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When is it OK for children to start drinking fruit juice?
Children should be at least 6 months of age (strength of recommendation [SOR]: C, expert opinion) and parents should provide only 100% fruit juice in a cup (not a bottle). Intake should be limited to 4 to 6 oz a day until 12 months of age (SOR: C, expert opinion). It’s important to reiterate to parents that breastfeeding is the preferred source of infant nutrition for the first 6 (preferably 12) months of life (SOR: A, systematic reviews).
Sugar-sweetened fruit drinks have been linked to excess weight gain and obesity (SOR: B, cohort studies with mixed results). Sugar-sweetened beverages provide little nutritional benefit to children and should be restricted (SOR: C, expert opinion). See the TABLE for definitions of fruit juice, fruit drinks, and sugar-sweetened beverages.
TABLE
What’s fruit juice and what’s not
| TERM | DEFINITION |
|---|---|
| Fruit juice | Beverage containing 100% fruit juice from the liquid naturally occurring in the fruit tissue; contains no artificial sweetener |
| Fruit drink | Beverage containing <100% natural fruit juice. Includes sweetened fruit juice reconstituted from concentrate and fruit-flavored drinks |
| Sugar-sweetened beverage | Fruit drinks, fruit “ades,” and carbonated beverages (including sodas and cola beverages) to which sweeteners have been added |
Evidence summary
One of every 6 American children is overweight or at risk of becoming overweight.1 Overweight children are more likely than normal-weight children to be overweight as adults; they’re at significant risk for morbidity and mortality from hypertension, cardiovascular disease, and diabetes in adulthood. Establishing sound nutritional habits—including appropriate consumption of fruit juices, fruit drinks, and other sugar-sweetened beverages—early in life plays an important role in preventing overweight in later childhood and adulthood.2
Fruit juice/obesity link is controversial
During the transition to table foods between 4 and 11 months of age, the top 3 nonmilk sources of carbohydrate in an infant’s diet are infant cereal, 100% juice, and bananas.2 One in 5 infants routinely drinks juice before 6 months of age.3 Consuming 100% juice and fruit-flavored drinks can contribute to excess energy intake and displace other nutrient-dense foods in the child’s diet.
The role of fruit juice consumption in childhood obesity is controversial. In 1 group of 168 children 2 to 5 years of age, 9% of children who drank >12 oz of fruit juice per day were overweight, compared with 3% of those who drank <12 oz daily.4
A recent review of 21 studies found 6 (3 longitudinal and 3 cross-sectional) that supported a relationship between juice intake and weight and 15 (9 longitudinal and 6 cross-sectional) that suggested no link between 100% fruit juice consumption and overweight in children or adolescents.5
Regardless of the relationship between fruit juice and obesity, it is important to emphasize that breast milk provides essential nutrients and immune protection for the growing infant. Breast milk should remain the recommended source of nutrition through the first year of life.6,7
Sugar-sweetened drinks: Short on nutrition, long on risk
Sugar-sweetened beverages (labeled as fruit drinks) often replace whole fruits in childhood diets.8 As a result, children may fail to meet recommendations for intake of whole fruits and vegetables, which contain fiber and nutrients essential to growth.
Consumption of fruit drinks and other sugar-sweetened beverages by American children has increased 135% since 1977; such drinks account for roughly 9% of daily energy intake.9 Data from the Feeding Infants and Toddlers Survey (FITS) indicate that 100% fruit juice and sugar-sweetened beverages are now the second and third leading sources, respectively, of energy (and carbohydrates) for American children between 1 and 2 years of age.3
Data from the National Health and Nutrition Examination Survey (NHANES) suggest that overweight children and adolescents consume more sugar-sweetened beverages than those who are not overweight.10 Other cohort data show that children who regularly consume sugar-sweetened beverages are twice as likely to be overweight by 5 years of age as children who don’t.11 However, 1 cohort of 521 children followed longitudinally from 5 to 9 years showed no association between sugar-sweetened beverage intake and body fat.12
A recent systematic review of 30 studies (15 cross-sectional, 10 prospective cohort, and 5 experimental trials) supports a link between consumption of sugar-sweetened beverages and childhood obesity.13
What about tooth decay?
Excess intake of both sugar-sweetened beverages14 and fruit juice15 has been associated with increased risk of dental caries. Excess intake is defined as more than 6 oz per day in children 1 to 6 years of age and more than 12 oz per day in children 7 to 18 years. To help reduce the risk for dental caries, children should drink juice from a cup.
Recommendations
The American Academy of Family Physicians,16 American Academy of Pediatrics,6 American Heart Association,17 and World Health Organization18 all recommend breast milk as the preferred source of infant nutrition for the first 6 (preferably 12) months of life. The US Preventive Services Task Force recently emphasized the need for primary care physicians to further promote breastfeeding efforts.19
Infants shouldn’t be given fruit juice before 6 months of age.17 If juice is offered, it should be 100% fruit juice in a cup, not a bottle. Children 1 to 6 years of age should drink no more than 4 to 6 oz of 100% fruit juice per day. Children 7 to 18 years of age should limit intake to 12 oz of 100% fruit juice per day.17 Infants, children, and adolescents shouldn’t drink unpasteurized juice.20
The American Heart Association recommends that children 1 to 3 years of age consume the equivalent of 1 cup of whole fruit per day. Children from 4 to 13 years should consume 1.5 cups per day.17
1. Ogden CL, Carroll MD, Curtin LR, et al. Prevalence of overweight and obesity in the United States. JAMA. 2006;295:1549-1555.
2. Skinner JD, Ziegler P, Ponza M. Transitions in infants’ and toddlers’ beverage patterns. J Am Diet Assoc. 2004;104(suppl 1):s45-s50.
3. Briefel RR, Reidy K, Karwe V, et al. Feeding infants and toddlers study: improvements needed in meeting infant feeding recommendations. J Am Diet Assoc. 2004;104(suppl 1):s31-s37.
4. Dennison BA, Rockwell HL, Baker SL. Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity [published correction appears in Pediatrics. 1997;100:733]. Pediatrics. 1997;99:15-22.
5. O’Neil CE, Nicklas TA. A review of the relationship between 100% fruit juice consumption and weight in children and adolescents. Am J Lifestyle Med. 2008;2:315-354.
6. Garner LM, Morton J, Lawrence RA, et al. Breastfeeding and the use of human milk. Pediatrics. 2005;115:496-506.
7. Kramer MS, Kakuma R. The optimal duration of exclusive breastfeeding: a systematic review. Adv Exp Med Biol. 2004;554:63-77.
8. Rampersaud GC, Bailey LB, Kauwell GP. National survey beverage consumption data for children and adolescents indicate the need to encourage a shift toward more nutritive beverages. J Am Diet Assoc. 2003;103:97-100.
9. Nielsen SJ, Popkin BM. Changes in beverage intake between 1977 and 2001. Am J Prev Med. 2004;27:205-210.
10. O’Connor TM, Yang SJ, Nicklas TA. Beverage intake among preschool children and its effect on weight status. Pediatrics. 2006;118:e1010-e1018.
11. Dubois L, Farmer A, Girard M, et al. Regular sugar-sweetened beverage consumption between meals increases risk of overweight among preschool-aged children. J Am Diet Assoc. 2007;107:924-934.
12. Johnson L, Mander AP, Jones LR, et al. Is sugar-sweetened beverage consumption associated with increased fatness in children? Nutrition. 2007;23:557-563.
13. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr. 2006;84:274-288.
14. Sohn W, Burt BA, Sowers MR. Carbonated soft drinks and dental caries in the primary dentition. J Dent Res. 2006;85:262-266.
15. Marshall TA, Levy SM, Broffitt B, et al. Dental caries and beverage consumption in young children. Pediatrics. 2003;112:e184-e191.
