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Does warfarin prevent deep venous thrombosis in high-risk patients?
Warfarin (Coumadin) is effective in preventing deep venous thrombosis (DVT) among patients with a history of DVT. Conventional dosing and longer durations are the most effective, but the ideal length of therapy is unknown (strength of recommendation [SOR]: A, based on large randomized controlled trials and meta-analysis).
Warfarin is useful in preventing DVT in patients with cancer, specifically those treated with chemotherapy (SOR: B, based on small randomized controlled trials). Warfarin may be effective in pre-venting DVT in immobilized patients such as those with trauma, spinal cord injury, or stroke (SOR: B, based on an underpowered randomized controlled trial and uncontrolled studies).
Evidence summary
Warfarin, at both low and conventional doses, has been shown to be effective in preventing recurrence of DVT. A large, 4-year placebo-controlled randomized controlled trial showed that long-term low-dose warfarin (international normalized ratio [INR], 1.5-1.9) was more effective than placebo for prevention of DVT (hazard ratio=0.36; 95% confidence interval [CI], 0.19-0.67).1
A double-blind randomized controlled trial of 738 patients demonstrated that conventional-intensity warfarin therapy (INR=2.0-3.0) was more effective than low-intensity therapy (INR=1.5-1.9) in prevention of recurrent DVT. There were 1.9 vs 0.7 DVTs per 100 person-years in the low-intensity vs conventional-intensity therapy groups (hazard ratio=2.8; 95% CI, 1.1-7.0; number needed to treat [NNT]=37). No significant difference was seen in the frequency of bleeding complications between the groups.2 This and other studies suggest that low-intensity warfarin therapy reduces the relative risk of thrombosis by about 75%, and conventional-intensity therapy reduces this risk by over 90%.2
Several studies have examined the duration of warfarin therapy. A meta-analysis found treatment with warfarin for 12 to 24 weeks decreased DVT recurrence compared with 2- to 6-week regimens (relative risk [RR]=0.60; 95% CI, 0.45-0.79; NNT=21).3 A multicenter randomized controlled trial found extending warfarin treatment for 12 months vs 3 months resulted in a 95% relative risk reduction (RRR) in risk of DVT recurrence (95% CI, 63-99; NNT=5).4 A multicenter randomized trial showed similar results, but risk for recurrence was the same after treatment was stopped, regardless of the length of treatment.5
In patients with cancer, warfarin was shown to be more effective than placebo in prevention of DVT. In a trial of 311 breast cancer patients receiving chemotherapy, treatment with very-low-dose warfarin (INR=1.3-1.9) decreased thrombotic events compared with placebo, with no increase in bleeding complications (RRR=85%; P=.031; NNT=27).6 A later cost analysis showed that very-low-dose warfarin can be used in prevention of DVT in breast cancer patients on chemotherapy without an increase in health care costs.7
Although immobilized patients are at high risk for DVT, no randomized controlled trials exist for the use of warfarin in these patients. A few small studies suggest that warfarin reduces DVT rates in spinal-cord-injured patients.8 A small trial randomized stroke patients undergoing rehabilitation to placebo or fixed 1- or 2-mg doses of warfarin. This underpowered study showed a nonsignificant decrease in the risk of development of DVT (RR=0.39; 95% CI, 0.13-1.37).8
Recommendations from others
The 6th American College of Chest Physicians Consensus Conference on Antithrombotic Therapy makes these recommendations:9
Prior DVT: Oral anticoagulation therapy (INR=2.0-3.0) is indicated for at least 3 months for patients with proximal DVT or for at least 6 months in those with idiopathic proximal vein thrombosis or recurrent venous thrombosis. Indefinite anticoagulation is indicated for patients with more than 1 episode of idiopathic proximal vein thrombosis or pulmonary embolus.
Malignancy: Indefinite anticoagulation (INR= 2.0-3.0) is indicated for patients with thrombosis complicating malignancy. Prophylaxis with low-intensity warfarin in ambulatory patients with cancer to prevent initial DVT warrants further study.
Acute spinal cord injuries: Low-molecular-weight heparin or switch to full-dose oral anti-coagulation (INR=2.0-3.0) for the duration of the rehabilitation phase.
Routine prophylaxis dramatically reduces DVT cases
John P. Langlois, MD
MAHEC Family Practice Residency, Asheville, NC
I can clearly recall the dramatic reduction in the number of our patients who developed DVT when our orthopedic colleagues embraced routine prophylaxis for the high-risk surgical patients with hip surgery and knee replacements. This answer indicates that we may also be able to reduce the risk of DVT in our high-risk nonsurgical patients with previous DVT or breast cancer. Note that much of the evidence is based on the use of low-dose and very-low-dose warfarin. This may help mitigate our fear of substituting bleeding complications for the prevention of clots.
1. Ridker PM, Goldhaber SZ, Danielson E, et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med 2003;348:1425-1434.
2. Kearon C, Ginsberg JS, Kovacs MJ, et al. Comparison of low-intensity warfarin therapy with conventional-intensity war-farin therapy for long-term prevention of recurrent venous thromboembolism. N Engl J Med 2003;349:631-639.
3. Pinede L, Duhaut P, Cucherat M, Ninet J, Pasquier J, Boissel JP. Comparison of long versus short duration of anticoagulant therapy after a first episode of venous thromboembolism: a meta-analysis of randomized, controlled trials. J Intern Med 2000;247:553-562.
4. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med 1999;340:901-907.
5. Agnelli G, Prandoni P, Santamaria MG, et al. Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. Warfarin Optimal Duration Italian Trial Investigators. N Engl J Med 2001;345:165-169.
6. Levine M, Hirsh J, Gent M, et al. Double-blind randomised trial of a very-low-dose warfarin for prevention of throm-boembolism in stage IV breast cancer. Lancet 1994;343:886-889.
7. Rajan R, Gafni A, Levine M, Hirsh J, Gent M. Very low-dose warfarin prophylaxis to prevent thromboembolism in women with metastatic breast cancer receiving chemotherapy: an economic evaluation. J Clin Oncol 1995;13:42-46.
8. Ginsberg JS, Bates SM, Oczkowski W, et al. Low-dose warfarin in rehabilitating stroke survivors. Thromb Res 2002;107:287-290.
9. Hirsh J, Dalen J, Guyatt G. American College of Chest Physicians. The sixth (2000) ACCP guidelines for antithrombotic therapy for prevention and treatment of thrombosis. American College of Chest Physicians. Chest 2001;119(1 Suppl):132S-193S.
Warfarin (Coumadin) is effective in preventing deep venous thrombosis (DVT) among patients with a history of DVT. Conventional dosing and longer durations are the most effective, but the ideal length of therapy is unknown (strength of recommendation [SOR]: A, based on large randomized controlled trials and meta-analysis).
Warfarin is useful in preventing DVT in patients with cancer, specifically those treated with chemotherapy (SOR: B, based on small randomized controlled trials). Warfarin may be effective in pre-venting DVT in immobilized patients such as those with trauma, spinal cord injury, or stroke (SOR: B, based on an underpowered randomized controlled trial and uncontrolled studies).
