The Journal of Family Practice

Early childhood caries (ECCs) are a preventable public health challenge. Breastfeeding may provide early protection from ECCs. In addition, oral hygiene that begins in infancy, regular dental care visits, and a healthy diet can minimize ECC risk.

In this article we review the critical role of the family physician (FP) in reducing ECCs by promoting breastfeeding and infant oral health and addressing dental health concerns.

How ECCs develop

ECCs represent decayed, missing, or filled areas in the primary dentition of the tooth surface. The bacteria that cause them (most often Streptococcus mutans¹) strongly adhere to teeth and produce acids as waste products of fermentable carbohydrate metabolism that demineralize tooth enamel and progress into the dentin. Weakened enamel and dentin can result in cavitation (ie, a dental cavity). Left untreated, caries can extend to the pulp and destroy the entire tooth. ECCs are a risk factor not only for dental caries in primary teeth, but in permanent dentition as well.

ECCs are the most common chronic disease affecting young children.¹ Dental disease may begin soon after tooth eruption with detrimental effects on oral development. Almost half of children have dental caries by 5 years of age.²

ECCs represent a complex and multifactorial disease that is impacted by biomedical factors and unmet social needs. Children who are most at risk include those with low socioeconomic status, a high-sugar diet, exposure to household smoke, and limited dental care access.³ In addition, women with low education, poor oral health, and/or a lack of fluoride exposure are more likely to have children with ECCs.³ This is partly because of vertical transmission of cariogenic bacteria from caregiver to child. Horizontal transmission in daycare settings can also occur. Paternal and child oral health have not been linked.

Support breastfeeding; keep oral microbiome changes in mind

The American Academy of Pediatrics (AAP) recommends exclusive breastfeeding for the first 6 months of life, a combination of breastfeeding and complementary foods until 12 months of age, and continued breastfeeding for as long as mutually desired by mother and baby.⁴ The World Health Organization (WHO) recommends continued breastfeeding until 2 years of age or beyond.⁵ In fact, the WHO global nutrition targets for 2025 include increasing the rate of exclusive breastfeeding in the first 6 months of life to at least 50%.⁶

Early childhood caries are the most common chronic disease affecting young children.

In addition to maternal, financial, and societal benefits, human milk offers nutritional and other health-related advantages for children that optimize growth and development into adulthood.⁴ Breastfed infants may benefit from reduction in infections and diseases, including asthma, diabetes mellitus, childhood cancer, and obesity.⁷ Improved neurocognitive development, intelligence, and education attainment in adulthood have also been described.⁸ And the rich microbiome of human milk helps to establish oral and intestinal floras⁹ and may mediate protection from ECCs.³

Continue to: However, as a child's oral microbiome changes...

However, as a child’s oral microbiome changes with the emergence of primary teeth and exposure to more and varied bacteria and dietary sugars, the natural sugars in human milk may become the substrate for cariogenic bacteria.³ ECCs can develop and progress rapidly. Importantly, both the practice of breastfeeding and ECC risk are modified by socioeconomic status, maternal oral health and education, and exposure to household smoking.^3,7 Understanding these relationships may help you better target risk assessment and counseling efforts.

What the research tells us about breastfeeding and ECCs

Breastfeeding is hypothesized to be one of many factors that influence ECC development. However, studies on this association have had conflicting results and have not adequately controlled for major confounders, such as dietary composition, maternal and infant oral hygiene, and maternal oral health status.

So here is what we know.

Breastfeeding during the first year. In one meta-analysis involving children who breastfed for up to 12 months, those who breastfed longer within the 12-month period had a reduced risk of ECCs compared with those who breastfed for a shorter period of time,³ which implies that breast milk may be protective in the first year of life.³

Further, a 2014 study with about 500 participants found that children were more likely to have caries by 5 years of age if they breastfed for <6 months than if they breastfed for at least 6 months.¹⁰

Continue to: After the first year

After the first year. A Canadian study found an increased risk of ECCs associated with breastfeeding for longer periods of time. The study of healthy urban children reported that breastfeeding for >24 months was associated with a 2- to 3-fold increased odds of ECCs compared with shorter breastfeeding duration.¹¹

No relationship? Lastly, a US study using National Health and Nutrition Examination Survey data found there was no evidence to suggest that breastfeeding duration was an independent risk factor for ECCs.¹²

A possible explanation for a link

An initial protective effect of breastfeeding against ECCs may be related to breast milk’s immunomodulatory factors and rich microbiome. Breast milk contains Lactobacilli and substances, including human casein and secretory IgA, that inhibit growth and attachment of bacteria,⁹ particularly the caries pathogen S mutans. Early defense against ECCs may be mediated through the establishment of a healthy oral and gut microbiome that results from exposure to breastfeeding and contact with skin, gut, and breast milk microbiomes. Later on, the child’s oral microbiome changes with the emergence of teeth and the introduction of complementary foods andother drinks.

A look at the role vitamin D plays

Vitamin D status may influence childhood dental health.¹³ Low maternal vitamin D levels have been associated with ECCs,¹⁴ and mothers with higher prenatal vitamin D intakes were more likely to report that their children were caries-free compared with women who had lower vitamin D intake.¹⁵ Additionally, children with severe ECCs were found to have lower vitamin D levels than cavity-free children.¹⁶ Unfortunately, only a minority of infants who are predominantly breastfed for > 6 months receive vitamin D supplementation.¹⁷

Other factors at work: Carbohydrate exposure, nocturnal feedings

Exposure to carbohydrates—the essential substrate for cariogenic bacteria—is a key factor in ECC development. Refined sugars contribute considerably to tooth decay. Frequency of feeding and feeding practices, such as prolonged nocturnal feeding (either breast or bottle) may increase ECC risk.³ Further, a major determinant of ECC risk is colonization of the infant’s mouth by cariogenic bacteria. Finally, ECC risk depends on socioeconomic status, oral hygiene, exposure to fluoride, and the mother’s oral health, education, and smoking status.³ Even birth order plays a role, with those born first having lower risk than subsequent children.¹⁸

Continue to: Breastfeeding and another area of oral health...

Breastfeeding and another area of oral health: Malocclusion

In addition to its relationship with ECCs, breastfeeding promotes adequate development of craniofacial structures (comprising the tongue, facial muscles, and jaw), which are important for smiling, emotion, and social contact. Breastfeeding may prevent the development of malocclusion (ie, a misalignment of the teeth) in primary dentition, which is a risk factor for malocclusion in adulthood.⁷ Although previous studies had conflicting results, a large prospective study found that breastfeeding significantly reduced the risk of moderate and severe malocclusion; however, this effect was nullified by nonnutritive sucking and pacifier use.¹⁹

Oral health recommendations: The FP’s role

ECCs are theoretically preventable. To optimize the benefits of breastfeeding and minimize ECC risk, parents should follow recommendations for their children regarding proper oral hygiene, appropriate fluoride exposure, regular dental visits, and a healthy diet.¹

Be sure to advise parents to:

• avoid saliva-sharing behaviors (eg, sharing utensils with their children or cleaning a pacifier with their mouth), as these may increase early colonization of S mutans in infants;
• seek regular preventive dental care and attend to caries—both for their children and themselves; and
• use antimicrobial oral care products including xylitol-containing chewing gum to lower levels of cariogenic microorganisms in themselves and, in turn, reduce mother–child vertical transmission of S mutans.¹

In addition, make sure your prenatal counseling includes a discussion of the importance of good maternal oral health and diet—including an adequate vitamin D intake—to prevent ECCs in their children.

It’s never too early to start

Providing guidance on children’s oral health can start with the first well-infant visit. FPs should perform an oral health risk assessment by 6 months of age (see the AAP’s Oral Health Risk Assessment Tool at https://www.aap.org/en-us/Documents/oralhealth_RiskAssessmentTool.pdf) and evaluate fluoride exposure. Advise parents to establish a dental home by the time the child is 12 months of age; to clean their children’s mouths after feedings (before teeth arrive) with a clean, wet, soft washcloth; and to brush their children’s teeth, once they erupt, twice daily using a soft toothbrush (TABLE 1²⁰).

Continue to: Talk to parents about...

Talk to parents about how to provide optimal exposure to fluoride, which is known to be safe and effective for the prevention of ECCs.¹ Use of fluoridated toothpaste in small amounts provides the benefits of fluoride without increasing the risk of fluorosis, especially for children at risk for caries (see TABLE 2²¹).

The rich microbiome of human milk helps to establish oral and intestinal floras and may mediate protection from early childhood caries.

The US Preventive Services Task Force recommends that primary care practitioners apply fluoride varnish biannually for at least 2 years to the primary teeth of all children up to 5 years of age (Grade B evidence).²² This is particularly important for high-risk children, such as those with low-income or minority status. However, practitioners should also take into account that high cumulative fluoride intake can lead to dental fluorosis.¹ Finally, tell parents to avoid giving their children sugar-containing snacks and drinks to reduce ECC risk.

CORRESPONDENCE
Peter D. Wong, MD, 303-89 Humber College Boulevard, Toronto, Ontario, Canada M9V 4B8; peter.wong@sickkids.ca.

Early childhood caries (ECCs) are a preventable public health challenge. Breastfeeding may provide early protection from ECCs. In addition, oral hygiene that begins in infancy, regular dental care visits, and a healthy diet can minimize ECC risk.

In this article we review the critical role of the family physician (FP) in reducing ECCs by promoting breastfeeding and infant oral health and addressing dental health concerns.

How ECCs develop

ECCs represent decayed, missing, or filled areas in the primary dentition of the tooth surface. The bacteria that cause them (most often Streptococcus mutans¹) strongly adhere to teeth and produce acids as waste products of fermentable carbohydrate metabolism that demineralize tooth enamel and progress into the dentin. Weakened enamel and dentin can result in cavitation (ie, a dental cavity). Left untreated, caries can extend to the pulp and destroy the entire tooth. ECCs are a risk factor not only for dental caries in primary teeth, but in permanent dentition as well.

ECCs are the most common chronic disease affecting young children.¹ Dental disease may begin soon after tooth eruption with detrimental effects on oral development. Almost half of children have dental caries by 5 years of age.²

ECCs represent a complex and multifactorial disease that is impacted by biomedical factors and unmet social needs. Children who are most at risk include those with low socioeconomic status, a high-sugar diet, exposure to household smoke, and limited dental care access.³ In addition, women with low education, poor oral health, and/or a lack of fluoride exposure are more likely to have children with ECCs.³ This is partly because of vertical transmission of cariogenic bacteria from caregiver to child. Horizontal transmission in daycare settings can also occur. Paternal and child oral health have not been linked.

Support breastfeeding; keep oral microbiome changes in mind

The American Academy of Pediatrics (AAP) recommends exclusive breastfeeding for the first 6 months of life, a combination of breastfeeding and complementary foods until 12 months of age, and continued breastfeeding for as long as mutually desired by mother and baby.⁴ The World Health Organization (WHO) recommends continued breastfeeding until 2 years of age or beyond.⁵ In fact, the WHO global nutrition targets for 2025 include increasing the rate of exclusive breastfeeding in the first 6 months of life to at least 50%.⁶

Early childhood caries are the most common chronic disease affecting young children.

In addition to maternal, financial, and societal benefits, human milk offers nutritional and other health-related advantages for children that optimize growth and development into adulthood.⁴ Breastfed infants may benefit from reduction in infections and diseases, including asthma, diabetes mellitus, childhood cancer, and obesity.⁷ Improved neurocognitive development, intelligence, and education attainment in adulthood have also been described.⁸ And the rich microbiome of human milk helps to establish oral and intestinal floras⁹ and may mediate protection from ECCs.³

Continue to: However, as a child's oral microbiome changes...

However, as a child’s oral microbiome changes with the emergence of primary teeth and exposure to more and varied bacteria and dietary sugars, the natural sugars in human milk may become the substrate for cariogenic bacteria.³ ECCs can develop and progress rapidly. Importantly, both the practice of breastfeeding and ECC risk are modified by socioeconomic status, maternal oral health and education, and exposure to household smoking.^3,7 Understanding these relationships may help you better target risk assessment and counseling efforts.

What the research tells us about breastfeeding and ECCs

Breastfeeding is hypothesized to be one of many factors that influence ECC development. However, studies on this association have had conflicting results and have not adequately controlled for major confounders, such as dietary composition, maternal and infant oral hygiene, and maternal oral health status.

So here is what we know.

Breastfeeding during the first year. In one meta-analysis involving children who breastfed for up to 12 months, those who breastfed longer within the 12-month period had a reduced risk of ECCs compared with those who breastfed for a shorter period of time,³ which implies that breast milk may be protective in the first year of life.³

Further, a 2014 study with about 500 participants found that children were more likely to have caries by 5 years of age if they breastfed for <6 months than if they breastfed for at least 6 months.¹⁰

Continue to: After the first year

After the first year. A Canadian study found an increased risk of ECCs associated with breastfeeding for longer periods of time. The study of healthy urban children reported that breastfeeding for >24 months was associated with a 2- to 3-fold increased odds of ECCs compared with shorter breastfeeding duration.¹¹

No relationship? Lastly, a US study using National Health and Nutrition Examination Survey data found there was no evidence to suggest that breastfeeding duration was an independent risk factor for ECCs.¹²

A possible explanation for a link

An initial protective effect of breastfeeding against ECCs may be related to breast milk’s immunomodulatory factors and rich microbiome. Breast milk contains Lactobacilli and substances, including human casein and secretory IgA, that inhibit growth and attachment of bacteria,⁹ particularly the caries pathogen S mutans. Early defense against ECCs may be mediated through the establishment of a healthy oral and gut microbiome that results from exposure to breastfeeding and contact with skin, gut, and breast milk microbiomes. Later on, the child’s oral microbiome changes with the emergence of teeth and the introduction of complementary foods andother drinks.

