are low and the satisfaction rates are high.¹⁶

The ethical conundrum of reinfibulation

Reinfibulation is defined as the restitching or reapproximation of scar tissue or the labia after delivery or a gynecologic procedure, and it is often performed routinely after every delivery in patients’ countries of origin.¹⁷

Postpartum reinfibulation on patient request raises legal and ethical issues for the ObGyn. In the United Kingdom, reinfibulation is illegal, and some international organizations, including the International Federation of Gynecology and Obstetrics and the WHO, have recommended against the practice. In the United States, reinfibulation of an adult is legal, as it falls under the umbrella of elective female genital cosmetic surgery.^18,19

The procedure could create or exacerbate long-term complications and should generally be discouraged. However, if despite extensive counseling (preferably in the prenatal period) a patient insists on having the procedure, the ObGyn may need to elevate the principle of patient autonomy and either comply or find a practitioner who is comfortable performing it. One retrospective review in Switzerland suggested that specific care and informative counseling prenatally with the inclusion of a patient’s partner in the discussion can improve the acceptability of defibulation without reinfibulation.²⁰

Conclusion

It is important for ObGyns to be familiar with the practice of FGC and to be trained in its recognition on examination and care for the long-term complications that can result from the practice. At the same time, ObGyns should be especially conscious of their biases in order to provide culturally competent care and reduce health care stigmatization and inequities for these patients.