CASE: Stress and chest pain

A primary care physician refers Mr. J, age 40, to our mental health clinic for evaluation of anxiety symptoms. Almost a decade ago Mr. J presented to his primary care physician with anxiety and panic attacks that included chest pain and shortness of breath. Various pharmacologic treatments, including paroxetine, were only moderately successful until 4 years ago, when Mr. J began nighttime continuous positive airway pressure (CPAP) therapy and pramipexole, 0.25 to 0.5 mg/d, for obstructive sleep apnea (OSA), at which point his anxiety completely resolved.

Mr. J reported no anxiety for many years, but when shortness of breath, palpitations, and chest pain re-emerge, he consults his primary care physician. After a negative workup for myocardial infarction, Mr. J is started on short-term beta-blocker therapy and restarted on paroxetine, 20 mg/d. A sleep medicine specialist repeats polysomnography and makes slight adjustments to Mr. J’s CPAP therapy. Mr. J relocates to our city and his new primary care physician refers Mr. J to our mental health clinic.

In addition to OSA, Mr. J has mild anemia, hyperlipidemia, and vitamin D deficiency. Mr. J was adopted and has no knowledge of his family psychiatric or medical history. His mental status is normal. Mr. J is not obese, exercises regularly, and has slight micrognathia. His current medications include paroxetine, 20 mg/d, modafinil, 200 mg/d, and ergocalciferol, 50,000 units/week for vitamin D deficiency.

Mr. J says he experienced a single panic attack 7 months ago, but none since then. However, he complains of chronic chest pressure and mild intermittent anxiety associated with the stress of his new job and recent relocation.

The authors’ observations

Mr. J’s anxiety resolved fully only after receiving treatment for OSA, which is characterized by episodes of blocked breathing during sleep (Table 1).¹ Multiple studies show a significant association between OSA and panic attacks.^2-5 In a survey of 301 sleep apnea patients, Edlund et al⁶ demonstrated that OSA may cause nocturnal panic attacks. Untreated OSA can worsen anxiety symptoms. In a study of 242 OSA patients, those who were not compliant with CPAP therapy had significantly higher anxiety scores as measured on the Hospital Anxiety and Depression Scale_.⁷

OSA treatment options include CPAP, oral appliance, and surgery; weight loss and positional therapy may help. Thyroid function, B12, folate, ferritin, and iron studies, and complete blood count can rule out secondary causes of OSA.

Table 1

Obstructive sleep apnea risk factors, symptoms, and features

HISTORY: A succession of diagnoses

Approximately 9 years ago, Mr. J experienced several episodes of waking in the middle of the night from a bad dream with severe shortness of breath and chest pain. He also reported increasing fatigue, anxiety, and stress regarding work, graduate school, and his wife’s recent miscarriage. After negative cardiac workups, his primary care physician diagnosed panic attacks. He referred Mr. J to stress management classes and prescribed clonazepam, 1.5 mg/d, which was discontinued after 2 months.

One week after discontinuing clonazepam, Mr. J experienced chest pain, shortness of breath, and anxiety while awake. A cardiologist ruled out cardiac pathology. Mr. J’s primary care physician prescribed sertraline, 25 mg/d, and propranolol, 60 mg/d and 10 mg as needed, for anxiety.

Shortly after, Mr. J moved to a different city. His new primary care physician discontinued sertraline and propranolol and started paroxetine, titrated to 20 mg/d. A psychiatrist diagnosed Mr. J with panic disorder without agoraphobia, continued paroxetine, and added alprazolam, 1 mg/d as needed. Mr. J’s anxiety symptoms were moderately controlled for several years.

After his son was diagnosed with attention-deficit/hyperactivity disorder (ADHD), Mr. J also was evaluated and found to have ADHD and major depressive disorder, single episode. Mr. J received methylphenidate, 54 mg/d, and paroxetine was titrated to 40 mg/d, with moderate results.

Approximately 6 years before presenting to our clinic, Mr. J reported worsening daytime fatigue, which was treated with modafinil, 200 mg/d. He experienced significant improvement. The next year methylphenidate was switched to amphetamine/dextroamphetamine, then discontinued because of side effects. His physician started Mr. J on atomoxetine, which also was discontinued because of side effects.

