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When should patients with asymptomatic aortic stenosis be evaluated for valve replacement?
For patients whose echocardiograms show advanced calcification of the aortic valves, a jet velocity of > 4.0 m/s, or a progression in jet velocity of 0.3m/s/year; and for patients who have an abnormal exercise response or an impaired functional status, consider referral for valve replacement prior to the onset of symptoms (Grade of Recommendation: C).
Evidence summary
Aortic stenosis is a narrowing of the aortic valve. Degree of severity is judged by valve area: mild (1.5–2.0 cm2), moderate (1.0–1.5 cm2), severe (< 1.0 cm2). Alternatively, stenosis may be classified by transvalvular gradient or jet velocity, the latter being the easier quantity to measure by echocardiogram. Prevalence of aortic stenosis increases with age; one series of 1243 elderly women (mean age of 82) found mild stenosis in 10%, moderate stenosis in 6%, and severe stenosis in 2%.1 Natural history studies show that once classic symptoms develop, average survival decreases to 5 years with the onset of angina, 3 years after cardiac syncope, and 2 years after heart failure.2 The incidence of sudden death increases from < 1% annually among asymptomatic patients to 15% to 20% among symptomatic patients.3,4
Aortic stenosis is suggested by such findings as a harsh systolic murmur at the right upper sternal border, pulsus parvus et tardus, and a sustained point of maximal impulse. Exercise stress testing may provide additional information. In one prospective study of 123 patients, those who had a greater increase in valve area, cardiac output, and blood pressure and a smaller decrease in stroke volume on stress echocardiogram were more likely to remain asymptomatic for the entire length of their time in the study, an average of 2.5 years.5
Asymptomatic patients with aortic stenosis who undergo coronary artery bypass grafting (CABG) often have their aortic valve replaced at the same time; the timing of aortic valve replacement in patients not requiring CABG is controversial. One prospective study found the severity of stenosis at baseline to be the strongest prognostic predictor. Patients with a jet velocity of < 3.0 m/s were unlikely to develop symptoms within 5 years; those with a jet velocity of 4.0 m/s had a > 50% likelihood of developing symptoms or dying within 2 years.5 Another study followed 128 patients for 4 years and found that moderate to severe valvular calcification and an increase in jet velocity of 0.3 m/s/year were the best prognostic predictors.6 Almost 80% of those with both calcification and a rapid change in jet velocity underwent surgery or died within 2 years6 (Table).
TABLE
Indications for possible valve replacement with asymptomatic aortic stenosis
| Predicting factor | Marker of worse prognosis |
|---|---|
| Calcification | Moderate to severe (multiple large calcified areas to extensive calcification of all cusps) |
| Jet velocity | > 4.0 m/s |
| Rate of jet velocity progression | ≥0.3 m/s/year |
| Exercise response | Minimal to no change in valve area, cardiac output, and blood pressure; marked decrease in stroke volume |
| Functional status | Impaired initially or declining |
Recommendations from others
The American College of Cardiology/American Heart Association Task Force on Practice Guidelines recommends echocardiograms every 5 years for mild stenosis, every 2 years for moderate stenosis, and annually for severe stenosis.4 There is no guideline for exercise testing. Aortic valve replacement is recommended for symptomatic patients and patients with severe stenosis undergoing CABG or other valvular or aortic surgery.
Clinical Commentary by Ken Grauer, MD; and search strategy, at www.fpin.org.
1. Aronow WS, Ahn C, Kronzon I. Am J Cardiol 1997;79:379-80.
2. Ross J, Jr., Braunwald E. Circulation 1968;38(1 Suppl ):61-7.
3. Balentine J, Eisenhart A. Aortic Stenosis. EMedicine Journal 2002;3:1.-
4. Bonow RO, Carabello B, deLeon AC, Jr., et al. Circulation 1998;98:1949-84.
5. Otto CM, Burwash IG, Legget ME, et al. Circulation 1997;95:2262-70.
6. Rosenhek R, Binder T, Porenta G, et al. N Engl J Med 2000;343:611-7.
For patients whose echocardiograms show advanced calcification of the aortic valves, a jet velocity of > 4.0 m/s, or a progression in jet velocity of 0.3m/s/year; and for patients who have an abnormal exercise response or an impaired functional status, consider referral for valve replacement prior to the onset of symptoms (Grade of Recommendation: C).
Evidence summary
Aortic stenosis is a narrowing of the aortic valve. Degree of severity is judged by valve area: mild (1.5–2.0 cm2), moderate (1.0–1.5 cm2), severe (< 1.0 cm2). Alternatively, stenosis may be classified by transvalvular gradient or jet velocity, the latter being the easier quantity to measure by echocardiogram. Prevalence of aortic stenosis increases with age; one series of 1243 elderly women (mean age of 82) found mild stenosis in 10%, moderate stenosis in 6%, and severe stenosis in 2%.1 Natural history studies show that once classic symptoms develop, average survival decreases to 5 years with the onset of angina, 3 years after cardiac syncope, and 2 years after heart failure.2 The incidence of sudden death increases from < 1% annually among asymptomatic patients to 15% to 20% among symptomatic patients.3,4
Aortic stenosis is suggested by such findings as a harsh systolic murmur at the right upper sternal border, pulsus parvus et tardus, and a sustained point of maximal impulse. Exercise stress testing may provide additional information. In one prospective study of 123 patients, those who had a greater increase in valve area, cardiac output, and blood pressure and a smaller decrease in stroke volume on stress echocardiogram were more likely to remain asymptomatic for the entire length of their time in the study, an average of 2.5 years.5
Asymptomatic patients with aortic stenosis who undergo coronary artery bypass grafting (CABG) often have their aortic valve replaced at the same time; the timing of aortic valve replacement in patients not requiring CABG is controversial. One prospective study found the severity of stenosis at baseline to be the strongest prognostic predictor. Patients with a jet velocity of < 3.0 m/s were unlikely to develop symptoms within 5 years; those with a jet velocity of 4.0 m/s had a > 50% likelihood of developing symptoms or dying within 2 years.5 Another study followed 128 patients for 4 years and found that moderate to severe valvular calcification and an increase in jet velocity of 0.3 m/s/year were the best prognostic predictors.6 Almost 80% of those with both calcification and a rapid change in jet velocity underwent surgery or died within 2 years6 (Table).
