The Journal of Family Practice

Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.

The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.

Take your pick of candidates, but don't expect a difference in your practice "hassle factor"—or paycheck.

Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.¹ These programs have bipartisan support and are not going away.

In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.

What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign² (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.

In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.

Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.

The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.

Take your pick of candidates, but don't expect a difference in your practice "hassle factor"—or paycheck.

Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.¹ These programs have bipartisan support and are not going away.

In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.

What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign² (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.

In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.

Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.

The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.

Take your pick of candidates, but don't expect a difference in your practice "hassle factor"—or paycheck.

Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.¹ These programs have bipartisan support and are not going away.

In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.

What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign² (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.

In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.

The FP noted patchy alopecia with scaling of the scalp and made the presumptive diagnosis of tinea capitis. A woods lamp examination did not demonstrate fluorescence. The child was very cooperative and the doctor was able to perform a potassium hydroxide (KOH) preparation by scraping the areas of alopecia with the edge of one glass slide while catching the scale on another slide. Microscopic examination revealed branching hyphae and some broken hairs with fungal elements within the hair shaft. (See video on how to perform a KOH preparation.) This microscopic picture was consistent with Trichophyton tonsurans, the most common cause of tinea capitis in the United States. The reason that the infected area did not fluoresce was that the dermatophyte was within the hair shaft (endothrix) rather than external to the hair (exothrix).

Topical antifungal therapy is not adequate for tinea capitis; oral treatment is needed. Oral antifungal choices include griseofulvin, terbinafine, and fluconazole. Griseofulvin comes in an oral suspension making it a desirable option for children who can’t swallow pills. However, at least 6 to 8 weeks of treatment (20 mg/kg/d) is required. Oral terbinafine tablets are less expensive and shorter courses of therapy may be used. Tablets of 250 mg terbinafine (most affordable of all the choices) can be broken in half for younger children and the dose should always be calculated based on weight. Fluconazole comes in various tablets, strengths, and liquid formulations and can be prescribed for 3 to 6 weeks, as needed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Yao C. Tinea capitis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill;2013:782-787.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP noted patchy alopecia with scaling of the scalp and made the presumptive diagnosis of tinea capitis. A woods lamp examination did not demonstrate fluorescence. The child was very cooperative and the doctor was able to perform a potassium hydroxide (KOH) preparation by scraping the areas of alopecia with the edge of one glass slide while catching the scale on another slide. Microscopic examination revealed branching hyphae and some broken hairs with fungal elements within the hair shaft. (See video on how to perform a KOH preparation.) This microscopic picture was consistent with Trichophyton tonsurans, the most common cause of tinea capitis in the United States. The reason that the infected area did not fluoresce was that the dermatophyte was within the hair shaft (endothrix) rather than external to the hair (exothrix).

Topical antifungal therapy is not adequate for tinea capitis; oral treatment is needed. Oral antifungal choices include griseofulvin, terbinafine, and fluconazole. Griseofulvin comes in an oral suspension making it a desirable option for children who can’t swallow pills. However, at least 6 to 8 weeks of treatment (20 mg/kg/d) is required. Oral terbinafine tablets are less expensive and shorter courses of therapy may be used. Tablets of 250 mg terbinafine (most affordable of all the choices) can be broken in half for younger children and the dose should always be calculated based on weight. Fluconazole comes in various tablets, strengths, and liquid formulations and can be prescribed for 3 to 6 weeks, as needed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Yao C. Tinea capitis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill;2013:782-787.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP noted patchy alopecia with scaling of the scalp and made the presumptive diagnosis of tinea capitis. A woods lamp examination did not demonstrate fluorescence. The child was very cooperative and the doctor was able to perform a potassium hydroxide (KOH) preparation by scraping the areas of alopecia with the edge of one glass slide while catching the scale on another slide. Microscopic examination revealed branching hyphae and some broken hairs with fungal elements within the hair shaft. (See video on how to perform a KOH preparation.) This microscopic picture was consistent with Trichophyton tonsurans, the most common cause of tinea capitis in the United States. The reason that the infected area did not fluoresce was that the dermatophyte was within the hair shaft (endothrix) rather than external to the hair (exothrix).

Topical antifungal therapy is not adequate for tinea capitis; oral treatment is needed. Oral antifungal choices include griseofulvin, terbinafine, and fluconazole. Griseofulvin comes in an oral suspension making it a desirable option for children who can’t swallow pills. However, at least 6 to 8 weeks of treatment (20 mg/kg/d) is required. Oral terbinafine tablets are less expensive and shorter courses of therapy may be used. Tablets of 250 mg terbinafine (most affordable of all the choices) can be broken in half for younger children and the dose should always be calculated based on weight. Fluconazole comes in various tablets, strengths, and liquid formulations and can be prescribed for 3 to 6 weeks, as needed.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Yao C. Tinea capitis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill;2013:782-787.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

CASE › Mary, a 34-year-old woman, is a new patient to your practice after moving to the area for a job. She has a history of migraine headaches triggered by her menstrual periods. She has been taking combined oral contraceptives (COCs) since she was 17, with a few years off when she had 2 children. Her migraines improved when she was pregnant, but worsened postpartum with each of her daughters to a point where she had to stop breastfeeding at 4 months to go back on the pills.

On the COCs, she gets one or 2 mild-to-moderate headaches a month. She uses sumatriptan for abortive treatment with good relief. She has not missed work in the past 4 years because of her migraines. During the 6 months she was off COCs when trying to get pregnant, she routinely missed 2 to 3 workdays per month due to migraines. She knows when she is going to get a headache because she sees flashing lights in her left visual field. She has no other neurologic symptoms with the headaches, and the character of the headaches has not changed. She is a non-smoker, has normal blood pressure and lipid levels, and no other vascular risk factors.

You review her history and talk to her about the risk of stroke with migraines and with COCs. She is almost 35 years of age and you recommend stopping the COCs due to the risk. She feels strongly that she wants to continue taking the COCs, saying her quality of life is poor when she is off the pills. What should you do?

Migraine headaches are 2 to 3 times more prevalent in women than in men,¹ with a lifetime risk of 43% vs 18%, respectively.² Women account for about 80% of the $1 billion spent each year in the United States in medical expenses and lost work productivity related to migraines.^1,2

Clinical patterns suggestive of menstrual migraine. About half of women affected by migraine have menstrually-related migraines (MRM); 3% to 12% have pure menstrual migraines (PMM).³ MRM and PMM are both characterized by the presence of symptoms in at least 2 to 3 consecutive cycles, with symptoms occurring from between 2 days before to 3 days after the onset of menstruation. However, in PMM, symptoms do not occur at any other time of the menstrual cycle; in MRM, symptoms can occur at other times of the cycle. PMM is more likely to respond to hormone therapy than is MRM.

Multiple studies in the United States, Europe, and Asia have noted that migraines related to menses typically last longer, are more severe, less likely to be associated with aura, and more likely to be recurrent and recalcitrant to treatment than non-menstrual migraines.¹ TABLE 1³ describes diagnostic criteria for migraine without aura.

Prevalence patterns point to the role of estrogen. The prevalence of migraines in women increases around puberty, peaks between ages 30 and 40, and decreases after natural menopause.⁶ Migraine prevalence increases during the first week postpartum, when levels of estrogen and progesterone decrease suddenly and significantly.¹ Migraine frequency and intensity decrease in the second and third trimesters of pregnancy and after menopause, when estrogen levels fluctuate significantly less.¹ In the Women’s Health Initiative study, women who used hormone replacement therapy (HRT) had a 42% increased risk of migraines compared with women in the study who had never used HRT.⁸

Migraines related to menses typically last longer, are more severe, less likely to be associated with aura, and more likely to be recalcitrant to treatment than non-menstrual migraines.The association of migraine with female hormones was further supported by a Dutch study of male-to-female transgender patients on estrogen therapy, who had a 26% incidence of migraine, equivalent to the 25% prevalence in natal female controls in this study, compared with just 7.5% in male controls.⁹ The association between migraine and estrogen withdrawal was investigated in studies performed more than 40 years ago, when women experiencing migraines around the time of menses were given intramuscular estradiol and experienced a delay in symptom onset.¹⁰

Abortive and prophylactic treatments: Factors that guide selection

In considering probable menstrual migraine, take a detailed history, review headache diaries if available to determine association of headaches with menses, and perform a thorough neurologic examination. If a diagnosis of menstrual migraine is established, discuss the benefits of different treatment options, both abortive and prophylactic.

For the patient with MRM, take into account frequency of symptoms, predictability of menstruation, medication costs, and comorbidities. Both triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) can be effective treatments for MRM.¹¹ Abortive therapy may be appropriate if a patient prefers to take medication intermittently, if her menses are unpredictable, or if she does not get migraine headaches with every menses. Mefenamic acid, sumatriptan, and rizatriptan have category B recommendations for abortive treatment for menstrual migraines (TABLE 2^11-16). (For the patient who has regular MRM but unpredictable menses, ovulation predictor kits can be used to help predict the onset of menses, although this would involve additional cost.)