Two years later, Mr. J complained of gradual worsening daytime sleepiness. Polysomnography revealed that Mr. J had severe OSA and periodic limb movement disorder. After he began nighttime CPAP and pramipexole, 0.25 to 0.5 mg/d, and continued modafinil, 200 mg/d, his anxiety symptoms completely resolved. Several months later Mr. J’s physician discontinued paroxetine because Mr. J reported it caused mildly decreased concentration.

The authors’ observations

The etiology of Mr. J’s anxiety is unclear; however, he does not meet criteria for:

• panic disorder, because he denies persistent concern about having more attacks or the implications or consequences of panic attacks, or significant change in behavior related to panic attacks (Table 2)⁸
• generalized anxiety disorder, because between panic attacks Mr. J’s baseline anxiety related to “real-world” stressors is mild, intermittent, and easily controllable⁸
• substance-induced anxiety disorder, because Mr. J denies using caffeine, tobacco, alcohol, or illicit drugs. Also, for many years he worked for a company that performed random drug screening.

Table 2

Diagnostic criteria for panic disorder without agoraphobia

Although it is difficult to draw a conclusion from a single case, Mr. J’s dramatic improvement with CPAP warrants speculation about possible etiologic relationships among daytime panic attacks, nighttime panic attacks, and OSA.

According to DSM-IV-TR, a panic attack has a distinct period of intense fear or discomfort (Table 3).⁸ Recurrent panic attacks can lead to anticipatory anxiety, which is an intense fear and/or dread of having another panic attack.⁹ According to Steven Reiss’ expectancy theory, anxiety sensitivity—ie, the fear of anxiety or fear of fear—may be a risk factor for panic disorder.¹⁰ Therefore, past panic attacks may increase the likelihood of future panic attacks.

Table 3

Diagnostic criteria for panic attack*

Mr. J’s panic symptoms may be caused by multiple OSA-induced nocturnal panic attacks. These nighttime panic attacks may predispose him to daytime attacks. It is possible that Mr. J had subclinical panic disorder before developing OSA. In this scenario, his OSA-induced nocturnal panic attacks may have worsened his panic disorder. Unfortunately, we do not know precisely how long Mr. J has had OSA—only that he was diagnosed with the condition 4 years before presenting to our clinic.

Mr. J responded moderately to paroxetine monotherapy but experienced rapid resolution of his panic attacks with a combination of paroxetine and CPAP. CPAP monotherapy sufficiently prevented panic attacks for 4 years. Finally, when Mr. J experienced a single panic attack several months before presenting to our clinic—at the end of a very stressful year—reintroducing paroxetine prevented subsequent attacks. This supports our hypothesis that OSA may predispose or indirectly cause patients to develop daytime panic attacks. Alternately, this case suggests that OSA may cause subclinical panic disorder to present as an acute condition.

We rule out anxiety disorder secondary to a general medical condition (OSA) and diagnose Mr. J with anxiety disorder not otherwise specified.

The authors’ observations

We continue paroxetine at 20 mg/d because it was working fairly well with minimal side effects. The sleep medicine specialist maintained modafinil, 200 mg/d. Laboratory studies—including a comprehensive metabolic panel, complete blood count with differential, and thyroid stimulating hormone—were within normal limits except a fasting blood glucose of 123 mg/dL, for which we referred Mr. J to his primary care physician.

OUTCOME: Discontinue paroxetine?

One month later, Mr. J denies panic attacks, other anxiety symptoms, or other psychiatric symptoms and is sleeping well. However, he reports that his mildly decreased concentration persists and he wants to stop paroxetine.

After discussing the risks and benefits, Mr. J and the treatment team decide to continue paroxetine at 20 mg/d. We cite peer-reviewed literature that recommends continuing antidepressants for at least 1 year and possibly indefinitely after symptom resolution to control panic disorder symptoms.⁹ In addition, we discuss the lack of studies comparing different lengths of treatment with SSRIs for apparent OSA-induced panic attacks that respond to SSRI/CPAP therapy. Because Mr. J was doing well and experiencing minimal side effects, he feels he would be better served with a longer period of psychopharmacologic treatment.

