Although it is often taken for granted, the ability to initiate and maintain sleep throughout the night is elusive for many. About one-third of adults experience a troublesome episode of insomnia.¹ In most, it is transient, but in 10% to 15% (roughly 30 million people), the problem becomes self-perpetuating and chronic.² Chronic insomnia is one of the most prevalent conditions that family physicians (FPs) encounter, a function of it being so closely associated with comorbid conditions that FPs deal with every day, such as depression, chronic pain, and polypharmacy.^3,4

Insomnia can be vexing for a number of reasons. Because it is not acutely dangerous, patients may present it as an “add-on” concern at the end of an already lengthy visit. And because insomnia is often a symptom of multiple underlying physiologic and psychological factors, it requires the FP to engage in a thorough and time-consuming exploration of possible causes and comorbidities. Finally, standard treatment options have drawbacks: reports show that use of pharmacotherapy is troubling to prescribers primarily because of concerns about adverse effects and dependence;^5-7 the other major therapeutic avenue, cognitive behavioral therapy for insomnia (CBT-I), requires training and is time-consuming to deliver in the context of an office visit.^8,9

Despite these obstacles, successful evaluation and treatment of insomnia can be highly rewarding. Chronic insomnia is associated with great individual misery and negative consequences for long-term health. Specifically, it is associated with reduced quality of life and daytime functioning,¹⁰ depression,^11,12 hypertension,^13,14 increased workplace accidents and absenteeism,^15-17 and exacerbations of chronic pain.¹⁸ And while the evaluation and management of insomnia can be laborious, a systematic method can streamline the process.

Insomnia: Symptom or cause?

The International Classification of Sleep Disorders defines chronic insomnia as an inability to sleep sufficiently despite creating adequate opportunity. It occurs at least 3 nights per week for >3 months with perceived negative consequences during the day. Patients typically complain about symptoms including fatigue, diminished cog­nitive performance, and mood disturbance.¹⁹ Acute insomnia triggered by one or more biopsychosocial stresses is, by definition, self-limited and has different underlying mechanisms. As such, it will not be described in this review.

The chief risk factors are female gender, low socioeconomic status, and increasing age.²⁰ However, cohorts of healthy seniors show preserved good sleep; the increase in prevalence of insomnia in the elderly is likely linked more specifically to age-related accumulation of medical/mental health disorders and polypharmacy than aging per se.²¹

Research over the past 20 years has shown that comorbidities have a bidirectional relationship with insomnia, rather than a one-way cause and effect.

In the past, insomnia was viewed as a symptom, occurring secondarily to an underlying cause, usually an acute biopsychosocial stressor or depression. It was assumed that if the primary cause was effectively treated, then healthy sleep would return.

But research over the past 20 years has changed this paradigm in 2 ways. First, when comorbidities such as depression or chronic pain are present, they have a bidirectional relationship with insomnia rather than a one-way cause and effect. For example, instead of depression being a primary disorder from which insomnia can result, it is now recognized that insomnia can be present first and is a risk factor for new-onset depression. When depression and insomnia coexist, they may exacerbate each other in a bidirectional pattern.

Secondly, an estimated 15% of chronic insomnia sufferers have no targetable comorbidity; rather, they are unable to get sufficient sleep in large part because of a trait-like predisposition to fragile sleep, called hyperarousal brain physiology.²² These people used to be described as having “primary insomnia,” although the term has been dropped from the 5th edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM).²³

Assess comorbidities, obtain sleep logs

The evaluation of the chronic form of insomnia should begin with a thorough medical his­tory to assess for comorbid conditions that can exacerbate disturbed sleep. These are generally grouped into medical disorders (TABLE 1²⁰), medications/substances (eg, antidepressants, stimulants, decongestants, narcotic analgesics, cardiovascular drugs, pulmonary agents, alcohol), and mental health disorders (especially depression and anxiety). It’s important to consider whether such comorbidities are contributing to the insomnia and optimize treatment that addresses them.

Take particular care to evaluate signs and symptoms of comorbid primary sleep disorders such as obstructive sleep apnea, restless legs syndrome (RLS), and circadian rhythm disorders since any of these can present with a complaint of insomnia. RLS, usually classified as a sleep disorder because of its circadian pattern (it is experienced more at night than during the day), is present to a troublesome degree in about 3% to 4% of all adults.²⁴ It is important to inquire about symptoms of RLS (urge to move legs in the night more than during the day; relieved with movement; worsened with inactivity) so as not to miss this treatable cause of insomnia.

The physical exam should focus on signs that suggest sleep-disordered breathing—obesity, large neck girth, hypertension, and crowded oropharynx—because people with sleep apnea often present with the complaint of frequent awakenings.

Sleep logs can present a powerful picture

In addition to a history and physical exam, physicians should ask their patients with chronic insomnia to complete sleep logs for 2 to 3 weeks.²⁰ A sleep log with midnight near the middle of the page is preferred by many because it places the typical sleeping hours in the middle of the page, showing relevant information in a way that can be grasped immediately (FIGURE 1). To save time, nurses can provide sleep logs to patients along with instructions about how to complete them.

Patient-completed sleep logs often illuminate obvious detrimental behaviors that reinforce insomnia (eg, spending excessive time in bed, having irregular bed/wake times, daytime napping that diminishes sleep drive in the evening). In addition, they sometimes reveal circadian rhythm abnormalities such as delayed sleep phase syndrome in which the patient attempts to sleep at a normal bedtime, but exhibits a marked delay in falling asleep/waking up compared to societal norms. Seeing such information graphically represented is often a powerful learning experience for both physician and patient.

Sleep studies aren't usually warranted

In its most recent (2008) clinical guideline on the evaluation and management of chronic insomnia, the American Academy of Sleep Medicine (AASM) stated that “routine testing in the sleep lab is not warranted for most cases of insomnia.” Instead, it is reserved for individuals in whom there is a suspicion of a comorbid sleep disorder. FPs should refer patients for formal sleep studies only if, in addition to the insomnia complaint, there is suspicion of:²⁰

• obstructive sleep apnea (based upon some combination of loud snoring, obesity, hypertension, and/or excessive daytime sleepiness),
• narcolepsy (based upon excessive daytime sleepiness without a readily identifiable cause), or
• arousals with the potential for self-injurious behavior (parasomnias).

Treatments: Sleep hygiene, CBT-I, and medication

Sleep hygiene, cognitive/behavioral techniques, and pharmacotherapy serve as the core of therapy for chronic insomnia.

Sleep hygiene: Common-sense strategies

Most FPs are familiar with sleep hygiene instructions; these are simple, common-sense behavioral techniques such as limiting caffeine and screen (television, computer) time at night, avoiding daytime naps, and maintaining regular bed- and out-of-bed times. (See “A sleep hygiene checklist.”) Although it is a logical starting point for behavioral modification, sleep hygiene has not been studied rigorously as a monotherapy for insomnia and, therefore, doesn’t have an evidence rating in terms of effectiveness.²⁰

CBT-I: Treatment of choice

CBT-I seeks to lower cognitive and somatic arousal. Taken together, cognitive and behavioral techniques are effective in 70% to 80% of people, whether they have primary insomnia or comorbidities.^25-27 Furthermore, the benefits are sustained with the passage of time.²⁷ CBT-I is regarded as the treatment of choice for chronic insomnia.²⁰

An experience of successful sleep initiation and maintenance is important psychologically: It renews patients' confidence in the ability to sleep.

When provided by a highly trained mental health professional, CBT-I usually takes the form of a series of 6 to 8 weekly appointments. Descriptions and manuals for CBT-I abound and online programs have also proliferated.^28,29 However, there is a shortage of highly trained providers, and most FPs do not feel proficient to engage fully in CBT-I.^8,9 Nevertheless, some behavioral elements of CBT-I, such as stimulus control and sleep restriction, can be utilized in the family medicine setting and may be effective for a significant subset of patients.

Stimulus control and sleep restriction. Two behavioral techniques for insomnia that can be applied in the family medicine setting are stimulus control and sleep restriction therapy.²⁰

With stimulus control, patients attempt to eliminate stimuli that weaken the psychological association between the bed and successful sleep, namely wakeful activities in bed such as watching television, reading, or even “tossing and turning.” Instead, they are instructed to use their bed only for sleep (and intimacy), to vacate it if awake and not clearly on the verge of sleep, and to avoid looking at a clock during the night. Patients are also advised to sleep only in their own bed and not in other places in their home.

Sleep restriction is predicated on the observation that many people with insomnia habitually spend too much time awake in bed, and this creates a conditioned arousal response to the bed. With sleep restriction, the patient is assigned a narrow window of “allowed time in bed,” usually a 6-hour interval of their choosing, and is instructed to adhere to this schedule for a period of 2 to 4 weeks. Many patients find that they fall asleep more rapidly and stay asleep longer after a few weeks. This experience of “successful” sleep initiation and maintenance is important psychologically; it renews their confidence in their ability to sleep, which is missing in most people with chronic insomnia.

If you use this approach with a patient, be sure to acknowledge that sleep restriction usually engenders some sleep deprivation in the first few weeks. But it is only a short-term intervention designed to change the expectation of nightly insomnia that is so ingrained in these patients. While they engage in sleep restriction, patients should keep sleep logs to track their “sleep efficiency” (ie, estimated time asleep vs time in bed). Once good sleep efficiency (>85%) is achieved, they may gradually lengthen their allowed time in bed by 15 minutes each week until they are obtaining 7 to 9 hours of sleep per night. (See “Breaking the cycle of insomnia by employing sleep restriction.”)

Cognitive therapy. Cognitive therapies for insomnia are usually provided by psychologists with special training. Three specific techniques that have evidence ratings* from the AASM are:²⁰

1. Relaxation training, including progressive muscle relaxation, guided imagery, and abdominal breathing to lower somatic and cognitive arousal states that interfere with sleep (strength of recommendation [SOR]: A).
2. Biofeedback therapy trains patients to control some physiologic variable through visual or auditory feedback. The objective is to reduce somatic arousal (SOR: B).
3. Paradoxical intention in which the patient is trained to confront the fear of staying awake and its potential effects. The objective is to eliminate a patient’s anxiety about sleep performance (SOR: B).

Pharmacotherapy: Overused? Addictive?

For patients who continue to struggle with insomnia despite attempting CBT-I, or for those who prefer a different approach, pharmacotherapy is a reasonable therapeutic option. While hypnotic medications are no guarantee of success, they sometimes provide meaningful benefit when supplied to a patient who has successfully established good cognitive and behavioral techniques, but is still struggling with insomnia.

Use of hypnotic medications has increased dramatically in recent years. Prescriptions for sleep medications approached 60 million in 2008, up 54% from 2004, with sales topping $2 billion.^30,31 A National Health and Nutrition Examination Survey looking at the period between 2005 and 2010 found that about 4% of adults ages 20 and older used prescription sleep aids in the past month.³²

Meta-analyses of pharmacotherapy for chronic insomnia show small to moderate effect sizes for sleep variables such as latency to sleep onset, total sleep time, and wake time after sleep onset.^33,34 Treatment of chronic insomnia with hypnotic medications is of comparable effectiveness to CBT-I in the early phase, but the benefits of CBT-I are more enduring.²⁷

A controversial approach. The appropriateness of hypnotic medications for chronic insomnia is controversial. While their use by health care professionals has been increasing, some authors have raised concerns about sleeping pills, citing a lack of effectiveness and possible adverse effects such as falls, driving impairment, and the potential for addiction, tolerance, and dependence.^33,35 The Beers Criteria of the American Geriatric Society recommends against the use of benzodiazepines in the elderly due to the risks of falls, cognitive impairment, and motor vehicle accidents and advises against the use of benzodiazepine agonists (such as zolpidem) for >90 days.³⁶

Two behavioral techniques for insomnia that can be easily applied in the family medicine setting are stimulus control and sleep restriction therapy.

Despite these concerns, the potential benefits of hypnotic medications for chronic insomnia should not be dismissed. The common strategy of simply addressing comorbidities and advising good sleep hygiene is insufficient for many patients. And some patients prefer the ease of using a hypnotic agent to the commitment required by CBT-I. Several reports suggest that the risk of hypnotic medication misuse in people with no history of substance abuse is overestimated.^37,38 And a panel of insomnia experts convened for the New Clinical Drug Evaluation Unit symposium in 2001 concluded, “Patients with chronic insomnia tend to exhibit therapy-seeking behavior, not drug-seeking behavior.”³⁹

Which hypnotic agent to choose?

US Food and Drug Administration (FDA)-approved hypnotic medications fall into 5 families (TABLE 2⁴⁰): benzodiazepines (BDZs), benzodiazepine agonists (BDZAs, sometimes called “Z drugs”), melatonin agonists (eg, ramelteon), tricyclic antidepressants (eg, low-dose doxepin), and orexin antagonists (eg, suvorexant). BDZs, BDZAs, and melatonin agonists potentiate sleep-promoting systems, while orexin antagonists and antihistaminergics suppress wake-promoting systems.

"Patients with chronic insomnia tend to exhibit therapy-seeking behavior, not drug-seeking behavior."

Studies of physician prescribing patterns show that among prescription medications for insomnia, zolpidem is the most popular, followed by trazodone (off-label use), other benzodiazepines, quetiapine (off-label use), and doxepin.⁴¹ Overall, over-the-counter melatonin may be more widely used than any of the prescription choices.⁴²

One useful basis for selection of an agent is whether the patient complains of difficulty with sleep initiation at the beginning of the night vs sleep maintenance, or both. For sleep initiation complaints, short-acting/sleep-promoting agents are preferred. For sleep maintenance complaints, longer-acting/wake-inhibiting medications that work at the end of the sleep phase may be necessary.

The AASM has recently concluded an exhaustive review of the literature regarding hypnotic medications for chronic insomnia.⁴³ The authors acknowledge important methodologic limitations, most notably a paucity of data on effectiveness and adverse effects, along with industry sponsorship of most studies and publication bias. Nevertheless, their conclusions favor the use of FDA-approved agents to off-label use of trazodone or over-the-counter use of melatonin or diphenhydramine. To summarize the AASM guidelines:³⁸

1. Medications recommended for sleep onset insomnia include: eszopiclone, ramelteon, temazepam, triazolam, zaleplon, and zolpidem.
2. Medications recommended for treating sleep maintenance insomnia include: doxepin, eszopiclone, suvorexant, zolpidem, and temazepam.
3. Medications not recommended for treating either sleep initiation or sleep maintenance insomnia include: diphenhydramine, melatonin, tiagabine, trazodone, tryptophan, and valerian.

These recommendations are similar to a review of hypnotics published by The Medical Letter in 2015.⁴⁰
 

Trazodone, an antidepressant medication with sedating properties, is not FDA-approved for the treatment of insomnia, yet ranks second to zolpidem in the number of prescriptions written for insomnia. Its popularity may be due to a perception of safety implied by its unscheduled FDA status and the lack of restrictions on prescribing duration. However, several reviews point out that its evidence base is weak.^44,45 There is only one placebo-controlled study involving trazodone use for "primary insomnia" (other studies have been in people with comorbid depression) and it showed insignificant improvements in sleep parameters and less effectiveness compared to zolpidem.⁴⁶

Trazadone, an antidepressant with sedating properties, is not FDA-approved for the treatment of insomnia, yet ranks second to zolpidem in the number of prescriptions written for insomnia.

Trazodone’s mechanisms of action are thought to be serotonin reuptake inhibition and alpha blockade, which might explain adverse effects such as orthostatic hypotension and psychomotor impairment. The frequency of such adverse effects is difficult to estimate since most studies of trazodone have used higher doses than are commonly used for insomnia in order to address comorbid depression. However, some experts have cautioned against its use—especially in the elderly.

The AASM guidelines recommend against use of trazodone. Others assert that it is probably best reserved for people in whom the complaint of insomnia is linked to comorbid depression.^43,44 

Is long-term use ever appropriate? There are no published guidelines about dosing strategies for hypnotics and whether nightly or intermittent use is preferred. All FDA-approved hypnotic agents are for short-term use, but this designation stems from a lack of long-term studies demonstrating continuing efficacy rather than actual proof of loss of effect. Although tolerance to over-the-counter sleep aids does occur, it has not been demonstrated to occur with FDA-approved agents. Studies of eszopiclone and zolpidem indicate continuing effectiveness as hypnotics with nightly use over a time-frame of several months to one year.^47,48

Regarding the thorny question of long-term use of hypnotics for chronic insomnia, the AASM concluded that long-term use should be reserved for “individuals in whom CBT-I is inaccessible or ineffective, who have been appropriately screened for contraindications to such treatment, who maintain long-term gains with medication, and who are followed regularly.”⁴³

CORRESPONDENCE
Adam J. Sorscher, MD, Dartmouth-Hitchcock Medical Center, 18 Old Etna Road, Lebanon, NH 03766; [email protected].