Triptans are contraindicated for women with a history of cardiac disease or uncontrolled hypertension. For the patient who has predictable menses and regularly occurring menstrual migraine, some data show that a short-term prophylactic regimen with triptans started 2 to 3 days before the onset of menses and continued for 5 to 7 days total can reduce the incidence of menstrual migraine (TABLE 2^11-16). At least one high-quality randomized controlled trial (RCT) showed a significant reduction in the incidence of MRM when women were treated prophylactically with frovatriptan, a long-acting triptan with a half-life of approximately 26 hours. Participants received frovatriptan 2.5 mg once a day or twice a day or placebo in the perimenstrual period (day -2 to +3). The incidence of MRM was 52%, 41%, and 67%, respectively (P<.0001).^11,17

Another RCT of fair quality examined the effect of naratriptan (half-life 6-8 hours) on the median number of menstrual migraines over 4 menstrual cycles. Women who received 1 mg of naratriptan BID for 2 to 3 days before menses had 2 MRM episodes over the 4 cycles compared with 4 MRM episodes in women who received placebo over the same time period (P<.05).^11,18 A third RCT, also of fair quality, compared 2 different regimens of zolmitriptan (half-life 3 hours) with placebo and found that women who received 2.5 mg of zolmitriptan either BID or TID 2 to 3 days prior to menses had a reduction both in frequency of menstrual migraines and in the mean number of breakthrough headaches per menstrual cycle, as well as a reduction in the need for rescue medications.^12,19 Triptans are contraindicated in women with a history of cardiac disease or uncontrolled hypertension. Also, triptans can be expensive, precluding their use for some patients.

Evidence is insufficient to recommend for or against the use of NSAIDs as prophylaxis for MRM.¹¹ NSAIDs may be contraindicated in women with a history of peptic ulcer disease or gastrointestinal bleeding. That said, if NSAIDs are not contraindicated, a trial may be reasonable given their low cost.

Data are sparse on the use of vitamins and supplements in treating and preventing PMM or MRM. In one very small double-blind, placebo-controlled study in 1991 (N=24, with efficacy data for 20), participants received a 2-week course of oral magnesium premenstrually. There was a statistically significant reduction in the number of days with headache per month (from 4.7±3.1 days to 2.4±2.2 days; P<.01) and in the total pain index (P<.03).²⁰ A number of studies have demonstrated a correlation between hypomagnesemia and migraine headaches.^5,21 The exact mechanism for this relationship is unclear.

Some recent evidence-based reviews have examined the efficacy of nutraceuticals such as magnesium, feverfew, butterbur, coenzyme Q10, and riboflavin on typical migraine, but it is not clear if these results are translatable to the treatment and prophylaxis of menstrual migraine.^11,22 A multicenter, single-blind, RCT is underway to examine the efficacy of acupuncture as prophylaxis for MRM.²³

The association between MRM and hormonal variation makes exogenous hormone therapy a tempting prophylactic treatment. A study by Somerville showed that using exogenous estrogen to mitigate the decrease in estrogen through the menstrual cycle can raise the headache threshold and thereby decrease the frequency and severity of MRM.¹⁰ Progesterone levels also vary throughout the menstrual cycle; however, this variation has not been shown to correlate with MRM. Some investigators have speculated that continuous exogenous progesterone may decrease the frequency of MRM through the blunting of estrogen cycles.^5,10,24

Most studies examining the role of exogenous estrogen in reducing menstrual migraines have used topical estrogen (either in patch or gel formulations) in the perimenstrual window (TABLE 2^11-16). The topical estrogen route has been examined, in particular, as it is presumed to confer less risk of hypercoagulability by avoiding first-pass metabolism. However, there is conflicting evidence on this issue, in particular regarding premenopausal women.^13,25 Additionally, many of the studies of estrogen supplementation show a trend toward increased headache once estrogen is discontinued, presumably due to estrogen withdrawal.^10,24

That said, one study by MacGregor, et al demonstrates that the use of estradiol gel in the perimenstrual window leads to a 22% reduction in migraine days as well as less severe migrainous symptoms.²⁶ This trend has been demonstrated in other studies examining estrogen supplementation. Of note, the estrogen studies generally are small, older, and of fair to poor quality.¹¹ These studies have used higher doses of estrogen than are commonly used for contraception today because lower doses of estrogen seem not to have the same impact on migraine.^5,24

As for COCs, with either normal or extended cycling, data are more mixed than for estrogen supplementation alone; equivalent numbers of women experience improvement, no change, or worsening of their headache pattern. Many women have continuing or worsening migraines in the hormone-free week, and thus most studies have examined the use of extended cycling COCs.⁵ Sulak, et al demonstrated a statistically significant reduction in headache frequency using extended-cycling COCs, though they did not examine MRM in particular.²⁷ The efficacy of extended-cycling COCs for reduction of MRM was confirmed by Coffee and colleagues with a small but statistically significant decrease in daily headache scores.²⁸

Evidence is insufficient to recommend for or against the use of NSAIDs as prophylaxis for menstrually-related migraines.

Adverse effects. All estrogen therapies pose the risk of adverse effects (deep vein thrombosis, hypertension, breast tenderness, nausea, etc). Additionally, estrogen supplementation may actually trigger migraines in some women if, when it is discontinued, the blood estrogen level does not remain above a threshold concentration.^5,10,24 Estrogen may also trigger migraine in previously headache-free women and may convert migraine without aura into migraine with aura. In either case, therapy should be stopped.^5,24

There is promising evidence from 2 small RCTs and one observational trial that progestin-only contraceptive pills (POP) may reduce the frequency and severity of menstrual migraines (TABLE 2^11-16). More prospective data are needed to confirm this reduction, as there have not been specific studies examining other progesterone-only preparations to prevent menstrual migraines.

Risk of ischemic stroke. Unfortunately, there are population data showing that second-generation and, to a smaller degree, third-generation progestins, which include the desogestrel used in the above studies, may increase the risk of ischemic stroke. This is a particular concern in women who experience migraine.²⁹ Second-generation progestins include levonorgestrel, which is in the levonorgestrel IUD; however, there is no direct evidence for increased ischemic stroke in this particular preparation, and the circulating plasma levels are low. Etonorgestrel, the active ingredient in the contraceptive implant, is a third-generation progestin, though there is no direct evidence of increased ischemic stroke with use of the etonorgestrel implant.

There is a 2- to 4-fold increased risk of ischemic stroke in women who experience migraine.^1,5,30 As stated above, this risk may be further increased by some progesterone formulations. But there is also a demonstrable increase in ischemic stroke risk with the use of estrogen, particularly at the higher concentrations that have been shown to prevent MRM.^31,32 The overall incidence of ischemic stroke in menstrual-age women is low, which has limited the number of studies with enough power to quantify the absolute increased risk of stroke in conjunction with estrogen use. Nevertheless, exogenous estrogen is thought to increase the risk of ischemic stroke an additional 2- to 4-fold.^{1,5,29,30,32-34}

A number of studies have demonstrated a correlation between hypomagnesemia and migraine headaches. The exact mechanism for this relationship is unclear.Women who experience aura. MRM, as it is defined, typically excludes women who experience aura; however, the number of women who experience aura with migraine either in proximity to their menses or throughout the month has not been well documented. The risk of ischemic stroke is higher for women who experience migraine with aura than those with migraine alone, possibly because aura is associated with reduced regional vascular flow leading to hypoperfusion, which sets the stage for a possible ischemic event.^4,5,35 The risk of ischemic stroke is amplified further for women who are over 35, who smoke, or who have additional vascular risk factors (eg, uncontrolled hypertension, diabetes, or known vascular or cardiac disease).^1,5,34 This array of evidence serves as the basis for the US Medical Eligibility Criteria (USMEC) recommendations³⁶ for hormonal contraceptive use, in particular the absolute contraindication for estrogen use in women who experience migraine with aura (TABLE 3^36-38).

CASE ›  Given Mary’s experience of aura with migraine, you talk with her at length about the risk of ischemic stroke and the USMEC recommendation that she absolutely should not be taking COCs. You suggest a progestin-only method of contraception such as depot medroxyprogesterone acetate, a progestin intrauterine device, or a hormonal implant, which may suppress ovulation and decrease her headaches. You discuss that while some women may have headaches with these progestin-only methods, stroke risk is significantly reduced. You also suggest a trial of prophylactic triptans as another possible option.