A look at the role vitamin D plays

Vitamin D status may influence childhood dental health.¹³ Low maternal vitamin D levels have been associated with ECCs,¹⁴ and mothers with higher prenatal vitamin D intakes were more likely to report that their children were caries-free compared with women who had lower vitamin D intake.¹⁵ Additionally, children with severe ECCs were found to have lower vitamin D levels than cavity-free children.¹⁶ Unfortunately, only a minority of infants who are predominantly breastfed for > 6 months receive vitamin D supplementation.¹⁷

Other factors at work: Carbohydrate exposure, nocturnal feedings

Exposure to carbohydrates—the essential substrate for cariogenic bacteria—is a key factor in ECC development. Refined sugars contribute considerably to tooth decay. Frequency of feeding and feeding practices, such as prolonged nocturnal feeding (either breast or bottle) may increase ECC risk.³ Further, a major determinant of ECC risk is colonization of the infant’s mouth by cariogenic bacteria. Finally, ECC risk depends on socioeconomic status, oral hygiene, exposure to fluoride, and the mother’s oral health, education, and smoking status.³ Even birth order plays a role, with those born first having lower risk than subsequent children.¹⁸

Continue to: Breastfeeding and another area of oral health...

Breastfeeding and another area of oral health: Malocclusion

In addition to its relationship with ECCs, breastfeeding promotes adequate development of craniofacial structures (comprising the tongue, facial muscles, and jaw), which are important for smiling, emotion, and social contact. Breastfeeding may prevent the development of malocclusion (ie, a misalignment of the teeth) in primary dentition, which is a risk factor for malocclusion in adulthood.⁷ Although previous studies had conflicting results, a large prospective study found that breastfeeding significantly reduced the risk of moderate and severe malocclusion; however, this effect was nullified by nonnutritive sucking and pacifier use.¹⁹

Oral health recommendations: The FP’s role

ECCs are theoretically preventable. To optimize the benefits of breastfeeding and minimize ECC risk, parents should follow recommendations for their children regarding proper oral hygiene, appropriate fluoride exposure, regular dental visits, and a healthy diet.¹

Be sure to advise parents to:

• avoid saliva-sharing behaviors (eg, sharing utensils with their children or cleaning a pacifier with their mouth), as these may increase early colonization of S mutans in infants;
• seek regular preventive dental care and attend to caries—both for their children and themselves; and
• use antimicrobial oral care products including xylitol-containing chewing gum to lower levels of cariogenic microorganisms in themselves and, in turn, reduce mother–child vertical transmission of S mutans.¹

In addition, make sure your prenatal counseling includes a discussion of the importance of good maternal oral health and diet—including an adequate vitamin D intake—to prevent ECCs in their children.

It’s never too early to start

Providing guidance on children’s oral health can start with the first well-infant visit. FPs should perform an oral health risk assessment by 6 months of age (see the AAP’s Oral Health Risk Assessment Tool at https://www.aap.org/en-us/Documents/oralhealth_RiskAssessmentTool.pdf) and evaluate fluoride exposure. Advise parents to establish a dental home by the time the child is 12 months of age; to clean their children’s mouths after feedings (before teeth arrive) with a clean, wet, soft washcloth; and to brush their children’s teeth, once they erupt, twice daily using a soft toothbrush (TABLE 1²⁰).

Continue to: Talk to parents about...

Talk to parents about how to provide optimal exposure to fluoride, which is known to be safe and effective for the prevention of ECCs.¹ Use of fluoridated toothpaste in small amounts provides the benefits of fluoride without increasing the risk of fluorosis, especially for children at risk for caries (see TABLE 2²¹).

The rich microbiome of human milk helps to establish oral and intestinal floras and may mediate protection from early childhood caries.

The US Preventive Services Task Force recommends that primary care practitioners apply fluoride varnish biannually for at least 2 years to the primary teeth of all children up to 5 years of age (Grade B evidence).²² This is particularly important for high-risk children, such as those with low-income or minority status. However, practitioners should also take into account that high cumulative fluoride intake can lead to dental fluorosis.¹ Finally, tell parents to avoid giving their children sugar-containing snacks and drinks to reduce ECC risk.

CORRESPONDENCE
Peter D. Wong, MD, 303-89 Humber College Boulevard, Toronto, Ontario, Canada M9V 4B8; peter.wong@sickkids.ca.

Early childhood caries (ECCs) are a preventable public health challenge. Breastfeeding may provide early protection from ECCs. In addition, oral hygiene that begins in infancy, regular dental care visits, and a healthy diet can minimize ECC risk.

In this article we review the critical role of the family physician (FP) in reducing ECCs by promoting breastfeeding and infant oral health and addressing dental health concerns.

How ECCs develop

ECCs represent decayed, missing, or filled areas in the primary dentition of the tooth surface. The bacteria that cause them (most often Streptococcus mutans¹) strongly adhere to teeth and produce acids as waste products of fermentable carbohydrate metabolism that demineralize tooth enamel and progress into the dentin. Weakened enamel and dentin can result in cavitation (ie, a dental cavity). Left untreated, caries can extend to the pulp and destroy the entire tooth. ECCs are a risk factor not only for dental caries in primary teeth, but in permanent dentition as well.

ECCs are the most common chronic disease affecting young children.¹ Dental disease may begin soon after tooth eruption with detrimental effects on oral development. Almost half of children have dental caries by 5 years of age.²

ECCs represent a complex and multifactorial disease that is impacted by biomedical factors and unmet social needs. Children who are most at risk include those with low socioeconomic status, a high-sugar diet, exposure to household smoke, and limited dental care access.³ In addition, women with low education, poor oral health, and/or a lack of fluoride exposure are more likely to have children with ECCs.³ This is partly because of vertical transmission of cariogenic bacteria from caregiver to child. Horizontal transmission in daycare settings can also occur. Paternal and child oral health have not been linked.

Support breastfeeding; keep oral microbiome changes in mind

The American Academy of Pediatrics (AAP) recommends exclusive breastfeeding for the first 6 months of life, a combination of breastfeeding and complementary foods until 12 months of age, and continued breastfeeding for as long as mutually desired by mother and baby.⁴ The World Health Organization (WHO) recommends continued breastfeeding until 2 years of age or beyond.⁵ In fact, the WHO global nutrition targets for 2025 include increasing the rate of exclusive breastfeeding in the first 6 months of life to at least 50%.⁶

Early childhood caries are the most common chronic disease affecting young children.

In addition to maternal, financial, and societal benefits, human milk offers nutritional and other health-related advantages for children that optimize growth and development into adulthood.⁴ Breastfed infants may benefit from reduction in infections and diseases, including asthma, diabetes mellitus, childhood cancer, and obesity.⁷ Improved neurocognitive development, intelligence, and education attainment in adulthood have also been described.⁸ And the rich microbiome of human milk helps to establish oral and intestinal floras⁹ and may mediate protection from ECCs.³

Continue to: However, as a child's oral microbiome changes...

However, as a child’s oral microbiome changes with the emergence of primary teeth and exposure to more and varied bacteria and dietary sugars, the natural sugars in human milk may become the substrate for cariogenic bacteria.³ ECCs can develop and progress rapidly. Importantly, both the practice of breastfeeding and ECC risk are modified by socioeconomic status, maternal oral health and education, and exposure to household smoking.^3,7 Understanding these relationships may help you better target risk assessment and counseling efforts.

What the research tells us about breastfeeding and ECCs

Breastfeeding is hypothesized to be one of many factors that influence ECC development. However, studies on this association have had conflicting results and have not adequately controlled for major confounders, such as dietary composition, maternal and infant oral hygiene, and maternal oral health status.

So here is what we know.

Breastfeeding during the first year. In one meta-analysis involving children who breastfed for up to 12 months, those who breastfed longer within the 12-month period had a reduced risk of ECCs compared with those who breastfed for a shorter period of time,³ which implies that breast milk may be protective in the first year of life.³

Further, a 2014 study with about 500 participants found that children were more likely to have caries by 5 years of age if they breastfed for <6 months than if they breastfed for at least 6 months.¹⁰

Continue to: After the first year

After the first year. A Canadian study found an increased risk of ECCs associated with breastfeeding for longer periods of time. The study of healthy urban children reported that breastfeeding for >24 months was associated with a 2- to 3-fold increased odds of ECCs compared with shorter breastfeeding duration.¹¹

No relationship? Lastly, a US study using National Health and Nutrition Examination Survey data found there was no evidence to suggest that breastfeeding duration was an independent risk factor for ECCs.¹²

A possible explanation for a link

An initial protective effect of breastfeeding against ECCs may be related to breast milk’s immunomodulatory factors and rich microbiome. Breast milk contains Lactobacilli and substances, including human casein and secretory IgA, that inhibit growth and attachment of bacteria,⁹ particularly the caries pathogen S mutans. Early defense against ECCs may be mediated through the establishment of a healthy oral and gut microbiome that results from exposure to breastfeeding and contact with skin, gut, and breast milk microbiomes. Later on, the child’s oral microbiome changes with the emergence of teeth and the introduction of complementary foods andother drinks.

A look at the role vitamin D plays

Vitamin D status may influence childhood dental health.¹³ Low maternal vitamin D levels have been associated with ECCs,¹⁴ and mothers with higher prenatal vitamin D intakes were more likely to report that their children were caries-free compared with women who had lower vitamin D intake.¹⁵ Additionally, children with severe ECCs were found to have lower vitamin D levels than cavity-free children.¹⁶ Unfortunately, only a minority of infants who are predominantly breastfed for > 6 months receive vitamin D supplementation.¹⁷

Other factors at work: Carbohydrate exposure, nocturnal feedings

Exposure to carbohydrates—the essential substrate for cariogenic bacteria—is a key factor in ECC development. Refined sugars contribute considerably to tooth decay. Frequency of feeding and feeding practices, such as prolonged nocturnal feeding (either breast or bottle) may increase ECC risk.³ Further, a major determinant of ECC risk is colonization of the infant’s mouth by cariogenic bacteria. Finally, ECC risk depends on socioeconomic status, oral hygiene, exposure to fluoride, and the mother’s oral health, education, and smoking status.³ Even birth order plays a role, with those born first having lower risk than subsequent children.¹⁸

Continue to: Breastfeeding and another area of oral health...

Breastfeeding and another area of oral health: Malocclusion

In addition to its relationship with ECCs, breastfeeding promotes adequate development of craniofacial structures (comprising the tongue, facial muscles, and jaw), which are important for smiling, emotion, and social contact. Breastfeeding may prevent the development of malocclusion (ie, a misalignment of the teeth) in primary dentition, which is a risk factor for malocclusion in adulthood.⁷ Although previous studies had conflicting results, a large prospective study found that breastfeeding significantly reduced the risk of moderate and severe malocclusion; however, this effect was nullified by nonnutritive sucking and pacifier use.¹⁹

Oral health recommendations: The FP’s role

ECCs are theoretically preventable. To optimize the benefits of breastfeeding and minimize ECC risk, parents should follow recommendations for their children regarding proper oral hygiene, appropriate fluoride exposure, regular dental visits, and a healthy diet.¹

Be sure to advise parents to:

• avoid saliva-sharing behaviors (eg, sharing utensils with their children or cleaning a pacifier with their mouth), as these may increase early colonization of S mutans in infants;
• seek regular preventive dental care and attend to caries—both for their children and themselves; and
• use antimicrobial oral care products including xylitol-containing chewing gum to lower levels of cariogenic microorganisms in themselves and, in turn, reduce mother–child vertical transmission of S mutans.¹

In addition, make sure your prenatal counseling includes a discussion of the importance of good maternal oral health and diet—including an adequate vitamin D intake—to prevent ECCs in their children.

It’s never too early to start

Providing guidance on children’s oral health can start with the first well-infant visit. FPs should perform an oral health risk assessment by 6 months of age (see the AAP’s Oral Health Risk Assessment Tool at https://www.aap.org/en-us/Documents/oralhealth_RiskAssessmentTool.pdf) and evaluate fluoride exposure. Advise parents to establish a dental home by the time the child is 12 months of age; to clean their children’s mouths after feedings (before teeth arrive) with a clean, wet, soft washcloth; and to brush their children’s teeth, once they erupt, twice daily using a soft toothbrush (TABLE 1²⁰).

Continue to: Talk to parents about...

Talk to parents about how to provide optimal exposure to fluoride, which is known to be safe and effective for the prevention of ECCs.¹ Use of fluoridated toothpaste in small amounts provides the benefits of fluoride without increasing the risk of fluorosis, especially for children at risk for caries (see TABLE 2²¹).

The rich microbiome of human milk helps to establish oral and intestinal floras and may mediate protection from early childhood caries.

The US Preventive Services Task Force recommends that primary care practitioners apply fluoride varnish biannually for at least 2 years to the primary teeth of all children up to 5 years of age (Grade B evidence).²² This is particularly important for high-risk children, such as those with low-income or minority status. However, practitioners should also take into account that high cumulative fluoride intake can lead to dental fluorosis.¹ Finally, tell parents to avoid giving their children sugar-containing snacks and drinks to reduce ECC risk.

CORRESPONDENCE
Peter D. Wong, MD, 303-89 Humber College Boulevard, Toronto, Ontario, Canada M9V 4B8; peter.wong@sickkids.ca.

Acetylsalicylic acid has been around for nearly 200 years. It traces its history back to a French chemist (Charles Frederic Gerhardt) and 2 German chemists (Felix Hoffmann and Arthur Eichengrün) who worked at Bayer, the company that launched the pain reliever under the name “aspirin” in 1899. It is now one of the most commonly used medications in the world.

No wonder our patients are confused!

With aspirin's anti-inflammatory properties in mind, researchers conducted randomized trials for secondary prevention of heart attacks in the 1970s; low-dose aspirin was proven effective in reducing risk for a second myocardial infarction. These trials led to speculation that aspirin might be effective for primary prevention as well. Indeed, in the 1980s the large Physicians' Health Study found aspirin reduced the incidence of first heart attack in healthy physicians by 44%.¹ Unfortunately, there was no reduction in mortality from heart disease and it was only effective for those older than 50.