TABLE
Indications for possible valve replacement with asymptomatic aortic stenosis
| Predicting factor | Marker of worse prognosis |
|---|---|
| Calcification | Moderate to severe (multiple large calcified areas to extensive calcification of all cusps) |
| Jet velocity | > 4.0 m/s |
| Rate of jet velocity progression | ≥0.3 m/s/year |
| Exercise response | Minimal to no change in valve area, cardiac output, and blood pressure; marked decrease in stroke volume |
| Functional status | Impaired initially or declining |
Recommendations from others
The American College of Cardiology/American Heart Association Task Force on Practice Guidelines recommends echocardiograms every 5 years for mild stenosis, every 2 years for moderate stenosis, and annually for severe stenosis.4 There is no guideline for exercise testing. Aortic valve replacement is recommended for symptomatic patients and patients with severe stenosis undergoing CABG or other valvular or aortic surgery.
Clinical Commentary by Ken Grauer, MD; and search strategy, at www.fpin.org.
For patients whose echocardiograms show advanced calcification of the aortic valves, a jet velocity of > 4.0 m/s, or a progression in jet velocity of 0.3m/s/year; and for patients who have an abnormal exercise response or an impaired functional status, consider referral for valve replacement prior to the onset of symptoms (Grade of Recommendation: C).
Evidence summary
Aortic stenosis is a narrowing of the aortic valve. Degree of severity is judged by valve area: mild (1.5–2.0 cm2), moderate (1.0–1.5 cm2), severe (< 1.0 cm2). Alternatively, stenosis may be classified by transvalvular gradient or jet velocity, the latter being the easier quantity to measure by echocardiogram. Prevalence of aortic stenosis increases with age; one series of 1243 elderly women (mean age of 82) found mild stenosis in 10%, moderate stenosis in 6%, and severe stenosis in 2%.1 Natural history studies show that once classic symptoms develop, average survival decreases to 5 years with the onset of angina, 3 years after cardiac syncope, and 2 years after heart failure.2 The incidence of sudden death increases from < 1% annually among asymptomatic patients to 15% to 20% among symptomatic patients.3,4
Aortic stenosis is suggested by such findings as a harsh systolic murmur at the right upper sternal border, pulsus parvus et tardus, and a sustained point of maximal impulse. Exercise stress testing may provide additional information. In one prospective study of 123 patients, those who had a greater increase in valve area, cardiac output, and blood pressure and a smaller decrease in stroke volume on stress echocardiogram were more likely to remain asymptomatic for the entire length of their time in the study, an average of 2.5 years.5
Asymptomatic patients with aortic stenosis who undergo coronary artery bypass grafting (CABG) often have their aortic valve replaced at the same time; the timing of aortic valve replacement in patients not requiring CABG is controversial. One prospective study found the severity of stenosis at baseline to be the strongest prognostic predictor. Patients with a jet velocity of < 3.0 m/s were unlikely to develop symptoms within 5 years; those with a jet velocity of 4.0 m/s had a > 50% likelihood of developing symptoms or dying within 2 years.5 Another study followed 128 patients for 4 years and found that moderate to severe valvular calcification and an increase in jet velocity of 0.3 m/s/year were the best prognostic predictors.6 Almost 80% of those with both calcification and a rapid change in jet velocity underwent surgery or died within 2 years6 (Table).
TABLE
Indications for possible valve replacement with asymptomatic aortic stenosis
| Predicting factor | Marker of worse prognosis |
|---|---|
| Calcification | Moderate to severe (multiple large calcified areas to extensive calcification of all cusps) |
| Jet velocity | > 4.0 m/s |
| Rate of jet velocity progression | ≥0.3 m/s/year |
| Exercise response | Minimal to no change in valve area, cardiac output, and blood pressure; marked decrease in stroke volume |
| Functional status | Impaired initially or declining |
Recommendations from others
The American College of Cardiology/American Heart Association Task Force on Practice Guidelines recommends echocardiograms every 5 years for mild stenosis, every 2 years for moderate stenosis, and annually for severe stenosis.4 There is no guideline for exercise testing. Aortic valve replacement is recommended for symptomatic patients and patients with severe stenosis undergoing CABG or other valvular or aortic surgery.
Clinical Commentary by Ken Grauer, MD; and search strategy, at www.fpin.org.
1. Aronow WS, Ahn C, Kronzon I. Am J Cardiol 1997;79:379-80.
2. Ross J, Jr., Braunwald E. Circulation 1968;38(1 Suppl ):61-7.
3. Balentine J, Eisenhart A. Aortic Stenosis. EMedicine Journal 2002;3:1.-
4. Bonow RO, Carabello B, deLeon AC, Jr., et al. Circulation 1998;98:1949-84.
5. Otto CM, Burwash IG, Legget ME, et al. Circulation 1997;95:2262-70.
6. Rosenhek R, Binder T, Porenta G, et al. N Engl J Med 2000;343:611-7.
1. Aronow WS, Ahn C, Kronzon I. Am J Cardiol 1997;79:379-80.
2. Ross J, Jr., Braunwald E. Circulation 1968;38(1 Suppl ):61-7.
3. Balentine J, Eisenhart A. Aortic Stenosis. EMedicine Journal 2002;3:1.-
4. Bonow RO, Carabello B, deLeon AC, Jr., et al. Circulation 1998;98:1949-84.
5. Otto CM, Burwash IG, Legget ME, et al. Circulation 1997;95:2262-70.
6. Rosenhek R, Binder T, Porenta G, et al. N Engl J Med 2000;343:611-7.
Evidence-based answers from the Family Physicians Inquiries Network
What is the best therapy for constipation in infants?
The best treatment for minor, self-limited constipation (infant dyschezia) may be observation and parental education about its benign nature. (Grade of recommendation: D, expert opinion.) For cases requiring treatment, limited evidence suggests that 2 weeks of 2% or 4% lactulose normalizes stool passage and consistency. (Grade of recommendation: C, single cohort study.) No data are available about the benefits or harms of rectal thermometer stimulation, glycerin suppositories, sorbitol or sorbitol-containing juices, barley malt extract, or corn syrup. The significant risks of sodium phosphate enemas and mineral oil consumption make their use contraindicated. (Grade of recommendation: D, case reports and expert opinion.)
Evidence summary
Infants experience normal physiologic variation in stool frequency and consistency, moderated in part by diet.1 Childhood functional defecation disorders represent a continuum from infant dyschezia, to functional constipation, to functional fecal retention2,3 (Table 1). Most infants have dyschezia or functional constipation. Infant dyschezia, a self-limited condition related to immature muscle coordination, requires only parental reassurance.
We found no placebo-controlled trials of osmotic laxatives in infants. One uncontrolled trial of 220 functionally constipated, bottle-fed infants younger than 6 months showed normalization of stools in 90% of infants within 2 weeks of treatment with 2% or 4% lactulose.4 No other evidence has been published about the benefits or harms of sorbitol-containing juices, fiber, osmotic laxatives, formula switching, rectal stimulation with rectal thermometers, or glycerin suppositories.