She says she understands the increased risk of stroke but is still unwilling to try anything else right now due to worries about her quality of life. You decide jointly to refill COCs for 3 months, and you document the shared decision process in the chart. After advising the patient that you will not continue to prescribe COCs for an extended period of time, you also schedule a follow-up appointment to further discuss risks and benefits of migraine treatment and means of reducing other risk factors for stroke.

CORRESPONDENCE
Sarina Schrager, MD, MS, University of Wisconsin, Department of Family Medicine, 1100 Delaplaine Ct, Madison, WI 53715; [email protected].

CASE › Mary, a 34-year-old woman, is a new patient to your practice after moving to the area for a job. She has a history of migraine headaches triggered by her menstrual periods. She has been taking combined oral contraceptives (COCs) since she was 17, with a few years off when she had 2 children. Her migraines improved when she was pregnant, but worsened postpartum with each of her daughters to a point where she had to stop breastfeeding at 4 months to go back on the pills.

On the COCs, she gets one or 2 mild-to-moderate headaches a month. She uses sumatriptan for abortive treatment with good relief. She has not missed work in the past 4 years because of her migraines. During the 6 months she was off COCs when trying to get pregnant, she routinely missed 2 to 3 workdays per month due to migraines. She knows when she is going to get a headache because she sees flashing lights in her left visual field. She has no other neurologic symptoms with the headaches, and the character of the headaches has not changed. She is a non-smoker, has normal blood pressure and lipid levels, and no other vascular risk factors.

You review her history and talk to her about the risk of stroke with migraines and with COCs. She is almost 35 years of age and you recommend stopping the COCs due to the risk. She feels strongly that she wants to continue taking the COCs, saying her quality of life is poor when she is off the pills. What should you do?

Migraine headaches are 2 to 3 times more prevalent in women than in men,¹ with a lifetime risk of 43% vs 18%, respectively.² Women account for about 80% of the $1 billion spent each year in the United States in medical expenses and lost work productivity related to migraines.^1,2

Clinical patterns suggestive of menstrual migraine. About half of women affected by migraine have menstrually-related migraines (MRM); 3% to 12% have pure menstrual migraines (PMM).³ MRM and PMM are both characterized by the presence of symptoms in at least 2 to 3 consecutive cycles, with symptoms occurring from between 2 days before to 3 days after the onset of menstruation. However, in PMM, symptoms do not occur at any other time of the menstrual cycle; in MRM, symptoms can occur at other times of the cycle. PMM is more likely to respond to hormone therapy than is MRM.

Multiple studies in the United States, Europe, and Asia have noted that migraines related to menses typically last longer, are more severe, less likely to be associated with aura, and more likely to be recurrent and recalcitrant to treatment than non-menstrual migraines.¹ TABLE 1³ describes diagnostic criteria for migraine without aura.

Prevalence patterns point to the role of estrogen. The prevalence of migraines in women increases around puberty, peaks between ages 30 and 40, and decreases after natural menopause.⁶ Migraine prevalence increases during the first week postpartum, when levels of estrogen and progesterone decrease suddenly and significantly.¹ Migraine frequency and intensity decrease in the second and third trimesters of pregnancy and after menopause, when estrogen levels fluctuate significantly less.¹ In the Women’s Health Initiative study, women who used hormone replacement therapy (HRT) had a 42% increased risk of migraines compared with women in the study who had never used HRT.⁸

Migraines related to menses typically last longer, are more severe, less likely to be associated with aura, and more likely to be recalcitrant to treatment than non-menstrual migraines.The association of migraine with female hormones was further supported by a Dutch study of male-to-female transgender patients on estrogen therapy, who had a 26% incidence of migraine, equivalent to the 25% prevalence in natal female controls in this study, compared with just 7.5% in male controls.⁹ The association between migraine and estrogen withdrawal was investigated in studies performed more than 40 years ago, when women experiencing migraines around the time of menses were given intramuscular estradiol and experienced a delay in symptom onset.¹⁰

Abortive and prophylactic treatments: Factors that guide selection

In considering probable menstrual migraine, take a detailed history, review headache diaries if available to determine association of headaches with menses, and perform a thorough neurologic examination. If a diagnosis of menstrual migraine is established, discuss the benefits of different treatment options, both abortive and prophylactic.

For the patient with MRM, take into account frequency of symptoms, predictability of menstruation, medication costs, and comorbidities. Both triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) can be effective treatments for MRM.¹¹ Abortive therapy may be appropriate if a patient prefers to take medication intermittently, if her menses are unpredictable, or if she does not get migraine headaches with every menses. Mefenamic acid, sumatriptan, and rizatriptan have category B recommendations for abortive treatment for menstrual migraines (TABLE 2^11-16). (For the patient who has regular MRM but unpredictable menses, ovulation predictor kits can be used to help predict the onset of menses, although this would involve additional cost.)

Triptans are contraindicated for women with a history of cardiac disease or uncontrolled hypertension. For the patient who has predictable menses and regularly occurring menstrual migraine, some data show that a short-term prophylactic regimen with triptans started 2 to 3 days before the onset of menses and continued for 5 to 7 days total can reduce the incidence of menstrual migraine (TABLE 2^11-16). At least one high-quality randomized controlled trial (RCT) showed a significant reduction in the incidence of MRM when women were treated prophylactically with frovatriptan, a long-acting triptan with a half-life of approximately 26 hours. Participants received frovatriptan 2.5 mg once a day or twice a day or placebo in the perimenstrual period (day -2 to +3). The incidence of MRM was 52%, 41%, and 67%, respectively (P<.0001).^11,17

Another RCT of fair quality examined the effect of naratriptan (half-life 6-8 hours) on the median number of menstrual migraines over 4 menstrual cycles. Women who received 1 mg of naratriptan BID for 2 to 3 days before menses had 2 MRM episodes over the 4 cycles compared with 4 MRM episodes in women who received placebo over the same time period (P<.05).^11,18 A third RCT, also of fair quality, compared 2 different regimens of zolmitriptan (half-life 3 hours) with placebo and found that women who received 2.5 mg of zolmitriptan either BID or TID 2 to 3 days prior to menses had a reduction both in frequency of menstrual migraines and in the mean number of breakthrough headaches per menstrual cycle, as well as a reduction in the need for rescue medications.^12,19 Triptans are contraindicated in women with a history of cardiac disease or uncontrolled hypertension. Also, triptans can be expensive, precluding their use for some patients.

Evidence is insufficient to recommend for or against the use of NSAIDs as prophylaxis for MRM.¹¹ NSAIDs may be contraindicated in women with a history of peptic ulcer disease or gastrointestinal bleeding. That said, if NSAIDs are not contraindicated, a trial may be reasonable given their low cost.

Data are sparse on the use of vitamins and supplements in treating and preventing PMM or MRM. In one very small double-blind, placebo-controlled study in 1991 (N=24, with efficacy data for 20), participants received a 2-week course of oral magnesium premenstrually. There was a statistically significant reduction in the number of days with headache per month (from 4.7±3.1 days to 2.4±2.2 days; P<.01) and in the total pain index (P<.03).²⁰ A number of studies have demonstrated a correlation between hypomagnesemia and migraine headaches.^5,21 The exact mechanism for this relationship is unclear.

Some recent evidence-based reviews have examined the efficacy of nutraceuticals such as magnesium, feverfew, butterbur, coenzyme Q10, and riboflavin on typical migraine, but it is not clear if these results are translatable to the treatment and prophylaxis of menstrual migraine.^11,22 A multicenter, single-blind, RCT is underway to examine the efficacy of acupuncture as prophylaxis for MRM.²³

The association between MRM and hormonal variation makes exogenous hormone therapy a tempting prophylactic treatment. A study by Somerville showed that using exogenous estrogen to mitigate the decrease in estrogen through the menstrual cycle can raise the headache threshold and thereby decrease the frequency and severity of MRM.¹⁰ Progesterone levels also vary throughout the menstrual cycle; however, this variation has not been shown to correlate with MRM. Some investigators have speculated that continuous exogenous progesterone may decrease the frequency of MRM through the blunting of estrogen cycles.^5,10,24

Most studies examining the role of exogenous estrogen in reducing menstrual migraines have used topical estrogen (either in patch or gel formulations) in the perimenstrual window (TABLE 2^11-16). The topical estrogen route has been examined, in particular, as it is presumed to confer less risk of hypercoagulability by avoiding first-pass metabolism. However, there is conflicting evidence on this issue, in particular regarding premenopausal women.^13,25 Additionally, many of the studies of estrogen supplementation show a trend toward increased headache once estrogen is discontinued, presumably due to estrogen withdrawal.^10,24

That said, one study by MacGregor, et al demonstrates that the use of estradiol gel in the perimenstrual window leads to a 22% reduction in migraine days as well as less severe migrainous symptoms.²⁶ This trend has been demonstrated in other studies examining estrogen supplementation. Of note, the estrogen studies generally are small, older, and of fair to poor quality.¹¹ These studies have used higher doses of estrogen than are commonly used for contraception today because lower doses of estrogen seem not to have the same impact on migraine.^5,24

As for COCs, with either normal or extended cycling, data are more mixed than for estrogen supplementation alone; equivalent numbers of women experience improvement, no change, or worsening of their headache pattern. Many women have continuing or worsening migraines in the hormone-free week, and thus most studies have examined the use of extended cycling COCs.⁵ Sulak, et al demonstrated a statistically significant reduction in headache frequency using extended-cycling COCs, though they did not examine MRM in particular.²⁷ The efficacy of extended-cycling COCs for reduction of MRM was confirmed by Coffee and colleagues with a small but statistically significant decrease in daily headache scores.²⁸

Evidence is insufficient to recommend for or against the use of NSAIDs as prophylaxis for menstrually-related migraines.