Although it is often taken for granted, the ability to initiate and maintain sleep throughout the night is elusive for many. About one-third of adults experience a troublesome episode of insomnia.¹ In most, it is transient, but in 10% to 15% (roughly 30 million people), the problem becomes self-perpetuating and chronic.² Chronic insomnia is one of the most prevalent conditions that family physicians (FPs) encounter, a function of it being so closely associated with comorbid conditions that FPs deal with every day, such as depression, chronic pain, and polypharmacy.^3,4

Insomnia can be vexing for a number of reasons. Because it is not acutely dangerous, patients may present it as an “add-on” concern at the end of an already lengthy visit. And because insomnia is often a symptom of multiple underlying physiologic and psychological factors, it requires the FP to engage in a thorough and time-consuming exploration of possible causes and comorbidities. Finally, standard treatment options have drawbacks: reports show that use of pharmacotherapy is troubling to prescribers primarily because of concerns about adverse effects and dependence;^5-7 the other major therapeutic avenue, cognitive behavioral therapy for insomnia (CBT-I), requires training and is time-consuming to deliver in the context of an office visit.^8,9

Despite these obstacles, successful evaluation and treatment of insomnia can be highly rewarding. Chronic insomnia is associated with great individual misery and negative consequences for long-term health. Specifically, it is associated with reduced quality of life and daytime functioning,¹⁰ depression,^11,12 hypertension,^13,14 increased workplace accidents and absenteeism,^15-17 and exacerbations of chronic pain.¹⁸ And while the evaluation and management of insomnia can be laborious, a systematic method can streamline the process.

Insomnia: Symptom or cause?

The International Classification of Sleep Disorders defines chronic insomnia as an inability to sleep sufficiently despite creating adequate opportunity. It occurs at least 3 nights per week for >3 months with perceived negative consequences during the day. Patients typically complain about symptoms including fatigue, diminished cog­nitive performance, and mood disturbance.¹⁹ Acute insomnia triggered by one or more biopsychosocial stresses is, by definition, self-limited and has different underlying mechanisms. As such, it will not be described in this review.

The chief risk factors are female gender, low socioeconomic status, and increasing age.²⁰ However, cohorts of healthy seniors show preserved good sleep; the increase in prevalence of insomnia in the elderly is likely linked more specifically to age-related accumulation of medical/mental health disorders and polypharmacy than aging per se.²¹

Research over the past 20 years has shown that comorbidities have a bidirectional relationship with insomnia, rather than a one-way cause and effect.

In the past, insomnia was viewed as a symptom, occurring secondarily to an underlying cause, usually an acute biopsychosocial stressor or depression. It was assumed that if the primary cause was effectively treated, then healthy sleep would return.

But research over the past 20 years has changed this paradigm in 2 ways. First, when comorbidities such as depression or chronic pain are present, they have a bidirectional relationship with insomnia rather than a one-way cause and effect. For example, instead of depression being a primary disorder from which insomnia can result, it is now recognized that insomnia can be present first and is a risk factor for new-onset depression. When depression and insomnia coexist, they may exacerbate each other in a bidirectional pattern.

Secondly, an estimated 15% of chronic insomnia sufferers have no targetable comorbidity; rather, they are unable to get sufficient sleep in large part because of a trait-like predisposition to fragile sleep, called hyperarousal brain physiology.²² These people used to be described as having “primary insomnia,” although the term has been dropped from the 5th edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM).²³

Assess comorbidities, obtain sleep logs

The evaluation of the chronic form of insomnia should begin with a thorough medical his­tory to assess for comorbid conditions that can exacerbate disturbed sleep. These are generally grouped into medical disorders (TABLE 1²⁰), medications/substances (eg, antidepressants, stimulants, decongestants, narcotic analgesics, cardiovascular drugs, pulmonary agents, alcohol), and mental health disorders (especially depression and anxiety). It’s important to consider whether such comorbidities are contributing to the insomnia and optimize treatment that addresses them.

Take particular care to evaluate signs and symptoms of comorbid primary sleep disorders such as obstructive sleep apnea, restless legs syndrome (RLS), and circadian rhythm disorders since any of these can present with a complaint of insomnia. RLS, usually classified as a sleep disorder because of its circadian pattern (it is experienced more at night than during the day), is present to a troublesome degree in about 3% to 4% of all adults.²⁴ It is important to inquire about symptoms of RLS (urge to move legs in the night more than during the day; relieved with movement; worsened with inactivity) so as not to miss this treatable cause of insomnia.

The physical exam should focus on signs that suggest sleep-disordered breathing—obesity, large neck girth, hypertension, and crowded oropharynx—because people with sleep apnea often present with the complaint of frequent awakenings.

Sleep logs can present a powerful picture

In addition to a history and physical exam, physicians should ask their patients with chronic insomnia to complete sleep logs for 2 to 3 weeks.²⁰ A sleep log with midnight near the middle of the page is preferred by many because it places the typical sleeping hours in the middle of the page, showing relevant information in a way that can be grasped immediately (FIGURE 1). To save time, nurses can provide sleep logs to patients along with instructions about how to complete them.

Patient-completed sleep logs often illuminate obvious detrimental behaviors that reinforce insomnia (eg, spending excessive time in bed, having irregular bed/wake times, daytime napping that diminishes sleep drive in the evening). In addition, they sometimes reveal circadian rhythm abnormalities such as delayed sleep phase syndrome in which the patient attempts to sleep at a normal bedtime, but exhibits a marked delay in falling asleep/waking up compared to societal norms. Seeing such information graphically represented is often a powerful learning experience for both physician and patient.

Sleep studies aren't usually warranted

In its most recent (2008) clinical guideline on the evaluation and management of chronic insomnia, the American Academy of Sleep Medicine (AASM) stated that “routine testing in the sleep lab is not warranted for most cases of insomnia.” Instead, it is reserved for individuals in whom there is a suspicion of a comorbid sleep disorder. FPs should refer patients for formal sleep studies only if, in addition to the insomnia complaint, there is suspicion of:²⁰

• obstructive sleep apnea (based upon some combination of loud snoring, obesity, hypertension, and/or excessive daytime sleepiness),
• narcolepsy (based upon excessive daytime sleepiness without a readily identifiable cause), or
• arousals with the potential for self-injurious behavior (parasomnias).

Treatments: Sleep hygiene, CBT-I, and medication

Sleep hygiene, cognitive/behavioral techniques, and pharmacotherapy serve as the core of therapy for chronic insomnia.

Sleep hygiene: Common-sense strategies

Most FPs are familiar with sleep hygiene instructions; these are simple, common-sense behavioral techniques such as limiting caffeine and screen (television, computer) time at night, avoiding daytime naps, and maintaining regular bed- and out-of-bed times. (See “A sleep hygiene checklist.”) Although it is a logical starting point for behavioral modification, sleep hygiene has not been studied rigorously as a monotherapy for insomnia and, therefore, doesn’t have an evidence rating in terms of effectiveness.²⁰

CBT-I: Treatment of choice

CBT-I seeks to lower cognitive and somatic arousal. Taken together, cognitive and behavioral techniques are effective in 70% to 80% of people, whether they have primary insomnia or comorbidities.^25-27 Furthermore, the benefits are sustained with the passage of time.²⁷ CBT-I is regarded as the treatment of choice for chronic insomnia.²⁰

An experience of successful sleep initiation and maintenance is important psychologically: It renews patients' confidence in the ability to sleep.

When provided by a highly trained mental health professional, CBT-I usually takes the form of a series of 6 to 8 weekly appointments. Descriptions and manuals for CBT-I abound and online programs have also proliferated.^28,29 However, there is a shortage of highly trained providers, and most FPs do not feel proficient to engage fully in CBT-I.^8,9 Nevertheless, some behavioral elements of CBT-I, such as stimulus control and sleep restriction, can be utilized in the family medicine setting and may be effective for a significant subset of patients.

Stimulus control and sleep restriction. Two behavioral techniques for insomnia that can be applied in the family medicine setting are stimulus control and sleep restriction therapy.²⁰

With stimulus control, patients attempt to eliminate stimuli that weaken the psychological association between the bed and successful sleep, namely wakeful activities in bed such as watching television, reading, or even “tossing and turning.” Instead, they are instructed to use their bed only for sleep (and intimacy), to vacate it if awake and not clearly on the verge of sleep, and to avoid looking at a clock during the night. Patients are also advised to sleep only in their own bed and not in other places in their home.

Sleep restriction is predicated on the observation that many people with insomnia habitually spend too much time awake in bed, and this creates a conditioned arousal response to the bed. With sleep restriction, the patient is assigned a narrow window of “allowed time in bed,” usually a 6-hour interval of their choosing, and is instructed to adhere to this schedule for a period of 2 to 4 weeks. Many patients find that they fall asleep more rapidly and stay asleep longer after a few weeks. This experience of “successful” sleep initiation and maintenance is important psychologically; it renews their confidence in their ability to sleep, which is missing in most people with chronic insomnia.

If you use this approach with a patient, be sure to acknowledge that sleep restriction usually engenders some sleep deprivation in the first few weeks. But it is only a short-term intervention designed to change the expectation of nightly insomnia that is so ingrained in these patients. While they engage in sleep restriction, patients should keep sleep logs to track their “sleep efficiency” (ie, estimated time asleep vs time in bed). Once good sleep efficiency (>85%) is achieved, they may gradually lengthen their allowed time in bed by 15 minutes each week until they are obtaining 7 to 9 hours of sleep per night. (See “Breaking the cycle of insomnia by employing sleep restriction.”)

Cognitive therapy. Cognitive therapies for insomnia are usually provided by psychologists with special training. Three specific techniques that have evidence ratings* from the AASM are:²⁰

1. Relaxation training, including progressive muscle relaxation, guided imagery, and abdominal breathing to lower somatic and cognitive arousal states that interfere with sleep (strength of recommendation [SOR]: A).
2. Biofeedback therapy trains patients to control some physiologic variable through visual or auditory feedback. The objective is to reduce somatic arousal (SOR: B).
3. Paradoxical intention in which the patient is trained to confront the fear of staying awake and its potential effects. The objective is to eliminate a patient’s anxiety about sleep performance (SOR: B).

Pharmacotherapy: Overused? Addictive?

For patients who continue to struggle with insomnia despite attempting CBT-I, or for those who prefer a different approach, pharmacotherapy is a reasonable therapeutic option. While hypnotic medications are no guarantee of success, they sometimes provide meaningful benefit when supplied to a patient who has successfully established good cognitive and behavioral techniques, but is still struggling with insomnia.

Use of hypnotic medications has increased dramatically in recent years. Prescriptions for sleep medications approached 60 million in 2008, up 54% from 2004, with sales topping $2 billion.^30,31 A National Health and Nutrition Examination Survey looking at the period between 2005 and 2010 found that about 4% of adults ages 20 and older used prescription sleep aids in the past month.³²

Meta-analyses of pharmacotherapy for chronic insomnia show small to moderate effect sizes for sleep variables such as latency to sleep onset, total sleep time, and wake time after sleep onset.^33,34 Treatment of chronic insomnia with hypnotic medications is of comparable effectiveness to CBT-I in the early phase, but the benefits of CBT-I are more enduring.²⁷

A controversial approach. The appropriateness of hypnotic medications for chronic insomnia is controversial. While their use by health care professionals has been increasing, some authors have raised concerns about sleeping pills, citing a lack of effectiveness and possible adverse effects such as falls, driving impairment, and the potential for addiction, tolerance, and dependence.^33,35 The Beers Criteria of the American Geriatric Society recommends against the use of benzodiazepines in the elderly due to the risks of falls, cognitive impairment, and motor vehicle accidents and advises against the use of benzodiazepine agonists (such as zolpidem) for >90 days.³⁶

Two behavioral techniques for insomnia that can be easily applied in the family medicine setting are stimulus control and sleep restriction therapy.

Despite these concerns, the potential benefits of hypnotic medications for chronic insomnia should not be dismissed. The common strategy of simply addressing comorbidities and advising good sleep hygiene is insufficient for many patients. And some patients prefer the ease of using a hypnotic agent to the commitment required by CBT-I. Several reports suggest that the risk of hypnotic medication misuse in people with no history of substance abuse is overestimated.^37,38 And a panel of insomnia experts convened for the New Clinical Drug Evaluation Unit symposium in 2001 concluded, “Patients with chronic insomnia tend to exhibit therapy-seeking behavior, not drug-seeking behavior.”³⁹

Which hypnotic agent to choose?

US Food and Drug Administration (FDA)-approved hypnotic medications fall into 5 families (TABLE 2⁴⁰): benzodiazepines (BDZs), benzodiazepine agonists (BDZAs, sometimes called “Z drugs”), melatonin agonists (eg, ramelteon), tricyclic antidepressants (eg, low-dose doxepin), and orexin antagonists (eg, suvorexant). BDZs, BDZAs, and melatonin agonists potentiate sleep-promoting systems, while orexin antagonists and antihistaminergics suppress wake-promoting systems.

"Patients with chronic insomnia tend to exhibit therapy-seeking behavior, not drug-seeking behavior."

Studies of physician prescribing patterns show that among prescription medications for insomnia, zolpidem is the most popular, followed by trazodone (off-label use), other benzodiazepines, quetiapine (off-label use), and doxepin.⁴¹ Overall, over-the-counter melatonin may be more widely used than any of the prescription choices.⁴²

One useful basis for selection of an agent is whether the patient complains of difficulty with sleep initiation at the beginning of the night vs sleep maintenance, or both. For sleep initiation complaints, short-acting/sleep-promoting agents are preferred. For sleep maintenance complaints, longer-acting/wake-inhibiting medications that work at the end of the sleep phase may be necessary.

The AASM has recently concluded an exhaustive review of the literature regarding hypnotic medications for chronic insomnia.⁴³ The authors acknowledge important methodologic limitations, most notably a paucity of data on effectiveness and adverse effects, along with industry sponsorship of most studies and publication bias. Nevertheless, their conclusions favor the use of FDA-approved agents to off-label use of trazodone or over-the-counter use of melatonin or diphenhydramine. To summarize the AASM guidelines:³⁸

1. Medications recommended for sleep onset insomnia include: eszopiclone, ramelteon, temazepam, triazolam, zaleplon, and zolpidem.
2. Medications recommended for treating sleep maintenance insomnia include: doxepin, eszopiclone, suvorexant, zolpidem, and temazepam.
3. Medications not recommended for treating either sleep initiation or sleep maintenance insomnia include: diphenhydramine, melatonin, tiagabine, trazodone, tryptophan, and valerian.

These recommendations are similar to a review of hypnotics published by The Medical Letter in 2015.⁴⁰
 

Trazodone, an antidepressant medication with sedating properties, is not FDA-approved for the treatment of insomnia, yet ranks second to zolpidem in the number of prescriptions written for insomnia. Its popularity may be due to a perception of safety implied by its unscheduled FDA status and the lack of restrictions on prescribing duration. However, several reviews point out that its evidence base is weak.^44,45 There is only one placebo-controlled study involving trazodone use for "primary insomnia" (other studies have been in people with comorbid depression) and it showed insignificant improvements in sleep parameters and less effectiveness compared to zolpidem.⁴⁶

Trazadone, an antidepressant with sedating properties, is not FDA-approved for the treatment of insomnia, yet ranks second to zolpidem in the number of prescriptions written for insomnia.

Trazodone’s mechanisms of action are thought to be serotonin reuptake inhibition and alpha blockade, which might explain adverse effects such as orthostatic hypotension and psychomotor impairment. The frequency of such adverse effects is difficult to estimate since most studies of trazodone have used higher doses than are commonly used for insomnia in order to address comorbid depression. However, some experts have cautioned against its use—especially in the elderly.