We found no trials of mineral oil or sodium phosphate enemas in constipated infants. Mineral oil has been associated with lipoid aspiration pneumonia in infants less than 1 year of age.5,6 Sodium phosphate enemas in children under 2 years of age have been associated with electrolyte disturbances, dehydration, and cardiac arrest.7
TABLE 1
Rome II childhood functional defecation disorders2
| Disorder, by age | Characteristics |
|---|---|
| Infant dyschezia (< 6 months old) | 10+ minutes of straining and crying before successful passage of stools. |
| Functional constipation (infancy to preschool years) | 2+ weeks of mostly pebble-like, hard stools for stools; or firm stools 2 times/wk; and no evidence of structural, endocrine, or metabolic disease. |
| Functional fecal retention (infancy to age 16) | 12+ weeks of passage of large-diameter stools at intervals < 2 times/wk; and retentive posturing, avoiding defecation by purposefully contracting the pelvic floor, then gluteal muscles. |
Recommendations from others
The North American Society for Pediatric Gastroenterology and Nutrition recommends glycerin suppositories for rectal disimpaction for acutely constipated infants; sorbitol-containing juices, such as prune, pear, and apple, for decreasing constipation; barley malt extract, corn syrup, lactulose, or sorbitol (osmotic laxatives) as stool softeners; and avoidance of enemas, mineral oil, and stimulant laxatives due to potential adverse effects8 (Table 2).
TABLE 2
Recommended interventions for infant constipation8
| Laxative | Dosage | Side effects | Comment |
|---|---|---|---|
| Glycerin suppositories | Standard | None reported | For rectal disimpaction |
| Sorbitol-containing juices | Variable | None reported | Prune, apple, pear |
| Barley malt extract | 2–10 mL/240 mL milk or juice | Unpleasant odor | Suitable for bottle-feeding |
| Corn syrup | Variable (light or dark) | None reported | Not considered source of C. botulinum spores |
| Lactulose (70% solution) | 1–3 mL/kg per day, divided doses | Flatulence, abdominal cramps, hypernatremia | Well-tolerated long-term |
| Sorbitol | 1–3 mg/kg per day, divided doses | Same as lactulose | Less expensive than lactulose |
Clinical Commentaries by Brian T. Easton, MD, and Susan E. Graves, MD, at http://www.fpin.org.
1. Hyams JS, Treem WR, Etienne NL, et al. Pediatrics 1995;95:50-4.
2. Rasquin-Weber A, Hyman PE, Cucchiara S, et al. Gut 1999;45(suppl 2):II60-8.
3. Felt B, Wise CG, Olson A, et al. Arch Pediatr Adolesc Med 1999;153:380-5.
4. Hejlp M, Kamper J, Ebbesen J, et al. Treatment of infantile constipation in infants fed with breast milk substitutes: a controlled trial of 2% and 4% allominlactulose. Ugeskr Laeger 1990;152:1819-22.
5. Wolfson BJ, Allen JL, Panitch HB, et al. Pediatr Radiol 1989;19:545-7.
6. Sharif F, Crushell E, O’Driscoll K, et al. Arch Dis Child 2001;85:121-4.
7. Harrington L, Schuh S. Pediatr Emerg Care 1997;13:225-6.
8. Baker SS, Liptak GS, Colletti RB, et al. J Pediatr Gastroenterol Nutr 1999;29:612-6.
The best treatment for minor, self-limited constipation (infant dyschezia) may be observation and parental education about its benign nature. (Grade of recommendation: D, expert opinion.) For cases requiring treatment, limited evidence suggests that 2 weeks of 2% or 4% lactulose normalizes stool passage and consistency. (Grade of recommendation: C, single cohort study.) No data are available about the benefits or harms of rectal thermometer stimulation, glycerin suppositories, sorbitol or sorbitol-containing juices, barley malt extract, or corn syrup. The significant risks of sodium phosphate enemas and mineral oil consumption make their use contraindicated. (Grade of recommendation: D, case reports and expert opinion.)
Evidence summary
Infants experience normal physiologic variation in stool frequency and consistency, moderated in part by diet.1 Childhood functional defecation disorders represent a continuum from infant dyschezia, to functional constipation, to functional fecal retention2,3 (Table 1). Most infants have dyschezia or functional constipation. Infant dyschezia, a self-limited condition related to immature muscle coordination, requires only parental reassurance.
We found no placebo-controlled trials of osmotic laxatives in infants. One uncontrolled trial of 220 functionally constipated, bottle-fed infants younger than 6 months showed normalization of stools in 90% of infants within 2 weeks of treatment with 2% or 4% lactulose.4 No other evidence has been published about the benefits or harms of sorbitol-containing juices, fiber, osmotic laxatives, formula switching, rectal stimulation with rectal thermometers, or glycerin suppositories.
We found no trials of mineral oil or sodium phosphate enemas in constipated infants. Mineral oil has been associated with lipoid aspiration pneumonia in infants less than 1 year of age.5,6 Sodium phosphate enemas in children under 2 years of age have been associated with electrolyte disturbances, dehydration, and cardiac arrest.7
TABLE 1
Rome II childhood functional defecation disorders2
| Disorder, by age | Characteristics |
|---|---|
| Infant dyschezia (< 6 months old) | 10+ minutes of straining and crying before successful passage of stools. |
| Functional constipation (infancy to preschool years) | 2+ weeks of mostly pebble-like, hard stools for stools; or firm stools 2 times/wk; and no evidence of structural, endocrine, or metabolic disease. |
| Functional fecal retention (infancy to age 16) | 12+ weeks of passage of large-diameter stools at intervals < 2 times/wk; and retentive posturing, avoiding defecation by purposefully contracting the pelvic floor, then gluteal muscles. |
Recommendations from others
The North American Society for Pediatric Gastroenterology and Nutrition recommends glycerin suppositories for rectal disimpaction for acutely constipated infants; sorbitol-containing juices, such as prune, pear, and apple, for decreasing constipation; barley malt extract, corn syrup, lactulose, or sorbitol (osmotic laxatives) as stool softeners; and avoidance of enemas, mineral oil, and stimulant laxatives due to potential adverse effects8 (Table 2).