The downside of aspirin was a slight increase in the incidence of hemorrhagic stroke and bleeding requiring transfusion. Nonetheless, many healthy adults started taking daily aspirin hoping to prevent a heart attack.

In this issue of JFP, Smith and colleagues summarize the 2016 recommendations of the US Preventive Services Task Force (USPSTF) regarding aspirin for primary prevention, as well as the 4 large aspirin prevention trials published in 2018 subsequent to the USPSTF recommendations. The USPSTF recommended aspirin for adults ages 50 to 59 with a 10-year cardiovascular risk of at least 10% (B recommendation). For those ages 60-69, the USPSTF recommendation for aspirin as primary prevention has a “C” rating, meaning that patient preference is important to consider in balancing benefit and harms. For those 70 and older, the USPSTF gave aspirin an “I” (insufficient evidence) rating because of increased risk for bleeding. It is important to note that the positive B recommendation for those ages 50-59 is based not only on cardiovascular risk reduction but also on a slight risk reduction for colon cancer for those taking aspirin for at least 10 years.

The 4 new, large randomized trials published in 2018, however, cast doubt on the USPSTF recommendations because the results of these trials were negative for the most part. The bottom line is that daily aspirin for prevention is definitely not for everyone and perhaps not for anyone except those who have established vascular disease or are at high risk for vascular disease and low risk for bleeding.

No wonder patients are confused!
Smith recommends that, before prescribing aspirin to healthy adults for prevention, we assess each individual’s personal cardiovascular and bleeding risk using an online decision tool called Aspirin-Guide (www.aspiringuide.com). I agree.

Acetylsalicylic acid has been around for nearly 200 years. It traces its history back to a French chemist (Charles Frederic Gerhardt) and 2 German chemists (Felix Hoffmann and Arthur Eichengrün) who worked at Bayer, the company that launched the pain reliever under the name “aspirin” in 1899. It is now one of the most commonly used medications in the world.

No wonder our patients are confused!

With aspirin's anti-inflammatory properties in mind, researchers conducted randomized trials for secondary prevention of heart attacks in the 1970s; low-dose aspirin was proven effective in reducing risk for a second myocardial infarction. These trials led to speculation that aspirin might be effective for primary prevention as well. Indeed, in the 1980s the large Physicians' Health Study found aspirin reduced the incidence of first heart attack in healthy physicians by 44%.¹ Unfortunately, there was no reduction in mortality from heart disease and it was only effective for those older than 50.

The downside of aspirin was a slight increase in the incidence of hemorrhagic stroke and bleeding requiring transfusion. Nonetheless, many healthy adults started taking daily aspirin hoping to prevent a heart attack.

In this issue of JFP, Smith and colleagues summarize the 2016 recommendations of the US Preventive Services Task Force (USPSTF) regarding aspirin for primary prevention, as well as the 4 large aspirin prevention trials published in 2018 subsequent to the USPSTF recommendations. The USPSTF recommended aspirin for adults ages 50 to 59 with a 10-year cardiovascular risk of at least 10% (B recommendation). For those ages 60-69, the USPSTF recommendation for aspirin as primary prevention has a “C” rating, meaning that patient preference is important to consider in balancing benefit and harms. For those 70 and older, the USPSTF gave aspirin an “I” (insufficient evidence) rating because of increased risk for bleeding. It is important to note that the positive B recommendation for those ages 50-59 is based not only on cardiovascular risk reduction but also on a slight risk reduction for colon cancer for those taking aspirin for at least 10 years.

The 4 new, large randomized trials published in 2018, however, cast doubt on the USPSTF recommendations because the results of these trials were negative for the most part. The bottom line is that daily aspirin for prevention is definitely not for everyone and perhaps not for anyone except those who have established vascular disease or are at high risk for vascular disease and low risk for bleeding.

No wonder patients are confused!
Smith recommends that, before prescribing aspirin to healthy adults for prevention, we assess each individual’s personal cardiovascular and bleeding risk using an online decision tool called Aspirin-Guide (www.aspiringuide.com). I agree.

Acetylsalicylic acid has been around for nearly 200 years. It traces its history back to a French chemist (Charles Frederic Gerhardt) and 2 German chemists (Felix Hoffmann and Arthur Eichengrün) who worked at Bayer, the company that launched the pain reliever under the name “aspirin” in 1899. It is now one of the most commonly used medications in the world.

No wonder our patients are confused!

With aspirin's anti-inflammatory properties in mind, researchers conducted randomized trials for secondary prevention of heart attacks in the 1970s; low-dose aspirin was proven effective in reducing risk for a second myocardial infarction. These trials led to speculation that aspirin might be effective for primary prevention as well. Indeed, in the 1980s the large Physicians' Health Study found aspirin reduced the incidence of first heart attack in healthy physicians by 44%.¹ Unfortunately, there was no reduction in mortality from heart disease and it was only effective for those older than 50.

The downside of aspirin was a slight increase in the incidence of hemorrhagic stroke and bleeding requiring transfusion. Nonetheless, many healthy adults started taking daily aspirin hoping to prevent a heart attack.

In this issue of JFP, Smith and colleagues summarize the 2016 recommendations of the US Preventive Services Task Force (USPSTF) regarding aspirin for primary prevention, as well as the 4 large aspirin prevention trials published in 2018 subsequent to the USPSTF recommendations. The USPSTF recommended aspirin for adults ages 50 to 59 with a 10-year cardiovascular risk of at least 10% (B recommendation). For those ages 60-69, the USPSTF recommendation for aspirin as primary prevention has a “C” rating, meaning that patient preference is important to consider in balancing benefit and harms. For those 70 and older, the USPSTF gave aspirin an “I” (insufficient evidence) rating because of increased risk for bleeding. It is important to note that the positive B recommendation for those ages 50-59 is based not only on cardiovascular risk reduction but also on a slight risk reduction for colon cancer for those taking aspirin for at least 10 years.

The 4 new, large randomized trials published in 2018, however, cast doubt on the USPSTF recommendations because the results of these trials were negative for the most part. The bottom line is that daily aspirin for prevention is definitely not for everyone and perhaps not for anyone except those who have established vascular disease or are at high risk for vascular disease and low risk for bleeding.

No wonder patients are confused!
Smith recommends that, before prescribing aspirin to healthy adults for prevention, we assess each individual’s personal cardiovascular and bleeding risk using an online decision tool called Aspirin-Guide (www.aspiringuide.com). I agree.

A 9-day-old boy was brought to the emergency department by his mother. The infant had been doing well until his most recent diaper change when his mother noticed a rash around the umbilicus (FIGURE), genitalia, and anus.

The infant was born at term via spontaneous vaginal delivery. The pregnancy was uncomplicated; the infant’s mother was group B strep negative. Following a routine postpartum course, the infant underwent an elective circumcision before hospital discharge on his second day of life. There were no interval reports of irritability, poor feeding, fevers, vomiting, or changes in urine or stool output.

The mother denied any recent unusual exposures, sick contacts, or travel. However, upon further questioning, the mother noted that she herself had several small open wounds on the torso that she attributed to untreated methicillin-resistant Staphylococcus aureus (MRSA).

On physical examination, the infant was overall well-appearing and was breastfeeding vigorously without respiratory distress or cyanosis. He was afebrile with normal vital signs. The majority of the physical examination was normal; however, there was erythematous desquamation around the umbilical stump and genitalia with no vesicles noted. The umbilical stump had a small amount of purulent drainage and necrosis centrally. The infant had a 1-cm round, peeling lesion on the left temple (FIGURE) with a small amount of dried serosanguinous drainage and similar superficial peeling lesions at the left preauricular area and anterior chest. There was no underlying fluctuance and only minimal surrounding erythema.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Based on the age of the patient, clinical presentation, and suspected maternal MRSA infection (with possible transmission to the infant), we diagnosed staphylococcal scalded skin syndrome (SSSS) in this patient. SSSS is rare, with annual incidence of 45 cases per million US infants under the age of 2.¹ Newborns with a generalized form of SSSS commonly present with fever, poor feeding, irritability, and lethargy. This is followed by a generalized erythematous rash that initially may appear on the head and neck and spread to the rest of the body. Large, fragile blisters subsequently appear. These blisters rupture on gentle pressure, which is known as a positive Nikolsky sign. Ultimately, large sheets of skin easily slough off, leaving raw, denuded skin.²

S aureus is not part of normal skin flora, yet it is found on the skin and mucous membranes of 19% to 55% of healthy adults and children.³S aureus can cause a wide range of infections ranging from abscesses to cellulitis; SSSS is caused by hematogenous spread of S aureus exfoliative toxin. Newborns and immunocompromised patients are particularly susceptible.

Staphylococcal scalded skin syndrome should be considered a pediatric emergency due to potential complications such as sepsis.

Neonatal patients with SSSS most commonly present at 3 to 16 days of age.² The lack of antitoxin antibody in neonates allows the toxin to reach the epidermis where it acts locally to produce the characteristic fragile skin lesions that often rupture prior to clinical presentation.^2,4 During progression of the disease, flaky skin desquamation will occur as the lesions heal.

A retrospective review of 39 cases of SSSS identified pneumonia as the most frequent complication, occurring in 74.4% of the cases.⁵ The mortality rate of SSSS is up to 5%, and is associated with sepsis, superinfection, electrolyte imbalances, and extensive skin involvement.^2,6

If SSSS is suspected, obtain cultures from the blood, urine, eyes, nose, throat, and skin lesions to identify the primary focus of infection.⁷ However, the retrospective review of 39 cases (noted above) found a positive rate of S aureus isolation of only 23.5%.⁵ Physicians will often have to make a diagnosis based on clinical presentation and empirically initiate broad-spectrum antibiotics while considering alternative diagnoses.

Continue to: A clinical diagnosis with a large differential

A clinical diagnosis with a large differential

While biopsy rarely is required, it may be helpful to distinguish SSSS from other entities in the differential diagnosis (TABLE^2,3,7-13).

Toxic epidermal necrolysis (TEN) is a rare and life-threatening desquamating disease nearly always caused by a reaction to medications, including antibiotics. TEN can occur at any age. Fever, diffuse erythema, and extensive epidermal involvement (>30% of skin) differentiate TEN from Stevens-Johnson syndrome (SJS), which affects less than 10% of the epidermis. It is worth mentioning that TEN and SJS are now considered to be a spectrum of one disease, and an overlap syndrome has been described with 10% to 30% of skin affected.⁸ Diagnosis is made clinically, although skin biopsy routinely is performed.^7,9

Congenital syphilis features a red or pink maculopapular rash followed by desquamation. Lesions are more common on the soles.¹⁰ Desquamation or ulcerative skin lesions should be examined for spirochetes.¹¹ A quantitative, nontreponemal test such as the rapid plasma reagin (RPR) or the Venereal Disease Research Laboratory (VDRL) will be positive in most infants if exposed through the placenta, but antibodies will disappear in uninfected infants by 6 months of age.⁸

Congenital cutaneous candidiasis presents with a generalized eruption of erythematous macules, papules, and/or pustules with widespread desquamating and/or erosive dermatitis. Premature neonates with extremely low birth weight are at higher risk.¹³ Diagnosis is confirmed on microscopy by the presence of Candida albicans spores in skin scrapings.¹³

Neonatal herpes simplex virus (HSV) symptoms typically appear between 1 and 3 weeks of life, with 60% to 70% of cases presenting with classic clustering vesicles on an erythematous base.¹⁴ Diagnosis is made with HSV viral culture or polymerase chain reaction (PCR).

Continue to: SSSS should be considered a pediatrics emergency

SSSS should be considered a pediatric emergency due to potential complications. Core measures of SSSS treatment include immediate administration of intravenous (IV) antibiotics. US population studies suggest clindamycin and penicillinase-resistant penicillin as empiric therapy.¹⁵ However, local strains and resistance patterns, including the prevalence of MRSA, as well as age, comorbidities, and severity of illness should influence antibiotic selection.

IV nafcillin or oxacillin may be used with pediatric dosing of 150 mg/kg daily divided every 6 hours for methicillin-sensitive Staphylococcus aureus (MSSA). For suspected MRSA, IV vancomycin should be considered, with an infant dose of 40 to 60 mg/kg daily divided every 6 hours.¹⁶ Fluid, electrolyte, and nutritional management should be addressed immediately. Ongoing fluid losses due to exfoliated skin must be replaced, and skin care to desquamated areas also should be addressed urgently.

Our patient. Phone consultation with an infectious disease specialist at a local children’s hospital resulted in a recommendation to treat for sepsis empirically with IV vancomycin, cefotaxime, and acyclovir. Acyclovir was discontinued once the HSV PCR came back negative. The antibiotic coverage was narrowed to IV ampicillin 50 mg/kg every 8 hours when cerebrospinal fluid and blood cultures returned negative at 48 hours, wound culture sensitivity grew MSSA, and the patient’s clinical condition stabilized. Our patient received 10 days of IV antibiotics and was discharged on oral amoxicillin 50 mg/kg divided twice daily for a total of 14 days of treatment per recommendations by the infectious disease specialist. Our patient fully recovered without any residual skin findings after completion of the antibiotic course.

CORRESPONDENCE
Jennifer J. Walker, MD, MPH, Hawaii Island Family Health Center at Hilo Medical Center, 1190 Waianuenue Ave, Hilo, HI 96720; jjwalker@hhsc.org

A 9-day-old boy was brought to the emergency department by his mother. The infant had been doing well until his most recent diaper change when his mother noticed a rash around the umbilicus (FIGURE), genitalia, and anus.

The infant was born at term via spontaneous vaginal delivery. The pregnancy was uncomplicated; the infant’s mother was group B strep negative. Following a routine postpartum course, the infant underwent an elective circumcision before hospital discharge on his second day of life. There were no interval reports of irritability, poor feeding, fevers, vomiting, or changes in urine or stool output.