The AASM guidelines recommend against use of trazodone. Others assert that it is probably best reserved for people in whom the complaint of insomnia is linked to comorbid depression.^43,44 

Is long-term use ever appropriate? There are no published guidelines about dosing strategies for hypnotics and whether nightly or intermittent use is preferred. All FDA-approved hypnotic agents are for short-term use, but this designation stems from a lack of long-term studies demonstrating continuing efficacy rather than actual proof of loss of effect. Although tolerance to over-the-counter sleep aids does occur, it has not been demonstrated to occur with FDA-approved agents. Studies of eszopiclone and zolpidem indicate continuing effectiveness as hypnotics with nightly use over a time-frame of several months to one year.^47,48

Regarding the thorny question of long-term use of hypnotics for chronic insomnia, the AASM concluded that long-term use should be reserved for “individuals in whom CBT-I is inaccessible or ineffective, who have been appropriately screened for contraindications to such treatment, who maintain long-term gains with medication, and who are followed regularly.”⁴³

CORRESPONDENCE
Adam J. Sorscher, MD, Dartmouth-Hitchcock Medical Center, 18 Old Etna Road, Lebanon, NH 03766; [email protected].

Although it is often taken for granted, the ability to initiate and maintain sleep throughout the night is elusive for many. About one-third of adults experience a troublesome episode of insomnia.¹ In most, it is transient, but in 10% to 15% (roughly 30 million people), the problem becomes self-perpetuating and chronic.² Chronic insomnia is one of the most prevalent conditions that family physicians (FPs) encounter, a function of it being so closely associated with comorbid conditions that FPs deal with every day, such as depression, chronic pain, and polypharmacy.^3,4

Insomnia can be vexing for a number of reasons. Because it is not acutely dangerous, patients may present it as an “add-on” concern at the end of an already lengthy visit. And because insomnia is often a symptom of multiple underlying physiologic and psychological factors, it requires the FP to engage in a thorough and time-consuming exploration of possible causes and comorbidities. Finally, standard treatment options have drawbacks: reports show that use of pharmacotherapy is troubling to prescribers primarily because of concerns about adverse effects and dependence;^5-7 the other major therapeutic avenue, cognitive behavioral therapy for insomnia (CBT-I), requires training and is time-consuming to deliver in the context of an office visit.^8,9

Despite these obstacles, successful evaluation and treatment of insomnia can be highly rewarding. Chronic insomnia is associated with great individual misery and negative consequences for long-term health. Specifically, it is associated with reduced quality of life and daytime functioning,¹⁰ depression,^11,12 hypertension,^13,14 increased workplace accidents and absenteeism,^15-17 and exacerbations of chronic pain.¹⁸ And while the evaluation and management of insomnia can be laborious, a systematic method can streamline the process.

Insomnia: Symptom or cause?

The International Classification of Sleep Disorders defines chronic insomnia as an inability to sleep sufficiently despite creating adequate opportunity. It occurs at least 3 nights per week for >3 months with perceived negative consequences during the day. Patients typically complain about symptoms including fatigue, diminished cog­nitive performance, and mood disturbance.¹⁹ Acute insomnia triggered by one or more biopsychosocial stresses is, by definition, self-limited and has different underlying mechanisms. As such, it will not be described in this review.

The chief risk factors are female gender, low socioeconomic status, and increasing age.²⁰ However, cohorts of healthy seniors show preserved good sleep; the increase in prevalence of insomnia in the elderly is likely linked more specifically to age-related accumulation of medical/mental health disorders and polypharmacy than aging per se.²¹

Research over the past 20 years has shown that comorbidities have a bidirectional relationship with insomnia, rather than a one-way cause and effect.

In the past, insomnia was viewed as a symptom, occurring secondarily to an underlying cause, usually an acute biopsychosocial stressor or depression. It was assumed that if the primary cause was effectively treated, then healthy sleep would return.

But research over the past 20 years has changed this paradigm in 2 ways. First, when comorbidities such as depression or chronic pain are present, they have a bidirectional relationship with insomnia rather than a one-way cause and effect. For example, instead of depression being a primary disorder from which insomnia can result, it is now recognized that insomnia can be present first and is a risk factor for new-onset depression. When depression and insomnia coexist, they may exacerbate each other in a bidirectional pattern.

Secondly, an estimated 15% of chronic insomnia sufferers have no targetable comorbidity; rather, they are unable to get sufficient sleep in large part because of a trait-like predisposition to fragile sleep, called hyperarousal brain physiology.²² These people used to be described as having “primary insomnia,” although the term has been dropped from the 5th edition of The Diagnostic and Statistical Manual of Mental Disorders (DSM).²³

Assess comorbidities, obtain sleep logs

The evaluation of the chronic form of insomnia should begin with a thorough medical his­tory to assess for comorbid conditions that can exacerbate disturbed sleep. These are generally grouped into medical disorders (TABLE 1²⁰), medications/substances (eg, antidepressants, stimulants, decongestants, narcotic analgesics, cardiovascular drugs, pulmonary agents, alcohol), and mental health disorders (especially depression and anxiety). It’s important to consider whether such comorbidities are contributing to the insomnia and optimize treatment that addresses them.

Take particular care to evaluate signs and symptoms of comorbid primary sleep disorders such as obstructive sleep apnea, restless legs syndrome (RLS), and circadian rhythm disorders since any of these can present with a complaint of insomnia. RLS, usually classified as a sleep disorder because of its circadian pattern (it is experienced more at night than during the day), is present to a troublesome degree in about 3% to 4% of all adults.²⁴ It is important to inquire about symptoms of RLS (urge to move legs in the night more than during the day; relieved with movement; worsened with inactivity) so as not to miss this treatable cause of insomnia.

The physical exam should focus on signs that suggest sleep-disordered breathing—obesity, large neck girth, hypertension, and crowded oropharynx—because people with sleep apnea often present with the complaint of frequent awakenings.

Sleep logs can present a powerful picture

In addition to a history and physical exam, physicians should ask their patients with chronic insomnia to complete sleep logs for 2 to 3 weeks.²⁰ A sleep log with midnight near the middle of the page is preferred by many because it places the typical sleeping hours in the middle of the page, showing relevant information in a way that can be grasped immediately (FIGURE 1). To save time, nurses can provide sleep logs to patients along with instructions about how to complete them.

Patient-completed sleep logs often illuminate obvious detrimental behaviors that reinforce insomnia (eg, spending excessive time in bed, having irregular bed/wake times, daytime napping that diminishes sleep drive in the evening). In addition, they sometimes reveal circadian rhythm abnormalities such as delayed sleep phase syndrome in which the patient attempts to sleep at a normal bedtime, but exhibits a marked delay in falling asleep/waking up compared to societal norms. Seeing such information graphically represented is often a powerful learning experience for both physician and patient.

Sleep studies aren't usually warranted

In its most recent (2008) clinical guideline on the evaluation and management of chronic insomnia, the American Academy of Sleep Medicine (AASM) stated that “routine testing in the sleep lab is not warranted for most cases of insomnia.” Instead, it is reserved for individuals in whom there is a suspicion of a comorbid sleep disorder. FPs should refer patients for formal sleep studies only if, in addition to the insomnia complaint, there is suspicion of:²⁰

• obstructive sleep apnea (based upon some combination of loud snoring, obesity, hypertension, and/or excessive daytime sleepiness),
• narcolepsy (based upon excessive daytime sleepiness without a readily identifiable cause), or
• arousals with the potential for self-injurious behavior (parasomnias).

Treatments: Sleep hygiene, CBT-I, and medication

Sleep hygiene, cognitive/behavioral techniques, and pharmacotherapy serve as the core of therapy for chronic insomnia.

Sleep hygiene: Common-sense strategies

Most FPs are familiar with sleep hygiene instructions; these are simple, common-sense behavioral techniques such as limiting caffeine and screen (television, computer) time at night, avoiding daytime naps, and maintaining regular bed- and out-of-bed times. (See “A sleep hygiene checklist.”) Although it is a logical starting point for behavioral modification, sleep hygiene has not been studied rigorously as a monotherapy for insomnia and, therefore, doesn’t have an evidence rating in terms of effectiveness.²⁰

CBT-I: Treatment of choice

CBT-I seeks to lower cognitive and somatic arousal. Taken together, cognitive and behavioral techniques are effective in 70% to 80% of people, whether they have primary insomnia or comorbidities.^25-27 Furthermore, the benefits are sustained with the passage of time.²⁷ CBT-I is regarded as the treatment of choice for chronic insomnia.²⁰

An experience of successful sleep initiation and maintenance is important psychologically: It renews patients' confidence in the ability to sleep.

When provided by a highly trained mental health professional, CBT-I usually takes the form of a series of 6 to 8 weekly appointments. Descriptions and manuals for CBT-I abound and online programs have also proliferated.^28,29 However, there is a shortage of highly trained providers, and most FPs do not feel proficient to engage fully in CBT-I.^8,9 Nevertheless, some behavioral elements of CBT-I, such as stimulus control and sleep restriction, can be utilized in the family medicine setting and may be effective for a significant subset of patients.

Stimulus control and sleep restriction. Two behavioral techniques for insomnia that can be applied in the family medicine setting are stimulus control and sleep restriction therapy.²⁰

With stimulus control, patients attempt to eliminate stimuli that weaken the psychological association between the bed and successful sleep, namely wakeful activities in bed such as watching television, reading, or even “tossing and turning.” Instead, they are instructed to use their bed only for sleep (and intimacy), to vacate it if awake and not clearly on the verge of sleep, and to avoid looking at a clock during the night. Patients are also advised to sleep only in their own bed and not in other places in their home.

Sleep restriction is predicated on the observation that many people with insomnia habitually spend too much time awake in bed, and this creates a conditioned arousal response to the bed. With sleep restriction, the patient is assigned a narrow window of “allowed time in bed,” usually a 6-hour interval of their choosing, and is instructed to adhere to this schedule for a period of 2 to 4 weeks. Many patients find that they fall asleep more rapidly and stay asleep longer after a few weeks. This experience of “successful” sleep initiation and maintenance is important psychologically; it renews their confidence in their ability to sleep, which is missing in most people with chronic insomnia.

If you use this approach with a patient, be sure to acknowledge that sleep restriction usually engenders some sleep deprivation in the first few weeks. But it is only a short-term intervention designed to change the expectation of nightly insomnia that is so ingrained in these patients. While they engage in sleep restriction, patients should keep sleep logs to track their “sleep efficiency” (ie, estimated time asleep vs time in bed). Once good sleep efficiency (>85%) is achieved, they may gradually lengthen their allowed time in bed by 15 minutes each week until they are obtaining 7 to 9 hours of sleep per night. (See “Breaking the cycle of insomnia by employing sleep restriction.”)

Cognitive therapy. Cognitive therapies for insomnia are usually provided by psychologists with special training. Three specific techniques that have evidence ratings* from the AASM are:²⁰

1. Relaxation training, including progressive muscle relaxation, guided imagery, and abdominal breathing to lower somatic and cognitive arousal states that interfere with sleep (strength of recommendation [SOR]: A).
2. Biofeedback therapy trains patients to control some physiologic variable through visual or auditory feedback. The objective is to reduce somatic arousal (SOR: B).
3. Paradoxical intention in which the patient is trained to confront the fear of staying awake and its potential effects. The objective is to eliminate a patient’s anxiety about sleep performance (SOR: B).

Pharmacotherapy: Overused? Addictive?

For patients who continue to struggle with insomnia despite attempting CBT-I, or for those who prefer a different approach, pharmacotherapy is a reasonable therapeutic option. While hypnotic medications are no guarantee of success, they sometimes provide meaningful benefit when supplied to a patient who has successfully established good cognitive and behavioral techniques, but is still struggling with insomnia.

Use of hypnotic medications has increased dramatically in recent years. Prescriptions for sleep medications approached 60 million in 2008, up 54% from 2004, with sales topping $2 billion.^30,31 A National Health and Nutrition Examination Survey looking at the period between 2005 and 2010 found that about 4% of adults ages 20 and older used prescription sleep aids in the past month.³²

Meta-analyses of pharmacotherapy for chronic insomnia show small to moderate effect sizes for sleep variables such as latency to sleep onset, total sleep time, and wake time after sleep onset.^33,34 Treatment of chronic insomnia with hypnotic medications is of comparable effectiveness to CBT-I in the early phase, but the benefits of CBT-I are more enduring.²⁷

A controversial approach. The appropriateness of hypnotic medications for chronic insomnia is controversial. While their use by health care professionals has been increasing, some authors have raised concerns about sleeping pills, citing a lack of effectiveness and possible adverse effects such as falls, driving impairment, and the potential for addiction, tolerance, and dependence.^33,35 The Beers Criteria of the American Geriatric Society recommends against the use of benzodiazepines in the elderly due to the risks of falls, cognitive impairment, and motor vehicle accidents and advises against the use of benzodiazepine agonists (such as zolpidem) for >90 days.³⁶

Two behavioral techniques for insomnia that can be easily applied in the family medicine setting are stimulus control and sleep restriction therapy.

Despite these concerns, the potential benefits of hypnotic medications for chronic insomnia should not be dismissed. The common strategy of simply addressing comorbidities and advising good sleep hygiene is insufficient for many patients. And some patients prefer the ease of using a hypnotic agent to the commitment required by CBT-I. Several reports suggest that the risk of hypnotic medication misuse in people with no history of substance abuse is overestimated.^37,38 And a panel of insomnia experts convened for the New Clinical Drug Evaluation Unit symposium in 2001 concluded, “Patients with chronic insomnia tend to exhibit therapy-seeking behavior, not drug-seeking behavior.”³⁹

Which hypnotic agent to choose?

US Food and Drug Administration (FDA)-approved hypnotic medications fall into 5 families (TABLE 2⁴⁰): benzodiazepines (BDZs), benzodiazepine agonists (BDZAs, sometimes called “Z drugs”), melatonin agonists (eg, ramelteon), tricyclic antidepressants (eg, low-dose doxepin), and orexin antagonists (eg, suvorexant). BDZs, BDZAs, and melatonin agonists potentiate sleep-promoting systems, while orexin antagonists and antihistaminergics suppress wake-promoting systems.

"Patients with chronic insomnia tend to exhibit therapy-seeking behavior, not drug-seeking behavior."

Studies of physician prescribing patterns show that among prescription medications for insomnia, zolpidem is the most popular, followed by trazodone (off-label use), other benzodiazepines, quetiapine (off-label use), and doxepin.⁴¹ Overall, over-the-counter melatonin may be more widely used than any of the prescription choices.⁴²

One useful basis for selection of an agent is whether the patient complains of difficulty with sleep initiation at the beginning of the night vs sleep maintenance, or both. For sleep initiation complaints, short-acting/sleep-promoting agents are preferred. For sleep maintenance complaints, longer-acting/wake-inhibiting medications that work at the end of the sleep phase may be necessary.

The AASM has recently concluded an exhaustive review of the literature regarding hypnotic medications for chronic insomnia.⁴³ The authors acknowledge important methodologic limitations, most notably a paucity of data on effectiveness and adverse effects, along with industry sponsorship of most studies and publication bias. Nevertheless, their conclusions favor the use of FDA-approved agents to off-label use of trazodone or over-the-counter use of melatonin or diphenhydramine. To summarize the AASM guidelines:³⁸

1. Medications recommended for sleep onset insomnia include: eszopiclone, ramelteon, temazepam, triazolam, zaleplon, and zolpidem.
2. Medications recommended for treating sleep maintenance insomnia include: doxepin, eszopiclone, suvorexant, zolpidem, and temazepam.
3. Medications not recommended for treating either sleep initiation or sleep maintenance insomnia include: diphenhydramine, melatonin, tiagabine, trazodone, tryptophan, and valerian.

These recommendations are similar to a review of hypnotics published by The Medical Letter in 2015.⁴⁰
 

Trazodone, an antidepressant medication with sedating properties, is not FDA-approved for the treatment of insomnia, yet ranks second to zolpidem in the number of prescriptions written for insomnia. Its popularity may be due to a perception of safety implied by its unscheduled FDA status and the lack of restrictions on prescribing duration. However, several reviews point out that its evidence base is weak.^44,45 There is only one placebo-controlled study involving trazodone use for "primary insomnia" (other studies have been in people with comorbid depression) and it showed insignificant improvements in sleep parameters and less effectiveness compared to zolpidem.⁴⁶

Trazadone, an antidepressant with sedating properties, is not FDA-approved for the treatment of insomnia, yet ranks second to zolpidem in the number of prescriptions written for insomnia.