Adverse effects. All estrogen therapies pose the risk of adverse effects (deep vein thrombosis, hypertension, breast tenderness, nausea, etc). Additionally, estrogen supplementation may actually trigger migraines in some women if, when it is discontinued, the blood estrogen level does not remain above a threshold concentration.^5,10,24 Estrogen may also trigger migraine in previously headache-free women and may convert migraine without aura into migraine with aura. In either case, therapy should be stopped.^5,24

There is promising evidence from 2 small RCTs and one observational trial that progestin-only contraceptive pills (POP) may reduce the frequency and severity of menstrual migraines (TABLE 2^11-16). More prospective data are needed to confirm this reduction, as there have not been specific studies examining other progesterone-only preparations to prevent menstrual migraines.

Risk of ischemic stroke. Unfortunately, there are population data showing that second-generation and, to a smaller degree, third-generation progestins, which include the desogestrel used in the above studies, may increase the risk of ischemic stroke. This is a particular concern in women who experience migraine.²⁹ Second-generation progestins include levonorgestrel, which is in the levonorgestrel IUD; however, there is no direct evidence for increased ischemic stroke in this particular preparation, and the circulating plasma levels are low. Etonorgestrel, the active ingredient in the contraceptive implant, is a third-generation progestin, though there is no direct evidence of increased ischemic stroke with use of the etonorgestrel implant.

There is a 2- to 4-fold increased risk of ischemic stroke in women who experience migraine.^1,5,30 As stated above, this risk may be further increased by some progesterone formulations. But there is also a demonstrable increase in ischemic stroke risk with the use of estrogen, particularly at the higher concentrations that have been shown to prevent MRM.^31,32 The overall incidence of ischemic stroke in menstrual-age women is low, which has limited the number of studies with enough power to quantify the absolute increased risk of stroke in conjunction with estrogen use. Nevertheless, exogenous estrogen is thought to increase the risk of ischemic stroke an additional 2- to 4-fold.^{1,5,29,30,32-34}

A number of studies have demonstrated a correlation between hypomagnesemia and migraine headaches. The exact mechanism for this relationship is unclear.Women who experience aura. MRM, as it is defined, typically excludes women who experience aura; however, the number of women who experience aura with migraine either in proximity to their menses or throughout the month has not been well documented. The risk of ischemic stroke is higher for women who experience migraine with aura than those with migraine alone, possibly because aura is associated with reduced regional vascular flow leading to hypoperfusion, which sets the stage for a possible ischemic event.^4,5,35 The risk of ischemic stroke is amplified further for women who are over 35, who smoke, or who have additional vascular risk factors (eg, uncontrolled hypertension, diabetes, or known vascular or cardiac disease).^1,5,34 This array of evidence serves as the basis for the US Medical Eligibility Criteria (USMEC) recommendations³⁶ for hormonal contraceptive use, in particular the absolute contraindication for estrogen use in women who experience migraine with aura (TABLE 3^36-38).

CASE ›  Given Mary’s experience of aura with migraine, you talk with her at length about the risk of ischemic stroke and the USMEC recommendation that she absolutely should not be taking COCs. You suggest a progestin-only method of contraception such as depot medroxyprogesterone acetate, a progestin intrauterine device, or a hormonal implant, which may suppress ovulation and decrease her headaches. You discuss that while some women may have headaches with these progestin-only methods, stroke risk is significantly reduced. You also suggest a trial of prophylactic triptans as another possible option.

She says she understands the increased risk of stroke but is still unwilling to try anything else right now due to worries about her quality of life. You decide jointly to refill COCs for 3 months, and you document the shared decision process in the chart. After advising the patient that you will not continue to prescribe COCs for an extended period of time, you also schedule a follow-up appointment to further discuss risks and benefits of migraine treatment and means of reducing other risk factors for stroke.

CORRESPONDENCE
Sarina Schrager, MD, MS, University of Wisconsin, Department of Family Medicine, 1100 Delaplaine Ct, Madison, WI 53715; [email protected].

CASE › Mary, a 34-year-old woman, is a new patient to your practice after moving to the area for a job. She has a history of migraine headaches triggered by her menstrual periods. She has been taking combined oral contraceptives (COCs) since she was 17, with a few years off when she had 2 children. Her migraines improved when she was pregnant, but worsened postpartum with each of her daughters to a point where she had to stop breastfeeding at 4 months to go back on the pills.

On the COCs, she gets one or 2 mild-to-moderate headaches a month. She uses sumatriptan for abortive treatment with good relief. She has not missed work in the past 4 years because of her migraines. During the 6 months she was off COCs when trying to get pregnant, she routinely missed 2 to 3 workdays per month due to migraines. She knows when she is going to get a headache because she sees flashing lights in her left visual field. She has no other neurologic symptoms with the headaches, and the character of the headaches has not changed. She is a non-smoker, has normal blood pressure and lipid levels, and no other vascular risk factors.

You review her history and talk to her about the risk of stroke with migraines and with COCs. She is almost 35 years of age and you recommend stopping the COCs due to the risk. She feels strongly that she wants to continue taking the COCs, saying her quality of life is poor when she is off the pills. What should you do?

Migraine headaches are 2 to 3 times more prevalent in women than in men,¹ with a lifetime risk of 43% vs 18%, respectively.² Women account for about 80% of the $1 billion spent each year in the United States in medical expenses and lost work productivity related to migraines.^1,2

Clinical patterns suggestive of menstrual migraine. About half of women affected by migraine have menstrually-related migraines (MRM); 3% to 12% have pure menstrual migraines (PMM).³ MRM and PMM are both characterized by the presence of symptoms in at least 2 to 3 consecutive cycles, with symptoms occurring from between 2 days before to 3 days after the onset of menstruation. However, in PMM, symptoms do not occur at any other time of the menstrual cycle; in MRM, symptoms can occur at other times of the cycle. PMM is more likely to respond to hormone therapy than is MRM.

Multiple studies in the United States, Europe, and Asia have noted that migraines related to menses typically last longer, are more severe, less likely to be associated with aura, and more likely to be recurrent and recalcitrant to treatment than non-menstrual migraines.¹ TABLE 1³ describes diagnostic criteria for migraine without aura.

Prevalence patterns point to the role of estrogen. The prevalence of migraines in women increases around puberty, peaks between ages 30 and 40, and decreases after natural menopause.⁶ Migraine prevalence increases during the first week postpartum, when levels of estrogen and progesterone decrease suddenly and significantly.¹ Migraine frequency and intensity decrease in the second and third trimesters of pregnancy and after menopause, when estrogen levels fluctuate significantly less.¹ In the Women’s Health Initiative study, women who used hormone replacement therapy (HRT) had a 42% increased risk of migraines compared with women in the study who had never used HRT.⁸

Migraines related to menses typically last longer, are more severe, less likely to be associated with aura, and more likely to be recalcitrant to treatment than non-menstrual migraines.The association of migraine with female hormones was further supported by a Dutch study of male-to-female transgender patients on estrogen therapy, who had a 26% incidence of migraine, equivalent to the 25% prevalence in natal female controls in this study, compared with just 7.5% in male controls.⁹ The association between migraine and estrogen withdrawal was investigated in studies performed more than 40 years ago, when women experiencing migraines around the time of menses were given intramuscular estradiol and experienced a delay in symptom onset.¹⁰

Abortive and prophylactic treatments: Factors that guide selection

In considering probable menstrual migraine, take a detailed history, review headache diaries if available to determine association of headaches with menses, and perform a thorough neurologic examination. If a diagnosis of menstrual migraine is established, discuss the benefits of different treatment options, both abortive and prophylactic.

For the patient with MRM, take into account frequency of symptoms, predictability of menstruation, medication costs, and comorbidities. Both triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) can be effective treatments for MRM.¹¹ Abortive therapy may be appropriate if a patient prefers to take medication intermittently, if her menses are unpredictable, or if she does not get migraine headaches with every menses. Mefenamic acid, sumatriptan, and rizatriptan have category B recommendations for abortive treatment for menstrual migraines (TABLE 2^11-16). (For the patient who has regular MRM but unpredictable menses, ovulation predictor kits can be used to help predict the onset of menses, although this would involve additional cost.)