The mother denied any recent unusual exposures, sick contacts, or travel. However, upon further questioning, the mother noted that she herself had several small open wounds on the torso that she attributed to untreated methicillin-resistant Staphylococcus aureus (MRSA).

On physical examination, the infant was overall well-appearing and was breastfeeding vigorously without respiratory distress or cyanosis. He was afebrile with normal vital signs. The majority of the physical examination was normal; however, there was erythematous desquamation around the umbilical stump and genitalia with no vesicles noted. The umbilical stump had a small amount of purulent drainage and necrosis centrally. The infant had a 1-cm round, peeling lesion on the left temple (FIGURE) with a small amount of dried serosanguinous drainage and similar superficial peeling lesions at the left preauricular area and anterior chest. There was no underlying fluctuance and only minimal surrounding erythema.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Based on the age of the patient, clinical presentation, and suspected maternal MRSA infection (with possible transmission to the infant), we diagnosed staphylococcal scalded skin syndrome (SSSS) in this patient. SSSS is rare, with annual incidence of 45 cases per million US infants under the age of 2.¹ Newborns with a generalized form of SSSS commonly present with fever, poor feeding, irritability, and lethargy. This is followed by a generalized erythematous rash that initially may appear on the head and neck and spread to the rest of the body. Large, fragile blisters subsequently appear. These blisters rupture on gentle pressure, which is known as a positive Nikolsky sign. Ultimately, large sheets of skin easily slough off, leaving raw, denuded skin.²

S aureus is not part of normal skin flora, yet it is found on the skin and mucous membranes of 19% to 55% of healthy adults and children.³S aureus can cause a wide range of infections ranging from abscesses to cellulitis; SSSS is caused by hematogenous spread of S aureus exfoliative toxin. Newborns and immunocompromised patients are particularly susceptible.

Staphylococcal scalded skin syndrome should be considered a pediatric emergency due to potential complications such as sepsis.

Neonatal patients with SSSS most commonly present at 3 to 16 days of age.² The lack of antitoxin antibody in neonates allows the toxin to reach the epidermis where it acts locally to produce the characteristic fragile skin lesions that often rupture prior to clinical presentation.^2,4 During progression of the disease, flaky skin desquamation will occur as the lesions heal.

A retrospective review of 39 cases of SSSS identified pneumonia as the most frequent complication, occurring in 74.4% of the cases.⁵ The mortality rate of SSSS is up to 5%, and is associated with sepsis, superinfection, electrolyte imbalances, and extensive skin involvement.^2,6

If SSSS is suspected, obtain cultures from the blood, urine, eyes, nose, throat, and skin lesions to identify the primary focus of infection.⁷ However, the retrospective review of 39 cases (noted above) found a positive rate of S aureus isolation of only 23.5%.⁵ Physicians will often have to make a diagnosis based on clinical presentation and empirically initiate broad-spectrum antibiotics while considering alternative diagnoses.

Continue to: A clinical diagnosis with a large differential

A clinical diagnosis with a large differential

While biopsy rarely is required, it may be helpful to distinguish SSSS from other entities in the differential diagnosis (TABLE^2,3,7-13).

Toxic epidermal necrolysis (TEN) is a rare and life-threatening desquamating disease nearly always caused by a reaction to medications, including antibiotics. TEN can occur at any age. Fever, diffuse erythema, and extensive epidermal involvement (>30% of skin) differentiate TEN from Stevens-Johnson syndrome (SJS), which affects less than 10% of the epidermis. It is worth mentioning that TEN and SJS are now considered to be a spectrum of one disease, and an overlap syndrome has been described with 10% to 30% of skin affected.⁸ Diagnosis is made clinically, although skin biopsy routinely is performed.^7,9

Congenital syphilis features a red or pink maculopapular rash followed by desquamation. Lesions are more common on the soles.¹⁰ Desquamation or ulcerative skin lesions should be examined for spirochetes.¹¹ A quantitative, nontreponemal test such as the rapid plasma reagin (RPR) or the Venereal Disease Research Laboratory (VDRL) will be positive in most infants if exposed through the placenta, but antibodies will disappear in uninfected infants by 6 months of age.⁸

Congenital cutaneous candidiasis presents with a generalized eruption of erythematous macules, papules, and/or pustules with widespread desquamating and/or erosive dermatitis. Premature neonates with extremely low birth weight are at higher risk.¹³ Diagnosis is confirmed on microscopy by the presence of Candida albicans spores in skin scrapings.¹³

Neonatal herpes simplex virus (HSV) symptoms typically appear between 1 and 3 weeks of life, with 60% to 70% of cases presenting with classic clustering vesicles on an erythematous base.¹⁴ Diagnosis is made with HSV viral culture or polymerase chain reaction (PCR).

Continue to: SSSS should be considered a pediatrics emergency

SSSS should be considered a pediatric emergency due to potential complications. Core measures of SSSS treatment include immediate administration of intravenous (IV) antibiotics. US population studies suggest clindamycin and penicillinase-resistant penicillin as empiric therapy.¹⁵ However, local strains and resistance patterns, including the prevalence of MRSA, as well as age, comorbidities, and severity of illness should influence antibiotic selection.

IV nafcillin or oxacillin may be used with pediatric dosing of 150 mg/kg daily divided every 6 hours for methicillin-sensitive Staphylococcus aureus (MSSA). For suspected MRSA, IV vancomycin should be considered, with an infant dose of 40 to 60 mg/kg daily divided every 6 hours.¹⁶ Fluid, electrolyte, and nutritional management should be addressed immediately. Ongoing fluid losses due to exfoliated skin must be replaced, and skin care to desquamated areas also should be addressed urgently.

Our patient. Phone consultation with an infectious disease specialist at a local children’s hospital resulted in a recommendation to treat for sepsis empirically with IV vancomycin, cefotaxime, and acyclovir. Acyclovir was discontinued once the HSV PCR came back negative. The antibiotic coverage was narrowed to IV ampicillin 50 mg/kg every 8 hours when cerebrospinal fluid and blood cultures returned negative at 48 hours, wound culture sensitivity grew MSSA, and the patient’s clinical condition stabilized. Our patient received 10 days of IV antibiotics and was discharged on oral amoxicillin 50 mg/kg divided twice daily for a total of 14 days of treatment per recommendations by the infectious disease specialist. Our patient fully recovered without any residual skin findings after completion of the antibiotic course.

CORRESPONDENCE
Jennifer J. Walker, MD, MPH, Hawaii Island Family Health Center at Hilo Medical Center, 1190 Waianuenue Ave, Hilo, HI 96720; jjwalker@hhsc.org

A 9-day-old boy was brought to the emergency department by his mother. The infant had been doing well until his most recent diaper change when his mother noticed a rash around the umbilicus (FIGURE), genitalia, and anus.

The infant was born at term via spontaneous vaginal delivery. The pregnancy was uncomplicated; the infant’s mother was group B strep negative. Following a routine postpartum course, the infant underwent an elective circumcision before hospital discharge on his second day of life. There were no interval reports of irritability, poor feeding, fevers, vomiting, or changes in urine or stool output.

The mother denied any recent unusual exposures, sick contacts, or travel. However, upon further questioning, the mother noted that she herself had several small open wounds on the torso that she attributed to untreated methicillin-resistant Staphylococcus aureus (MRSA).

On physical examination, the infant was overall well-appearing and was breastfeeding vigorously without respiratory distress or cyanosis. He was afebrile with normal vital signs. The majority of the physical examination was normal; however, there was erythematous desquamation around the umbilical stump and genitalia with no vesicles noted. The umbilical stump had a small amount of purulent drainage and necrosis centrally. The infant had a 1-cm round, peeling lesion on the left temple (FIGURE) with a small amount of dried serosanguinous drainage and similar superficial peeling lesions at the left preauricular area and anterior chest. There was no underlying fluctuance and only minimal surrounding erythema.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Based on the age of the patient, clinical presentation, and suspected maternal MRSA infection (with possible transmission to the infant), we diagnosed staphylococcal scalded skin syndrome (SSSS) in this patient. SSSS is rare, with annual incidence of 45 cases per million US infants under the age of 2.¹ Newborns with a generalized form of SSSS commonly present with fever, poor feeding, irritability, and lethargy. This is followed by a generalized erythematous rash that initially may appear on the head and neck and spread to the rest of the body. Large, fragile blisters subsequently appear. These blisters rupture on gentle pressure, which is known as a positive Nikolsky sign. Ultimately, large sheets of skin easily slough off, leaving raw, denuded skin.²

S aureus is not part of normal skin flora, yet it is found on the skin and mucous membranes of 19% to 55% of healthy adults and children.³S aureus can cause a wide range of infections ranging from abscesses to cellulitis; SSSS is caused by hematogenous spread of S aureus exfoliative toxin. Newborns and immunocompromised patients are particularly susceptible.

Staphylococcal scalded skin syndrome should be considered a pediatric emergency due to potential complications such as sepsis.

Neonatal patients with SSSS most commonly present at 3 to 16 days of age.² The lack of antitoxin antibody in neonates allows the toxin to reach the epidermis where it acts locally to produce the characteristic fragile skin lesions that often rupture prior to clinical presentation.^2,4 During progression of the disease, flaky skin desquamation will occur as the lesions heal.

A retrospective review of 39 cases of SSSS identified pneumonia as the most frequent complication, occurring in 74.4% of the cases.⁵ The mortality rate of SSSS is up to 5%, and is associated with sepsis, superinfection, electrolyte imbalances, and extensive skin involvement.^2,6

If SSSS is suspected, obtain cultures from the blood, urine, eyes, nose, throat, and skin lesions to identify the primary focus of infection.⁷ However, the retrospective review of 39 cases (noted above) found a positive rate of S aureus isolation of only 23.5%.⁵ Physicians will often have to make a diagnosis based on clinical presentation and empirically initiate broad-spectrum antibiotics while considering alternative diagnoses.

Continue to: A clinical diagnosis with a large differential

A clinical diagnosis with a large differential

While biopsy rarely is required, it may be helpful to distinguish SSSS from other entities in the differential diagnosis (TABLE^2,3,7-13).

Toxic epidermal necrolysis (TEN) is a rare and life-threatening desquamating disease nearly always caused by a reaction to medications, including antibiotics. TEN can occur at any age. Fever, diffuse erythema, and extensive epidermal involvement (>30% of skin) differentiate TEN from Stevens-Johnson syndrome (SJS), which affects less than 10% of the epidermis. It is worth mentioning that TEN and SJS are now considered to be a spectrum of one disease, and an overlap syndrome has been described with 10% to 30% of skin affected.⁸ Diagnosis is made clinically, although skin biopsy routinely is performed.^7,9

Congenital syphilis features a red or pink maculopapular rash followed by desquamation. Lesions are more common on the soles.¹⁰ Desquamation or ulcerative skin lesions should be examined for spirochetes.¹¹ A quantitative, nontreponemal test such as the rapid plasma reagin (RPR) or the Venereal Disease Research Laboratory (VDRL) will be positive in most infants if exposed through the placenta, but antibodies will disappear in uninfected infants by 6 months of age.⁸

Congenital cutaneous candidiasis presents with a generalized eruption of erythematous macules, papules, and/or pustules with widespread desquamating and/or erosive dermatitis. Premature neonates with extremely low birth weight are at higher risk.¹³ Diagnosis is confirmed on microscopy by the presence of Candida albicans spores in skin scrapings.¹³

Neonatal herpes simplex virus (HSV) symptoms typically appear between 1 and 3 weeks of life, with 60% to 70% of cases presenting with classic clustering vesicles on an erythematous base.¹⁴ Diagnosis is made with HSV viral culture or polymerase chain reaction (PCR).

Continue to: SSSS should be considered a pediatrics emergency

SSSS should be considered a pediatric emergency due to potential complications. Core measures of SSSS treatment include immediate administration of intravenous (IV) antibiotics. US population studies suggest clindamycin and penicillinase-resistant penicillin as empiric therapy.¹⁵ However, local strains and resistance patterns, including the prevalence of MRSA, as well as age, comorbidities, and severity of illness should influence antibiotic selection.

IV nafcillin or oxacillin may be used with pediatric dosing of 150 mg/kg daily divided every 6 hours for methicillin-sensitive Staphylococcus aureus (MSSA). For suspected MRSA, IV vancomycin should be considered, with an infant dose of 40 to 60 mg/kg daily divided every 6 hours.¹⁶ Fluid, electrolyte, and nutritional management should be addressed immediately. Ongoing fluid losses due to exfoliated skin must be replaced, and skin care to desquamated areas also should be addressed urgently.

Our patient. Phone consultation with an infectious disease specialist at a local children’s hospital resulted in a recommendation to treat for sepsis empirically with IV vancomycin, cefotaxime, and acyclovir. Acyclovir was discontinued once the HSV PCR came back negative. The antibiotic coverage was narrowed to IV ampicillin 50 mg/kg every 8 hours when cerebrospinal fluid and blood cultures returned negative at 48 hours, wound culture sensitivity grew MSSA, and the patient’s clinical condition stabilized. Our patient received 10 days of IV antibiotics and was discharged on oral amoxicillin 50 mg/kg divided twice daily for a total of 14 days of treatment per recommendations by the infectious disease specialist. Our patient fully recovered without any residual skin findings after completion of the antibiotic course.

CORRESPONDENCE
Jennifer J. Walker, MD, MPH, Hawaii Island Family Health Center at Hilo Medical Center, 1190 Waianuenue Ave, Hilo, HI 96720; jjwalker@hhsc.org

THE CASE

A 78-year-old woman with a history of anxiety and hypertension presented to our family medicine residency practice in Massachusetts with subacute polyarticular arthralgias that had been present for 2 months. She complained of pain and swelling of both ankles and the right knee. She noted that her symptoms had started on a recent trip to the Dominican Republic, where she developed generalized joint pain and a fever that lasted 1 to 2 weeks and subsequently resolved with the lingering polyarthralgias. She denied any rash, constitutional symptoms, photosensitivity, headaches, photophobia, or history of tick bite. Physical examination revealed normal vital signs, notable warmth and swelling of the bilateral ankles that was worse on the right side, and swelling of the right knee with effusion—but no tenderness—to palpation.

