Clinical Review

The author reports no financial relationships relevant to this article.

CASE: No relief, despite multiple therapies

A 20-year-old woman is referred to your practice for evaluation of persistent dyspareunia. She describes the pain as “excruciating” and reports that it occurs with attempted penile insertion.

Her symptoms began 1 year ago when she noted some postcoital soreness at the introitus, as well as external dysuria. The symptoms have become so pronounced that she now avoids sexual intercourse altogether. She experiences similar pain when she inserts a tampon, wears tight jeans, or rides a bicycle. She has no history of recurrent vaginitis.

So far, she has tried, sequentially, topical steroids, vitamin D ointment, topical gabapentin, and oral amitriptyline—without improvement.

What is the differential diagnosis? And what can you do to ease her pain?

Although vulvar pain has many causes, women who have a chronic vulvar pain syndrome generally fall into one of three diagnostic categories (i.e., McKay’s patterns):

• cyclic vulvovaginal candidiasis
• vestibulitis
• essential vulvodynia.¹

In this case, the diagnosis is vestibulitis, which is marked by focal erythema and, in some cases, focal erosion at the junction of the hymen and vestibule. Clinical findings in women who have vestibulitis are often subtle, but can be detected with careful examination.

This article outlines the diagnosis and management of vestibulitis and essential vulvodynia, including a basic classification of vulvar pain (TABLE). In the process, it also sheds light on the tricky diagnosis of cyclic vulvovaginal candidiasis, which can provoke vestibulitis in some cases.

A careful history, focused physical examination of the vulva and vagina, and microscopy of the vaginal secretions are the foundation of diagnosis of any vulvar pain syndrome.

TABLE

How vulvar pain is classified

Generalized Involvement of the entire vulva Provoked (sexual contact, nonsexual contact, or both) Unprovoked (spontaneous) Mixed (provoked and unprovoked)
Localized Involvement of a portion, or component, of the vulva, e.g., vestibulodynia, clitorodynia, hemivulvodynia, etc. Provoked (sexual contact, nonsexual contact, or both) Unprovoked Mixed (provoked or unprovoked)
International Society for the Study of Vulvar Diseases13

Anatomy of the vulva

The first step in adopting a practical approach to vulvar pain is developing familiarity with vulvar anatomy. I find it useful to divide the vulvovaginal anatomy into three discrete areas:

• vulva
• vestibule
• vagina.

The vulvar integument is keratinized and contains hair follicles and apocrine glands. The epithelium of the vestibule, on the other hand, is similar to the buccal mucosa: nonkeratinized and usually moist, with no adnexal structures. This highly innervated area extends from the hymenal ring to Hart’s line (FIGURE 1) and is the primary site of concern in women who have a vulvar pain syndrome.

The vagina begins at the hymenal ring and extends proximally to the cervix. The vagina is uniformly normal in patients who complain of chronic vulvar pain unless yeast vaginitis is one of the causes.

Cyclic vulvovaginitis can lead to dyspareunia

Women who have cyclic vulvovaginal candidiasis initially complain of symptoms of yeast vaginitis, e.g., vulvovaginal itching and a cheesy white vaginal discharge. Most women experience infrequent episodes of yeast vaginitis, but those who have cyclic candidiasis relapse after a short course of topical or systemic antifungal therapy. When they relapse, they tend to experience mild irritative symptoms and de novo entry dyspareunia.

Many of these women will have been treated with intermittent antifungal medication and antibiotics because their clinician assumed that a bacterial infection was present when the antifungal therapy did not solve the problem. Another challenge in evaluating these women is the inability of point-of-care testing to guide the diagnosis—or the omission of such testing altogether.

The basic profile of these patients remains the same, however: relapsing introital symptoms that are relatively mild but lead to worsening entry dyspareunia, a sign of vestibulitis. The patient may also report postcoital soreness and burning after micturition when the urine drops onto the vestibule (“splash dysuria”). These symptoms may reflect the presence of small vestibular fissures.

 

Evaluation can be tricky

The key to evaluation of a patient with these complaints is to schedule her appointment once she has been off therapy for at least 2 weeks and has not used any intravaginal medication during that interval. This drug holiday serves two functions:

• It eliminates adverse reactions to medications from the differential diagnosis.
• It allows adequate evaluation of vaginal secretions, including a reliable vaginal culture for Candida species.

During this initial encounter, the exam may well be normal. Ask the patient to grade her vulvovaginal symptoms on a scale of 0 to 10, with 10 representing the worst symptoms experienced and 0 being a complete lack of symptoms. Many patients at the initial encounter will grade their symptoms as minimal, in the range of 2 to 3 out of 10.

If the exam is normal, ask the patient to return for a repeat evaluation when her symptoms reach 8 or greater on the 10-point scale, and instruct her not to self-treat with a topical or systemic antimicrobial. When she returns, vulvovaginal candidiasis can usually be diagnosed by microscopy and confirmed by vaginal yeast culture to rule out non-albicans Candida. Patients who have recurrent vulvovaginal candidiasis tend to flare premenstrually.

Treatment may be lengthy

Treatment of cyclic vulvovaginal candidiasis involves an initial course of oral fluconazole (150 mg every 3 days for three doses), followed by suppressive therapy with weekly fluconazole (150 mg).² This treatment is effective in more than 90% of cases, easing the cyclicity of the patient’s symptoms. However, she may be left with some residual vestibulitis and discomfort with coitus, which may take as long as 2 months to resolve. Biweekly application of a topical steroid of modest strength may help, such as triamcinalone 0.1% ointment.

Vestibulitis is most common among young women

Women who have vestibulitis tend to be premenopausal and young—typically, in their 20s. They usually complain of worsening pain with coitus, as well as pain with tampon insertion and tenderness when riding a bike or wearing tight jeans, suggesting that touch to the vestibule provokes the pain.

Despite these other symptoms, however, it is the inability to have vaginal sexual intercourse that usually brings the patient to the physician. I generally ask a simple question: “If you did not engage in sexual intercourse, would you be normal?” In other words, would she avoid the pain if she avoided touch to the vestibule? Patients who have vestibulitis inevitably answer, “Yes!”

“The eye doesn’t see what the mind doesn’t know”

This caveat is important as you examine the patient (FIGURE 1). When vestibulitis is present, clinical findings are often subtle; careful examination, however, can elicit the source of the tenderness. Inspect the vulvar vestibule carefully circumferentially, and exert pressure at the junction of the hymen and vestibule using a moistened cotton swab.

As I mentioned earlier, women who have vestibulitis have evidence of focal erythema and, sometimes, focal erosion at the junction of the hymen and vestibule. They also experience exquisite tenderness as the cotton swab presses against this junction, with the pain most intense in the 3 to 9 o’clock region. Yeast vaginitis should be ruled out by microscopy and yeast culture.

Most patients have avoided coitus for some time before they see a physician, so vestibular fissures may not be obvious. The diagnosis of vestibulitis can be based on Friedrich’s criteria:

• severe pain at the vestibule upon touch or attempted vaginal entry
• tenderness to pressure localized within the vulvar vestibule
• physical findings confined to vestibular erythema of various degrees.³

FIGURE 1 Physical findings may be subtle

When vestibulitis is suspected, look for areas of erythema or fissuring at the junction of the hymen and vestibule and explore the entire vestibule out to Hart’s line.

Medical therapy is ineffective

Vestibulitis is a disease that renders the vestibular epithelium less resilient and more susceptible to fissures upon contact. For this reason, medical therapy is ineffective.

Although a 6-week trial of a topical steroid (triamcinalone 0.1% or desoximetasone 0.25% ointment twice daily) is commonly prescribed, it is rare for a patient to have a response sufficient to restore pain-free coitus.⁴

Some patients are adept at applying topical 5% xylocaine ointment to the vestibule 15 to 30 minutes before coitus to ease the discomfort associated with intercourse. Another alternative is injection of interferon into the vestibule, which can limit the percentage of patients who require vestibulectomy by almost 50%. However, interferon must be injected into the vestibule three times weekly for 4 weeks.⁵ Side effects include the pain of the needlestick and systemic fever and flu-like illness from the interferon.

 

Vestibulectomy is the treatment of choice

Multiple studies suggest 61% to 94% improvement or cure after vestibulectomy.⁶ A key predictor of surgical failure is constant vulvar pain in addition to pain with coitus.⁷ Such patients should probably be managed by an expert.

Before deciding on vestibulectomy, confirm that the patient has had persistent symptoms for more than 6 months. The reason? Spontaneous remission does sometimes occur within the first 6 months of vestibulitis.

In the OR, after induction of anesthesia, apply downward and lateral pressure to the posterior fourchette to bring small fissures to light. Vestibulectomy entails removal of the hymen and vestibular skin out to Hart’s line. This usually means removal of all of the vestibule except the part just lateral to the urethral meatus (FIGURE 2).

Once this tissue is removed, mobilize the vaginal epithelium, as in posterior colporrhaphy, and advance it to cover the surgical defect.

FIGURE 2 Excision of the vestibule

Vestibulectomy involves removal of the entire vestibule except the part just lateral to the urethral meatus.

Postoperative immobilization is required

After surgery, the patient should expect to be somewhat immobilized for 2 weeks and to require narcotic analgesia during this time. Healing should be apparent by 6 postoperative weeks, but the suture line at the introitus may still be slightly tender. I usually recommend that the patient avoid coitus until the 3-month postoperative visit. At this visit, the introitus should no longer be tender. If this is the case, the patient can be given the green light for coitus.

In older women, look for genital atrophy

Postmenopausal women are remaining sexually active in ever-increasing numbers. When dyspareunia occurs in this population, the cause is usually genital atrophy. Long-term treatment with systemic or topical estrogen will usually ease coital pain. Surgery is not a mainstay of treatment of dyspareunia in postmenopausal women. (For more on this population, see “Postmenopausal dyspareunia: A problem for the 21st century,” by Alan Altman, MD, in the March 2009 issue of OBG Management at www.obgmanagement.com.)

Essential vulvodynia is more common among older women

Women who have essential (dysesthetic) vulvodynia tend to be older and postmenopausal, although premenopausal women are sometimes affected. These women complain of chronic, unremitting, diffuse vulvar burning that is usually not limited to the vestibule. They may have similar symptoms in the region of the urethra and rectum. In general, dyspareunia is not a major problem.

In women who have essential vulvodynia, the pelvic examination is absolutely normal other than the presence of mild genital atrophy in the postmenopausal patient. There is no evidence of provoked tenderness and no focal erythema or erosion.

Treatment is medical

Women who have essential vulvodynia are not candidates for surgery. Optimal treatment of this neuralgia entails the use of low-dosage amitriptyline (25 to 50 mg nightly) or other antidepressants (e.g., venlafaxine, sertraline, duloxetine).⁸ I prefer low-dosage sertraline (25 mg daily) because it has a low incidence of side effects at this dosage.

Less is more in the pharmacotherapeutic management of essential vulvodynia. Women who do not respond to a lower dosage tend not to respond to a higher one, either.

Another option is gabapentin. It usually is administered orally but was recently studied in a topical formulation, both of which appear to be effective.^9,10

Counsel the patient that improvement, not cure, is the therapeutic goal with these drugs and that her response will be gradual, with improvement usually noticed after 2 weeks of therapy, continuing until her 6-week revisit. At that time, the dosage can be maintained or increased, depending on the patient’s response. If the patient is happy with that response, treatment should continue for 4 months, at which point she can be weaned from therapy. Relapse is uncommon.

CASE: OUTCOME

Upon examination, the patient exhibits focal erythema at the junction of the hymen and vestibule. Palpation of these areas with a moist cotton swab causes extreme tenderness, recreating the patient’s introital pain. Microscopy of the vaginal secretions is normal, and a vaginal yeast culture is negative.

Because she is an excellent candidate for vestibulectomy, the patient undergoes resection of the vulvar vestibule from the hymenal ring to Hart’s line, from the 1 o’clock to 11 o’clock positions, and recovers slowly.

At her 6-week postoperative checkup, the surgical site is healed but tender. At her 3-month visit, the introitus is no longer tender, erythema has resolved, and she resumes coital activity.

The author reports no financial relationships relevant to this article.

CASE: No relief, despite multiple therapies

A 20-year-old woman is referred to your practice for evaluation of persistent dyspareunia. She describes the pain as “excruciating” and reports that it occurs with attempted penile insertion.

Her symptoms began 1 year ago when she noted some postcoital soreness at the introitus, as well as external dysuria. The symptoms have become so pronounced that she now avoids sexual intercourse altogether. She experiences similar pain when she inserts a tampon, wears tight jeans, or rides a bicycle. She has no history of recurrent vaginitis.

So far, she has tried, sequentially, topical steroids, vitamin D ointment, topical gabapentin, and oral amitriptyline—without improvement.

What is the differential diagnosis? And what can you do to ease her pain?

Although vulvar pain has many causes, women who have a chronic vulvar pain syndrome generally fall into one of three diagnostic categories (i.e., McKay’s patterns):

• cyclic vulvovaginal candidiasis
• vestibulitis
• essential vulvodynia.¹

In this case, the diagnosis is vestibulitis, which is marked by focal erythema and, in some cases, focal erosion at the junction of the hymen and vestibule. Clinical findings in women who have vestibulitis are often subtle, but can be detected with careful examination.

This article outlines the diagnosis and management of vestibulitis and essential vulvodynia, including a basic classification of vulvar pain (TABLE). In the process, it also sheds light on the tricky diagnosis of cyclic vulvovaginal candidiasis, which can provoke vestibulitis in some cases.

A careful history, focused physical examination of the vulva and vagina, and microscopy of the vaginal secretions are the foundation of diagnosis of any vulvar pain syndrome.

TABLE

How vulvar pain is classified

Generalized Involvement of the entire vulva Provoked (sexual contact, nonsexual contact, or both) Unprovoked (spontaneous) Mixed (provoked and unprovoked)
Localized Involvement of a portion, or component, of the vulva, e.g., vestibulodynia, clitorodynia, hemivulvodynia, etc. Provoked (sexual contact, nonsexual contact, or both) Unprovoked Mixed (provoked or unprovoked)
International Society for the Study of Vulvar Diseases13

Anatomy of the vulva

The first step in adopting a practical approach to vulvar pain is developing familiarity with vulvar anatomy. I find it useful to divide the vulvovaginal anatomy into three discrete areas:

• vulva
• vestibule
• vagina.

The vulvar integument is keratinized and contains hair follicles and apocrine glands. The epithelium of the vestibule, on the other hand, is similar to the buccal mucosa: nonkeratinized and usually moist, with no adnexal structures. This highly innervated area extends from the hymenal ring to Hart’s line (FIGURE 1) and is the primary site of concern in women who have a vulvar pain syndrome.

The vagina begins at the hymenal ring and extends proximally to the cervix. The vagina is uniformly normal in patients who complain of chronic vulvar pain unless yeast vaginitis is one of the causes.

Cyclic vulvovaginitis can lead to dyspareunia

Women who have cyclic vulvovaginal candidiasis initially complain of symptoms of yeast vaginitis, e.g., vulvovaginal itching and a cheesy white vaginal discharge. Most women experience infrequent episodes of yeast vaginitis, but those who have cyclic candidiasis relapse after a short course of topical or systemic antifungal therapy. When they relapse, they tend to experience mild irritative symptoms and de novo entry dyspareunia.

Many of these women will have been treated with intermittent antifungal medication and antibiotics because their clinician assumed that a bacterial infection was present when the antifungal therapy did not solve the problem. Another challenge in evaluating these women is the inability of point-of-care testing to guide the diagnosis—or the omission of such testing altogether.

The basic profile of these patients remains the same, however: relapsing introital symptoms that are relatively mild but lead to worsening entry dyspareunia, a sign of vestibulitis. The patient may also report postcoital soreness and burning after micturition when the urine drops onto the vestibule (“splash dysuria”). These symptoms may reflect the presence of small vestibular fissures.