Trazodone’s mechanisms of action are thought to be serotonin reuptake inhibition and alpha blockade, which might explain adverse effects such as orthostatic hypotension and psychomotor impairment. The frequency of such adverse effects is difficult to estimate since most studies of trazodone have used higher doses than are commonly used for insomnia in order to address comorbid depression. However, some experts have cautioned against its use—especially in the elderly.

The AASM guidelines recommend against use of trazodone. Others assert that it is probably best reserved for people in whom the complaint of insomnia is linked to comorbid depression.^43,44 

Is long-term use ever appropriate? There are no published guidelines about dosing strategies for hypnotics and whether nightly or intermittent use is preferred. All FDA-approved hypnotic agents are for short-term use, but this designation stems from a lack of long-term studies demonstrating continuing efficacy rather than actual proof of loss of effect. Although tolerance to over-the-counter sleep aids does occur, it has not been demonstrated to occur with FDA-approved agents. Studies of eszopiclone and zolpidem indicate continuing effectiveness as hypnotics with nightly use over a time-frame of several months to one year.^47,48

Regarding the thorny question of long-term use of hypnotics for chronic insomnia, the AASM concluded that long-term use should be reserved for “individuals in whom CBT-I is inaccessible or ineffective, who have been appropriately screened for contraindications to such treatment, who maintain long-term gains with medication, and who are followed regularly.”⁴³

CORRESPONDENCE
Adam J. Sorscher, MD, Dartmouth-Hitchcock Medical Center, 18 Old Etna Road, Lebanon, NH 03766; [email protected].

Photo by Rhoda Baer

A report on cancer in the US suggests the incidence of leukemia and myeloma has been on the rise in recent years, but the incidence of non-Hodgkin lymphoma (NHL) has been on the decline.

Meanwhile, annual death rates for leukemia and NHL have decreased, and annual death rates for myeloma have decreased in men but not in women.

Furthermore, patients with leukemia, NHL, and myeloma have seen a substantial improvement in 5-year survival rates in recent years relative to patients in the late 1970s.

These findings are part of the Annual Report to the Nation on the Status of Cancer, 1975-2014, which has been published in the Journal of the National Cancer Institute.

This report is released each year, but the current edition includes a special section focused on survival.

“While trends in death rates are the most commonly used measure to assess progress against cancer, survival trends are also an important measure to evaluate progress in improvement of cancer outcomes,” said Ahmedin Jemal, DVM, PhD, of the American Cancer Society.

“We last included a special section on cancer survival in 2004, and, as we found then, survival improved over time for almost all cancers at every stage of diagnosis.”

For the current report, researchers calculated the 5-year average annual percent changes (AAPCs) for 2009 to 2013 for cancer incidence and for 2010 to 2014 for cancer mortality.

Cancer incidence (2009-2013)

In women, the AAPC increased 1.5% for leukemia (P<0.05), decreased 0.5% for NHL (P<0.05), and increased 2.2% for myeloma (P<0.05).

In men, the AAPC increased 1.7% for leukemia (P<0.05), decreased 0.2% for NHL, and increased 2.8% for myeloma (P<0.05).

Cancer mortality (2010-2014)

In women, the AAPC decreased 1.2% for leukemia (P<0.05), decreased 2.2% for NHL (P<0.05), and increased 0.5% for myeloma.

In men, the AAPC decreased 1.0% for leukemia (P<0.05), decreased 2.0% for NHL (P<0.05), and decreased 0.9% for myeloma (P<0.05).

5-year survival

The researchers compared 5-year relative survival for cancers diagnosed from 1975 to 1977 and those diagnosed from 2006 to 2012.

The absolute percentage change over time (for both sexes combined) was 26.1% for NHL, 25.7% for myeloma, and 28.5% for leukemia.

Five-year survival for patients diagnosed in 1975-1977 was 46.5% for NHL, 24.6% for myeloma, and 34.2% for leukemia.

Five-year survival for patients diagnosed in 2006-2012 was 72.6% for NHL, 50.2% for myeloma, and 62.7% for leukemia.

Photo by Rhoda Baer

A report on cancer in the US suggests the incidence of leukemia and myeloma has been on the rise in recent years, but the incidence of non-Hodgkin lymphoma (NHL) has been on the decline.

Meanwhile, annual death rates for leukemia and NHL have decreased, and annual death rates for myeloma have decreased in men but not in women.

Furthermore, patients with leukemia, NHL, and myeloma have seen a substantial improvement in 5-year survival rates in recent years relative to patients in the late 1970s.

These findings are part of the Annual Report to the Nation on the Status of Cancer, 1975-2014, which has been published in the Journal of the National Cancer Institute.

This report is released each year, but the current edition includes a special section focused on survival.

“While trends in death rates are the most commonly used measure to assess progress against cancer, survival trends are also an important measure to evaluate progress in improvement of cancer outcomes,” said Ahmedin Jemal, DVM, PhD, of the American Cancer Society.

“We last included a special section on cancer survival in 2004, and, as we found then, survival improved over time for almost all cancers at every stage of diagnosis.”

For the current report, researchers calculated the 5-year average annual percent changes (AAPCs) for 2009 to 2013 for cancer incidence and for 2010 to 2014 for cancer mortality.

Cancer incidence (2009-2013)

In women, the AAPC increased 1.5% for leukemia (P<0.05), decreased 0.5% for NHL (P<0.05), and increased 2.2% for myeloma (P<0.05).

In men, the AAPC increased 1.7% for leukemia (P<0.05), decreased 0.2% for NHL, and increased 2.8% for myeloma (P<0.05).

Cancer mortality (2010-2014)

In women, the AAPC decreased 1.2% for leukemia (P<0.05), decreased 2.2% for NHL (P<0.05), and increased 0.5% for myeloma.

In men, the AAPC decreased 1.0% for leukemia (P<0.05), decreased 2.0% for NHL (P<0.05), and decreased 0.9% for myeloma (P<0.05).

5-year survival

The researchers compared 5-year relative survival for cancers diagnosed from 1975 to 1977 and those diagnosed from 2006 to 2012.

The absolute percentage change over time (for both sexes combined) was 26.1% for NHL, 25.7% for myeloma, and 28.5% for leukemia.

Five-year survival for patients diagnosed in 1975-1977 was 46.5% for NHL, 24.6% for myeloma, and 34.2% for leukemia.

Five-year survival for patients diagnosed in 2006-2012 was 72.6% for NHL, 50.2% for myeloma, and 62.7% for leukemia.

Photo by Rhoda Baer

A report on cancer in the US suggests the incidence of leukemia and myeloma has been on the rise in recent years, but the incidence of non-Hodgkin lymphoma (NHL) has been on the decline.

Meanwhile, annual death rates for leukemia and NHL have decreased, and annual death rates for myeloma have decreased in men but not in women.

Furthermore, patients with leukemia, NHL, and myeloma have seen a substantial improvement in 5-year survival rates in recent years relative to patients in the late 1970s.

These findings are part of the Annual Report to the Nation on the Status of Cancer, 1975-2014, which has been published in the Journal of the National Cancer Institute.

This report is released each year, but the current edition includes a special section focused on survival.

“While trends in death rates are the most commonly used measure to assess progress against cancer, survival trends are also an important measure to evaluate progress in improvement of cancer outcomes,” said Ahmedin Jemal, DVM, PhD, of the American Cancer Society.

“We last included a special section on cancer survival in 2004, and, as we found then, survival improved over time for almost all cancers at every stage of diagnosis.”

For the current report, researchers calculated the 5-year average annual percent changes (AAPCs) for 2009 to 2013 for cancer incidence and for 2010 to 2014 for cancer mortality.

Cancer incidence (2009-2013)

In women, the AAPC increased 1.5% for leukemia (P<0.05), decreased 0.5% for NHL (P<0.05), and increased 2.2% for myeloma (P<0.05).

In men, the AAPC increased 1.7% for leukemia (P<0.05), decreased 0.2% for NHL, and increased 2.8% for myeloma (P<0.05).

Cancer mortality (2010-2014)

In women, the AAPC decreased 1.2% for leukemia (P<0.05), decreased 2.2% for NHL (P<0.05), and increased 0.5% for myeloma.

In men, the AAPC decreased 1.0% for leukemia (P<0.05), decreased 2.0% for NHL (P<0.05), and decreased 0.9% for myeloma (P<0.05).

5-year survival

The researchers compared 5-year relative survival for cancers diagnosed from 1975 to 1977 and those diagnosed from 2006 to 2012.

The absolute percentage change over time (for both sexes combined) was 26.1% for NHL, 25.7% for myeloma, and 28.5% for leukemia.

Five-year survival for patients diagnosed in 1975-1977 was 46.5% for NHL, 24.6% for myeloma, and 34.2% for leukemia.

Five-year survival for patients diagnosed in 2006-2012 was 72.6% for NHL, 50.2% for myeloma, and 62.7% for leukemia.

Influenza vaccination was associated with reduced risk of laboratory-confirmed influenza-associated death in children, a case-cohort analysis found.

“These results support current recommendations for annual influenza vaccination for all children 6 months of age” and older, wrote Brendan Flannery, PhD, and his coauthors at the Centers for Disease Control and Prevention, Atlanta. “To our knowledge, this is the first study to use laboratory-confirmed outcomes to investigate influenza vaccine effectiveness against influenza-associated deaths.”

KatarzynaBialasiewicz/Thinkstock

[email protected]

Influenza vaccination was associated with reduced risk of laboratory-confirmed influenza-associated death in children, a case-cohort analysis found.

“These results support current recommendations for annual influenza vaccination for all children 6 months of age” and older, wrote Brendan Flannery, PhD, and his coauthors at the Centers for Disease Control and Prevention, Atlanta. “To our knowledge, this is the first study to use laboratory-confirmed outcomes to investigate influenza vaccine effectiveness against influenza-associated deaths.”

KatarzynaBialasiewicz/Thinkstock

[email protected]

Influenza vaccination was associated with reduced risk of laboratory-confirmed influenza-associated death in children, a case-cohort analysis found.

“These results support current recommendations for annual influenza vaccination for all children 6 months of age” and older, wrote Brendan Flannery, PhD, and his coauthors at the Centers for Disease Control and Prevention, Atlanta. “To our knowledge, this is the first study to use laboratory-confirmed outcomes to investigate influenza vaccine effectiveness against influenza-associated deaths.”

KatarzynaBialasiewicz/Thinkstock

[email protected]

Mentorship, whether through a formal or informal system, plays a significant role in a professional’s life; it fosters the development of professional expertise and is associated with increased job satisfaction. An effective mentor guides a less-experienced colleague by modeling positive behaviors and building trust, while being cognizant that his or her role is to be dependable, engaged, authentic, and attuned to the needs of the mentee. You can probably name one of your mentors off the top of your head right now!

The original “mentor” was a character of that name in Homer’s epic poem The Odyssey, but the word is now used to refer to a trusted advisor, friend, teacher, or wise person. In the story, Mentor served as a friend and advocate to Telemachus, the son of the king of Ithaca, while his father, Odysseus, was away fighting in the Trojan War. In 1699, the novel The Adventures of Telemachus portrayed Mentor as Telemachus’ tutor, and he became the hero of the story.^1,2

History holds many examples of mentoring relationships: Socrates and Plato, Haydn and Beethoven, and Freud and Jung. Modern-day duos include Kobe Bryant and Shaquille O’Neal, Kirk and Spock, and—dare I say it?—Brady and Belichick. During the Middle Ages, mentorship—particularly in medicine and nursing—was practiced via apprenticeship, which incorporated support, guidance, socialization, well-being, empowerment, education, and career progression.³

Throughout my career as a PA, I have been fortunate to be guided by competent and willing mentors. What have they had in common? For starters, an internal desire (sometimes called generosity of spirit) to mentor and a commitment to my growth and development as their mentee. Successful professional mentors must also possess the necessary knowledge to help effectively develop their mentee’s skills. Discussions with my colleagues and previous mentors inspired the following compilation of the essential responsibilities and traits of a mentor.

Initiating new ideas. A main aspect of a mentor’s role involves assisting in acquiring the confidence and tools to function and excel in our competitive professional world.^4-6 In the early 1970s, when I was a young PA, a wonderful physician and friend, Dr. Burton Brasher, took me under his wing and exemplified what it means to be a clinician. I learned from him that it was also my obligation to mentor others, and I have tried to do this frequently in my four decades as a PA. Through his example, I was shown the importance of cultivating emotional intelligence and sensitivity while still providing an honest assessment of strengths and weaknesses. Here was a physician who was unencumbered by ego. We met often to discuss the care of both of our patients.

Staying the course. In 1995, I mentored James Cannon—a young financial comptroller who desperately wanted to be a PA. I’ve (hopefully) helped him navigate PA school, our mutual time in the military, his time in academia, and his introduction to professional volunteer work. In each stage of his career, we had lengthy conversations about the pros and cons of his decisions. Now, 22 years later, he has become my mentor; he has matured in the profession and is at the forefront of taking it to the next level. It is now very common for me to call on him for his advice as I move into the home stretch of my career. A few years ago, he became a trustee of our university and his skills have advanced the success of our programs. Indeed, the student becomes the teacher.

Networking and articulating cultural norms. Dave Mittman, the co-founder and original publisher of Clinician Reviews, had the experience of hiring his very close friend and PA school classmate, Tom Yackeren. In 1985, Dave was publisher of Physician Assistant Journal (at that time, the official journal of the AAPA). Dave and Tom were business partners and relied on each other’s skills to grow their business. They shared trust, friendship, and a mutual knowledge of professional “culture.” They understood each other and how they could each contribute to their success. Their partnership maintained a complementary balance, each of them able to play to his strengths with the support and encouragement of the other. Tom has since used his knowledge and experience to mentor others.

Demonstrating honesty, integrity, and enthusiasm. Marie-Eileen Onieal, our NP editor-in-chief, grew up in a household where her father was a firefighter and union organizer. He taught her the value of always paying it forward. While she has mentored many people in her career, she fondly remembers mentoring Lori Fritz through her transition into academia—what Marie-Eileen calls “the precarious journey of an educator.” When she met Lori, she says, they just “clicked,” and that bond has survived to this day. Lori is now an established academician, mentoring new students and professionals, and modeling her experience with Marie-Eileen’s involvement in the profession.

These are examples of when it works. But what happens when the relationship doesn’t “click”? Unfortunately, not all mentorships are fruitful. When mentor and mentee clash, it is paramount to acknowledge that the relationship is not working and to back away appropriately, without regard to ego. No one benefits when the parties are at odds—and this may explain why some of the greatest partnerships form organically.

Above all, in order for a mentorship to be prosperous, mentors must express compassion and remain genuine throughout all interactions with their mentee. It is a long-term commitment. Without this generosity of spirit, the influence and benefit of a professional mentor would be lost. If you have other ideas about what makes a great mentor, or how to foster a more satisfying mentor/mentee relationship, please share them with me at [email protected].

Mentorship, whether through a formal or informal system, plays a significant role in a professional’s life; it fosters the development of professional expertise and is associated with increased job satisfaction. An effective mentor guides a less-experienced colleague by modeling positive behaviors and building trust, while being cognizant that his or her role is to be dependable, engaged, authentic, and attuned to the needs of the mentee. You can probably name one of your mentors off the top of your head right now!

The original “mentor” was a character of that name in Homer’s epic poem The Odyssey, but the word is now used to refer to a trusted advisor, friend, teacher, or wise person. In the story, Mentor served as a friend and advocate to Telemachus, the son of the king of Ithaca, while his father, Odysseus, was away fighting in the Trojan War. In 1699, the novel The Adventures of Telemachus portrayed Mentor as Telemachus’ tutor, and he became the hero of the story.^1,2

History holds many examples of mentoring relationships: Socrates and Plato, Haydn and Beethoven, and Freud and Jung. Modern-day duos include Kobe Bryant and Shaquille O’Neal, Kirk and Spock, and—dare I say it?—Brady and Belichick. During the Middle Ages, mentorship—particularly in medicine and nursing—was practiced via apprenticeship, which incorporated support, guidance, socialization, well-being, empowerment, education, and career progression.³

Throughout my career as a PA, I have been fortunate to be guided by competent and willing mentors. What have they had in common? For starters, an internal desire (sometimes called generosity of spirit) to mentor and a commitment to my growth and development as their mentee. Successful professional mentors must also possess the necessary knowledge to help effectively develop their mentee’s skills. Discussions with my colleagues and previous mentors inspired the following compilation of the essential responsibilities and traits of a mentor.