Triptans are contraindicated for women with a history of cardiac disease or uncontrolled hypertension. For the patient who has predictable menses and regularly occurring menstrual migraine, some data show that a short-term prophylactic regimen with triptans started 2 to 3 days before the onset of menses and continued for 5 to 7 days total can reduce the incidence of menstrual migraine (TABLE 2^11-16). At least one high-quality randomized controlled trial (RCT) showed a significant reduction in the incidence of MRM when women were treated prophylactically with frovatriptan, a long-acting triptan with a half-life of approximately 26 hours. Participants received frovatriptan 2.5 mg once a day or twice a day or placebo in the perimenstrual period (day -2 to +3). The incidence of MRM was 52%, 41%, and 67%, respectively (P<.0001).^11,17

Another RCT of fair quality examined the effect of naratriptan (half-life 6-8 hours) on the median number of menstrual migraines over 4 menstrual cycles. Women who received 1 mg of naratriptan BID for 2 to 3 days before menses had 2 MRM episodes over the 4 cycles compared with 4 MRM episodes in women who received placebo over the same time period (P<.05).^11,18 A third RCT, also of fair quality, compared 2 different regimens of zolmitriptan (half-life 3 hours) with placebo and found that women who received 2.5 mg of zolmitriptan either BID or TID 2 to 3 days prior to menses had a reduction both in frequency of menstrual migraines and in the mean number of breakthrough headaches per menstrual cycle, as well as a reduction in the need for rescue medications.^12,19 Triptans are contraindicated in women with a history of cardiac disease or uncontrolled hypertension. Also, triptans can be expensive, precluding their use for some patients.

Evidence is insufficient to recommend for or against the use of NSAIDs as prophylaxis for MRM.¹¹ NSAIDs may be contraindicated in women with a history of peptic ulcer disease or gastrointestinal bleeding. That said, if NSAIDs are not contraindicated, a trial may be reasonable given their low cost.

Data are sparse on the use of vitamins and supplements in treating and preventing PMM or MRM. In one very small double-blind, placebo-controlled study in 1991 (N=24, with efficacy data for 20), participants received a 2-week course of oral magnesium premenstrually. There was a statistically significant reduction in the number of days with headache per month (from 4.7±3.1 days to 2.4±2.2 days; P<.01) and in the total pain index (P<.03).²⁰ A number of studies have demonstrated a correlation between hypomagnesemia and migraine headaches.^5,21 The exact mechanism for this relationship is unclear.

Some recent evidence-based reviews have examined the efficacy of nutraceuticals such as magnesium, feverfew, butterbur, coenzyme Q10, and riboflavin on typical migraine, but it is not clear if these results are translatable to the treatment and prophylaxis of menstrual migraine.^11,22 A multicenter, single-blind, RCT is underway to examine the efficacy of acupuncture as prophylaxis for MRM.²³

The association between MRM and hormonal variation makes exogenous hormone therapy a tempting prophylactic treatment. A study by Somerville showed that using exogenous estrogen to mitigate the decrease in estrogen through the menstrual cycle can raise the headache threshold and thereby decrease the frequency and severity of MRM.¹⁰ Progesterone levels also vary throughout the menstrual cycle; however, this variation has not been shown to correlate with MRM. Some investigators have speculated that continuous exogenous progesterone may decrease the frequency of MRM through the blunting of estrogen cycles.^5,10,24

Most studies examining the role of exogenous estrogen in reducing menstrual migraines have used topical estrogen (either in patch or gel formulations) in the perimenstrual window (TABLE 2^11-16). The topical estrogen route has been examined, in particular, as it is presumed to confer less risk of hypercoagulability by avoiding first-pass metabolism. However, there is conflicting evidence on this issue, in particular regarding premenopausal women.^13,25 Additionally, many of the studies of estrogen supplementation show a trend toward increased headache once estrogen is discontinued, presumably due to estrogen withdrawal.^10,24

That said, one study by MacGregor, et al demonstrates that the use of estradiol gel in the perimenstrual window leads to a 22% reduction in migraine days as well as less severe migrainous symptoms.²⁶ This trend has been demonstrated in other studies examining estrogen supplementation. Of note, the estrogen studies generally are small, older, and of fair to poor quality.¹¹ These studies have used higher doses of estrogen than are commonly used for contraception today because lower doses of estrogen seem not to have the same impact on migraine.^5,24

As for COCs, with either normal or extended cycling, data are more mixed than for estrogen supplementation alone; equivalent numbers of women experience improvement, no change, or worsening of their headache pattern. Many women have continuing or worsening migraines in the hormone-free week, and thus most studies have examined the use of extended cycling COCs.⁵ Sulak, et al demonstrated a statistically significant reduction in headache frequency using extended-cycling COCs, though they did not examine MRM in particular.²⁷ The efficacy of extended-cycling COCs for reduction of MRM was confirmed by Coffee and colleagues with a small but statistically significant decrease in daily headache scores.²⁸

Evidence is insufficient to recommend for or against the use of NSAIDs as prophylaxis for menstrually-related migraines.

Adverse effects. All estrogen therapies pose the risk of adverse effects (deep vein thrombosis, hypertension, breast tenderness, nausea, etc). Additionally, estrogen supplementation may actually trigger migraines in some women if, when it is discontinued, the blood estrogen level does not remain above a threshold concentration.^5,10,24 Estrogen may also trigger migraine in previously headache-free women and may convert migraine without aura into migraine with aura. In either case, therapy should be stopped.^5,24

There is promising evidence from 2 small RCTs and one observational trial that progestin-only contraceptive pills (POP) may reduce the frequency and severity of menstrual migraines (TABLE 2^11-16). More prospective data are needed to confirm this reduction, as there have not been specific studies examining other progesterone-only preparations to prevent menstrual migraines.

Risk of ischemic stroke. Unfortunately, there are population data showing that second-generation and, to a smaller degree, third-generation progestins, which include the desogestrel used in the above studies, may increase the risk of ischemic stroke. This is a particular concern in women who experience migraine.²⁹ Second-generation progestins include levonorgestrel, which is in the levonorgestrel IUD; however, there is no direct evidence for increased ischemic stroke in this particular preparation, and the circulating plasma levels are low. Etonorgestrel, the active ingredient in the contraceptive implant, is a third-generation progestin, though there is no direct evidence of increased ischemic stroke with use of the etonorgestrel implant.

There is a 2- to 4-fold increased risk of ischemic stroke in women who experience migraine.^1,5,30 As stated above, this risk may be further increased by some progesterone formulations. But there is also a demonstrable increase in ischemic stroke risk with the use of estrogen, particularly at the higher concentrations that have been shown to prevent MRM.^31,32 The overall incidence of ischemic stroke in menstrual-age women is low, which has limited the number of studies with enough power to quantify the absolute increased risk of stroke in conjunction with estrogen use. Nevertheless, exogenous estrogen is thought to increase the risk of ischemic stroke an additional 2- to 4-fold.^{1,5,29,30,32-34}

A number of studies have demonstrated a correlation between hypomagnesemia and migraine headaches. The exact mechanism for this relationship is unclear.Women who experience aura. MRM, as it is defined, typically excludes women who experience aura; however, the number of women who experience aura with migraine either in proximity to their menses or throughout the month has not been well documented. The risk of ischemic stroke is higher for women who experience migraine with aura than those with migraine alone, possibly because aura is associated with reduced regional vascular flow leading to hypoperfusion, which sets the stage for a possible ischemic event.^4,5,35 The risk of ischemic stroke is amplified further for women who are over 35, who smoke, or who have additional vascular risk factors (eg, uncontrolled hypertension, diabetes, or known vascular or cardiac disease).^1,5,34 This array of evidence serves as the basis for the US Medical Eligibility Criteria (USMEC) recommendations³⁶ for hormonal contraceptive use, in particular the absolute contraindication for estrogen use in women who experience migraine with aura (TABLE 3^36-38).

CASE ›  Given Mary’s experience of aura with migraine, you talk with her at length about the risk of ischemic stroke and the USMEC recommendation that she absolutely should not be taking COCs. You suggest a progestin-only method of contraception such as depot medroxyprogesterone acetate, a progestin intrauterine device, or a hormonal implant, which may suppress ovulation and decrease her headaches. You discuss that while some women may have headaches with these progestin-only methods, stroke risk is significantly reduced. You also suggest a trial of prophylactic triptans as another possible option.

She says she understands the increased risk of stroke but is still unwilling to try anything else right now due to worries about her quality of life. You decide jointly to refill COCs for 3 months, and you document the shared decision process in the chart. After advising the patient that you will not continue to prescribe COCs for an extended period of time, you also schedule a follow-up appointment to further discuss risks and benefits of migraine treatment and means of reducing other risk factors for stroke.