 

Evaluation can be tricky

The key to evaluation of a patient with these complaints is to schedule her appointment once she has been off therapy for at least 2 weeks and has not used any intravaginal medication during that interval. This drug holiday serves two functions:

• It eliminates adverse reactions to medications from the differential diagnosis.
• It allows adequate evaluation of vaginal secretions, including a reliable vaginal culture for Candida species.

During this initial encounter, the exam may well be normal. Ask the patient to grade her vulvovaginal symptoms on a scale of 0 to 10, with 10 representing the worst symptoms experienced and 0 being a complete lack of symptoms. Many patients at the initial encounter will grade their symptoms as minimal, in the range of 2 to 3 out of 10.

If the exam is normal, ask the patient to return for a repeat evaluation when her symptoms reach 8 or greater on the 10-point scale, and instruct her not to self-treat with a topical or systemic antimicrobial. When she returns, vulvovaginal candidiasis can usually be diagnosed by microscopy and confirmed by vaginal yeast culture to rule out non-albicans Candida. Patients who have recurrent vulvovaginal candidiasis tend to flare premenstrually.

Treatment may be lengthy

Treatment of cyclic vulvovaginal candidiasis involves an initial course of oral fluconazole (150 mg every 3 days for three doses), followed by suppressive therapy with weekly fluconazole (150 mg).² This treatment is effective in more than 90% of cases, easing the cyclicity of the patient’s symptoms. However, she may be left with some residual vestibulitis and discomfort with coitus, which may take as long as 2 months to resolve. Biweekly application of a topical steroid of modest strength may help, such as triamcinalone 0.1% ointment.

Vestibulitis is most common among young women

Women who have vestibulitis tend to be premenopausal and young—typically, in their 20s. They usually complain of worsening pain with coitus, as well as pain with tampon insertion and tenderness when riding a bike or wearing tight jeans, suggesting that touch to the vestibule provokes the pain.

Despite these other symptoms, however, it is the inability to have vaginal sexual intercourse that usually brings the patient to the physician. I generally ask a simple question: “If you did not engage in sexual intercourse, would you be normal?” In other words, would she avoid the pain if she avoided touch to the vestibule? Patients who have vestibulitis inevitably answer, “Yes!”

“The eye doesn’t see what the mind doesn’t know”

This caveat is important as you examine the patient (FIGURE 1). When vestibulitis is present, clinical findings are often subtle; careful examination, however, can elicit the source of the tenderness. Inspect the vulvar vestibule carefully circumferentially, and exert pressure at the junction of the hymen and vestibule using a moistened cotton swab.

As I mentioned earlier, women who have vestibulitis have evidence of focal erythema and, sometimes, focal erosion at the junction of the hymen and vestibule. They also experience exquisite tenderness as the cotton swab presses against this junction, with the pain most intense in the 3 to 9 o’clock region. Yeast vaginitis should be ruled out by microscopy and yeast culture.

Most patients have avoided coitus for some time before they see a physician, so vestibular fissures may not be obvious. The diagnosis of vestibulitis can be based on Friedrich’s criteria:

• severe pain at the vestibule upon touch or attempted vaginal entry
• tenderness to pressure localized within the vulvar vestibule
• physical findings confined to vestibular erythema of various degrees.³

FIGURE 1 Physical findings may be subtle

When vestibulitis is suspected, look for areas of erythema or fissuring at the junction of the hymen and vestibule and explore the entire vestibule out to Hart’s line.

Medical therapy is ineffective

Vestibulitis is a disease that renders the vestibular epithelium less resilient and more susceptible to fissures upon contact. For this reason, medical therapy is ineffective.

Although a 6-week trial of a topical steroid (triamcinalone 0.1% or desoximetasone 0.25% ointment twice daily) is commonly prescribed, it is rare for a patient to have a response sufficient to restore pain-free coitus.⁴

Some patients are adept at applying topical 5% xylocaine ointment to the vestibule 15 to 30 minutes before coitus to ease the discomfort associated with intercourse. Another alternative is injection of interferon into the vestibule, which can limit the percentage of patients who require vestibulectomy by almost 50%. However, interferon must be injected into the vestibule three times weekly for 4 weeks.⁵ Side effects include the pain of the needlestick and systemic fever and flu-like illness from the interferon.

 

Vestibulectomy is the treatment of choice

Multiple studies suggest 61% to 94% improvement or cure after vestibulectomy.⁶ A key predictor of surgical failure is constant vulvar pain in addition to pain with coitus.⁷ Such patients should probably be managed by an expert.

Before deciding on vestibulectomy, confirm that the patient has had persistent symptoms for more than 6 months. The reason? Spontaneous remission does sometimes occur within the first 6 months of vestibulitis.

In the OR, after induction of anesthesia, apply downward and lateral pressure to the posterior fourchette to bring small fissures to light. Vestibulectomy entails removal of the hymen and vestibular skin out to Hart’s line. This usually means removal of all of the vestibule except the part just lateral to the urethral meatus (FIGURE 2).

Once this tissue is removed, mobilize the vaginal epithelium, as in posterior colporrhaphy, and advance it to cover the surgical defect.

FIGURE 2 Excision of the vestibule

Vestibulectomy involves removal of the entire vestibule except the part just lateral to the urethral meatus.

Postoperative immobilization is required

After surgery, the patient should expect to be somewhat immobilized for 2 weeks and to require narcotic analgesia during this time. Healing should be apparent by 6 postoperative weeks, but the suture line at the introitus may still be slightly tender. I usually recommend that the patient avoid coitus until the 3-month postoperative visit. At this visit, the introitus should no longer be tender. If this is the case, the patient can be given the green light for coitus.

In older women, look for genital atrophy

Postmenopausal women are remaining sexually active in ever-increasing numbers. When dyspareunia occurs in this population, the cause is usually genital atrophy. Long-term treatment with systemic or topical estrogen will usually ease coital pain. Surgery is not a mainstay of treatment of dyspareunia in postmenopausal women. (For more on this population, see “Postmenopausal dyspareunia: A problem for the 21st century,” by Alan Altman, MD, in the March 2009 issue of OBG Management at www.obgmanagement.com.)

Essential vulvodynia is more common among older women

Women who have essential (dysesthetic) vulvodynia tend to be older and postmenopausal, although premenopausal women are sometimes affected. These women complain of chronic, unremitting, diffuse vulvar burning that is usually not limited to the vestibule. They may have similar symptoms in the region of the urethra and rectum. In general, dyspareunia is not a major problem.

In women who have essential vulvodynia, the pelvic examination is absolutely normal other than the presence of mild genital atrophy in the postmenopausal patient. There is no evidence of provoked tenderness and no focal erythema or erosion.

Treatment is medical

Women who have essential vulvodynia are not candidates for surgery. Optimal treatment of this neuralgia entails the use of low-dosage amitriptyline (25 to 50 mg nightly) or other antidepressants (e.g., venlafaxine, sertraline, duloxetine).⁸ I prefer low-dosage sertraline (25 mg daily) because it has a low incidence of side effects at this dosage.

Less is more in the pharmacotherapeutic management of essential vulvodynia. Women who do not respond to a lower dosage tend not to respond to a higher one, either.

Another option is gabapentin. It usually is administered orally but was recently studied in a topical formulation, both of which appear to be effective.^9,10

Counsel the patient that improvement, not cure, is the therapeutic goal with these drugs and that her response will be gradual, with improvement usually noticed after 2 weeks of therapy, continuing until her 6-week revisit. At that time, the dosage can be maintained or increased, depending on the patient’s response. If the patient is happy with that response, treatment should continue for 4 months, at which point she can be weaned from therapy. Relapse is uncommon.

CASE: OUTCOME

Upon examination, the patient exhibits focal erythema at the junction of the hymen and vestibule. Palpation of these areas with a moist cotton swab causes extreme tenderness, recreating the patient’s introital pain. Microscopy of the vaginal secretions is normal, and a vaginal yeast culture is negative.

Because she is an excellent candidate for vestibulectomy, the patient undergoes resection of the vulvar vestibule from the hymenal ring to Hart’s line, from the 1 o’clock to 11 o’clock positions, and recovers slowly.

At her 6-week postoperative checkup, the surgical site is healed but tender. At her 3-month visit, the introitus is no longer tender, erythema has resolved, and she resumes coital activity.

The author reports no financial relationships relevant to this article.

CASE: No relief, despite multiple therapies

A 20-year-old woman is referred to your practice for evaluation of persistent dyspareunia. She describes the pain as “excruciating” and reports that it occurs with attempted penile insertion.

Her symptoms began 1 year ago when she noted some postcoital soreness at the introitus, as well as external dysuria. The symptoms have become so pronounced that she now avoids sexual intercourse altogether. She experiences similar pain when she inserts a tampon, wears tight jeans, or rides a bicycle. She has no history of recurrent vaginitis.

So far, she has tried, sequentially, topical steroids, vitamin D ointment, topical gabapentin, and oral amitriptyline—without improvement.

What is the differential diagnosis? And what can you do to ease her pain?

Although vulvar pain has many causes, women who have a chronic vulvar pain syndrome generally fall into one of three diagnostic categories (i.e., McKay’s patterns):

• cyclic vulvovaginal candidiasis
• vestibulitis
• essential vulvodynia.¹

In this case, the diagnosis is vestibulitis, which is marked by focal erythema and, in some cases, focal erosion at the junction of the hymen and vestibule. Clinical findings in women who have vestibulitis are often subtle, but can be detected with careful examination.

This article outlines the diagnosis and management of vestibulitis and essential vulvodynia, including a basic classification of vulvar pain (TABLE). In the process, it also sheds light on the tricky diagnosis of cyclic vulvovaginal candidiasis, which can provoke vestibulitis in some cases.

A careful history, focused physical examination of the vulva and vagina, and microscopy of the vaginal secretions are the foundation of diagnosis of any vulvar pain syndrome.

TABLE

How vulvar pain is classified

Generalized Involvement of the entire vulva Provoked (sexual contact, nonsexual contact, or both) Unprovoked (spontaneous) Mixed (provoked and unprovoked)
Localized Involvement of a portion, or component, of the vulva, e.g., vestibulodynia, clitorodynia, hemivulvodynia, etc. Provoked (sexual contact, nonsexual contact, or both) Unprovoked Mixed (provoked or unprovoked)
International Society for the Study of Vulvar Diseases13

Anatomy of the vulva

The first step in adopting a practical approach to vulvar pain is developing familiarity with vulvar anatomy. I find it useful to divide the vulvovaginal anatomy into three discrete areas:

• vulva
• vestibule
• vagina.

The vulvar integument is keratinized and contains hair follicles and apocrine glands. The epithelium of the vestibule, on the other hand, is similar to the buccal mucosa: nonkeratinized and usually moist, with no adnexal structures. This highly innervated area extends from the hymenal ring to Hart’s line (FIGURE 1) and is the primary site of concern in women who have a vulvar pain syndrome.

The vagina begins at the hymenal ring and extends proximally to the cervix. The vagina is uniformly normal in patients who complain of chronic vulvar pain unless yeast vaginitis is one of the causes.

Cyclic vulvovaginitis can lead to dyspareunia

Women who have cyclic vulvovaginal candidiasis initially complain of symptoms of yeast vaginitis, e.g., vulvovaginal itching and a cheesy white vaginal discharge. Most women experience infrequent episodes of yeast vaginitis, but those who have cyclic candidiasis relapse after a short course of topical or systemic antifungal therapy. When they relapse, they tend to experience mild irritative symptoms and de novo entry dyspareunia.

Many of these women will have been treated with intermittent antifungal medication and antibiotics because their clinician assumed that a bacterial infection was present when the antifungal therapy did not solve the problem. Another challenge in evaluating these women is the inability of point-of-care testing to guide the diagnosis—or the omission of such testing altogether.

The basic profile of these patients remains the same, however: relapsing introital symptoms that are relatively mild but lead to worsening entry dyspareunia, a sign of vestibulitis. The patient may also report postcoital soreness and burning after micturition when the urine drops onto the vestibule (“splash dysuria”). These symptoms may reflect the presence of small vestibular fissures.

 

Evaluation can be tricky

The key to evaluation of a patient with these complaints is to schedule her appointment once she has been off therapy for at least 2 weeks and has not used any intravaginal medication during that interval. This drug holiday serves two functions:

• It eliminates adverse reactions to medications from the differential diagnosis.
• It allows adequate evaluation of vaginal secretions, including a reliable vaginal culture for Candida species.

During this initial encounter, the exam may well be normal. Ask the patient to grade her vulvovaginal symptoms on a scale of 0 to 10, with 10 representing the worst symptoms experienced and 0 being a complete lack of symptoms. Many patients at the initial encounter will grade their symptoms as minimal, in the range of 2 to 3 out of 10.

If the exam is normal, ask the patient to return for a repeat evaluation when her symptoms reach 8 or greater on the 10-point scale, and instruct her not to self-treat with a topical or systemic antimicrobial. When she returns, vulvovaginal candidiasis can usually be diagnosed by microscopy and confirmed by vaginal yeast culture to rule out non-albicans Candida. Patients who have recurrent vulvovaginal candidiasis tend to flare premenstrually.

Treatment may be lengthy

Treatment of cyclic vulvovaginal candidiasis involves an initial course of oral fluconazole (150 mg every 3 days for three doses), followed by suppressive therapy with weekly fluconazole (150 mg).² This treatment is effective in more than 90% of cases, easing the cyclicity of the patient’s symptoms. However, she may be left with some residual vestibulitis and discomfort with coitus, which may take as long as 2 months to resolve. Biweekly application of a topical steroid of modest strength may help, such as triamcinalone 0.1% ointment.

Vestibulitis is most common among young women

Women who have vestibulitis tend to be premenopausal and young—typically, in their 20s. They usually complain of worsening pain with coitus, as well as pain with tampon insertion and tenderness when riding a bike or wearing tight jeans, suggesting that touch to the vestibule provokes the pain.

Despite these other symptoms, however, it is the inability to have vaginal sexual intercourse that usually brings the patient to the physician. I generally ask a simple question: “If you did not engage in sexual intercourse, would you be normal?” In other words, would she avoid the pain if she avoided touch to the vestibule? Patients who have vestibulitis inevitably answer, “Yes!”

“The eye doesn’t see what the mind doesn’t know”

This caveat is important as you examine the patient (FIGURE 1). When vestibulitis is present, clinical findings are often subtle; careful examination, however, can elicit the source of the tenderness. Inspect the vulvar vestibule carefully circumferentially, and exert pressure at the junction of the hymen and vestibule using a moistened cotton swab.

As I mentioned earlier, women who have vestibulitis have evidence of focal erythema and, sometimes, focal erosion at the junction of the hymen and vestibule. They also experience exquisite tenderness as the cotton swab presses against this junction, with the pain most intense in the 3 to 9 o’clock region. Yeast vaginitis should be ruled out by microscopy and yeast culture.

Most patients have avoided coitus for some time before they see a physician, so vestibular fissures may not be obvious. The diagnosis of vestibulitis can be based on Friedrich’s criteria:

• severe pain at the vestibule upon touch or attempted vaginal entry
• tenderness to pressure localized within the vulvar vestibule
• physical findings confined to vestibular erythema of various degrees.³

FIGURE 1 Physical findings may be subtle

When vestibulitis is suspected, look for areas of erythema or fissuring at the junction of the hymen and vestibule and explore the entire vestibule out to Hart’s line.

Medical therapy is ineffective

Vestibulitis is a disease that renders the vestibular epithelium less resilient and more susceptible to fissures upon contact. For this reason, medical therapy is ineffective.

Although a 6-week trial of a topical steroid (triamcinalone 0.1% or desoximetasone 0.25% ointment twice daily) is commonly prescribed, it is rare for a patient to have a response sufficient to restore pain-free coitus.⁴

Some patients are adept at applying topical 5% xylocaine ointment to the vestibule 15 to 30 minutes before coitus to ease the discomfort associated with intercourse. Another alternative is injection of interferon into the vestibule, which can limit the percentage of patients who require vestibulectomy by almost 50%. However, interferon must be injected into the vestibule three times weekly for 4 weeks.⁵ Side effects include the pain of the needlestick and systemic fever and flu-like illness from the interferon.