16. American Academy of Family Physicians. Breastfeeding policy statement. 2007. Available at: http://www.aafp.org/online/en/home/policy/policies/b/breastfeedingpolicy.html. Accessed March 25, 2008.
17. Gidding SS, Dennison BA, Birch LL, et al. Dietary recommendations for children and adolescents: a guide for practitioners: consensus statement from the American Heart Association [published corrections appear in Circulation. 2005;112:2375; Circulation. 2006;113:e857]. Circulation. 2005;112:2061-2075.
18. World Health Organization. The optimal duration of exclusive breastfeeding: results of a WHO systematic review. Indian Pediatr. 2001;38:565-567.
19. US Preventive Services Task Force. Primary care interventions to promote breastfeeding: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:560-564.
20. American Academy of Pediatrics. The use and misuse of fruit juice in pediatrics. Pediatrics. 2001;107:1210-1213.
Children should be at least 6 months of age (strength of recommendation [SOR]: C, expert opinion) and parents should provide only 100% fruit juice in a cup (not a bottle). Intake should be limited to 4 to 6 oz a day until 12 months of age (SOR: C, expert opinion). It’s important to reiterate to parents that breastfeeding is the preferred source of infant nutrition for the first 6 (preferably 12) months of life (SOR: A, systematic reviews).
Sugar-sweetened fruit drinks have been linked to excess weight gain and obesity (SOR: B, cohort studies with mixed results). Sugar-sweetened beverages provide little nutritional benefit to children and should be restricted (SOR: C, expert opinion). See the TABLE for definitions of fruit juice, fruit drinks, and sugar-sweetened beverages.
TABLE
What’s fruit juice and what’s not
| TERM | DEFINITION |
|---|---|
| Fruit juice | Beverage containing 100% fruit juice from the liquid naturally occurring in the fruit tissue; contains no artificial sweetener |
| Fruit drink | Beverage containing <100% natural fruit juice. Includes sweetened fruit juice reconstituted from concentrate and fruit-flavored drinks |
| Sugar-sweetened beverage | Fruit drinks, fruit “ades,” and carbonated beverages (including sodas and cola beverages) to which sweeteners have been added |
Evidence summary
One of every 6 American children is overweight or at risk of becoming overweight.1 Overweight children are more likely than normal-weight children to be overweight as adults; they’re at significant risk for morbidity and mortality from hypertension, cardiovascular disease, and diabetes in adulthood. Establishing sound nutritional habits—including appropriate consumption of fruit juices, fruit drinks, and other sugar-sweetened beverages—early in life plays an important role in preventing overweight in later childhood and adulthood.2
Fruit juice/obesity link is controversial
During the transition to table foods between 4 and 11 months of age, the top 3 nonmilk sources of carbohydrate in an infant’s diet are infant cereal, 100% juice, and bananas.2 One in 5 infants routinely drinks juice before 6 months of age.3 Consuming 100% juice and fruit-flavored drinks can contribute to excess energy intake and displace other nutrient-dense foods in the child’s diet.
The role of fruit juice consumption in childhood obesity is controversial. In 1 group of 168 children 2 to 5 years of age, 9% of children who drank >12 oz of fruit juice per day were overweight, compared with 3% of those who drank <12 oz daily.4
A recent review of 21 studies found 6 (3 longitudinal and 3 cross-sectional) that supported a relationship between juice intake and weight and 15 (9 longitudinal and 6 cross-sectional) that suggested no link between 100% fruit juice consumption and overweight in children or adolescents.5
Regardless of the relationship between fruit juice and obesity, it is important to emphasize that breast milk provides essential nutrients and immune protection for the growing infant. Breast milk should remain the recommended source of nutrition through the first year of life.6,7
Sugar-sweetened drinks: Short on nutrition, long on risk
Sugar-sweetened beverages (labeled as fruit drinks) often replace whole fruits in childhood diets.8 As a result, children may fail to meet recommendations for intake of whole fruits and vegetables, which contain fiber and nutrients essential to growth.
Consumption of fruit drinks and other sugar-sweetened beverages by American children has increased 135% since 1977; such drinks account for roughly 9% of daily energy intake.9 Data from the Feeding Infants and Toddlers Survey (FITS) indicate that 100% fruit juice and sugar-sweetened beverages are now the second and third leading sources, respectively, of energy (and carbohydrates) for American children between 1 and 2 years of age.3
Data from the National Health and Nutrition Examination Survey (NHANES) suggest that overweight children and adolescents consume more sugar-sweetened beverages than those who are not overweight.10 Other cohort data show that children who regularly consume sugar-sweetened beverages are twice as likely to be overweight by 5 years of age as children who don’t.11 However, 1 cohort of 521 children followed longitudinally from 5 to 9 years showed no association between sugar-sweetened beverage intake and body fat.12
A recent systematic review of 30 studies (15 cross-sectional, 10 prospective cohort, and 5 experimental trials) supports a link between consumption of sugar-sweetened beverages and childhood obesity.13
What about tooth decay?
Excess intake of both sugar-sweetened beverages14 and fruit juice15 has been associated with increased risk of dental caries. Excess intake is defined as more than 6 oz per day in children 1 to 6 years of age and more than 12 oz per day in children 7 to 18 years. To help reduce the risk for dental caries, children should drink juice from a cup.
Recommendations
The American Academy of Family Physicians,16 American Academy of Pediatrics,6 American Heart Association,17 and World Health Organization18 all recommend breast milk as the preferred source of infant nutrition for the first 6 (preferably 12) months of life. The US Preventive Services Task Force recently emphasized the need for primary care physicians to further promote breastfeeding efforts.19
Infants shouldn’t be given fruit juice before 6 months of age.17 If juice is offered, it should be 100% fruit juice in a cup, not a bottle. Children 1 to 6 years of age should drink no more than 4 to 6 oz of 100% fruit juice per day. Children 7 to 18 years of age should limit intake to 12 oz of 100% fruit juice per day.17 Infants, children, and adolescents shouldn’t drink unpasteurized juice.20
The American Heart Association recommends that children 1 to 3 years of age consume the equivalent of 1 cup of whole fruit per day. Children from 4 to 13 years should consume 1.5 cups per day.17
Children should be at least 6 months of age (strength of recommendation [SOR]: C, expert opinion) and parents should provide only 100% fruit juice in a cup (not a bottle). Intake should be limited to 4 to 6 oz a day until 12 months of age (SOR: C, expert opinion). It’s important to reiterate to parents that breastfeeding is the preferred source of infant nutrition for the first 6 (preferably 12) months of life (SOR: A, systematic reviews).
Sugar-sweetened fruit drinks have been linked to excess weight gain and obesity (SOR: B, cohort studies with mixed results). Sugar-sweetened beverages provide little nutritional benefit to children and should be restricted (SOR: C, expert opinion). See the TABLE for definitions of fruit juice, fruit drinks, and sugar-sweetened beverages.
TABLE
What’s fruit juice and what’s not
| TERM | DEFINITION |
|---|---|
| Fruit juice | Beverage containing 100% fruit juice from the liquid naturally occurring in the fruit tissue; contains no artificial sweetener |
| Fruit drink | Beverage containing <100% natural fruit juice. Includes sweetened fruit juice reconstituted from concentrate and fruit-flavored drinks |
| Sugar-sweetened beverage | Fruit drinks, fruit “ades,” and carbonated beverages (including sodas and cola beverages) to which sweeteners have been added |
Evidence summary
One of every 6 American children is overweight or at risk of becoming overweight.1 Overweight children are more likely than normal-weight children to be overweight as adults; they’re at significant risk for morbidity and mortality from hypertension, cardiovascular disease, and diabetes in adulthood. Establishing sound nutritional habits—including appropriate consumption of fruit juices, fruit drinks, and other sugar-sweetened beverages—early in life plays an important role in preventing overweight in later childhood and adulthood.2
Fruit juice/obesity link is controversial
During the transition to table foods between 4 and 11 months of age, the top 3 nonmilk sources of carbohydrate in an infant’s diet are infant cereal, 100% juice, and bananas.2 One in 5 infants routinely drinks juice before 6 months of age.3 Consuming 100% juice and fruit-flavored drinks can contribute to excess energy intake and displace other nutrient-dense foods in the child’s diet.