Initiating new ideas. A main aspect of a mentor’s role involves assisting in acquiring the confidence and tools to function and excel in our competitive professional world.^4-6 In the early 1970s, when I was a young PA, a wonderful physician and friend, Dr. Burton Brasher, took me under his wing and exemplified what it means to be a clinician. I learned from him that it was also my obligation to mentor others, and I have tried to do this frequently in my four decades as a PA. Through his example, I was shown the importance of cultivating emotional intelligence and sensitivity while still providing an honest assessment of strengths and weaknesses. Here was a physician who was unencumbered by ego. We met often to discuss the care of both of our patients.

Staying the course. In 1995, I mentored James Cannon—a young financial comptroller who desperately wanted to be a PA. I’ve (hopefully) helped him navigate PA school, our mutual time in the military, his time in academia, and his introduction to professional volunteer work. In each stage of his career, we had lengthy conversations about the pros and cons of his decisions. Now, 22 years later, he has become my mentor; he has matured in the profession and is at the forefront of taking it to the next level. It is now very common for me to call on him for his advice as I move into the home stretch of my career. A few years ago, he became a trustee of our university and his skills have advanced the success of our programs. Indeed, the student becomes the teacher.

Networking and articulating cultural norms. Dave Mittman, the co-founder and original publisher of Clinician Reviews, had the experience of hiring his very close friend and PA school classmate, Tom Yackeren. In 1985, Dave was publisher of Physician Assistant Journal (at that time, the official journal of the AAPA). Dave and Tom were business partners and relied on each other’s skills to grow their business. They shared trust, friendship, and a mutual knowledge of professional “culture.” They understood each other and how they could each contribute to their success. Their partnership maintained a complementary balance, each of them able to play to his strengths with the support and encouragement of the other. Tom has since used his knowledge and experience to mentor others.

Demonstrating honesty, integrity, and enthusiasm. Marie-Eileen Onieal, our NP editor-in-chief, grew up in a household where her father was a firefighter and union organizer. He taught her the value of always paying it forward. While she has mentored many people in her career, she fondly remembers mentoring Lori Fritz through her transition into academia—what Marie-Eileen calls “the precarious journey of an educator.” When she met Lori, she says, they just “clicked,” and that bond has survived to this day. Lori is now an established academician, mentoring new students and professionals, and modeling her experience with Marie-Eileen’s involvement in the profession.

These are examples of when it works. But what happens when the relationship doesn’t “click”? Unfortunately, not all mentorships are fruitful. When mentor and mentee clash, it is paramount to acknowledge that the relationship is not working and to back away appropriately, without regard to ego. No one benefits when the parties are at odds—and this may explain why some of the greatest partnerships form organically.

Above all, in order for a mentorship to be prosperous, mentors must express compassion and remain genuine throughout all interactions with their mentee. It is a long-term commitment. Without this generosity of spirit, the influence and benefit of a professional mentor would be lost. If you have other ideas about what makes a great mentor, or how to foster a more satisfying mentor/mentee relationship, please share them with me at [email protected].

Mentorship, whether through a formal or informal system, plays a significant role in a professional’s life; it fosters the development of professional expertise and is associated with increased job satisfaction. An effective mentor guides a less-experienced colleague by modeling positive behaviors and building trust, while being cognizant that his or her role is to be dependable, engaged, authentic, and attuned to the needs of the mentee. You can probably name one of your mentors off the top of your head right now!

The original “mentor” was a character of that name in Homer’s epic poem The Odyssey, but the word is now used to refer to a trusted advisor, friend, teacher, or wise person. In the story, Mentor served as a friend and advocate to Telemachus, the son of the king of Ithaca, while his father, Odysseus, was away fighting in the Trojan War. In 1699, the novel The Adventures of Telemachus portrayed Mentor as Telemachus’ tutor, and he became the hero of the story.^1,2

History holds many examples of mentoring relationships: Socrates and Plato, Haydn and Beethoven, and Freud and Jung. Modern-day duos include Kobe Bryant and Shaquille O’Neal, Kirk and Spock, and—dare I say it?—Brady and Belichick. During the Middle Ages, mentorship—particularly in medicine and nursing—was practiced via apprenticeship, which incorporated support, guidance, socialization, well-being, empowerment, education, and career progression.³

Throughout my career as a PA, I have been fortunate to be guided by competent and willing mentors. What have they had in common? For starters, an internal desire (sometimes called generosity of spirit) to mentor and a commitment to my growth and development as their mentee. Successful professional mentors must also possess the necessary knowledge to help effectively develop their mentee’s skills. Discussions with my colleagues and previous mentors inspired the following compilation of the essential responsibilities and traits of a mentor.

Initiating new ideas. A main aspect of a mentor’s role involves assisting in acquiring the confidence and tools to function and excel in our competitive professional world.^4-6 In the early 1970s, when I was a young PA, a wonderful physician and friend, Dr. Burton Brasher, took me under his wing and exemplified what it means to be a clinician. I learned from him that it was also my obligation to mentor others, and I have tried to do this frequently in my four decades as a PA. Through his example, I was shown the importance of cultivating emotional intelligence and sensitivity while still providing an honest assessment of strengths and weaknesses. Here was a physician who was unencumbered by ego. We met often to discuss the care of both of our patients.

Staying the course. In 1995, I mentored James Cannon—a young financial comptroller who desperately wanted to be a PA. I’ve (hopefully) helped him navigate PA school, our mutual time in the military, his time in academia, and his introduction to professional volunteer work. In each stage of his career, we had lengthy conversations about the pros and cons of his decisions. Now, 22 years later, he has become my mentor; he has matured in the profession and is at the forefront of taking it to the next level. It is now very common for me to call on him for his advice as I move into the home stretch of my career. A few years ago, he became a trustee of our university and his skills have advanced the success of our programs. Indeed, the student becomes the teacher.

Networking and articulating cultural norms. Dave Mittman, the co-founder and original publisher of Clinician Reviews, had the experience of hiring his very close friend and PA school classmate, Tom Yackeren. In 1985, Dave was publisher of Physician Assistant Journal (at that time, the official journal of the AAPA). Dave and Tom were business partners and relied on each other’s skills to grow their business. They shared trust, friendship, and a mutual knowledge of professional “culture.” They understood each other and how they could each contribute to their success. Their partnership maintained a complementary balance, each of them able to play to his strengths with the support and encouragement of the other. Tom has since used his knowledge and experience to mentor others.

Demonstrating honesty, integrity, and enthusiasm. Marie-Eileen Onieal, our NP editor-in-chief, grew up in a household where her father was a firefighter and union organizer. He taught her the value of always paying it forward. While she has mentored many people in her career, she fondly remembers mentoring Lori Fritz through her transition into academia—what Marie-Eileen calls “the precarious journey of an educator.” When she met Lori, she says, they just “clicked,” and that bond has survived to this day. Lori is now an established academician, mentoring new students and professionals, and modeling her experience with Marie-Eileen’s involvement in the profession.

These are examples of when it works. But what happens when the relationship doesn’t “click”? Unfortunately, not all mentorships are fruitful. When mentor and mentee clash, it is paramount to acknowledge that the relationship is not working and to back away appropriately, without regard to ego. No one benefits when the parties are at odds—and this may explain why some of the greatest partnerships form organically.

Above all, in order for a mentorship to be prosperous, mentors must express compassion and remain genuine throughout all interactions with their mentee. It is a long-term commitment. Without this generosity of spirit, the influence and benefit of a professional mentor would be lost. If you have other ideas about what makes a great mentor, or how to foster a more satisfying mentor/mentee relationship, please share them with me at [email protected].

In this month’s issue of The Journal of Family Practice, we are pleased to launch a new department called “Behavioral Health Consult.” This bimonthly column will feature behavioral and mental health topics such as depression, anxiety, obesity, and substance abuse.

Drawn from real patient encounters. As you read the inaugural item on depression, written by Michael Maksimowski, MD, and Michael Raddock, MD, you'll notice that the article starts with a brief case report. Cases will play an important role in this column and will either describe a single patient whom the author(s) cared for or be an amalgam of several (as was the case this month).

Practical and to the point. We have asked the authors, who are family physicians (FPs) and psychiatrists or psychologists who work closely with FPs, to provide a concentrated and practical summary of the elements of diagnosis and treatment that are most important and pertinent to primary care clinicians.

The column will address topics like depression and substance abuse.

Addressing an overwhelming need. The need for FPs and other primary care clinicians to stay current on the management of mental and behavioral health issues is obvious. Mood and anxiety disorders (eg, depression, anxiety, panic disorder, agoraphobia) affect almost 30% of the US adult population¹ and many of these patients are seen at least initially by their primary care physicians. According to the Centers for Disease Control and Prevention, 4 health risk behaviors—tobacco use, poor nutrition, excess alcohol consumption, and insufficient exercise—cause much of the illness, suffering, and early death related to chronic diseases and conditions.² My personal experience in our urban Chicago clinic definitely supports these statistics.

No lack of research. I teach several evidence-based medicine courses each year that focus on the review of recent randomized trials and meta-analyses that are important for FPs to know about. Every year, one of my talks is about either mental health or behavioral health research. Every year I wonder whether there will be enough new research to report on, and every year, I find that there is an abundance of research that helps us to better manage these common problems. “Behavioral Health Consult” is this journal’s way of helping to keep you current and informed.

In an effort to make this addition as useful to you as possible, please feel free to email me at [email protected] with suggestions for topics you would like to see in “Behavioral Health Consult.” We look forward to your reactions—and your comments.

In this month’s issue of The Journal of Family Practice, we are pleased to launch a new department called “Behavioral Health Consult.” This bimonthly column will feature behavioral and mental health topics such as depression, anxiety, obesity, and substance abuse.

Drawn from real patient encounters. As you read the inaugural item on depression, written by Michael Maksimowski, MD, and Michael Raddock, MD, you'll notice that the article starts with a brief case report. Cases will play an important role in this column and will either describe a single patient whom the author(s) cared for or be an amalgam of several (as was the case this month).

Practical and to the point. We have asked the authors, who are family physicians (FPs) and psychiatrists or psychologists who work closely with FPs, to provide a concentrated and practical summary of the elements of diagnosis and treatment that are most important and pertinent to primary care clinicians.

The column will address topics like depression and substance abuse.

Addressing an overwhelming need. The need for FPs and other primary care clinicians to stay current on the management of mental and behavioral health issues is obvious. Mood and anxiety disorders (eg, depression, anxiety, panic disorder, agoraphobia) affect almost 30% of the US adult population¹ and many of these patients are seen at least initially by their primary care physicians. According to the Centers for Disease Control and Prevention, 4 health risk behaviors—tobacco use, poor nutrition, excess alcohol consumption, and insufficient exercise—cause much of the illness, suffering, and early death related to chronic diseases and conditions.² My personal experience in our urban Chicago clinic definitely supports these statistics.

No lack of research. I teach several evidence-based medicine courses each year that focus on the review of recent randomized trials and meta-analyses that are important for FPs to know about. Every year, one of my talks is about either mental health or behavioral health research. Every year I wonder whether there will be enough new research to report on, and every year, I find that there is an abundance of research that helps us to better manage these common problems. “Behavioral Health Consult” is this journal’s way of helping to keep you current and informed.

In an effort to make this addition as useful to you as possible, please feel free to email me at [email protected] with suggestions for topics you would like to see in “Behavioral Health Consult.” We look forward to your reactions—and your comments.

In this month’s issue of The Journal of Family Practice, we are pleased to launch a new department called “Behavioral Health Consult.” This bimonthly column will feature behavioral and mental health topics such as depression, anxiety, obesity, and substance abuse.

Drawn from real patient encounters. As you read the inaugural item on depression, written by Michael Maksimowski, MD, and Michael Raddock, MD, you'll notice that the article starts with a brief case report. Cases will play an important role in this column and will either describe a single patient whom the author(s) cared for or be an amalgam of several (as was the case this month).

Practical and to the point. We have asked the authors, who are family physicians (FPs) and psychiatrists or psychologists who work closely with FPs, to provide a concentrated and practical summary of the elements of diagnosis and treatment that are most important and pertinent to primary care clinicians.

The column will address topics like depression and substance abuse.

Addressing an overwhelming need. The need for FPs and other primary care clinicians to stay current on the management of mental and behavioral health issues is obvious. Mood and anxiety disorders (eg, depression, anxiety, panic disorder, agoraphobia) affect almost 30% of the US adult population¹ and many of these patients are seen at least initially by their primary care physicians. According to the Centers for Disease Control and Prevention, 4 health risk behaviors—tobacco use, poor nutrition, excess alcohol consumption, and insufficient exercise—cause much of the illness, suffering, and early death related to chronic diseases and conditions.² My personal experience in our urban Chicago clinic definitely supports these statistics.

No lack of research. I teach several evidence-based medicine courses each year that focus on the review of recent randomized trials and meta-analyses that are important for FPs to know about. Every year, one of my talks is about either mental health or behavioral health research. Every year I wonder whether there will be enough new research to report on, and every year, I find that there is an abundance of research that helps us to better manage these common problems. “Behavioral Health Consult” is this journal’s way of helping to keep you current and informed.

In an effort to make this addition as useful to you as possible, please feel free to email me at [email protected] with suggestions for topics you would like to see in “Behavioral Health Consult.” We look forward to your reactions—and your comments.

I read the article, “What family physicians can do to combat bullying” (J Fam Pract. 2017;66:82-89) and Dr. Hickner’s editorial, “It’s time to screen for bullying” (J Fam Pract. 2017;66:66) with great interest. I’m a bullying prevention researcher and the creator of a new bullying prevention program, CirclePoint, which is being piloted in Boston Public Schools. I’m also a featured speaker on bullying in the Massachusetts General Hospital’s life skills after-school program that runs in a dozen area schools.

My work in schools has taught me that as important as it is to identify bullying problems, it is equally important for doctors to know how to counsel patients and caregivers on how to resolve these problems.

Identifying bullying without providing further guidance can actually do more harm than good, both to the child’s health and to the child-physician relationship.

Children often don’t tell adults they are being bullied because the actions that adults take—while well-intended—can sometimes make the situation worse. Further, some caregivers may actually blame the child for being bullied. And a doctor who simply identifies the problem and leaves the next steps to an ill-informed caregiver may lose the patient’s trust.

Also worth noting: Some children who are bullied may not have a clear understanding of what the term “bullying” means. I strongly suggest asking patients about how others are treating them and if anyone is making them upset. Questions about behaviors and feelings are more effective at identifying a bullying problem than questions that use the term “bullying.”

Our program has a free resource that was developed for educators, but can easily be used by physicians to counsel patients and caregivers. It’s designed to convey recommended actions for both the student and caregiver in a matter of minutes.

Doctors who identify a bullying problem bear a responsibility to counsel both the patient and caregiver(s) on what bullying is, why it happens, and, most critically, recommended actions to take to effectively resolve the problem.

Ari Magnusson
Charlestown, Mass

I read the article, “What family physicians can do to combat bullying” (J Fam Pract. 2017;66:82-89) and Dr. Hickner’s editorial, “It’s time to screen for bullying” (J Fam Pract. 2017;66:66) with great interest. I’m a bullying prevention researcher and the creator of a new bullying prevention program, CirclePoint, which is being piloted in Boston Public Schools. I’m also a featured speaker on bullying in the Massachusetts General Hospital’s life skills after-school program that runs in a dozen area schools.

My work in schools has taught me that as important as it is to identify bullying problems, it is equally important for doctors to know how to counsel patients and caregivers on how to resolve these problems.

Identifying bullying without providing further guidance can actually do more harm than good, both to the child’s health and to the child-physician relationship.

Children often don’t tell adults they are being bullied because the actions that adults take—while well-intended—can sometimes make the situation worse. Further, some caregivers may actually blame the child for being bullied. And a doctor who simply identifies the problem and leaves the next steps to an ill-informed caregiver may lose the patient’s trust.

