Although vulvovaginitis has several possible causes, the typical presenting symptoms are similar regardless of the cause: itching, burning, and vaginal discharge. Physical examination often reveals atrophy, redness, excoriations, and fissures in the vulvovaginal and perianal areas. Determining the cause is key to successful treatment.

This article reviews the diagnosis and treatment of many common and less common infectious and noninfectious causes of vulvovaginitis, the use of special tests, and the management of persistent cases.

DIAGNOSIS CAN BE CHALLENGING

Vulvar and vaginal symptoms are most commonly caused by local infections, but other causes must be also be considered, including several noninfectious ones (Table 1). Challenges in diagnosing vulvovaginitis are many and include distinguishing contact from allergic dermatitis, recognizing vaginal atrophy, and recognizing a parasitic infection. Determining whether a patient has an infectious process is important so that antibiotics can be used only when truly needed.

Foreign bodies in the vagina should also be considered, especially in children,¹ as should sexual abuse. A 15-year retrospective review of prepubertal girls presenting with recurrent vaginal discharge found that sexual abuse might have been involved in about 5% of cases.²

Systemic diseases, such as eczema and psoriasis, may also present with gynecologic symptoms.

Heavy vaginal discharge may also be normal. This situation is a diagnosis of exclusion but is important to recognize in order to allay the patient’s anxiety and avoid unnecessary treatment.

SIMPLE OFFICE-BASED ASSESSMENT

A thorough history and physical examination are always warranted.

Simple tests of vaginal secretions can often determine the diagnosis (Table 2). Vaginal secretions should be analyzed in the following order: 

Testing the pH. The pH can help determine likely diagnoses and streamline further testing (Figure 1). 

Saline microscopy. Some of the vaginal discharge sample should be diluted with 1 or 2 drops of normal saline and examined under a microscope, first at × 10 magnification, then at × 40. The sample should be searched for epithelial cells, blood cells, “clue” cells (ie, epithelial cells with borders studded or obscured by bacteria), and motile trichomonads.

10% KOH whiff test and microscopy. To a second vaginal sample, a small amount of 10% potassium hydroxide should be added, and the examiner should sniff it. An amine or fishy odor is a sign of bacterial vaginosis.

If pH paper, KOH, and a microscope are unavailable, other point-of-care tests can be used for specific conditions as discussed below.

INFECTIOUS CAUSES

Infectious causes of vulvovaginitis include bacterial vaginosis, candidiasis, trichomoniasis, and herpes simplex virus (HSV) infection.

BACTERIAL VAGINOSIS

Bacterial vaginosis is the most common vaginal disorder worldwide. It has been linked to preterm delivery, intra-amniotic infection, endometritis, postabortion infection, and vaginal cuff cellulitis after hysterectomy.³ It may also be a risk factor for human immunodeficiency virus (HIV) infection.⁴

The condition reflects a microbial imbalance in the vaginal ecosystem, characterized by depletion of the dominant hydrogen peroxide-producing lactobacilli and overgrowth of anaerobic and facultative aerobic organisms such as Gardnerella vaginalis, Mycoplasma hominis, Atopobium vaginae, and Prevotella and Mobiluncus species.

Diagnosis of bacterial vaginosis

The Amsel criteria consist of the following:

• pH greater than 4.5
• Positive whiff test
• Homogeneous discharge
• Clue cells.

Three of the four criteria must be present for a diagnosis of bacterial vaginosis. This method is inexpensive and provides immediate results in the clinic.

The Nugent score, based on seeing certain bacteria from a vaginal swab on Gram stain microscopy, is the diagnostic standard for research.⁵

DNA tests. Affirm VPIII (BD Diagnostics, Sparks, MD) is a nonamplified nucleic acid probe hybridization test that detects Trichomonas vaginalis, Candida albicans, and G vaginalis. Although it is more expensive than testing for the Amsel criteria, it is commonly used in private offices because it is simple to use, gives rapid results, and does not require a microscope.⁶ Insurance pays for it when the test is indicated, but we know of a patient who received a bill for approximately $500 when the insurance company thought the test was not indicated.

In a study of 109 patients with symptoms of vulvovaginitis, the Affirm VPIII was found comparable to saline microscopy when tested on residual vaginal samples. Compared with Gram stain using Nugent scoring, the test has a sensitivity of 87.7% to 95.2% and a specificity of 81% to 99.1% for bacterial vaginosis.⁷

In 323 symptomatic women, a polymerase chain reaction (PCR) assay for bacterial vaginosis was 96.9% sensitive and 92.6% specific for bacterial vaginosis, and Affirm VPIII was 90.1% sensitive and 67.6% specific, compared with a reference standard incorporating Nugent Gram-stain scores and Amsel criteria.⁸ The test is commercially available.

Management of bacterial vaginosis

Initial treatment. Bacterial vaginosis can be treated with oral or topical metronidazole, oral tinidazole, or oral or topical clindamycin.⁹ All options offer equivalent efficacy as initial treatments, so the choice may be based on cost and preferred route of administration.

Treatment for recurrent disease. Women who have 3 or more episodes in 12 months should receive initial treatment each time as described above and should then be offered additional suppressive therapy with 0.75% metronidazole intravaginal gel 2 times a week for 4 months. A side effect of therapy is vulvovaginal candidiasis, which should be treated as needed.

In a multicenter study, Sobel et al¹⁰ randomized patients who had recurrent bacterial vaginosis to twice-weekly metronidazole gel or placebo for 16 weeks after their initial treatment. During the 28 weeks of follow-up, recurrences occurred in 51% of treated women vs 75% of those on placebo.

Another option for chronic therapy is oral metronidazole and boric acid vaginal suppositories.

Reichman et al¹¹ treated women with oral metronidazole or tinidazole 500 mg twice a day for 7 days, followed by vaginal boric acid 600 mg daily for 21 days. This was followed by twice-weekly vaginal metronidazole gel for 16 weeks. At follow-up, the cure rate was 92% at 7 weeks, dropping to 88% at 12 weeks and 50% at 36 weeks.

Patients with recurrent bacterial vaginosis despite therapy should be referred to a vulvovaginal or infectious disease specialist.

VULVOVAGINAL CANDIDIASIS

Vulvovaginal candidiasis is the second most common cause of vaginitis.

Diagnosis can be clinical

Vulvovaginal candidiasis can be clinically diagnosed on the basis of cottage cheese-like clumpy discharge; external dysuria (a burning sensation when urine comes in contact with the vulva); and vulvar itching, pain, swelling, and redness. Edema, fissures, and excoriations may be seen on examination of the vulva. (Figure 3).

Saline microscopy (Figure 2) with the addition of 10% KOH may reveal the characteristic fungal elements, but its sensitivity is only 50%.

Fungal culture remains the gold standard for diagnosis and is needed to determine the sensitivity of specific strains of Candida to therapy.¹²

DNA tests can also be helpful. In a study of patients with symptomatic vaginitis, Affirm VPIII detected Candida in 11% of samples, whereas microscopy detected it in only 7%.¹³ Another study⁷ found that Affirm VPIII produced comparable results whether the sample was collected from residual vaginal discharge found on the speculum or was collected in the traditional way (by swabbing).

Cartwright et al⁸ compared the performance of a multiplexed, real-time PCR assay and Affirm VPIII in 102 patients. PCR was much more sensitive (97.7% vs 58.1%) but less specific (93.2% vs 100%), with culture serving as the gold standard.

Management of candidiasis

Uncomplicated cases can be managed with prescription or over-the-counter topical or oral antifungal medications for 1 to 7 days, depending on the medication.⁹ However, most of the common antifungals may not be effective against non-albicans Candida.

In immunosuppressed patients and diabetic patients, if symptoms do not improve with regular treatment, a vaginal sample should be cultured for C albicans. If the culture is positive, the patient should be treated with fluconazole 150 mg orally every 3 days for 3 doses.¹⁴

Patients with recurrent episodes (3 or more in 12 months) should follow initial treatment with maintenance therapy of weekly fluconazole 150 mg orally for 6 months.¹⁵

Non-albicans Candida may be azole-resistant, and fungal culture and sensitivity should be obtained. Sobel et al¹³ documented successful treatment of non-albicans Candida using boric acid and flucytosine. Phillips¹⁶ documented successful use of compounded amphotericin B in a 50-mg vaginal suppository for 14 days. Therefore, in patients who have Candida species other than C albicans, treatment should be one of the following:

• Vaginal boric acid 600 mg daily for 14 to 21 days
• Flucytosine in 15.5% vaginal cream, intravaginally administered as 5 g for 14 days 
• Amphotericin B 50 mg vaginal suppositories for 14 days.

Boric acid is readily available, but flucytosine vaginal cream and amphotericin B vaginal suppositories must usually be compounded by a pharmacist.

Of note: All that itches is not yeast. Patients with persistent itching despite treatment should be referred to a specialist to search for another cause.

TRICHOMONIASIS

The incidence of T vaginalis infection is higher than that of Neisseria gonorrhoeae and Chlamydia trachomatis combined, with an estimated 7.4 million new cases occurring in the year 2000 in the United States.¹⁷ Infection increases the sexual transmission of HIV.^18–20 It is often asymptomatic and so is likely underdiagnosed.

Diagnosis of trichomoniasis

Vaginal pH may be normal or elevated (> 4.5).

Direct microscopy. Observation by saline microscopy of motile trichomonads with their characteristic jerky movements is 100% specific but only 50% sensitive. Sensitivity is reduced by delaying microscopy on the sample by as little as 10 minutes.²¹

The incidental finding of T vaginalis on a conventional Papanicolaou (Pap) smear has poor sensitivity and specificity, and patients diagnosed with T vaginalis by conventional Pap smear should have a second test performed. The liquid-based Pap test is more accurate for microscopic diagnosis, and its results can be used to determine if treatment is needed (sensitivity 60%–90%; specificity 98%–100%).^22,23

Culture. Amplification of T vaginalis in liquid culture usually provides results within 3 days.²⁴ It is more sensitive than microscopy but less sensitive than a nucleic acid amplification test: compared with a nucleic acid amplification test, culture is 44% to 75% sensitive for detecting T vaginalis and 100% specific.¹⁹ Culture is the preferred test for resistant strains.

Non–culture-based or nucleic acid tests do not require viable organisms, so they allow for a wider range of specimen storage temperatures and time intervals between collection and processing. This quality limits them for testing treatment success; if performed too early, they may detect nonviable organisms. A 2-week interval is recommended between the end of treatment and retesting.²⁵

Nonamplified tests such as Affirm VPIII and the Osom Trichomonas Test (Sekisui Diagnostics, Lexington, MA) are 40% to 95% sensitive, depending on the test and reference standard used, and 92% to 100% specific.^26,27

Nucleic acid amplification tests are usually not performed as point-of-care tests. They are more expensive and require special equipment with trained personnel. Sensitivities range from 76% to 100%, making these tests more suitable for screening and testing of asymptomatic women, in whom the concentration of organisms may be lower.

Treatment of trichomoniasis

Treatment is a single 2-g oral dose of metronidazole or tinidazole.⁹

If initial treatment is ineffective, an additional regimen can be either of the following:

• Oral metronidazole 500 mg twice a day for 7 days
• Oral metronidazole or tinidazole, 2 g daily for 5 days.