The role of fruit juice consumption in childhood obesity is controversial. In 1 group of 168 children 2 to 5 years of age, 9% of children who drank >12 oz of fruit juice per day were overweight, compared with 3% of those who drank <12 oz daily.4
A recent review of 21 studies found 6 (3 longitudinal and 3 cross-sectional) that supported a relationship between juice intake and weight and 15 (9 longitudinal and 6 cross-sectional) that suggested no link between 100% fruit juice consumption and overweight in children or adolescents.5
Regardless of the relationship between fruit juice and obesity, it is important to emphasize that breast milk provides essential nutrients and immune protection for the growing infant. Breast milk should remain the recommended source of nutrition through the first year of life.6,7
Sugar-sweetened drinks: Short on nutrition, long on risk
Sugar-sweetened beverages (labeled as fruit drinks) often replace whole fruits in childhood diets.8 As a result, children may fail to meet recommendations for intake of whole fruits and vegetables, which contain fiber and nutrients essential to growth.
Consumption of fruit drinks and other sugar-sweetened beverages by American children has increased 135% since 1977; such drinks account for roughly 9% of daily energy intake.9 Data from the Feeding Infants and Toddlers Survey (FITS) indicate that 100% fruit juice and sugar-sweetened beverages are now the second and third leading sources, respectively, of energy (and carbohydrates) for American children between 1 and 2 years of age.3
Data from the National Health and Nutrition Examination Survey (NHANES) suggest that overweight children and adolescents consume more sugar-sweetened beverages than those who are not overweight.10 Other cohort data show that children who regularly consume sugar-sweetened beverages are twice as likely to be overweight by 5 years of age as children who don’t.11 However, 1 cohort of 521 children followed longitudinally from 5 to 9 years showed no association between sugar-sweetened beverage intake and body fat.12
A recent systematic review of 30 studies (15 cross-sectional, 10 prospective cohort, and 5 experimental trials) supports a link between consumption of sugar-sweetened beverages and childhood obesity.13
What about tooth decay?
Excess intake of both sugar-sweetened beverages14 and fruit juice15 has been associated with increased risk of dental caries. Excess intake is defined as more than 6 oz per day in children 1 to 6 years of age and more than 12 oz per day in children 7 to 18 years. To help reduce the risk for dental caries, children should drink juice from a cup.
Recommendations
The American Academy of Family Physicians,16 American Academy of Pediatrics,6 American Heart Association,17 and World Health Organization18 all recommend breast milk as the preferred source of infant nutrition for the first 6 (preferably 12) months of life. The US Preventive Services Task Force recently emphasized the need for primary care physicians to further promote breastfeeding efforts.19
Infants shouldn’t be given fruit juice before 6 months of age.17 If juice is offered, it should be 100% fruit juice in a cup, not a bottle. Children 1 to 6 years of age should drink no more than 4 to 6 oz of 100% fruit juice per day. Children 7 to 18 years of age should limit intake to 12 oz of 100% fruit juice per day.17 Infants, children, and adolescents shouldn’t drink unpasteurized juice.20
The American Heart Association recommends that children 1 to 3 years of age consume the equivalent of 1 cup of whole fruit per day. Children from 4 to 13 years should consume 1.5 cups per day.17
1. Ogden CL, Carroll MD, Curtin LR, et al. Prevalence of overweight and obesity in the United States. JAMA. 2006;295:1549-1555.
2. Skinner JD, Ziegler P, Ponza M. Transitions in infants’ and toddlers’ beverage patterns. J Am Diet Assoc. 2004;104(suppl 1):s45-s50.
3. Briefel RR, Reidy K, Karwe V, et al. Feeding infants and toddlers study: improvements needed in meeting infant feeding recommendations. J Am Diet Assoc. 2004;104(suppl 1):s31-s37.
4. Dennison BA, Rockwell HL, Baker SL. Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity [published correction appears in Pediatrics. 1997;100:733]. Pediatrics. 1997;99:15-22.
5. O’Neil CE, Nicklas TA. A review of the relationship between 100% fruit juice consumption and weight in children and adolescents. Am J Lifestyle Med. 2008;2:315-354.
6. Garner LM, Morton J, Lawrence RA, et al. Breastfeeding and the use of human milk. Pediatrics. 2005;115:496-506.
7. Kramer MS, Kakuma R. The optimal duration of exclusive breastfeeding: a systematic review. Adv Exp Med Biol. 2004;554:63-77.
8. Rampersaud GC, Bailey LB, Kauwell GP. National survey beverage consumption data for children and adolescents indicate the need to encourage a shift toward more nutritive beverages. J Am Diet Assoc. 2003;103:97-100.
9. Nielsen SJ, Popkin BM. Changes in beverage intake between 1977 and 2001. Am J Prev Med. 2004;27:205-210.
10. O’Connor TM, Yang SJ, Nicklas TA. Beverage intake among preschool children and its effect on weight status. Pediatrics. 2006;118:e1010-e1018.
11. Dubois L, Farmer A, Girard M, et al. Regular sugar-sweetened beverage consumption between meals increases risk of overweight among preschool-aged children. J Am Diet Assoc. 2007;107:924-934.
12. Johnson L, Mander AP, Jones LR, et al. Is sugar-sweetened beverage consumption associated with increased fatness in children? Nutrition. 2007;23:557-563.
13. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr. 2006;84:274-288.
14. Sohn W, Burt BA, Sowers MR. Carbonated soft drinks and dental caries in the primary dentition. J Dent Res. 2006;85:262-266.
15. Marshall TA, Levy SM, Broffitt B, et al. Dental caries and beverage consumption in young children. Pediatrics. 2003;112:e184-e191.
16. American Academy of Family Physicians. Breastfeeding policy statement. 2007. Available at: http://www.aafp.org/online/en/home/policy/policies/b/breastfeedingpolicy.html. Accessed March 25, 2008.
17. Gidding SS, Dennison BA, Birch LL, et al. Dietary recommendations for children and adolescents: a guide for practitioners: consensus statement from the American Heart Association [published corrections appear in Circulation. 2005;112:2375; Circulation. 2006;113:e857]. Circulation. 2005;112:2061-2075.
18. World Health Organization. The optimal duration of exclusive breastfeeding: results of a WHO systematic review. Indian Pediatr. 2001;38:565-567.
19. US Preventive Services Task Force. Primary care interventions to promote breastfeeding: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:560-564.
20. American Academy of Pediatrics. The use and misuse of fruit juice in pediatrics. Pediatrics. 2001;107:1210-1213.
1. Ogden CL, Carroll MD, Curtin LR, et al. Prevalence of overweight and obesity in the United States. JAMA. 2006;295:1549-1555.
2. Skinner JD, Ziegler P, Ponza M. Transitions in infants’ and toddlers’ beverage patterns. J Am Diet Assoc. 2004;104(suppl 1):s45-s50.
3. Briefel RR, Reidy K, Karwe V, et al. Feeding infants and toddlers study: improvements needed in meeting infant feeding recommendations. J Am Diet Assoc. 2004;104(suppl 1):s31-s37.