Evidence summary
Warfarin, at both low and conventional doses, has been shown to be effective in preventing recurrence of DVT. A large, 4-year placebo-controlled randomized controlled trial showed that long-term low-dose warfarin (international normalized ratio [INR], 1.5-1.9) was more effective than placebo for prevention of DVT (hazard ratio=0.36; 95% confidence interval [CI], 0.19-0.67).1
A double-blind randomized controlled trial of 738 patients demonstrated that conventional-intensity warfarin therapy (INR=2.0-3.0) was more effective than low-intensity therapy (INR=1.5-1.9) in prevention of recurrent DVT. There were 1.9 vs 0.7 DVTs per 100 person-years in the low-intensity vs conventional-intensity therapy groups (hazard ratio=2.8; 95% CI, 1.1-7.0; number needed to treat [NNT]=37). No significant difference was seen in the frequency of bleeding complications between the groups.2 This and other studies suggest that low-intensity warfarin therapy reduces the relative risk of thrombosis by about 75%, and conventional-intensity therapy reduces this risk by over 90%.2
Several studies have examined the duration of warfarin therapy. A meta-analysis found treatment with warfarin for 12 to 24 weeks decreased DVT recurrence compared with 2- to 6-week regimens (relative risk [RR]=0.60; 95% CI, 0.45-0.79; NNT=21).3 A multicenter randomized controlled trial found extending warfarin treatment for 12 months vs 3 months resulted in a 95% relative risk reduction (RRR) in risk of DVT recurrence (95% CI, 63-99; NNT=5).4 A multicenter randomized trial showed similar results, but risk for recurrence was the same after treatment was stopped, regardless of the length of treatment.5
In patients with cancer, warfarin was shown to be more effective than placebo in prevention of DVT. In a trial of 311 breast cancer patients receiving chemotherapy, treatment with very-low-dose warfarin (INR=1.3-1.9) decreased thrombotic events compared with placebo, with no increase in bleeding complications (RRR=85%; P=.031; NNT=27).6 A later cost analysis showed that very-low-dose warfarin can be used in prevention of DVT in breast cancer patients on chemotherapy without an increase in health care costs.7
Although immobilized patients are at high risk for DVT, no randomized controlled trials exist for the use of warfarin in these patients. A few small studies suggest that warfarin reduces DVT rates in spinal-cord-injured patients.8 A small trial randomized stroke patients undergoing rehabilitation to placebo or fixed 1- or 2-mg doses of warfarin. This underpowered study showed a nonsignificant decrease in the risk of development of DVT (RR=0.39; 95% CI, 0.13-1.37).8
Recommendations from others
The 6th American College of Chest Physicians Consensus Conference on Antithrombotic Therapy makes these recommendations:9
Prior DVT: Oral anticoagulation therapy (INR=2.0-3.0) is indicated for at least 3 months for patients with proximal DVT or for at least 6 months in those with idiopathic proximal vein thrombosis or recurrent venous thrombosis. Indefinite anticoagulation is indicated for patients with more than 1 episode of idiopathic proximal vein thrombosis or pulmonary embolus.
Malignancy: Indefinite anticoagulation (INR= 2.0-3.0) is indicated for patients with thrombosis complicating malignancy. Prophylaxis with low-intensity warfarin in ambulatory patients with cancer to prevent initial DVT warrants further study.
Acute spinal cord injuries: Low-molecular-weight heparin or switch to full-dose oral anti-coagulation (INR=2.0-3.0) for the duration of the rehabilitation phase.
Routine prophylaxis dramatically reduces DVT cases
John P. Langlois, MD
MAHEC Family Practice Residency, Asheville, NC
I can clearly recall the dramatic reduction in the number of our patients who developed DVT when our orthopedic colleagues embraced routine prophylaxis for the high-risk surgical patients with hip surgery and knee replacements. This answer indicates that we may also be able to reduce the risk of DVT in our high-risk nonsurgical patients with previous DVT or breast cancer. Note that much of the evidence is based on the use of low-dose and very-low-dose warfarin. This may help mitigate our fear of substituting bleeding complications for the prevention of clots.
Warfarin (Coumadin) is effective in preventing deep venous thrombosis (DVT) among patients with a history of DVT. Conventional dosing and longer durations are the most effective, but the ideal length of therapy is unknown (strength of recommendation [SOR]: A, based on large randomized controlled trials and meta-analysis).
Warfarin is useful in preventing DVT in patients with cancer, specifically those treated with chemotherapy (SOR: B, based on small randomized controlled trials). Warfarin may be effective in pre-venting DVT in immobilized patients such as those with trauma, spinal cord injury, or stroke (SOR: B, based on an underpowered randomized controlled trial and uncontrolled studies).
Evidence summary
Warfarin, at both low and conventional doses, has been shown to be effective in preventing recurrence of DVT. A large, 4-year placebo-controlled randomized controlled trial showed that long-term low-dose warfarin (international normalized ratio [INR], 1.5-1.9) was more effective than placebo for prevention of DVT (hazard ratio=0.36; 95% confidence interval [CI], 0.19-0.67).1
A double-blind randomized controlled trial of 738 patients demonstrated that conventional-intensity warfarin therapy (INR=2.0-3.0) was more effective than low-intensity therapy (INR=1.5-1.9) in prevention of recurrent DVT. There were 1.9 vs 0.7 DVTs per 100 person-years in the low-intensity vs conventional-intensity therapy groups (hazard ratio=2.8; 95% CI, 1.1-7.0; number needed to treat [NNT]=37). No significant difference was seen in the frequency of bleeding complications between the groups.2 This and other studies suggest that low-intensity warfarin therapy reduces the relative risk of thrombosis by about 75%, and conventional-intensity therapy reduces this risk by over 90%.2
Several studies have examined the duration of warfarin therapy. A meta-analysis found treatment with warfarin for 12 to 24 weeks decreased DVT recurrence compared with 2- to 6-week regimens (relative risk [RR]=0.60; 95% CI, 0.45-0.79; NNT=21).3 A multicenter randomized controlled trial found extending warfarin treatment for 12 months vs 3 months resulted in a 95% relative risk reduction (RRR) in risk of DVT recurrence (95% CI, 63-99; NNT=5).4 A multicenter randomized trial showed similar results, but risk for recurrence was the same after treatment was stopped, regardless of the length of treatment.5
In patients with cancer, warfarin was shown to be more effective than placebo in prevention of DVT. In a trial of 311 breast cancer patients receiving chemotherapy, treatment with very-low-dose warfarin (INR=1.3-1.9) decreased thrombotic events compared with placebo, with no increase in bleeding complications (RRR=85%; P=.031; NNT=27).6 A later cost analysis showed that very-low-dose warfarin can be used in prevention of DVT in breast cancer patients on chemotherapy without an increase in health care costs.7
Although immobilized patients are at high risk for DVT, no randomized controlled trials exist for the use of warfarin in these patients. A few small studies suggest that warfarin reduces DVT rates in spinal-cord-injured patients.8 A small trial randomized stroke patients undergoing rehabilitation to placebo or fixed 1- or 2-mg doses of warfarin. This underpowered study showed a nonsignificant decrease in the risk of development of DVT (RR=0.39; 95% CI, 0.13-1.37).8
Recommendations from others
The 6th American College of Chest Physicians Consensus Conference on Antithrombotic Therapy makes these recommendations:9
Prior DVT: Oral anticoagulation therapy (INR=2.0-3.0) is indicated for at least 3 months for patients with proximal DVT or for at least 6 months in those with idiopathic proximal vein thrombosis or recurrent venous thrombosis. Indefinite anticoagulation is indicated for patients with more than 1 episode of idiopathic proximal vein thrombosis or pulmonary embolus.