Patients allergic to nitroimidazoles should be referred for desensitization.

If these treatments are unsuccessful, the patient should be referred to an infectious disease specialist or gynecologist who specializes in vulvovaginal disorders. Treatment failure is uncommon and is usually related to noncompliance, reinfection, or metronidazole resistance.²⁸ The US Centers for Disease Control and Prevention offers testing for resistance by request.

Reportedly successful regimens for refractory trichomoniasis include 14 days of either:

• Oral tinidazole 500 mg 4 times daily plus vaginal tinidazole 500 mg twice daily²⁹
• Oral tinidazole 1 g 3 times daily plus compounded 5% intravaginal paromomycin 5 g nightly.³⁰

HERPES SIMPLEX VIRUS INFECTION

HSV (HSV-1 and HSV-2) causes lifelong infection. About 50 million people in the United States are infected with HSV-2, the most common cause of recurrent infections.³¹ Owing to changes in sexual practices, an increasing number of young people are acquiring anogenital HSV-1 infection.^32,33

Diagnosis of herpes

Diagnosis may be difficult because the painful vesicular or ulcerative lesions (Figure 4) may not be visible at the time of presentation. Diagnosis is based on specific virologic and serologic tests. Nonspecific tests (eg, Tzanck smear, direct immunofluorescence) are neither sensitive nor specific and should not be relied on for diagnosis.³⁴ HSV culture or HSV-PCR testing of a lesion is preferred. The sensitivity of viral culture can be low and is dependent on the stage of healing of a lesion and obtaining an adequate sample.

Accurate type-specific HSV serologic assays are based on HSV-specific glycoprotein G1 (HSV-1) and glycoprotein G2 (HSV-2). Unless a patient’s serologic status has already been determined, serologic testing should be done concurrently with HSV culture or PCR testing. Serologic testing enables classification of an infection as primary, nonprimary, or recurrent. For example, a patient with a positive HSV culture and negative serology most likely has primary HSV infection, and serologic study should be repeated after 6 to 8 weeks to assess for seroconversion.

Immunoglobulin M (IgM) testing for HSV-1 or HSV-2 is not diagnostic or type-specific and may be positive during recurrent genital or oral episodes of herpes.³⁵

Treatment of herpes

In general, antiviral medications (eg, acyclovir, valacyclovir, famciclovir) are effective for managing HSV.¹² Episodic or continuous suppression therapy may be needed for patients experiencing more than four outbreaks in 12 months. Patients who do not respond to treatment should be referred to an infectious disease specialist and undergo a viral culture with sensitivities.

NONINFECTIOUS CAUSES

Desquamative inflammatory vaginitis

Desquamative inflammatory vaginitis is a chronic vaginal disorder of unknown cause. It is a diagnosis of exclusion, and some patients may have a superimposed bacterial infection. It occurs mostly in perimenopausal woman and is often associated with low estrogen levels.

Diagnosis. Patients may report copious green-yellow mucoid discharge, vulvar or vaginal pain, and dyspareunia. On examination, the vulva may be erythematous, friable, and tender to the touch. The vagina may have ecchymoses, be diffusely erythematous, and have linear lesions. Mucoid or purulent discharge may be seen.

The vaginal pH is greater than 4.5.

Saline microscopy shows increased parabasal cells and leukorrhea (Figure 5).

Diagnosis is based on all of the following:

• At least 1 symptom (ie, vaginal discharge, dyspareunia, pruritus, pain, irritation, or burning)
• Vaginal inflammation on examination
• pH higher than 4.5
• Presence of parabasal cells and leukorrhea on microscopy (a ratio of leukocytes to vaginal epithelial cells > 1:1).³⁶

Treatment involves use of 2% intravaginal clindamycin or 10% intravaginal compounded hydrocortisone cream for 4 to 6 weeks. Patients who are not cured with single-agent therapy may benefit from compounded clindamycin and hydrocortisone, with estrogen added to the formulation for hypoestrogenic patients.

Atrophic vaginitis

Atrophic vaginitis is often seen in menopausal or hypoestrogenic women. Presenting symptoms include vulvar or vaginal pain and dyspareunia.

Diagnosis. On physical examination, the vulva appears pale and atrophic, with narrowing of the introitus. Vaginal examination may reveal a pale mucosa that lacks elasticity and rugation. The examination should be performed with caution, as the vagina may bleed easily.

The vaginal pH is usually elevated.  

Saline microscopy may show parabasal cells and a paucity of epithelial cells. (Figure 6).

The Vaginal Maturation Index is an indicator of the maturity of the epithelial cell types being exfoliated; these normally include parabasal (immature) cells, intermediate, and superficial (mature) cells. A predominance of immature cells indicates a hypoestrogenic state.

Infection should be considered and treated as needed.

Treatment. Patients with no contraindication may benefit from systemic hormone therapy or topical estrogen, or both.

Contact dermatitis

Contact dermatitis is classified into two types:

Irritant dermatitis, caused by the destructive action of contactants, eg, urine, feces, topical agents, feminine wipes               

Allergic dermatitis, also contactant-induced, but immunologically mediated.

If a diagnosis cannot be made from the patient history and physical examination, biopsy should be performed.

Treatment of contact dermatitis involves removing the irritant, hydrating the skin with sitz baths, and using an emollient (eg, petroleum jelly) and midpotent topical steroids until resolution. Some patients benefit from topical immunosuppressive agents (eg, tacrolimus). Patients with severe symptoms may be treated with a tapering course of oral steroids for 5 to 7 days. Recalcitrant cases should be referred to a specialist.

Lichen planus

Lichen sclerosus is a benign, chronic, progressive dermatologic condition characterized by marked inflammation, epithelial thinning, and distinctive dermal changes accompanied by pruritus and pain (Figures 7 and 8).

Treatment. High-potency topical steroids are the mainstay of therapy for lichen disease. Although these are not infectious processes, superimposed infections (mostly bacterial and fungal) may also be present and should be treated.

Although vulvovaginitis has several possible causes, the typical presenting symptoms are similar regardless of the cause: itching, burning, and vaginal discharge. Physical examination often reveals atrophy, redness, excoriations, and fissures in the vulvovaginal and perianal areas. Determining the cause is key to successful treatment.

This article reviews the diagnosis and treatment of many common and less common infectious and noninfectious causes of vulvovaginitis, the use of special tests, and the management of persistent cases.

DIAGNOSIS CAN BE CHALLENGING

Vulvar and vaginal symptoms are most commonly caused by local infections, but other causes must be also be considered, including several noninfectious ones (Table 1). Challenges in diagnosing vulvovaginitis are many and include distinguishing contact from allergic dermatitis, recognizing vaginal atrophy, and recognizing a parasitic infection. Determining whether a patient has an infectious process is important so that antibiotics can be used only when truly needed.

Foreign bodies in the vagina should also be considered, especially in children,¹ as should sexual abuse. A 15-year retrospective review of prepubertal girls presenting with recurrent vaginal discharge found that sexual abuse might have been involved in about 5% of cases.²

Systemic diseases, such as eczema and psoriasis, may also present with gynecologic symptoms.

Heavy vaginal discharge may also be normal. This situation is a diagnosis of exclusion but is important to recognize in order to allay the patient’s anxiety and avoid unnecessary treatment.

SIMPLE OFFICE-BASED ASSESSMENT

A thorough history and physical examination are always warranted.

Simple tests of vaginal secretions can often determine the diagnosis (Table 2). Vaginal secretions should be analyzed in the following order: 

Testing the pH. The pH can help determine likely diagnoses and streamline further testing (Figure 1). 

Saline microscopy. Some of the vaginal discharge sample should be diluted with 1 or 2 drops of normal saline and examined under a microscope, first at × 10 magnification, then at × 40. The sample should be searched for epithelial cells, blood cells, “clue” cells (ie, epithelial cells with borders studded or obscured by bacteria), and motile trichomonads.

10% KOH whiff test and microscopy. To a second vaginal sample, a small amount of 10% potassium hydroxide should be added, and the examiner should sniff it. An amine or fishy odor is a sign of bacterial vaginosis.

If pH paper, KOH, and a microscope are unavailable, other point-of-care tests can be used for specific conditions as discussed below.

INFECTIOUS CAUSES

Infectious causes of vulvovaginitis include bacterial vaginosis, candidiasis, trichomoniasis, and herpes simplex virus (HSV) infection.

BACTERIAL VAGINOSIS

Bacterial vaginosis is the most common vaginal disorder worldwide. It has been linked to preterm delivery, intra-amniotic infection, endometritis, postabortion infection, and vaginal cuff cellulitis after hysterectomy.³ It may also be a risk factor for human immunodeficiency virus (HIV) infection.⁴

The condition reflects a microbial imbalance in the vaginal ecosystem, characterized by depletion of the dominant hydrogen peroxide-producing lactobacilli and overgrowth of anaerobic and facultative aerobic organisms such as Gardnerella vaginalis, Mycoplasma hominis, Atopobium vaginae, and Prevotella and Mobiluncus species.

Diagnosis of bacterial vaginosis

The Amsel criteria consist of the following:

• pH greater than 4.5
• Positive whiff test
• Homogeneous discharge
• Clue cells.

Three of the four criteria must be present for a diagnosis of bacterial vaginosis. This method is inexpensive and provides immediate results in the clinic.

The Nugent score, based on seeing certain bacteria from a vaginal swab on Gram stain microscopy, is the diagnostic standard for research.⁵

DNA tests. Affirm VPIII (BD Diagnostics, Sparks, MD) is a nonamplified nucleic acid probe hybridization test that detects Trichomonas vaginalis, Candida albicans, and G vaginalis. Although it is more expensive than testing for the Amsel criteria, it is commonly used in private offices because it is simple to use, gives rapid results, and does not require a microscope.⁶ Insurance pays for it when the test is indicated, but we know of a patient who received a bill for approximately $500 when the insurance company thought the test was not indicated.

In a study of 109 patients with symptoms of vulvovaginitis, the Affirm VPIII was found comparable to saline microscopy when tested on residual vaginal samples. Compared with Gram stain using Nugent scoring, the test has a sensitivity of 87.7% to 95.2% and a specificity of 81% to 99.1% for bacterial vaginosis.⁷

In 323 symptomatic women, a polymerase chain reaction (PCR) assay for bacterial vaginosis was 96.9% sensitive and 92.6% specific for bacterial vaginosis, and Affirm VPIII was 90.1% sensitive and 67.6% specific, compared with a reference standard incorporating Nugent Gram-stain scores and Amsel criteria.⁸ The test is commercially available.

Management of bacterial vaginosis

Initial treatment. Bacterial vaginosis can be treated with oral or topical metronidazole, oral tinidazole, or oral or topical clindamycin.⁹ All options offer equivalent efficacy as initial treatments, so the choice may be based on cost and preferred route of administration.

Treatment for recurrent disease. Women who have 3 or more episodes in 12 months should receive initial treatment each time as described above and should then be offered additional suppressive therapy with 0.75% metronidazole intravaginal gel 2 times a week for 4 months. A side effect of therapy is vulvovaginal candidiasis, which should be treated as needed.