4. Dennison BA, Rockwell HL, Baker SL. Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity [published correction appears in Pediatrics. 1997;100:733]. Pediatrics. 1997;99:15-22.
5. O’Neil CE, Nicklas TA. A review of the relationship between 100% fruit juice consumption and weight in children and adolescents. Am J Lifestyle Med. 2008;2:315-354.
6. Garner LM, Morton J, Lawrence RA, et al. Breastfeeding and the use of human milk. Pediatrics. 2005;115:496-506.
7. Kramer MS, Kakuma R. The optimal duration of exclusive breastfeeding: a systematic review. Adv Exp Med Biol. 2004;554:63-77.
8. Rampersaud GC, Bailey LB, Kauwell GP. National survey beverage consumption data for children and adolescents indicate the need to encourage a shift toward more nutritive beverages. J Am Diet Assoc. 2003;103:97-100.
9. Nielsen SJ, Popkin BM. Changes in beverage intake between 1977 and 2001. Am J Prev Med. 2004;27:205-210.
10. O’Connor TM, Yang SJ, Nicklas TA. Beverage intake among preschool children and its effect on weight status. Pediatrics. 2006;118:e1010-e1018.
11. Dubois L, Farmer A, Girard M, et al. Regular sugar-sweetened beverage consumption between meals increases risk of overweight among preschool-aged children. J Am Diet Assoc. 2007;107:924-934.
12. Johnson L, Mander AP, Jones LR, et al. Is sugar-sweetened beverage consumption associated with increased fatness in children? Nutrition. 2007;23:557-563.
13. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr. 2006;84:274-288.
14. Sohn W, Burt BA, Sowers MR. Carbonated soft drinks and dental caries in the primary dentition. J Dent Res. 2006;85:262-266.
15. Marshall TA, Levy SM, Broffitt B, et al. Dental caries and beverage consumption in young children. Pediatrics. 2003;112:e184-e191.
16. American Academy of Family Physicians. Breastfeeding policy statement. 2007. Available at: http://www.aafp.org/online/en/home/policy/policies/b/breastfeedingpolicy.html. Accessed March 25, 2008.
17. Gidding SS, Dennison BA, Birch LL, et al. Dietary recommendations for children and adolescents: a guide for practitioners: consensus statement from the American Heart Association [published corrections appear in Circulation. 2005;112:2375; Circulation. 2006;113:e857]. Circulation. 2005;112:2061-2075.
18. World Health Organization. The optimal duration of exclusive breastfeeding: results of a WHO systematic review. Indian Pediatr. 2001;38:565-567.
19. US Preventive Services Task Force. Primary care interventions to promote breastfeeding: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:560-564.
20. American Academy of Pediatrics. The use and misuse of fruit juice in pediatrics. Pediatrics. 2001;107:1210-1213.
Evidence-based answers from the Family Physicians Inquiries Network
Does ambulatory blood pressure monitoring aid in the management of patients with hypertension?
Twenty-four hour ambulatory blood pressure monitoring (ABPM) has a higher correlation with target end-organ damage than standard office measurements and is superior for risk stratification. Because it is more complicated to implement than office-based measurements, it should be reserved for: establishing the diagnosis of white-coat hypertension or borderline hypertension in previously untreated patients; evaluating previously treated patients with resistant hypertension; diagnosing and treating hypertension disorders of pregnancy; and identifying nocturnal hypertension. (Grade of recommendation: B, based on consistent cohort studies and trials, requiring extrapolation in certain clinical circumstances)
Evidence summary
The accuracy of ABPM has been validated for use in the adult, pediatric, and pregnant populations.1 Community-based cohort studies have consistently shown ABPM to be more reproducible than office blood pressure measurements.2,3 Also, ABPM correlates better with disease-oriented outcomes, such as left ventricular mass, retinopathy, and microalbuminuria than does office measurement.4,5
ABPM also has a better correlation with several patient-oriented outcomes. A cohort study of 1076 patients found that an elevation in ABPM was a better predictor of cardiovascular events and overall mortality than office measurements.6 Another cohort study of 1464 patients found ABPM was linearly related to stroke risk and more predictive of a cerebrovascular event than was screening blood pressure over an average of 6.4 years.7
In a randomized parallel-group trial, 419 untreated patients were followed up using either ABPM or conventional office measurements to initiate and adjust antihypertensive therapy.8 When compared with standard office measurement, management with ABPM led to less intensive antihypertensive drug therapy without loss of blood pressure control. Evidence from these and other studies indicates that ABPM can be useful for risk stratification of patients in whom the diagnosis of hypertension is not clear.9 However, trials studying the long-term outcomes of the treatment of ambulatory blood pressure levels are still lacking.
Recommendations from others
An ad hoc committee of the American Society of Hypertension, the Canadian Hypertension Society, and the British Hypertension Society all agree that ABPM is useful in excluding the diagnosis of white-coat hypertension and evaluating resistant hypertension or episodic hypertension.1 The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of Hypertension and the National High Blood Pressure Education Program working group on ambulatory blood pressure monitoring add that ABPM plays a limited role in the routine evaluation of patients with suspected hypertension.1
Frank deGruy, MD
Department of Family Medicine University of Colorado
Why has ABPM not supplanted office-based sphyngomanometry as a preferred measurement technique? Because it is inconvenient. The first barrier to eliminating hypertension is getting blood pressure readings in the first place, and ABPM is not well suited for this. But in borderline or difficult situations (eg, white-coat or nocturnal hypertension), where multiple determinations are necessary, ABPM has something to offer. Perhaps its greatest value is in developing more parsimonious and effective treatment regimens for treatment-resistant patients, or those for whom side effects are a problem.
1. See www.jfponline.com for the Joint National Committee reference, validation studies, and for recommendations from others.
2. Pearce KA, Evans GW, Summerson J, Rao JS. J Fam Pract 1997;45:426-33.
3. Hietanen E, Wendelin-Saarenhovi M. Scand J Clin Lab Invest 1996;56:471-80.
4. Verdecchia P, Clement D, Fagard R, Palatini P, Parati G. Blood Press Monit 1999;4:03-317.
5. Ozdemir FN, Guz G, Sezer S, Arat Z, Haberal M. Nephrol Dial Transplant 2000;15:1038-40.
6. Perloff D, Sokolow M, Cowan R. JAMA 1983;249:2792-98.
7. Ohkubo T, Hozawa A, Nagai K, et al. J Hypertens 2000;18:847-54.
8. Staessen JA, Byttebier G, Buntinx F, Celis H, O’Brien ET, Fagard R. JAMA 1997;278:1065-72.
9. Khattar RS, Senior R, Lahiri A. J Clin Hypertens (Greenwich) 2001;3:90-98.
Twenty-four hour ambulatory blood pressure monitoring (ABPM) has a higher correlation with target end-organ damage than standard office measurements and is superior for risk stratification. Because it is more complicated to implement than office-based measurements, it should be reserved for: establishing the diagnosis of white-coat hypertension or borderline hypertension in previously untreated patients; evaluating previously treated patients with resistant hypertension; diagnosing and treating hypertension disorders of pregnancy; and identifying nocturnal hypertension. (Grade of recommendation: B, based on consistent cohort studies and trials, requiring extrapolation in certain clinical circumstances)
Evidence summary
The accuracy of ABPM has been validated for use in the adult, pediatric, and pregnant populations.1 Community-based cohort studies have consistently shown ABPM to be more reproducible than office blood pressure measurements.2,3 Also, ABPM correlates better with disease-oriented outcomes, such as left ventricular mass, retinopathy, and microalbuminuria than does office measurement.4,5
ABPM also has a better correlation with several patient-oriented outcomes. A cohort study of 1076 patients found that an elevation in ABPM was a better predictor of cardiovascular events and overall mortality than office measurements.6 Another cohort study of 1464 patients found ABPM was linearly related to stroke risk and more predictive of a cerebrovascular event than was screening blood pressure over an average of 6.4 years.7
In a randomized parallel-group trial, 419 untreated patients were followed up using either ABPM or conventional office measurements to initiate and adjust antihypertensive therapy.8 When compared with standard office measurement, management with ABPM led to less intensive antihypertensive drug therapy without loss of blood pressure control. Evidence from these and other studies indicates that ABPM can be useful for risk stratification of patients in whom the diagnosis of hypertension is not clear.9 However, trials studying the long-term outcomes of the treatment of ambulatory blood pressure levels are still lacking.