Six months later, Mr. J says his anxiety symptoms are well controlled and generally unchanged except for an occasional “little flutter” of anxiety every 3 or 4 days that lasts several seconds. For 1 year, he reports no recurrence of panic attacks, compliance with CPAP, and stable OSA.

Related resource

• Saunamäki T, Jehkonen M. Depression and anxiety in obstructive sleep apnea syndrome: a review. Acta Neurol Scand. 2007;116(5):277-288.

Drug brand names

• Alprazolam • Xanax
• Amphetamine/dextroamphetamine • Adderall
• Atomoxetine • Strattera
• Clonazepam • Klonopin
• Ergocalciferol • Calciferol
• Modafinil • Provigil
• Methylphenidate extended release • Concerta
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Propranolol • Inderal
• Sertraline • Zoloft

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Stress and chest pain

A primary care physician refers Mr. J, age 40, to our mental health clinic for evaluation of anxiety symptoms. Almost a decade ago Mr. J presented to his primary care physician with anxiety and panic attacks that included chest pain and shortness of breath. Various pharmacologic treatments, including paroxetine, were only moderately successful until 4 years ago, when Mr. J began nighttime continuous positive airway pressure (CPAP) therapy and pramipexole, 0.25 to 0.5 mg/d, for obstructive sleep apnea (OSA), at which point his anxiety completely resolved.

Mr. J reported no anxiety for many years, but when shortness of breath, palpitations, and chest pain re-emerge, he consults his primary care physician. After a negative workup for myocardial infarction, Mr. J is started on short-term beta-blocker therapy and restarted on paroxetine, 20 mg/d. A sleep medicine specialist repeats polysomnography and makes slight adjustments to Mr. J’s CPAP therapy. Mr. J relocates to our city and his new primary care physician refers Mr. J to our mental health clinic.

In addition to OSA, Mr. J has mild anemia, hyperlipidemia, and vitamin D deficiency. Mr. J was adopted and has no knowledge of his family psychiatric or medical history. His mental status is normal. Mr. J is not obese, exercises regularly, and has slight micrognathia. His current medications include paroxetine, 20 mg/d, modafinil, 200 mg/d, and ergocalciferol, 50,000 units/week for vitamin D deficiency.

Mr. J says he experienced a single panic attack 7 months ago, but none since then. However, he complains of chronic chest pressure and mild intermittent anxiety associated with the stress of his new job and recent relocation.

The authors’ observations

Mr. J’s anxiety resolved fully only after receiving treatment for OSA, which is characterized by episodes of blocked breathing during sleep (Table 1).¹ Multiple studies show a significant association between OSA and panic attacks.^2-5 In a survey of 301 sleep apnea patients, Edlund et al⁶ demonstrated that OSA may cause nocturnal panic attacks. Untreated OSA can worsen anxiety symptoms. In a study of 242 OSA patients, those who were not compliant with CPAP therapy had significantly higher anxiety scores as measured on the Hospital Anxiety and Depression Scale_.⁷

OSA treatment options include CPAP, oral appliance, and surgery; weight loss and positional therapy may help. Thyroid function, B12, folate, ferritin, and iron studies, and complete blood count can rule out secondary causes of OSA.

Table 1

Obstructive sleep apnea risk factors, symptoms, and features

HISTORY: A succession of diagnoses

Approximately 9 years ago, Mr. J experienced several episodes of waking in the middle of the night from a bad dream with severe shortness of breath and chest pain. He also reported increasing fatigue, anxiety, and stress regarding work, graduate school, and his wife’s recent miscarriage. After negative cardiac workups, his primary care physician diagnosed panic attacks. He referred Mr. J to stress management classes and prescribed clonazepam, 1.5 mg/d, which was discontinued after 2 months.