 

Vestibulectomy is the treatment of choice

Multiple studies suggest 61% to 94% improvement or cure after vestibulectomy.⁶ A key predictor of surgical failure is constant vulvar pain in addition to pain with coitus.⁷ Such patients should probably be managed by an expert.

Before deciding on vestibulectomy, confirm that the patient has had persistent symptoms for more than 6 months. The reason? Spontaneous remission does sometimes occur within the first 6 months of vestibulitis.

In the OR, after induction of anesthesia, apply downward and lateral pressure to the posterior fourchette to bring small fissures to light. Vestibulectomy entails removal of the hymen and vestibular skin out to Hart’s line. This usually means removal of all of the vestibule except the part just lateral to the urethral meatus (FIGURE 2).

Once this tissue is removed, mobilize the vaginal epithelium, as in posterior colporrhaphy, and advance it to cover the surgical defect.

FIGURE 2 Excision of the vestibule

Vestibulectomy involves removal of the entire vestibule except the part just lateral to the urethral meatus.

Postoperative immobilization is required

After surgery, the patient should expect to be somewhat immobilized for 2 weeks and to require narcotic analgesia during this time. Healing should be apparent by 6 postoperative weeks, but the suture line at the introitus may still be slightly tender. I usually recommend that the patient avoid coitus until the 3-month postoperative visit. At this visit, the introitus should no longer be tender. If this is the case, the patient can be given the green light for coitus.

In older women, look for genital atrophy

Postmenopausal women are remaining sexually active in ever-increasing numbers. When dyspareunia occurs in this population, the cause is usually genital atrophy. Long-term treatment with systemic or topical estrogen will usually ease coital pain. Surgery is not a mainstay of treatment of dyspareunia in postmenopausal women. (For more on this population, see “Postmenopausal dyspareunia: A problem for the 21st century,” by Alan Altman, MD, in the March 2009 issue of OBG Management at www.obgmanagement.com.)

Essential vulvodynia is more common among older women

Women who have essential (dysesthetic) vulvodynia tend to be older and postmenopausal, although premenopausal women are sometimes affected. These women complain of chronic, unremitting, diffuse vulvar burning that is usually not limited to the vestibule. They may have similar symptoms in the region of the urethra and rectum. In general, dyspareunia is not a major problem.

In women who have essential vulvodynia, the pelvic examination is absolutely normal other than the presence of mild genital atrophy in the postmenopausal patient. There is no evidence of provoked tenderness and no focal erythema or erosion.

Treatment is medical

Women who have essential vulvodynia are not candidates for surgery. Optimal treatment of this neuralgia entails the use of low-dosage amitriptyline (25 to 50 mg nightly) or other antidepressants (e.g., venlafaxine, sertraline, duloxetine).⁸ I prefer low-dosage sertraline (25 mg daily) because it has a low incidence of side effects at this dosage.

Less is more in the pharmacotherapeutic management of essential vulvodynia. Women who do not respond to a lower dosage tend not to respond to a higher one, either.

Another option is gabapentin. It usually is administered orally but was recently studied in a topical formulation, both of which appear to be effective.^9,10

Counsel the patient that improvement, not cure, is the therapeutic goal with these drugs and that her response will be gradual, with improvement usually noticed after 2 weeks of therapy, continuing until her 6-week revisit. At that time, the dosage can be maintained or increased, depending on the patient’s response. If the patient is happy with that response, treatment should continue for 4 months, at which point she can be weaned from therapy. Relapse is uncommon.

CASE: OUTCOME

Upon examination, the patient exhibits focal erythema at the junction of the hymen and vestibule. Palpation of these areas with a moist cotton swab causes extreme tenderness, recreating the patient’s introital pain. Microscopy of the vaginal secretions is normal, and a vaginal yeast culture is negative.

Because she is an excellent candidate for vestibulectomy, the patient undergoes resection of the vulvar vestibule from the hymenal ring to Hart’s line, from the 1 o’clock to 11 o’clock positions, and recovers slowly.

At her 6-week postoperative checkup, the surgical site is healed but tender. At her 3-month visit, the introitus is no longer tender, erythema has resolved, and she resumes coital activity.

The author reports that he is President and Chief Executive Officer of digiChart, Inc., which develops, sells, and supports digiChart OB-GYN, an electronic health record specific to ObGyn practice.

It’s no longer news—this past February 17, President Barack Obama signed a $787 billion economic stimulus package—the American Recovery and Reinvestment Act of 2009—into law.^1,2 But did you know that, of the approximately $150 billion in the Act allocated for health care, $19.2 billion is for healthcare information technology, including $17 billion earmarked for incentive payments to hospitals and physicians for adopting electronic health records (EHR)?

In 2004, President George W. Bush set a goal of having a majority of US physicians using EHR within 10 years. But the march to get there has been at a snail’s pace: By July 2008, only 13% of physicians were using a basic EHR system and barely a third of those adopters—that’s only 4% percent of all physicians—had an extensive, fully functional EHR.³

The stimulus legislation dangles a carrot in front of providers for using EHR, but that’s not all the news: In the near future, the Act will also begin wielding a stick. Here’s an explanation of the situation, and how your practice may benefit—or be pinched—if you see Medicare or Medicaid patients.

First, what isn’t true

Sorry—contrary to the belief (and expectations) of many physicians, the Federal government isn’t going to pay for your purchase of an EHR system. Instead, an incentive payment will be made to physicians who have demonstrated “meaningful use” of a certified EHR. But what does that mean?

First, only one EHR certifying body is recognized today: CCHIT, the Certification Commission for Healthcare Information Technology. It’s unclear what certification standards the Office of the National Coordinator for Health Information Technology (ONCHIT)—an agency of the US Department of Health and Human Services (HHS)—will set for the future.

Second, under current standards of the Act, “meaningful use” comprises three functions of an EHR application:

• e-prescribing that meets the standards of HHS
  
• connectivity to other providers for full access to a patient’s history
  
• the ability to report the use of technology to HHS.⁴
  

The incentive is based on the percentage of Medicare and Medicaid patients who receive care from a recipient physician. A physician who accepts Medicare assignment for her (his) patients can receive an incentive as high as $44,000 over 5 years. Physicians who provide care to Medicaid patients that represents more than 30% of their practice can receive as much as $64,000, again, over 5 years.^4,5 See “Key dates and calculations for the Federal EHR incentive.”

What does this mean for your practice?

 

If you do not see Medicare patients, or if fewer than 30% of your patients are Medicaid patients, there is no rush to adopt EHR: You won’t receive any stimulus money for doing so. But if you do meet either of those qualifying criteria, there is urgency—you will lose money by delaying. For a practice that receives $44,000 in stimulus money because it qualifies under Medicare ($64,000 under Medicaid), that incentive will off set much of the cost of adopting EHR.

But such economic urgency begs the question, in my opinion. Today, EHR applications can streamline the workflow and operations of a practice. They can improve the quality of the care that you provide, return at least three times the cost of ownership (in my experience, working with numerous medical practices that use EHR), and calm the frenetic pace of your working day. Applications are robust, turning a practice “paperless” over 18 to 24 months.

The Bush baton is passed to Obama. Stand clear!

There’s no doubt: The Obama administration intends to realize the goal set by President George W. Bush to drive near-universal adoption of EHR by 2014.

True, little was accomplished to achieve that goal from 2004 through 2008. Why not? Was the physician community to blame? Yes, in part, because:

• many physicians were waiting—for the Federal government to pay them for their purchase of EHR or to give them a government-developed EHR
  
• Physicians are resistant to change—many insist that they are more efficient and productive in a paper-based system
  
• Physicians have claimed that EHR applications lack features that enable a “paperless” practice
  
• Physicians have complained about the expense of EHR applications.
  

Many pebbles, many ripples are likely

The Federal government won’t be the only driving force in EHR—so will academic medical centers, healthcare systems, community hospitals, and large physician networks. They’ll do so through implementation of so-called enterprise systems that are linked to private-practice EHR applications.

Last, take note that reimbursement schemes introduced by the Centers for Medicare & Medicaid Services (CMS) are quickly adopted by private insurance payers. Some physicians already see a decrease in premiums for their professional liability insurance because they use EHR.

I strongly believe that, for a number of reasons that make medical and management sense in a practice, now is the time to adopt EHR. Incentives offered by this year’s stimulus Act are just one more reason.

The author reports that he is President and Chief Executive Officer of digiChart, Inc., which develops, sells, and supports digiChart OB-GYN, an electronic health record specific to ObGyn practice.

It’s no longer news—this past February 17, President Barack Obama signed a $787 billion economic stimulus package—the American Recovery and Reinvestment Act of 2009—into law.^1,2 But did you know that, of the approximately $150 billion in the Act allocated for health care, $19.2 billion is for healthcare information technology, including $17 billion earmarked for incentive payments to hospitals and physicians for adopting electronic health records (EHR)?

In 2004, President George W. Bush set a goal of having a majority of US physicians using EHR within 10 years. But the march to get there has been at a snail’s pace: By July 2008, only 13% of physicians were using a basic EHR system and barely a third of those adopters—that’s only 4% percent of all physicians—had an extensive, fully functional EHR.³

The stimulus legislation dangles a carrot in front of providers for using EHR, but that’s not all the news: In the near future, the Act will also begin wielding a stick. Here’s an explanation of the situation, and how your practice may benefit—or be pinched—if you see Medicare or Medicaid patients.

First, what isn’t true

Sorry—contrary to the belief (and expectations) of many physicians, the Federal government isn’t going to pay for your purchase of an EHR system. Instead, an incentive payment will be made to physicians who have demonstrated “meaningful use” of a certified EHR. But what does that mean?

First, only one EHR certifying body is recognized today: CCHIT, the Certification Commission for Healthcare Information Technology. It’s unclear what certification standards the Office of the National Coordinator for Health Information Technology (ONCHIT)—an agency of the US Department of Health and Human Services (HHS)—will set for the future.

Second, under current standards of the Act, “meaningful use” comprises three functions of an EHR application:

• e-prescribing that meets the standards of HHS
  
• connectivity to other providers for full access to a patient’s history
  
• the ability to report the use of technology to HHS.⁴
  

The incentive is based on the percentage of Medicare and Medicaid patients who receive care from a recipient physician. A physician who accepts Medicare assignment for her (his) patients can receive an incentive as high as $44,000 over 5 years. Physicians who provide care to Medicaid patients that represents more than 30% of their practice can receive as much as $64,000, again, over 5 years.^4,5 See “Key dates and calculations for the Federal EHR incentive.”

What does this mean for your practice?

 

If you do not see Medicare patients, or if fewer than 30% of your patients are Medicaid patients, there is no rush to adopt EHR: You won’t receive any stimulus money for doing so. But if you do meet either of those qualifying criteria, there is urgency—you will lose money by delaying. For a practice that receives $44,000 in stimulus money because it qualifies under Medicare ($64,000 under Medicaid), that incentive will off set much of the cost of adopting EHR.

But such economic urgency begs the question, in my opinion. Today, EHR applications can streamline the workflow and operations of a practice. They can improve the quality of the care that you provide, return at least three times the cost of ownership (in my experience, working with numerous medical practices that use EHR), and calm the frenetic pace of your working day. Applications are robust, turning a practice “paperless” over 18 to 24 months.

The Bush baton is passed to Obama. Stand clear!

There’s no doubt: The Obama administration intends to realize the goal set by President George W. Bush to drive near-universal adoption of EHR by 2014.

True, little was accomplished to achieve that goal from 2004 through 2008. Why not? Was the physician community to blame? Yes, in part, because:

• many physicians were waiting—for the Federal government to pay them for their purchase of EHR or to give them a government-developed EHR
  
• Physicians are resistant to change—many insist that they are more efficient and productive in a paper-based system
  
• Physicians have claimed that EHR applications lack features that enable a “paperless” practice
  
• Physicians have complained about the expense of EHR applications.
  

Many pebbles, many ripples are likely

The Federal government won’t be the only driving force in EHR—so will academic medical centers, healthcare systems, community hospitals, and large physician networks. They’ll do so through implementation of so-called enterprise systems that are linked to private-practice EHR applications.

Last, take note that reimbursement schemes introduced by the Centers for Medicare & Medicaid Services (CMS) are quickly adopted by private insurance payers. Some physicians already see a decrease in premiums for their professional liability insurance because they use EHR.

I strongly believe that, for a number of reasons that make medical and management sense in a practice, now is the time to adopt EHR. Incentives offered by this year’s stimulus Act are just one more reason.

The author reports that he is President and Chief Executive Officer of digiChart, Inc., which develops, sells, and supports digiChart OB-GYN, an electronic health record specific to ObGyn practice.

It’s no longer news—this past February 17, President Barack Obama signed a $787 billion economic stimulus package—the American Recovery and Reinvestment Act of 2009—into law.^1,2 But did you know that, of the approximately $150 billion in the Act allocated for health care, $19.2 billion is for healthcare information technology, including $17 billion earmarked for incentive payments to hospitals and physicians for adopting electronic health records (EHR)?

In 2004, President George W. Bush set a goal of having a majority of US physicians using EHR within 10 years. But the march to get there has been at a snail’s pace: By July 2008, only 13% of physicians were using a basic EHR system and barely a third of those adopters—that’s only 4% percent of all physicians—had an extensive, fully functional EHR.³

The stimulus legislation dangles a carrot in front of providers for using EHR, but that’s not all the news: In the near future, the Act will also begin wielding a stick. Here’s an explanation of the situation, and how your practice may benefit—or be pinched—if you see Medicare or Medicaid patients.

First, what isn’t true

Sorry—contrary to the belief (and expectations) of many physicians, the Federal government isn’t going to pay for your purchase of an EHR system. Instead, an incentive payment will be made to physicians who have demonstrated “meaningful use” of a certified EHR. But what does that mean?

First, only one EHR certifying body is recognized today: CCHIT, the Certification Commission for Healthcare Information Technology. It’s unclear what certification standards the Office of the National Coordinator for Health Information Technology (ONCHIT)—an agency of the US Department of Health and Human Services (HHS)—will set for the future.

Second, under current standards of the Act, “meaningful use” comprises three functions of an EHR application:

• e-prescribing that meets the standards of HHS
  
• connectivity to other providers for full access to a patient’s history
  
• the ability to report the use of technology to HHS.⁴
  

The incentive is based on the percentage of Medicare and Medicaid patients who receive care from a recipient physician. A physician who accepts Medicare assignment for her (his) patients can receive an incentive as high as $44,000 over 5 years. Physicians who provide care to Medicaid patients that represents more than 30% of their practice can receive as much as $64,000, again, over 5 years.^4,5 See “Key dates and calculations for the Federal EHR incentive.”

What does this mean for your practice?

 

If you do not see Medicare patients, or if fewer than 30% of your patients are Medicaid patients, there is no rush to adopt EHR: You won’t receive any stimulus money for doing so. But if you do meet either of those qualifying criteria, there is urgency—you will lose money by delaying. For a practice that receives $44,000 in stimulus money because it qualifies under Medicare ($64,000 under Medicaid), that incentive will off set much of the cost of adopting EHR.

But such economic urgency begs the question, in my opinion. Today, EHR applications can streamline the workflow and operations of a practice. They can improve the quality of the care that you provide, return at least three times the cost of ownership (in my experience, working with numerous medical practices that use EHR), and calm the frenetic pace of your working day. Applications are robust, turning a practice “paperless” over 18 to 24 months.

The Bush baton is passed to Obama. Stand clear!

There’s no doubt: The Obama administration intends to realize the goal set by President George W. Bush to drive near-universal adoption of EHR by 2014.