THE DIAGNOSIS

The patient’s labwork revealed a white blood cell count of 5900/mcL (reference range, 4500–11,000/mcL), hemoglobin count of 12.5 g/dL (reference range, 14–17.5 g/dL), and a platelet count of 230×10³/mcL. Electrolytes and renal function were normal. She had an elevated erythrocyte sedimentation rate of 34 mm/h (reference range, 0–20 mm/h) and a positive antinuclear antibody (ANA) test, but no titer was reported. Anti-chikungunya IgG and IgM antibodies were positive on enzyme-linked immunosorbent assay (ELISA) serologic testing.

DISCUSSION

Chikungunya is an infectious disease that is relatively rare in the United States. Chikungunya was rarely identified in American travelers prior to 2006, but incidence increased over the next decade. In 2014, a total of 2811 cases were reported.¹ Chikungunya is an RNA arbovirus that is transmitted by Aedes aegypti and Aedes albopictus mosquitoes and is endemic to West Africa. Within the last 2 decades, there has been an increasing number of outbreaks in India, Asia, Europe, and the Americas, where the highest incidence is in South America, followed by Central America. In the United States, almost all reported cases of chikungunya infection have been in travelers returning from endemic areas.² The first 2 known cases of local transmission in the United States were reported in Florida in July 2014.³ Local transmission of chikungunya is significant in that it represents the possibility of a local reservoir for sustained transmission.

Disease presentation. Patients will initially complain of a high fever and severe distal polyarthralgias that usually are symmetric. The most common symptoms are polyarthralgias (87%–98% of patients), myalgias (46%–59%), and a maculopapular rash involving the palms and soles (40%–50%).⁴ Other associated symptoms include headaches, photophobia, and digestive symptoms. Respiratory symptoms are not present in chikungunya.⁵

The term chikungunya is derived from a Kimakonde (central Bantu) word meaning “that which bends up” because of the arthralgia caused by the disease. Fever usually lasts 3 to 7 days; polyarthralgia begins shortly after the onset of fever.⁴ Frank arthritis also may be present. Infection often exacerbates a previously damaged or diseased joint. Acute symptoms usually persist for 1 to 2 weeks, but arthralgias and arthritis can persist for months to years following resolution of the acute disease.⁶ In one study of 47 patients with acute chikungunya in Marseilles, France, the number of patients who were symptomatic declined from 88% to 86%, 48%, and 4% at 1, 3, 6, and 15 months, respectively.⁷

The differential diagnosis includes tropical infectious diseases (dengue, chikungunya, Zika, and leptospirosis) in patients who have recently traveled to the tropics and who complain of subacute polyarticular arthralgias or arthritis; locally acquired infections associated with arthralgia/arthritis such as Lyme disease and other tick-borne diseases and rickettsial infections; parvovirus B19 and other postinfectious arthritides; and rheumatologic conditions such as systemic lupus.

Chikungunya virus is increasingly common in American travelers returning from tropical and subtropical regions.

Clinical differentiation among dengue, chikungunya, and Zika may be difficult, although persistent frank arthritis is much more common in chikungunya than in dengue or Zika. Furthermore, conjunctivitis is present in Zika but is absent in chikungunya. Chikungunya also is more likely to cause high fever, severe arthralgia, arthritis, rash, and lymphopenia than Zika or dengue. Dengue is more likely to cause lymphopenia and hemorrhagic consequences than is chikungunya or Zika.⁸

Continue to: In our patient...

In our patient, dengue titers were not obtained because the duration of symptoms was thought to be more consistent with chikungunya, but testing for dengue also would have been appropriate. If present, fever typically is low-grade in Zika and is shorter in duration than in chikungunya (approximately 2–3 days vs 5–7 days).⁹ Coinfection with chikungunya and Zika sometimes occurs because the same mosquito species transmit both diseases.

The most common test for diagnosing acute chikungunya is ELISA serologic testing for IgM antibodies, which develop toward the end of the first week of infection; earlier in that first week, serum testing for viral RNA may be performed by polymerase chain reaction.

Treatment is largely supportive

Treatment of acute chikungunya is largely supportive and includes anti-inflammatory agents. To our knowledge, no antiviral agents have been shown to be effective. Postacute or chronic symptoms may require treatment with glucocorticoids or other immunomodulatory medications. A 2017 literature review of treatments for chikungunya-associated rheumatic disorders showed evidence that chloroquine was more effective than placebo for chronic pain relief. Also, adding a disease-modifying antirheumatic agent in combination with chloroquine was more effective for controlling pain and reducing disability than hydroxychloroquine monotherapy.¹⁰

Our patient was treated with ibuprofen only and experienced resolution of joint symptoms several months after the initial presentation. A repeat ANA test 12 months later was negative.

A 2009 review of the medical literature revealed a single case report of chikungunya associated with positive ANA.⁸ Although a positive ANA may be associated with acute viral infections, significantly elevated ANA levels typically are associated with autoimmunity. Resolution of the patient’s serum ANA 1 year later suggested that the positive ANA was not secondary to a pre-existing rheumatologic condition but rather a consequence of her body’s response to the chikungunya infection itself. Our case raises the hypothesis that, at least in some cases, chikungunya somehow stimulates a temporary autoimmune response, which may help explain why immunomodulatory medications can be effective treatment options.

Continue to: THE TAKEAWAY

Chikungunya is increasingly common in tropical and subtropical regions. Family physicians practicing in the United States should become familiar with the common patterns of presentation of viruses such as chikungunya, dengue, and Zika. Obtaining a travel history for patients presenting with arthritis improves the differential diagnosis and may even reveal the cause of the condition.

CORRESPONDENCE
Jeremy Golding, MD, 279 Lincoln Street, Worcester, MA 01605; Jeremy.Golding@umassmemorial.org

THE CASE

A 78-year-old woman with a history of anxiety and hypertension presented to our family medicine residency practice in Massachusetts with subacute polyarticular arthralgias that had been present for 2 months. She complained of pain and swelling of both ankles and the right knee. She noted that her symptoms had started on a recent trip to the Dominican Republic, where she developed generalized joint pain and a fever that lasted 1 to 2 weeks and subsequently resolved with the lingering polyarthralgias. She denied any rash, constitutional symptoms, photosensitivity, headaches, photophobia, or history of tick bite. Physical examination revealed normal vital signs, notable warmth and swelling of the bilateral ankles that was worse on the right side, and swelling of the right knee with effusion—but no tenderness—to palpation.

THE DIAGNOSIS

The patient’s labwork revealed a white blood cell count of 5900/mcL (reference range, 4500–11,000/mcL), hemoglobin count of 12.5 g/dL (reference range, 14–17.5 g/dL), and a platelet count of 230×10³/mcL. Electrolytes and renal function were normal. She had an elevated erythrocyte sedimentation rate of 34 mm/h (reference range, 0–20 mm/h) and a positive antinuclear antibody (ANA) test, but no titer was reported. Anti-chikungunya IgG and IgM antibodies were positive on enzyme-linked immunosorbent assay (ELISA) serologic testing.

DISCUSSION

Chikungunya is an infectious disease that is relatively rare in the United States. Chikungunya was rarely identified in American travelers prior to 2006, but incidence increased over the next decade. In 2014, a total of 2811 cases were reported.¹ Chikungunya is an RNA arbovirus that is transmitted by Aedes aegypti and Aedes albopictus mosquitoes and is endemic to West Africa. Within the last 2 decades, there has been an increasing number of outbreaks in India, Asia, Europe, and the Americas, where the highest incidence is in South America, followed by Central America. In the United States, almost all reported cases of chikungunya infection have been in travelers returning from endemic areas.² The first 2 known cases of local transmission in the United States were reported in Florida in July 2014.³ Local transmission of chikungunya is significant in that it represents the possibility of a local reservoir for sustained transmission.

Disease presentation. Patients will initially complain of a high fever and severe distal polyarthralgias that usually are symmetric. The most common symptoms are polyarthralgias (87%–98% of patients), myalgias (46%–59%), and a maculopapular rash involving the palms and soles (40%–50%).⁴ Other associated symptoms include headaches, photophobia, and digestive symptoms. Respiratory symptoms are not present in chikungunya.⁵

The term chikungunya is derived from a Kimakonde (central Bantu) word meaning “that which bends up” because of the arthralgia caused by the disease. Fever usually lasts 3 to 7 days; polyarthralgia begins shortly after the onset of fever.⁴ Frank arthritis also may be present. Infection often exacerbates a previously damaged or diseased joint. Acute symptoms usually persist for 1 to 2 weeks, but arthralgias and arthritis can persist for months to years following resolution of the acute disease.⁶ In one study of 47 patients with acute chikungunya in Marseilles, France, the number of patients who were symptomatic declined from 88% to 86%, 48%, and 4% at 1, 3, 6, and 15 months, respectively.⁷

The differential diagnosis includes tropical infectious diseases (dengue, chikungunya, Zika, and leptospirosis) in patients who have recently traveled to the tropics and who complain of subacute polyarticular arthralgias or arthritis; locally acquired infections associated with arthralgia/arthritis such as Lyme disease and other tick-borne diseases and rickettsial infections; parvovirus B19 and other postinfectious arthritides; and rheumatologic conditions such as systemic lupus.

Chikungunya virus is increasingly common in American travelers returning from tropical and subtropical regions.

Clinical differentiation among dengue, chikungunya, and Zika may be difficult, although persistent frank arthritis is much more common in chikungunya than in dengue or Zika. Furthermore, conjunctivitis is present in Zika but is absent in chikungunya. Chikungunya also is more likely to cause high fever, severe arthralgia, arthritis, rash, and lymphopenia than Zika or dengue. Dengue is more likely to cause lymphopenia and hemorrhagic consequences than is chikungunya or Zika.⁸

Continue to: In our patient...

In our patient, dengue titers were not obtained because the duration of symptoms was thought to be more consistent with chikungunya, but testing for dengue also would have been appropriate. If present, fever typically is low-grade in Zika and is shorter in duration than in chikungunya (approximately 2–3 days vs 5–7 days).⁹ Coinfection with chikungunya and Zika sometimes occurs because the same mosquito species transmit both diseases.

The most common test for diagnosing acute chikungunya is ELISA serologic testing for IgM antibodies, which develop toward the end of the first week of infection; earlier in that first week, serum testing for viral RNA may be performed by polymerase chain reaction.

Treatment is largely supportive

Treatment of acute chikungunya is largely supportive and includes anti-inflammatory agents. To our knowledge, no antiviral agents have been shown to be effective. Postacute or chronic symptoms may require treatment with glucocorticoids or other immunomodulatory medications. A 2017 literature review of treatments for chikungunya-associated rheumatic disorders showed evidence that chloroquine was more effective than placebo for chronic pain relief. Also, adding a disease-modifying antirheumatic agent in combination with chloroquine was more effective for controlling pain and reducing disability than hydroxychloroquine monotherapy.¹⁰

Our patient was treated with ibuprofen only and experienced resolution of joint symptoms several months after the initial presentation. A repeat ANA test 12 months later was negative.

A 2009 review of the medical literature revealed a single case report of chikungunya associated with positive ANA.⁸ Although a positive ANA may be associated with acute viral infections, significantly elevated ANA levels typically are associated with autoimmunity. Resolution of the patient’s serum ANA 1 year later suggested that the positive ANA was not secondary to a pre-existing rheumatologic condition but rather a consequence of her body’s response to the chikungunya infection itself. Our case raises the hypothesis that, at least in some cases, chikungunya somehow stimulates a temporary autoimmune response, which may help explain why immunomodulatory medications can be effective treatment options.

Continue to: THE TAKEAWAY

Chikungunya is increasingly common in tropical and subtropical regions. Family physicians practicing in the United States should become familiar with the common patterns of presentation of viruses such as chikungunya, dengue, and Zika. Obtaining a travel history for patients presenting with arthritis improves the differential diagnosis and may even reveal the cause of the condition.

CORRESPONDENCE
Jeremy Golding, MD, 279 Lincoln Street, Worcester, MA 01605; Jeremy.Golding@umassmemorial.org

THE CASE

A 78-year-old woman with a history of anxiety and hypertension presented to our family medicine residency practice in Massachusetts with subacute polyarticular arthralgias that had been present for 2 months. She complained of pain and swelling of both ankles and the right knee. She noted that her symptoms had started on a recent trip to the Dominican Republic, where she developed generalized joint pain and a fever that lasted 1 to 2 weeks and subsequently resolved with the lingering polyarthralgias. She denied any rash, constitutional symptoms, photosensitivity, headaches, photophobia, or history of tick bite. Physical examination revealed normal vital signs, notable warmth and swelling of the bilateral ankles that was worse on the right side, and swelling of the right knee with effusion—but no tenderness—to palpation.

THE DIAGNOSIS

The patient’s labwork revealed a white blood cell count of 5900/mcL (reference range, 4500–11,000/mcL), hemoglobin count of 12.5 g/dL (reference range, 14–17.5 g/dL), and a platelet count of 230×10³/mcL. Electrolytes and renal function were normal. She had an elevated erythrocyte sedimentation rate of 34 mm/h (reference range, 0–20 mm/h) and a positive antinuclear antibody (ANA) test, but no titer was reported. Anti-chikungunya IgG and IgM antibodies were positive on enzyme-linked immunosorbent assay (ELISA) serologic testing.