Recommendations from others
An ad hoc committee of the American Society of Hypertension, the Canadian Hypertension Society, and the British Hypertension Society all agree that ABPM is useful in excluding the diagnosis of white-coat hypertension and evaluating resistant hypertension or episodic hypertension.1 The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of Hypertension and the National High Blood Pressure Education Program working group on ambulatory blood pressure monitoring add that ABPM plays a limited role in the routine evaluation of patients with suspected hypertension.1
Frank deGruy, MD
Department of Family Medicine University of Colorado
Why has ABPM not supplanted office-based sphyngomanometry as a preferred measurement technique? Because it is inconvenient. The first barrier to eliminating hypertension is getting blood pressure readings in the first place, and ABPM is not well suited for this. But in borderline or difficult situations (eg, white-coat or nocturnal hypertension), where multiple determinations are necessary, ABPM has something to offer. Perhaps its greatest value is in developing more parsimonious and effective treatment regimens for treatment-resistant patients, or those for whom side effects are a problem.
Twenty-four hour ambulatory blood pressure monitoring (ABPM) has a higher correlation with target end-organ damage than standard office measurements and is superior for risk stratification. Because it is more complicated to implement than office-based measurements, it should be reserved for: establishing the diagnosis of white-coat hypertension or borderline hypertension in previously untreated patients; evaluating previously treated patients with resistant hypertension; diagnosing and treating hypertension disorders of pregnancy; and identifying nocturnal hypertension. (Grade of recommendation: B, based on consistent cohort studies and trials, requiring extrapolation in certain clinical circumstances)
Evidence summary
The accuracy of ABPM has been validated for use in the adult, pediatric, and pregnant populations.1 Community-based cohort studies have consistently shown ABPM to be more reproducible than office blood pressure measurements.2,3 Also, ABPM correlates better with disease-oriented outcomes, such as left ventricular mass, retinopathy, and microalbuminuria than does office measurement.4,5
ABPM also has a better correlation with several patient-oriented outcomes. A cohort study of 1076 patients found that an elevation in ABPM was a better predictor of cardiovascular events and overall mortality than office measurements.6 Another cohort study of 1464 patients found ABPM was linearly related to stroke risk and more predictive of a cerebrovascular event than was screening blood pressure over an average of 6.4 years.7
In a randomized parallel-group trial, 419 untreated patients were followed up using either ABPM or conventional office measurements to initiate and adjust antihypertensive therapy.8 When compared with standard office measurement, management with ABPM led to less intensive antihypertensive drug therapy without loss of blood pressure control. Evidence from these and other studies indicates that ABPM can be useful for risk stratification of patients in whom the diagnosis of hypertension is not clear.9 However, trials studying the long-term outcomes of the treatment of ambulatory blood pressure levels are still lacking.
Recommendations from others
An ad hoc committee of the American Society of Hypertension, the Canadian Hypertension Society, and the British Hypertension Society all agree that ABPM is useful in excluding the diagnosis of white-coat hypertension and evaluating resistant hypertension or episodic hypertension.1 The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of Hypertension and the National High Blood Pressure Education Program working group on ambulatory blood pressure monitoring add that ABPM plays a limited role in the routine evaluation of patients with suspected hypertension.1
Frank deGruy, MD
Department of Family Medicine University of Colorado
Why has ABPM not supplanted office-based sphyngomanometry as a preferred measurement technique? Because it is inconvenient. The first barrier to eliminating hypertension is getting blood pressure readings in the first place, and ABPM is not well suited for this. But in borderline or difficult situations (eg, white-coat or nocturnal hypertension), where multiple determinations are necessary, ABPM has something to offer. Perhaps its greatest value is in developing more parsimonious and effective treatment regimens for treatment-resistant patients, or those for whom side effects are a problem.
1. See www.jfponline.com for the Joint National Committee reference, validation studies, and for recommendations from others.
2. Pearce KA, Evans GW, Summerson J, Rao JS. J Fam Pract 1997;45:426-33.
3. Hietanen E, Wendelin-Saarenhovi M. Scand J Clin Lab Invest 1996;56:471-80.
4. Verdecchia P, Clement D, Fagard R, Palatini P, Parati G. Blood Press Monit 1999;4:03-317.
5. Ozdemir FN, Guz G, Sezer S, Arat Z, Haberal M. Nephrol Dial Transplant 2000;15:1038-40.
6. Perloff D, Sokolow M, Cowan R. JAMA 1983;249:2792-98.
7. Ohkubo T, Hozawa A, Nagai K, et al. J Hypertens 2000;18:847-54.
8. Staessen JA, Byttebier G, Buntinx F, Celis H, O’Brien ET, Fagard R. JAMA 1997;278:1065-72.
9. Khattar RS, Senior R, Lahiri A. J Clin Hypertens (Greenwich) 2001;3:90-98.
1. See www.jfponline.com for the Joint National Committee reference, validation studies, and for recommendations from others.
2. Pearce KA, Evans GW, Summerson J, Rao JS. J Fam Pract 1997;45:426-33.
3. Hietanen E, Wendelin-Saarenhovi M. Scand J Clin Lab Invest 1996;56:471-80.
4. Verdecchia P, Clement D, Fagard R, Palatini P, Parati G. Blood Press Monit 1999;4:03-317.
5. Ozdemir FN, Guz G, Sezer S, Arat Z, Haberal M. Nephrol Dial Transplant 2000;15:1038-40.
6. Perloff D, Sokolow M, Cowan R. JAMA 1983;249:2792-98.
7. Ohkubo T, Hozawa A, Nagai K, et al. J Hypertens 2000;18:847-54.
8. Staessen JA, Byttebier G, Buntinx F, Celis H, O’Brien ET, Fagard R. JAMA 1997;278:1065-72.
9. Khattar RS, Senior R, Lahiri A. J Clin Hypertens (Greenwich) 2001;3:90-98.
Evidence-based answers from the Family Physicians Inquiries Network
Does delaying placement of tympanostomy tubes have an adverse effect on developmental outcomes in children with persistent middle ear effusions?
BACKGROUND: Fluid in the middle ear creates a conductive hearing loss. This has historically raised concern for potential delays in child development. Persistent otitis media with effusion (OME) is, therefore, the primary indication for tympanostomy tube placement. This study re-examines the link between middle ear effusions, developmental outcomes, and the ability of this surgical intervention to affect these outcomes.
POPULATION STUDIED: Healthy newborns were recruited to participate from a variety of practice settings in the greater Pittsburgh area. Exclusion criteria included: birth weight less than 2270 g, congenital malformation or significant neonatal illness, multiple birth, maternal illness, maternal drug abuse, and several social limitations (foster care, inability to give informed consent, younger than 18 years, English as a second language).