True, little was accomplished to achieve that goal from 2004 through 2008. Why not? Was the physician community to blame? Yes, in part, because:

• many physicians were waiting—for the Federal government to pay them for their purchase of EHR or to give them a government-developed EHR
  
• Physicians are resistant to change—many insist that they are more efficient and productive in a paper-based system
  
• Physicians have claimed that EHR applications lack features that enable a “paperless” practice
  
• Physicians have complained about the expense of EHR applications.
  

Many pebbles, many ripples are likely

The Federal government won’t be the only driving force in EHR—so will academic medical centers, healthcare systems, community hospitals, and large physician networks. They’ll do so through implementation of so-called enterprise systems that are linked to private-practice EHR applications.

Last, take note that reimbursement schemes introduced by the Centers for Medicare & Medicaid Services (CMS) are quickly adopted by private insurance payers. Some physicians already see a decrease in premiums for their professional liability insurance because they use EHR.

I strongly believe that, for a number of reasons that make medical and management sense in a practice, now is the time to adopt EHR. Incentives offered by this year’s stimulus Act are just one more reason.

The author reports no financial relationships relevant to this article.

The therapeutic success of any medication depends on the interaction between its specific biochemical effects and nonspecific factors.¹ Therefore, clinical trial designers may view the placebo effect as undesirable, but it can be a valuable response that improves outcomes in medical practice. As Freud stated: “Expectation colored by hope and faith is an effective force with which we have to reckon…in all our attempts at treatment and cure.”²

This article describes how experienced clinicians make use of the placebo effect and three other powerful, nonspecific elements of successful pharmacotherapy.

The placebo effect

Any effect attributable to a pill or potion that does not originate from its specific pharmaceutical properties is known as the placebo effect.³ Its clinical value has been trivialized, in part because of misconceptions (TABLE 1). For example, the placebo effect is commonly believed to be short-lived; in fact, it can last a long time.⁴

In practice, our goal is to enhance the placebo effect to maximize a desirable therapeutic outcome (TABLE 2).⁵ Therefore, before I prescribe a medication, I tell my patient that I have selected a particular medication because I have had good results with it in many other patients and I believe it will work well for her, too.

Too often, physicians feel pessimistic about a medication’s potential therapeutic result, and communicate that pessimism. What the patient hears is: “There’s nothing else I can do for you; why not try this medication, even though I don’t believe it’s going to work.” This may create a negative placebo effect⁶—termed the “nocebo” effect— which gives the patient a negative expectation about the treatment’s outcome. The patient internalizes the physician’s statement and belief, and lives out this negative expectation.

TABLE 1

Correcting misconceptions about the placebo effect⁴

Misconception	What the evidence shows
Placebo effects are short-lived	The placebo effect has been documented to last for a long time
Only complaints of psychological origin respond to placebo	Changes after placebo have been documented for most symptoms, including those originating from somatic disease
Placebo responders and nonresponders are distinctly different	There is no difference between placebo responders and nonresponders
The placebo effect is only about one third of the total therapeutic effect	The placebo effect can be as much as 100% of the total therapeutic effect
Only about one third of the population responds to placebo	The placebo response is context-dependent, and may include more than 90% of the patient population

TABLE 2

Strategies to enhance the placebo effect⁵

Develop a sustained therapeutic partnership with the patient
Listen effectively and verify that she feels listened to
Provide comprehensible explanations of health problems therapeutically tailored to her needs and personality style
Show empathy, care, and concern for her as a person
Enhance her sense of control and mastery over her predicament

CASE 1: Predicting positive results

Mrs. A. J. is a 38-year-old mother of two. She has symptoms of anxiety and depression, crying spells, poor appetite, and insomnia.

After taking a detailed history and examination, I recommend treatment with a combination of counseling and the antidepressant mirtazapine. I tell Mrs. A. J. that this medication has very good potential to help her recover. I also inform her that improved sleep and appetite may well be the first effects she’ll experience—even accompanied by restored hope and optimism. I then give her an appointment for the following week.

When Mrs. A. J. comes for the follow-up appointment, she reports improvement in appetite, sleep, and mood—as predicted.

Even though studies of antidepressants rarely show mood improvement within the first 7 days, it is not unusual to hear patients report feeling less depressed within days after they start a new antidepressant. The drug’s specific chemical effects on the brain may not be sufficient to explain this phenomenon; the explanation for such improvement probably lies in nonspecific effects, such as the patient expecting that this medication will make her feel better. The placebo effect can occur as soon as a patient starts a medication. Experienced clinicians understand the placebo effect’s power and harness it for their patients.

Conditioned responses

Many biologic responses can be associated with visual, auditory, tactile, olfactory, and gustatory stimuli. Nonconditioned physiologic responses paired with conditioned stimuli induce the same biologic effects as a drug. Evidence supporting this phenomenon includes successful conditioning of the immune system.^7-10 Conditioned responses—as demonstrated in glycemia regulation¹⁰ and with psychopharmacology¹¹—also can enhance the desirable results of pharmacotherapy.

 

CASE 2: A soothing drink

Ms. L. G. is a 24-year-old single college student who complains of irritability, short temper, and anxiety associated with obsessive worries about her health and her studies. Her symptoms become significantly worse before her menstrual period. Repeated diagnostic workups and pelvic examinations by her ObGyn have all been unremarkable.

At the beginning of this visit, Ms. L. G. is short of breath and looks anxious and worried. The nurse offers her a cup of tea; she asks for water instead, and is asked to bring it into the consultation-therapy room.

After a comprehensive interview and mental status examination, I recommend treatment with a combination of cognitive behavior therapy (CBT) and medication. Considering Ms. L. G.’s history of treatment with other medications, we agree to start treatment with sertraline. We review the potential benefits and therapeutic expectations of alleviating her symptoms of anxiety and obsessive worries. She is also told that she can expect an improvement in mood.

I then give her a sample of 50-mg sertraline and ask her to take it right there in the office, sipping from the glass of water. As she swallows, I compliment her on her wise decision to start treatment. She thanks me for being attentive to her needs. She is instructed to call me in 1 week, even if she feels better, and report changes in her condition.

Seven days later, Ms. L. G. calls to report significant improvement in her symptoms. She reports no side effects.

Often, patients come to my office feeling thirsty. My staff or I offer them a glass of water or a cup of tea. As patients sip, they swallow and incorporate the liquid into their body. At the same time, I use verbal interventions to make them feel listened to and understood. They internalize this emotional experience in connection with swallowing the liquid.

Later, when swallowing the new medication as instructed, the patient again experiences the positive therapeutic effect that was internalized in the physician’s office.

The power of suggestion

It has been shown that the power of suggestion can positively—or negatively—affect treatment outcome.^12,13 In practice, most clinicians give unintentional suggestions by how and what they communicate to the patient.

We make predictions about the patient’s disease in terms of progress, severity of symptoms, and expected treatment outcomes, including possible side effects. The patient consciously and subconsciously internalizes these predictions, and then exhibits the outcome predicted by the medical expert. This is compatible with Watzlawick’s principle that the prediction of an event may lead to events fulfilling the prediction.¹⁴ In practice, be aware of the power in your words and body language and learn to use them wisely to enhance the positive outcome of pharmacotherapy.

CASE 3: Predicting improvement

Mrs. J. C., 48 years old, has had premenstrual dysphoric disorder (PMDD) and fibromyalgia for many years. She describes to me how specialists have tried to alleviate her depression and chronic pain. Follow-up questioning reveals that, whenever she received a new prescription, the physician would alert her to all the possible side effects and instruct her to call the office if she developed a problem with the new medication.

Invariably, Mrs. J. C. would call as instructed and describe side effects she developed with the new medication. Often, the physician would discontinue the medication, depriving her of benefits she might have obtained later.

My approach is different. Although I answer all of Mrs. J. C.’s questions about potential side effects, I also emphasize this prescription’s potential benefits—improved sleep, appetite, thoughts, and mood. I tell her she may experience improved sleep before improved mood. I then make a request: “Promise to call me by Tuesday next week, even if you begin to feel better?”

When Mrs. J. C. calls to report her status, she mentions that she is sleeping better and has begun to feel better during the day.

This vignette illustrates the importance of suggesting to the patient a positive outcome of pharmacotherapy associated with a particular action (calling the physician’s office to report results). When the patient promised to call, she internalized the suggestion that calling would be associated with feeling better—and that is what happened. Contrast that with saying to her: “Call me if you have a problem with any of these side effects,” which gives her a suggestion to report a problem.

The suggestion effect also can be used to reframe a predictable side effect as a positive sign that indicates the beginning of change leading to recovery (see “Using suggestion to reframe initial side effects as positive signs”).

 

Participatory pharmacotherapy

Many patients seek ownership in making decisions about their treatment and medications. In participatory pharmacotherapy, patients provide you with data and valuable information—family history, personal medical history, experience with treatment—and inform you about which medications worked best. You invite patients to predict how they see themselves getting better and into recovery.

Based on this information and your knowledge, training, and experience, you and the patient jointly create a treatment plan that includes tailored pharmacotherapy. The next case illustrates the use of participatory pharmacotherapy to enhance treatment.

CASE 4: All in the family

Mrs. B. R., age 52, suffers from diabetic polyneuropathy, with tingling, numbness, and pain in her legs, feet, and hands. These symptoms are associated with anxiety, sadness, and worry. A detailed history reveals that these symptoms persist even though her blood glucose level has been in the target range and she has already achieved her goal of weight control with proper diet and exercise.

Mrs. B. R. then reports to me that her cousin, who has the same diagnosis, recently started to take venlafaxine with very good results. She asks me if we can consider this medication as part of her treatment.

I compliment Mrs. B. R. for her knowledge of her condition and her cousin’s treatment results. She responds by elaborating on her readings about venlafaxine on the Web and how convinced she is that this medication will help her as it helped her cousin.

I also reassure Mrs. B. R. that, together, we will make decisions about what medications to use and what to avoid based on her experiences. Her input into this process of choosing the best medications for her is valuable and will also be considered in future situations. She smiles and thanks me for considering her suggestions.

Inviting patients to be partners in diagnosing their illness and formulating a treatment plan improves the likelihood of a successful therapeutic alliance; adherence with prescribed medication; and the best possible outcome of pharmacotherapy.

Not all patients are candidates for participatory pharmacotherapy (TABLE 3), but many respond well. Avoid medications that the patient has already found unhelpful, ineffective, or associated with intolerable side effects. If possible, choose medications that the patient associates with a positive experience or expectation, based on family and personal history.

In patients with a defiant-oppositional personality, consider framing the treatment decision as a choice between two equally efficacious medications. This gives the patient the sense of control in choosing her medication, which is jointly monitored.

Related resources See Dr. Torem’s accompanying reading list

TABLE 3

Choosing patients for participatory pharmacotherapy

Good candidates	Exclusionary qualities
Adults	Children, adolescents, and prison inmates
No history of alcoholism or drug addiction	Alcohol dependence or drug addiction
Average or above-average intelligence	Below-average intelligence
Intact cognitive function	Cognitive deficits, such as dementia
Not psychotic	Actively psychotic
Good comprehension of diagnosis and treatment	Poor comprehension of diagnosis and treatment
Therapeutic alliance is present	Therapeutic alliance is absent
Personality style or disorder with a need to be in control of treatment, such as obsessive–compulsive personality	Passive, dependent personality style or disorder (these patients may view a participatory approach as reflecting the physician’s lack of confidence)

The author reports no financial relationships relevant to this article.

The therapeutic success of any medication depends on the interaction between its specific biochemical effects and nonspecific factors.¹ Therefore, clinical trial designers may view the placebo effect as undesirable, but it can be a valuable response that improves outcomes in medical practice. As Freud stated: “Expectation colored by hope and faith is an effective force with which we have to reckon…in all our attempts at treatment and cure.”²

This article describes how experienced clinicians make use of the placebo effect and three other powerful, nonspecific elements of successful pharmacotherapy.

The placebo effect

Any effect attributable to a pill or potion that does not originate from its specific pharmaceutical properties is known as the placebo effect.³ Its clinical value has been trivialized, in part because of misconceptions (TABLE 1). For example, the placebo effect is commonly believed to be short-lived; in fact, it can last a long time.⁴

In practice, our goal is to enhance the placebo effect to maximize a desirable therapeutic outcome (TABLE 2).⁵ Therefore, before I prescribe a medication, I tell my patient that I have selected a particular medication because I have had good results with it in many other patients and I believe it will work well for her, too.

Too often, physicians feel pessimistic about a medication’s potential therapeutic result, and communicate that pessimism. What the patient hears is: “There’s nothing else I can do for you; why not try this medication, even though I don’t believe it’s going to work.” This may create a negative placebo effect⁶—termed the “nocebo” effect— which gives the patient a negative expectation about the treatment’s outcome. The patient internalizes the physician’s statement and belief, and lives out this negative expectation.

TABLE 1

Correcting misconceptions about the placebo effect⁴

Misconception	What the evidence shows
Placebo effects are short-lived	The placebo effect has been documented to last for a long time
Only complaints of psychological origin respond to placebo	Changes after placebo have been documented for most symptoms, including those originating from somatic disease
Placebo responders and nonresponders are distinctly different	There is no difference between placebo responders and nonresponders
The placebo effect is only about one third of the total therapeutic effect	The placebo effect can be as much as 100% of the total therapeutic effect
Only about one third of the population responds to placebo	The placebo response is context-dependent, and may include more than 90% of the patient population

TABLE 2

Strategies to enhance the placebo effect⁵

Develop a sustained therapeutic partnership with the patient
Listen effectively and verify that she feels listened to
Provide comprehensible explanations of health problems therapeutically tailored to her needs and personality style
Show empathy, care, and concern for her as a person
Enhance her sense of control and mastery over her predicament

CASE 1: Predicting positive results

Mrs. A. J. is a 38-year-old mother of two. She has symptoms of anxiety and depression, crying spells, poor appetite, and insomnia.

After taking a detailed history and examination, I recommend treatment with a combination of counseling and the antidepressant mirtazapine. I tell Mrs. A. J. that this medication has very good potential to help her recover. I also inform her that improved sleep and appetite may well be the first effects she’ll experience—even accompanied by restored hope and optimism. I then give her an appointment for the following week.

When Mrs. A. J. comes for the follow-up appointment, she reports improvement in appetite, sleep, and mood—as predicted.

Even though studies of antidepressants rarely show mood improvement within the first 7 days, it is not unusual to hear patients report feeling less depressed within days after they start a new antidepressant. The drug’s specific chemical effects on the brain may not be sufficient to explain this phenomenon; the explanation for such improvement probably lies in nonspecific effects, such as the patient expecting that this medication will make her feel better. The placebo effect can occur as soon as a patient starts a medication. Experienced clinicians understand the placebo effect’s power and harness it for their patients.

Conditioned responses

Many biologic responses can be associated with visual, auditory, tactile, olfactory, and gustatory stimuli. Nonconditioned physiologic responses paired with conditioned stimuli induce the same biologic effects as a drug. Evidence supporting this phenomenon includes successful conditioning of the immune system.^7-10 Conditioned responses—as demonstrated in glycemia regulation¹⁰ and with psychopharmacology¹¹—also can enhance the desirable results of pharmacotherapy.

 

CASE 2: A soothing drink

Ms. L. G. is a 24-year-old single college student who complains of irritability, short temper, and anxiety associated with obsessive worries about her health and her studies. Her symptoms become significantly worse before her menstrual period. Repeated diagnostic workups and pelvic examinations by her ObGyn have all been unremarkable.

At the beginning of this visit, Ms. L. G. is short of breath and looks anxious and worried. The nurse offers her a cup of tea; she asks for water instead, and is asked to bring it into the consultation-therapy room.

After a comprehensive interview and mental status examination, I recommend treatment with a combination of cognitive behavior therapy (CBT) and medication. Considering Ms. L. G.’s history of treatment with other medications, we agree to start treatment with sertraline. We review the potential benefits and therapeutic expectations of alleviating her symptoms of anxiety and obsessive worries. She is also told that she can expect an improvement in mood.