DISCUSSION

Chikungunya is an infectious disease that is relatively rare in the United States. Chikungunya was rarely identified in American travelers prior to 2006, but incidence increased over the next decade. In 2014, a total of 2811 cases were reported.¹ Chikungunya is an RNA arbovirus that is transmitted by Aedes aegypti and Aedes albopictus mosquitoes and is endemic to West Africa. Within the last 2 decades, there has been an increasing number of outbreaks in India, Asia, Europe, and the Americas, where the highest incidence is in South America, followed by Central America. In the United States, almost all reported cases of chikungunya infection have been in travelers returning from endemic areas.² The first 2 known cases of local transmission in the United States were reported in Florida in July 2014.³ Local transmission of chikungunya is significant in that it represents the possibility of a local reservoir for sustained transmission.

Disease presentation. Patients will initially complain of a high fever and severe distal polyarthralgias that usually are symmetric. The most common symptoms are polyarthralgias (87%–98% of patients), myalgias (46%–59%), and a maculopapular rash involving the palms and soles (40%–50%).⁴ Other associated symptoms include headaches, photophobia, and digestive symptoms. Respiratory symptoms are not present in chikungunya.⁵

The term chikungunya is derived from a Kimakonde (central Bantu) word meaning “that which bends up” because of the arthralgia caused by the disease. Fever usually lasts 3 to 7 days; polyarthralgia begins shortly after the onset of fever.⁴ Frank arthritis also may be present. Infection often exacerbates a previously damaged or diseased joint. Acute symptoms usually persist for 1 to 2 weeks, but arthralgias and arthritis can persist for months to years following resolution of the acute disease.⁶ In one study of 47 patients with acute chikungunya in Marseilles, France, the number of patients who were symptomatic declined from 88% to 86%, 48%, and 4% at 1, 3, 6, and 15 months, respectively.⁷

The differential diagnosis includes tropical infectious diseases (dengue, chikungunya, Zika, and leptospirosis) in patients who have recently traveled to the tropics and who complain of subacute polyarticular arthralgias or arthritis; locally acquired infections associated with arthralgia/arthritis such as Lyme disease and other tick-borne diseases and rickettsial infections; parvovirus B19 and other postinfectious arthritides; and rheumatologic conditions such as systemic lupus.

Chikungunya virus is increasingly common in American travelers returning from tropical and subtropical regions.

Clinical differentiation among dengue, chikungunya, and Zika may be difficult, although persistent frank arthritis is much more common in chikungunya than in dengue or Zika. Furthermore, conjunctivitis is present in Zika but is absent in chikungunya. Chikungunya also is more likely to cause high fever, severe arthralgia, arthritis, rash, and lymphopenia than Zika or dengue. Dengue is more likely to cause lymphopenia and hemorrhagic consequences than is chikungunya or Zika.⁸

Continue to: In our patient...

In our patient, dengue titers were not obtained because the duration of symptoms was thought to be more consistent with chikungunya, but testing for dengue also would have been appropriate. If present, fever typically is low-grade in Zika and is shorter in duration than in chikungunya (approximately 2–3 days vs 5–7 days).⁹ Coinfection with chikungunya and Zika sometimes occurs because the same mosquito species transmit both diseases.

The most common test for diagnosing acute chikungunya is ELISA serologic testing for IgM antibodies, which develop toward the end of the first week of infection; earlier in that first week, serum testing for viral RNA may be performed by polymerase chain reaction.

Treatment is largely supportive

Treatment of acute chikungunya is largely supportive and includes anti-inflammatory agents. To our knowledge, no antiviral agents have been shown to be effective. Postacute or chronic symptoms may require treatment with glucocorticoids or other immunomodulatory medications. A 2017 literature review of treatments for chikungunya-associated rheumatic disorders showed evidence that chloroquine was more effective than placebo for chronic pain relief. Also, adding a disease-modifying antirheumatic agent in combination with chloroquine was more effective for controlling pain and reducing disability than hydroxychloroquine monotherapy.¹⁰

Our patient was treated with ibuprofen only and experienced resolution of joint symptoms several months after the initial presentation. A repeat ANA test 12 months later was negative.

A 2009 review of the medical literature revealed a single case report of chikungunya associated with positive ANA.⁸ Although a positive ANA may be associated with acute viral infections, significantly elevated ANA levels typically are associated with autoimmunity. Resolution of the patient’s serum ANA 1 year later suggested that the positive ANA was not secondary to a pre-existing rheumatologic condition but rather a consequence of her body’s response to the chikungunya infection itself. Our case raises the hypothesis that, at least in some cases, chikungunya somehow stimulates a temporary autoimmune response, which may help explain why immunomodulatory medications can be effective treatment options.

Continue to: THE TAKEAWAY

Chikungunya is increasingly common in tropical and subtropical regions. Family physicians practicing in the United States should become familiar with the common patterns of presentation of viruses such as chikungunya, dengue, and Zika. Obtaining a travel history for patients presenting with arthritis improves the differential diagnosis and may even reveal the cause of the condition.

CORRESPONDENCE
Jeremy Golding, MD, 279 Lincoln Street, Worcester, MA 01605; Jeremy.Golding@umassmemorial.org

THE CASE

Julia* is a 31-year-old woman, gravida 3 para 3, who presents to your office for evaluation after a recent emergency department (ED) visit. Her husband and children are with her. She is 4 months postpartum after an uncomplicated normal spontaneous vaginal delivery. She is breastfeeding her healthy baby boy and is using an intrauterine device for birth control. She went to the ED last week after “choking on a chip” while having lunch with her children. It felt like she “couldn’t breathe.” She called 911 herself. The ED evaluation was unremarkable. Her discharge diagnosis was “panic attack,” and she was sent home with a prescription for lorazepam.

Since the incident, she has been unable to eat any solid foods and has lost 7 pounds. She also reports a globus sensation, extreme fear of swallowing, insomnia, and pervasive thoughts that she could die at any moment and leave her children motherless. She has not taken the lorazepam.

She has a history of self-reported anxiety dating back to high school but no history of panic attacks. She has never been diagnosed with an anxiety disorder and has never before been prescribed anti-anxiety medication. She doesn’t have a history of postpartum depression in prior pregnancies, and a depression screening at her postpartum visit 2 months ago was negative.

● How would you proceed with this patient?

*The patient’s name has been changed to protect her identity.

During the perinatal period, women are particularly vulnerable to affective disorders, and primary care physicians are encouraged to routinely screen for and treat depression in pregnant and postpartum women.¹ However, anxiety disorders have a higher incidence than mood disorders in the general population,² and perinatal anxiety may be more widely underrecognized and undertreated than depression.³ In addition, higher depression scores early in pregnancy have been shown to predict higher anxiety later in pregnancy.⁴

As family physicians, we are well-trained to recognize and treat anxiety disorders in the general patient population; however, we may lack the awareness and tools to identify these conditions in the perinatal period. Given our frequent encounters with both mom and baby in a child’s first year of life, we are uniquely positioned to promptly recognize, diagnose, and treat postpartum anxiety and thereby improve health outcomes for families.

DEFINING PERINATAL ANXIETY

Anxiety disorders (including generalized anxiety disorder, panic, phobia, and social anxiety) are the most common mental health disorders evaluated and treated in the primary care setting, with a lifetime prevalence of close to 30%.²

Continue to: A recent report from...

A recent report from the Centers for Disease Control and Prevention (CDC) estimates that 1 in 9 women experience symptoms of postpartum depression.⁵ The prevalence of anxiety disorders during pregnancy and the early postpartum period is not as well-known, but studies suggest that perinatal anxiety is much more prevalent than depression. In one study, generalized anxiety disorder (GAD) in the pre- and postnatal periods was 15.8% and 17.1%, respectively; an incidence far exceeding that of perinatal depression (3.9% and 4.8%, for the same periods).⁶ Additional evidence suggests that even more women in the postnatal period experience clinically significant levels of anxiety but do not meet full diagnostic criteria for an anxiety disorder.⁷

Consider screening for postpartum anxiety with the GAD-7 or the Edinburgh Postnatal Depression Scale (questions 3-5).

In another study, 9.5% of women met criteria for GAD at some point during pregnancy, with highest anxiety levels in the first trimester.⁸ Women with a history of GAD, lower education, lack of social support, and personal history of child abuse have the highest risk for postpartum anxiety. Women with a history of posttraumatic stress disorder (PTSD) may be twice as likely to develop postpartum anxiety as healthy women.⁹

It has been well-documented that sleep disruption—which is very common in new mothers in the postnatal period—contributes to mood and anxiety disorders.^10,11

Clarifying a diagnosis of postpartum anxiety

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5)¹² specifies no diagnosis of postpartum anxiety disorder. And no standardized diagnostic criteria exist. It is likely that in some cases, postpartum anxiety represents an exacerbation of underlying GAD, and in other cases it is a situational disorder brought about by specific circumstances of the peripartum period.

The DSM-5 does, however, provide a helpful diagnostic approach. It defines a diagnosis of postpartum depression as being a variant of major depressive disorder (MDD) in which a woman must 1) meet criteria for a major depressive episode; and 2) occur during pregnancy or within 4 weeks of delivery. In practice, many clinicians extend the second requirement to include the first year postpartum.¹³ There is a “with anxious distress” specifier for major depression in the DSM-5, but the 2 disorders are otherwise unlinked.

Continue to: To apply the...

To apply the DSM-5 principles for postpartum depression to postpartum anxiety, a patient would need to 1) meet the diagnostic criteria for an anxiety disorder that 2) have their onset within a specified perinatal period. Variant presentations of anxiety in the postpartum period might include panic disorder and phobias, which could also interfere with a woman’s ability to care for her child.

The DSM-5 offers the following criteria for GAD¹²:

• excessive worry about a variety of topics
• worry that is experienced as hard to control
• worry associated with at least 3 physical or cognitive symptoms: edginess/restlessness, tiring easily, impaired concentration, irritability
• anxiety, worry, or associated symptoms that make it hard to carry out day-to-day activities and responsibilities
• symptoms that are unrelated to any other medical conditions and cannot be explained by the effect of substances including a prescription medication, alcohol, or recreational drugs
• symptoms that are not better explained by a different mental disorder.

Debilitating effects of postpartum anxiety

Many women experience some level of anxiety during pregnancy and early postpartum—anxiety that may range from normal and adaptive to debilitating.¹⁴ While the challenges of caring for a newborn are likely to bring some level of anxiety, these symptoms should be transient and not interfere with a woman’s capacity to care for her infant, herself, or her family.

Postpartum anxiety has been associated with a prior fear of giving birth, fear of death (of both mother and baby), lack of control, lack of self-confidence, and lack of confidence in the medical system.⁹ The experience of such ongoing disturbing thoughts or feelings of worry and tension that affect a woman’s ability to manage from day to day should indicate an illness state that deserves medical attention.

Consider diagnosing postpartum anxiety when DSM-5 criteria for generalized anxiety disorder are met during the first year postpartum.

Mothers with postpartum anxiety disorders report significantly less bonding with their infants than do mothers without anxiety.¹⁵ A recent narrative review describes numerous studies that illustrate the negative effects of postpartum anxiety on bonding, breastfeeding, infant temperament, early childhood development, and conduct disorders.¹⁶ Anxious women may be less likely to initiate breastfeeding, have more challenges with breastfeeding, and even have a different milk composition.¹⁷ Women with prenatal anxiety are also more likely to stop breastfeeding prematurely.¹⁸ Children of anxious mothers may be more likely to have a difficult temperament and to display more distress.¹⁹ There are small studies demonstrating deficits in early infant development and increases in conduct disorder in the male offspring of anxious women.²⁰

Continue to: SCREENING FOR POSTPARTUM ANXIETY

SCREENING FOR POSTPARTUM ANXIETY

Screening for perinatal depression has become standard of care, and the Edinburgh Postnatal Depression Scale (EPDS) is a widely used instrument.¹ The EPDS, a 10-question self-report scale, was created and validated to screen for perinatal depression, with a cutoff of > 10/30 usually considered a positive result.

Researchers have investigated the utility of the EPDS as a screening tool for perinatal anxiety as well.^21-23 These studies show some promise, but there are questions as to whether a total score or a subscale score of the EPDS is most accurate in detecting anxiety. Women with perinatal anxiety may score low on the total EPDS, yet score higher on 3 anxiety-specific questions (TABLE 1²³). For this reason, several studies propose an EPDS anxiety subscore or subscale (referred to as EPDS-3A).

Of note, there are some women who will score high on the subscale who do not ultimately meet the criteria for an anxiety disorder diagnosis. Clinicians should not over-interpret these scores and should always use sound clinical judgment when making a diagnosis.

Research has also focused on using the GAD 7-item (GAD-7) scale (TABLE 2²⁴),²⁵ and on the development of new tools and screening tools designed specifically for perinatal anxiety, including the Postpartum Worry Scale²⁶ and the Postpartum Specific Anxiety Scale (PSAS).²⁷

Family physicians may consider using the EPDS subscale if they are already using the EPDS, or adding the GAD-7 as a separate screening instrument during a postpartum visit. To date there is no one standard recommendation or screening tool.

Continue to: NONPHARMACOLOGIC TREATMENT

As one would with any patient who has situational anxiety, help new mothers find ways to increase their coping skills, reduce stress, and mobilize social supports and family resources. Given the association between sleep disruption and perinatal anxiety, counsel new mothers, especially those at high risk for postpartum anxiety, to prioritize sleep during this vulnerable time. To that end, consider recommending that they ask partners, family members, or friends to help them take care of the infant at night (or during the day). Such nonmedical interventions may be sufficient for women with mild anxiety.

Very few studies have addressed nonpharmacologic management of postpartum anxiety, but cognitive behavioral therapy (CBT) has been shown to help in managing and treating anxiety disorders outside of pregnancy.²⁸ A few small studies indicate promise for CBT and for mindfulness-based interventions (MBIs) during pregnancy.²⁹

A 2016 systematic review of pharmacologic and nonpharmacologic treatment of anxiety in the perinatal period found support for the use of CBT for panic disorder and specific phobias both in pregnancy and postpartum.³⁰ A very small study found that teaching mothers to massage their preterm infants decreased maternal anxiety.³¹

If the patient is amenable, it is reasonable to start with behavioral interventions like CBT or MBI before pharmacologic treatment—particularly when physicians have mental health professionals embedded in their primary care team.