One week after discontinuing clonazepam, Mr. J experienced chest pain, shortness of breath, and anxiety while awake. A cardiologist ruled out cardiac pathology. Mr. J’s primary care physician prescribed sertraline, 25 mg/d, and propranolol, 60 mg/d and 10 mg as needed, for anxiety.

Shortly after, Mr. J moved to a different city. His new primary care physician discontinued sertraline and propranolol and started paroxetine, titrated to 20 mg/d. A psychiatrist diagnosed Mr. J with panic disorder without agoraphobia, continued paroxetine, and added alprazolam, 1 mg/d as needed. Mr. J’s anxiety symptoms were moderately controlled for several years.

After his son was diagnosed with attention-deficit/hyperactivity disorder (ADHD), Mr. J also was evaluated and found to have ADHD and major depressive disorder, single episode. Mr. J received methylphenidate, 54 mg/d, and paroxetine was titrated to 40 mg/d, with moderate results.

Approximately 6 years before presenting to our clinic, Mr. J reported worsening daytime fatigue, which was treated with modafinil, 200 mg/d. He experienced significant improvement. The next year methylphenidate was switched to amphetamine/dextroamphetamine, then discontinued because of side effects. His physician started Mr. J on atomoxetine, which also was discontinued because of side effects.

Two years later, Mr. J complained of gradual worsening daytime sleepiness. Polysomnography revealed that Mr. J had severe OSA and periodic limb movement disorder. After he began nighttime CPAP and pramipexole, 0.25 to 0.5 mg/d, and continued modafinil, 200 mg/d, his anxiety symptoms completely resolved. Several months later Mr. J’s physician discontinued paroxetine because Mr. J reported it caused mildly decreased concentration.

The authors’ observations

The etiology of Mr. J’s anxiety is unclear; however, he does not meet criteria for:

• panic disorder, because he denies persistent concern about having more attacks or the implications or consequences of panic attacks, or significant change in behavior related to panic attacks (Table 2)⁸
• generalized anxiety disorder, because between panic attacks Mr. J’s baseline anxiety related to “real-world” stressors is mild, intermittent, and easily controllable⁸
• substance-induced anxiety disorder, because Mr. J denies using caffeine, tobacco, alcohol, or illicit drugs. Also, for many years he worked for a company that performed random drug screening.

Table 2

Diagnostic criteria for panic disorder without agoraphobia

Although it is difficult to draw a conclusion from a single case, Mr. J’s dramatic improvement with CPAP warrants speculation about possible etiologic relationships among daytime panic attacks, nighttime panic attacks, and OSA.

According to DSM-IV-TR, a panic attack has a distinct period of intense fear or discomfort (Table 3).⁸ Recurrent panic attacks can lead to anticipatory anxiety, which is an intense fear and/or dread of having another panic attack.⁹ According to Steven Reiss’ expectancy theory, anxiety sensitivity—ie, the fear of anxiety or fear of fear—may be a risk factor for panic disorder.¹⁰ Therefore, past panic attacks may increase the likelihood of future panic attacks.

Table 3

Diagnostic criteria for panic attack*

Mr. J’s panic symptoms may be caused by multiple OSA-induced nocturnal panic attacks. These nighttime panic attacks may predispose him to daytime attacks. It is possible that Mr. J had subclinical panic disorder before developing OSA. In this scenario, his OSA-induced nocturnal panic attacks may have worsened his panic disorder. Unfortunately, we do not know precisely how long Mr. J has had OSA—only that he was diagnosed with the condition 4 years before presenting to our clinic.

Mr. J responded moderately to paroxetine monotherapy but experienced rapid resolution of his panic attacks with a combination of paroxetine and CPAP. CPAP monotherapy sufficiently prevented panic attacks for 4 years. Finally, when Mr. J experienced a single panic attack several months before presenting to our clinic—at the end of a very stressful year—reintroducing paroxetine prevented subsequent attacks. This supports our hypothesis that OSA may predispose or indirectly cause patients to develop daytime panic attacks. Alternately, this case suggests that OSA may cause subclinical panic disorder to present as an acute condition.