I then give her a sample of 50-mg sertraline and ask her to take it right there in the office, sipping from the glass of water. As she swallows, I compliment her on her wise decision to start treatment. She thanks me for being attentive to her needs. She is instructed to call me in 1 week, even if she feels better, and report changes in her condition.

Seven days later, Ms. L. G. calls to report significant improvement in her symptoms. She reports no side effects.

Often, patients come to my office feeling thirsty. My staff or I offer them a glass of water or a cup of tea. As patients sip, they swallow and incorporate the liquid into their body. At the same time, I use verbal interventions to make them feel listened to and understood. They internalize this emotional experience in connection with swallowing the liquid.

Later, when swallowing the new medication as instructed, the patient again experiences the positive therapeutic effect that was internalized in the physician’s office.

The power of suggestion

It has been shown that the power of suggestion can positively—or negatively—affect treatment outcome.^12,13 In practice, most clinicians give unintentional suggestions by how and what they communicate to the patient.

We make predictions about the patient’s disease in terms of progress, severity of symptoms, and expected treatment outcomes, including possible side effects. The patient consciously and subconsciously internalizes these predictions, and then exhibits the outcome predicted by the medical expert. This is compatible with Watzlawick’s principle that the prediction of an event may lead to events fulfilling the prediction.¹⁴ In practice, be aware of the power in your words and body language and learn to use them wisely to enhance the positive outcome of pharmacotherapy.

CASE 3: Predicting improvement

Mrs. J. C., 48 years old, has had premenstrual dysphoric disorder (PMDD) and fibromyalgia for many years. She describes to me how specialists have tried to alleviate her depression and chronic pain. Follow-up questioning reveals that, whenever she received a new prescription, the physician would alert her to all the possible side effects and instruct her to call the office if she developed a problem with the new medication.

Invariably, Mrs. J. C. would call as instructed and describe side effects she developed with the new medication. Often, the physician would discontinue the medication, depriving her of benefits she might have obtained later.

My approach is different. Although I answer all of Mrs. J. C.’s questions about potential side effects, I also emphasize this prescription’s potential benefits—improved sleep, appetite, thoughts, and mood. I tell her she may experience improved sleep before improved mood. I then make a request: “Promise to call me by Tuesday next week, even if you begin to feel better?”

When Mrs. J. C. calls to report her status, she mentions that she is sleeping better and has begun to feel better during the day.

This vignette illustrates the importance of suggesting to the patient a positive outcome of pharmacotherapy associated with a particular action (calling the physician’s office to report results). When the patient promised to call, she internalized the suggestion that calling would be associated with feeling better—and that is what happened. Contrast that with saying to her: “Call me if you have a problem with any of these side effects,” which gives her a suggestion to report a problem.

The suggestion effect also can be used to reframe a predictable side effect as a positive sign that indicates the beginning of change leading to recovery (see “Using suggestion to reframe initial side effects as positive signs”).

 

Participatory pharmacotherapy

Many patients seek ownership in making decisions about their treatment and medications. In participatory pharmacotherapy, patients provide you with data and valuable information—family history, personal medical history, experience with treatment—and inform you about which medications worked best. You invite patients to predict how they see themselves getting better and into recovery.

Based on this information and your knowledge, training, and experience, you and the patient jointly create a treatment plan that includes tailored pharmacotherapy. The next case illustrates the use of participatory pharmacotherapy to enhance treatment.

CASE 4: All in the family

Mrs. B. R., age 52, suffers from diabetic polyneuropathy, with tingling, numbness, and pain in her legs, feet, and hands. These symptoms are associated with anxiety, sadness, and worry. A detailed history reveals that these symptoms persist even though her blood glucose level has been in the target range and she has already achieved her goal of weight control with proper diet and exercise.

Mrs. B. R. then reports to me that her cousin, who has the same diagnosis, recently started to take venlafaxine with very good results. She asks me if we can consider this medication as part of her treatment.

I compliment Mrs. B. R. for her knowledge of her condition and her cousin’s treatment results. She responds by elaborating on her readings about venlafaxine on the Web and how convinced she is that this medication will help her as it helped her cousin.

I also reassure Mrs. B. R. that, together, we will make decisions about what medications to use and what to avoid based on her experiences. Her input into this process of choosing the best medications for her is valuable and will also be considered in future situations. She smiles and thanks me for considering her suggestions.

Inviting patients to be partners in diagnosing their illness and formulating a treatment plan improves the likelihood of a successful therapeutic alliance; adherence with prescribed medication; and the best possible outcome of pharmacotherapy.

Not all patients are candidates for participatory pharmacotherapy (TABLE 3), but many respond well. Avoid medications that the patient has already found unhelpful, ineffective, or associated with intolerable side effects. If possible, choose medications that the patient associates with a positive experience or expectation, based on family and personal history.

In patients with a defiant-oppositional personality, consider framing the treatment decision as a choice between two equally efficacious medications. This gives the patient the sense of control in choosing her medication, which is jointly monitored.

Related resources See Dr. Torem’s accompanying reading list

TABLE 3

Choosing patients for participatory pharmacotherapy

Good candidates	Exclusionary qualities
Adults	Children, adolescents, and prison inmates
No history of alcoholism or drug addiction	Alcohol dependence or drug addiction
Average or above-average intelligence	Below-average intelligence
Intact cognitive function	Cognitive deficits, such as dementia
Not psychotic	Actively psychotic
Good comprehension of diagnosis and treatment	Poor comprehension of diagnosis and treatment
Therapeutic alliance is present	Therapeutic alliance is absent
Personality style or disorder with a need to be in control of treatment, such as obsessive–compulsive personality	Passive, dependent personality style or disorder (these patients may view a participatory approach as reflecting the physician’s lack of confidence)

The author reports no financial relationships relevant to this article.

The therapeutic success of any medication depends on the interaction between its specific biochemical effects and nonspecific factors.¹ Therefore, clinical trial designers may view the placebo effect as undesirable, but it can be a valuable response that improves outcomes in medical practice. As Freud stated: “Expectation colored by hope and faith is an effective force with which we have to reckon…in all our attempts at treatment and cure.”²

This article describes how experienced clinicians make use of the placebo effect and three other powerful, nonspecific elements of successful pharmacotherapy.

The placebo effect

Any effect attributable to a pill or potion that does not originate from its specific pharmaceutical properties is known as the placebo effect.³ Its clinical value has been trivialized, in part because of misconceptions (TABLE 1). For example, the placebo effect is commonly believed to be short-lived; in fact, it can last a long time.⁴

In practice, our goal is to enhance the placebo effect to maximize a desirable therapeutic outcome (TABLE 2).⁵ Therefore, before I prescribe a medication, I tell my patient that I have selected a particular medication because I have had good results with it in many other patients and I believe it will work well for her, too.

Too often, physicians feel pessimistic about a medication’s potential therapeutic result, and communicate that pessimism. What the patient hears is: “There’s nothing else I can do for you; why not try this medication, even though I don’t believe it’s going to work.” This may create a negative placebo effect⁶—termed the “nocebo” effect— which gives the patient a negative expectation about the treatment’s outcome. The patient internalizes the physician’s statement and belief, and lives out this negative expectation.

TABLE 1

Correcting misconceptions about the placebo effect⁴

Misconception	What the evidence shows
Placebo effects are short-lived	The placebo effect has been documented to last for a long time
Only complaints of psychological origin respond to placebo	Changes after placebo have been documented for most symptoms, including those originating from somatic disease
Placebo responders and nonresponders are distinctly different	There is no difference between placebo responders and nonresponders
The placebo effect is only about one third of the total therapeutic effect	The placebo effect can be as much as 100% of the total therapeutic effect
Only about one third of the population responds to placebo	The placebo response is context-dependent, and may include more than 90% of the patient population

TABLE 2

Strategies to enhance the placebo effect⁵

Develop a sustained therapeutic partnership with the patient
Listen effectively and verify that she feels listened to
Provide comprehensible explanations of health problems therapeutically tailored to her needs and personality style
Show empathy, care, and concern for her as a person
Enhance her sense of control and mastery over her predicament

CASE 1: Predicting positive results

Mrs. A. J. is a 38-year-old mother of two. She has symptoms of anxiety and depression, crying spells, poor appetite, and insomnia.

After taking a detailed history and examination, I recommend treatment with a combination of counseling and the antidepressant mirtazapine. I tell Mrs. A. J. that this medication has very good potential to help her recover. I also inform her that improved sleep and appetite may well be the first effects she’ll experience—even accompanied by restored hope and optimism. I then give her an appointment for the following week.

When Mrs. A. J. comes for the follow-up appointment, she reports improvement in appetite, sleep, and mood—as predicted.

Even though studies of antidepressants rarely show mood improvement within the first 7 days, it is not unusual to hear patients report feeling less depressed within days after they start a new antidepressant. The drug’s specific chemical effects on the brain may not be sufficient to explain this phenomenon; the explanation for such improvement probably lies in nonspecific effects, such as the patient expecting that this medication will make her feel better. The placebo effect can occur as soon as a patient starts a medication. Experienced clinicians understand the placebo effect’s power and harness it for their patients.

Conditioned responses

Many biologic responses can be associated with visual, auditory, tactile, olfactory, and gustatory stimuli. Nonconditioned physiologic responses paired with conditioned stimuli induce the same biologic effects as a drug. Evidence supporting this phenomenon includes successful conditioning of the immune system.^7-10 Conditioned responses—as demonstrated in glycemia regulation¹⁰ and with psychopharmacology¹¹—also can enhance the desirable results of pharmacotherapy.

 

CASE 2: A soothing drink

Ms. L. G. is a 24-year-old single college student who complains of irritability, short temper, and anxiety associated with obsessive worries about her health and her studies. Her symptoms become significantly worse before her menstrual period. Repeated diagnostic workups and pelvic examinations by her ObGyn have all been unremarkable.

At the beginning of this visit, Ms. L. G. is short of breath and looks anxious and worried. The nurse offers her a cup of tea; she asks for water instead, and is asked to bring it into the consultation-therapy room.

After a comprehensive interview and mental status examination, I recommend treatment with a combination of cognitive behavior therapy (CBT) and medication. Considering Ms. L. G.’s history of treatment with other medications, we agree to start treatment with sertraline. We review the potential benefits and therapeutic expectations of alleviating her symptoms of anxiety and obsessive worries. She is also told that she can expect an improvement in mood.

I then give her a sample of 50-mg sertraline and ask her to take it right there in the office, sipping from the glass of water. As she swallows, I compliment her on her wise decision to start treatment. She thanks me for being attentive to her needs. She is instructed to call me in 1 week, even if she feels better, and report changes in her condition.

Seven days later, Ms. L. G. calls to report significant improvement in her symptoms. She reports no side effects.

Often, patients come to my office feeling thirsty. My staff or I offer them a glass of water or a cup of tea. As patients sip, they swallow and incorporate the liquid into their body. At the same time, I use verbal interventions to make them feel listened to and understood. They internalize this emotional experience in connection with swallowing the liquid.

Later, when swallowing the new medication as instructed, the patient again experiences the positive therapeutic effect that was internalized in the physician’s office.

The power of suggestion

It has been shown that the power of suggestion can positively—or negatively—affect treatment outcome.^12,13 In practice, most clinicians give unintentional suggestions by how and what they communicate to the patient.

We make predictions about the patient’s disease in terms of progress, severity of symptoms, and expected treatment outcomes, including possible side effects. The patient consciously and subconsciously internalizes these predictions, and then exhibits the outcome predicted by the medical expert. This is compatible with Watzlawick’s principle that the prediction of an event may lead to events fulfilling the prediction.¹⁴ In practice, be aware of the power in your words and body language and learn to use them wisely to enhance the positive outcome of pharmacotherapy.

CASE 3: Predicting improvement

Mrs. J. C., 48 years old, has had premenstrual dysphoric disorder (PMDD) and fibromyalgia for many years. She describes to me how specialists have tried to alleviate her depression and chronic pain. Follow-up questioning reveals that, whenever she received a new prescription, the physician would alert her to all the possible side effects and instruct her to call the office if she developed a problem with the new medication.

Invariably, Mrs. J. C. would call as instructed and describe side effects she developed with the new medication. Often, the physician would discontinue the medication, depriving her of benefits she might have obtained later.

My approach is different. Although I answer all of Mrs. J. C.’s questions about potential side effects, I also emphasize this prescription’s potential benefits—improved sleep, appetite, thoughts, and mood. I tell her she may experience improved sleep before improved mood. I then make a request: “Promise to call me by Tuesday next week, even if you begin to feel better?”

When Mrs. J. C. calls to report her status, she mentions that she is sleeping better and has begun to feel better during the day.

This vignette illustrates the importance of suggesting to the patient a positive outcome of pharmacotherapy associated with a particular action (calling the physician’s office to report results). When the patient promised to call, she internalized the suggestion that calling would be associated with feeling better—and that is what happened. Contrast that with saying to her: “Call me if you have a problem with any of these side effects,” which gives her a suggestion to report a problem.

The suggestion effect also can be used to reframe a predictable side effect as a positive sign that indicates the beginning of change leading to recovery (see “Using suggestion to reframe initial side effects as positive signs”).

 

Participatory pharmacotherapy

Many patients seek ownership in making decisions about their treatment and medications. In participatory pharmacotherapy, patients provide you with data and valuable information—family history, personal medical history, experience with treatment—and inform you about which medications worked best. You invite patients to predict how they see themselves getting better and into recovery.

Based on this information and your knowledge, training, and experience, you and the patient jointly create a treatment plan that includes tailored pharmacotherapy. The next case illustrates the use of participatory pharmacotherapy to enhance treatment.

CASE 4: All in the family

Mrs. B. R., age 52, suffers from diabetic polyneuropathy, with tingling, numbness, and pain in her legs, feet, and hands. These symptoms are associated with anxiety, sadness, and worry. A detailed history reveals that these symptoms persist even though her blood glucose level has been in the target range and she has already achieved her goal of weight control with proper diet and exercise.

Mrs. B. R. then reports to me that her cousin, who has the same diagnosis, recently started to take venlafaxine with very good results. She asks me if we can consider this medication as part of her treatment.

I compliment Mrs. B. R. for her knowledge of her condition and her cousin’s treatment results. She responds by elaborating on her readings about venlafaxine on the Web and how convinced she is that this medication will help her as it helped her cousin.

I also reassure Mrs. B. R. that, together, we will make decisions about what medications to use and what to avoid based on her experiences. Her input into this process of choosing the best medications for her is valuable and will also be considered in future situations. She smiles and thanks me for considering her suggestions.

Inviting patients to be partners in diagnosing their illness and formulating a treatment plan improves the likelihood of a successful therapeutic alliance; adherence with prescribed medication; and the best possible outcome of pharmacotherapy.

Not all patients are candidates for participatory pharmacotherapy (TABLE 3), but many respond well. Avoid medications that the patient has already found unhelpful, ineffective, or associated with intolerable side effects. If possible, choose medications that the patient associates with a positive experience or expectation, based on family and personal history.

In patients with a defiant-oppositional personality, consider framing the treatment decision as a choice between two equally efficacious medications. This gives the patient the sense of control in choosing her medication, which is jointly monitored.

Related resources See Dr. Torem’s accompanying reading list

TABLE 3

Choosing patients for participatory pharmacotherapy

Good candidates	Exclusionary qualities
Adults	Children, adolescents, and prison inmates
No history of alcoholism or drug addiction	Alcohol dependence or drug addiction
Average or above-average intelligence	Below-average intelligence
Intact cognitive function	Cognitive deficits, such as dementia
Not psychotic	Actively psychotic
Good comprehension of diagnosis and treatment	Poor comprehension of diagnosis and treatment
Therapeutic alliance is present	Therapeutic alliance is absent
Personality style or disorder with a need to be in control of treatment, such as obsessive–compulsive personality	Passive, dependent personality style or disorder (these patients may view a participatory approach as reflecting the physician’s lack of confidence)

Baby Boomers have transformed attitudes toward many aspects of aging. Menopause is no exception. Once a taboo topic, menopause is now openly discussed among women who seek information about vasomotor symptoms, hormones and their alternatives, and ways to maintain health as they move past midlife. ObGyns are treating more and more of these women, and fielding their many questions.