TABLE 2
Recommended interventions for infant constipation8
| Laxative | Dosage | Side effects | Comment |
|---|---|---|---|
| Glycerin suppositories | Standard | None reported | For rectal disimpaction |
| Sorbitol-containing juices | Variable | None reported | Prune, apple, pear |
| Barley malt extract | 2–10 mL/240 mL milk or juice | Unpleasant odor | Suitable for bottle-feeding |
| Corn syrup | Variable (light or dark) | None reported | Not considered source of C. botulinum spores |
| Lactulose (70% solution) | 1–3 mL/kg per day, divided doses | Flatulence, abdominal cramps, hypernatremia | Well-tolerated long-term |
| Sorbitol | 1–3 mg/kg per day, divided doses | Same as lactulose | Less expensive than lactulose |
Clinical Commentaries by Brian T. Easton, MD, and Susan E. Graves, MD, at http://www.fpin.org.
The best treatment for minor, self-limited constipation (infant dyschezia) may be observation and parental education about its benign nature. (Grade of recommendation: D, expert opinion.) For cases requiring treatment, limited evidence suggests that 2 weeks of 2% or 4% lactulose normalizes stool passage and consistency. (Grade of recommendation: C, single cohort study.) No data are available about the benefits or harms of rectal thermometer stimulation, glycerin suppositories, sorbitol or sorbitol-containing juices, barley malt extract, or corn syrup. The significant risks of sodium phosphate enemas and mineral oil consumption make their use contraindicated. (Grade of recommendation: D, case reports and expert opinion.)
Evidence summary
Infants experience normal physiologic variation in stool frequency and consistency, moderated in part by diet.1 Childhood functional defecation disorders represent a continuum from infant dyschezia, to functional constipation, to functional fecal retention2,3 (Table 1). Most infants have dyschezia or functional constipation. Infant dyschezia, a self-limited condition related to immature muscle coordination, requires only parental reassurance.
We found no placebo-controlled trials of osmotic laxatives in infants. One uncontrolled trial of 220 functionally constipated, bottle-fed infants younger than 6 months showed normalization of stools in 90% of infants within 2 weeks of treatment with 2% or 4% lactulose.4 No other evidence has been published about the benefits or harms of sorbitol-containing juices, fiber, osmotic laxatives, formula switching, rectal stimulation with rectal thermometers, or glycerin suppositories.
We found no trials of mineral oil or sodium phosphate enemas in constipated infants. Mineral oil has been associated with lipoid aspiration pneumonia in infants less than 1 year of age.5,6 Sodium phosphate enemas in children under 2 years of age have been associated with electrolyte disturbances, dehydration, and cardiac arrest.7
TABLE 1
Rome II childhood functional defecation disorders2
| Disorder, by age | Characteristics |
|---|---|
| Infant dyschezia (< 6 months old) | 10+ minutes of straining and crying before successful passage of stools. |
| Functional constipation (infancy to preschool years) | 2+ weeks of mostly pebble-like, hard stools for stools; or firm stools 2 times/wk; and no evidence of structural, endocrine, or metabolic disease. |
| Functional fecal retention (infancy to age 16) | 12+ weeks of passage of large-diameter stools at intervals < 2 times/wk; and retentive posturing, avoiding defecation by purposefully contracting the pelvic floor, then gluteal muscles. |
Recommendations from others
The North American Society for Pediatric Gastroenterology and Nutrition recommends glycerin suppositories for rectal disimpaction for acutely constipated infants; sorbitol-containing juices, such as prune, pear, and apple, for decreasing constipation; barley malt extract, corn syrup, lactulose, or sorbitol (osmotic laxatives) as stool softeners; and avoidance of enemas, mineral oil, and stimulant laxatives due to potential adverse effects8 (Table 2).
TABLE 2
Recommended interventions for infant constipation8
| Laxative | Dosage | Side effects | Comment |
|---|---|---|---|
| Glycerin suppositories | Standard | None reported | For rectal disimpaction |
| Sorbitol-containing juices | Variable | None reported | Prune, apple, pear |
| Barley malt extract | 2–10 mL/240 mL milk or juice | Unpleasant odor | Suitable for bottle-feeding |
| Corn syrup | Variable (light or dark) | None reported | Not considered source of C. botulinum spores |
| Lactulose (70% solution) | 1–3 mL/kg per day, divided doses | Flatulence, abdominal cramps, hypernatremia | Well-tolerated long-term |
| Sorbitol | 1–3 mg/kg per day, divided doses | Same as lactulose | Less expensive than lactulose |
Clinical Commentaries by Brian T. Easton, MD, and Susan E. Graves, MD, at http://www.fpin.org.
1. Hyams JS, Treem WR, Etienne NL, et al. Pediatrics 1995;95:50-4.
2. Rasquin-Weber A, Hyman PE, Cucchiara S, et al. Gut 1999;45(suppl 2):II60-8.
3. Felt B, Wise CG, Olson A, et al. Arch Pediatr Adolesc Med 1999;153:380-5.
4. Hejlp M, Kamper J, Ebbesen J, et al. Treatment of infantile constipation in infants fed with breast milk substitutes: a controlled trial of 2% and 4% allominlactulose. Ugeskr Laeger 1990;152:1819-22.
5. Wolfson BJ, Allen JL, Panitch HB, et al. Pediatr Radiol 1989;19:545-7.
6. Sharif F, Crushell E, O’Driscoll K, et al. Arch Dis Child 2001;85:121-4.
7. Harrington L, Schuh S. Pediatr Emerg Care 1997;13:225-6.
8. Baker SS, Liptak GS, Colletti RB, et al. J Pediatr Gastroenterol Nutr 1999;29:612-6.
1. Hyams JS, Treem WR, Etienne NL, et al. Pediatrics 1995;95:50-4.
2. Rasquin-Weber A, Hyman PE, Cucchiara S, et al. Gut 1999;45(suppl 2):II60-8.
3. Felt B, Wise CG, Olson A, et al. Arch Pediatr Adolesc Med 1999;153:380-5.
4. Hejlp M, Kamper J, Ebbesen J, et al. Treatment of infantile constipation in infants fed with breast milk substitutes: a controlled trial of 2% and 4% allominlactulose. Ugeskr Laeger 1990;152:1819-22.
5. Wolfson BJ, Allen JL, Panitch HB, et al. Pediatr Radiol 1989;19:545-7.
6. Sharif F, Crushell E, O’Driscoll K, et al. Arch Dis Child 2001;85:121-4.
7. Harrington L, Schuh S. Pediatr Emerg Care 1997;13:225-6.
8. Baker SS, Liptak GS, Colletti RB, et al. J Pediatr Gastroenterol Nutr 1999;29:612-6.
Evidence-based answers from the Family Physicians Inquiries Network
What levels of cholesterol should be treated for primary prevention?