CORRESPONDENCE
Sarina Schrager, MD, MS, University of Wisconsin, Department of Family Medicine, 1100 Delaplaine Ct, Madison, WI 53715; [email protected].

Eliminating routine glucometer readings makes primary care visits more efficient, according to a 6-month review of activity at a primary care clinic. The results were published online Sept. 26 in JAMA Internal Medicine.

“The routine tasks that are components of rooming the clinic patient are increasing in number,” wrote James L Wofford, MD, of Wake Forest University, Winston-Salem, N.C., and his colleagues (JAMA Intern Med. 2016 Sep 26. doi: 10.1001/jamainternmed.2016.5769). Routine glucometer readings are costly in terms of time, money, and mental energy of clinicians, and do not add value, they wrote.

©Boarding1Now/Thinkstock

The researchers compared data from a primary care clinic in North Carolina for 3 months before and 3 months after the clinic eliminated routine glucometer readings (Jan. 1, 2015, to March 15, 2015, and March 16, 2015, to June 30, 2015). After a 1-week trial during which no routine clinical glucometry was performed, the option remained available at the request of a nurse or patient.

The number of glucometer readings decreased from approximately 400 per month to 100 per month after the change in policy, yielded a cost savings of at least $2,000 per month, and time saving of 25 hours of nursing time per month.

“Despite the fear of missing an occasional markedly elevated glucose level, clinicians gradually grew comfortable and never reconsidered reinstitution of routine glucometer readings,” Dr. Wofford and his associates wrote. However, some patient education was needed to reassure those who were disappointed by the change.

“As important as the lesson that routine glucometer readings in the clinic is a wasteful practice, the more important lesson is that examining office routines for foolish consistencies should be a regular component of making primary care more efficient,” the researchers added.

They had no financial conflicts to disclose.

Eliminating routine glucometer readings makes primary care visits more efficient, according to a 6-month review of activity at a primary care clinic. The results were published online Sept. 26 in JAMA Internal Medicine.

“The routine tasks that are components of rooming the clinic patient are increasing in number,” wrote James L Wofford, MD, of Wake Forest University, Winston-Salem, N.C., and his colleagues (JAMA Intern Med. 2016 Sep 26. doi: 10.1001/jamainternmed.2016.5769). Routine glucometer readings are costly in terms of time, money, and mental energy of clinicians, and do not add value, they wrote.

©Boarding1Now/Thinkstock

The researchers compared data from a primary care clinic in North Carolina for 3 months before and 3 months after the clinic eliminated routine glucometer readings (Jan. 1, 2015, to March 15, 2015, and March 16, 2015, to June 30, 2015). After a 1-week trial during which no routine clinical glucometry was performed, the option remained available at the request of a nurse or patient.

The number of glucometer readings decreased from approximately 400 per month to 100 per month after the change in policy, yielded a cost savings of at least $2,000 per month, and time saving of 25 hours of nursing time per month.

“Despite the fear of missing an occasional markedly elevated glucose level, clinicians gradually grew comfortable and never reconsidered reinstitution of routine glucometer readings,” Dr. Wofford and his associates wrote. However, some patient education was needed to reassure those who were disappointed by the change.

“As important as the lesson that routine glucometer readings in the clinic is a wasteful practice, the more important lesson is that examining office routines for foolish consistencies should be a regular component of making primary care more efficient,” the researchers added.

They had no financial conflicts to disclose.

Eliminating routine glucometer readings makes primary care visits more efficient, according to a 6-month review of activity at a primary care clinic. The results were published online Sept. 26 in JAMA Internal Medicine.

“The routine tasks that are components of rooming the clinic patient are increasing in number,” wrote James L Wofford, MD, of Wake Forest University, Winston-Salem, N.C., and his colleagues (JAMA Intern Med. 2016 Sep 26. doi: 10.1001/jamainternmed.2016.5769). Routine glucometer readings are costly in terms of time, money, and mental energy of clinicians, and do not add value, they wrote.

©Boarding1Now/Thinkstock

The researchers compared data from a primary care clinic in North Carolina for 3 months before and 3 months after the clinic eliminated routine glucometer readings (Jan. 1, 2015, to March 15, 2015, and March 16, 2015, to June 30, 2015). After a 1-week trial during which no routine clinical glucometry was performed, the option remained available at the request of a nurse or patient.

The number of glucometer readings decreased from approximately 400 per month to 100 per month after the change in policy, yielded a cost savings of at least $2,000 per month, and time saving of 25 hours of nursing time per month.

“Despite the fear of missing an occasional markedly elevated glucose level, clinicians gradually grew comfortable and never reconsidered reinstitution of routine glucometer readings,” Dr. Wofford and his associates wrote. However, some patient education was needed to reassure those who were disappointed by the change.

“As important as the lesson that routine glucometer readings in the clinic is a wasteful practice, the more important lesson is that examining office routines for foolish consistencies should be a regular component of making primary care more efficient,” the researchers added.

They had no financial conflicts to disclose.

Grants made possible by the “Million Dollar Bike Ride” and rare disease patient organizations are now available through the University of Pennsylvania Orphan Disease Center. September 16 is the deadline for letters of intent.

The diseases for which research funding is available are: adult polyglucosan body disease; ataxia-telangiectasia; Castleman disease; CFTR nonsense mutations; congenital hyperinsulinism; congenital muscular dystrophy; CRB1 degenerative retinal disease; nonsense mutations in cystic fibrosis; dyskeratosis congenital & telomere biology disorders; fibrous dysplasia/McCune Albright syndrome; generalized lymphatic anomaly and Gorham-Stout disease; Glut 1 deficiency; lymphangioleiomyomatosis; mucolipidosis type IV; mucopolysaccharidoses; Niemann Pick type C; Pitt Hopkins syndrome; RASopathies; Tay-Sachs, Sandhoff, GM1, or Canavan disease; and Snyder-Robinson syndrome.

Grants made possible by the “Million Dollar Bike Ride” and rare disease patient organizations are now available through the University of Pennsylvania Orphan Disease Center. September 16 is the deadline for letters of intent.

The diseases for which research funding is available are: adult polyglucosan body disease; ataxia-telangiectasia; Castleman disease; CFTR nonsense mutations; congenital hyperinsulinism; congenital muscular dystrophy; CRB1 degenerative retinal disease; nonsense mutations in cystic fibrosis; dyskeratosis congenital & telomere biology disorders; fibrous dysplasia/McCune Albright syndrome; generalized lymphatic anomaly and Gorham-Stout disease; Glut 1 deficiency; lymphangioleiomyomatosis; mucolipidosis type IV; mucopolysaccharidoses; Niemann Pick type C; Pitt Hopkins syndrome; RASopathies; Tay-Sachs, Sandhoff, GM1, or Canavan disease; and Snyder-Robinson syndrome.

Grants made possible by the “Million Dollar Bike Ride” and rare disease patient organizations are now available through the University of Pennsylvania Orphan Disease Center. September 16 is the deadline for letters of intent.

The diseases for which research funding is available are: adult polyglucosan body disease; ataxia-telangiectasia; Castleman disease; CFTR nonsense mutations; congenital hyperinsulinism; congenital muscular dystrophy; CRB1 degenerative retinal disease; nonsense mutations in cystic fibrosis; dyskeratosis congenital & telomere biology disorders; fibrous dysplasia/McCune Albright syndrome; generalized lymphatic anomaly and Gorham-Stout disease; Glut 1 deficiency; lymphangioleiomyomatosis; mucolipidosis type IV; mucopolysaccharidoses; Niemann Pick type C; Pitt Hopkins syndrome; RASopathies; Tay-Sachs, Sandhoff, GM1, or Canavan disease; and Snyder-Robinson syndrome.

The family physician (FP) suspected that the patient had some type of fungal infection under her breasts. The FP scraped the edge and performed a potassium hydroxide (KOH) preparation that showed pseudohyphae and budding yeast forms, indicating a candida infection. (See video on how to perform a KOH preparation.) The FP also noted that there appeared to be some satellite lesions around the edge of the hyperpigmented area. Under the left breast was a small fissure and some white coloration at the skinfold. The differential diagnosis included tinea corporis and inverse psoriasis.

The FP prescribed topical clotrimazole cream 1% over the counter to be applied twice daily until at least one week after the rash resolved. While nystatin would be another option, it required a prescription and would not cover any possible dermatophyte in the area. The FP also explained that the dark pigmentation is the result of a longstanding inflammatory process related to the infection and would not go away immediately with treatment. In fact, the postinflammatory hyperpigmentation might remain for life.

The FP also spent time counseling the patient on an improved diet, increased exercise, and adherence to her diabetes medicines. A follow-up appointment for one month was set to review the patient's general health and to see if the candida infection resolved.