In this Update, I examine recent data on three important aspects of menopause:

• how to reduce the risk of cardiovascular disease among women who enter menopause surgically, through oophorectomy
• what to offer women who ask for nonhormonal relief from vasomotor symptoms
• a new drug on the horizon to combat osteoporosis.

Bilateral oophorectomy raises young women’s risk of cardiovascular death

Rivera CM, Grossardt BR, Rhodes DJ, et al. Increased cardiovascular mortality after early bilateral oophorectomy. Menopause. 2009;16:15–23.

Parker WH, Manson JE. Oophorectomy and cardiovascular mortality: is there a link? Menopause. 2009;16:1–2.

Cardiovascular mortality does not increase among women who undergo unilateral oophorectomy, but it does rise among women who undergo bilateral oophorectomy before 45 years of age. However, among women who initiate estrogen therapy at the time of bilateral oophorectomy and continue that therapy through at least 45 years of age, no excess cardiovascular mortality occurs.

Those are the findings of a unique retrospective cohort study performed by investigators from the Mayo Clinic. In the study, investigators reviewed the death certificates of more than 2,300 women who underwent unilateral or bilateral oophorectomy for benign disease before menopause in Olmstead County, Minnesota, from 1950 to 1987. They also followed a similar number of age-matched women for several decades.

These results support the findings of other studies that have observed that menopausal hormone therapy is associated with a lower incidence of cardiovascular death in “young” menopausal women, including those in their 50s or within one decade of the onset of menopause.^1,2

More than 500,000 women undergo bilateral oophorectomy each year in the United States, usually in association with hysterectomy for benign disease.

Induced menopause merits special attention

Spontaneous menopause is physiologic. In contrast, induced menopause (whether associated with surgery, radiation therapy, or chemotherapy) and premature ovarian failure are pathologic conditions.³ Unless they are managed appropriately, induced menopause and premature ovarian failure raise the risk of cardiovascular disease.

Since the initial findings of the Women’s Health Initiative trial of estrogen–progestin therapy were published in 2002, many women and clinicians have become wary about the use of hormone therapy, even among young women who have no ovarian function and who lack a contraindication to hormone therapy.⁴ Unless hormonal management is contraindicated, it is recommended in this setting.

In addition, Parker and Manson recommend that gynecologic surgeons who routinely perform bilateral oophorectomy at the time of hysterectomy for benign disease in premenopausal women who do not have an elevated risk of ovarian cancer should consider updating their therapeutic recommendations and, whenever possible, preserving the ovaries.

Interest in nonhormonal therapies for hot flashes remains high

Bair YA, Gold EB, Zhang G, et al. Use of complementary and alternative medicine during the menopausal transition: longitudinal results from the Study of Women’s Health Across the Nation. Menopause. 2008;15:32–43.

Butt DA, Lock M, Lewis JE, Ross S, Moineddin R. Gabapentin for the treatment of menopausal hot flashes: a randomized trial. Menopause. 2008;15:310–318.

More than three quarters of women use some type of complementary and alternative medicine (CAM) during the menopausal transition. So found a survey conducted as part of the Study of Women’s Health Across the Nation (SWAN), which involved more than 2,000 premenopausal and perimenopausal women.

More than one third of all US women use one or more forms of CAM, spending more than $600 million a year.

In the SWAN survey, Japanese and white women were significantly more likely to report use of CAM than were Chinese, African-American, and Hispanic women during menopause.

Some women use both CAM and hormones

A notable finding of this report from SWAN is that concomitant use of menopausal hormone therapy and CAM is common among symptomatic women, even though herbal therapies have not been proved to be more effective than placebo in the treatment of vasomotor symptoms.⁵

Given the high prevalence of use of CAM, ObGyns should recognize that symptomatic patients especially bothered by vasomotor symptoms may seek relief with both CAM and a prescription medication. For this reason, it is wise to ask perimenopausal and postmenopausal women to list all the remedies they use—both prescription and over the counter.

 

Gabapentin eases symptoms in some women

Along with the antidepressants paroxetine and venlafaxine, gabapentin is the most widely studied prescription agent used in the nonhormonal treatment of menopausal vasomotor symptoms.

Canadian investigators performed a double-blind, placebo-controlled trial involving 197 symptomatic, spontaneously menopausal women (age range: 45 to 65 years). Participants were randomized to gabapentin (300 mg) or placebo, given three times daily for 4 weeks.

Ten of the 99 women who were randomized to gabapentin and six of the 98 women who were randomized to placebo dropped out of the study because of adverse effects. Hot-flash scores decreased by 51% among women taking gabapentin and by 26% among women in the placebo arm (p<.001). Women who used gabapentin were significantly more likely to report dizziness, drowsiness, and unsteadiness than those who received placebo.

Despite its proven efficacy, gabapentin does not appear to equal estrogen in its ability to alleviate vasomotor symptoms. Further, gabapentin’s side-effect profile and the need for thrice-daily administration also limit its appeal. Nevertheless, symptomatic women who are interested in nonhormonal treatment may wish to consider this option.

Anti-osteoporosis arsenal may gain a new weapon

Cummings S, McClung M, Christiansen C, et al. A phase III study of the effects of denosumab on vertebral, nonvertebral, and hip fracture in women with osteoporosis: results from the FREEDOM Trial. Paper presented at: Annual Meeting of the American Society for Bone and Mineral Research; September 16, 2008; Montreal, Canada.

Miller PD, Bolognese MA, Lewiecki EM, et al; AMG Bone Loss Study Group. Effect of denosumab on bone density and turnover in postmenopausal women with low bone mass after long-term continued, discontinued, and restarting of therapy: a randomized, blinded phase 2 clinical trial. Bone. 2008;43:222–229.

In a 3-year study in which more than 7,800 women 60 to 90 years old were randomized to denosumab (60 mg) or placebo, denosumab reduced the risk of vertebral fracture by 68% and the risk of hip fracture by 40%.

FIGURE A new agent to inhibit bone resorption

RankL is a protein that controls osteoclast maturation, activity, and survival. Denosumab mimics the endogenous decoy receptor OPG to inhibit RankL and reduce osteoclast proliferation, differentiation, and function. Denosumab is a monoclonal antibody to RankL, a mediator of osteoclast function ( FIGURE ). In contrast to alendronate, which enhances trabecular bone density (e.g., that found in the spine), denosumab increases cortical (as in long bones) as well as trabecular bone density.⁶ If the agent obtains approval by the US Food and Drug Administration, it will be an important new approach to the treatment of osteoporosis in menopausal women.⁷

The drug is administered every 6 months by subcutaneous injection.

Like estrogen, denosumab has rapidly reversible effects

The trial by Miller and associates found that the effects of denosumab are rapidly reversible after discontinuation of therapy, in contrast to alendronate. As Goldstein noted in “Update on Osteoporosis” in the November 2008 issue of OBG Management, clinicians are still exploring the relationships between alendronate and osteonecrosis of the jaw and proximal femoral-shaft fracture.⁷ Only further research and surveillance will clarify the clinical pros and cons of denosumab’s swift reversibility.

Baby Boomers have transformed attitudes toward many aspects of aging. Menopause is no exception. Once a taboo topic, menopause is now openly discussed among women who seek information about vasomotor symptoms, hormones and their alternatives, and ways to maintain health as they move past midlife. ObGyns are treating more and more of these women, and fielding their many questions.

In this Update, I examine recent data on three important aspects of menopause:

• how to reduce the risk of cardiovascular disease among women who enter menopause surgically, through oophorectomy
• what to offer women who ask for nonhormonal relief from vasomotor symptoms
• a new drug on the horizon to combat osteoporosis.

Bilateral oophorectomy raises young women’s risk of cardiovascular death

Rivera CM, Grossardt BR, Rhodes DJ, et al. Increased cardiovascular mortality after early bilateral oophorectomy. Menopause. 2009;16:15–23.

Parker WH, Manson JE. Oophorectomy and cardiovascular mortality: is there a link? Menopause. 2009;16:1–2.

Cardiovascular mortality does not increase among women who undergo unilateral oophorectomy, but it does rise among women who undergo bilateral oophorectomy before 45 years of age. However, among women who initiate estrogen therapy at the time of bilateral oophorectomy and continue that therapy through at least 45 years of age, no excess cardiovascular mortality occurs.

Those are the findings of a unique retrospective cohort study performed by investigators from the Mayo Clinic. In the study, investigators reviewed the death certificates of more than 2,300 women who underwent unilateral or bilateral oophorectomy for benign disease before menopause in Olmstead County, Minnesota, from 1950 to 1987. They also followed a similar number of age-matched women for several decades.

These results support the findings of other studies that have observed that menopausal hormone therapy is associated with a lower incidence of cardiovascular death in “young” menopausal women, including those in their 50s or within one decade of the onset of menopause.^1,2

More than 500,000 women undergo bilateral oophorectomy each year in the United States, usually in association with hysterectomy for benign disease.

Induced menopause merits special attention

Spontaneous menopause is physiologic. In contrast, induced menopause (whether associated with surgery, radiation therapy, or chemotherapy) and premature ovarian failure are pathologic conditions.³ Unless they are managed appropriately, induced menopause and premature ovarian failure raise the risk of cardiovascular disease.

Since the initial findings of the Women’s Health Initiative trial of estrogen–progestin therapy were published in 2002, many women and clinicians have become wary about the use of hormone therapy, even among young women who have no ovarian function and who lack a contraindication to hormone therapy.⁴ Unless hormonal management is contraindicated, it is recommended in this setting.

In addition, Parker and Manson recommend that gynecologic surgeons who routinely perform bilateral oophorectomy at the time of hysterectomy for benign disease in premenopausal women who do not have an elevated risk of ovarian cancer should consider updating their therapeutic recommendations and, whenever possible, preserving the ovaries.

Interest in nonhormonal therapies for hot flashes remains high

Bair YA, Gold EB, Zhang G, et al. Use of complementary and alternative medicine during the menopausal transition: longitudinal results from the Study of Women’s Health Across the Nation. Menopause. 2008;15:32–43.

Butt DA, Lock M, Lewis JE, Ross S, Moineddin R. Gabapentin for the treatment of menopausal hot flashes: a randomized trial. Menopause. 2008;15:310–318.

More than three quarters of women use some type of complementary and alternative medicine (CAM) during the menopausal transition. So found a survey conducted as part of the Study of Women’s Health Across the Nation (SWAN), which involved more than 2,000 premenopausal and perimenopausal women.

More than one third of all US women use one or more forms of CAM, spending more than $600 million a year.

In the SWAN survey, Japanese and white women were significantly more likely to report use of CAM than were Chinese, African-American, and Hispanic women during menopause.

Some women use both CAM and hormones

A notable finding of this report from SWAN is that concomitant use of menopausal hormone therapy and CAM is common among symptomatic women, even though herbal therapies have not been proved to be more effective than placebo in the treatment of vasomotor symptoms.⁵

Given the high prevalence of use of CAM, ObGyns should recognize that symptomatic patients especially bothered by vasomotor symptoms may seek relief with both CAM and a prescription medication. For this reason, it is wise to ask perimenopausal and postmenopausal women to list all the remedies they use—both prescription and over the counter.

 

Gabapentin eases symptoms in some women

Along with the antidepressants paroxetine and venlafaxine, gabapentin is the most widely studied prescription agent used in the nonhormonal treatment of menopausal vasomotor symptoms.

Canadian investigators performed a double-blind, placebo-controlled trial involving 197 symptomatic, spontaneously menopausal women (age range: 45 to 65 years). Participants were randomized to gabapentin (300 mg) or placebo, given three times daily for 4 weeks.

Ten of the 99 women who were randomized to gabapentin and six of the 98 women who were randomized to placebo dropped out of the study because of adverse effects. Hot-flash scores decreased by 51% among women taking gabapentin and by 26% among women in the placebo arm (p<.001). Women who used gabapentin were significantly more likely to report dizziness, drowsiness, and unsteadiness than those who received placebo.

Despite its proven efficacy, gabapentin does not appear to equal estrogen in its ability to alleviate vasomotor symptoms. Further, gabapentin’s side-effect profile and the need for thrice-daily administration also limit its appeal. Nevertheless, symptomatic women who are interested in nonhormonal treatment may wish to consider this option.

Anti-osteoporosis arsenal may gain a new weapon

Cummings S, McClung M, Christiansen C, et al. A phase III study of the effects of denosumab on vertebral, nonvertebral, and hip fracture in women with osteoporosis: results from the FREEDOM Trial. Paper presented at: Annual Meeting of the American Society for Bone and Mineral Research; September 16, 2008; Montreal, Canada.

Miller PD, Bolognese MA, Lewiecki EM, et al; AMG Bone Loss Study Group. Effect of denosumab on bone density and turnover in postmenopausal women with low bone mass after long-term continued, discontinued, and restarting of therapy: a randomized, blinded phase 2 clinical trial. Bone. 2008;43:222–229.

In a 3-year study in which more than 7,800 women 60 to 90 years old were randomized to denosumab (60 mg) or placebo, denosumab reduced the risk of vertebral fracture by 68% and the risk of hip fracture by 40%.

FIGURE A new agent to inhibit bone resorption

RankL is a protein that controls osteoclast maturation, activity, and survival. Denosumab mimics the endogenous decoy receptor OPG to inhibit RankL and reduce osteoclast proliferation, differentiation, and function. Denosumab is a monoclonal antibody to RankL, a mediator of osteoclast function ( FIGURE ). In contrast to alendronate, which enhances trabecular bone density (e.g., that found in the spine), denosumab increases cortical (as in long bones) as well as trabecular bone density.⁶ If the agent obtains approval by the US Food and Drug Administration, it will be an important new approach to the treatment of osteoporosis in menopausal women.⁷

The drug is administered every 6 months by subcutaneous injection.

Like estrogen, denosumab has rapidly reversible effects

The trial by Miller and associates found that the effects of denosumab are rapidly reversible after discontinuation of therapy, in contrast to alendronate. As Goldstein noted in “Update on Osteoporosis” in the November 2008 issue of OBG Management, clinicians are still exploring the relationships between alendronate and osteonecrosis of the jaw and proximal femoral-shaft fracture.⁷ Only further research and surveillance will clarify the clinical pros and cons of denosumab’s swift reversibility.

Baby Boomers have transformed attitudes toward many aspects of aging. Menopause is no exception. Once a taboo topic, menopause is now openly discussed among women who seek information about vasomotor symptoms, hormones and their alternatives, and ways to maintain health as they move past midlife. ObGyns are treating more and more of these women, and fielding their many questions.

In this Update, I examine recent data on three important aspects of menopause:

• how to reduce the risk of cardiovascular disease among women who enter menopause surgically, through oophorectomy
• what to offer women who ask for nonhormonal relief from vasomotor symptoms
• a new drug on the horizon to combat osteoporosis.

Bilateral oophorectomy raises young women’s risk of cardiovascular death

Rivera CM, Grossardt BR, Rhodes DJ, et al. Increased cardiovascular mortality after early bilateral oophorectomy. Menopause. 2009;16:15–23.

Parker WH, Manson JE. Oophorectomy and cardiovascular mortality: is there a link? Menopause. 2009;16:1–2.

Cardiovascular mortality does not increase among women who undergo unilateral oophorectomy, but it does rise among women who undergo bilateral oophorectomy before 45 years of age. However, among women who initiate estrogen therapy at the time of bilateral oophorectomy and continue that therapy through at least 45 years of age, no excess cardiovascular mortality occurs.

Those are the findings of a unique retrospective cohort study performed by investigators from the Mayo Clinic. In the study, investigators reviewed the death certificates of more than 2,300 women who underwent unilateral or bilateral oophorectomy for benign disease before menopause in Olmstead County, Minnesota, from 1950 to 1987. They also followed a similar number of age-matched women for several decades.