In a multicenter study, Sobel et al¹⁰ randomized patients who had recurrent bacterial vaginosis to twice-weekly metronidazole gel or placebo for 16 weeks after their initial treatment. During the 28 weeks of follow-up, recurrences occurred in 51% of treated women vs 75% of those on placebo.

Another option for chronic therapy is oral metronidazole and boric acid vaginal suppositories.

Reichman et al¹¹ treated women with oral metronidazole or tinidazole 500 mg twice a day for 7 days, followed by vaginal boric acid 600 mg daily for 21 days. This was followed by twice-weekly vaginal metronidazole gel for 16 weeks. At follow-up, the cure rate was 92% at 7 weeks, dropping to 88% at 12 weeks and 50% at 36 weeks.

Patients with recurrent bacterial vaginosis despite therapy should be referred to a vulvovaginal or infectious disease specialist.

VULVOVAGINAL CANDIDIASIS

Vulvovaginal candidiasis is the second most common cause of vaginitis.

Diagnosis can be clinical

Vulvovaginal candidiasis can be clinically diagnosed on the basis of cottage cheese-like clumpy discharge; external dysuria (a burning sensation when urine comes in contact with the vulva); and vulvar itching, pain, swelling, and redness. Edema, fissures, and excoriations may be seen on examination of the vulva. (Figure 3).

Saline microscopy (Figure 2) with the addition of 10% KOH may reveal the characteristic fungal elements, but its sensitivity is only 50%.

Fungal culture remains the gold standard for diagnosis and is needed to determine the sensitivity of specific strains of Candida to therapy.¹²

DNA tests can also be helpful. In a study of patients with symptomatic vaginitis, Affirm VPIII detected Candida in 11% of samples, whereas microscopy detected it in only 7%.¹³ Another study⁷ found that Affirm VPIII produced comparable results whether the sample was collected from residual vaginal discharge found on the speculum or was collected in the traditional way (by swabbing).

Cartwright et al⁸ compared the performance of a multiplexed, real-time PCR assay and Affirm VPIII in 102 patients. PCR was much more sensitive (97.7% vs 58.1%) but less specific (93.2% vs 100%), with culture serving as the gold standard.

Management of candidiasis

Uncomplicated cases can be managed with prescription or over-the-counter topical or oral antifungal medications for 1 to 7 days, depending on the medication.⁹ However, most of the common antifungals may not be effective against non-albicans Candida.

In immunosuppressed patients and diabetic patients, if symptoms do not improve with regular treatment, a vaginal sample should be cultured for C albicans. If the culture is positive, the patient should be treated with fluconazole 150 mg orally every 3 days for 3 doses.¹⁴

Patients with recurrent episodes (3 or more in 12 months) should follow initial treatment with maintenance therapy of weekly fluconazole 150 mg orally for 6 months.¹⁵

Non-albicans Candida may be azole-resistant, and fungal culture and sensitivity should be obtained. Sobel et al¹³ documented successful treatment of non-albicans Candida using boric acid and flucytosine. Phillips¹⁶ documented successful use of compounded amphotericin B in a 50-mg vaginal suppository for 14 days. Therefore, in patients who have Candida species other than C albicans, treatment should be one of the following:

• Vaginal boric acid 600 mg daily for 14 to 21 days
• Flucytosine in 15.5% vaginal cream, intravaginally administered as 5 g for 14 days 
• Amphotericin B 50 mg vaginal suppositories for 14 days.

Boric acid is readily available, but flucytosine vaginal cream and amphotericin B vaginal suppositories must usually be compounded by a pharmacist.

Of note: All that itches is not yeast. Patients with persistent itching despite treatment should be referred to a specialist to search for another cause.

TRICHOMONIASIS

The incidence of T vaginalis infection is higher than that of Neisseria gonorrhoeae and Chlamydia trachomatis combined, with an estimated 7.4 million new cases occurring in the year 2000 in the United States.¹⁷ Infection increases the sexual transmission of HIV.^18–20 It is often asymptomatic and so is likely underdiagnosed.

Diagnosis of trichomoniasis

Vaginal pH may be normal or elevated (> 4.5).

Direct microscopy. Observation by saline microscopy of motile trichomonads with their characteristic jerky movements is 100% specific but only 50% sensitive. Sensitivity is reduced by delaying microscopy on the sample by as little as 10 minutes.²¹

The incidental finding of T vaginalis on a conventional Papanicolaou (Pap) smear has poor sensitivity and specificity, and patients diagnosed with T vaginalis by conventional Pap smear should have a second test performed. The liquid-based Pap test is more accurate for microscopic diagnosis, and its results can be used to determine if treatment is needed (sensitivity 60%–90%; specificity 98%–100%).^22,23

Culture. Amplification of T vaginalis in liquid culture usually provides results within 3 days.²⁴ It is more sensitive than microscopy but less sensitive than a nucleic acid amplification test: compared with a nucleic acid amplification test, culture is 44% to 75% sensitive for detecting T vaginalis and 100% specific.¹⁹ Culture is the preferred test for resistant strains.

Non–culture-based or nucleic acid tests do not require viable organisms, so they allow for a wider range of specimen storage temperatures and time intervals between collection and processing. This quality limits them for testing treatment success; if performed too early, they may detect nonviable organisms. A 2-week interval is recommended between the end of treatment and retesting.²⁵

Nonamplified tests such as Affirm VPIII and the Osom Trichomonas Test (Sekisui Diagnostics, Lexington, MA) are 40% to 95% sensitive, depending on the test and reference standard used, and 92% to 100% specific.^26,27

Nucleic acid amplification tests are usually not performed as point-of-care tests. They are more expensive and require special equipment with trained personnel. Sensitivities range from 76% to 100%, making these tests more suitable for screening and testing of asymptomatic women, in whom the concentration of organisms may be lower.

Treatment of trichomoniasis

Treatment is a single 2-g oral dose of metronidazole or tinidazole.⁹

If initial treatment is ineffective, an additional regimen can be either of the following:

• Oral metronidazole 500 mg twice a day for 7 days
• Oral metronidazole or tinidazole, 2 g daily for 5 days.

Patients allergic to nitroimidazoles should be referred for desensitization.

If these treatments are unsuccessful, the patient should be referred to an infectious disease specialist or gynecologist who specializes in vulvovaginal disorders. Treatment failure is uncommon and is usually related to noncompliance, reinfection, or metronidazole resistance.²⁸ The US Centers for Disease Control and Prevention offers testing for resistance by request.

Reportedly successful regimens for refractory trichomoniasis include 14 days of either:

• Oral tinidazole 500 mg 4 times daily plus vaginal tinidazole 500 mg twice daily²⁹
• Oral tinidazole 1 g 3 times daily plus compounded 5% intravaginal paromomycin 5 g nightly.³⁰

HERPES SIMPLEX VIRUS INFECTION

HSV (HSV-1 and HSV-2) causes lifelong infection. About 50 million people in the United States are infected with HSV-2, the most common cause of recurrent infections.³¹ Owing to changes in sexual practices, an increasing number of young people are acquiring anogenital HSV-1 infection.^32,33

Diagnosis of herpes

Diagnosis may be difficult because the painful vesicular or ulcerative lesions (Figure 4) may not be visible at the time of presentation. Diagnosis is based on specific virologic and serologic tests. Nonspecific tests (eg, Tzanck smear, direct immunofluorescence) are neither sensitive nor specific and should not be relied on for diagnosis.³⁴ HSV culture or HSV-PCR testing of a lesion is preferred. The sensitivity of viral culture can be low and is dependent on the stage of healing of a lesion and obtaining an adequate sample.

Accurate type-specific HSV serologic assays are based on HSV-specific glycoprotein G1 (HSV-1) and glycoprotein G2 (HSV-2). Unless a patient’s serologic status has already been determined, serologic testing should be done concurrently with HSV culture or PCR testing. Serologic testing enables classification of an infection as primary, nonprimary, or recurrent. For example, a patient with a positive HSV culture and negative serology most likely has primary HSV infection, and serologic study should be repeated after 6 to 8 weeks to assess for seroconversion.

Immunoglobulin M (IgM) testing for HSV-1 or HSV-2 is not diagnostic or type-specific and may be positive during recurrent genital or oral episodes of herpes.³⁵

Treatment of herpes

In general, antiviral medications (eg, acyclovir, valacyclovir, famciclovir) are effective for managing HSV.¹² Episodic or continuous suppression therapy may be needed for patients experiencing more than four outbreaks in 12 months. Patients who do not respond to treatment should be referred to an infectious disease specialist and undergo a viral culture with sensitivities.

NONINFECTIOUS CAUSES

Desquamative inflammatory vaginitis

Desquamative inflammatory vaginitis is a chronic vaginal disorder of unknown cause. It is a diagnosis of exclusion, and some patients may have a superimposed bacterial infection. It occurs mostly in perimenopausal woman and is often associated with low estrogen levels.

Diagnosis. Patients may report copious green-yellow mucoid discharge, vulvar or vaginal pain, and dyspareunia. On examination, the vulva may be erythematous, friable, and tender to the touch. The vagina may have ecchymoses, be diffusely erythematous, and have linear lesions. Mucoid or purulent discharge may be seen.

The vaginal pH is greater than 4.5.

Saline microscopy shows increased parabasal cells and leukorrhea (Figure 5).

Diagnosis is based on all of the following:

• At least 1 symptom (ie, vaginal discharge, dyspareunia, pruritus, pain, irritation, or burning)
• Vaginal inflammation on examination
• pH higher than 4.5
• Presence of parabasal cells and leukorrhea on microscopy (a ratio of leukocytes to vaginal epithelial cells > 1:1).³⁶

Treatment involves use of 2% intravaginal clindamycin or 10% intravaginal compounded hydrocortisone cream for 4 to 6 weeks. Patients who are not cured with single-agent therapy may benefit from compounded clindamycin and hydrocortisone, with estrogen added to the formulation for hypoestrogenic patients.

Atrophic vaginitis

Atrophic vaginitis is often seen in menopausal or hypoestrogenic women. Presenting symptoms include vulvar or vaginal pain and dyspareunia.

Diagnosis. On physical examination, the vulva appears pale and atrophic, with narrowing of the introitus. Vaginal examination may reveal a pale mucosa that lacks elasticity and rugation. The examination should be performed with caution, as the vagina may bleed easily.

The vaginal pH is usually elevated.  

Saline microscopy may show parabasal cells and a paucity of epithelial cells. (Figure 6).

The Vaginal Maturation Index is an indicator of the maturity of the epithelial cell types being exfoliated; these normally include parabasal (immature) cells, intermediate, and superficial (mature) cells. A predominance of immature cells indicates a hypoestrogenic state.

Infection should be considered and treated as needed.

Treatment. Patients with no contraindication may benefit from systemic hormone therapy or topical estrogen, or both.

Contact dermatitis

Contact dermatitis is classified into two types:

Irritant dermatitis, caused by the destructive action of contactants, eg, urine, feces, topical agents, feminine wipes               

Allergic dermatitis, also contactant-induced, but immunologically mediated.

If a diagnosis cannot be made from the patient history and physical examination, biopsy should be performed.