Also worth noting: Some children who are bullied may not have a clear understanding of what the term “bullying” means. I strongly suggest asking patients about how others are treating them and if anyone is making them upset. Questions about behaviors and feelings are more effective at identifying a bullying problem than questions that use the term “bullying.”

Our program has a free resource that was developed for educators, but can easily be used by physicians to counsel patients and caregivers. It’s designed to convey recommended actions for both the student and caregiver in a matter of minutes.

Doctors who identify a bullying problem bear a responsibility to counsel both the patient and caregiver(s) on what bullying is, why it happens, and, most critically, recommended actions to take to effectively resolve the problem.

Ari Magnusson
Charlestown, Mass

I read the article, “What family physicians can do to combat bullying” (J Fam Pract. 2017;66:82-89) and Dr. Hickner’s editorial, “It’s time to screen for bullying” (J Fam Pract. 2017;66:66) with great interest. I’m a bullying prevention researcher and the creator of a new bullying prevention program, CirclePoint, which is being piloted in Boston Public Schools. I’m also a featured speaker on bullying in the Massachusetts General Hospital’s life skills after-school program that runs in a dozen area schools.

My work in schools has taught me that as important as it is to identify bullying problems, it is equally important for doctors to know how to counsel patients and caregivers on how to resolve these problems.

Identifying bullying without providing further guidance can actually do more harm than good, both to the child’s health and to the child-physician relationship.

Children often don’t tell adults they are being bullied because the actions that adults take—while well-intended—can sometimes make the situation worse. Further, some caregivers may actually blame the child for being bullied. And a doctor who simply identifies the problem and leaves the next steps to an ill-informed caregiver may lose the patient’s trust.

Also worth noting: Some children who are bullied may not have a clear understanding of what the term “bullying” means. I strongly suggest asking patients about how others are treating them and if anyone is making them upset. Questions about behaviors and feelings are more effective at identifying a bullying problem than questions that use the term “bullying.”

Our program has a free resource that was developed for educators, but can easily be used by physicians to counsel patients and caregivers. It’s designed to convey recommended actions for both the student and caregiver in a matter of minutes.

Doctors who identify a bullying problem bear a responsibility to counsel both the patient and caregiver(s) on what bullying is, why it happens, and, most critically, recommended actions to take to effectively resolve the problem.

Ari Magnusson
Charlestown, Mass

In a recent letter to the editor on the role of auscultation and echocardiography, “Point-of-care ultrasound: It’s no replacement for the stethoscope” (J Fam Pract. 2016;65:734), Dr. Fredricks claimed that “doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.” His citation for this claim was a review article from more than 20 years ago that offered no evidence in support of the superiority of auscultation over echocardiography to characterize murmurs.¹ The review did acknowledge the limitations and variability between examiners.

The notion that physical examination is superior to echocardiography is appealing, but likely incorrect. A study of medical students with basic training in echocardiography showed that they were able to characterize murmurs more accurately with point-of-care ultrasound than experienced cardiologists auscultating the murmur.²

The existence of a better test does not obviate the role of the physical examination, but it does highlight the need to understand its limits. Like an ultrasound study, physical examination maneuvers are tests, with sensitivities and specificities. We should approach them as such, and not romanticize their performance.

David Mackenzie, MD
Portland, Me

In a recent letter to the editor on the role of auscultation and echocardiography, “Point-of-care ultrasound: It’s no replacement for the stethoscope” (J Fam Pract. 2016;65:734), Dr. Fredricks claimed that “doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.” His citation for this claim was a review article from more than 20 years ago that offered no evidence in support of the superiority of auscultation over echocardiography to characterize murmurs.¹ The review did acknowledge the limitations and variability between examiners.

The notion that physical examination is superior to echocardiography is appealing, but likely incorrect. A study of medical students with basic training in echocardiography showed that they were able to characterize murmurs more accurately with point-of-care ultrasound than experienced cardiologists auscultating the murmur.²

The existence of a better test does not obviate the role of the physical examination, but it does highlight the need to understand its limits. Like an ultrasound study, physical examination maneuvers are tests, with sensitivities and specificities. We should approach them as such, and not romanticize their performance.

David Mackenzie, MD
Portland, Me

In a recent letter to the editor on the role of auscultation and echocardiography, “Point-of-care ultrasound: It’s no replacement for the stethoscope” (J Fam Pract. 2016;65:734), Dr. Fredricks claimed that “doppler ultrasound is not as precise as the stethoscope when used by a practiced listener for identifying the source and subtle characteristics of murmurs.” His citation for this claim was a review article from more than 20 years ago that offered no evidence in support of the superiority of auscultation over echocardiography to characterize murmurs.¹ The review did acknowledge the limitations and variability between examiners.

The notion that physical examination is superior to echocardiography is appealing, but likely incorrect. A study of medical students with basic training in echocardiography showed that they were able to characterize murmurs more accurately with point-of-care ultrasound than experienced cardiologists auscultating the murmur.²

The existence of a better test does not obviate the role of the physical examination, but it does highlight the need to understand its limits. Like an ultrasound study, physical examination maneuvers are tests, with sensitivities and specificities. We should approach them as such, and not romanticize their performance.

David Mackenzie, MD
Portland, Me

ILLUSTRATIVE CASE

A 48-year-old man presents to your office for follow-up of right knee pain that has been bothering him for the last 12 months. He denies any trauma or inciting incident for the pain. On physical exam, he does not have crepitus, but has medial joint line tenderness of his right knee. A magnetic resonance image (MRI) shows a partial, medial meniscal tear. Do you refer him to Physical Therapy (PT) or Orthopedics for arthroscopy and repair?

The meniscus—cartilage in the knee joint that provides support, stability, and lubrication to the joint during activity—can tear during a traumatic event or because of degeneration over time. Traumatic meniscal tears typically happen to younger adults and teens (<30 years of age) during sports, such as basketball and soccer,whereas degenerative meniscal tears generally present in patients ages 40 to 60 years.^2,3 The annual incidence of all meniscal tears is 79 per 100,000.⁴ While some physicians can diagnose traumatic meniscal tears based on history and physical examination, degenerative meniscal tears are generally more challenging, and typically warrant an MRI for confirmation.³

Meniscal tears can be treated either conservatively, with supportive care and exercise, or with surgery. Unfortunately, there are no national orthopedic guidelines available to help direct care. In one observational study of surgery as treatment for both traumatic and degenerative meniscal tears, 95 out of 117 patients (81.2%) were generally satisfied with this treatment at the 4-year follow-up, with higher satisfaction in the traumatic meniscal tear group than in the degenerative tear group.⁵

Two systematic reviews of surgery vs nonoperative management or sham therapies found no additional benefit of surgery for meniscal tears in a variety of patients with and without osteoarthritis.^6,7 However, both studies were of only moderate quality because of the number of patients in the nonoperative groups who ultimately obtained surgery. And neither of the studies directly compared surgery to nonoperative management.^6,7

Yet another investigation, a multicenter, randomized, double-blind, sham-controlled study conducted in Finland involving 146 patients, compared sham surgery to arthroscopic partial meniscectomy. Both groups received instruction on performing post-procedure exercises, and both groups had similar and marked improvement in pain and function.⁸

Clinical practice recommendations devised from a systematic and vast review of the literature recommend that the decision for surgery be based on patient-specific factors such as symptoms, age, mechanism of tear, extent of damage, and occupational/­social/activity needs.⁹

STUDY SUMMARY

Exercise is as good as—and in one way, better than—surgery

The current randomized controlled superiority trial compared exercise therapy to arthroscopic partial meniscectomy in patients ages 35 to 60 years presenting to the orthopedic departments of 2 hospitals in Norway with unilateral knee pain for more than 2 months and an MRI-delineated medial meniscal tear. Patients were included only if they had radiographic evidence of minimal osteoarthritis (Kellgren-Lawrence classification grade ≤2). Exclusion criteria were acute trauma, locked knee, ligament injury, and knee surgery in the same knee within the previous 2 years.

The primary outcomes were change in patient-reported knee function as determined by overall knee injury and osteoarthritis outcome score (KOOS₄) after 2 years and thigh muscle strength at 3 months as measured by physiotherapists. The KOOS₄ consists of 4 out of the 5 KOOS subscales: pain, other symptoms (swelling, grinding/noise from the joint, ability to straighten and bend), function in sports/recreation, and knee-related quality of life (QOL). This study utilized the average score of each subscale.

Secondary outcomes were the 5 individual KOOS subscales (the 4 previously mentioned plus activities of daily living [ADLs]), as well as thigh muscle strength and lower extremity performance test results.

Methods. Testing personnel were blinded to group allocation; participants wore pants or neoprene sleeves to cover surgical scars. A total of 140 patients were randomized to either 12 weeks (24-36 sessions) of exercise therapy alone or a standardized arthroscopic partial meniscectomy with written and oral encouragement upon discharge to perform simple exercises at home 2 to4 times daily (to regain range of motion and reduce swelling).

Results. The overall mean improvement in KOOS₄ score from baseline at 2 years was similar between the exercise group and the meniscectomy group (25.3 points vs 24.4 points, respectively; mean difference [MD], 0.9; 95% confidence interval [CI], -4.3 to 6.1; P=.72). Additionally, muscle strength (measured as peak torque flexion and extension and total work flexion and extension) at both 3 and 12 months showed significant objective improvements favoring exercise therapy.

Exercise therapy was as effective as surgery after a 2-year follow-up period and was superior in the short term for thigh muscle strength.

Secondary outcomes comparing the change from baseline of KOOS subscale scores showed 4 of the 5 having non-significant differences (pain, ADL, sports/­recreation, and QOL). Only the symptoms subscale had a significant difference favoring exercise therapy (MD, 5.3 points; 95% CI, 0.5 to 10.2; P=.03), which was likely clinically insignificant when using a grading scale of 0 to 100.

Of those patients allocated to exercise therapy alone, 19% crossed over and underwent surgery during the 2 years of the study.

WHAT'S NEW

Head-to-head comparison adds evidence to previous findings

This is the first trial to directly compare exercise therapy to surgery in patients with meniscal tears. Interestingly, exercise therapy was as effective after a 2-year follow-up period and was superior in the short term for thigh muscle strength.¹ The results of this study build on those from the smaller study conducted in Finland mentioned earlier.⁸ In that study, both groups received instruction for the same graduated exercise plan. The researchers found that exercise was comparable to surgery for meniscal tears in patients with no osteoarthritis.

CAVEATS

Results may not translate to those with more severe osteoarthritis

This trial included patients with only mild to no osteoarthritis in addition to their meniscal tear.¹ It is unclear if the results would be maintained in patients with more advanced disease. Additionally, 19% of patients crossed over from the exercise group to the surgery group, even though muscle strength improved. Therefore, education about the risks of surgery and the potential lack of benefit is important.

CHALLENGES TO IMPLEMENTATION

The cost and effort of physical therapy may be a deterrent

The cost of PT can be a barrier for some patients who have adequate insurance coverage for surgery, but inadequate coverage for PT. Additionally, exercise therapy requires significant and ongoing amounts of time and effort, which may be a deterrent for patients with busy lifestyles. Patients and physicians may view surgery as an “easier” fix.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 48-year-old man presents to your office for follow-up of right knee pain that has been bothering him for the last 12 months. He denies any trauma or inciting incident for the pain. On physical exam, he does not have crepitus, but has medial joint line tenderness of his right knee. A magnetic resonance image (MRI) shows a partial, medial meniscal tear. Do you refer him to Physical Therapy (PT) or Orthopedics for arthroscopy and repair?

The meniscus—cartilage in the knee joint that provides support, stability, and lubrication to the joint during activity—can tear during a traumatic event or because of degeneration over time. Traumatic meniscal tears typically happen to younger adults and teens (<30 years of age) during sports, such as basketball and soccer,whereas degenerative meniscal tears generally present in patients ages 40 to 60 years.^2,3 The annual incidence of all meniscal tears is 79 per 100,000.⁴ While some physicians can diagnose traumatic meniscal tears based on history and physical examination, degenerative meniscal tears are generally more challenging, and typically warrant an MRI for confirmation.³

Meniscal tears can be treated either conservatively, with supportive care and exercise, or with surgery. Unfortunately, there are no national orthopedic guidelines available to help direct care. In one observational study of surgery as treatment for both traumatic and degenerative meniscal tears, 95 out of 117 patients (81.2%) were generally satisfied with this treatment at the 4-year follow-up, with higher satisfaction in the traumatic meniscal tear group than in the degenerative tear group.⁵

Two systematic reviews of surgery vs nonoperative management or sham therapies found no additional benefit of surgery for meniscal tears in a variety of patients with and without osteoarthritis.^6,7 However, both studies were of only moderate quality because of the number of patients in the nonoperative groups who ultimately obtained surgery. And neither of the studies directly compared surgery to nonoperative management.^6,7

Yet another investigation, a multicenter, randomized, double-blind, sham-controlled study conducted in Finland involving 146 patients, compared sham surgery to arthroscopic partial meniscectomy. Both groups received instruction on performing post-procedure exercises, and both groups had similar and marked improvement in pain and function.⁸

Clinical practice recommendations devised from a systematic and vast review of the literature recommend that the decision for surgery be based on patient-specific factors such as symptoms, age, mechanism of tear, extent of damage, and occupational/­social/activity needs.⁹

STUDY SUMMARY

Exercise is as good as—and in one way, better than—surgery

The current randomized controlled superiority trial compared exercise therapy to arthroscopic partial meniscectomy in patients ages 35 to 60 years presenting to the orthopedic departments of 2 hospitals in Norway with unilateral knee pain for more than 2 months and an MRI-delineated medial meniscal tear. Patients were included only if they had radiographic evidence of minimal osteoarthritis (Kellgren-Lawrence classification grade ≤2). Exclusion criteria were acute trauma, locked knee, ligament injury, and knee surgery in the same knee within the previous 2 years.

The primary outcomes were change in patient-reported knee function as determined by overall knee injury and osteoarthritis outcome score (KOOS₄) after 2 years and thigh muscle strength at 3 months as measured by physiotherapists. The KOOS₄ consists of 4 out of the 5 KOOS subscales: pain, other symptoms (swelling, grinding/noise from the joint, ability to straighten and bend), function in sports/recreation, and knee-related quality of life (QOL). This study utilized the average score of each subscale.

Secondary outcomes were the 5 individual KOOS subscales (the 4 previously mentioned plus activities of daily living [ADLs]), as well as thigh muscle strength and lower extremity performance test results.

Methods. Testing personnel were blinded to group allocation; participants wore pants or neoprene sleeves to cover surgical scars. A total of 140 patients were randomized to either 12 weeks (24-36 sessions) of exercise therapy alone or a standardized arthroscopic partial meniscectomy with written and oral encouragement upon discharge to perform simple exercises at home 2 to4 times daily (to regain range of motion and reduce swelling).

Results. The overall mean improvement in KOOS₄ score from baseline at 2 years was similar between the exercise group and the meniscectomy group (25.3 points vs 24.4 points, respectively; mean difference [MD], 0.9; 95% confidence interval [CI], -4.3 to 6.1; P=.72). Additionally, muscle strength (measured as peak torque flexion and extension and total work flexion and extension) at both 3 and 12 months showed significant objective improvements favoring exercise therapy.

Exercise therapy was as effective as surgery after a 2-year follow-up period and was superior in the short term for thigh muscle strength.

Secondary outcomes comparing the change from baseline of KOOS subscale scores showed 4 of the 5 having non-significant differences (pain, ADL, sports/­recreation, and QOL). Only the symptoms subscale had a significant difference favoring exercise therapy (MD, 5.3 points; 95% CI, 0.5 to 10.2; P=.03), which was likely clinically insignificant when using a grading scale of 0 to 100.

Of those patients allocated to exercise therapy alone, 19% crossed over and underwent surgery during the 2 years of the study.

WHAT'S NEW

Head-to-head comparison adds evidence to previous findings

This is the first trial to directly compare exercise therapy to surgery in patients with meniscal tears. Interestingly, exercise therapy was as effective after a 2-year follow-up period and was superior in the short term for thigh muscle strength.¹ The results of this study build on those from the smaller study conducted in Finland mentioned earlier.⁸ In that study, both groups received instruction for the same graduated exercise plan. The researchers found that exercise was comparable to surgery for meniscal tears in patients with no osteoarthritis.