These results support the findings of other studies that have observed that menopausal hormone therapy is associated with a lower incidence of cardiovascular death in “young” menopausal women, including those in their 50s or within one decade of the onset of menopause.^1,2

More than 500,000 women undergo bilateral oophorectomy each year in the United States, usually in association with hysterectomy for benign disease.

Induced menopause merits special attention

Spontaneous menopause is physiologic. In contrast, induced menopause (whether associated with surgery, radiation therapy, or chemotherapy) and premature ovarian failure are pathologic conditions.³ Unless they are managed appropriately, induced menopause and premature ovarian failure raise the risk of cardiovascular disease.

Since the initial findings of the Women’s Health Initiative trial of estrogen–progestin therapy were published in 2002, many women and clinicians have become wary about the use of hormone therapy, even among young women who have no ovarian function and who lack a contraindication to hormone therapy.⁴ Unless hormonal management is contraindicated, it is recommended in this setting.

In addition, Parker and Manson recommend that gynecologic surgeons who routinely perform bilateral oophorectomy at the time of hysterectomy for benign disease in premenopausal women who do not have an elevated risk of ovarian cancer should consider updating their therapeutic recommendations and, whenever possible, preserving the ovaries.

Interest in nonhormonal therapies for hot flashes remains high

Bair YA, Gold EB, Zhang G, et al. Use of complementary and alternative medicine during the menopausal transition: longitudinal results from the Study of Women’s Health Across the Nation. Menopause. 2008;15:32–43.

Butt DA, Lock M, Lewis JE, Ross S, Moineddin R. Gabapentin for the treatment of menopausal hot flashes: a randomized trial. Menopause. 2008;15:310–318.

More than three quarters of women use some type of complementary and alternative medicine (CAM) during the menopausal transition. So found a survey conducted as part of the Study of Women’s Health Across the Nation (SWAN), which involved more than 2,000 premenopausal and perimenopausal women.

More than one third of all US women use one or more forms of CAM, spending more than $600 million a year.

In the SWAN survey, Japanese and white women were significantly more likely to report use of CAM than were Chinese, African-American, and Hispanic women during menopause.

Some women use both CAM and hormones

A notable finding of this report from SWAN is that concomitant use of menopausal hormone therapy and CAM is common among symptomatic women, even though herbal therapies have not been proved to be more effective than placebo in the treatment of vasomotor symptoms.⁵

Given the high prevalence of use of CAM, ObGyns should recognize that symptomatic patients especially bothered by vasomotor symptoms may seek relief with both CAM and a prescription medication. For this reason, it is wise to ask perimenopausal and postmenopausal women to list all the remedies they use—both prescription and over the counter.

 

Gabapentin eases symptoms in some women

Along with the antidepressants paroxetine and venlafaxine, gabapentin is the most widely studied prescription agent used in the nonhormonal treatment of menopausal vasomotor symptoms.

Canadian investigators performed a double-blind, placebo-controlled trial involving 197 symptomatic, spontaneously menopausal women (age range: 45 to 65 years). Participants were randomized to gabapentin (300 mg) or placebo, given three times daily for 4 weeks.

Ten of the 99 women who were randomized to gabapentin and six of the 98 women who were randomized to placebo dropped out of the study because of adverse effects. Hot-flash scores decreased by 51% among women taking gabapentin and by 26% among women in the placebo arm (p<.001). Women who used gabapentin were significantly more likely to report dizziness, drowsiness, and unsteadiness than those who received placebo.

Despite its proven efficacy, gabapentin does not appear to equal estrogen in its ability to alleviate vasomotor symptoms. Further, gabapentin’s side-effect profile and the need for thrice-daily administration also limit its appeal. Nevertheless, symptomatic women who are interested in nonhormonal treatment may wish to consider this option.

Anti-osteoporosis arsenal may gain a new weapon

Cummings S, McClung M, Christiansen C, et al. A phase III study of the effects of denosumab on vertebral, nonvertebral, and hip fracture in women with osteoporosis: results from the FREEDOM Trial. Paper presented at: Annual Meeting of the American Society for Bone and Mineral Research; September 16, 2008; Montreal, Canada.

Miller PD, Bolognese MA, Lewiecki EM, et al; AMG Bone Loss Study Group. Effect of denosumab on bone density and turnover in postmenopausal women with low bone mass after long-term continued, discontinued, and restarting of therapy: a randomized, blinded phase 2 clinical trial. Bone. 2008;43:222–229.

In a 3-year study in which more than 7,800 women 60 to 90 years old were randomized to denosumab (60 mg) or placebo, denosumab reduced the risk of vertebral fracture by 68% and the risk of hip fracture by 40%.

FIGURE A new agent to inhibit bone resorption

RankL is a protein that controls osteoclast maturation, activity, and survival. Denosumab mimics the endogenous decoy receptor OPG to inhibit RankL and reduce osteoclast proliferation, differentiation, and function. Denosumab is a monoclonal antibody to RankL, a mediator of osteoclast function ( FIGURE ). In contrast to alendronate, which enhances trabecular bone density (e.g., that found in the spine), denosumab increases cortical (as in long bones) as well as trabecular bone density.⁶ If the agent obtains approval by the US Food and Drug Administration, it will be an important new approach to the treatment of osteoporosis in menopausal women.⁷

The drug is administered every 6 months by subcutaneous injection.

Like estrogen, denosumab has rapidly reversible effects

The trial by Miller and associates found that the effects of denosumab are rapidly reversible after discontinuation of therapy, in contrast to alendronate. As Goldstein noted in “Update on Osteoporosis” in the November 2008 issue of OBG Management, clinicians are still exploring the relationships between alendronate and osteonecrosis of the jaw and proximal femoral-shaft fracture.⁷ Only further research and surveillance will clarify the clinical pros and cons of denosumab’s swift reversibility.

The author reports that he is a member and past board member of the Iowa Medical Society. He is a current board member of the Midwest Medical Insurance Company.

*This example is a bit disingenuous. In real life, the insurance industry has several mechanisms available to cushion a solitary large outlier like this in any given year (reinsurance, etc). However, the net effect as portrayed here is quite real.

The lessons we’ve learned from past malpractice insurance crises are worth reviewing so we can avoid the next one. In the mid-1970s, it was sky-rocketing malpractice insurance rates—100% to 150% increases year after year. In the 2000–2003 crisis, the number of actual claims fell but the payout per claim soared.

Through these crises, we’ve learned the value of physician-owned malpractice insurance companies, the importance of tort reform (most notably in California), the roles that inflation and technology play, and the need for policing our own ranks to root out incompetent physicians. In this article, I analyze those past crises and the solutions that led us out of them.

That ’70s show

Nobody knew whom to blame for what happened in the 1970s. Attorneys reproached bad physicians and greedy insurance companies. Insurance companies criticized inept physicians and unscrupulous attorneys. We physicians didn’t suddenly become incredibly stupid between 1976 and 1977, but we were at a disadvantage because we didn’t have access to unbiased data to assess the problem.

So state medical societies responded by organizing malpractice liability insurance companies, which became quite successful. This led to the creation of the Physicians Insurance Association of America (PIAA), organized to share solutions and data. These unbiased data have been invaluable in helping us analyze the numerous crises of the past 30 years.

The perfect storm

We analyzed the cause of the late 1970s crisis as the perfect storm: increased severity and increased frequency (see “A glossary of insurance-speak,”). In the 2000–2003 crisis, the severity of claims increased while the frequency of claims actually fell.

Tracking the combined ratios (losses to premiums) of PIAA companies demonstrates the devastating effects of the crisis years (FIGURE 1).¹ Combined ratios around 110, indicating a 10% loss, are tolerable. When the combined ratio inched up to 114 and then skyrocketed, as it did in 2000–2001, crisis ensued.

What this means in real dollars is quite telling. If an insurance company has $100 million income and combined ratios of 120, 134, 129, and 122 over 4 years, the company has lost $105 million (20+34+29+22=105)!

The fix, but not for you

As FIGURE 1 shows, the combined ratios came back into line as the crisis abated—for insurance companies, not physicians.

Insurance companies rectified their combined ratios by raising premiums. If losses rise (numerator), insurance companies can increase premiums (denominator) to bring their combined ratios back into line.

This is healthy for the insurance companies—and you, as an insured, want and need a healthy company—but it is very bad for your pocketbook. Rates increased 105% over 4 years and are likely to stay there until the next crisis, when they will rise even further.

FIGURE 1 10 years’ combined ratio of all PIAA companies ¹

The spike marks the 2000–2003 crisis.

Who’s to blame?

That depends on who controls frequency and severity. I will eliminate the “greedy” insurance companies from this discussion. Most physician-owned companies simply return any excess profit to their insured members. Two parties control frequency of claims:

The attorneys. They attempt to develop new theories of litigation and exploit weaknesses in our scientific knowledge. When it’s a bad baby, it must be the doctor’s fault. Lawsuits with no medical foundation remain an expensive problem; 70% of cases nationwide are closed without payment (FIGURE 2).²

The physicians. We are also culpable. In the 1970s, we believed all physicians were going to be sued (mostly true), and that we would all be sued equally (not true). In some jurisdictions, almost one half of all paid malpractice claims come from a fairly small number of habitual offenders.³

FIGURE 2 Outcome of malpractice cases closed in 2004²

A large majority of liability cases are closed without payment.

 

The peer-policing problem

Physician peer policing has become restrained and time consuming. You have to give the bad ones time to reform.

Juries, however, have no patience with peer policing. They extract impressive damages for allowing an inept physician to see even one patient, let alone practice for 6 months and hurt a number of people while under his or her peers’ watchful eyes.

Effects of growing severity

Frequency pales in comparison with the damage wrought by increasing severity. Two dynamics mainly control severity: 1) a combination of inflation and improved technology and 2) juries.

Inflation and improved technology

Compare how we have improved our care for injured parties versus the above-inflation cost of that care. Babies with cerebral palsy live longer and we are ever improving their care. This is good, but very expensive.

We should expect increases in severity to mimic increases in inflation and technology, to parallel the increase in health-care costs in general. However, the only place where this has happened is California.⁴

Most juries are reasonable…

Few states restrict the pain and suffering awards juries may grant. None restrict damage awards. Juries can award $100,000 or several million dollars for the same injury. They may disregard scientific data and expert testimony. Juries carry our wallets (and retirement plans, houses, cars, and kids’ educations) in their hip pocket.

Almost all jurors want to do the right thing, exhibiting an organic restraint. When interviewed after a case, jurors are typically sincere and responsible and want assurance that they made the right choice. The jury system usually works.⁵

…but there are outliers

The killers, however, are the outliers. Look what happens to our fairly strong insurance company’s combined ratio if a case that we thought was winnable results in a $15 million jury verdict. Our company shoots for a combined ratio of 105% to 110% (we plan to lose $5 million to $10 million a year, which our return on investments covers). All of a sudden, besides our planned losses, we’re assessed an extra $15 million. Then we are looking at a combined ratio in the crisis range: 125%. One case, one runaway jury. A volatile game.*

Jury awards have been increasing faster than inflation and technology together can support. Perhaps it is because the value of the “mega dollar” has risen far greater than inflation. Perhaps it’s the fault of the lottery, the exceptional millionaire of the 1960s being replaced by the billionaire of the 1990s (a thousandfold increase) and the multibillionaire of the 21st Century (another hundredfold increase). I speculate that jury awards more closely follow this trend.

What have we learned?

Sad to say, the modern function is too similar to that of the 1970s. We have ruled out the “greedy” insurance companies and developed solid unbiased data—good steps— but we have not been able to avoid crises nor have we stabilized premiums to match medical inflation.

Where physicians “healed thyselves”

Under these circumstances, well-run physician-owned and -governed companies with a nonprofit but sound financial goal should continue to offer the best long-term rates and security. Based on reasonable combined ratio goals (105 to 110), income from the company’s invested assets can reduce physician premiums.

Physician owners and physician input throughout the corporate structure sustain the business model. Professional medical expertise in reviewing claims, peer review of physicians’ performance, and support for physicians through the onerous lawsuit experience augment a medical malpractice insurance company. Claims committees of multispecialty physicians ensure that we fight when right and settle expeditiously when wrong, saving time and money.

A positive side effect

Physician-owned companies have created a cadre of physicians schooled in the medical malpractice insurance business. This makes us much less vulnerable in the political arena. Our pooled data enable us to negotiate from truly informed positions.

Four things we can do to fix it

If malpractice costs do hinge on inflation and technology, repeat offender doctors, aggressive attorneys, and runaway juries, then another crisis is imminent unless we can rein in attorneys and juries.

As physicians, if we hurt someone we expect them to be given reasonable restitution, and we strive to ensure the return of as much function as possible. We are making strides to find and limit incompetent physicians. Although frequency, which reflects frivolous lawsuits, has been stable recently, aggressive attorneys remain a threat.

Here are four ways to fix the problem:

Do your part. Remodeling juries is a political solution—with a capital “P.” In spite of our 30-year effort to hire lobbyists and, at times, an 85% approval rating by the general public for tort reform, most states have yet to enact truly effective limits on juries. To avoid the next crisis, we will need a grassroots, every-physician, hands-on movement to pass tort reform.

 

Copy California. The Medical Insurance Compensation Reform Act (MICRA) of 1975 has been quite successful in California (see the TABLE).² A cap on noneconomic damages is the most important aspect of the MICRA reforms—it limits the runaway jury’s ability to award excessive verdicts.⁴ It is also the most difficult reform to get passed because it is perceived to limit a plaintiff ’s right to fair and reasonable compensation.

TABLE

California’s MICRA reforms²

$250,000 cap on noneconomic damages
Collateral source offsets
Periodic payment of future damages
One-third-year statute of limitations/repose
Joint and several liability
Limit on contingency fees

Get ready for the next crisis. The most recent crisis has passed. Regrettably, we lost our best opportunity to have federally mandated reform in 2003 and 2004 when President Bush actively campaigned for caps and most of the MICRA reforms. When the next opportunity comes, we need to be ready.

Organize. Our malpractice premiums are up 925% since the 1970s. Our paid lobbyists and PACs have not gotten the job done. Obviously, throwing money at the problem doesn’t work. Next time, we must organize every physician nationwide to attain our political goal: to pass caps and MICRA reforms.

Your state medical society, your specialty society, and the PIAA (www.piaa.us) have the contact numbers and e-mail addresses of your legislators. The next time this is an issue, call your legislators. They seem to listen to constituents more than they listen to lobbyists.

The author reports that he is a member and past board member of the Iowa Medical Society. He is a current board member of the Midwest Medical Insurance Company.

*This example is a bit disingenuous. In real life, the insurance industry has several mechanisms available to cushion a solitary large outlier like this in any given year (reinsurance, etc). However, the net effect as portrayed here is quite real.

The lessons we’ve learned from past malpractice insurance crises are worth reviewing so we can avoid the next one. In the mid-1970s, it was sky-rocketing malpractice insurance rates—100% to 150% increases year after year. In the 2000–2003 crisis, the number of actual claims fell but the payout per claim soared.

Through these crises, we’ve learned the value of physician-owned malpractice insurance companies, the importance of tort reform (most notably in California), the roles that inflation and technology play, and the need for policing our own ranks to root out incompetent physicians. In this article, I analyze those past crises and the solutions that led us out of them.

That ’70s show

Nobody knew whom to blame for what happened in the 1970s. Attorneys reproached bad physicians and greedy insurance companies. Insurance companies criticized inept physicians and unscrupulous attorneys. We physicians didn’t suddenly become incredibly stupid between 1976 and 1977, but we were at a disadvantage because we didn’t have access to unbiased data to assess the problem.

So state medical societies responded by organizing malpractice liability insurance companies, which became quite successful. This led to the creation of the Physicians Insurance Association of America (PIAA), organized to share solutions and data. These unbiased data have been invaluable in helping us analyze the numerous crises of the past 30 years.