The levels of cholesterol that should be treated for primary prevention are based on low-density lipoprotein cholesterol (LDL-C) levels of > 100 mg/dL to > 190 mg/dL and vary according to whether the patient’s risk is high, moderate, or low. See the table to estimate risk. Grade of recommendation for medication indications: A (on the basis of high-quality randomized controlled trials). Grade of recommendation for lifestyle indications: B (on the basis of extrapolations from randomized controlled trials).
TABLE
Adult treatment recommendations from NCEP, Adult Treatment Panel III
| Risk category | LDL-C level | LDL-C goal* at which to consider medication |
|---|---|---|
| Coronary heart disease risk equivalents | < 100 mg/dL | ≥ 130 mg/dL; ≥100-129 mg/dL optional |
| 2 or more major risk factors† | < 130 mg/dL | 10-year risk‡ 10-20%: ≥ 130 mg/dL; 10-year risk‡ < 10%: ≥160 mg/dL |
| 0 or 1 major risk factor† | < 160 mg/dL | ≥ 190 mg/dL; 160-190 mg/dL optional |
| NOTE: CHD risk equivalents include symptomatic carotid artery disease, peripheral arterial disease, abdominal aortic aneurysm, diabetes, and a 10-year risk of > 20% (see ‡ below). The cutoff points for therapy for patients with clinical CHD are the same as for CHD risk equivalents. | ||
| * Initiate therapeutic lifestyle changes above these levels. | ||
| †Major risk factors include cigarette smoking, hypertension, HDL < 40 mg/dL, family history of premature CHD (CHD in first-degree male relative < 55 y; CHD in first-degree female relative < 65 y), age (men ≥ 45 y, women ≥ 55 y). | ||
| ‡To calculate 10-year risk, use the Framingham Tables, available at http://www.nhlbi.nih.gov/guidelines/cholesterol/risk_tbl.htm. | ||
Evidence summary
Statins are the most effective at reducing LDL-C and the associated cardiovascular risk. The 5-year West of Scotland study (WOSCOPS) showed that a 26% reduction in LDL-C (from a mean of 192 to 142 mg/dL) using pravastatin 40 mg per day reduced the risk of either nonfatal myocardial infarction (MI) or coronary heart disease (CHD) death (number needed to treat [NNT] = 42; relative risk [RR] = 31; 95% confidence interval [CI],17 - 43).1 This trial enrolled middle-aged men with an LDL-C level > 155 mg/dL without a history of prior MI, although subjects with stable angina (5% of the participants) were still eligible. Similar reductions were seen in cardiovascular death and in all-cause death (RR = 22; 95% CI = 0 - 40). Lovastatin reduced the risk of a first major acute coronary event (NNT = 24) in the 5-year AFCAPS/TexCAPS trial that enrolled 5608 men and 997 women with below-average high-density lipoprotein cholesterol (HDL-C) (men, 36 mg/dL; women, 40 mg/dL) without signs or symptoms of CHD.2 LDL-C was lowered 25% (from a mean of 156 to 115 mg/dL). Unpublished results suggest that simvastatin may have a similar effect. Primary prevention data are still lacking for atorvastatin and fluvastatin.
The 7-year Lipid Research Clinics Coronary Prevention Trial (LRC-CPPT) documented a reduction in CHD death and/or nonfatal MI (NNT = 59) with a 12.6% reduction in LDL-C with the use of cholestyramine, a bile acid resin, 24 g per day.3
Results of studies of the fibric acid derivatives are mixed. Subjects taking gemfibrozil 1200 mg per day in the 5-year Helsinki Heart Study had fewer coronary events compared with those taking a placebo (NNT = 71).4 Subsequent analysis suggests that patients with a high LDL-C/HDL-C ratio (> 5) plus hypertriglyceridemia ( 205 mg/dL) benefited the most.5 Clofibrate is no longer used because of an unexplained increase in deaths in the WHO Cooperative Trial.6 To date, outcomes in fenofibrate trials have only focused on surrogate markers and not long-term clinical outcomes.
Recommendations from others
The recommendations of the Third Report of the National Cholesterol Education Program7 (NCEP, Adult Treatment Panel III) are in the table. This report is an excellent source of additional information (http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf).
Read a clinical commentary by David Switzer, MD, at www.fpin.org.
1. Shepard J, Cobbe SM, Ford I, et al. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995;333:1301-7.
2. Downs JR, Clearfield M, Weis S, et al. JAMA 1998;279:1615-22.
3. The Lipid Research Clinics Coronary Primary Prevention Trial results. JAMA 1984;251:351-64,365-74.
4. Frick MH, Elo O, Happa K, et al. N Engl J Med 1987;317:1237-45.
5. Manninen V, Tenkanen L, Koskinen P, et al. Circulation 1992;85:37-45.
6. WHO cooperative trial. Lancet 1984;2:600-4.
7. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-97.
The levels of cholesterol that should be treated for primary prevention are based on low-density lipoprotein cholesterol (LDL-C) levels of > 100 mg/dL to > 190 mg/dL and vary according to whether the patient’s risk is high, moderate, or low. See the table to estimate risk. Grade of recommendation for medication indications: A (on the basis of high-quality randomized controlled trials). Grade of recommendation for lifestyle indications: B (on the basis of extrapolations from randomized controlled trials).
TABLE
Adult treatment recommendations from NCEP, Adult Treatment Panel III
| Risk category | LDL-C level | LDL-C goal* at which to consider medication |
|---|---|---|
| Coronary heart disease risk equivalents | < 100 mg/dL | ≥ 130 mg/dL; ≥100-129 mg/dL optional |
| 2 or more major risk factors† | < 130 mg/dL | 10-year risk‡ 10-20%: ≥ 130 mg/dL; 10-year risk‡ < 10%: ≥160 mg/dL |
| 0 or 1 major risk factor† | < 160 mg/dL | ≥ 190 mg/dL; 160-190 mg/dL optional |
| NOTE: CHD risk equivalents include symptomatic carotid artery disease, peripheral arterial disease, abdominal aortic aneurysm, diabetes, and a 10-year risk of > 20% (see ‡ below). The cutoff points for therapy for patients with clinical CHD are the same as for CHD risk equivalents. | ||
| * Initiate therapeutic lifestyle changes above these levels. | ||
| †Major risk factors include cigarette smoking, hypertension, HDL < 40 mg/dL, family history of premature CHD (CHD in first-degree male relative < 55 y; CHD in first-degree female relative < 65 y), age (men ≥ 45 y, women ≥ 55 y). | ||
| ‡To calculate 10-year risk, use the Framingham Tables, available at http://www.nhlbi.nih.gov/guidelines/cholesterol/risk_tbl.htm. | ||
Evidence summary
Statins are the most effective at reducing LDL-C and the associated cardiovascular risk. The 5-year West of Scotland study (WOSCOPS) showed that a 26% reduction in LDL-C (from a mean of 192 to 142 mg/dL) using pravastatin 40 mg per day reduced the risk of either nonfatal myocardial infarction (MI) or coronary heart disease (CHD) death (number needed to treat [NNT] = 42; relative risk [RR] = 31; 95% confidence interval [CI],17 - 43).1 This trial enrolled middle-aged men with an LDL-C level > 155 mg/dL without a history of prior MI, although subjects with stable angina (5% of the participants) were still eligible. Similar reductions were seen in cardiovascular death and in all-cause death (RR = 22; 95% CI = 0 - 40). Lovastatin reduced the risk of a first major acute coronary event (NNT = 24) in the 5-year AFCAPS/TexCAPS trial that enrolled 5608 men and 997 women with below-average high-density lipoprotein cholesterol (HDL-C) (men, 36 mg/dL; women, 40 mg/dL) without signs or symptoms of CHD.2 LDL-C was lowered 25% (from a mean of 156 to 115 mg/dL). Unpublished results suggest that simvastatin may have a similar effect. Primary prevention data are still lacking for atorvastatin and fluvastatin.