Malignancy: Indefinite anticoagulation (INR= 2.0-3.0) is indicated for patients with thrombosis complicating malignancy. Prophylaxis with low-intensity warfarin in ambulatory patients with cancer to prevent initial DVT warrants further study.
Acute spinal cord injuries: Low-molecular-weight heparin or switch to full-dose oral anti-coagulation (INR=2.0-3.0) for the duration of the rehabilitation phase.
Routine prophylaxis dramatically reduces DVT cases
John P. Langlois, MD
MAHEC Family Practice Residency, Asheville, NC
I can clearly recall the dramatic reduction in the number of our patients who developed DVT when our orthopedic colleagues embraced routine prophylaxis for the high-risk surgical patients with hip surgery and knee replacements. This answer indicates that we may also be able to reduce the risk of DVT in our high-risk nonsurgical patients with previous DVT or breast cancer. Note that much of the evidence is based on the use of low-dose and very-low-dose warfarin. This may help mitigate our fear of substituting bleeding complications for the prevention of clots.
1. Ridker PM, Goldhaber SZ, Danielson E, et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med 2003;348:1425-1434.
2. Kearon C, Ginsberg JS, Kovacs MJ, et al. Comparison of low-intensity warfarin therapy with conventional-intensity war-farin therapy for long-term prevention of recurrent venous thromboembolism. N Engl J Med 2003;349:631-639.
3. Pinede L, Duhaut P, Cucherat M, Ninet J, Pasquier J, Boissel JP. Comparison of long versus short duration of anticoagulant therapy after a first episode of venous thromboembolism: a meta-analysis of randomized, controlled trials. J Intern Med 2000;247:553-562.
4. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med 1999;340:901-907.
5. Agnelli G, Prandoni P, Santamaria MG, et al. Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. Warfarin Optimal Duration Italian Trial Investigators. N Engl J Med 2001;345:165-169.
6. Levine M, Hirsh J, Gent M, et al. Double-blind randomised trial of a very-low-dose warfarin for prevention of throm-boembolism in stage IV breast cancer. Lancet 1994;343:886-889.
7. Rajan R, Gafni A, Levine M, Hirsh J, Gent M. Very low-dose warfarin prophylaxis to prevent thromboembolism in women with metastatic breast cancer receiving chemotherapy: an economic evaluation. J Clin Oncol 1995;13:42-46.
8. Ginsberg JS, Bates SM, Oczkowski W, et al. Low-dose warfarin in rehabilitating stroke survivors. Thromb Res 2002;107:287-290.
9. Hirsh J, Dalen J, Guyatt G. American College of Chest Physicians. The sixth (2000) ACCP guidelines for antithrombotic therapy for prevention and treatment of thrombosis. American College of Chest Physicians. Chest 2001;119(1 Suppl):132S-193S.
1. Ridker PM, Goldhaber SZ, Danielson E, et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med 2003;348:1425-1434.
2. Kearon C, Ginsberg JS, Kovacs MJ, et al. Comparison of low-intensity warfarin therapy with conventional-intensity war-farin therapy for long-term prevention of recurrent venous thromboembolism. N Engl J Med 2003;349:631-639.
3. Pinede L, Duhaut P, Cucherat M, Ninet J, Pasquier J, Boissel JP. Comparison of long versus short duration of anticoagulant therapy after a first episode of venous thromboembolism: a meta-analysis of randomized, controlled trials. J Intern Med 2000;247:553-562.
4. Kearon C, Gent M, Hirsh J, et al. A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med 1999;340:901-907.
5. Agnelli G, Prandoni P, Santamaria MG, et al. Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. Warfarin Optimal Duration Italian Trial Investigators. N Engl J Med 2001;345:165-169.
6. Levine M, Hirsh J, Gent M, et al. Double-blind randomised trial of a very-low-dose warfarin for prevention of throm-boembolism in stage IV breast cancer. Lancet 1994;343:886-889.
7. Rajan R, Gafni A, Levine M, Hirsh J, Gent M. Very low-dose warfarin prophylaxis to prevent thromboembolism in women with metastatic breast cancer receiving chemotherapy: an economic evaluation. J Clin Oncol 1995;13:42-46.
8. Ginsberg JS, Bates SM, Oczkowski W, et al. Low-dose warfarin in rehabilitating stroke survivors. Thromb Res 2002;107:287-290.
9. Hirsh J, Dalen J, Guyatt G. American College of Chest Physicians. The sixth (2000) ACCP guidelines for antithrombotic therapy for prevention and treatment of thrombosis. American College of Chest Physicians. Chest 2001;119(1 Suppl):132S-193S.
Evidence-based answers from the Family Physicians Inquiries Network
The Mini Electronic Medical Record: A Low-Cost, Low-Risk Partial Solution
For several years our residency program had been considering the purchase of an electronic medicalrecord (EMR). We had seen demonstrations of the products and were aware that a few practices in our area were using full EMRs. We knew of their many advantages, as delineated in several recent articles.1-3
Our faculty had 3 major concerns about the purchase of an EMR. The first was price. The cost of implementation cited in the literature varies widely; one source estimates $15,000 per full-time physician.1 There is disagreement as to whether the operating expenses of paperless EMR systems are less than traditional paper systems.4 The savings in dictation and filing are often offset by fees for service agreements and technical support. Thus, it seemed unlikely that an EMR would significantly decrease our operating costs in the immediate future.
Our second concern was the potential for physician dissatisfaction and disruption of clinical flow. At least 10 residency programs had purchased commercial EMRs and discontinued using them.5-7 Our clinic was running smoothly, so we believed that the advantages of a full EMR would not compensate for the inconveniences and frustrations that seem to accompany a commercial product. Our third concern was the apparent lack of a dominant EMR vendor. A recent survey of the industry revealed tremendous turnover,8 and a survey of family medicine residencies reported that no vendor had more than 25% of the market.5 Consequently, we feared investing in a product when its vendor might go out of business.
Our foremost goal was quality improvement (QI). This should include electronic reminders for due prevention items, the ability to display our completion rates for key prevention items without the time and expense of pulling charts, and the ability to check on critical combinations of diagnoses and medications (eg, congestive heart failure and ß-blocker usage). Second, we wanted to improve the legibility and accessibility of key parts of a patient’s chart, particularly medications and chronic diagnoses. The ability to access the full chart electronically and to change our current dictation of daily SOAP Notes (SpeechStudio; Portland, Ore) were less important to us.
Development
Since we did not believe a commercial program would meet our goals, we decided to create our own partial or miniature electronic medical record (mini EMR). Several reports in the literature have described the value of mini EMRs.9,10 One of the authors with previous programming experience (R.D.C.) began writing the first version in May 1999. We found a formulary database, Multum (Multum Information Services, Denver, Colo) from which we could import generic and trade medication names and categories. We also created a list of 700 primary care International Classification of Diseases–9th revision (ICD-9) codes common in our practice.