In cases where intertriginous fungal infections are treated without KOH or fungal culture confirmation, be suspicious for inverse psoriasis if the patient does not respond to antifungal medications. With such a large area involved, an oral antifungal such as fluconazole might occasionally be needed. Terbinafine is not an effective medicine for cutaneous candidiasis. If psoriasis is suspected, it helps to look for clues, such as nail pitting or cutaneous involvement with plaques on the elbows, knees, or scalp. If all else fails, a punch biopsy can be used to determine the correct diagnosis.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R. Candidiasis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:777-781.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The family physician (FP) suspected that the patient had some type of fungal infection under her breasts. The FP scraped the edge and performed a potassium hydroxide (KOH) preparation that showed pseudohyphae and budding yeast forms, indicating a candida infection. (See video on how to perform a KOH preparation.) The FP also noted that there appeared to be some satellite lesions around the edge of the hyperpigmented area. Under the left breast was a small fissure and some white coloration at the skinfold. The differential diagnosis included tinea corporis and inverse psoriasis.

The FP prescribed topical clotrimazole cream 1% over the counter to be applied twice daily until at least one week after the rash resolved. While nystatin would be another option, it required a prescription and would not cover any possible dermatophyte in the area. The FP also explained that the dark pigmentation is the result of a longstanding inflammatory process related to the infection and would not go away immediately with treatment. In fact, the postinflammatory hyperpigmentation might remain for life.

The FP also spent time counseling the patient on an improved diet, increased exercise, and adherence to her diabetes medicines. A follow-up appointment for one month was set to review the patient's general health and to see if the candida infection resolved.

In cases where intertriginous fungal infections are treated without KOH or fungal culture confirmation, be suspicious for inverse psoriasis if the patient does not respond to antifungal medications. With such a large area involved, an oral antifungal such as fluconazole might occasionally be needed. Terbinafine is not an effective medicine for cutaneous candidiasis. If psoriasis is suspected, it helps to look for clues, such as nail pitting or cutaneous involvement with plaques on the elbows, knees, or scalp. If all else fails, a punch biopsy can be used to determine the correct diagnosis.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R. Candidiasis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:777-781.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The family physician (FP) suspected that the patient had some type of fungal infection under her breasts. The FP scraped the edge and performed a potassium hydroxide (KOH) preparation that showed pseudohyphae and budding yeast forms, indicating a candida infection. (See video on how to perform a KOH preparation.) The FP also noted that there appeared to be some satellite lesions around the edge of the hyperpigmented area. Under the left breast was a small fissure and some white coloration at the skinfold. The differential diagnosis included tinea corporis and inverse psoriasis.

The FP prescribed topical clotrimazole cream 1% over the counter to be applied twice daily until at least one week after the rash resolved. While nystatin would be another option, it required a prescription and would not cover any possible dermatophyte in the area. The FP also explained that the dark pigmentation is the result of a longstanding inflammatory process related to the infection and would not go away immediately with treatment. In fact, the postinflammatory hyperpigmentation might remain for life.

The FP also spent time counseling the patient on an improved diet, increased exercise, and adherence to her diabetes medicines. A follow-up appointment for one month was set to review the patient's general health and to see if the candida infection resolved.

In cases where intertriginous fungal infections are treated without KOH or fungal culture confirmation, be suspicious for inverse psoriasis if the patient does not respond to antifungal medications. With such a large area involved, an oral antifungal such as fluconazole might occasionally be needed. Terbinafine is not an effective medicine for cutaneous candidiasis. If psoriasis is suspected, it helps to look for clues, such as nail pitting or cutaneous involvement with plaques on the elbows, knees, or scalp. If all else fails, a punch biopsy can be used to determine the correct diagnosis.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R. Candidiasis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:777-781.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

MUNICH – When it comes to predicting mortality in diabetes patients, the foot may trump the heart.

Over a 5-year period, patients who had the most severe foot pathology were almost four times more likely to die than those who had a constellation of cardiovascular risk factors. The association with foot pathology stayed strong and, in a multivariate analysis, was the only factor that remained significantly associated with death in the cohort, Dragan Tesic, MD, said at the annual meeting of the European Association for the Study of Diabetes.

©donskarpo/thinkstockphotos.com

“On average, our patients with severe foot pathology had a 5-year shortening of their lifespan,” said Dr. Tesic of the University of Novi Sad, Serbia. This finding was even more pronounced in younger patients: Those aged 55 years and younger with severe foot pathology died a median of 14 years earlier than their normal expected lifespan would have ended.

Dr. Tesic and his colleagues conducted a 5-year mortality analysis of 244 patients with diabetes, 12% of whom had type 1 disease. The analysis included cardiovascular risk factors (hypertension, triglycerides, cholesterol levels, fibrinogen, proteinuria, and smoking); diabetes duration; coronary artery and cerebrovascular disease; and peripheral artery disease.

Foot pathology was determined according the recently published clinical guidelines by the International Working Group on the Diabetic Foot (IWGDF) (Diab Met Res Rev. 2016. doi: 10.1002/dmrr.2694).

The document parses the diabetic foot into four severity categories:

• 0: No peripheral neuropathy.

• 1: Peripheral neuropathy.

• 2: Peripheral neuropathy with peripheral artery disease and/or a foot deformity.

• 3: Peripheral neuropathy and a history of a foot ulcer or a lower-extremity amputation.

At baseline, patients were a median of 68 years old, though they ranged in age from 36 to 83 years. The mean duration of diabetes was 17 years, and the mean HbA_1c was 8.9%. About half had retinopathy; no one was on hemodialysis.

By 5 years, 53 patients (22%) had died. Their median age was 70 years – 5 years short of the Serbian national life expectancy. However, deaths were evenly distributed among the age groups, Dr. Tesic said: 30% of deceased patients were aged 40-64, 41% aged 65-74, and 28% aged 74 and older.

The causes of death were sudden cardiac death (38%), acute coronary syndrome (32%), stroke (11%), cancer (13%), and sepsis (6%).

There were no significant between-group differences in the type of diabetes; any lipid parameter; diabetic retinopathy; proteinuria; or cardiovascular or cerebrovascular disease. However, patients who died had significantly more severe foot pathology, with 71% scoring either a 2 or 3 on the IWGDF scale compared with 36% of those who were still alive. This level of foot pathology was seen in every age group of the deceased patients: 75% of those in the youngest, 54% of those in the middle group, and 73% of those in the oldest group.

Those who died had developed their foot lesions earlier (66 years vs. 69 years). They had poorer ankle reflexes, and worse results on the Neuropad, a visual indicator test for human diabetic neuropathy. Those who died were older (70 years vs. 66 years), had a longer diabetes duration (20 years vs. 17 years), and more hypertension (79% vs. 61%).

But in a multivariate analysis, only the IWGDF score remained a significant predictor of mortality (odds ratio, 3.78). All of the cardiovascular risk factors, as well as age, diabetes duration, and glucose measures, had no effect on survivalk in that analysis.

The study underscores the importance of preventing and treating diabetic neuropathy and foot complications, Dr. Tesic stressed.

“I like to say that I see an opportunity in every difficulty. The examination of the diabetic foot may be time-consuming, but without that we are not delivering adequate or appropriate care to our patients.”

He had no financial disclosures.

[email protected]

MUNICH – When it comes to predicting mortality in diabetes patients, the foot may trump the heart.

Over a 5-year period, patients who had the most severe foot pathology were almost four times more likely to die than those who had a constellation of cardiovascular risk factors. The association with foot pathology stayed strong and, in a multivariate analysis, was the only factor that remained significantly associated with death in the cohort, Dragan Tesic, MD, said at the annual meeting of the European Association for the Study of Diabetes.

©donskarpo/thinkstockphotos.com

“On average, our patients with severe foot pathology had a 5-year shortening of their lifespan,” said Dr. Tesic of the University of Novi Sad, Serbia. This finding was even more pronounced in younger patients: Those aged 55 years and younger with severe foot pathology died a median of 14 years earlier than their normal expected lifespan would have ended.

Dr. Tesic and his colleagues conducted a 5-year mortality analysis of 244 patients with diabetes, 12% of whom had type 1 disease. The analysis included cardiovascular risk factors (hypertension, triglycerides, cholesterol levels, fibrinogen, proteinuria, and smoking); diabetes duration; coronary artery and cerebrovascular disease; and peripheral artery disease.

Foot pathology was determined according the recently published clinical guidelines by the International Working Group on the Diabetic Foot (IWGDF) (Diab Met Res Rev. 2016. doi: 10.1002/dmrr.2694).

The document parses the diabetic foot into four severity categories:

• 0: No peripheral neuropathy.

• 1: Peripheral neuropathy.