STUDY DESIGN AND VALIDITY: This was a nonblinded randomized clinical trial. Of 6350 patients screened between the ages of 2 days and 2 months, 588 met eligibility criteria, and 429 ultimately participated. The subjects were examined monthly to assess for the presence of OME from age 2 months until 3 years. Children with significant effusions (defined either as bilateral effusions persisting 90 or more days or unilateral effusions persisting for more than 135 days) were randomized to an early intervention group (n=216) or a delayed treatment group (n=213). Children in the early treatment group received tympanostomy tubes as soon as possible. Children in the delayed treatment group had tubes placed either 6 months (for persistent bilateral OME) or 9 months (for persistent unilateral OME) after the initial diagnosis. Ninety-four percent of the subjects (402 of 429) successfully completed developmental testing at the age of 3 years. One of the particular strengths of this study is its methodologic attention to detail. The study groups are well defined and well described, and relevant outcomes are reported. Questions that were not adequately addressed, however, include: (1) Is 3 years an adequate length for follow-up in terms of reliable developmental outcomes?1 and (2) Could tympanostomy tube placement be delayed even longer than 9 months (or perhaps avoided completely)?
OUTCOMES MEASURED: Three sets of primary developmental outcomes were measured up to 3 years after randomization: formal norm-referenced tests to assess cognition and receptive language skills, conversational sampling to assess expressive language skills, and parental questionnaires to assess parental distress and child behavior.
RESULTS: By age 3 years, 82% of the early intervention group (n=169) and 34% of the delayed treatment group (n=66) had undergone tympanostomy tube placement. There were no significant differences between groups for receptive or expressive language skills, cognition, parental distress, or child behaviors.
This study provides compelling evidence that placement of tympanostomy tubes at the time of diagnosis in otherwise healthy children with persistent OME is no more effective than withholding treatment for up to 9 months. In this setting, early surgical intervention has no effect on cognitive development, language acquisition and development, or behavior.
BACKGROUND: Fluid in the middle ear creates a conductive hearing loss. This has historically raised concern for potential delays in child development. Persistent otitis media with effusion (OME) is, therefore, the primary indication for tympanostomy tube placement. This study re-examines the link between middle ear effusions, developmental outcomes, and the ability of this surgical intervention to affect these outcomes.
POPULATION STUDIED: Healthy newborns were recruited to participate from a variety of practice settings in the greater Pittsburgh area. Exclusion criteria included: birth weight less than 2270 g, congenital malformation or significant neonatal illness, multiple birth, maternal illness, maternal drug abuse, and several social limitations (foster care, inability to give informed consent, younger than 18 years, English as a second language).
STUDY DESIGN AND VALIDITY: This was a nonblinded randomized clinical trial. Of 6350 patients screened between the ages of 2 days and 2 months, 588 met eligibility criteria, and 429 ultimately participated. The subjects were examined monthly to assess for the presence of OME from age 2 months until 3 years. Children with significant effusions (defined either as bilateral effusions persisting 90 or more days or unilateral effusions persisting for more than 135 days) were randomized to an early intervention group (n=216) or a delayed treatment group (n=213). Children in the early treatment group received tympanostomy tubes as soon as possible. Children in the delayed treatment group had tubes placed either 6 months (for persistent bilateral OME) or 9 months (for persistent unilateral OME) after the initial diagnosis. Ninety-four percent of the subjects (402 of 429) successfully completed developmental testing at the age of 3 years. One of the particular strengths of this study is its methodologic attention to detail. The study groups are well defined and well described, and relevant outcomes are reported. Questions that were not adequately addressed, however, include: (1) Is 3 years an adequate length for follow-up in terms of reliable developmental outcomes?1 and (2) Could tympanostomy tube placement be delayed even longer than 9 months (or perhaps avoided completely)?
OUTCOMES MEASURED: Three sets of primary developmental outcomes were measured up to 3 years after randomization: formal norm-referenced tests to assess cognition and receptive language skills, conversational sampling to assess expressive language skills, and parental questionnaires to assess parental distress and child behavior.
RESULTS: By age 3 years, 82% of the early intervention group (n=169) and 34% of the delayed treatment group (n=66) had undergone tympanostomy tube placement. There were no significant differences between groups for receptive or expressive language skills, cognition, parental distress, or child behaviors.
This study provides compelling evidence that placement of tympanostomy tubes at the time of diagnosis in otherwise healthy children with persistent OME is no more effective than withholding treatment for up to 9 months. In this setting, early surgical intervention has no effect on cognitive development, language acquisition and development, or behavior.
BACKGROUND: Fluid in the middle ear creates a conductive hearing loss. This has historically raised concern for potential delays in child development. Persistent otitis media with effusion (OME) is, therefore, the primary indication for tympanostomy tube placement. This study re-examines the link between middle ear effusions, developmental outcomes, and the ability of this surgical intervention to affect these outcomes.
POPULATION STUDIED: Healthy newborns were recruited to participate from a variety of practice settings in the greater Pittsburgh area. Exclusion criteria included: birth weight less than 2270 g, congenital malformation or significant neonatal illness, multiple birth, maternal illness, maternal drug abuse, and several social limitations (foster care, inability to give informed consent, younger than 18 years, English as a second language).
STUDY DESIGN AND VALIDITY: This was a nonblinded randomized clinical trial. Of 6350 patients screened between the ages of 2 days and 2 months, 588 met eligibility criteria, and 429 ultimately participated. The subjects were examined monthly to assess for the presence of OME from age 2 months until 3 years. Children with significant effusions (defined either as bilateral effusions persisting 90 or more days or unilateral effusions persisting for more than 135 days) were randomized to an early intervention group (n=216) or a delayed treatment group (n=213). Children in the early treatment group received tympanostomy tubes as soon as possible. Children in the delayed treatment group had tubes placed either 6 months (for persistent bilateral OME) or 9 months (for persistent unilateral OME) after the initial diagnosis. Ninety-four percent of the subjects (402 of 429) successfully completed developmental testing at the age of 3 years. One of the particular strengths of this study is its methodologic attention to detail. The study groups are well defined and well described, and relevant outcomes are reported. Questions that were not adequately addressed, however, include: (1) Is 3 years an adequate length for follow-up in terms of reliable developmental outcomes?1 and (2) Could tympanostomy tube placement be delayed even longer than 9 months (or perhaps avoided completely)?
OUTCOMES MEASURED: Three sets of primary developmental outcomes were measured up to 3 years after randomization: formal norm-referenced tests to assess cognition and receptive language skills, conversational sampling to assess expressive language skills, and parental questionnaires to assess parental distress and child behavior.
RESULTS: By age 3 years, 82% of the early intervention group (n=169) and 34% of the delayed treatment group (n=66) had undergone tympanostomy tube placement. There were no significant differences between groups for receptive or expressive language skills, cognition, parental distress, or child behaviors.
This study provides compelling evidence that placement of tympanostomy tubes at the time of diagnosis in otherwise healthy children with persistent OME is no more effective than withholding treatment for up to 9 months. In this setting, early surgical intervention has no effect on cognitive development, language acquisition and development, or behavior.
Is there a clinical difference in outcomes when b-agonist therapy is delivered through metered-dose inhaler (MDI) with a spacing device compared with standard nebulizer treatments in acutely wheezing children?
BACKGROUND: Asthma remains a leading cause of hospitalization in children. It has been determined that the MDI is equally as effective as nebulized wet aerosol therapy for treatment of acute asthma in adults, and may even work better in children older than 2 years.1 The authors of this study investigated whether the same relationship holds true in children between the ages of 10 months and 4 years.
POPULATION STUDIED: The investigators enrolled 42 children aged 10 months to 4 years presenting to the emergency department of a large hospital in Israel. Children were not included if they had a history of cardiac disease or chronic respiratory disease (other than asthma), had an altered level of consciousness, or were in respiratory failure. Most subjects were referred from their primary care physicians to the emergency department because of the severity of their presentation.