Current Use
Starting in May 2000, all of our 6.5 full-time equivalent physicians began using the mini EMR. Our patients’ demographic data were initially imported from our billing program into the mini EMR from a delimited text file. This same method is used to update phone numbers monthly. We had traditionally placed a preprinted sheet of paper for notes and orders on the front of each patient’s chart at each visit. This sheet was replaced with a printout from the mini EMR that included current ICD-9 codes, medications, and reminders for age- and sex-appropriate due prevention items. Front sheets are batch-printed each morning, then placed in the patient’s chart where it remains until the next visit, to be replaced by the most current printed version. When dictating the visit, the physician also updates the mini EMR entry for that patient on the computer. It takes approximately 30 seconds to call up a patient record and enter or change several diagnoses or medications or to add prevention item dates. This is not additional time, since most physicians would otherwise have to update the problem and medication lists in the paper chart. However, it does require that the physician be at a computer terminal. Physicians or nurses also update the mini EMR as data from Papanicolaou tests, laboratory values, and so forth, become available.
Microsoft Access has proved to be very stable, and we have not experienced any system crashes or lockups. Security issues are addressed in 3 ways. First, Access allows group and individual log-in names and passwords for both individual and networked computers. Second, it can generate an audit trail for any changes made to the database. Finally, the database should be used on a standalone network or behind a firewall.
Six months after full implementation of the mini EMR, more than 75% of our patients older than 50 years (N=1912) had been entered into the mini EMR. Acceptance has been very high, even by care providers who were admittedly computer phobic. Since we can easily query the mini EMR and determine our adherence rates for prevention items and medication usage, we are planning a number of QI projects, including improving mammography rates, using β-blockers in patients with congestive heart failure, and lowering low-density lipoprotein levels.
Using the Mini EMR in Other Practices
There are several lessons we learned from developing and implementing the mini EMR. The first is to start with a subset of your most committed practitioners. This group will be most forgiving of the inevitable growing pains associated with adopting a new system. Such an approach may also induce nonuser envy. Second, the development of a sense of ownership of the program was very important. We believe implementing users’ suggestions increased acceptance.
Although a general purpose relational database may be inappropriate for practice networks with many providers and locations, adopting the mini EMR in a smaller practice should be relatively easy. A person with good knowledge of Access would be required for initial setup, for the link to your current computer system, and for any desired modifications. A small network can easily be created, as described by Levin.11 Although we have not attempted to import data from the mini EMR into a commercial EMR, the widespread use of Access should make interfacing with a commercial EMR relatively simple.
Conclusions
The mini EMR has given our practice many of the advantages of a full EMR with few of the accompanying disruptions and at a much lower price. The simplicity of the design, coupled with the many attributes of Microsoft Access, make it easy to maintain and modify. We believe this program will serve our practice well for several years and then act as a bridge to a full commercial EMR once that software market has matured.
1. Ornstein SM. Electronic medical records in family practice: the time is now. J Fam Pract 1997;44:45-48.
2. Jerant AF, Hill DB. Does the use of electronic medical records improve surrogate patient outcomes in outpatient settings? J Fam Pract 2000;49:349-57.
3. Rehm S, Kraft S. How to select a computer system for a family physician’s office. 2nd ed. Shawnee Mission, Kan: American Academy of Family Physicians Committee on Health Care Services; 1999. Available at: www.aafp.org/fpnet/guide/index.html.
4. Field C. Steps to a paperless office: weigh carefully the pros and cons of an EMR. Physicians and computers. 2000;18:26,-29-30,32.-
5. Lenhart JG, Honess K, Covington D, Johnson KE. An analysis of trends, perceptions, and use patterns of electronic medical records among US family practice residency programs. Med Informatics 2000;32:109-14.
6. Lawler F, Cacy JR, Viviani N, Hamm RM, Cobb SW. Implementation and termination of a computerized medical information system. J Fam Pract 1996;42:233-36.
7. Dambro MR, Weiss BD, McClure CL, Vuturo AF. An unsuccessful experience with computerized medical records in an academic medical center. J Med Educ 1988;63:617-23.
8. Rehm S, Kraft S. Electronic medical records: the FPM vendor survey. Fam Pract Manage 2001;8:45-54.Available at: www.aafp.org/fpm/20010100/4Selec.html.
9. Carey TS, Thomas D, Woolsey A, et al. Half a loaf is better than waiting for the bread truck. A computerized mini-medical record for outpatient care. Arch Intern Med 1992;152:1845-49.
10. Whiting O, E. KQ, Simborg DW, Epstein WV. A controlled experiment to evaluate the use of a time-oriented summary medical record. Med Care 1980;18:842-52.
11. Levin MW. How a salaried FP computerized his practice—on his own. Fam Pract Manage 2000;7:[6 screens].-Available at: www.aafp.org/fpm/20000600/43howa.html.
For several years our residency program had been considering the purchase of an electronic medicalrecord (EMR). We had seen demonstrations of the products and were aware that a few practices in our area were using full EMRs. We knew of their many advantages, as delineated in several recent articles.1-3
Our faculty had 3 major concerns about the purchase of an EMR. The first was price. The cost of implementation cited in the literature varies widely; one source estimates $15,000 per full-time physician.1 There is disagreement as to whether the operating expenses of paperless EMR systems are less than traditional paper systems.4 The savings in dictation and filing are often offset by fees for service agreements and technical support. Thus, it seemed unlikely that an EMR would significantly decrease our operating costs in the immediate future.
Our second concern was the potential for physician dissatisfaction and disruption of clinical flow. At least 10 residency programs had purchased commercial EMRs and discontinued using them.5-7 Our clinic was running smoothly, so we believed that the advantages of a full EMR would not compensate for the inconveniences and frustrations that seem to accompany a commercial product. Our third concern was the apparent lack of a dominant EMR vendor. A recent survey of the industry revealed tremendous turnover,8 and a survey of family medicine residencies reported that no vendor had more than 25% of the market.5 Consequently, we feared investing in a product when its vendor might go out of business.
Our foremost goal was quality improvement (QI). This should include electronic reminders for due prevention items, the ability to display our completion rates for key prevention items without the time and expense of pulling charts, and the ability to check on critical combinations of diagnoses and medications (eg, congestive heart failure and ß-blocker usage). Second, we wanted to improve the legibility and accessibility of key parts of a patient’s chart, particularly medications and chronic diagnoses. The ability to access the full chart electronically and to change our current dictation of daily SOAP Notes (SpeechStudio; Portland, Ore) were less important to us.
Development
Since we did not believe a commercial program would meet our goals, we decided to create our own partial or miniature electronic medical record (mini EMR). Several reports in the literature have described the value of mini EMRs.9,10 One of the authors with previous programming experience (R.D.C.) began writing the first version in May 1999. We found a formulary database, Multum (Multum Information Services, Denver, Colo) from which we could import generic and trade medication names and categories. We also created a list of 700 primary care International Classification of Diseases–9th revision (ICD-9) codes common in our practice.