Treatment of contact dermatitis involves removing the irritant, hydrating the skin with sitz baths, and using an emollient (eg, petroleum jelly) and midpotent topical steroids until resolution. Some patients benefit from topical immunosuppressive agents (eg, tacrolimus). Patients with severe symptoms may be treated with a tapering course of oral steroids for 5 to 7 days. Recalcitrant cases should be referred to a specialist.

Lichen planus

Lichen sclerosus is a benign, chronic, progressive dermatologic condition characterized by marked inflammation, epithelial thinning, and distinctive dermal changes accompanied by pruritus and pain (Figures 7 and 8).

Treatment. High-potency topical steroids are the mainstay of therapy for lichen disease. Although these are not infectious processes, superimposed infections (mostly bacterial and fungal) may also be present and should be treated.

Although vulvovaginitis has several possible causes, the typical presenting symptoms are similar regardless of the cause: itching, burning, and vaginal discharge. Physical examination often reveals atrophy, redness, excoriations, and fissures in the vulvovaginal and perianal areas. Determining the cause is key to successful treatment.

This article reviews the diagnosis and treatment of many common and less common infectious and noninfectious causes of vulvovaginitis, the use of special tests, and the management of persistent cases.

DIAGNOSIS CAN BE CHALLENGING

Vulvar and vaginal symptoms are most commonly caused by local infections, but other causes must be also be considered, including several noninfectious ones (Table 1). Challenges in diagnosing vulvovaginitis are many and include distinguishing contact from allergic dermatitis, recognizing vaginal atrophy, and recognizing a parasitic infection. Determining whether a patient has an infectious process is important so that antibiotics can be used only when truly needed.

Foreign bodies in the vagina should also be considered, especially in children,¹ as should sexual abuse. A 15-year retrospective review of prepubertal girls presenting with recurrent vaginal discharge found that sexual abuse might have been involved in about 5% of cases.²

Systemic diseases, such as eczema and psoriasis, may also present with gynecologic symptoms.

Heavy vaginal discharge may also be normal. This situation is a diagnosis of exclusion but is important to recognize in order to allay the patient’s anxiety and avoid unnecessary treatment.

SIMPLE OFFICE-BASED ASSESSMENT

A thorough history and physical examination are always warranted.

Simple tests of vaginal secretions can often determine the diagnosis (Table 2). Vaginal secretions should be analyzed in the following order: 

Testing the pH. The pH can help determine likely diagnoses and streamline further testing (Figure 1). 

Saline microscopy. Some of the vaginal discharge sample should be diluted with 1 or 2 drops of normal saline and examined under a microscope, first at × 10 magnification, then at × 40. The sample should be searched for epithelial cells, blood cells, “clue” cells (ie, epithelial cells with borders studded or obscured by bacteria), and motile trichomonads.

10% KOH whiff test and microscopy. To a second vaginal sample, a small amount of 10% potassium hydroxide should be added, and the examiner should sniff it. An amine or fishy odor is a sign of bacterial vaginosis.

If pH paper, KOH, and a microscope are unavailable, other point-of-care tests can be used for specific conditions as discussed below.

INFECTIOUS CAUSES

Infectious causes of vulvovaginitis include bacterial vaginosis, candidiasis, trichomoniasis, and herpes simplex virus (HSV) infection.

BACTERIAL VAGINOSIS

Bacterial vaginosis is the most common vaginal disorder worldwide. It has been linked to preterm delivery, intra-amniotic infection, endometritis, postabortion infection, and vaginal cuff cellulitis after hysterectomy.³ It may also be a risk factor for human immunodeficiency virus (HIV) infection.⁴

The condition reflects a microbial imbalance in the vaginal ecosystem, characterized by depletion of the dominant hydrogen peroxide-producing lactobacilli and overgrowth of anaerobic and facultative aerobic organisms such as Gardnerella vaginalis, Mycoplasma hominis, Atopobium vaginae, and Prevotella and Mobiluncus species.

Diagnosis of bacterial vaginosis

The Amsel criteria consist of the following:

• pH greater than 4.5
• Positive whiff test
• Homogeneous discharge
• Clue cells.

Three of the four criteria must be present for a diagnosis of bacterial vaginosis. This method is inexpensive and provides immediate results in the clinic.

The Nugent score, based on seeing certain bacteria from a vaginal swab on Gram stain microscopy, is the diagnostic standard for research.⁵

DNA tests. Affirm VPIII (BD Diagnostics, Sparks, MD) is a nonamplified nucleic acid probe hybridization test that detects Trichomonas vaginalis, Candida albicans, and G vaginalis. Although it is more expensive than testing for the Amsel criteria, it is commonly used in private offices because it is simple to use, gives rapid results, and does not require a microscope.⁶ Insurance pays for it when the test is indicated, but we know of a patient who received a bill for approximately $500 when the insurance company thought the test was not indicated.

In a study of 109 patients with symptoms of vulvovaginitis, the Affirm VPIII was found comparable to saline microscopy when tested on residual vaginal samples. Compared with Gram stain using Nugent scoring, the test has a sensitivity of 87.7% to 95.2% and a specificity of 81% to 99.1% for bacterial vaginosis.⁷

In 323 symptomatic women, a polymerase chain reaction (PCR) assay for bacterial vaginosis was 96.9% sensitive and 92.6% specific for bacterial vaginosis, and Affirm VPIII was 90.1% sensitive and 67.6% specific, compared with a reference standard incorporating Nugent Gram-stain scores and Amsel criteria.⁸ The test is commercially available.

Management of bacterial vaginosis

Initial treatment. Bacterial vaginosis can be treated with oral or topical metronidazole, oral tinidazole, or oral or topical clindamycin.⁹ All options offer equivalent efficacy as initial treatments, so the choice may be based on cost and preferred route of administration.

Treatment for recurrent disease. Women who have 3 or more episodes in 12 months should receive initial treatment each time as described above and should then be offered additional suppressive therapy with 0.75% metronidazole intravaginal gel 2 times a week for 4 months. A side effect of therapy is vulvovaginal candidiasis, which should be treated as needed.

In a multicenter study, Sobel et al¹⁰ randomized patients who had recurrent bacterial vaginosis to twice-weekly metronidazole gel or placebo for 16 weeks after their initial treatment. During the 28 weeks of follow-up, recurrences occurred in 51% of treated women vs 75% of those on placebo.

Another option for chronic therapy is oral metronidazole and boric acid vaginal suppositories.

Reichman et al¹¹ treated women with oral metronidazole or tinidazole 500 mg twice a day for 7 days, followed by vaginal boric acid 600 mg daily for 21 days. This was followed by twice-weekly vaginal metronidazole gel for 16 weeks. At follow-up, the cure rate was 92% at 7 weeks, dropping to 88% at 12 weeks and 50% at 36 weeks.

Patients with recurrent bacterial vaginosis despite therapy should be referred to a vulvovaginal or infectious disease specialist.

VULVOVAGINAL CANDIDIASIS

Vulvovaginal candidiasis is the second most common cause of vaginitis.

Diagnosis can be clinical

Vulvovaginal candidiasis can be clinically diagnosed on the basis of cottage cheese-like clumpy discharge; external dysuria (a burning sensation when urine comes in contact with the vulva); and vulvar itching, pain, swelling, and redness. Edema, fissures, and excoriations may be seen on examination of the vulva. (Figure 3).

Saline microscopy (Figure 2) with the addition of 10% KOH may reveal the characteristic fungal elements, but its sensitivity is only 50%.

Fungal culture remains the gold standard for diagnosis and is needed to determine the sensitivity of specific strains of Candida to therapy.¹²

DNA tests can also be helpful. In a study of patients with symptomatic vaginitis, Affirm VPIII detected Candida in 11% of samples, whereas microscopy detected it in only 7%.¹³ Another study⁷ found that Affirm VPIII produced comparable results whether the sample was collected from residual vaginal discharge found on the speculum or was collected in the traditional way (by swabbing).

Cartwright et al⁸ compared the performance of a multiplexed, real-time PCR assay and Affirm VPIII in 102 patients. PCR was much more sensitive (97.7% vs 58.1%) but less specific (93.2% vs 100%), with culture serving as the gold standard.

Management of candidiasis

Uncomplicated cases can be managed with prescription or over-the-counter topical or oral antifungal medications for 1 to 7 days, depending on the medication.⁹ However, most of the common antifungals may not be effective against non-albicans Candida.

In immunosuppressed patients and diabetic patients, if symptoms do not improve with regular treatment, a vaginal sample should be cultured for C albicans. If the culture is positive, the patient should be treated with fluconazole 150 mg orally every 3 days for 3 doses.¹⁴

Patients with recurrent episodes (3 or more in 12 months) should follow initial treatment with maintenance therapy of weekly fluconazole 150 mg orally for 6 months.¹⁵

Non-albicans Candida may be azole-resistant, and fungal culture and sensitivity should be obtained. Sobel et al¹³ documented successful treatment of non-albicans Candida using boric acid and flucytosine. Phillips¹⁶ documented successful use of compounded amphotericin B in a 50-mg vaginal suppository for 14 days. Therefore, in patients who have Candida species other than C albicans, treatment should be one of the following:

• Vaginal boric acid 600 mg daily for 14 to 21 days
• Flucytosine in 15.5% vaginal cream, intravaginally administered as 5 g for 14 days 
• Amphotericin B 50 mg vaginal suppositories for 14 days.

Boric acid is readily available, but flucytosine vaginal cream and amphotericin B vaginal suppositories must usually be compounded by a pharmacist.

Of note: All that itches is not yeast. Patients with persistent itching despite treatment should be referred to a specialist to search for another cause.

TRICHOMONIASIS

The incidence of T vaginalis infection is higher than that of Neisseria gonorrhoeae and Chlamydia trachomatis combined, with an estimated 7.4 million new cases occurring in the year 2000 in the United States.¹⁷ Infection increases the sexual transmission of HIV.^18–20 It is often asymptomatic and so is likely underdiagnosed.

Diagnosis of trichomoniasis

Vaginal pH may be normal or elevated (> 4.5).

Direct microscopy. Observation by saline microscopy of motile trichomonads with their characteristic jerky movements is 100% specific but only 50% sensitive. Sensitivity is reduced by delaying microscopy on the sample by as little as 10 minutes.²¹

The incidental finding of T vaginalis on a conventional Papanicolaou (Pap) smear has poor sensitivity and specificity, and patients diagnosed with T vaginalis by conventional Pap smear should have a second test performed. The liquid-based Pap test is more accurate for microscopic diagnosis, and its results can be used to determine if treatment is needed (sensitivity 60%–90%; specificity 98%–100%).^22,23

Culture. Amplification of T vaginalis in liquid culture usually provides results within 3 days.²⁴ It is more sensitive than microscopy but less sensitive than a nucleic acid amplification test: compared with a nucleic acid amplification test, culture is 44% to 75% sensitive for detecting T vaginalis and 100% specific.¹⁹ Culture is the preferred test for resistant strains.