PHARMACOLOGIC TREATMENT

Selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) are considered first-line treatment for moderate to severe anxiety disorders in the perinatal and postnatal period.

Continue to: SSRIs in pregnancy

SSRIs in pregnancy. Lacking support of randomized controlled trials, most recommendations regarding SSRIs in pregnancy come from expert consensus or cohort and case control studies. Studies have raised concerns for an increased rate of congenital heart defects among fetuses exposed to paroxetine³² and primary pulmonary hypertension with all SSRIs.³³ But the absolute risks are quite small. There have also been concerns regarding low birth weight and preterm birth, but it is possible that these outcomes result from the depression itself rather than the medication.³⁴

Many experts believe that not treating anxiety/ depression is more harmful than the fetal effects of SSRIs.

Unfortunately, there are very few studies evaluating the efficacy of SSRIs in treating postpartum depression³⁵ and even fewer that specifically evaluate their effect on perinatal anxiety. Many experts believe that not treating anxiety/depression is actually more harmful than the fetal effects of SSRIs, and that SSRIs are largely safe in both pregnancy and while breastfeeding, with benefits outweighing the risks.

SSRIs while breastfeeding. SSRIs have been found to be present in varying levels in breastmilk but may or may not be present in the serum of nursing infants.³⁶ A 2008 guideline from the American College of Obstetricians and Gynecologists lists paroxetine, sertraline, and fluvoxamine as slightly safer than fluoxetine, escitalopram, and citalopram.³⁷ A 2015 systematic review similarly concluded that sertraline and paroxetine have the most safety data on lactation.³⁸ Lowest effective dose is always recommended to minimize exposure.

Benzodiazepines. As in the general population, benzodiazepines should be reserved for short-term use in acute anxiety and panic because they are associated with such adverse effects as worsening of depression/anxiety and risk of dependence and overdose. Longer-acting benzodiazepines (eg, clonazepam) are generally not recommended in lactation because of reported effects on infants, including sedation. Shorter-acting benzodiazepines (eg, lorazepam) are considered safer in lactation.³⁹

THE CASE

Julia saw her family physician 4 more times, was evaluated by an ear-nose-and-throat specialist for her throat complaints, saw a therapist for CBT and a psychiatrist for medication, had 3 more ED visits, and lost 23 pounds before she finally agreed to start an SSRI for postpartum anxiety. She screened high on the EPDS-3A (9/9) despite scoring low on the full EPDS for perinatal depression (total, 9/30).

Continue to: Because of her swallowing impediments...

Because of her swallowing impediments and because she was breastfeeding, sertraline solution was started at very small doses. It was titrated weekly to obtain therapeutic levels. By 4 weeks, her weight stabilized. By 8 weeks, she started gaining weight and sleeping better. She saw the therapist regularly to continue CBT techniques. Over the next several months she started eating a normal diet. She is currently maintained on her SSRI, is still breastfeeding, and has achieved insight into her perinatal anxiety disorder.

CORRESPONDENCE
Veronica Jordan, MD, 3569 Round Barn Cir #200, Santa Rosa, CA 95403; veronica.a.jordan@gmail.com.

THE CASE

Julia* is a 31-year-old woman, gravida 3 para 3, who presents to your office for evaluation after a recent emergency department (ED) visit. Her husband and children are with her. She is 4 months postpartum after an uncomplicated normal spontaneous vaginal delivery. She is breastfeeding her healthy baby boy and is using an intrauterine device for birth control. She went to the ED last week after “choking on a chip” while having lunch with her children. It felt like she “couldn’t breathe.” She called 911 herself. The ED evaluation was unremarkable. Her discharge diagnosis was “panic attack,” and she was sent home with a prescription for lorazepam.

Since the incident, she has been unable to eat any solid foods and has lost 7 pounds. She also reports a globus sensation, extreme fear of swallowing, insomnia, and pervasive thoughts that she could die at any moment and leave her children motherless. She has not taken the lorazepam.

She has a history of self-reported anxiety dating back to high school but no history of panic attacks. She has never been diagnosed with an anxiety disorder and has never before been prescribed anti-anxiety medication. She doesn’t have a history of postpartum depression in prior pregnancies, and a depression screening at her postpartum visit 2 months ago was negative.

● How would you proceed with this patient?

*The patient’s name has been changed to protect her identity.

During the perinatal period, women are particularly vulnerable to affective disorders, and primary care physicians are encouraged to routinely screen for and treat depression in pregnant and postpartum women.¹ However, anxiety disorders have a higher incidence than mood disorders in the general population,² and perinatal anxiety may be more widely underrecognized and undertreated than depression.³ In addition, higher depression scores early in pregnancy have been shown to predict higher anxiety later in pregnancy.⁴

As family physicians, we are well-trained to recognize and treat anxiety disorders in the general patient population; however, we may lack the awareness and tools to identify these conditions in the perinatal period. Given our frequent encounters with both mom and baby in a child’s first year of life, we are uniquely positioned to promptly recognize, diagnose, and treat postpartum anxiety and thereby improve health outcomes for families.

DEFINING PERINATAL ANXIETY

Anxiety disorders (including generalized anxiety disorder, panic, phobia, and social anxiety) are the most common mental health disorders evaluated and treated in the primary care setting, with a lifetime prevalence of close to 30%.²

Continue to: A recent report from...

A recent report from the Centers for Disease Control and Prevention (CDC) estimates that 1 in 9 women experience symptoms of postpartum depression.⁵ The prevalence of anxiety disorders during pregnancy and the early postpartum period is not as well-known, but studies suggest that perinatal anxiety is much more prevalent than depression. In one study, generalized anxiety disorder (GAD) in the pre- and postnatal periods was 15.8% and 17.1%, respectively; an incidence far exceeding that of perinatal depression (3.9% and 4.8%, for the same periods).⁶ Additional evidence suggests that even more women in the postnatal period experience clinically significant levels of anxiety but do not meet full diagnostic criteria for an anxiety disorder.⁷

Consider screening for postpartum anxiety with the GAD-7 or the Edinburgh Postnatal Depression Scale (questions 3-5).

In another study, 9.5% of women met criteria for GAD at some point during pregnancy, with highest anxiety levels in the first trimester.⁸ Women with a history of GAD, lower education, lack of social support, and personal history of child abuse have the highest risk for postpartum anxiety. Women with a history of posttraumatic stress disorder (PTSD) may be twice as likely to develop postpartum anxiety as healthy women.⁹

It has been well-documented that sleep disruption—which is very common in new mothers in the postnatal period—contributes to mood and anxiety disorders.^10,11

Clarifying a diagnosis of postpartum anxiety

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5)¹² specifies no diagnosis of postpartum anxiety disorder. And no standardized diagnostic criteria exist. It is likely that in some cases, postpartum anxiety represents an exacerbation of underlying GAD, and in other cases it is a situational disorder brought about by specific circumstances of the peripartum period.

The DSM-5 does, however, provide a helpful diagnostic approach. It defines a diagnosis of postpartum depression as being a variant of major depressive disorder (MDD) in which a woman must 1) meet criteria for a major depressive episode; and 2) occur during pregnancy or within 4 weeks of delivery. In practice, many clinicians extend the second requirement to include the first year postpartum.¹³ There is a “with anxious distress” specifier for major depression in the DSM-5, but the 2 disorders are otherwise unlinked.

Continue to: To apply the...

To apply the DSM-5 principles for postpartum depression to postpartum anxiety, a patient would need to 1) meet the diagnostic criteria for an anxiety disorder that 2) have their onset within a specified perinatal period. Variant presentations of anxiety in the postpartum period might include panic disorder and phobias, which could also interfere with a woman’s ability to care for her child.

The DSM-5 offers the following criteria for GAD¹²:

• excessive worry about a variety of topics
• worry that is experienced as hard to control
• worry associated with at least 3 physical or cognitive symptoms: edginess/restlessness, tiring easily, impaired concentration, irritability
• anxiety, worry, or associated symptoms that make it hard to carry out day-to-day activities and responsibilities
• symptoms that are unrelated to any other medical conditions and cannot be explained by the effect of substances including a prescription medication, alcohol, or recreational drugs
• symptoms that are not better explained by a different mental disorder.

Debilitating effects of postpartum anxiety

Many women experience some level of anxiety during pregnancy and early postpartum—anxiety that may range from normal and adaptive to debilitating.¹⁴ While the challenges of caring for a newborn are likely to bring some level of anxiety, these symptoms should be transient and not interfere with a woman’s capacity to care for her infant, herself, or her family.

Postpartum anxiety has been associated with a prior fear of giving birth, fear of death (of both mother and baby), lack of control, lack of self-confidence, and lack of confidence in the medical system.⁹ The experience of such ongoing disturbing thoughts or feelings of worry and tension that affect a woman’s ability to manage from day to day should indicate an illness state that deserves medical attention.

Consider diagnosing postpartum anxiety when DSM-5 criteria for generalized anxiety disorder are met during the first year postpartum.

Mothers with postpartum anxiety disorders report significantly less bonding with their infants than do mothers without anxiety.¹⁵ A recent narrative review describes numerous studies that illustrate the negative effects of postpartum anxiety on bonding, breastfeeding, infant temperament, early childhood development, and conduct disorders.¹⁶ Anxious women may be less likely to initiate breastfeeding, have more challenges with breastfeeding, and even have a different milk composition.¹⁷ Women with prenatal anxiety are also more likely to stop breastfeeding prematurely.¹⁸ Children of anxious mothers may be more likely to have a difficult temperament and to display more distress.¹⁹ There are small studies demonstrating deficits in early infant development and increases in conduct disorder in the male offspring of anxious women.²⁰

Continue to: SCREENING FOR POSTPARTUM ANXIETY

SCREENING FOR POSTPARTUM ANXIETY

Screening for perinatal depression has become standard of care, and the Edinburgh Postnatal Depression Scale (EPDS) is a widely used instrument.¹ The EPDS, a 10-question self-report scale, was created and validated to screen for perinatal depression, with a cutoff of > 10/30 usually considered a positive result.

Researchers have investigated the utility of the EPDS as a screening tool for perinatal anxiety as well.^21-23 These studies show some promise, but there are questions as to whether a total score or a subscale score of the EPDS is most accurate in detecting anxiety. Women with perinatal anxiety may score low on the total EPDS, yet score higher on 3 anxiety-specific questions (TABLE 1²³). For this reason, several studies propose an EPDS anxiety subscore or subscale (referred to as EPDS-3A).

Of note, there are some women who will score high on the subscale who do not ultimately meet the criteria for an anxiety disorder diagnosis. Clinicians should not over-interpret these scores and should always use sound clinical judgment when making a diagnosis.

Research has also focused on using the GAD 7-item (GAD-7) scale (TABLE 2²⁴),²⁵ and on the development of new tools and screening tools designed specifically for perinatal anxiety, including the Postpartum Worry Scale²⁶ and the Postpartum Specific Anxiety Scale (PSAS).²⁷

Family physicians may consider using the EPDS subscale if they are already using the EPDS, or adding the GAD-7 as a separate screening instrument during a postpartum visit. To date there is no one standard recommendation or screening tool.

Continue to: NONPHARMACOLOGIC TREATMENT

As one would with any patient who has situational anxiety, help new mothers find ways to increase their coping skills, reduce stress, and mobilize social supports and family resources. Given the association between sleep disruption and perinatal anxiety, counsel new mothers, especially those at high risk for postpartum anxiety, to prioritize sleep during this vulnerable time. To that end, consider recommending that they ask partners, family members, or friends to help them take care of the infant at night (or during the day). Such nonmedical interventions may be sufficient for women with mild anxiety.

Very few studies have addressed nonpharmacologic management of postpartum anxiety, but cognitive behavioral therapy (CBT) has been shown to help in managing and treating anxiety disorders outside of pregnancy.²⁸ A few small studies indicate promise for CBT and for mindfulness-based interventions (MBIs) during pregnancy.²⁹

A 2016 systematic review of pharmacologic and nonpharmacologic treatment of anxiety in the perinatal period found support for the use of CBT for panic disorder and specific phobias both in pregnancy and postpartum.³⁰ A very small study found that teaching mothers to massage their preterm infants decreased maternal anxiety.³¹

If the patient is amenable, it is reasonable to start with behavioral interventions like CBT or MBI before pharmacologic treatment—particularly when physicians have mental health professionals embedded in their primary care team.

PHARMACOLOGIC TREATMENT

Selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) are considered first-line treatment for moderate to severe anxiety disorders in the perinatal and postnatal period.

Continue to: SSRIs in pregnancy

SSRIs in pregnancy. Lacking support of randomized controlled trials, most recommendations regarding SSRIs in pregnancy come from expert consensus or cohort and case control studies. Studies have raised concerns for an increased rate of congenital heart defects among fetuses exposed to paroxetine³² and primary pulmonary hypertension with all SSRIs.³³ But the absolute risks are quite small. There have also been concerns regarding low birth weight and preterm birth, but it is possible that these outcomes result from the depression itself rather than the medication.³⁴

Many experts believe that not treating anxiety/ depression is more harmful than the fetal effects of SSRIs.

Unfortunately, there are very few studies evaluating the efficacy of SSRIs in treating postpartum depression³⁵ and even fewer that specifically evaluate their effect on perinatal anxiety. Many experts believe that not treating anxiety/depression is actually more harmful than the fetal effects of SSRIs, and that SSRIs are largely safe in both pregnancy and while breastfeeding, with benefits outweighing the risks.

SSRIs while breastfeeding. SSRIs have been found to be present in varying levels in breastmilk but may or may not be present in the serum of nursing infants.³⁶ A 2008 guideline from the American College of Obstetricians and Gynecologists lists paroxetine, sertraline, and fluvoxamine as slightly safer than fluoxetine, escitalopram, and citalopram.³⁷ A 2015 systematic review similarly concluded that sertraline and paroxetine have the most safety data on lactation.³⁸ Lowest effective dose is always recommended to minimize exposure.