Current Use
Starting in May 2000, all of our 6.5 full-time equivalent physicians began using the mini EMR. Our patients’ demographic data were initially imported from our billing program into the mini EMR from a delimited text file. This same method is used to update phone numbers monthly. We had traditionally placed a preprinted sheet of paper for notes and orders on the front of each patient’s chart at each visit. This sheet was replaced with a printout from the mini EMR that included current ICD-9 codes, medications, and reminders for age- and sex-appropriate due prevention items. Front sheets are batch-printed each morning, then placed in the patient’s chart where it remains until the next visit, to be replaced by the most current printed version. When dictating the visit, the physician also updates the mini EMR entry for that patient on the computer. It takes approximately 30 seconds to call up a patient record and enter or change several diagnoses or medications or to add prevention item dates. This is not additional time, since most physicians would otherwise have to update the problem and medication lists in the paper chart. However, it does require that the physician be at a computer terminal. Physicians or nurses also update the mini EMR as data from Papanicolaou tests, laboratory values, and so forth, become available.
Microsoft Access has proved to be very stable, and we have not experienced any system crashes or lockups. Security issues are addressed in 3 ways. First, Access allows group and individual log-in names and passwords for both individual and networked computers. Second, it can generate an audit trail for any changes made to the database. Finally, the database should be used on a standalone network or behind a firewall.
Six months after full implementation of the mini EMR, more than 75% of our patients older than 50 years (N=1912) had been entered into the mini EMR. Acceptance has been very high, even by care providers who were admittedly computer phobic. Since we can easily query the mini EMR and determine our adherence rates for prevention items and medication usage, we are planning a number of QI projects, including improving mammography rates, using β-blockers in patients with congestive heart failure, and lowering low-density lipoprotein levels.
Using the Mini EMR in Other Practices
There are several lessons we learned from developing and implementing the mini EMR. The first is to start with a subset of your most committed practitioners. This group will be most forgiving of the inevitable growing pains associated with adopting a new system. Such an approach may also induce nonuser envy. Second, the development of a sense of ownership of the program was very important. We believe implementing users’ suggestions increased acceptance.
Although a general purpose relational database may be inappropriate for practice networks with many providers and locations, adopting the mini EMR in a smaller practice should be relatively easy. A person with good knowledge of Access would be required for initial setup, for the link to your current computer system, and for any desired modifications. A small network can easily be created, as described by Levin.11 Although we have not attempted to import data from the mini EMR into a commercial EMR, the widespread use of Access should make interfacing with a commercial EMR relatively simple.
Conclusions
The mini EMR has given our practice many of the advantages of a full EMR with few of the accompanying disruptions and at a much lower price. The simplicity of the design, coupled with the many attributes of Microsoft Access, make it easy to maintain and modify. We believe this program will serve our practice well for several years and then act as a bridge to a full commercial EMR once that software market has matured.
For several years our residency program had been considering the purchase of an electronic medicalrecord (EMR). We had seen demonstrations of the products and were aware that a few practices in our area were using full EMRs. We knew of their many advantages, as delineated in several recent articles.1-3
Our faculty had 3 major concerns about the purchase of an EMR. The first was price. The cost of implementation cited in the literature varies widely; one source estimates $15,000 per full-time physician.1 There is disagreement as to whether the operating expenses of paperless EMR systems are less than traditional paper systems.4 The savings in dictation and filing are often offset by fees for service agreements and technical support. Thus, it seemed unlikely that an EMR would significantly decrease our operating costs in the immediate future.
Our second concern was the potential for physician dissatisfaction and disruption of clinical flow. At least 10 residency programs had purchased commercial EMRs and discontinued using them.5-7 Our clinic was running smoothly, so we believed that the advantages of a full EMR would not compensate for the inconveniences and frustrations that seem to accompany a commercial product. Our third concern was the apparent lack of a dominant EMR vendor. A recent survey of the industry revealed tremendous turnover,8 and a survey of family medicine residencies reported that no vendor had more than 25% of the market.5 Consequently, we feared investing in a product when its vendor might go out of business.
Our foremost goal was quality improvement (QI). This should include electronic reminders for due prevention items, the ability to display our completion rates for key prevention items without the time and expense of pulling charts, and the ability to check on critical combinations of diagnoses and medications (eg, congestive heart failure and ß-blocker usage). Second, we wanted to improve the legibility and accessibility of key parts of a patient’s chart, particularly medications and chronic diagnoses. The ability to access the full chart electronically and to change our current dictation of daily SOAP Notes (SpeechStudio; Portland, Ore) were less important to us.
Development
Since we did not believe a commercial program would meet our goals, we decided to create our own partial or miniature electronic medical record (mini EMR). Several reports in the literature have described the value of mini EMRs.9,10 One of the authors with previous programming experience (R.D.C.) began writing the first version in May 1999. We found a formulary database, Multum (Multum Information Services, Denver, Colo) from which we could import generic and trade medication names and categories. We also created a list of 700 primary care International Classification of Diseases–9th revision (ICD-9) codes common in our practice.
Current Use
Starting in May 2000, all of our 6.5 full-time equivalent physicians began using the mini EMR. Our patients’ demographic data were initially imported from our billing program into the mini EMR from a delimited text file. This same method is used to update phone numbers monthly. We had traditionally placed a preprinted sheet of paper for notes and orders on the front of each patient’s chart at each visit. This sheet was replaced with a printout from the mini EMR that included current ICD-9 codes, medications, and reminders for age- and sex-appropriate due prevention items. Front sheets are batch-printed each morning, then placed in the patient’s chart where it remains until the next visit, to be replaced by the most current printed version. When dictating the visit, the physician also updates the mini EMR entry for that patient on the computer. It takes approximately 30 seconds to call up a patient record and enter or change several diagnoses or medications or to add prevention item dates. This is not additional time, since most physicians would otherwise have to update the problem and medication lists in the paper chart. However, it does require that the physician be at a computer terminal. Physicians or nurses also update the mini EMR as data from Papanicolaou tests, laboratory values, and so forth, become available.
Microsoft Access has proved to be very stable, and we have not experienced any system crashes or lockups. Security issues are addressed in 3 ways. First, Access allows group and individual log-in names and passwords for both individual and networked computers. Second, it can generate an audit trail for any changes made to the database. Finally, the database should be used on a standalone network or behind a firewall.
Six months after full implementation of the mini EMR, more than 75% of our patients older than 50 years (N=1912) had been entered into the mini EMR. Acceptance has been very high, even by care providers who were admittedly computer phobic. Since we can easily query the mini EMR and determine our adherence rates for prevention items and medication usage, we are planning a number of QI projects, including improving mammography rates, using β-blockers in patients with congestive heart failure, and lowering low-density lipoprotein levels.
Using the Mini EMR in Other Practices
There are several lessons we learned from developing and implementing the mini EMR. The first is to start with a subset of your most committed practitioners. This group will be most forgiving of the inevitable growing pains associated with adopting a new system. Such an approach may also induce nonuser envy. Second, the development of a sense of ownership of the program was very important. We believe implementing users’ suggestions increased acceptance.
Although a general purpose relational database may be inappropriate for practice networks with many providers and locations, adopting the mini EMR in a smaller practice should be relatively easy. A person with good knowledge of Access would be required for initial setup, for the link to your current computer system, and for any desired modifications. A small network can easily be created, as described by Levin.11 Although we have not attempted to import data from the mini EMR into a commercial EMR, the widespread use of Access should make interfacing with a commercial EMR relatively simple.
Conclusions
The mini EMR has given our practice many of the advantages of a full EMR with few of the accompanying disruptions and at a much lower price. The simplicity of the design, coupled with the many attributes of Microsoft Access, make it easy to maintain and modify. We believe this program will serve our practice well for several years and then act as a bridge to a full commercial EMR once that software market has matured.