We rule out anxiety disorder secondary to a general medical condition (OSA) and diagnose Mr. J with anxiety disorder not otherwise specified.

The authors’ observations

We continue paroxetine at 20 mg/d because it was working fairly well with minimal side effects. The sleep medicine specialist maintained modafinil, 200 mg/d. Laboratory studies—including a comprehensive metabolic panel, complete blood count with differential, and thyroid stimulating hormone—were within normal limits except a fasting blood glucose of 123 mg/dL, for which we referred Mr. J to his primary care physician.

OUTCOME: Discontinue paroxetine?

One month later, Mr. J denies panic attacks, other anxiety symptoms, or other psychiatric symptoms and is sleeping well. However, he reports that his mildly decreased concentration persists and he wants to stop paroxetine.

After discussing the risks and benefits, Mr. J and the treatment team decide to continue paroxetine at 20 mg/d. We cite peer-reviewed literature that recommends continuing antidepressants for at least 1 year and possibly indefinitely after symptom resolution to control panic disorder symptoms.⁹ In addition, we discuss the lack of studies comparing different lengths of treatment with SSRIs for apparent OSA-induced panic attacks that respond to SSRI/CPAP therapy. Because Mr. J was doing well and experiencing minimal side effects, he feels he would be better served with a longer period of psychopharmacologic treatment.

Six months later, Mr. J says his anxiety symptoms are well controlled and generally unchanged except for an occasional “little flutter” of anxiety every 3 or 4 days that lasts several seconds. For 1 year, he reports no recurrence of panic attacks, compliance with CPAP, and stable OSA.

Related resource

• Saunamäki T, Jehkonen M. Depression and anxiety in obstructive sleep apnea syndrome: a review. Acta Neurol Scand. 2007;116(5):277-288.

Drug brand names

• Alprazolam • Xanax
• Amphetamine/dextroamphetamine • Adderall
• Atomoxetine • Strattera
• Clonazepam • Klonopin
• Ergocalciferol • Calciferol
• Modafinil • Provigil
• Methylphenidate extended release • Concerta
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Propranolol • Inderal
• Sertraline • Zoloft

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Stress and chest pain

A primary care physician refers Mr. J, age 40, to our mental health clinic for evaluation of anxiety symptoms. Almost a decade ago Mr. J presented to his primary care physician with anxiety and panic attacks that included chest pain and shortness of breath. Various pharmacologic treatments, including paroxetine, were only moderately successful until 4 years ago, when Mr. J began nighttime continuous positive airway pressure (CPAP) therapy and pramipexole, 0.25 to 0.5 mg/d, for obstructive sleep apnea (OSA), at which point his anxiety completely resolved.

Mr. J reported no anxiety for many years, but when shortness of breath, palpitations, and chest pain re-emerge, he consults his primary care physician. After a negative workup for myocardial infarction, Mr. J is started on short-term beta-blocker therapy and restarted on paroxetine, 20 mg/d. A sleep medicine specialist repeats polysomnography and makes slight adjustments to Mr. J’s CPAP therapy. Mr. J relocates to our city and his new primary care physician refers Mr. J to our mental health clinic.

In addition to OSA, Mr. J has mild anemia, hyperlipidemia, and vitamin D deficiency. Mr. J was adopted and has no knowledge of his family psychiatric or medical history. His mental status is normal. Mr. J is not obese, exercises regularly, and has slight micrognathia. His current medications include paroxetine, 20 mg/d, modafinil, 200 mg/d, and ergocalciferol, 50,000 units/week for vitamin D deficiency.

Mr. J says he experienced a single panic attack 7 months ago, but none since then. However, he complains of chronic chest pressure and mild intermittent anxiety associated with the stress of his new job and recent relocation.

The authors’ observations

Mr. J’s anxiety resolved fully only after receiving treatment for OSA, which is characterized by episodes of blocked breathing during sleep (Table 1).¹ Multiple studies show a significant association between OSA and panic attacks.^2-5 In a survey of 301 sleep apnea patients, Edlund et al⁶ demonstrated that OSA may cause nocturnal panic attacks. Untreated OSA can worsen anxiety symptoms. In a study of 242 OSA patients, those who were not compliant with CPAP therapy had significantly higher anxiety scores as measured on the Hospital Anxiety and Depression Scale_.⁷

OSA treatment options include CPAP, oral appliance, and surgery; weight loss and positional therapy may help. Thyroid function, B12, folate, ferritin, and iron studies, and complete blood count can rule out secondary causes of OSA.