The perfect storm

We analyzed the cause of the late 1970s crisis as the perfect storm: increased severity and increased frequency (see “A glossary of insurance-speak,”). In the 2000–2003 crisis, the severity of claims increased while the frequency of claims actually fell.

Tracking the combined ratios (losses to premiums) of PIAA companies demonstrates the devastating effects of the crisis years (FIGURE 1).¹ Combined ratios around 110, indicating a 10% loss, are tolerable. When the combined ratio inched up to 114 and then skyrocketed, as it did in 2000–2001, crisis ensued.

What this means in real dollars is quite telling. If an insurance company has $100 million income and combined ratios of 120, 134, 129, and 122 over 4 years, the company has lost $105 million (20+34+29+22=105)!

The fix, but not for you

As FIGURE 1 shows, the combined ratios came back into line as the crisis abated—for insurance companies, not physicians.

Insurance companies rectified their combined ratios by raising premiums. If losses rise (numerator), insurance companies can increase premiums (denominator) to bring their combined ratios back into line.

This is healthy for the insurance companies—and you, as an insured, want and need a healthy company—but it is very bad for your pocketbook. Rates increased 105% over 4 years and are likely to stay there until the next crisis, when they will rise even further.

FIGURE 1 10 years’ combined ratio of all PIAA companies ¹

The spike marks the 2000–2003 crisis.

Who’s to blame?

That depends on who controls frequency and severity. I will eliminate the “greedy” insurance companies from this discussion. Most physician-owned companies simply return any excess profit to their insured members. Two parties control frequency of claims:

The attorneys. They attempt to develop new theories of litigation and exploit weaknesses in our scientific knowledge. When it’s a bad baby, it must be the doctor’s fault. Lawsuits with no medical foundation remain an expensive problem; 70% of cases nationwide are closed without payment (FIGURE 2).²

The physicians. We are also culpable. In the 1970s, we believed all physicians were going to be sued (mostly true), and that we would all be sued equally (not true). In some jurisdictions, almost one half of all paid malpractice claims come from a fairly small number of habitual offenders.³

FIGURE 2 Outcome of malpractice cases closed in 2004²

A large majority of liability cases are closed without payment.

 

The peer-policing problem

Physician peer policing has become restrained and time consuming. You have to give the bad ones time to reform.

Juries, however, have no patience with peer policing. They extract impressive damages for allowing an inept physician to see even one patient, let alone practice for 6 months and hurt a number of people while under his or her peers’ watchful eyes.

Effects of growing severity

Frequency pales in comparison with the damage wrought by increasing severity. Two dynamics mainly control severity: 1) a combination of inflation and improved technology and 2) juries.

Inflation and improved technology

Compare how we have improved our care for injured parties versus the above-inflation cost of that care. Babies with cerebral palsy live longer and we are ever improving their care. This is good, but very expensive.

We should expect increases in severity to mimic increases in inflation and technology, to parallel the increase in health-care costs in general. However, the only place where this has happened is California.⁴

Most juries are reasonable…

Few states restrict the pain and suffering awards juries may grant. None restrict damage awards. Juries can award $100,000 or several million dollars for the same injury. They may disregard scientific data and expert testimony. Juries carry our wallets (and retirement plans, houses, cars, and kids’ educations) in their hip pocket.

Almost all jurors want to do the right thing, exhibiting an organic restraint. When interviewed after a case, jurors are typically sincere and responsible and want assurance that they made the right choice. The jury system usually works.⁵

…but there are outliers

The killers, however, are the outliers. Look what happens to our fairly strong insurance company’s combined ratio if a case that we thought was winnable results in a $15 million jury verdict. Our company shoots for a combined ratio of 105% to 110% (we plan to lose $5 million to $10 million a year, which our return on investments covers). All of a sudden, besides our planned losses, we’re assessed an extra $15 million. Then we are looking at a combined ratio in the crisis range: 125%. One case, one runaway jury. A volatile game.*

Jury awards have been increasing faster than inflation and technology together can support. Perhaps it is because the value of the “mega dollar” has risen far greater than inflation. Perhaps it’s the fault of the lottery, the exceptional millionaire of the 1960s being replaced by the billionaire of the 1990s (a thousandfold increase) and the multibillionaire of the 21st Century (another hundredfold increase). I speculate that jury awards more closely follow this trend.

What have we learned?

Sad to say, the modern function is too similar to that of the 1970s. We have ruled out the “greedy” insurance companies and developed solid unbiased data—good steps— but we have not been able to avoid crises nor have we stabilized premiums to match medical inflation.

Where physicians “healed thyselves”

Under these circumstances, well-run physician-owned and -governed companies with a nonprofit but sound financial goal should continue to offer the best long-term rates and security. Based on reasonable combined ratio goals (105 to 110), income from the company’s invested assets can reduce physician premiums.

Physician owners and physician input throughout the corporate structure sustain the business model. Professional medical expertise in reviewing claims, peer review of physicians’ performance, and support for physicians through the onerous lawsuit experience augment a medical malpractice insurance company. Claims committees of multispecialty physicians ensure that we fight when right and settle expeditiously when wrong, saving time and money.

A positive side effect

Physician-owned companies have created a cadre of physicians schooled in the medical malpractice insurance business. This makes us much less vulnerable in the political arena. Our pooled data enable us to negotiate from truly informed positions.

Four things we can do to fix it

If malpractice costs do hinge on inflation and technology, repeat offender doctors, aggressive attorneys, and runaway juries, then another crisis is imminent unless we can rein in attorneys and juries.

As physicians, if we hurt someone we expect them to be given reasonable restitution, and we strive to ensure the return of as much function as possible. We are making strides to find and limit incompetent physicians. Although frequency, which reflects frivolous lawsuits, has been stable recently, aggressive attorneys remain a threat.

Here are four ways to fix the problem:

Do your part. Remodeling juries is a political solution—with a capital “P.” In spite of our 30-year effort to hire lobbyists and, at times, an 85% approval rating by the general public for tort reform, most states have yet to enact truly effective limits on juries. To avoid the next crisis, we will need a grassroots, every-physician, hands-on movement to pass tort reform.

 

Copy California. The Medical Insurance Compensation Reform Act (MICRA) of 1975 has been quite successful in California (see the TABLE).² A cap on noneconomic damages is the most important aspect of the MICRA reforms—it limits the runaway jury’s ability to award excessive verdicts.⁴ It is also the most difficult reform to get passed because it is perceived to limit a plaintiff ’s right to fair and reasonable compensation.

TABLE

California’s MICRA reforms²

$250,000 cap on noneconomic damages
Collateral source offsets
Periodic payment of future damages
One-third-year statute of limitations/repose
Joint and several liability
Limit on contingency fees

Get ready for the next crisis. The most recent crisis has passed. Regrettably, we lost our best opportunity to have federally mandated reform in 2003 and 2004 when President Bush actively campaigned for caps and most of the MICRA reforms. When the next opportunity comes, we need to be ready.

Organize. Our malpractice premiums are up 925% since the 1970s. Our paid lobbyists and PACs have not gotten the job done. Obviously, throwing money at the problem doesn’t work. Next time, we must organize every physician nationwide to attain our political goal: to pass caps and MICRA reforms.

Your state medical society, your specialty society, and the PIAA (www.piaa.us) have the contact numbers and e-mail addresses of your legislators. The next time this is an issue, call your legislators. They seem to listen to constituents more than they listen to lobbyists.

The author reports that he is a member and past board member of the Iowa Medical Society. He is a current board member of the Midwest Medical Insurance Company.

*This example is a bit disingenuous. In real life, the insurance industry has several mechanisms available to cushion a solitary large outlier like this in any given year (reinsurance, etc). However, the net effect as portrayed here is quite real.

The lessons we’ve learned from past malpractice insurance crises are worth reviewing so we can avoid the next one. In the mid-1970s, it was sky-rocketing malpractice insurance rates—100% to 150% increases year after year. In the 2000–2003 crisis, the number of actual claims fell but the payout per claim soared.

Through these crises, we’ve learned the value of physician-owned malpractice insurance companies, the importance of tort reform (most notably in California), the roles that inflation and technology play, and the need for policing our own ranks to root out incompetent physicians. In this article, I analyze those past crises and the solutions that led us out of them.

That ’70s show

Nobody knew whom to blame for what happened in the 1970s. Attorneys reproached bad physicians and greedy insurance companies. Insurance companies criticized inept physicians and unscrupulous attorneys. We physicians didn’t suddenly become incredibly stupid between 1976 and 1977, but we were at a disadvantage because we didn’t have access to unbiased data to assess the problem.

So state medical societies responded by organizing malpractice liability insurance companies, which became quite successful. This led to the creation of the Physicians Insurance Association of America (PIAA), organized to share solutions and data. These unbiased data have been invaluable in helping us analyze the numerous crises of the past 30 years.

The perfect storm

We analyzed the cause of the late 1970s crisis as the perfect storm: increased severity and increased frequency (see “A glossary of insurance-speak,”). In the 2000–2003 crisis, the severity of claims increased while the frequency of claims actually fell.

Tracking the combined ratios (losses to premiums) of PIAA companies demonstrates the devastating effects of the crisis years (FIGURE 1).¹ Combined ratios around 110, indicating a 10% loss, are tolerable. When the combined ratio inched up to 114 and then skyrocketed, as it did in 2000–2001, crisis ensued.

What this means in real dollars is quite telling. If an insurance company has $100 million income and combined ratios of 120, 134, 129, and 122 over 4 years, the company has lost $105 million (20+34+29+22=105)!

The fix, but not for you

As FIGURE 1 shows, the combined ratios came back into line as the crisis abated—for insurance companies, not physicians.

Insurance companies rectified their combined ratios by raising premiums. If losses rise (numerator), insurance companies can increase premiums (denominator) to bring their combined ratios back into line.

This is healthy for the insurance companies—and you, as an insured, want and need a healthy company—but it is very bad for your pocketbook. Rates increased 105% over 4 years and are likely to stay there until the next crisis, when they will rise even further.

FIGURE 1 10 years’ combined ratio of all PIAA companies ¹

The spike marks the 2000–2003 crisis.

Who’s to blame?

That depends on who controls frequency and severity. I will eliminate the “greedy” insurance companies from this discussion. Most physician-owned companies simply return any excess profit to their insured members. Two parties control frequency of claims:

The attorneys. They attempt to develop new theories of litigation and exploit weaknesses in our scientific knowledge. When it’s a bad baby, it must be the doctor’s fault. Lawsuits with no medical foundation remain an expensive problem; 70% of cases nationwide are closed without payment (FIGURE 2).²

The physicians. We are also culpable. In the 1970s, we believed all physicians were going to be sued (mostly true), and that we would all be sued equally (not true). In some jurisdictions, almost one half of all paid malpractice claims come from a fairly small number of habitual offenders.³

FIGURE 2 Outcome of malpractice cases closed in 2004²

A large majority of liability cases are closed without payment.

 

The peer-policing problem

Physician peer policing has become restrained and time consuming. You have to give the bad ones time to reform.

Juries, however, have no patience with peer policing. They extract impressive damages for allowing an inept physician to see even one patient, let alone practice for 6 months and hurt a number of people while under his or her peers’ watchful eyes.

Effects of growing severity

Frequency pales in comparison with the damage wrought by increasing severity. Two dynamics mainly control severity: 1) a combination of inflation and improved technology and 2) juries.

Inflation and improved technology

Compare how we have improved our care for injured parties versus the above-inflation cost of that care. Babies with cerebral palsy live longer and we are ever improving their care. This is good, but very expensive.

We should expect increases in severity to mimic increases in inflation and technology, to parallel the increase in health-care costs in general. However, the only place where this has happened is California.⁴

Most juries are reasonable…

Few states restrict the pain and suffering awards juries may grant. None restrict damage awards. Juries can award $100,000 or several million dollars for the same injury. They may disregard scientific data and expert testimony. Juries carry our wallets (and retirement plans, houses, cars, and kids’ educations) in their hip pocket.

Almost all jurors want to do the right thing, exhibiting an organic restraint. When interviewed after a case, jurors are typically sincere and responsible and want assurance that they made the right choice. The jury system usually works.⁵

…but there are outliers

The killers, however, are the outliers. Look what happens to our fairly strong insurance company’s combined ratio if a case that we thought was winnable results in a $15 million jury verdict. Our company shoots for a combined ratio of 105% to 110% (we plan to lose $5 million to $10 million a year, which our return on investments covers). All of a sudden, besides our planned losses, we’re assessed an extra $15 million. Then we are looking at a combined ratio in the crisis range: 125%. One case, one runaway jury. A volatile game.*

Jury awards have been increasing faster than inflation and technology together can support. Perhaps it is because the value of the “mega dollar” has risen far greater than inflation. Perhaps it’s the fault of the lottery, the exceptional millionaire of the 1960s being replaced by the billionaire of the 1990s (a thousandfold increase) and the multibillionaire of the 21st Century (another hundredfold increase). I speculate that jury awards more closely follow this trend.

What have we learned?

Sad to say, the modern function is too similar to that of the 1970s. We have ruled out the “greedy” insurance companies and developed solid unbiased data—good steps— but we have not been able to avoid crises nor have we stabilized premiums to match medical inflation.

Where physicians “healed thyselves”

Under these circumstances, well-run physician-owned and -governed companies with a nonprofit but sound financial goal should continue to offer the best long-term rates and security. Based on reasonable combined ratio goals (105 to 110), income from the company’s invested assets can reduce physician premiums.

Physician owners and physician input throughout the corporate structure sustain the business model. Professional medical expertise in reviewing claims, peer review of physicians’ performance, and support for physicians through the onerous lawsuit experience augment a medical malpractice insurance company. Claims committees of multispecialty physicians ensure that we fight when right and settle expeditiously when wrong, saving time and money.

A positive side effect

Physician-owned companies have created a cadre of physicians schooled in the medical malpractice insurance business. This makes us much less vulnerable in the political arena. Our pooled data enable us to negotiate from truly informed positions.

Four things we can do to fix it

If malpractice costs do hinge on inflation and technology, repeat offender doctors, aggressive attorneys, and runaway juries, then another crisis is imminent unless we can rein in attorneys and juries.

As physicians, if we hurt someone we expect them to be given reasonable restitution, and we strive to ensure the return of as much function as possible. We are making strides to find and limit incompetent physicians. Although frequency, which reflects frivolous lawsuits, has been stable recently, aggressive attorneys remain a threat.

Here are four ways to fix the problem:

Do your part. Remodeling juries is a political solution—with a capital “P.” In spite of our 30-year effort to hire lobbyists and, at times, an 85% approval rating by the general public for tort reform, most states have yet to enact truly effective limits on juries. To avoid the next crisis, we will need a grassroots, every-physician, hands-on movement to pass tort reform.

 

Copy California. The Medical Insurance Compensation Reform Act (MICRA) of 1975 has been quite successful in California (see the TABLE).² A cap on noneconomic damages is the most important aspect of the MICRA reforms—it limits the runaway jury’s ability to award excessive verdicts.⁴ It is also the most difficult reform to get passed because it is perceived to limit a plaintiff ’s right to fair and reasonable compensation.

TABLE

California’s MICRA reforms²

$250,000 cap on noneconomic damages
Collateral source offsets
Periodic payment of future damages
One-third-year statute of limitations/repose
Joint and several liability
Limit on contingency fees

Get ready for the next crisis. The most recent crisis has passed. Regrettably, we lost our best opportunity to have federally mandated reform in 2003 and 2004 when President Bush actively campaigned for caps and most of the MICRA reforms. When the next opportunity comes, we need to be ready.

Organize. Our malpractice premiums are up 925% since the 1970s. Our paid lobbyists and PACs have not gotten the job done. Obviously, throwing money at the problem doesn’t work. Next time, we must organize every physician nationwide to attain our political goal: to pass caps and MICRA reforms.

Your state medical society, your specialty society, and the PIAA (www.piaa.us) have the contact numbers and e-mail addresses of your legislators. The next time this is an issue, call your legislators. They seem to listen to constituents more than they listen to lobbyists.