Non–culture-based or nucleic acid tests do not require viable organisms, so they allow for a wider range of specimen storage temperatures and time intervals between collection and processing. This quality limits them for testing treatment success; if performed too early, they may detect nonviable organisms. A 2-week interval is recommended between the end of treatment and retesting.²⁵

Nonamplified tests such as Affirm VPIII and the Osom Trichomonas Test (Sekisui Diagnostics, Lexington, MA) are 40% to 95% sensitive, depending on the test and reference standard used, and 92% to 100% specific.^26,27

Nucleic acid amplification tests are usually not performed as point-of-care tests. They are more expensive and require special equipment with trained personnel. Sensitivities range from 76% to 100%, making these tests more suitable for screening and testing of asymptomatic women, in whom the concentration of organisms may be lower.

Treatment of trichomoniasis

Treatment is a single 2-g oral dose of metronidazole or tinidazole.⁹

If initial treatment is ineffective, an additional regimen can be either of the following:

• Oral metronidazole 500 mg twice a day for 7 days
• Oral metronidazole or tinidazole, 2 g daily for 5 days.

Patients allergic to nitroimidazoles should be referred for desensitization.

If these treatments are unsuccessful, the patient should be referred to an infectious disease specialist or gynecologist who specializes in vulvovaginal disorders. Treatment failure is uncommon and is usually related to noncompliance, reinfection, or metronidazole resistance.²⁸ The US Centers for Disease Control and Prevention offers testing for resistance by request.

Reportedly successful regimens for refractory trichomoniasis include 14 days of either:

• Oral tinidazole 500 mg 4 times daily plus vaginal tinidazole 500 mg twice daily²⁹
• Oral tinidazole 1 g 3 times daily plus compounded 5% intravaginal paromomycin 5 g nightly.³⁰

HERPES SIMPLEX VIRUS INFECTION

HSV (HSV-1 and HSV-2) causes lifelong infection. About 50 million people in the United States are infected with HSV-2, the most common cause of recurrent infections.³¹ Owing to changes in sexual practices, an increasing number of young people are acquiring anogenital HSV-1 infection.^32,33

Diagnosis of herpes

Diagnosis may be difficult because the painful vesicular or ulcerative lesions (Figure 4) may not be visible at the time of presentation. Diagnosis is based on specific virologic and serologic tests. Nonspecific tests (eg, Tzanck smear, direct immunofluorescence) are neither sensitive nor specific and should not be relied on for diagnosis.³⁴ HSV culture or HSV-PCR testing of a lesion is preferred. The sensitivity of viral culture can be low and is dependent on the stage of healing of a lesion and obtaining an adequate sample.

Accurate type-specific HSV serologic assays are based on HSV-specific glycoprotein G1 (HSV-1) and glycoprotein G2 (HSV-2). Unless a patient’s serologic status has already been determined, serologic testing should be done concurrently with HSV culture or PCR testing. Serologic testing enables classification of an infection as primary, nonprimary, or recurrent. For example, a patient with a positive HSV culture and negative serology most likely has primary HSV infection, and serologic study should be repeated after 6 to 8 weeks to assess for seroconversion.

Immunoglobulin M (IgM) testing for HSV-1 or HSV-2 is not diagnostic or type-specific and may be positive during recurrent genital or oral episodes of herpes.³⁵

Treatment of herpes

In general, antiviral medications (eg, acyclovir, valacyclovir, famciclovir) are effective for managing HSV.¹² Episodic or continuous suppression therapy may be needed for patients experiencing more than four outbreaks in 12 months. Patients who do not respond to treatment should be referred to an infectious disease specialist and undergo a viral culture with sensitivities.

NONINFECTIOUS CAUSES

Desquamative inflammatory vaginitis

Desquamative inflammatory vaginitis is a chronic vaginal disorder of unknown cause. It is a diagnosis of exclusion, and some patients may have a superimposed bacterial infection. It occurs mostly in perimenopausal woman and is often associated with low estrogen levels.

Diagnosis. Patients may report copious green-yellow mucoid discharge, vulvar or vaginal pain, and dyspareunia. On examination, the vulva may be erythematous, friable, and tender to the touch. The vagina may have ecchymoses, be diffusely erythematous, and have linear lesions. Mucoid or purulent discharge may be seen.

The vaginal pH is greater than 4.5.

Saline microscopy shows increased parabasal cells and leukorrhea (Figure 5).

Diagnosis is based on all of the following:

• At least 1 symptom (ie, vaginal discharge, dyspareunia, pruritus, pain, irritation, or burning)
• Vaginal inflammation on examination
• pH higher than 4.5
• Presence of parabasal cells and leukorrhea on microscopy (a ratio of leukocytes to vaginal epithelial cells > 1:1).³⁶

Treatment involves use of 2% intravaginal clindamycin or 10% intravaginal compounded hydrocortisone cream for 4 to 6 weeks. Patients who are not cured with single-agent therapy may benefit from compounded clindamycin and hydrocortisone, with estrogen added to the formulation for hypoestrogenic patients.

Atrophic vaginitis

Atrophic vaginitis is often seen in menopausal or hypoestrogenic women. Presenting symptoms include vulvar or vaginal pain and dyspareunia.

Diagnosis. On physical examination, the vulva appears pale and atrophic, with narrowing of the introitus. Vaginal examination may reveal a pale mucosa that lacks elasticity and rugation. The examination should be performed with caution, as the vagina may bleed easily.

The vaginal pH is usually elevated.  

Saline microscopy may show parabasal cells and a paucity of epithelial cells. (Figure 6).

The Vaginal Maturation Index is an indicator of the maturity of the epithelial cell types being exfoliated; these normally include parabasal (immature) cells, intermediate, and superficial (mature) cells. A predominance of immature cells indicates a hypoestrogenic state.

Infection should be considered and treated as needed.

Treatment. Patients with no contraindication may benefit from systemic hormone therapy or topical estrogen, or both.

Contact dermatitis

Contact dermatitis is classified into two types:

Irritant dermatitis, caused by the destructive action of contactants, eg, urine, feces, topical agents, feminine wipes               

Allergic dermatitis, also contactant-induced, but immunologically mediated.

If a diagnosis cannot be made from the patient history and physical examination, biopsy should be performed.

Treatment of contact dermatitis involves removing the irritant, hydrating the skin with sitz baths, and using an emollient (eg, petroleum jelly) and midpotent topical steroids until resolution. Some patients benefit from topical immunosuppressive agents (eg, tacrolimus). Patients with severe symptoms may be treated with a tapering course of oral steroids for 5 to 7 days. Recalcitrant cases should be referred to a specialist.

Lichen planus

Lichen sclerosus is a benign, chronic, progressive dermatologic condition characterized by marked inflammation, epithelial thinning, and distinctive dermal changes accompanied by pruritus and pain (Figures 7 and 8).

Treatment. High-potency topical steroids are the mainstay of therapy for lichen disease. Although these are not infectious processes, superimposed infections (mostly bacterial and fungal) may also be present and should be treated.

New, changing technologies are being incorporated into every aspect of medical care and education, and the impact cannot be overstated. While the ultimate qualitative impact (beneficial, intrusive, efficient, obstructive, or neutral) of specific individual implementations remains to be seen, there is no doubt that the faces of patient care and the financial management of healthcare delivery have been forever altered.

The amount of information now literally at our fingertips is overwhelming. Some of my patients bring the latest from www.clinicaltrials.gov to their appointments. One patient recently brought downloaded online testimony from patients who were being given an oil supplement to treat disorders including gout, neuropathy, carpal tunnel, sinusitis, headache, and postop hip and knee pain and wanted to know why I hadn’t suggested it for her. Accessing the information pipeline is like drinking from a firehose, and there is no perfect valve that can adjust the flow to every thirst.

Lest we think that only patients use sites of variable reliability in getting their online medical information, in a recent survey by Kantar Media, when 508 physicians were asked which of 49 sites they looked at most often, Wikipedia came in at number 3 (UpToDate was number 1 and Cleveland Clinic Journal of Medicine was number 25). But when asked to rate the 49 sites for “quality clinical content,” responders listed Wikipedia as 47 (UpToDate was still number 1 and CCJM was number 6).

We healthcare providers can assess the accuracy and quality of clinical content. But it is not always easy, especially when trying to access, digest, and utilize information within the real-time constraints of an office visit or inpatient consultation. The now almost universal use of electronic medical records (EMRs) in major health systems provides access to true point-of-care information to assist in clinical decision-making, but how we filter and channel this information and apply it to the patient sitting in the exam room is not always straightforward. It is naïve to think that one source can fit all of our information needs.

A “smart” EMR can reflexively direct me to diagnosis-linked clinical guidelines or care paths. But without knowing the specifics of how the guidelines were written, I can’t know if they are ideally applicable to the patient in front of me. Guidelines based solely on clinical trial data may not be ideal for a given patient due to constraints of the clinical trial design and the tested clinical populations. There are times in areas outside my clinical field that I seek clinically nuanced expertise in interpreting clinical trials rather than the actual clinical trial data. Other times, when approaching problems within my own expertise, I want to see the raw data to reach a conclusion on its applicability and likely magnitude of effect in a specific patient. Using a trusted source of predigested, summarized data (as opposed to the raw data), knowing whether an author has a relationship with a specific company, and knowing that the clinical trials of a specific therapy are not intrinsically bad or good—all of these contribute to contextual decisions that lead to my clinical recommendations. I always want to know the nature of authors’ commercial relationships, as well as the track record of my information sources.

It is in this context that the paper by Andrews et al in this issue of the Journal addresses in a very practical way some of the nuances in using several popular point-of-care information resources. This is the second of 2 papers that these authors have contributed to the CCJM in an effort to inform and direct us how to quench our thirst for information without getting bloated.

New, changing technologies are being incorporated into every aspect of medical care and education, and the impact cannot be overstated. While the ultimate qualitative impact (beneficial, intrusive, efficient, obstructive, or neutral) of specific individual implementations remains to be seen, there is no doubt that the faces of patient care and the financial management of healthcare delivery have been forever altered.

The amount of information now literally at our fingertips is overwhelming. Some of my patients bring the latest from www.clinicaltrials.gov to their appointments. One patient recently brought downloaded online testimony from patients who were being given an oil supplement to treat disorders including gout, neuropathy, carpal tunnel, sinusitis, headache, and postop hip and knee pain and wanted to know why I hadn’t suggested it for her. Accessing the information pipeline is like drinking from a firehose, and there is no perfect valve that can adjust the flow to every thirst.

Lest we think that only patients use sites of variable reliability in getting their online medical information, in a recent survey by Kantar Media, when 508 physicians were asked which of 49 sites they looked at most often, Wikipedia came in at number 3 (UpToDate was number 1 and Cleveland Clinic Journal of Medicine was number 25). But when asked to rate the 49 sites for “quality clinical content,” responders listed Wikipedia as 47 (UpToDate was still number 1 and CCJM was number 6).

We healthcare providers can assess the accuracy and quality of clinical content. But it is not always easy, especially when trying to access, digest, and utilize information within the real-time constraints of an office visit or inpatient consultation. The now almost universal use of electronic medical records (EMRs) in major health systems provides access to true point-of-care information to assist in clinical decision-making, but how we filter and channel this information and apply it to the patient sitting in the exam room is not always straightforward. It is naïve to think that one source can fit all of our information needs.