The 7-year Lipid Research Clinics Coronary Prevention Trial (LRC-CPPT) documented a reduction in CHD death and/or nonfatal MI (NNT = 59) with a 12.6% reduction in LDL-C with the use of cholestyramine, a bile acid resin, 24 g per day.3
Results of studies of the fibric acid derivatives are mixed. Subjects taking gemfibrozil 1200 mg per day in the 5-year Helsinki Heart Study had fewer coronary events compared with those taking a placebo (NNT = 71).4 Subsequent analysis suggests that patients with a high LDL-C/HDL-C ratio (> 5) plus hypertriglyceridemia ( 205 mg/dL) benefited the most.5 Clofibrate is no longer used because of an unexplained increase in deaths in the WHO Cooperative Trial.6 To date, outcomes in fenofibrate trials have only focused on surrogate markers and not long-term clinical outcomes.
Recommendations from others
The recommendations of the Third Report of the National Cholesterol Education Program7 (NCEP, Adult Treatment Panel III) are in the table. This report is an excellent source of additional information (http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf).
Read a clinical commentary by David Switzer, MD, at www.fpin.org.
The levels of cholesterol that should be treated for primary prevention are based on low-density lipoprotein cholesterol (LDL-C) levels of > 100 mg/dL to > 190 mg/dL and vary according to whether the patient’s risk is high, moderate, or low. See the table to estimate risk. Grade of recommendation for medication indications: A (on the basis of high-quality randomized controlled trials). Grade of recommendation for lifestyle indications: B (on the basis of extrapolations from randomized controlled trials).
TABLE
Adult treatment recommendations from NCEP, Adult Treatment Panel III
| Risk category | LDL-C level | LDL-C goal* at which to consider medication |
|---|---|---|
| Coronary heart disease risk equivalents | < 100 mg/dL | ≥ 130 mg/dL; ≥100-129 mg/dL optional |
| 2 or more major risk factors† | < 130 mg/dL | 10-year risk‡ 10-20%: ≥ 130 mg/dL; 10-year risk‡ < 10%: ≥160 mg/dL |
| 0 or 1 major risk factor† | < 160 mg/dL | ≥ 190 mg/dL; 160-190 mg/dL optional |
| NOTE: CHD risk equivalents include symptomatic carotid artery disease, peripheral arterial disease, abdominal aortic aneurysm, diabetes, and a 10-year risk of > 20% (see ‡ below). The cutoff points for therapy for patients with clinical CHD are the same as for CHD risk equivalents. | ||
| * Initiate therapeutic lifestyle changes above these levels. | ||
| †Major risk factors include cigarette smoking, hypertension, HDL < 40 mg/dL, family history of premature CHD (CHD in first-degree male relative < 55 y; CHD in first-degree female relative < 65 y), age (men ≥ 45 y, women ≥ 55 y). | ||
| ‡To calculate 10-year risk, use the Framingham Tables, available at http://www.nhlbi.nih.gov/guidelines/cholesterol/risk_tbl.htm. | ||
Evidence summary
Statins are the most effective at reducing LDL-C and the associated cardiovascular risk. The 5-year West of Scotland study (WOSCOPS) showed that a 26% reduction in LDL-C (from a mean of 192 to 142 mg/dL) using pravastatin 40 mg per day reduced the risk of either nonfatal myocardial infarction (MI) or coronary heart disease (CHD) death (number needed to treat [NNT] = 42; relative risk [RR] = 31; 95% confidence interval [CI],17 - 43).1 This trial enrolled middle-aged men with an LDL-C level > 155 mg/dL without a history of prior MI, although subjects with stable angina (5% of the participants) were still eligible. Similar reductions were seen in cardiovascular death and in all-cause death (RR = 22; 95% CI = 0 - 40). Lovastatin reduced the risk of a first major acute coronary event (NNT = 24) in the 5-year AFCAPS/TexCAPS trial that enrolled 5608 men and 997 women with below-average high-density lipoprotein cholesterol (HDL-C) (men, 36 mg/dL; women, 40 mg/dL) without signs or symptoms of CHD.2 LDL-C was lowered 25% (from a mean of 156 to 115 mg/dL). Unpublished results suggest that simvastatin may have a similar effect. Primary prevention data are still lacking for atorvastatin and fluvastatin.
The 7-year Lipid Research Clinics Coronary Prevention Trial (LRC-CPPT) documented a reduction in CHD death and/or nonfatal MI (NNT = 59) with a 12.6% reduction in LDL-C with the use of cholestyramine, a bile acid resin, 24 g per day.3
Results of studies of the fibric acid derivatives are mixed. Subjects taking gemfibrozil 1200 mg per day in the 5-year Helsinki Heart Study had fewer coronary events compared with those taking a placebo (NNT = 71).4 Subsequent analysis suggests that patients with a high LDL-C/HDL-C ratio (> 5) plus hypertriglyceridemia ( 205 mg/dL) benefited the most.5 Clofibrate is no longer used because of an unexplained increase in deaths in the WHO Cooperative Trial.6 To date, outcomes in fenofibrate trials have only focused on surrogate markers and not long-term clinical outcomes.
Recommendations from others
The recommendations of the Third Report of the National Cholesterol Education Program7 (NCEP, Adult Treatment Panel III) are in the table. This report is an excellent source of additional information (http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf).
Read a clinical commentary by David Switzer, MD, at www.fpin.org.