CAVEATS

Results may not translate to those with more severe osteoarthritis

This trial included patients with only mild to no osteoarthritis in addition to their meniscal tear.¹ It is unclear if the results would be maintained in patients with more advanced disease. Additionally, 19% of patients crossed over from the exercise group to the surgery group, even though muscle strength improved. Therefore, education about the risks of surgery and the potential lack of benefit is important.

CHALLENGES TO IMPLEMENTATION

The cost and effort of physical therapy may be a deterrent

The cost of PT can be a barrier for some patients who have adequate insurance coverage for surgery, but inadequate coverage for PT. Additionally, exercise therapy requires significant and ongoing amounts of time and effort, which may be a deterrent for patients with busy lifestyles. Patients and physicians may view surgery as an “easier” fix.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

ILLUSTRATIVE CASE

A 48-year-old man presents to your office for follow-up of right knee pain that has been bothering him for the last 12 months. He denies any trauma or inciting incident for the pain. On physical exam, he does not have crepitus, but has medial joint line tenderness of his right knee. A magnetic resonance image (MRI) shows a partial, medial meniscal tear. Do you refer him to Physical Therapy (PT) or Orthopedics for arthroscopy and repair?

The meniscus—cartilage in the knee joint that provides support, stability, and lubrication to the joint during activity—can tear during a traumatic event or because of degeneration over time. Traumatic meniscal tears typically happen to younger adults and teens (<30 years of age) during sports, such as basketball and soccer,whereas degenerative meniscal tears generally present in patients ages 40 to 60 years.^2,3 The annual incidence of all meniscal tears is 79 per 100,000.⁴ While some physicians can diagnose traumatic meniscal tears based on history and physical examination, degenerative meniscal tears are generally more challenging, and typically warrant an MRI for confirmation.³

Meniscal tears can be treated either conservatively, with supportive care and exercise, or with surgery. Unfortunately, there are no national orthopedic guidelines available to help direct care. In one observational study of surgery as treatment for both traumatic and degenerative meniscal tears, 95 out of 117 patients (81.2%) were generally satisfied with this treatment at the 4-year follow-up, with higher satisfaction in the traumatic meniscal tear group than in the degenerative tear group.⁵

Two systematic reviews of surgery vs nonoperative management or sham therapies found no additional benefit of surgery for meniscal tears in a variety of patients with and without osteoarthritis.^6,7 However, both studies were of only moderate quality because of the number of patients in the nonoperative groups who ultimately obtained surgery. And neither of the studies directly compared surgery to nonoperative management.^6,7

Yet another investigation, a multicenter, randomized, double-blind, sham-controlled study conducted in Finland involving 146 patients, compared sham surgery to arthroscopic partial meniscectomy. Both groups received instruction on performing post-procedure exercises, and both groups had similar and marked improvement in pain and function.⁸

Clinical practice recommendations devised from a systematic and vast review of the literature recommend that the decision for surgery be based on patient-specific factors such as symptoms, age, mechanism of tear, extent of damage, and occupational/­social/activity needs.⁹

STUDY SUMMARY

Exercise is as good as—and in one way, better than—surgery

The current randomized controlled superiority trial compared exercise therapy to arthroscopic partial meniscectomy in patients ages 35 to 60 years presenting to the orthopedic departments of 2 hospitals in Norway with unilateral knee pain for more than 2 months and an MRI-delineated medial meniscal tear. Patients were included only if they had radiographic evidence of minimal osteoarthritis (Kellgren-Lawrence classification grade ≤2). Exclusion criteria were acute trauma, locked knee, ligament injury, and knee surgery in the same knee within the previous 2 years.

The primary outcomes were change in patient-reported knee function as determined by overall knee injury and osteoarthritis outcome score (KOOS₄) after 2 years and thigh muscle strength at 3 months as measured by physiotherapists. The KOOS₄ consists of 4 out of the 5 KOOS subscales: pain, other symptoms (swelling, grinding/noise from the joint, ability to straighten and bend), function in sports/recreation, and knee-related quality of life (QOL). This study utilized the average score of each subscale.

Secondary outcomes were the 5 individual KOOS subscales (the 4 previously mentioned plus activities of daily living [ADLs]), as well as thigh muscle strength and lower extremity performance test results.

Methods. Testing personnel were blinded to group allocation; participants wore pants or neoprene sleeves to cover surgical scars. A total of 140 patients were randomized to either 12 weeks (24-36 sessions) of exercise therapy alone or a standardized arthroscopic partial meniscectomy with written and oral encouragement upon discharge to perform simple exercises at home 2 to4 times daily (to regain range of motion and reduce swelling).

Results. The overall mean improvement in KOOS₄ score from baseline at 2 years was similar between the exercise group and the meniscectomy group (25.3 points vs 24.4 points, respectively; mean difference [MD], 0.9; 95% confidence interval [CI], -4.3 to 6.1; P=.72). Additionally, muscle strength (measured as peak torque flexion and extension and total work flexion and extension) at both 3 and 12 months showed significant objective improvements favoring exercise therapy.

Exercise therapy was as effective as surgery after a 2-year follow-up period and was superior in the short term for thigh muscle strength.

Secondary outcomes comparing the change from baseline of KOOS subscale scores showed 4 of the 5 having non-significant differences (pain, ADL, sports/­recreation, and QOL). Only the symptoms subscale had a significant difference favoring exercise therapy (MD, 5.3 points; 95% CI, 0.5 to 10.2; P=.03), which was likely clinically insignificant when using a grading scale of 0 to 100.

Of those patients allocated to exercise therapy alone, 19% crossed over and underwent surgery during the 2 years of the study.

WHAT'S NEW

Head-to-head comparison adds evidence to previous findings

This is the first trial to directly compare exercise therapy to surgery in patients with meniscal tears. Interestingly, exercise therapy was as effective after a 2-year follow-up period and was superior in the short term for thigh muscle strength.¹ The results of this study build on those from the smaller study conducted in Finland mentioned earlier.⁸ In that study, both groups received instruction for the same graduated exercise plan. The researchers found that exercise was comparable to surgery for meniscal tears in patients with no osteoarthritis.

CAVEATS

Results may not translate to those with more severe osteoarthritis

This trial included patients with only mild to no osteoarthritis in addition to their meniscal tear.¹ It is unclear if the results would be maintained in patients with more advanced disease. Additionally, 19% of patients crossed over from the exercise group to the surgery group, even though muscle strength improved. Therefore, education about the risks of surgery and the potential lack of benefit is important.

CHALLENGES TO IMPLEMENTATION

The cost and effort of physical therapy may be a deterrent

The cost of PT can be a barrier for some patients who have adequate insurance coverage for surgery, but inadequate coverage for PT. Additionally, exercise therapy requires significant and ongoing amounts of time and effort, which may be a deterrent for patients with busy lifestyles. Patients and physicians may view surgery as an “easier” fix.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

EVIDENCE SUMMARY

A 2011 meta-analysis of 5 RCTs (total 2975 patients) that compared ACE inhibitor therapy with placebo in diabetic patients without hypertension and albuminuria found that ACE inhibitors reduced the risk of new-onset microalbuminuria or macroalbuminuria by 18% (relative risk [RR]=0.82; 95% confidence interval [CI], 0.73-0.92).¹ Normal albuminuria was defined in all included studies as an albumin excretion rate of <30 mg/d on a timed specimen confirmed with 3 serial measurements.

The RCTs included patients treated with lisinopril, enalapril, and perindopril. All but one examined patients with type 1 diabetes (2781 patients). The study that evaluated type 2 diabetes (194 patients) assessed patients with hypertension who used other antihypertensives to achieve normal blood pressure targets before ACE inhibitor initiation, a potential limitation.

Compared with placebo or no treatment, ACE inhibitor therapy reduced the risk of death from any cause (6 studies; 11,350 patients; RR=0.84; 95% CI, 0.73-0.97).¹ Patient populations across pooled RCTs were heterogeneous, including subjects with type 1 and type 2 diabetes, with or without hypertension, and with or without albuminuria.

ACE inhibitors increase risk of cough

Patients taking an ACE inhibitor have an increased risk of cough (6 studies; 11,791 patients; RR=1.84; 95% CI, 1.24-2.72).¹ ACE inhibitor therapy doesn’t increase the risk of headache or hyperkalemia.

ARBs don’t help prevent diabetic kidney disease in normotensive patients

The 2011 meta-analysis also included 5 RCTs (4604 patients, approximately 3000 with type 2 diabetes and more than 1000 with type 1 diabetes) that compared ARBs with placebo in patients without hypertension.¹ Unlike ACE inhibitor therapy, ARB treatment didn’t significantly affect new-onset microalbuminuria or macroalbuminuria (RR=1.06; 95% CI, 0.67-1.69).

The trials evaluated losartan, candesartan, olmesartan, and valsartan. One study used other antihypertensives to achieve target blood pressure, and another included patients of any albuminuria status.

Compared with placebo or no treatment, ARBs didn’t reduce the risk of death (5 studies; 7653 patients; RR=1.12; 95% CI, 0.88-1.41).¹ All 5 RCTs assessed normoalbuminuric patients. Three of the 5 studies examined normotensive patients; one evaluated only hypertensive patients, and another assessed mostly hypertensive patients.

ARBs usually don’t produce significant adverse effects

Within the meta-analysis, ARBs didn’t increase risk of cough, headache, or hyperkalemia.¹

EVIDENCE SUMMARY

A 2011 meta-analysis of 5 RCTs (total 2975 patients) that compared ACE inhibitor therapy with placebo in diabetic patients without hypertension and albuminuria found that ACE inhibitors reduced the risk of new-onset microalbuminuria or macroalbuminuria by 18% (relative risk [RR]=0.82; 95% confidence interval [CI], 0.73-0.92).¹ Normal albuminuria was defined in all included studies as an albumin excretion rate of <30 mg/d on a timed specimen confirmed with 3 serial measurements.

The RCTs included patients treated with lisinopril, enalapril, and perindopril. All but one examined patients with type 1 diabetes (2781 patients). The study that evaluated type 2 diabetes (194 patients) assessed patients with hypertension who used other antihypertensives to achieve normal blood pressure targets before ACE inhibitor initiation, a potential limitation.

Compared with placebo or no treatment, ACE inhibitor therapy reduced the risk of death from any cause (6 studies; 11,350 patients; RR=0.84; 95% CI, 0.73-0.97).¹ Patient populations across pooled RCTs were heterogeneous, including subjects with type 1 and type 2 diabetes, with or without hypertension, and with or without albuminuria.

ACE inhibitors increase risk of cough

Patients taking an ACE inhibitor have an increased risk of cough (6 studies; 11,791 patients; RR=1.84; 95% CI, 1.24-2.72).¹ ACE inhibitor therapy doesn’t increase the risk of headache or hyperkalemia.

ARBs don’t help prevent diabetic kidney disease in normotensive patients

The 2011 meta-analysis also included 5 RCTs (4604 patients, approximately 3000 with type 2 diabetes and more than 1000 with type 1 diabetes) that compared ARBs with placebo in patients without hypertension.¹ Unlike ACE inhibitor therapy, ARB treatment didn’t significantly affect new-onset microalbuminuria or macroalbuminuria (RR=1.06; 95% CI, 0.67-1.69).

The trials evaluated losartan, candesartan, olmesartan, and valsartan. One study used other antihypertensives to achieve target blood pressure, and another included patients of any albuminuria status.

Compared with placebo or no treatment, ARBs didn’t reduce the risk of death (5 studies; 7653 patients; RR=1.12; 95% CI, 0.88-1.41).¹ All 5 RCTs assessed normoalbuminuric patients. Three of the 5 studies examined normotensive patients; one evaluated only hypertensive patients, and another assessed mostly hypertensive patients.

ARBs usually don’t produce significant adverse effects

Within the meta-analysis, ARBs didn’t increase risk of cough, headache, or hyperkalemia.¹

EVIDENCE SUMMARY

A 2011 meta-analysis of 5 RCTs (total 2975 patients) that compared ACE inhibitor therapy with placebo in diabetic patients without hypertension and albuminuria found that ACE inhibitors reduced the risk of new-onset microalbuminuria or macroalbuminuria by 18% (relative risk [RR]=0.82; 95% confidence interval [CI], 0.73-0.92).¹ Normal albuminuria was defined in all included studies as an albumin excretion rate of <30 mg/d on a timed specimen confirmed with 3 serial measurements.

The RCTs included patients treated with lisinopril, enalapril, and perindopril. All but one examined patients with type 1 diabetes (2781 patients). The study that evaluated type 2 diabetes (194 patients) assessed patients with hypertension who used other antihypertensives to achieve normal blood pressure targets before ACE inhibitor initiation, a potential limitation.

Compared with placebo or no treatment, ACE inhibitor therapy reduced the risk of death from any cause (6 studies; 11,350 patients; RR=0.84; 95% CI, 0.73-0.97).¹ Patient populations across pooled RCTs were heterogeneous, including subjects with type 1 and type 2 diabetes, with or without hypertension, and with or without albuminuria.

ACE inhibitors increase risk of cough

Patients taking an ACE inhibitor have an increased risk of cough (6 studies; 11,791 patients; RR=1.84; 95% CI, 1.24-2.72).¹ ACE inhibitor therapy doesn’t increase the risk of headache or hyperkalemia.

ARBs don’t help prevent diabetic kidney disease in normotensive patients

The 2011 meta-analysis also included 5 RCTs (4604 patients, approximately 3000 with type 2 diabetes and more than 1000 with type 1 diabetes) that compared ARBs with placebo in patients without hypertension.¹ Unlike ACE inhibitor therapy, ARB treatment didn’t significantly affect new-onset microalbuminuria or macroalbuminuria (RR=1.06; 95% CI, 0.67-1.69).

The trials evaluated losartan, candesartan, olmesartan, and valsartan. One study used other antihypertensives to achieve target blood pressure, and another included patients of any albuminuria status.

Compared with placebo or no treatment, ARBs didn’t reduce the risk of death (5 studies; 7653 patients; RR=1.12; 95% CI, 0.88-1.41).¹ All 5 RCTs assessed normoalbuminuric patients. Three of the 5 studies examined normotensive patients; one evaluated only hypertensive patients, and another assessed mostly hypertensive patients.

ARBs usually don’t produce significant adverse effects

Within the meta-analysis, ARBs didn’t increase risk of cough, headache, or hyperkalemia.¹

A 42-year-old gay man sought care for a nonhealing lesion on his penis that he’d had for 6 weeks. The patient acknowledged having unprotected sex with several partners in the month prior to the onset of the lesion. The lesion was asymptomatic and small, but rapidly developed into a superficial ulcer. The examination revealed a 1-cm ulcerated, erythematous plaque with raised and indurated edges on the glans (FIGURE). There was minimal drainage in the periurethral area. The patient didn’t have any other rashes or lesions on the skin or mucous membranes, or any regional lymphadenopathies.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Primary syphilis

The patient was given a diagnosis of primary syphilis based on his history and the clinical appearance of a syphilitic chancre. While chancres often occur on the shaft of the penis, they can also occur in the periurethral area, as was the case with this patient. The diagnosis of syphilis was confirmed with a positive Treponema pallidum particle agglutination assay (TPPA).

Although the primary route of transmission is sexual contact, syphilis may also be transmitted from mother to fetus during pregnancy or birth, resulting in congenital syphilis. In addition, a considerable number of men who are diagnosed with syphilis are positive for human immunodeficiency virus (HIV) antibodies.¹ (Our patient was tested for HIV; the result was negative.)

The resurgence of syphilis. In 2000 and 2001, rates of syphilis cases reached a historic low (2.1 cases per 100,000).² Since then, however, there has been a resurgence of syphilis—not just in men who have sex with men—but in all sexually active populations. In the United States during 2014 to 2015, the rate of primary and secondary syphilis increased to 7.5 cases per 100,000, which is the highest reported rate since 1994. From 2000 to 2015, this increase was primarily attributable to cases among men and, specifically, among gay, bisexual, and other men who have sex with men. But while the rate increased 18% among men during 2014 to 2015, it also increased by 27% among women.²

There has been a resurgence of syphilis—not just in men who have sex with men, but in all sexually active populations.

Social, epidemiologic, and individual risk factors can lead to higher levels of sexually transmitted diseases (STDs) in gay and bisexual men. In addition, lack of access to quality health care, homophobia, or stigma can all contribute to greater risk for this population.³ For these reasons, it is important for family physicians to immediately recognize this disease. (To learn more about the resurgence of syphilis, listen to the audiocast from Doug Campos-Outcalt, MD, MPA at http://bit.ly/2mRvYQe.)