A “smart” EMR can reflexively direct me to diagnosis-linked clinical guidelines or care paths. But without knowing the specifics of how the guidelines were written, I can’t know if they are ideally applicable to the patient in front of me. Guidelines based solely on clinical trial data may not be ideal for a given patient due to constraints of the clinical trial design and the tested clinical populations. There are times in areas outside my clinical field that I seek clinically nuanced expertise in interpreting clinical trials rather than the actual clinical trial data. Other times, when approaching problems within my own expertise, I want to see the raw data to reach a conclusion on its applicability and likely magnitude of effect in a specific patient. Using a trusted source of predigested, summarized data (as opposed to the raw data), knowing whether an author has a relationship with a specific company, and knowing that the clinical trials of a specific therapy are not intrinsically bad or good—all of these contribute to contextual decisions that lead to my clinical recommendations. I always want to know the nature of authors’ commercial relationships, as well as the track record of my information sources.

It is in this context that the paper by Andrews et al in this issue of the Journal addresses in a very practical way some of the nuances in using several popular point-of-care information resources. This is the second of 2 papers that these authors have contributed to the CCJM in an effort to inform and direct us how to quench our thirst for information without getting bloated.

New, changing technologies are being incorporated into every aspect of medical care and education, and the impact cannot be overstated. While the ultimate qualitative impact (beneficial, intrusive, efficient, obstructive, or neutral) of specific individual implementations remains to be seen, there is no doubt that the faces of patient care and the financial management of healthcare delivery have been forever altered.

The amount of information now literally at our fingertips is overwhelming. Some of my patients bring the latest from www.clinicaltrials.gov to their appointments. One patient recently brought downloaded online testimony from patients who were being given an oil supplement to treat disorders including gout, neuropathy, carpal tunnel, sinusitis, headache, and postop hip and knee pain and wanted to know why I hadn’t suggested it for her. Accessing the information pipeline is like drinking from a firehose, and there is no perfect valve that can adjust the flow to every thirst.

Lest we think that only patients use sites of variable reliability in getting their online medical information, in a recent survey by Kantar Media, when 508 physicians were asked which of 49 sites they looked at most often, Wikipedia came in at number 3 (UpToDate was number 1 and Cleveland Clinic Journal of Medicine was number 25). But when asked to rate the 49 sites for “quality clinical content,” responders listed Wikipedia as 47 (UpToDate was still number 1 and CCJM was number 6).

We healthcare providers can assess the accuracy and quality of clinical content. But it is not always easy, especially when trying to access, digest, and utilize information within the real-time constraints of an office visit or inpatient consultation. The now almost universal use of electronic medical records (EMRs) in major health systems provides access to true point-of-care information to assist in clinical decision-making, but how we filter and channel this information and apply it to the patient sitting in the exam room is not always straightforward. It is naïve to think that one source can fit all of our information needs.

A “smart” EMR can reflexively direct me to diagnosis-linked clinical guidelines or care paths. But without knowing the specifics of how the guidelines were written, I can’t know if they are ideally applicable to the patient in front of me. Guidelines based solely on clinical trial data may not be ideal for a given patient due to constraints of the clinical trial design and the tested clinical populations. There are times in areas outside my clinical field that I seek clinically nuanced expertise in interpreting clinical trials rather than the actual clinical trial data. Other times, when approaching problems within my own expertise, I want to see the raw data to reach a conclusion on its applicability and likely magnitude of effect in a specific patient. Using a trusted source of predigested, summarized data (as opposed to the raw data), knowing whether an author has a relationship with a specific company, and knowing that the clinical trials of a specific therapy are not intrinsically bad or good—all of these contribute to contextual decisions that lead to my clinical recommendations. I always want to know the nature of authors’ commercial relationships, as well as the track record of my information sources.

It is in this context that the paper by Andrews et al in this issue of the Journal addresses in a very practical way some of the nuances in using several popular point-of-care information resources. This is the second of 2 papers that these authors have contributed to the CCJM in an effort to inform and direct us how to quench our thirst for information without getting bloated.

To the Editor: We read with great interest the article by Drs. Cawcutt and Wilson on caring for international patients.¹ They provide an overview of the challenges of delivering medical care for these patients (eg, cultural differences) and the likely benefits from such interactions (eg, gaining cultural knowledge). Having practiced medicine in 3 different continents and experienced working in various medical centers caring for international patients, we would like to offer a slightly different viewpoint.

First, gaining cultural knowledge should be regarded as a prerequisite for healthcare workers involved in the care of international patients, rather than the expected benefit and consequence of such encounters. Healthcare workers with some knowledge of an international patient’s culture are best able to serve that patient.² Indeed, unless knowledge of cultural differences is obtained before such interactions, there is a significant risk of stereotyping by amplifying the sense of “otherness,” which is unfortunately too often mistaken for cultural sensitivity. The perception of the stereotypes and prejudices during the second stage of cultural adaptation (ie, irritation, hostility) often stems from the host’s lack of cultural knowledge. Table 1 of their article clearly reflects such risk: the authors have tried to exemplify the concepts they discussed through a number of real-life scenarios. But indeed some of those cases (eg, the man from Saudi Arabia) could be interpreted more as examples of stereotyping than cultural sensitivity.

Second, the authors do not mention requests by family members of international patients for nondisclosure of serious medical diagnoses, one we have frequently received from family members from different cultural backgrounds. These requests represent another challenge of caring for these patients as they counter our obligation for full disclosure and the patients’ right to know in order to be able to make informed decisions regarding their medical care.³

To the Editor: We read with great interest the article by Drs. Cawcutt and Wilson on caring for international patients.¹ They provide an overview of the challenges of delivering medical care for these patients (eg, cultural differences) and the likely benefits from such interactions (eg, gaining cultural knowledge). Having practiced medicine in 3 different continents and experienced working in various medical centers caring for international patients, we would like to offer a slightly different viewpoint.

First, gaining cultural knowledge should be regarded as a prerequisite for healthcare workers involved in the care of international patients, rather than the expected benefit and consequence of such encounters. Healthcare workers with some knowledge of an international patient’s culture are best able to serve that patient.² Indeed, unless knowledge of cultural differences is obtained before such interactions, there is a significant risk of stereotyping by amplifying the sense of “otherness,” which is unfortunately too often mistaken for cultural sensitivity. The perception of the stereotypes and prejudices during the second stage of cultural adaptation (ie, irritation, hostility) often stems from the host’s lack of cultural knowledge. Table 1 of their article clearly reflects such risk: the authors have tried to exemplify the concepts they discussed through a number of real-life scenarios. But indeed some of those cases (eg, the man from Saudi Arabia) could be interpreted more as examples of stereotyping than cultural sensitivity.

Second, the authors do not mention requests by family members of international patients for nondisclosure of serious medical diagnoses, one we have frequently received from family members from different cultural backgrounds. These requests represent another challenge of caring for these patients as they counter our obligation for full disclosure and the patients’ right to know in order to be able to make informed decisions regarding their medical care.³

To the Editor: We read with great interest the article by Drs. Cawcutt and Wilson on caring for international patients.¹ They provide an overview of the challenges of delivering medical care for these patients (eg, cultural differences) and the likely benefits from such interactions (eg, gaining cultural knowledge). Having practiced medicine in 3 different continents and experienced working in various medical centers caring for international patients, we would like to offer a slightly different viewpoint.

First, gaining cultural knowledge should be regarded as a prerequisite for healthcare workers involved in the care of international patients, rather than the expected benefit and consequence of such encounters. Healthcare workers with some knowledge of an international patient’s culture are best able to serve that patient.² Indeed, unless knowledge of cultural differences is obtained before such interactions, there is a significant risk of stereotyping by amplifying the sense of “otherness,” which is unfortunately too often mistaken for cultural sensitivity. The perception of the stereotypes and prejudices during the second stage of cultural adaptation (ie, irritation, hostility) often stems from the host’s lack of cultural knowledge. Table 1 of their article clearly reflects such risk: the authors have tried to exemplify the concepts they discussed through a number of real-life scenarios. But indeed some of those cases (eg, the man from Saudi Arabia) could be interpreted more as examples of stereotyping than cultural sensitivity.

Second, the authors do not mention requests by family members of international patients for nondisclosure of serious medical diagnoses, one we have frequently received from family members from different cultural backgrounds. These requests represent another challenge of caring for these patients as they counter our obligation for full disclosure and the patients’ right to know in order to be able to make informed decisions regarding their medical care.³

In Reply: We appreciate the comments, and we fully agree about the dangers of blurring sensitivity and stereotyping in medicine. We also recognize that health providers working around the world have distinct backgrounds and unique perspectives, which serve to enrich the discussion.

We agree that gaining cultural knowledge should be a prerequisite for healthcare workers. However, healthcare providers may not uniformly have the opportunity, time, or resources for this training. Additionally, providers working in large group practices including referral and academic medical centers often do not have control over scheduling of patient appointments. Therefore, rather than prohibiting the evaluations of international patients, we advocate for the utilization of a few guiding and common principles to optimize a mutually beneficial patient care experience. Despite inherent inadequacies and potential prejudices, healthcare providers do learn through patient encounters. Within this learning environment, mistakes will be made, but there are also opportunities for further self-improvement.

We agree there is a fine line between sensitivity and stereotyping, along with common misunderstandings regarding patient labeling. Identifying the geographic homeland of a patient could be misconstrued as intent to stereotype patients. However, numerous infectious diseases and many noncommunicable syndromes are disproportionately represented within select countries. Thus, we feel the identification of a patient’s homeland along with ethnicity, age, gender, and pertinent socioeconomic details can be done respectfully and remain an important collective part of the active medical history and serve to optimize care for each patient. Within medical education, we often find ourselves generalizing patient presentations and symptom profiles. 

Yet we must recognize that the generalized concepts cannot apply to everyone. Medicine remains a profession of humility—both in our willingness to consider additional diagnoses and in our openness to care for patients of different backgrounds. With this humility, we hope to avoid the pitfalls of patient stereotyping, misjudgments, and misunderstandings.

Finally, the nondisclosure of serious medical diagnoses at the request of family members can be a tricky issue. It can be most difficult to balance unique wishes of a family with the ethics of accurate patient communication and compliance with legal statutes and medical center policies. We advocate a team approach with family members of international patients as a way to avoid breaches in medical ethics or breaks in mutual family trust. 

In Reply: We appreciate the comments, and we fully agree about the dangers of blurring sensitivity and stereotyping in medicine. We also recognize that health providers working around the world have distinct backgrounds and unique perspectives, which serve to enrich the discussion.

We agree that gaining cultural knowledge should be a prerequisite for healthcare workers. However, healthcare providers may not uniformly have the opportunity, time, or resources for this training. Additionally, providers working in large group practices including referral and academic medical centers often do not have control over scheduling of patient appointments. Therefore, rather than prohibiting the evaluations of international patients, we advocate for the utilization of a few guiding and common principles to optimize a mutually beneficial patient care experience. Despite inherent inadequacies and potential prejudices, healthcare providers do learn through patient encounters. Within this learning environment, mistakes will be made, but there are also opportunities for further self-improvement.