1. Shepard J, Cobbe SM, Ford I, et al. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995;333:1301-7.
2. Downs JR, Clearfield M, Weis S, et al. JAMA 1998;279:1615-22.
3. The Lipid Research Clinics Coronary Primary Prevention Trial results. JAMA 1984;251:351-64,365-74.
4. Frick MH, Elo O, Happa K, et al. N Engl J Med 1987;317:1237-45.
5. Manninen V, Tenkanen L, Koskinen P, et al. Circulation 1992;85:37-45.
6. WHO cooperative trial. Lancet 1984;2:600-4.
7. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-97.
1. Shepard J, Cobbe SM, Ford I, et al. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995;333:1301-7.
2. Downs JR, Clearfield M, Weis S, et al. JAMA 1998;279:1615-22.
3. The Lipid Research Clinics Coronary Primary Prevention Trial results. JAMA 1984;251:351-64,365-74.
4. Frick MH, Elo O, Happa K, et al. N Engl J Med 1987;317:1237-45.
5. Manninen V, Tenkanen L, Koskinen P, et al. Circulation 1992;85:37-45.
6. WHO cooperative trial. Lancet 1984;2:600-4.
7. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-97.
Evidence-based answers from the Family Physicians Inquiries Network
When should acute nonvenereal conjunctivitis be treated with topical antibiotics?
Children with suspected or culture-proven acute nonvenereal bacterial conjunctivitis should be treated with topical antibiotics, which hastens clinical and microbiological remission and may prevent potentially serious morbidity. In light of recent evidence regarding the self-limiting nature of conjunctivitis in adults and the development of antibiotic resistance, a “wait-and-see” approach with careful follow-up may be reasonable for adults, but this approach has not been evaluated. (Grade of recommendation: C, based on extrapolation from systematic reviews of specialty clinic trials and cohort studies.)
Evidence summary
Conjunctivitis accounts for 1% to 2% of office visits to primary care practitioners.1 Conjunctivitis is more commonly caused by bacteria in children (50% in 1 study2) than in adults, in whom viral conjunctivitis predominates.3 Treating suspected or culture-proven acute bacterial conjunctivitis with topical antibiotics significantly shortens the clinical course of the disease and results in higher microbiological cure rates than placebo.1,4,5 A meta-analysis of 3 trials based in specialty clinics or hospitals reported significant clinical cure or improvement of bacterial conjunctivitis with 2 to 5 days of topical antibiotics compared with placebo (RR = 1.31, 95% CI, 1.11-1.55, number needed to treat = 5).1 Other articles have reported corneal or systemic complications of bacterial conjunctivitis. For example, 1 review reports that 25% of children with Haemophilus influenzae conjunctivitis develop otitis media.2
Although there is a small risk of complications and longer time course when bacterial conjunctivitis is left untreated, the disease is often self-limited, with a 64% clinical remission rate in patients treated for 2 to 5 days with placebo.1 The rate of spontaneous remission is much higher for adults than for children (71.6% vs 28%, respectively). The Cochrane meta-analysis reported a similar clinical cure rate in children for 6 to 10 days of treatment with topical antibiotics versus placebo. A systematic review of 5 placebo-controlled RCTs reported no serious adverse outcomes in conjunctivitis patients regardless of treatment group.4
Antibiotic resistance is a growing problem. Studies of fluoroquinolone resistance rates report a range of 4% to 50% for ocular bacteria.6 The 50% resistance rate occurred after 4 weeks of topical treatment in postcataract surgery patients.
Overall, this evidence suggests that for adults, watchful waiting rather than initially treating with antibiotics is reasonable, given the self-limited nature and lack of serious outcomes in untreated patients as well as growing concern about antibiotic resistance. Note that this recommendation applies only to acute nonvenereal conjunctivitis. It is generally accepted that conjunctivitis caused by gonococcus or chlamydia should be suspected in all newborns and in severe cases in sexually active young adults. These cases warrant culturing and antibiotic treatment to prevent serious complications.7
Recommendations from others
The American Optometric Association consensus guideline states that ideal treatment should be based on the specific causative organism. The guideline concludes that treatment of bacterial conjunctivitis with antibiotics can reduce symptoms, duration of illness, and chances of recurrence.8
Clinical Commentary by Carin Reust, MD, MSPH, at http://www.fpin.org.
1. Sheikh A, Hurwitz B, Cave J. Antibiotics versus placebo for acute bacterial conjunctivitis (Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford, England: Update Software.
2. Gigliotti F, Hendley JO, Morgan J, Michaels R, Dickens M, Lohr J. J Pediatr 1984;104:623-6.
3. Chung CW, Cohen EJ. West J Med 2000;173:202-5.
4. Sheikh A, Hurwitz B. Br J Gen Pract 2001;51:473-7.
5. Chung C, Cohen E. Bacterial conjunctivitis. Clinical evidence. London: BMJ Publishing Group, 2001: 436-41.
6. Baum J, Barza M. The evolution of antibiotic therapy for bacterial conjunctivitis and keratitis: 1970-2000. Cornea 2000;19:659-72.
7. Morrow GL, Abbott RL. Conjunctivitis. Am Fam Physician 1998;57:735-46.
8. American Optometric Association consensus panel on the care of the patient with conjunctivitis. Optometric clinical practice guideline no. 11, 1996.
Children with suspected or culture-proven acute nonvenereal bacterial conjunctivitis should be treated with topical antibiotics, which hastens clinical and microbiological remission and may prevent potentially serious morbidity. In light of recent evidence regarding the self-limiting nature of conjunctivitis in adults and the development of antibiotic resistance, a “wait-and-see” approach with careful follow-up may be reasonable for adults, but this approach has not been evaluated. (Grade of recommendation: C, based on extrapolation from systematic reviews of specialty clinic trials and cohort studies.)
Evidence summary
Conjunctivitis accounts for 1% to 2% of office visits to primary care practitioners.1 Conjunctivitis is more commonly caused by bacteria in children (50% in 1 study2) than in adults, in whom viral conjunctivitis predominates.3 Treating suspected or culture-proven acute bacterial conjunctivitis with topical antibiotics significantly shortens the clinical course of the disease and results in higher microbiological cure rates than placebo.1,4,5 A meta-analysis of 3 trials based in specialty clinics or hospitals reported significant clinical cure or improvement of bacterial conjunctivitis with 2 to 5 days of topical antibiotics compared with placebo (RR = 1.31, 95% CI, 1.11-1.55, number needed to treat = 5).1 Other articles have reported corneal or systemic complications of bacterial conjunctivitis. For example, 1 review reports that 25% of children with Haemophilus influenzae conjunctivitis develop otitis media.2
Although there is a small risk of complications and longer time course when bacterial conjunctivitis is left untreated, the disease is often self-limited, with a 64% clinical remission rate in patients treated for 2 to 5 days with placebo.1 The rate of spontaneous remission is much higher for adults than for children (71.6% vs 28%, respectively). The Cochrane meta-analysis reported a similar clinical cure rate in children for 6 to 10 days of treatment with topical antibiotics versus placebo. A systematic review of 5 placebo-controlled RCTs reported no serious adverse outcomes in conjunctivitis patients regardless of treatment group.4
Antibiotic resistance is a growing problem. Studies of fluoroquinolone resistance rates report a range of 4% to 50% for ocular bacteria.6 The 50% resistance rate occurred after 4 weeks of topical treatment in postcataract surgery patients.