1. Ornstein SM. Electronic medical records in family practice: the time is now. J Fam Pract 1997;44:45-48.
2. Jerant AF, Hill DB. Does the use of electronic medical records improve surrogate patient outcomes in outpatient settings? J Fam Pract 2000;49:349-57.
3. Rehm S, Kraft S. How to select a computer system for a family physician’s office. 2nd ed. Shawnee Mission, Kan: American Academy of Family Physicians Committee on Health Care Services; 1999. Available at: www.aafp.org/fpnet/guide/index.html.
4. Field C. Steps to a paperless office: weigh carefully the pros and cons of an EMR. Physicians and computers. 2000;18:26,-29-30,32.-
5. Lenhart JG, Honess K, Covington D, Johnson KE. An analysis of trends, perceptions, and use patterns of electronic medical records among US family practice residency programs. Med Informatics 2000;32:109-14.
6. Lawler F, Cacy JR, Viviani N, Hamm RM, Cobb SW. Implementation and termination of a computerized medical information system. J Fam Pract 1996;42:233-36.
7. Dambro MR, Weiss BD, McClure CL, Vuturo AF. An unsuccessful experience with computerized medical records in an academic medical center. J Med Educ 1988;63:617-23.
8. Rehm S, Kraft S. Electronic medical records: the FPM vendor survey. Fam Pract Manage 2001;8:45-54.Available at: www.aafp.org/fpm/20010100/4Selec.html.
9. Carey TS, Thomas D, Woolsey A, et al. Half a loaf is better than waiting for the bread truck. A computerized mini-medical record for outpatient care. Arch Intern Med 1992;152:1845-49.
10. Whiting O, E. KQ, Simborg DW, Epstein WV. A controlled experiment to evaluate the use of a time-oriented summary medical record. Med Care 1980;18:842-52.
11. Levin MW. How a salaried FP computerized his practice—on his own. Fam Pract Manage 2000;7:[6 screens].-Available at: www.aafp.org/fpm/20000600/43howa.html.
1. Ornstein SM. Electronic medical records in family practice: the time is now. J Fam Pract 1997;44:45-48.
2. Jerant AF, Hill DB. Does the use of electronic medical records improve surrogate patient outcomes in outpatient settings? J Fam Pract 2000;49:349-57.
3. Rehm S, Kraft S. How to select a computer system for a family physician’s office. 2nd ed. Shawnee Mission, Kan: American Academy of Family Physicians Committee on Health Care Services; 1999. Available at: www.aafp.org/fpnet/guide/index.html.
4. Field C. Steps to a paperless office: weigh carefully the pros and cons of an EMR. Physicians and computers. 2000;18:26,-29-30,32.-
5. Lenhart JG, Honess K, Covington D, Johnson KE. An analysis of trends, perceptions, and use patterns of electronic medical records among US family practice residency programs. Med Informatics 2000;32:109-14.
6. Lawler F, Cacy JR, Viviani N, Hamm RM, Cobb SW. Implementation and termination of a computerized medical information system. J Fam Pract 1996;42:233-36.
7. Dambro MR, Weiss BD, McClure CL, Vuturo AF. An unsuccessful experience with computerized medical records in an academic medical center. J Med Educ 1988;63:617-23.
8. Rehm S, Kraft S. Electronic medical records: the FPM vendor survey. Fam Pract Manage 2001;8:45-54.Available at: www.aafp.org/fpm/20010100/4Selec.html.
9. Carey TS, Thomas D, Woolsey A, et al. Half a loaf is better than waiting for the bread truck. A computerized mini-medical record for outpatient care. Arch Intern Med 1992;152:1845-49.
10. Whiting O, E. KQ, Simborg DW, Epstein WV. A controlled experiment to evaluate the use of a time-oriented summary medical record. Med Care 1980;18:842-52.
11. Levin MW. How a salaried FP computerized his practice—on his own. Fam Pract Manage 2000;7:[6 screens].-Available at: www.aafp.org/fpm/20000600/43howa.html.
What is the best oral antifungal medication for tinea capitis?
Terbinafine is effective, safe for use in children, and relatively inexpensive, and it offers a shorter course of therapy than griseofulvin. Unfortunately, it is not available in liquid form. Fluconazole is available in liquid form and appears to be effective and safe, but fewer clinical trials have been published about it. Griseofulvin taken for 6 to 8 weeks remains an effective therapy for tinea capitis. There are insufficient randomized controlled trials directly comparing these agents to clearly establish a superior medication. (Grade of Recommendation: B [small randomized controlled trials with limited head-to-head comparisons of drugs])
Recommendations From Others
Major pediatric and infectious disease textbooks continue to recommend griseofulvin as first-line therapy for tinea capitis but recognize that other safe and effective treatments exist.1-4 A recent practice guideline from the British Association of Dermatologists did not recommend any oral antifungal agent as clearly superior.5
Evidence Summary
Tinea capitis is one of the most common dermatophyte infections in the pediatric population, affecting up to 4% of all children. The peak age is 4 to 6 years; infection is rare after puberty. Systemic therapy is generally required.6 The exact efficacy of any agent is difficult to determine, because most studies were small, used different doses and definitions of cure, and were conducted in different populations. With the exception of ketoconazole, all agents seem to have roughly similar efficacy and cure rates of approximately 70% to 80%. None of these agents require laboratory monitoring at the recommended lengths of treatment for tinea capitis Table.7
Griseofulvin’s safety and long history of use in children are its best assets. Recommended dosages and treatment duration have been increased because of fears of developing resistance.8 Tablets are approximately one third the cost of the liquid preparations.
Ketoconazole was one of the first “-azoles” studied for the treatment of tinea in children. It is not as efficacious or as safe as other available treatments, making it unsuitable for the treatment of tinea capitis in children.5
Itraconazole has been associated with several abnormalities of bone and soft tissue at doses exceeding normal human exposure. Additionally, at more normal doses a component of the liquid formulation causes pancreatic adenocarcinoma in rats.6 It has had mixed efficacy in clinical trials, with cure rates ranging from 40% to 89%.9-11
Fluconazole is another broad-spectrum antifungal in the triazole class. It has been approved by the Food and Drug Administration (FDA) for use in children with systemic fungal infections. The safety profile is very good; it has no known significant carcinogenic potential. Fluconazole is available in both tablet and liquid formulations that make dosing in young children convenient. There are very few clinical studies comparing fluconazole with other antifungal drugs, and no head-to-head prospective randomized controlled trials with griseofulvin have been published to date.5
Terbinafine is an allyamine antifungal drug that has a very good safety profile. Unfortunately, there is no liquid formulation of terbinafine, but tablets may be hidden in food.12 Although terbinafine is efficacious against Trichophyton tonsurans and Trichophyton violaceum, it does not work as well against Microsporum canis, which accounts for approximately 3% of the infections.12-15 Terbinafine is the most attractively priced treatment for tinea capitis, particularly if a short course is used.
John DeSpain, MD (Dermatology)
Columbia, MissourI
In the near future I suspect the controversy will not be whether to use the newer antifungals (terbinafine, itraconazole, and fluconazole) but rather which one to use. Despite abundant literature documenting the apparent safety of the newer agents, only the makers of griseofulvin have obtained FDA approval for treating pediatric tinea infections. (Fluconazole is approved for the treatment of thrush.) More than 90% of the cases of tinea capitis in the United States are caused by Trichophyton tonsurans; thus, concern about resistant Microsporum canis is probably overemphasized.