• 2: Peripheral neuropathy with peripheral artery disease and/or a foot deformity.

• 3: Peripheral neuropathy and a history of a foot ulcer or a lower-extremity amputation.

At baseline, patients were a median of 68 years old, though they ranged in age from 36 to 83 years. The mean duration of diabetes was 17 years, and the mean HbA_1c was 8.9%. About half had retinopathy; no one was on hemodialysis.

By 5 years, 53 patients (22%) had died. Their median age was 70 years – 5 years short of the Serbian national life expectancy. However, deaths were evenly distributed among the age groups, Dr. Tesic said: 30% of deceased patients were aged 40-64, 41% aged 65-74, and 28% aged 74 and older.

The causes of death were sudden cardiac death (38%), acute coronary syndrome (32%), stroke (11%), cancer (13%), and sepsis (6%).

There were no significant between-group differences in the type of diabetes; any lipid parameter; diabetic retinopathy; proteinuria; or cardiovascular or cerebrovascular disease. However, patients who died had significantly more severe foot pathology, with 71% scoring either a 2 or 3 on the IWGDF scale compared with 36% of those who were still alive. This level of foot pathology was seen in every age group of the deceased patients: 75% of those in the youngest, 54% of those in the middle group, and 73% of those in the oldest group.

Those who died had developed their foot lesions earlier (66 years vs. 69 years). They had poorer ankle reflexes, and worse results on the Neuropad, a visual indicator test for human diabetic neuropathy. Those who died were older (70 years vs. 66 years), had a longer diabetes duration (20 years vs. 17 years), and more hypertension (79% vs. 61%).

But in a multivariate analysis, only the IWGDF score remained a significant predictor of mortality (odds ratio, 3.78). All of the cardiovascular risk factors, as well as age, diabetes duration, and glucose measures, had no effect on survivalk in that analysis.

The study underscores the importance of preventing and treating diabetic neuropathy and foot complications, Dr. Tesic stressed.

“I like to say that I see an opportunity in every difficulty. The examination of the diabetic foot may be time-consuming, but without that we are not delivering adequate or appropriate care to our patients.”

He had no financial disclosures.

[email protected]

MUNICH – When it comes to predicting mortality in diabetes patients, the foot may trump the heart.

Over a 5-year period, patients who had the most severe foot pathology were almost four times more likely to die than those who had a constellation of cardiovascular risk factors. The association with foot pathology stayed strong and, in a multivariate analysis, was the only factor that remained significantly associated with death in the cohort, Dragan Tesic, MD, said at the annual meeting of the European Association for the Study of Diabetes.

©donskarpo/thinkstockphotos.com

“On average, our patients with severe foot pathology had a 5-year shortening of their lifespan,” said Dr. Tesic of the University of Novi Sad, Serbia. This finding was even more pronounced in younger patients: Those aged 55 years and younger with severe foot pathology died a median of 14 years earlier than their normal expected lifespan would have ended.

Dr. Tesic and his colleagues conducted a 5-year mortality analysis of 244 patients with diabetes, 12% of whom had type 1 disease. The analysis included cardiovascular risk factors (hypertension, triglycerides, cholesterol levels, fibrinogen, proteinuria, and smoking); diabetes duration; coronary artery and cerebrovascular disease; and peripheral artery disease.

Foot pathology was determined according the recently published clinical guidelines by the International Working Group on the Diabetic Foot (IWGDF) (Diab Met Res Rev. 2016. doi: 10.1002/dmrr.2694).

The document parses the diabetic foot into four severity categories:

• 0: No peripheral neuropathy.

• 1: Peripheral neuropathy.

• 2: Peripheral neuropathy with peripheral artery disease and/or a foot deformity.

• 3: Peripheral neuropathy and a history of a foot ulcer or a lower-extremity amputation.

At baseline, patients were a median of 68 years old, though they ranged in age from 36 to 83 years. The mean duration of diabetes was 17 years, and the mean HbA_1c was 8.9%. About half had retinopathy; no one was on hemodialysis.

By 5 years, 53 patients (22%) had died. Their median age was 70 years – 5 years short of the Serbian national life expectancy. However, deaths were evenly distributed among the age groups, Dr. Tesic said: 30% of deceased patients were aged 40-64, 41% aged 65-74, and 28% aged 74 and older.

The causes of death were sudden cardiac death (38%), acute coronary syndrome (32%), stroke (11%), cancer (13%), and sepsis (6%).

There were no significant between-group differences in the type of diabetes; any lipid parameter; diabetic retinopathy; proteinuria; or cardiovascular or cerebrovascular disease. However, patients who died had significantly more severe foot pathology, with 71% scoring either a 2 or 3 on the IWGDF scale compared with 36% of those who were still alive. This level of foot pathology was seen in every age group of the deceased patients: 75% of those in the youngest, 54% of those in the middle group, and 73% of those in the oldest group.

Those who died had developed their foot lesions earlier (66 years vs. 69 years). They had poorer ankle reflexes, and worse results on the Neuropad, a visual indicator test for human diabetic neuropathy. Those who died were older (70 years vs. 66 years), had a longer diabetes duration (20 years vs. 17 years), and more hypertension (79% vs. 61%).

But in a multivariate analysis, only the IWGDF score remained a significant predictor of mortality (odds ratio, 3.78). All of the cardiovascular risk factors, as well as age, diabetes duration, and glucose measures, had no effect on survivalk in that analysis.

The study underscores the importance of preventing and treating diabetic neuropathy and foot complications, Dr. Tesic stressed.

“I like to say that I see an opportunity in every difficulty. The examination of the diabetic foot may be time-consuming, but without that we are not delivering adequate or appropriate care to our patients.”

He had no financial disclosures.

[email protected]

The FP diagnosed thrush or candidiasis of the oral mucosa. To make sure it was not just milk, the FP gently drew a tongue blade over the tongue and the white exudate was mostly adherent (milk wipes away rather easily). The tongue blade was then rubbed onto a glass slide and 2 drops of potassium hydroxide (KOH) solution were applied. Microscopic evaluation revealed pseudohyphae and budding yeasts consistent with Candida albicans. (See video on how to perform a KOH preparation.)

Thrush is a common condition in infants with normal immune systems and does not require work-up for immunosuppression if this is the only finding at this age. Of course, thrush is seen in people who are immunosuppressed from various diseases (such as human immunodeficiency virus) and medications (like chemotherapy).

The FP chose to treat the child with oral nystatin suspension 2 mL 4 times a day. The directions were to give 1 mL in each side of the infant’s mouth and to continue this until 48 hours after signs and symptoms resolved. The mother was not having any symptoms or erythema of the nipples, but if she was, a topical antifungal agent (to be washed off before breastfeeding) could be used.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R. Candidiasis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill;2013:777-781.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed thrush or candidiasis of the oral mucosa. To make sure it was not just milk, the FP gently drew a tongue blade over the tongue and the white exudate was mostly adherent (milk wipes away rather easily). The tongue blade was then rubbed onto a glass slide and 2 drops of potassium hydroxide (KOH) solution were applied. Microscopic evaluation revealed pseudohyphae and budding yeasts consistent with Candida albicans. (See video on how to perform a KOH preparation.)

Thrush is a common condition in infants with normal immune systems and does not require work-up for immunosuppression if this is the only finding at this age. Of course, thrush is seen in people who are immunosuppressed from various diseases (such as human immunodeficiency virus) and medications (like chemotherapy).

The FP chose to treat the child with oral nystatin suspension 2 mL 4 times a day. The directions were to give 1 mL in each side of the infant’s mouth and to continue this until 48 hours after signs and symptoms resolved. The mother was not having any symptoms or erythema of the nipples, but if she was, a topical antifungal agent (to be washed off before breastfeeding) could be used.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R. Candidiasis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill;2013:777-781.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed thrush or candidiasis of the oral mucosa. To make sure it was not just milk, the FP gently drew a tongue blade over the tongue and the white exudate was mostly adherent (milk wipes away rather easily). The tongue blade was then rubbed onto a glass slide and 2 drops of potassium hydroxide (KOH) solution were applied. Microscopic evaluation revealed pseudohyphae and budding yeasts consistent with Candida albicans. (See video on how to perform a KOH preparation.)

Thrush is a common condition in infants with normal immune systems and does not require work-up for immunosuppression if this is the only finding at this age. Of course, thrush is seen in people who are immunosuppressed from various diseases (such as human immunodeficiency virus) and medications (like chemotherapy).

The FP chose to treat the child with oral nystatin suspension 2 mL 4 times a day. The directions were to give 1 mL in each side of the infant’s mouth and to continue this until 48 hours after signs and symptoms resolved. The mother was not having any symptoms or erythema of the nipples, but if she was, a topical antifungal agent (to be washed off before breastfeeding) could be used.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R. Candidiasis. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill;2013:777-781.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com