Table 1

Obstructive sleep apnea risk factors, symptoms, and features

HISTORY: A succession of diagnoses

Approximately 9 years ago, Mr. J experienced several episodes of waking in the middle of the night from a bad dream with severe shortness of breath and chest pain. He also reported increasing fatigue, anxiety, and stress regarding work, graduate school, and his wife’s recent miscarriage. After negative cardiac workups, his primary care physician diagnosed panic attacks. He referred Mr. J to stress management classes and prescribed clonazepam, 1.5 mg/d, which was discontinued after 2 months.

One week after discontinuing clonazepam, Mr. J experienced chest pain, shortness of breath, and anxiety while awake. A cardiologist ruled out cardiac pathology. Mr. J’s primary care physician prescribed sertraline, 25 mg/d, and propranolol, 60 mg/d and 10 mg as needed, for anxiety.

Shortly after, Mr. J moved to a different city. His new primary care physician discontinued sertraline and propranolol and started paroxetine, titrated to 20 mg/d. A psychiatrist diagnosed Mr. J with panic disorder without agoraphobia, continued paroxetine, and added alprazolam, 1 mg/d as needed. Mr. J’s anxiety symptoms were moderately controlled for several years.

After his son was diagnosed with attention-deficit/hyperactivity disorder (ADHD), Mr. J also was evaluated and found to have ADHD and major depressive disorder, single episode. Mr. J received methylphenidate, 54 mg/d, and paroxetine was titrated to 40 mg/d, with moderate results.

Approximately 6 years before presenting to our clinic, Mr. J reported worsening daytime fatigue, which was treated with modafinil, 200 mg/d. He experienced significant improvement. The next year methylphenidate was switched to amphetamine/dextroamphetamine, then discontinued because of side effects. His physician started Mr. J on atomoxetine, which also was discontinued because of side effects.

Two years later, Mr. J complained of gradual worsening daytime sleepiness. Polysomnography revealed that Mr. J had severe OSA and periodic limb movement disorder. After he began nighttime CPAP and pramipexole, 0.25 to 0.5 mg/d, and continued modafinil, 200 mg/d, his anxiety symptoms completely resolved. Several months later Mr. J’s physician discontinued paroxetine because Mr. J reported it caused mildly decreased concentration.

The authors’ observations

The etiology of Mr. J’s anxiety is unclear; however, he does not meet criteria for:

• panic disorder, because he denies persistent concern about having more attacks or the implications or consequences of panic attacks, or significant change in behavior related to panic attacks (Table 2)⁸
• generalized anxiety disorder, because between panic attacks Mr. J’s baseline anxiety related to “real-world” stressors is mild, intermittent, and easily controllable⁸
• substance-induced anxiety disorder, because Mr. J denies using caffeine, tobacco, alcohol, or illicit drugs. Also, for many years he worked for a company that performed random drug screening.

Table 2

Diagnostic criteria for panic disorder without agoraphobia

Although it is difficult to draw a conclusion from a single case, Mr. J’s dramatic improvement with CPAP warrants speculation about possible etiologic relationships among daytime panic attacks, nighttime panic attacks, and OSA.

According to DSM-IV-TR, a panic attack has a distinct period of intense fear or discomfort (Table 3).⁸ Recurrent panic attacks can lead to anticipatory anxiety, which is an intense fear and/or dread of having another panic attack.⁹ According to Steven Reiss’ expectancy theory, anxiety sensitivity—ie, the fear of anxiety or fear of fear—may be a risk factor for panic disorder.¹⁰ Therefore, past panic attacks may increase the likelihood of future panic attacks.