Benzodiazepines. As in the general population, benzodiazepines should be reserved for short-term use in acute anxiety and panic because they are associated with such adverse effects as worsening of depression/anxiety and risk of dependence and overdose. Longer-acting benzodiazepines (eg, clonazepam) are generally not recommended in lactation because of reported effects on infants, including sedation. Shorter-acting benzodiazepines (eg, lorazepam) are considered safer in lactation.³⁹

THE CASE

Julia saw her family physician 4 more times, was evaluated by an ear-nose-and-throat specialist for her throat complaints, saw a therapist for CBT and a psychiatrist for medication, had 3 more ED visits, and lost 23 pounds before she finally agreed to start an SSRI for postpartum anxiety. She screened high on the EPDS-3A (9/9) despite scoring low on the full EPDS for perinatal depression (total, 9/30).

Continue to: Because of her swallowing impediments...

Because of her swallowing impediments and because she was breastfeeding, sertraline solution was started at very small doses. It was titrated weekly to obtain therapeutic levels. By 4 weeks, her weight stabilized. By 8 weeks, she started gaining weight and sleeping better. She saw the therapist regularly to continue CBT techniques. Over the next several months she started eating a normal diet. She is currently maintained on her SSRI, is still breastfeeding, and has achieved insight into her perinatal anxiety disorder.

CORRESPONDENCE
Veronica Jordan, MD, 3569 Round Barn Cir #200, Santa Rosa, CA 95403; veronica.a.jordan@gmail.com.

THE CASE

Julia* is a 31-year-old woman, gravida 3 para 3, who presents to your office for evaluation after a recent emergency department (ED) visit. Her husband and children are with her. She is 4 months postpartum after an uncomplicated normal spontaneous vaginal delivery. She is breastfeeding her healthy baby boy and is using an intrauterine device for birth control. She went to the ED last week after “choking on a chip” while having lunch with her children. It felt like she “couldn’t breathe.” She called 911 herself. The ED evaluation was unremarkable. Her discharge diagnosis was “panic attack,” and she was sent home with a prescription for lorazepam.

Since the incident, she has been unable to eat any solid foods and has lost 7 pounds. She also reports a globus sensation, extreme fear of swallowing, insomnia, and pervasive thoughts that she could die at any moment and leave her children motherless. She has not taken the lorazepam.

She has a history of self-reported anxiety dating back to high school but no history of panic attacks. She has never been diagnosed with an anxiety disorder and has never before been prescribed anti-anxiety medication. She doesn’t have a history of postpartum depression in prior pregnancies, and a depression screening at her postpartum visit 2 months ago was negative.

● How would you proceed with this patient?

*The patient’s name has been changed to protect her identity.

During the perinatal period, women are particularly vulnerable to affective disorders, and primary care physicians are encouraged to routinely screen for and treat depression in pregnant and postpartum women.¹ However, anxiety disorders have a higher incidence than mood disorders in the general population,² and perinatal anxiety may be more widely underrecognized and undertreated than depression.³ In addition, higher depression scores early in pregnancy have been shown to predict higher anxiety later in pregnancy.⁴

As family physicians, we are well-trained to recognize and treat anxiety disorders in the general patient population; however, we may lack the awareness and tools to identify these conditions in the perinatal period. Given our frequent encounters with both mom and baby in a child’s first year of life, we are uniquely positioned to promptly recognize, diagnose, and treat postpartum anxiety and thereby improve health outcomes for families.

DEFINING PERINATAL ANXIETY

Anxiety disorders (including generalized anxiety disorder, panic, phobia, and social anxiety) are the most common mental health disorders evaluated and treated in the primary care setting, with a lifetime prevalence of close to 30%.²

Continue to: A recent report from...

A recent report from the Centers for Disease Control and Prevention (CDC) estimates that 1 in 9 women experience symptoms of postpartum depression.⁵ The prevalence of anxiety disorders during pregnancy and the early postpartum period is not as well-known, but studies suggest that perinatal anxiety is much more prevalent than depression. In one study, generalized anxiety disorder (GAD) in the pre- and postnatal periods was 15.8% and 17.1%, respectively; an incidence far exceeding that of perinatal depression (3.9% and 4.8%, for the same periods).⁶ Additional evidence suggests that even more women in the postnatal period experience clinically significant levels of anxiety but do not meet full diagnostic criteria for an anxiety disorder.⁷

Consider screening for postpartum anxiety with the GAD-7 or the Edinburgh Postnatal Depression Scale (questions 3-5).

In another study, 9.5% of women met criteria for GAD at some point during pregnancy, with highest anxiety levels in the first trimester.⁸ Women with a history of GAD, lower education, lack of social support, and personal history of child abuse have the highest risk for postpartum anxiety. Women with a history of posttraumatic stress disorder (PTSD) may be twice as likely to develop postpartum anxiety as healthy women.⁹

It has been well-documented that sleep disruption—which is very common in new mothers in the postnatal period—contributes to mood and anxiety disorders.^10,11

Clarifying a diagnosis of postpartum anxiety

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5)¹² specifies no diagnosis of postpartum anxiety disorder. And no standardized diagnostic criteria exist. It is likely that in some cases, postpartum anxiety represents an exacerbation of underlying GAD, and in other cases it is a situational disorder brought about by specific circumstances of the peripartum period.

The DSM-5 does, however, provide a helpful diagnostic approach. It defines a diagnosis of postpartum depression as being a variant of major depressive disorder (MDD) in which a woman must 1) meet criteria for a major depressive episode; and 2) occur during pregnancy or within 4 weeks of delivery. In practice, many clinicians extend the second requirement to include the first year postpartum.¹³ There is a “with anxious distress” specifier for major depression in the DSM-5, but the 2 disorders are otherwise unlinked.

Continue to: To apply the...

To apply the DSM-5 principles for postpartum depression to postpartum anxiety, a patient would need to 1) meet the diagnostic criteria for an anxiety disorder that 2) have their onset within a specified perinatal period. Variant presentations of anxiety in the postpartum period might include panic disorder and phobias, which could also interfere with a woman’s ability to care for her child.

The DSM-5 offers the following criteria for GAD¹²:

• excessive worry about a variety of topics
• worry that is experienced as hard to control
• worry associated with at least 3 physical or cognitive symptoms: edginess/restlessness, tiring easily, impaired concentration, irritability
• anxiety, worry, or associated symptoms that make it hard to carry out day-to-day activities and responsibilities
• symptoms that are unrelated to any other medical conditions and cannot be explained by the effect of substances including a prescription medication, alcohol, or recreational drugs
• symptoms that are not better explained by a different mental disorder.

Debilitating effects of postpartum anxiety

Many women experience some level of anxiety during pregnancy and early postpartum—anxiety that may range from normal and adaptive to debilitating.¹⁴ While the challenges of caring for a newborn are likely to bring some level of anxiety, these symptoms should be transient and not interfere with a woman’s capacity to care for her infant, herself, or her family.

Postpartum anxiety has been associated with a prior fear of giving birth, fear of death (of both mother and baby), lack of control, lack of self-confidence, and lack of confidence in the medical system.⁹ The experience of such ongoing disturbing thoughts or feelings of worry and tension that affect a woman’s ability to manage from day to day should indicate an illness state that deserves medical attention.

Consider diagnosing postpartum anxiety when DSM-5 criteria for generalized anxiety disorder are met during the first year postpartum.

Mothers with postpartum anxiety disorders report significantly less bonding with their infants than do mothers without anxiety.¹⁵ A recent narrative review describes numerous studies that illustrate the negative effects of postpartum anxiety on bonding, breastfeeding, infant temperament, early childhood development, and conduct disorders.¹⁶ Anxious women may be less likely to initiate breastfeeding, have more challenges with breastfeeding, and even have a different milk composition.¹⁷ Women with prenatal anxiety are also more likely to stop breastfeeding prematurely.¹⁸ Children of anxious mothers may be more likely to have a difficult temperament and to display more distress.¹⁹ There are small studies demonstrating deficits in early infant development and increases in conduct disorder in the male offspring of anxious women.²⁰

Continue to: SCREENING FOR POSTPARTUM ANXIETY

SCREENING FOR POSTPARTUM ANXIETY

Screening for perinatal depression has become standard of care, and the Edinburgh Postnatal Depression Scale (EPDS) is a widely used instrument.¹ The EPDS, a 10-question self-report scale, was created and validated to screen for perinatal depression, with a cutoff of > 10/30 usually considered a positive result.

Researchers have investigated the utility of the EPDS as a screening tool for perinatal anxiety as well.^21-23 These studies show some promise, but there are questions as to whether a total score or a subscale score of the EPDS is most accurate in detecting anxiety. Women with perinatal anxiety may score low on the total EPDS, yet score higher on 3 anxiety-specific questions (TABLE 1²³). For this reason, several studies propose an EPDS anxiety subscore or subscale (referred to as EPDS-3A).

Of note, there are some women who will score high on the subscale who do not ultimately meet the criteria for an anxiety disorder diagnosis. Clinicians should not over-interpret these scores and should always use sound clinical judgment when making a diagnosis.

Research has also focused on using the GAD 7-item (GAD-7) scale (TABLE 2²⁴),²⁵ and on the development of new tools and screening tools designed specifically for perinatal anxiety, including the Postpartum Worry Scale²⁶ and the Postpartum Specific Anxiety Scale (PSAS).²⁷

Family physicians may consider using the EPDS subscale if they are already using the EPDS, or adding the GAD-7 as a separate screening instrument during a postpartum visit. To date there is no one standard recommendation or screening tool.

Continue to: NONPHARMACOLOGIC TREATMENT

As one would with any patient who has situational anxiety, help new mothers find ways to increase their coping skills, reduce stress, and mobilize social supports and family resources. Given the association between sleep disruption and perinatal anxiety, counsel new mothers, especially those at high risk for postpartum anxiety, to prioritize sleep during this vulnerable time. To that end, consider recommending that they ask partners, family members, or friends to help them take care of the infant at night (or during the day). Such nonmedical interventions may be sufficient for women with mild anxiety.

Very few studies have addressed nonpharmacologic management of postpartum anxiety, but cognitive behavioral therapy (CBT) has been shown to help in managing and treating anxiety disorders outside of pregnancy.²⁸ A few small studies indicate promise for CBT and for mindfulness-based interventions (MBIs) during pregnancy.²⁹

A 2016 systematic review of pharmacologic and nonpharmacologic treatment of anxiety in the perinatal period found support for the use of CBT for panic disorder and specific phobias both in pregnancy and postpartum.³⁰ A very small study found that teaching mothers to massage their preterm infants decreased maternal anxiety.³¹

If the patient is amenable, it is reasonable to start with behavioral interventions like CBT or MBI before pharmacologic treatment—particularly when physicians have mental health professionals embedded in their primary care team.

PHARMACOLOGIC TREATMENT

Selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) are considered first-line treatment for moderate to severe anxiety disorders in the perinatal and postnatal period.

Continue to: SSRIs in pregnancy

SSRIs in pregnancy. Lacking support of randomized controlled trials, most recommendations regarding SSRIs in pregnancy come from expert consensus or cohort and case control studies. Studies have raised concerns for an increased rate of congenital heart defects among fetuses exposed to paroxetine³² and primary pulmonary hypertension with all SSRIs.³³ But the absolute risks are quite small. There have also been concerns regarding low birth weight and preterm birth, but it is possible that these outcomes result from the depression itself rather than the medication.³⁴

Many experts believe that not treating anxiety/ depression is more harmful than the fetal effects of SSRIs.

Unfortunately, there are very few studies evaluating the efficacy of SSRIs in treating postpartum depression³⁵ and even fewer that specifically evaluate their effect on perinatal anxiety. Many experts believe that not treating anxiety/depression is actually more harmful than the fetal effects of SSRIs, and that SSRIs are largely safe in both pregnancy and while breastfeeding, with benefits outweighing the risks.

SSRIs while breastfeeding. SSRIs have been found to be present in varying levels in breastmilk but may or may not be present in the serum of nursing infants.³⁶ A 2008 guideline from the American College of Obstetricians and Gynecologists lists paroxetine, sertraline, and fluvoxamine as slightly safer than fluoxetine, escitalopram, and citalopram.³⁷ A 2015 systematic review similarly concluded that sertraline and paroxetine have the most safety data on lactation.³⁸ Lowest effective dose is always recommended to minimize exposure.

Benzodiazepines. As in the general population, benzodiazepines should be reserved for short-term use in acute anxiety and panic because they are associated with such adverse effects as worsening of depression/anxiety and risk of dependence and overdose. Longer-acting benzodiazepines (eg, clonazepam) are generally not recommended in lactation because of reported effects on infants, including sedation. Shorter-acting benzodiazepines (eg, lorazepam) are considered safer in lactation.³⁹

THE CASE

Julia saw her family physician 4 more times, was evaluated by an ear-nose-and-throat specialist for her throat complaints, saw a therapist for CBT and a psychiatrist for medication, had 3 more ED visits, and lost 23 pounds before she finally agreed to start an SSRI for postpartum anxiety. She screened high on the EPDS-3A (9/9) despite scoring low on the full EPDS for perinatal depression (total, 9/30).

Continue to: Because of her swallowing impediments...

Because of her swallowing impediments and because she was breastfeeding, sertraline solution was started at very small doses. It was titrated weekly to obtain therapeutic levels. By 4 weeks, her weight stabilized. By 8 weeks, she started gaining weight and sleeping better. She saw the therapist regularly to continue CBT techniques. Over the next several months she started eating a normal diet. She is currently maintained on her SSRI, is still breastfeeding, and has achieved insight into her perinatal anxiety disorder.

CORRESPONDENCE
Veronica Jordan, MD, 3569 Round Barn Cir #200, Santa Rosa, CA 95403; veronica.a.jordan@gmail.com.