STUDY DESIGN AND VALIDITY: This study was a randomized controlled double-blind double-dummy clinical trial. Subjects were randomly assigned to 2 groups. Randomization assignment was concealed. The first group received a standard dose of salbutamol (2.5 mg in 1.5 cc of normal saline) by nebulized aerosol therapy along with 4 puffs of placebo by MDI with a spacing device and facemask. The second group received 4 puffs of salbutamol (400 μg) by MDI with spacer and facemask along with 2 mL of normal saline by nebulized aerosol. Clinical scores (respiratory rate, pulse rate, pulse oximetry, wheezing, breath sounds, and retractions) were calculated at baseline and also 15 minutes after the conclusion of each respiratory treatment. Each patient received a total of 3 treatments delivered at 20-minute intervals. The study is well designed. The authors do not mention if any treatments were rendered by the referring physicians before arrival in the emergency department. The presence of antecedent b-agonist therapy could have affected the outcomes. This study was large enough to find a difference in the major outcomes (if one exists) but not to determine whether MDI therapy results in a change in the rate of hospitalization.
OUTCOMES MEASURED: The 2 major outcomes were respiratory rate and the patient’s clinical score. Minor outcomes included pulse rate and room air pulse oximetry. Hospitalization rates between the groups were also compared.
RESULTS: The study groups were similar at baseline. The reduction in respiratory rate and the improvement in patients’ clinical scores were similar between groups. Side effect rates were similar in the 2 groups. A total of 31% required hospitalization, but there was no difference in the rate of hospitalization between groups.
The use of a MDI with spacer and facemask is clinically equal to the use of nebulized aerosol for the delivery of b-agonist therapy in acutely wheezing infants between the ages of 10 months and 4 years. Symptoms resolve similarly with the 2 methods. This study was not large enough to determine whether one administration method is superior with regard to hospitalization rate, although a recent meta-analysis1 involving studies of older children demonstrated shorter stays in MDI-treated children. Education regarding the proper use of the MDI-spacer-facemask combination (ie, the facemask should cover the mouth and nose) in infants and children is a key component to ensuring therapeutic success.
BACKGROUND: Asthma remains a leading cause of hospitalization in children. It has been determined that the MDI is equally as effective as nebulized wet aerosol therapy for treatment of acute asthma in adults, and may even work better in children older than 2 years.1 The authors of this study investigated whether the same relationship holds true in children between the ages of 10 months and 4 years.
POPULATION STUDIED: The investigators enrolled 42 children aged 10 months to 4 years presenting to the emergency department of a large hospital in Israel. Children were not included if they had a history of cardiac disease or chronic respiratory disease (other than asthma), had an altered level of consciousness, or were in respiratory failure. Most subjects were referred from their primary care physicians to the emergency department because of the severity of their presentation.
STUDY DESIGN AND VALIDITY: This study was a randomized controlled double-blind double-dummy clinical trial. Subjects were randomly assigned to 2 groups. Randomization assignment was concealed. The first group received a standard dose of salbutamol (2.5 mg in 1.5 cc of normal saline) by nebulized aerosol therapy along with 4 puffs of placebo by MDI with a spacing device and facemask. The second group received 4 puffs of salbutamol (400 μg) by MDI with spacer and facemask along with 2 mL of normal saline by nebulized aerosol. Clinical scores (respiratory rate, pulse rate, pulse oximetry, wheezing, breath sounds, and retractions) were calculated at baseline and also 15 minutes after the conclusion of each respiratory treatment. Each patient received a total of 3 treatments delivered at 20-minute intervals. The study is well designed. The authors do not mention if any treatments were rendered by the referring physicians before arrival in the emergency department. The presence of antecedent b-agonist therapy could have affected the outcomes. This study was large enough to find a difference in the major outcomes (if one exists) but not to determine whether MDI therapy results in a change in the rate of hospitalization.
OUTCOMES MEASURED: The 2 major outcomes were respiratory rate and the patient’s clinical score. Minor outcomes included pulse rate and room air pulse oximetry. Hospitalization rates between the groups were also compared.
RESULTS: The study groups were similar at baseline. The reduction in respiratory rate and the improvement in patients’ clinical scores were similar between groups. Side effect rates were similar in the 2 groups. A total of 31% required hospitalization, but there was no difference in the rate of hospitalization between groups.
The use of a MDI with spacer and facemask is clinically equal to the use of nebulized aerosol for the delivery of b-agonist therapy in acutely wheezing infants between the ages of 10 months and 4 years. Symptoms resolve similarly with the 2 methods. This study was not large enough to determine whether one administration method is superior with regard to hospitalization rate, although a recent meta-analysis1 involving studies of older children demonstrated shorter stays in MDI-treated children. Education regarding the proper use of the MDI-spacer-facemask combination (ie, the facemask should cover the mouth and nose) in infants and children is a key component to ensuring therapeutic success.
BACKGROUND: Asthma remains a leading cause of hospitalization in children. It has been determined that the MDI is equally as effective as nebulized wet aerosol therapy for treatment of acute asthma in adults, and may even work better in children older than 2 years.1 The authors of this study investigated whether the same relationship holds true in children between the ages of 10 months and 4 years.
POPULATION STUDIED: The investigators enrolled 42 children aged 10 months to 4 years presenting to the emergency department of a large hospital in Israel. Children were not included if they had a history of cardiac disease or chronic respiratory disease (other than asthma), had an altered level of consciousness, or were in respiratory failure. Most subjects were referred from their primary care physicians to the emergency department because of the severity of their presentation.
STUDY DESIGN AND VALIDITY: This study was a randomized controlled double-blind double-dummy clinical trial. Subjects were randomly assigned to 2 groups. Randomization assignment was concealed. The first group received a standard dose of salbutamol (2.5 mg in 1.5 cc of normal saline) by nebulized aerosol therapy along with 4 puffs of placebo by MDI with a spacing device and facemask. The second group received 4 puffs of salbutamol (400 μg) by MDI with spacer and facemask along with 2 mL of normal saline by nebulized aerosol. Clinical scores (respiratory rate, pulse rate, pulse oximetry, wheezing, breath sounds, and retractions) were calculated at baseline and also 15 minutes after the conclusion of each respiratory treatment. Each patient received a total of 3 treatments delivered at 20-minute intervals. The study is well designed. The authors do not mention if any treatments were rendered by the referring physicians before arrival in the emergency department. The presence of antecedent b-agonist therapy could have affected the outcomes. This study was large enough to find a difference in the major outcomes (if one exists) but not to determine whether MDI therapy results in a change in the rate of hospitalization.
OUTCOMES MEASURED: The 2 major outcomes were respiratory rate and the patient’s clinical score. Minor outcomes included pulse rate and room air pulse oximetry. Hospitalization rates between the groups were also compared.
RESULTS: The study groups were similar at baseline. The reduction in respiratory rate and the improvement in patients’ clinical scores were similar between groups. Side effect rates were similar in the 2 groups. A total of 31% required hospitalization, but there was no difference in the rate of hospitalization between groups.
The use of a MDI with spacer and facemask is clinically equal to the use of nebulized aerosol for the delivery of b-agonist therapy in acutely wheezing infants between the ages of 10 months and 4 years. Symptoms resolve similarly with the 2 methods. This study was not large enough to determine whether one administration method is superior with regard to hospitalization rate, although a recent meta-analysis1 involving studies of older children demonstrated shorter stays in MDI-treated children. Education regarding the proper use of the MDI-spacer-facemask combination (ie, the facemask should cover the mouth and nose) in infants and children is a key component to ensuring therapeutic success.
Is electron-beam computed tomography (EBCT) a reliable tool for predicting coronary outcomes in an asymptomatic population?