We agree there is a fine line between sensitivity and stereotyping, along with common misunderstandings regarding patient labeling. Identifying the geographic homeland of a patient could be misconstrued as intent to stereotype patients. However, numerous infectious diseases and many noncommunicable syndromes are disproportionately represented within select countries. Thus, we feel the identification of a patient’s homeland along with ethnicity, age, gender, and pertinent socioeconomic details can be done respectfully and remain an important collective part of the active medical history and serve to optimize care for each patient. Within medical education, we often find ourselves generalizing patient presentations and symptom profiles. 

Yet we must recognize that the generalized concepts cannot apply to everyone. Medicine remains a profession of humility—both in our willingness to consider additional diagnoses and in our openness to care for patients of different backgrounds. With this humility, we hope to avoid the pitfalls of patient stereotyping, misjudgments, and misunderstandings.

Finally, the nondisclosure of serious medical diagnoses at the request of family members can be a tricky issue. It can be most difficult to balance unique wishes of a family with the ethics of accurate patient communication and compliance with legal statutes and medical center policies. We advocate a team approach with family members of international patients as a way to avoid breaches in medical ethics or breaks in mutual family trust. 

In Reply: We appreciate the comments, and we fully agree about the dangers of blurring sensitivity and stereotyping in medicine. We also recognize that health providers working around the world have distinct backgrounds and unique perspectives, which serve to enrich the discussion.

We agree that gaining cultural knowledge should be a prerequisite for healthcare workers. However, healthcare providers may not uniformly have the opportunity, time, or resources for this training. Additionally, providers working in large group practices including referral and academic medical centers often do not have control over scheduling of patient appointments. Therefore, rather than prohibiting the evaluations of international patients, we advocate for the utilization of a few guiding and common principles to optimize a mutually beneficial patient care experience. Despite inherent inadequacies and potential prejudices, healthcare providers do learn through patient encounters. Within this learning environment, mistakes will be made, but there are also opportunities for further self-improvement.

We agree there is a fine line between sensitivity and stereotyping, along with common misunderstandings regarding patient labeling. Identifying the geographic homeland of a patient could be misconstrued as intent to stereotype patients. However, numerous infectious diseases and many noncommunicable syndromes are disproportionately represented within select countries. Thus, we feel the identification of a patient’s homeland along with ethnicity, age, gender, and pertinent socioeconomic details can be done respectfully and remain an important collective part of the active medical history and serve to optimize care for each patient. Within medical education, we often find ourselves generalizing patient presentations and symptom profiles. 

Yet we must recognize that the generalized concepts cannot apply to everyone. Medicine remains a profession of humility—both in our willingness to consider additional diagnoses and in our openness to care for patients of different backgrounds. With this humility, we hope to avoid the pitfalls of patient stereotyping, misjudgments, and misunderstandings.

Finally, the nondisclosure of serious medical diagnoses at the request of family members can be a tricky issue. It can be most difficult to balance unique wishes of a family with the ethics of accurate patient communication and compliance with legal statutes and medical center policies. We advocate a team approach with family members of international patients as a way to avoid breaches in medical ethics or breaks in mutual family trust. 

To the Editor: In their article “A patient with altered mental status and an acid-base disturbance,”¹ Drs. Shylaja Mani and Gregory W. Rutecki state that 5-oxoproline or pyroglutamic acidosis is associated with an elevated osmol gap. This is not the case. The cited reference by Tan et al² describes a patient who most likely had ketoacidosis, perhaps complicated by isopropyl alcohol ingestion.

Those disorders can certainly generate an osmol gap. Although pyroglutamic acidosis was mentioned in the differential diagnosis of that case, that condition was never documented. The accumulation of 5-oxoproline or pyroglutamic acid should not elevate the serum osmolality or generate an osmol gap.

To the Editor: In their article “A patient with altered mental status and an acid-base disturbance,”¹ Drs. Shylaja Mani and Gregory W. Rutecki state that 5-oxoproline or pyroglutamic acidosis is associated with an elevated osmol gap. This is not the case. The cited reference by Tan et al² describes a patient who most likely had ketoacidosis, perhaps complicated by isopropyl alcohol ingestion.

Those disorders can certainly generate an osmol gap. Although pyroglutamic acidosis was mentioned in the differential diagnosis of that case, that condition was never documented. The accumulation of 5-oxoproline or pyroglutamic acid should not elevate the serum osmolality or generate an osmol gap.

To the Editor: In their article “A patient with altered mental status and an acid-base disturbance,”¹ Drs. Shylaja Mani and Gregory W. Rutecki state that 5-oxoproline or pyroglutamic acidosis is associated with an elevated osmol gap. This is not the case. The cited reference by Tan et al² describes a patient who most likely had ketoacidosis, perhaps complicated by isopropyl alcohol ingestion.

Those disorders can certainly generate an osmol gap. Although pyroglutamic acidosis was mentioned in the differential diagnosis of that case, that condition was never documented. The accumulation of 5-oxoproline or pyroglutamic acid should not elevate the serum osmolality or generate an osmol gap.

In Reply: We thank Dr. Emmett for his insightful comment. He is correct that in the case reported by Tan et al the elevated osmol gap was not a direct result of the patient’s presumed acetaminophen ingestion but more likely another unidentified toxic ingestion. The online version of our article has been modified accordingly (also see page 214 of this issue).

In Reply: We thank Dr. Emmett for his insightful comment. He is correct that in the case reported by Tan et al the elevated osmol gap was not a direct result of the patient’s presumed acetaminophen ingestion but more likely another unidentified toxic ingestion. The online version of our article has been modified accordingly (also see page 214 of this issue).

In Reply: We thank Dr. Emmett for his insightful comment. He is correct that in the case reported by Tan et al the elevated osmol gap was not a direct result of the patient’s presumed acetaminophen ingestion but more likely another unidentified toxic ingestion. The online version of our article has been modified accordingly (also see page 214 of this issue).

In the article “A patient with altered mental status and an acid-base disturbance” (Mani S, Rutecki GW, Cleve Clin J Med 2017; 84:27–34), 2 errors occurred in Table 2. The corrected table appears with corrections shown in red:

In addition, two sentences in the text regarding the osmol gap should be revised as follows:

On page 31, the last 3 lines should read as follows: “When the anion gap metabolic acidosis is multifactorial, as it was suspected to be in a case reported by Tan et al,²³ the osmol gap may be elevated as a consequence of additional toxic ingestions, as it was in the reported patient.”

And on page 33, the last sentence should read as follows: “As reflected in the revisions to MUD PILES and in the newer GOLD MARK acronym, the osmol gap has become more valuable in differential diagnosis of metabolic acidosis with an elevated anion gap consequent to an expanding array of toxic ingestions (methanol, propylene glycol, ethylene glycol, and diethylene glycol), which may accompany pyroglutamic acid-oxoproline.”

In the article “A patient with altered mental status and an acid-base disturbance” (Mani S, Rutecki GW, Cleve Clin J Med 2017; 84:27–34), 2 errors occurred in Table 2. The corrected table appears with corrections shown in red:

In addition, two sentences in the text regarding the osmol gap should be revised as follows:

On page 31, the last 3 lines should read as follows: “When the anion gap metabolic acidosis is multifactorial, as it was suspected to be in a case reported by Tan et al,²³ the osmol gap may be elevated as a consequence of additional toxic ingestions, as it was in the reported patient.”

And on page 33, the last sentence should read as follows: “As reflected in the revisions to MUD PILES and in the newer GOLD MARK acronym, the osmol gap has become more valuable in differential diagnosis of metabolic acidosis with an elevated anion gap consequent to an expanding array of toxic ingestions (methanol, propylene glycol, ethylene glycol, and diethylene glycol), which may accompany pyroglutamic acid-oxoproline.”

In the article “A patient with altered mental status and an acid-base disturbance” (Mani S, Rutecki GW, Cleve Clin J Med 2017; 84:27–34), 2 errors occurred in Table 2. The corrected table appears with corrections shown in red:

In addition, two sentences in the text regarding the osmol gap should be revised as follows:

On page 31, the last 3 lines should read as follows: “When the anion gap metabolic acidosis is multifactorial, as it was suspected to be in a case reported by Tan et al,²³ the osmol gap may be elevated as a consequence of additional toxic ingestions, as it was in the reported patient.”

And on page 33, the last sentence should read as follows: “As reflected in the revisions to MUD PILES and in the newer GOLD MARK acronym, the osmol gap has become more valuable in differential diagnosis of metabolic acidosis with an elevated anion gap consequent to an expanding array of toxic ingestions (methanol, propylene glycol, ethylene glycol, and diethylene glycol), which may accompany pyroglutamic acid-oxoproline.”

In the article, “Cardiopulmonary exercise testing: A contemporary and versatile clinical tool” (Leclerc K, Cleve Clin J Med 2017; 84:161–168), an error occurred in Table 1. Heart rate reserve was defined as maximum heart rate minus resting heart rate. It should be defined as (maximum heart rate minus resting heart rate) divided by (predicted maximum heart rate minus resting heart rate).

In the article, “Cardiopulmonary exercise testing: A contemporary and versatile clinical tool” (Leclerc K, Cleve Clin J Med 2017; 84:161–168), an error occurred in Table 1. Heart rate reserve was defined as maximum heart rate minus resting heart rate. It should be defined as (maximum heart rate minus resting heart rate) divided by (predicted maximum heart rate minus resting heart rate).

In the article, “Cardiopulmonary exercise testing: A contemporary and versatile clinical tool” (Leclerc K, Cleve Clin J Med 2017; 84:161–168), an error occurred in Table 1. Heart rate reserve was defined as maximum heart rate minus resting heart rate. It should be defined as (maximum heart rate minus resting heart rate) divided by (predicted maximum heart rate minus resting heart rate).

Flexibility and choice were key themes in the health care reform vision President Trump outlined in his first speech to a joint session of Congress on Feb. 28.

Specifically, Americans should be able to “purchase their own coverage through the use of tax credits and expanded health savings accounts, but it must be the plan they want, not the plan forced on them by our government,” Mr. Trump said. They also should be able to purchase insurance across state lines, which “will create a truly competitive national marketplace that will bring costs way down and provide far better care.”

Courtesy whitehouse.gov

Finally, Mr. Trump called for “legal reforms that protect patients and doctors from unnecessary costs that drive up the price of insurance and work to bring down the artificially high price of drugs and bring them down immediately,” he said, adding that the Food and Drug Administration needs to slash the time to approval for drugs and other medical treatments.

Some of these concepts were mirrored in a talking-points memo from the House Republican leadership earlier in February.

According to the memo, Republican efforts to repeal and replace the ACA will focus on the following areas:

• Repealing the ACA’s Medicaid expansion and allowing states to choose between block grands or per capita grants for Medicaid funding. States could choose to use those grants and per capita grants to keep expansion.

• Rebranding high-risk pools as “state innovation grants” to provide states with flexibility to design coverage that meets the needs of their populations. States could use the innovation grants to reduce patient out-of-pocket costs, lower the cost of providing care, stabilize the individual and small-group markets, provide access to preventive care, and promote participation in private health care plans.

• Promoting health savings accounts tied to high-deductible plans through increasing maximum contribution limits and other administrative fixes to allow for greater flexibility in their use.