Overall, this evidence suggests that for adults, watchful waiting rather than initially treating with antibiotics is reasonable, given the self-limited nature and lack of serious outcomes in untreated patients as well as growing concern about antibiotic resistance. Note that this recommendation applies only to acute nonvenereal conjunctivitis. It is generally accepted that conjunctivitis caused by gonococcus or chlamydia should be suspected in all newborns and in severe cases in sexually active young adults. These cases warrant culturing and antibiotic treatment to prevent serious complications.7
Recommendations from others
The American Optometric Association consensus guideline states that ideal treatment should be based on the specific causative organism. The guideline concludes that treatment of bacterial conjunctivitis with antibiotics can reduce symptoms, duration of illness, and chances of recurrence.8
Clinical Commentary by Carin Reust, MD, MSPH, at http://www.fpin.org.
Children with suspected or culture-proven acute nonvenereal bacterial conjunctivitis should be treated with topical antibiotics, which hastens clinical and microbiological remission and may prevent potentially serious morbidity. In light of recent evidence regarding the self-limiting nature of conjunctivitis in adults and the development of antibiotic resistance, a “wait-and-see” approach with careful follow-up may be reasonable for adults, but this approach has not been evaluated. (Grade of recommendation: C, based on extrapolation from systematic reviews of specialty clinic trials and cohort studies.)
Evidence summary
Conjunctivitis accounts for 1% to 2% of office visits to primary care practitioners.1 Conjunctivitis is more commonly caused by bacteria in children (50% in 1 study2) than in adults, in whom viral conjunctivitis predominates.3 Treating suspected or culture-proven acute bacterial conjunctivitis with topical antibiotics significantly shortens the clinical course of the disease and results in higher microbiological cure rates than placebo.1,4,5 A meta-analysis of 3 trials based in specialty clinics or hospitals reported significant clinical cure or improvement of bacterial conjunctivitis with 2 to 5 days of topical antibiotics compared with placebo (RR = 1.31, 95% CI, 1.11-1.55, number needed to treat = 5).1 Other articles have reported corneal or systemic complications of bacterial conjunctivitis. For example, 1 review reports that 25% of children with Haemophilus influenzae conjunctivitis develop otitis media.2
Although there is a small risk of complications and longer time course when bacterial conjunctivitis is left untreated, the disease is often self-limited, with a 64% clinical remission rate in patients treated for 2 to 5 days with placebo.1 The rate of spontaneous remission is much higher for adults than for children (71.6% vs 28%, respectively). The Cochrane meta-analysis reported a similar clinical cure rate in children for 6 to 10 days of treatment with topical antibiotics versus placebo. A systematic review of 5 placebo-controlled RCTs reported no serious adverse outcomes in conjunctivitis patients regardless of treatment group.4
Antibiotic resistance is a growing problem. Studies of fluoroquinolone resistance rates report a range of 4% to 50% for ocular bacteria.6 The 50% resistance rate occurred after 4 weeks of topical treatment in postcataract surgery patients.
Overall, this evidence suggests that for adults, watchful waiting rather than initially treating with antibiotics is reasonable, given the self-limited nature and lack of serious outcomes in untreated patients as well as growing concern about antibiotic resistance. Note that this recommendation applies only to acute nonvenereal conjunctivitis. It is generally accepted that conjunctivitis caused by gonococcus or chlamydia should be suspected in all newborns and in severe cases in sexually active young adults. These cases warrant culturing and antibiotic treatment to prevent serious complications.7
Recommendations from others
The American Optometric Association consensus guideline states that ideal treatment should be based on the specific causative organism. The guideline concludes that treatment of bacterial conjunctivitis with antibiotics can reduce symptoms, duration of illness, and chances of recurrence.8
Clinical Commentary by Carin Reust, MD, MSPH, at http://www.fpin.org.
1. Sheikh A, Hurwitz B, Cave J. Antibiotics versus placebo for acute bacterial conjunctivitis (Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford, England: Update Software.
2. Gigliotti F, Hendley JO, Morgan J, Michaels R, Dickens M, Lohr J. J Pediatr 1984;104:623-6.
3. Chung CW, Cohen EJ. West J Med 2000;173:202-5.
4. Sheikh A, Hurwitz B. Br J Gen Pract 2001;51:473-7.
5. Chung C, Cohen E. Bacterial conjunctivitis. Clinical evidence. London: BMJ Publishing Group, 2001: 436-41.
6. Baum J, Barza M. The evolution of antibiotic therapy for bacterial conjunctivitis and keratitis: 1970-2000. Cornea 2000;19:659-72.
7. Morrow GL, Abbott RL. Conjunctivitis. Am Fam Physician 1998;57:735-46.
8. American Optometric Association consensus panel on the care of the patient with conjunctivitis. Optometric clinical practice guideline no. 11, 1996.
1. Sheikh A, Hurwitz B, Cave J. Antibiotics versus placebo for acute bacterial conjunctivitis (Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford, England: Update Software.
2. Gigliotti F, Hendley JO, Morgan J, Michaels R, Dickens M, Lohr J. J Pediatr 1984;104:623-6.
3. Chung CW, Cohen EJ. West J Med 2000;173:202-5.
4. Sheikh A, Hurwitz B. Br J Gen Pract 2001;51:473-7.
5. Chung C, Cohen E. Bacterial conjunctivitis. Clinical evidence. London: BMJ Publishing Group, 2001: 436-41.
6. Baum J, Barza M. The evolution of antibiotic therapy for bacterial conjunctivitis and keratitis: 1970-2000. Cornea 2000;19:659-72.
7. Morrow GL, Abbott RL. Conjunctivitis. Am Fam Physician 1998;57:735-46.
8. American Optometric Association consensus panel on the care of the patient with conjunctivitis. Optometric clinical practice guideline no. 11, 1996.
Evidence-based answers from the Family Physicians Inquiries Network