BACKGROUND: Coronary artery disease remains the leading cause of death in the United States. Currently clinicians rely on traditional models of risk-factor analysis to predict coronary outcomes. EBCT has recently been identified as a tool for measuring calcium within the coronary arteries and promoted as a means of predicting coronary risk. The use of EBCT as a prognostic or screening tool is based on the premise of a causal and incremental association between coronary artery calcium and atherosclerosis.1,2 More coronary calcium means more atherosclerotic heart disease, which in turn means a higher risk for coronary events. The objective of this study was to review the literature on EBCT as a noninvasive method for predicting subsequent coronary events.
POPULATION STUDIED: The average age of a study participant in the 5 identified studies was 57 years, and 74% were men. The study setting (ie, primary care or referral) and the subject ethnicity were not reported. The baseline cardiovascular risk of participants was inconsistently reported.
STUDY DESIGN AND VALIDITY: This study was a meta-analysis. The authors searched the literature for articles pertaining to EBCT, heart disease, and prognosis. Studies were included if they were performed on an asymptomatic adult population with adequate follow-up (minimum of 36 months) and assessment of coronary outcomes (myocardial infarction [MI] or death) was reported. The authors included data from ongoing and unpublished studies. Incomplete data were imputed in a conservative fashion to limit bias toward the alternative hypothesis. Two authors independently reviewed the data, and differences were reconciled by group consensus. A random effects model was used to calculate summary estimates of the risk ratios.
OUTCOMES MEASURED: The primary outcome measures were risk ratios for hard coronary events (MI and cardiac death) and combined events (MI, cardiac death, and revascularization procedures).
RESULTS: Nine studies (4 published articles and 5 abstracts) were identified. Three were duplicate publications that reported the same data as another study, and one had only 33% follow-up; these were appropriately excluded. The remaining 5 studies with 4348 patients were included. There was significant heterogeneity between studies, with the best designed study having among the lowest risk ratios (2.3). The summary estimates calculated using a random effects model showed that patients with higher calcium scores by EBCT were at an increased risk of hard events (summary risk ratio=4.2; 95% confidence interval [CI], 1.6-11.3) and combined events (summary risk ratio=8.7; 95% CI, 2.7-28.1). However, these calculations should not have been reported in the first place because of the broad methodologic differences between studies and their significant heterogeneity. These major flaws greatly weaken the conclusions that can be drawn from this meta-analysis.
EBCT is a relatively costly test ($300-$400) in search of a clinical niche. It is no better at predicting coronary outcomes than traditional risk-factor modeling or the use of Framingham data. There is no evidence to support the routine use of EBCT as a screening tool for coronary disease in an asymptomatic population.
BACKGROUND: Coronary artery disease remains the leading cause of death in the United States. Currently clinicians rely on traditional models of risk-factor analysis to predict coronary outcomes. EBCT has recently been identified as a tool for measuring calcium within the coronary arteries and promoted as a means of predicting coronary risk. The use of EBCT as a prognostic or screening tool is based on the premise of a causal and incremental association between coronary artery calcium and atherosclerosis.1,2 More coronary calcium means more atherosclerotic heart disease, which in turn means a higher risk for coronary events. The objective of this study was to review the literature on EBCT as a noninvasive method for predicting subsequent coronary events.
POPULATION STUDIED: The average age of a study participant in the 5 identified studies was 57 years, and 74% were men. The study setting (ie, primary care or referral) and the subject ethnicity were not reported. The baseline cardiovascular risk of participants was inconsistently reported.
STUDY DESIGN AND VALIDITY: This study was a meta-analysis. The authors searched the literature for articles pertaining to EBCT, heart disease, and prognosis. Studies were included if they were performed on an asymptomatic adult population with adequate follow-up (minimum of 36 months) and assessment of coronary outcomes (myocardial infarction [MI] or death) was reported. The authors included data from ongoing and unpublished studies. Incomplete data were imputed in a conservative fashion to limit bias toward the alternative hypothesis. Two authors independently reviewed the data, and differences were reconciled by group consensus. A random effects model was used to calculate summary estimates of the risk ratios.
OUTCOMES MEASURED: The primary outcome measures were risk ratios for hard coronary events (MI and cardiac death) and combined events (MI, cardiac death, and revascularization procedures).
RESULTS: Nine studies (4 published articles and 5 abstracts) were identified. Three were duplicate publications that reported the same data as another study, and one had only 33% follow-up; these were appropriately excluded. The remaining 5 studies with 4348 patients were included. There was significant heterogeneity between studies, with the best designed study having among the lowest risk ratios (2.3). The summary estimates calculated using a random effects model showed that patients with higher calcium scores by EBCT were at an increased risk of hard events (summary risk ratio=4.2; 95% confidence interval [CI], 1.6-11.3) and combined events (summary risk ratio=8.7; 95% CI, 2.7-28.1). However, these calculations should not have been reported in the first place because of the broad methodologic differences between studies and their significant heterogeneity. These major flaws greatly weaken the conclusions that can be drawn from this meta-analysis.
EBCT is a relatively costly test ($300-$400) in search of a clinical niche. It is no better at predicting coronary outcomes than traditional risk-factor modeling or the use of Framingham data. There is no evidence to support the routine use of EBCT as a screening tool for coronary disease in an asymptomatic population.
BACKGROUND: Coronary artery disease remains the leading cause of death in the United States. Currently clinicians rely on traditional models of risk-factor analysis to predict coronary outcomes. EBCT has recently been identified as a tool for measuring calcium within the coronary arteries and promoted as a means of predicting coronary risk. The use of EBCT as a prognostic or screening tool is based on the premise of a causal and incremental association between coronary artery calcium and atherosclerosis.1,2 More coronary calcium means more atherosclerotic heart disease, which in turn means a higher risk for coronary events. The objective of this study was to review the literature on EBCT as a noninvasive method for predicting subsequent coronary events.
POPULATION STUDIED: The average age of a study participant in the 5 identified studies was 57 years, and 74% were men. The study setting (ie, primary care or referral) and the subject ethnicity were not reported. The baseline cardiovascular risk of participants was inconsistently reported.
STUDY DESIGN AND VALIDITY: This study was a meta-analysis. The authors searched the literature for articles pertaining to EBCT, heart disease, and prognosis. Studies were included if they were performed on an asymptomatic adult population with adequate follow-up (minimum of 36 months) and assessment of coronary outcomes (myocardial infarction [MI] or death) was reported. The authors included data from ongoing and unpublished studies. Incomplete data were imputed in a conservative fashion to limit bias toward the alternative hypothesis. Two authors independently reviewed the data, and differences were reconciled by group consensus. A random effects model was used to calculate summary estimates of the risk ratios.
OUTCOMES MEASURED: The primary outcome measures were risk ratios for hard coronary events (MI and cardiac death) and combined events (MI, cardiac death, and revascularization procedures).
RESULTS: Nine studies (4 published articles and 5 abstracts) were identified. Three were duplicate publications that reported the same data as another study, and one had only 33% follow-up; these were appropriately excluded. The remaining 5 studies with 4348 patients were included. There was significant heterogeneity between studies, with the best designed study having among the lowest risk ratios (2.3). The summary estimates calculated using a random effects model showed that patients with higher calcium scores by EBCT were at an increased risk of hard events (summary risk ratio=4.2; 95% confidence interval [CI], 1.6-11.3) and combined events (summary risk ratio=8.7; 95% CI, 2.7-28.1). However, these calculations should not have been reported in the first place because of the broad methodologic differences between studies and their significant heterogeneity. These major flaws greatly weaken the conclusions that can be drawn from this meta-analysis.
EBCT is a relatively costly test ($300-$400) in search of a clinical niche. It is no better at predicting coronary outcomes than traditional risk-factor modeling or the use of Framingham data. There is no evidence to support the routine use of EBCT as a screening tool for coronary disease in an asymptomatic population.