The 4 stages of syphilis

The signs and symptoms of syphilis vary by the stage of disease.

Primary syphilis is the stage of initial inoculation with T pallidum. It is during this stage that a firm, nonpruritic skin ulceration—a chancre—appears. Although the classic chancre is typically painless, it can be painful.

Secondary syphilis presents as a diffuse rash that frequently involves the palms and soles.

The third or latent stage of syphilis may last for 2 years with few, or no, symptoms. However, secondary and latent syphilis may entail a broad range of manifestations, which is why syphilis is known as the “great imitator.”

In the final stage—tertiary syphilis—gummas and neurologic or cardiac symptoms may be seen.

Differential includes fungal, bacterial infections

The differential diagnosis of syphilis includes other infections such as chancroid, condyloma acuminata, candidiasis, granuloma inguinale, and lymphogranuloma venereum.

Chancroid presents as multiple painful necrotizing genital ulcers that may be accompanied by inguinal lymphadenopathy. It is caused by the bacterium Haemophilus ducreyi.

Condyloma acuminata is characterized by skin-colored, nontender warts and is caused by the human papillomavirus (HPV).

Candidiasis is a fungal infection that is characterized by pruritus and whitish-colored patches on the penis.

Granuloma inguinale (Donovanosis) is a chronic bacterial infection caused by Klebsiella granulomatis. It initially appears as nodular lesions that evolve into ulcers, which progressively expand and are locally destructive.

Lymphogranuloma venereum is an STD that can be caused by 3 different types (serovars) of the bacteria Chlamydia trachomatis. It presents with self-limited genital papules and ulcers followed by painful inguinal and/or femoral lymphadenopathy.

Diagnosis can be confirmed with serologic tests

The diagnosis of syphilis can be made by direct identification of the bacterium or serologic tests. Direct tests include dark field microscopy of serous fluid from genital lesions. This provides an immediate diagnosis with a sensitivity rate of up to 97%.⁴ However, hospitals do not always have the equipment or experienced staff to perform this technique, which must be done within 10 minutes of acquiring a sample. A polymerase chain reaction test can also be used to detect T pallidum DNA from specimens of any lesion exudate, tissue, or body fluid, but these tests can be costly compared with other tests used to diagnose syphilis.⁵

Serologic tests are divided into 2 groups: treponemal (specific) and nontreponemal (nonspecific) tests. Treponemal tests, which include TPPA, T pallidum hemagglutination assays, and enzyme-linked immunosorbent assays, will yield a positive result for current or previously treated syphilis because a positive result remains so for life. Nontreponemal tests, such as the rapid plasma reagin (RPR) test and the venereal disease reference laboratory (VDRL) test, yield a titer that is a measure of disease activity (the titer drops with treatment and rises with reinfection). Because these are nonspecific tests, biological false positives may occur if the patient has other acute or chronic infections or autoimmune diseases.⁵

Treat with penicillin

The first-choice treatment for uncomplicated syphilis is a single dose of intramuscular (IM) penicillin G (2.4 million units). A single dose of oral azithromycin 2 g or doxycycline 100 mg orally twice a day for 14 days can be used for patients who are allergic to penicillin.^5-7 Ceftriaxone, either IM or intravenous 1 g/d for 10 to 14 days, is also effective.

Because nontreponemal tests are nonspecific, biological false positives may occur in patients with other acute or chronic infections or autoimmune diseases.

Our patient declined parenteral treatment, so he was treated with oral azithromycin 2 g in a single dose. His RPR titer was taken again one week after completing the azithromycin, at which time there was a 4-fold drop (1:32 to 1:8), indicating a good response to therapy. At a follow-up appointment 6 months later, the infection hadn’t recurred. We also educated the patient on the nature of the infection, how he became infected, and safe-sex practices to prevent reinfection.

CORRESPONDENCE
Husein Husein-ElAhmed, MD, PhD, Department of Dermatology, Hospital de Baza, Avda Murcia s/n, CP: 18800, Granada, Spain; [email protected].

A 42-year-old gay man sought care for a nonhealing lesion on his penis that he’d had for 6 weeks. The patient acknowledged having unprotected sex with several partners in the month prior to the onset of the lesion. The lesion was asymptomatic and small, but rapidly developed into a superficial ulcer. The examination revealed a 1-cm ulcerated, erythematous plaque with raised and indurated edges on the glans (FIGURE). There was minimal drainage in the periurethral area. The patient didn’t have any other rashes or lesions on the skin or mucous membranes, or any regional lymphadenopathies.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Primary syphilis

The patient was given a diagnosis of primary syphilis based on his history and the clinical appearance of a syphilitic chancre. While chancres often occur on the shaft of the penis, they can also occur in the periurethral area, as was the case with this patient. The diagnosis of syphilis was confirmed with a positive Treponema pallidum particle agglutination assay (TPPA).

Although the primary route of transmission is sexual contact, syphilis may also be transmitted from mother to fetus during pregnancy or birth, resulting in congenital syphilis. In addition, a considerable number of men who are diagnosed with syphilis are positive for human immunodeficiency virus (HIV) antibodies.¹ (Our patient was tested for HIV; the result was negative.)

The resurgence of syphilis. In 2000 and 2001, rates of syphilis cases reached a historic low (2.1 cases per 100,000).² Since then, however, there has been a resurgence of syphilis—not just in men who have sex with men—but in all sexually active populations. In the United States during 2014 to 2015, the rate of primary and secondary syphilis increased to 7.5 cases per 100,000, which is the highest reported rate since 1994. From 2000 to 2015, this increase was primarily attributable to cases among men and, specifically, among gay, bisexual, and other men who have sex with men. But while the rate increased 18% among men during 2014 to 2015, it also increased by 27% among women.²

There has been a resurgence of syphilis—not just in men who have sex with men, but in all sexually active populations.

Social, epidemiologic, and individual risk factors can lead to higher levels of sexually transmitted diseases (STDs) in gay and bisexual men. In addition, lack of access to quality health care, homophobia, or stigma can all contribute to greater risk for this population.³ For these reasons, it is important for family physicians to immediately recognize this disease. (To learn more about the resurgence of syphilis, listen to the audiocast from Doug Campos-Outcalt, MD, MPA at http://bit.ly/2mRvYQe.)

The 4 stages of syphilis

The signs and symptoms of syphilis vary by the stage of disease.

Primary syphilis is the stage of initial inoculation with T pallidum. It is during this stage that a firm, nonpruritic skin ulceration—a chancre—appears. Although the classic chancre is typically painless, it can be painful.

Secondary syphilis presents as a diffuse rash that frequently involves the palms and soles.

The third or latent stage of syphilis may last for 2 years with few, or no, symptoms. However, secondary and latent syphilis may entail a broad range of manifestations, which is why syphilis is known as the “great imitator.”

In the final stage—tertiary syphilis—gummas and neurologic or cardiac symptoms may be seen.

Differential includes fungal, bacterial infections

The differential diagnosis of syphilis includes other infections such as chancroid, condyloma acuminata, candidiasis, granuloma inguinale, and lymphogranuloma venereum.

Chancroid presents as multiple painful necrotizing genital ulcers that may be accompanied by inguinal lymphadenopathy. It is caused by the bacterium Haemophilus ducreyi.

Condyloma acuminata is characterized by skin-colored, nontender warts and is caused by the human papillomavirus (HPV).

Candidiasis is a fungal infection that is characterized by pruritus and whitish-colored patches on the penis.

Granuloma inguinale (Donovanosis) is a chronic bacterial infection caused by Klebsiella granulomatis. It initially appears as nodular lesions that evolve into ulcers, which progressively expand and are locally destructive.

Lymphogranuloma venereum is an STD that can be caused by 3 different types (serovars) of the bacteria Chlamydia trachomatis. It presents with self-limited genital papules and ulcers followed by painful inguinal and/or femoral lymphadenopathy.

Diagnosis can be confirmed with serologic tests

The diagnosis of syphilis can be made by direct identification of the bacterium or serologic tests. Direct tests include dark field microscopy of serous fluid from genital lesions. This provides an immediate diagnosis with a sensitivity rate of up to 97%.⁴ However, hospitals do not always have the equipment or experienced staff to perform this technique, which must be done within 10 minutes of acquiring a sample. A polymerase chain reaction test can also be used to detect T pallidum DNA from specimens of any lesion exudate, tissue, or body fluid, but these tests can be costly compared with other tests used to diagnose syphilis.⁵

Serologic tests are divided into 2 groups: treponemal (specific) and nontreponemal (nonspecific) tests. Treponemal tests, which include TPPA, T pallidum hemagglutination assays, and enzyme-linked immunosorbent assays, will yield a positive result for current or previously treated syphilis because a positive result remains so for life. Nontreponemal tests, such as the rapid plasma reagin (RPR) test and the venereal disease reference laboratory (VDRL) test, yield a titer that is a measure of disease activity (the titer drops with treatment and rises with reinfection). Because these are nonspecific tests, biological false positives may occur if the patient has other acute or chronic infections or autoimmune diseases.⁵

Treat with penicillin

The first-choice treatment for uncomplicated syphilis is a single dose of intramuscular (IM) penicillin G (2.4 million units). A single dose of oral azithromycin 2 g or doxycycline 100 mg orally twice a day for 14 days can be used for patients who are allergic to penicillin.^5-7 Ceftriaxone, either IM or intravenous 1 g/d for 10 to 14 days, is also effective.

Because nontreponemal tests are nonspecific, biological false positives may occur in patients with other acute or chronic infections or autoimmune diseases.

Our patient declined parenteral treatment, so he was treated with oral azithromycin 2 g in a single dose. His RPR titer was taken again one week after completing the azithromycin, at which time there was a 4-fold drop (1:32 to 1:8), indicating a good response to therapy. At a follow-up appointment 6 months later, the infection hadn’t recurred. We also educated the patient on the nature of the infection, how he became infected, and safe-sex practices to prevent reinfection.

CORRESPONDENCE
Husein Husein-ElAhmed, MD, PhD, Department of Dermatology, Hospital de Baza, Avda Murcia s/n, CP: 18800, Granada, Spain; [email protected].

A 42-year-old gay man sought care for a nonhealing lesion on his penis that he’d had for 6 weeks. The patient acknowledged having unprotected sex with several partners in the month prior to the onset of the lesion. The lesion was asymptomatic and small, but rapidly developed into a superficial ulcer. The examination revealed a 1-cm ulcerated, erythematous plaque with raised and indurated edges on the glans (FIGURE). There was minimal drainage in the periurethral area. The patient didn’t have any other rashes or lesions on the skin or mucous membranes, or any regional lymphadenopathies.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Primary syphilis

The patient was given a diagnosis of primary syphilis based on his history and the clinical appearance of a syphilitic chancre. While chancres often occur on the shaft of the penis, they can also occur in the periurethral area, as was the case with this patient. The diagnosis of syphilis was confirmed with a positive Treponema pallidum particle agglutination assay (TPPA).

Although the primary route of transmission is sexual contact, syphilis may also be transmitted from mother to fetus during pregnancy or birth, resulting in congenital syphilis. In addition, a considerable number of men who are diagnosed with syphilis are positive for human immunodeficiency virus (HIV) antibodies.¹ (Our patient was tested for HIV; the result was negative.)

The resurgence of syphilis. In 2000 and 2001, rates of syphilis cases reached a historic low (2.1 cases per 100,000).² Since then, however, there has been a resurgence of syphilis—not just in men who have sex with men—but in all sexually active populations. In the United States during 2014 to 2015, the rate of primary and secondary syphilis increased to 7.5 cases per 100,000, which is the highest reported rate since 1994. From 2000 to 2015, this increase was primarily attributable to cases among men and, specifically, among gay, bisexual, and other men who have sex with men. But while the rate increased 18% among men during 2014 to 2015, it also increased by 27% among women.²

There has been a resurgence of syphilis—not just in men who have sex with men, but in all sexually active populations.

Social, epidemiologic, and individual risk factors can lead to higher levels of sexually transmitted diseases (STDs) in gay and bisexual men. In addition, lack of access to quality health care, homophobia, or stigma can all contribute to greater risk for this population.³ For these reasons, it is important for family physicians to immediately recognize this disease. (To learn more about the resurgence of syphilis, listen to the audiocast from Doug Campos-Outcalt, MD, MPA at http://bit.ly/2mRvYQe.)

The 4 stages of syphilis

The signs and symptoms of syphilis vary by the stage of disease.

Primary syphilis is the stage of initial inoculation with T pallidum. It is during this stage that a firm, nonpruritic skin ulceration—a chancre—appears. Although the classic chancre is typically painless, it can be painful.

Secondary syphilis presents as a diffuse rash that frequently involves the palms and soles.

The third or latent stage of syphilis may last for 2 years with few, or no, symptoms. However, secondary and latent syphilis may entail a broad range of manifestations, which is why syphilis is known as the “great imitator.”

In the final stage—tertiary syphilis—gummas and neurologic or cardiac symptoms may be seen.

Differential includes fungal, bacterial infections

The differential diagnosis of syphilis includes other infections such as chancroid, condyloma acuminata, candidiasis, granuloma inguinale, and lymphogranuloma venereum.

Chancroid presents as multiple painful necrotizing genital ulcers that may be accompanied by inguinal lymphadenopathy. It is caused by the bacterium Haemophilus ducreyi.

Condyloma acuminata is characterized by skin-colored, nontender warts and is caused by the human papillomavirus (HPV).

Candidiasis is a fungal infection that is characterized by pruritus and whitish-colored patches on the penis.

Granuloma inguinale (Donovanosis) is a chronic bacterial infection caused by Klebsiella granulomatis. It initially appears as nodular lesions that evolve into ulcers, which progressively expand and are locally destructive.

Lymphogranuloma venereum is an STD that can be caused by 3 different types (serovars) of the bacteria Chlamydia trachomatis. It presents with self-limited genital papules and ulcers followed by painful inguinal and/or femoral lymphadenopathy.

Diagnosis can be confirmed with serologic tests

The diagnosis of syphilis can be made by direct identification of the bacterium or serologic tests. Direct tests include dark field microscopy of serous fluid from genital lesions. This provides an immediate diagnosis with a sensitivity rate of up to 97%.⁴ However, hospitals do not always have the equipment or experienced staff to perform this technique, which must be done within 10 minutes of acquiring a sample. A polymerase chain reaction test can also be used to detect T pallidum DNA from specimens of any lesion exudate, tissue, or body fluid, but these tests can be costly compared with other tests used to diagnose syphilis.⁵

Serologic tests are divided into 2 groups: treponemal (specific) and nontreponemal (nonspecific) tests. Treponemal tests, which include TPPA, T pallidum hemagglutination assays, and enzyme-linked immunosorbent assays, will yield a positive result for current or previously treated syphilis because a positive result remains so for life. Nontreponemal tests, such as the rapid plasma reagin (RPR) test and the venereal disease reference laboratory (VDRL) test, yield a titer that is a measure of disease activity (the titer drops with treatment and rises with reinfection). Because these are nonspecific tests, biological false positives may occur if the patient has other acute or chronic infections or autoimmune diseases.⁵

Treat with penicillin

The first-choice treatment for uncomplicated syphilis is a single dose of intramuscular (IM) penicillin G (2.4 million units). A single dose of oral azithromycin 2 g or doxycycline 100 mg orally twice a day for 14 days can be used for patients who are allergic to penicillin.^5-7 Ceftriaxone, either IM or intravenous 1 g/d for 10 to 14 days, is also effective.

Because nontreponemal tests are nonspecific, biological false positives may occur in patients with other acute or chronic infections or autoimmune diseases.

Our patient declined parenteral treatment, so he was treated with oral azithromycin 2 g in a single dose. His RPR titer was taken again one week after completing the azithromycin, at which time there was a 4-fold drop (1:32 to 1:8), indicating a good response to therapy. At a follow-up appointment 6 months later, the infection hadn’t recurred. We also educated the patient on the nature of the infection, how he became infected, and safe-sex practices to prevent reinfection.

CORRESPONDENCE
Husein Husein-ElAhmed, MD, PhD, Department of Dermatology, Hospital de Baza, Avda Murcia s/n, CP: 18800, Granada, Spain; [email protected].