• Replacing ACA premium subsides with refundable flat tax credits. Credit would be age-based, with younger recipients receiving smaller credits and older taxpayers being eligible for more. Tax credits would be available to those who are not eligible to receive coverage through other sources, such as an employer or government program.

Many of these provisions were included in a health reform plan known as A Better Way, which was announced in June 2016 by House Speaker Paul Ryan (R-Wis.).

Like Mr. Trump’s outline to Congress, the GOP talking-points memo was light on specifics, including how the bill will be paid for, how much money will be distributed to states for Medicaid, and how these provisions would alter current insurance coverage rates, which government actuaries project would reach 91.5% by 2025 under current law.

The GOP talking-points memo followed a Feb. 10 discussion draft that included the legislative language required to implement these concepts and allowed insurers to charge higher premiums to people with coverage lapses; repealed a number of taxes imposed on insurers, pharmaceutical companies, and device manufacturers; eliminated many of the ACA’s essential benefits; and ended tax penalties on companies that do not provide coverage to their employees.

This proposal, however, is already running into opposition from House Republicans, with reports stating that blocks of Republicans would not approve of the provisions.

It also could run aground in the Senate, where Sen. Lamar Alexander (R-Tenn.), chairman of the Committee on Health, Education, Labor, and Pensions, has expressed his intent to tackle heath care reform in pieces (public programs, the individual market, and employer market) to avoid getting bogged down in one overarching piece of legislation.

Getting Republicans on the same page is going to be a huge hurdle to get any legislation passed long before it comes down to trying to secure any Democratic votes to help pass any replacement legislation.

As former House Speaker John Boehner told physicians and health care IT leaders at the HIMSS annual conference on Feb. 23, “In the 25 years that I served in the Unites States Congress, Republicans never ever one time agreed on what a health care proposal should look like. Not once. … If you repeal without replace, anything that happens is your fault. You broke it. … If you pass repeal without replace, you’ll never pass replace because they will never ever agree on what the [replacement] bill should be.”

gtwachtman@frontlinemedcom.com
 

Flexibility and choice were key themes in the health care reform vision President Trump outlined in his first speech to a joint session of Congress on Feb. 28.

Specifically, Americans should be able to “purchase their own coverage through the use of tax credits and expanded health savings accounts, but it must be the plan they want, not the plan forced on them by our government,” Mr. Trump said. They also should be able to purchase insurance across state lines, which “will create a truly competitive national marketplace that will bring costs way down and provide far better care.”

Courtesy whitehouse.gov

Finally, Mr. Trump called for “legal reforms that protect patients and doctors from unnecessary costs that drive up the price of insurance and work to bring down the artificially high price of drugs and bring them down immediately,” he said, adding that the Food and Drug Administration needs to slash the time to approval for drugs and other medical treatments.

Some of these concepts were mirrored in a talking-points memo from the House Republican leadership earlier in February.

According to the memo, Republican efforts to repeal and replace the ACA will focus on the following areas:

• Repealing the ACA’s Medicaid expansion and allowing states to choose between block grands or per capita grants for Medicaid funding. States could choose to use those grants and per capita grants to keep expansion.

• Rebranding high-risk pools as “state innovation grants” to provide states with flexibility to design coverage that meets the needs of their populations. States could use the innovation grants to reduce patient out-of-pocket costs, lower the cost of providing care, stabilize the individual and small-group markets, provide access to preventive care, and promote participation in private health care plans.

• Promoting health savings accounts tied to high-deductible plans through increasing maximum contribution limits and other administrative fixes to allow for greater flexibility in their use.

• Replacing ACA premium subsides with refundable flat tax credits. Credit would be age-based, with younger recipients receiving smaller credits and older taxpayers being eligible for more. Tax credits would be available to those who are not eligible to receive coverage through other sources, such as an employer or government program.

Many of these provisions were included in a health reform plan known as A Better Way, which was announced in June 2016 by House Speaker Paul Ryan (R-Wis.).

Like Mr. Trump’s outline to Congress, the GOP talking-points memo was light on specifics, including how the bill will be paid for, how much money will be distributed to states for Medicaid, and how these provisions would alter current insurance coverage rates, which government actuaries project would reach 91.5% by 2025 under current law.

The GOP talking-points memo followed a Feb. 10 discussion draft that included the legislative language required to implement these concepts and allowed insurers to charge higher premiums to people with coverage lapses; repealed a number of taxes imposed on insurers, pharmaceutical companies, and device manufacturers; eliminated many of the ACA’s essential benefits; and ended tax penalties on companies that do not provide coverage to their employees.

This proposal, however, is already running into opposition from House Republicans, with reports stating that blocks of Republicans would not approve of the provisions.

It also could run aground in the Senate, where Sen. Lamar Alexander (R-Tenn.), chairman of the Committee on Health, Education, Labor, and Pensions, has expressed his intent to tackle heath care reform in pieces (public programs, the individual market, and employer market) to avoid getting bogged down in one overarching piece of legislation.

Getting Republicans on the same page is going to be a huge hurdle to get any legislation passed long before it comes down to trying to secure any Democratic votes to help pass any replacement legislation.

As former House Speaker John Boehner told physicians and health care IT leaders at the HIMSS annual conference on Feb. 23, “In the 25 years that I served in the Unites States Congress, Republicans never ever one time agreed on what a health care proposal should look like. Not once. … If you repeal without replace, anything that happens is your fault. You broke it. … If you pass repeal without replace, you’ll never pass replace because they will never ever agree on what the [replacement] bill should be.”

gtwachtman@frontlinemedcom.com
 

Flexibility and choice were key themes in the health care reform vision President Trump outlined in his first speech to a joint session of Congress on Feb. 28.

Specifically, Americans should be able to “purchase their own coverage through the use of tax credits and expanded health savings accounts, but it must be the plan they want, not the plan forced on them by our government,” Mr. Trump said. They also should be able to purchase insurance across state lines, which “will create a truly competitive national marketplace that will bring costs way down and provide far better care.”

Courtesy whitehouse.gov

Finally, Mr. Trump called for “legal reforms that protect patients and doctors from unnecessary costs that drive up the price of insurance and work to bring down the artificially high price of drugs and bring them down immediately,” he said, adding that the Food and Drug Administration needs to slash the time to approval for drugs and other medical treatments.

Some of these concepts were mirrored in a talking-points memo from the House Republican leadership earlier in February.

According to the memo, Republican efforts to repeal and replace the ACA will focus on the following areas:

• Repealing the ACA’s Medicaid expansion and allowing states to choose between block grands or per capita grants for Medicaid funding. States could choose to use those grants and per capita grants to keep expansion.

• Rebranding high-risk pools as “state innovation grants” to provide states with flexibility to design coverage that meets the needs of their populations. States could use the innovation grants to reduce patient out-of-pocket costs, lower the cost of providing care, stabilize the individual and small-group markets, provide access to preventive care, and promote participation in private health care plans.

• Promoting health savings accounts tied to high-deductible plans through increasing maximum contribution limits and other administrative fixes to allow for greater flexibility in their use.

• Replacing ACA premium subsides with refundable flat tax credits. Credit would be age-based, with younger recipients receiving smaller credits and older taxpayers being eligible for more. Tax credits would be available to those who are not eligible to receive coverage through other sources, such as an employer or government program.

Many of these provisions were included in a health reform plan known as A Better Way, which was announced in June 2016 by House Speaker Paul Ryan (R-Wis.).

Like Mr. Trump’s outline to Congress, the GOP talking-points memo was light on specifics, including how the bill will be paid for, how much money will be distributed to states for Medicaid, and how these provisions would alter current insurance coverage rates, which government actuaries project would reach 91.5% by 2025 under current law.

The GOP talking-points memo followed a Feb. 10 discussion draft that included the legislative language required to implement these concepts and allowed insurers to charge higher premiums to people with coverage lapses; repealed a number of taxes imposed on insurers, pharmaceutical companies, and device manufacturers; eliminated many of the ACA’s essential benefits; and ended tax penalties on companies that do not provide coverage to their employees.

This proposal, however, is already running into opposition from House Republicans, with reports stating that blocks of Republicans would not approve of the provisions.

It also could run aground in the Senate, where Sen. Lamar Alexander (R-Tenn.), chairman of the Committee on Health, Education, Labor, and Pensions, has expressed his intent to tackle heath care reform in pieces (public programs, the individual market, and employer market) to avoid getting bogged down in one overarching piece of legislation.

Getting Republicans on the same page is going to be a huge hurdle to get any legislation passed long before it comes down to trying to secure any Democratic votes to help pass any replacement legislation.

As former House Speaker John Boehner told physicians and health care IT leaders at the HIMSS annual conference on Feb. 23, “In the 25 years that I served in the Unites States Congress, Republicans never ever one time agreed on what a health care proposal should look like. Not once. … If you repeal without replace, anything that happens is your fault. You broke it. … If you pass repeal without replace, you’ll never pass replace because they will never ever agree on what the [replacement] bill should be.”

gtwachtman@frontlinemedcom.com
 

Because of a spate of mumps outbreaks over the last decade, adding a third dose of the mumps vaccine to the currently standard two-dose series was debated during a meeting of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices (ACIP).

“Data [on recent outbreaks] were presented to ACIP in 2012, and ACIP determined that the data were insufficient to recommend for or against the use of a third dose of MMR vaccine for mumps outbreak control,” explained Mona Marin, MD, of the CDC’s National Center for Immunization and Respiratory Diseases. “Subsequently, CDC issued guidance for consideration for use of a third dose in specifically identified target populations, along with criteria for public health departments to consider for decision-making. That includes settings with high two-dose coverage, intense exposure, and ongoing transmission.”

Steve Mann/thinkstock

dchitnis@frontlinemedcom.com

Because of a spate of mumps outbreaks over the last decade, adding a third dose of the mumps vaccine to the currently standard two-dose series was debated during a meeting of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices (ACIP).

“Data [on recent outbreaks] were presented to ACIP in 2012, and ACIP determined that the data were insufficient to recommend for or against the use of a third dose of MMR vaccine for mumps outbreak control,” explained Mona Marin, MD, of the CDC’s National Center for Immunization and Respiratory Diseases. “Subsequently, CDC issued guidance for consideration for use of a third dose in specifically identified target populations, along with criteria for public health departments to consider for decision-making. That includes settings with high two-dose coverage, intense exposure, and ongoing transmission.”

Steve Mann/thinkstock

dchitnis@frontlinemedcom.com

Because of a spate of mumps outbreaks over the last decade, adding a third dose of the mumps vaccine to the currently standard two-dose series was debated during a meeting of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices (ACIP).

“Data [on recent outbreaks] were presented to ACIP in 2012, and ACIP determined that the data were insufficient to recommend for or against the use of a third dose of MMR vaccine for mumps outbreak control,” explained Mona Marin, MD, of the CDC’s National Center for Immunization and Respiratory Diseases. “Subsequently, CDC issued guidance for consideration for use of a third dose in specifically identified target populations, along with criteria for public health departments to consider for decision-making. That includes settings with high two-dose coverage, intense exposure, and ongoing transmission.”

Steve Mann/thinkstock

dchitnis@frontlinemedcom.com