Table 3

Diagnostic criteria for panic attack*

Mr. J’s panic symptoms may be caused by multiple OSA-induced nocturnal panic attacks. These nighttime panic attacks may predispose him to daytime attacks. It is possible that Mr. J had subclinical panic disorder before developing OSA. In this scenario, his OSA-induced nocturnal panic attacks may have worsened his panic disorder. Unfortunately, we do not know precisely how long Mr. J has had OSA—only that he was diagnosed with the condition 4 years before presenting to our clinic.

Mr. J responded moderately to paroxetine monotherapy but experienced rapid resolution of his panic attacks with a combination of paroxetine and CPAP. CPAP monotherapy sufficiently prevented panic attacks for 4 years. Finally, when Mr. J experienced a single panic attack several months before presenting to our clinic—at the end of a very stressful year—reintroducing paroxetine prevented subsequent attacks. This supports our hypothesis that OSA may predispose or indirectly cause patients to develop daytime panic attacks. Alternately, this case suggests that OSA may cause subclinical panic disorder to present as an acute condition.

We rule out anxiety disorder secondary to a general medical condition (OSA) and diagnose Mr. J with anxiety disorder not otherwise specified.

The authors’ observations

We continue paroxetine at 20 mg/d because it was working fairly well with minimal side effects. The sleep medicine specialist maintained modafinil, 200 mg/d. Laboratory studies—including a comprehensive metabolic panel, complete blood count with differential, and thyroid stimulating hormone—were within normal limits except a fasting blood glucose of 123 mg/dL, for which we referred Mr. J to his primary care physician.

OUTCOME: Discontinue paroxetine?

One month later, Mr. J denies panic attacks, other anxiety symptoms, or other psychiatric symptoms and is sleeping well. However, he reports that his mildly decreased concentration persists and he wants to stop paroxetine.

After discussing the risks and benefits, Mr. J and the treatment team decide to continue paroxetine at 20 mg/d. We cite peer-reviewed literature that recommends continuing antidepressants for at least 1 year and possibly indefinitely after symptom resolution to control panic disorder symptoms.⁹ In addition, we discuss the lack of studies comparing different lengths of treatment with SSRIs for apparent OSA-induced panic attacks that respond to SSRI/CPAP therapy. Because Mr. J was doing well and experiencing minimal side effects, he feels he would be better served with a longer period of psychopharmacologic treatment.

Six months later, Mr. J says his anxiety symptoms are well controlled and generally unchanged except for an occasional “little flutter” of anxiety every 3 or 4 days that lasts several seconds. For 1 year, he reports no recurrence of panic attacks, compliance with CPAP, and stable OSA.

Related resource

• Saunamäki T, Jehkonen M. Depression and anxiety in obstructive sleep apnea syndrome: a review. Acta Neurol Scand. 2007;116(5):277-288.

Drug brand names

• Alprazolam • Xanax
• Amphetamine/dextroamphetamine • Adderall
• Atomoxetine • Strattera
• Clonazepam • Klonopin
• Ergocalciferol • Calciferol
• Modafinil • Provigil
• Methylphenidate extended release • Concerta
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Propranolol • Inderal
• Sertraline • Zoloft

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Because we will all be seeing more patients with stress urinary incontinence and other urogynecologic issues, it is critical that we keep abreast of the treatment options available—and their relative effectiveness.¹

In this exploration of nonsurgical approaches to stress incontinence, Richter and colleagues started with the premise that a combination of instructed pelvic floor exercises and an incontinence pessary would be better than either treatment alone. They (very appropriately) designated the following as primary outcome measures:

• patient-reported improvement
• symptoms of stress incontinence
• patient satisfaction, as measured using validated instruments.

As reported above, combination therapy did not prove to be superior to single-modality intervention. And although behavioral therapy was superior to a pessary at 3 months, by 12 months the modalities were roughly equivalent, and only about half of patients were still using the prescribed therapy: pessary (45%) or pelvic floor exercises (57%).