In my practice I no longer prescribe griseofulvin to adults for any type of fungal infection. Influenced by current FDA approval and the opinions of referring physicians, I still use griseofulvin to treat some children. However, I use the newer agents (itraconazole or terbinafine) in most cases.
1. Seidel HM, Barnett NK. Alopecia and hair shaft abnormalities. In: Hoekelman RA, Friedman SB, Nelson N, eds. Primary pediatric care. 3rd ed. St. Louis, Mo: Mosby; 1997:860.
2. Darmstadt GL. Cutaneous fungal infections. In: Behrman RE, ed. Nelson textbook of pediatrics. 16th ed. Philadelphia, Pa: W.B. Saunders Company; 2000:2038.
3. American Academy of Pediatrics Tinea capitis. In: 2000 Redbook: Report of the Committee on Infectious Diseases. 25th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1997;569-70.
4. Hay RJ. Dermatophytosis and other superficial mycoses. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s: Principles and practice of infectious diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:2762.
5. Higgins EM, Fuller LC, Smith CH. Guidelines for the management of tinea capitis. Br J Dermatol 2000;143:53-58.
6. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of the care for superficial mycotic infections of the skin: tinea capitis and tinea barbae. J Am Acad Derm 1996;34:290-94.
7. Bennett ML, Fleishcher AB, Loveless JW, Feldman SR. Oral griseolfulvin remains the treatment of choice for tinea capitis in children. Pediatr Dermatol 2000;17:304-09.
8. Friedlander SF. The optimal therapy for tinea capitis. Pediatr Dermatol 2000;17:325-26.
9. Degreef H. Itraconazole in the treatment of tinea capitis. Cutis 1996;58:90-93.
10. Jahangir M, Hussain I, Hasan M, Haroon TS. A double blind, randomized, comparative trial of itraconazole versus terbinafine for 2 weeks in tinea capitis. Br J Dermatol 1998;139:672-74.
11. Abdel-Rahman SM, Powell DA, Nahata MC. Efficacy of itraconazole in children with Trichophyton tonsurans tinea capitis. J Am Acad Derm 1998;38:443-46.
12. Freidlander SF. The evolving role of itraconazole, fluconazole and terbinafine in the treatment of tinea capitis. Pediatr Infect Dis J 1999;18:205-10.
13. Caceras-Rios H, Rueda M, Ballona R, Bustamonte B. Comparison of terbinafine and griseofulvin in the treatment of tinea capitis. J Am Acad Dermatol 2000;42:80-84.
14. Haroon TS, Hussain I, Aman S, et al. A randomized double blind comparative study of terbinafine for 1, 2 and 4 weeks in tinea capitis. Br J Dermatol 1996;135:86-88.
15. Dragos V, Lunder M. Lack of efficacy of 6-week treatment with oral terbinafine for tinea capitis due to Microsporum canis in children. Pediatr Dermatol 1997;14:46-48.
Terbinafine is effective, safe for use in children, and relatively inexpensive, and it offers a shorter course of therapy than griseofulvin. Unfortunately, it is not available in liquid form. Fluconazole is available in liquid form and appears to be effective and safe, but fewer clinical trials have been published about it. Griseofulvin taken for 6 to 8 weeks remains an effective therapy for tinea capitis. There are insufficient randomized controlled trials directly comparing these agents to clearly establish a superior medication. (Grade of Recommendation: B [small randomized controlled trials with limited head-to-head comparisons of drugs])
Recommendations From Others
Major pediatric and infectious disease textbooks continue to recommend griseofulvin as first-line therapy for tinea capitis but recognize that other safe and effective treatments exist.1-4 A recent practice guideline from the British Association of Dermatologists did not recommend any oral antifungal agent as clearly superior.5
Evidence Summary
Tinea capitis is one of the most common dermatophyte infections in the pediatric population, affecting up to 4% of all children. The peak age is 4 to 6 years; infection is rare after puberty. Systemic therapy is generally required.6 The exact efficacy of any agent is difficult to determine, because most studies were small, used different doses and definitions of cure, and were conducted in different populations. With the exception of ketoconazole, all agents seem to have roughly similar efficacy and cure rates of approximately 70% to 80%. None of these agents require laboratory monitoring at the recommended lengths of treatment for tinea capitis Table.7
Griseofulvin’s safety and long history of use in children are its best assets. Recommended dosages and treatment duration have been increased because of fears of developing resistance.8 Tablets are approximately one third the cost of the liquid preparations.
Ketoconazole was one of the first “-azoles” studied for the treatment of tinea in children. It is not as efficacious or as safe as other available treatments, making it unsuitable for the treatment of tinea capitis in children.5
Itraconazole has been associated with several abnormalities of bone and soft tissue at doses exceeding normal human exposure. Additionally, at more normal doses a component of the liquid formulation causes pancreatic adenocarcinoma in rats.6 It has had mixed efficacy in clinical trials, with cure rates ranging from 40% to 89%.9-11
Fluconazole is another broad-spectrum antifungal in the triazole class. It has been approved by the Food and Drug Administration (FDA) for use in children with systemic fungal infections. The safety profile is very good; it has no known significant carcinogenic potential. Fluconazole is available in both tablet and liquid formulations that make dosing in young children convenient. There are very few clinical studies comparing fluconazole with other antifungal drugs, and no head-to-head prospective randomized controlled trials with griseofulvin have been published to date.5
Terbinafine is an allyamine antifungal drug that has a very good safety profile. Unfortunately, there is no liquid formulation of terbinafine, but tablets may be hidden in food.12 Although terbinafine is efficacious against Trichophyton tonsurans and Trichophyton violaceum, it does not work as well against Microsporum canis, which accounts for approximately 3% of the infections.12-15 Terbinafine is the most attractively priced treatment for tinea capitis, particularly if a short course is used.
John DeSpain, MD (Dermatology)
Columbia, MissourI
In the near future I suspect the controversy will not be whether to use the newer antifungals (terbinafine, itraconazole, and fluconazole) but rather which one to use. Despite abundant literature documenting the apparent safety of the newer agents, only the makers of griseofulvin have obtained FDA approval for treating pediatric tinea infections. (Fluconazole is approved for the treatment of thrush.) More than 90% of the cases of tinea capitis in the United States are caused by Trichophyton tonsurans; thus, concern about resistant Microsporum canis is probably overemphasized.
In my practice I no longer prescribe griseofulvin to adults for any type of fungal infection. Influenced by current FDA approval and the opinions of referring physicians, I still use griseofulvin to treat some children. However, I use the newer agents (itraconazole or terbinafine) in most cases.
Terbinafine is effective, safe for use in children, and relatively inexpensive, and it offers a shorter course of therapy than griseofulvin. Unfortunately, it is not available in liquid form. Fluconazole is available in liquid form and appears to be effective and safe, but fewer clinical trials have been published about it. Griseofulvin taken for 6 to 8 weeks remains an effective therapy for tinea capitis. There are insufficient randomized controlled trials directly comparing these agents to clearly establish a superior medication. (Grade of Recommendation: B [small randomized controlled trials with limited head-to-head comparisons of drugs])
Recommendations From Others
Major pediatric and infectious disease textbooks continue to recommend griseofulvin as first-line therapy for tinea capitis but recognize that other safe and effective treatments exist.1-4 A recent practice guideline from the British Association of Dermatologists did not recommend any oral antifungal agent as clearly superior.5
Evidence Summary
Tinea capitis is one of the most common dermatophyte infections in the pediatric population, affecting up to 4% of all children. The peak age is 4 to 6 years; infection is rare after puberty. Systemic therapy is generally required.6 The exact efficacy of any agent is difficult to determine, because most studies were small, used different doses and definitions of cure, and were conducted in different populations. With the exception of ketoconazole, all agents seem to have roughly similar efficacy and cure rates of approximately 70% to 80%. None of these agents require laboratory monitoring at the recommended lengths of treatment for tinea capitis Table.7
Griseofulvin’s safety and long history of use in children are its best assets. Recommended dosages and treatment duration have been increased because of fears of developing resistance.8 Tablets are approximately one third the cost of the liquid preparations.
Ketoconazole was one of the first “-azoles” studied for the treatment of tinea in children. It is not as efficacious or as safe as other available treatments, making it unsuitable for the treatment of tinea capitis in children.5
Itraconazole has been associated with several abnormalities of bone and soft tissue at doses exceeding normal human exposure. Additionally, at more normal doses a component of the liquid formulation causes pancreatic adenocarcinoma in rats.6 It has had mixed efficacy in clinical trials, with cure rates ranging from 40% to 89%.9-11
Fluconazole is another broad-spectrum antifungal in the triazole class. It has been approved by the Food and Drug Administration (FDA) for use in children with systemic fungal infections. The safety profile is very good; it has no known significant carcinogenic potential. Fluconazole is available in both tablet and liquid formulations that make dosing in young children convenient. There are very few clinical studies comparing fluconazole with other antifungal drugs, and no head-to-head prospective randomized controlled trials with griseofulvin have been published to date.5
Terbinafine is an allyamine antifungal drug that has a very good safety profile. Unfortunately, there is no liquid formulation of terbinafine, but tablets may be hidden in food.12 Although terbinafine is efficacious against Trichophyton tonsurans and Trichophyton violaceum, it does not work as well against Microsporum canis, which accounts for approximately 3% of the infections.12-15 Terbinafine is the most attractively priced treatment for tinea capitis, particularly if a short course is used.
John DeSpain, MD (Dermatology)
Columbia, MissourI
In the near future I suspect the controversy will not be whether to use the newer antifungals (terbinafine, itraconazole, and fluconazole) but rather which one to use. Despite abundant literature documenting the apparent safety of the newer agents, only the makers of griseofulvin have obtained FDA approval for treating pediatric tinea infections. (Fluconazole is approved for the treatment of thrush.) More than 90% of the cases of tinea capitis in the United States are caused by Trichophyton tonsurans; thus, concern about resistant Microsporum canis is probably overemphasized.
In my practice I no longer prescribe griseofulvin to adults for any type of fungal infection. Influenced by current FDA approval and the opinions of referring physicians, I still use griseofulvin to treat some children. However, I use the newer agents (itraconazole or terbinafine) in most cases.
1. Seidel HM, Barnett NK. Alopecia and hair shaft abnormalities. In: Hoekelman RA, Friedman SB, Nelson N, eds. Primary pediatric care. 3rd ed. St. Louis, Mo: Mosby; 1997:860.
2. Darmstadt GL. Cutaneous fungal infections. In: Behrman RE, ed. Nelson textbook of pediatrics. 16th ed. Philadelphia, Pa: W.B. Saunders Company; 2000:2038.
3. American Academy of Pediatrics Tinea capitis. In: 2000 Redbook: Report of the Committee on Infectious Diseases. 25th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1997;569-70.
4. Hay RJ. Dermatophytosis and other superficial mycoses. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s: Principles and practice of infectious diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:2762.
5. Higgins EM, Fuller LC, Smith CH. Guidelines for the management of tinea capitis. Br J Dermatol 2000;143:53-58.
6. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of the care for superficial mycotic infections of the skin: tinea capitis and tinea barbae. J Am Acad Derm 1996;34:290-94.
7. Bennett ML, Fleishcher AB, Loveless JW, Feldman SR. Oral griseolfulvin remains the treatment of choice for tinea capitis in children. Pediatr Dermatol 2000;17:304-09.
8. Friedlander SF. The optimal therapy for tinea capitis. Pediatr Dermatol 2000;17:325-26.
9. Degreef H. Itraconazole in the treatment of tinea capitis. Cutis 1996;58:90-93.
10. Jahangir M, Hussain I, Hasan M, Haroon TS. A double blind, randomized, comparative trial of itraconazole versus terbinafine for 2 weeks in tinea capitis. Br J Dermatol 1998;139:672-74.
11. Abdel-Rahman SM, Powell DA, Nahata MC. Efficacy of itraconazole in children with Trichophyton tonsurans tinea capitis. J Am Acad Derm 1998;38:443-46.
12. Freidlander SF. The evolving role of itraconazole, fluconazole and terbinafine in the treatment of tinea capitis. Pediatr Infect Dis J 1999;18:205-10.
13. Caceras-Rios H, Rueda M, Ballona R, Bustamonte B. Comparison of terbinafine and griseofulvin in the treatment of tinea capitis. J Am Acad Dermatol 2000;42:80-84.
14. Haroon TS, Hussain I, Aman S, et al. A randomized double blind comparative study of terbinafine for 1, 2 and 4 weeks in tinea capitis. Br J Dermatol 1996;135:86-88.
15. Dragos V, Lunder M. Lack of efficacy of 6-week treatment with oral terbinafine for tinea capitis due to Microsporum canis in children. Pediatr Dermatol 1997;14:46-48.
1. Seidel HM, Barnett NK. Alopecia and hair shaft abnormalities. In: Hoekelman RA, Friedman SB, Nelson N, eds. Primary pediatric care. 3rd ed. St. Louis, Mo: Mosby; 1997:860.
2. Darmstadt GL. Cutaneous fungal infections. In: Behrman RE, ed. Nelson textbook of pediatrics. 16th ed. Philadelphia, Pa: W.B. Saunders Company; 2000:2038.
3. American Academy of Pediatrics Tinea capitis. In: 2000 Redbook: Report of the Committee on Infectious Diseases. 25th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1997;569-70.
4. Hay RJ. Dermatophytosis and other superficial mycoses. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s: Principles and practice of infectious diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:2762.
5. Higgins EM, Fuller LC, Smith CH. Guidelines for the management of tinea capitis. Br J Dermatol 2000;143:53-58.
6. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of the care for superficial mycotic infections of the skin: tinea capitis and tinea barbae. J Am Acad Derm 1996;34:290-94.
7. Bennett ML, Fleishcher AB, Loveless JW, Feldman SR. Oral griseolfulvin remains the treatment of choice for tinea capitis in children. Pediatr Dermatol 2000;17:304-09.
8. Friedlander SF. The optimal therapy for tinea capitis. Pediatr Dermatol 2000;17:325-26.
9. Degreef H. Itraconazole in the treatment of tinea capitis. Cutis 1996;58:90-93.
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Evidence-based answers from the Family Physicians Inquiries Network