This is not a real-world study

Most women who have stress incontinence and who select nonsurgical therapy choose only one option—pelvic floor exercises (if very motivated), a vaginal pessary or other device (if not so motivated), or another conservative option such as radiofrequency therapy (if even less motivated). In this study, women enrolled in behavioral therapy paid four visits (at roughly 2-week intervals) to approved “interventionists,” who instructed them in the technique for pelvic floor exercise and explained other skills and strategies to prevent urge and stress incontinence.

Many women find it difficult to attend the four to eight physiotherapy sessions that are necessary for behavioral intervention and are unwilling to devote 1 year to a therapy that they don’t find effective early on. (Physiotherapy is effective but requires a motivated patient.) Other women dislike inserting a vaginal device on a regular basis. ²

What’s more, very safe minimally invasive slings are available that offer more definitive therapy to patients who have stress incontinence. That said, a sling procedure should not be undertaken lightly. Patient selection should be based on preoperative testing, including an assessment of urethral function, for the transobturator sling.³ A retropubic sling requires a greater degree of expertise to tension appropriately but is suitable for a wider range of severity, including intrinsic sphincteric deficiency. The role of single-incision slings is unclear.

Bottom line: individualize care

The authors’ concluding statements are right on the money: “Individualization of care should continue to be the cornerstone of our approach to [stress incontinent] patients.” These women have several effective options available. We should help them make an educated choice based on symptom severity, lifestyle, and willingness to enroll in self-help intervention versus surgical therapy.

Because we will all be seeing more patients with stress urinary incontinence and other urogynecologic issues, it is critical that we keep abreast of the treatment options available—and their relative effectiveness.¹

In this exploration of nonsurgical approaches to stress incontinence, Richter and colleagues started with the premise that a combination of instructed pelvic floor exercises and an incontinence pessary would be better than either treatment alone. They (very appropriately) designated the following as primary outcome measures:

• patient-reported improvement
• symptoms of stress incontinence
• patient satisfaction, as measured using validated instruments.

As reported above, combination therapy did not prove to be superior to single-modality intervention. And although behavioral therapy was superior to a pessary at 3 months, by 12 months the modalities were roughly equivalent, and only about half of patients were still using the prescribed therapy: pessary (45%) or pelvic floor exercises (57%).

This is not a real-world study

Most women who have stress incontinence and who select nonsurgical therapy choose only one option—pelvic floor exercises (if very motivated), a vaginal pessary or other device (if not so motivated), or another conservative option such as radiofrequency therapy (if even less motivated). In this study, women enrolled in behavioral therapy paid four visits (at roughly 2-week intervals) to approved “interventionists,” who instructed them in the technique for pelvic floor exercise and explained other skills and strategies to prevent urge and stress incontinence.

Many women find it difficult to attend the four to eight physiotherapy sessions that are necessary for behavioral intervention and are unwilling to devote 1 year to a therapy that they don’t find effective early on. (Physiotherapy is effective but requires a motivated patient.) Other women dislike inserting a vaginal device on a regular basis. ²

What’s more, very safe minimally invasive slings are available that offer more definitive therapy to patients who have stress incontinence. That said, a sling procedure should not be undertaken lightly. Patient selection should be based on preoperative testing, including an assessment of urethral function, for the transobturator sling.³ A retropubic sling requires a greater degree of expertise to tension appropriately but is suitable for a wider range of severity, including intrinsic sphincteric deficiency. The role of single-incision slings is unclear.

Bottom line: individualize care

The authors’ concluding statements are right on the money: “Individualization of care should continue to be the cornerstone of our approach to [stress incontinent] patients.” These women have several effective options available. We should help them make an educated choice based on symptom severity, lifestyle, and willingness to enroll in self-help intervention versus surgical therapy.

Because we will all be seeing more patients with stress urinary incontinence and other urogynecologic issues, it is critical that we keep abreast of the treatment options available—and their relative effectiveness.¹

In this exploration of nonsurgical approaches to stress incontinence, Richter and colleagues started with the premise that a combination of instructed pelvic floor exercises and an incontinence pessary would be better than either treatment alone. They (very appropriately) designated the following as primary outcome measures:

• patient-reported improvement
• symptoms of stress incontinence
• patient satisfaction, as measured using validated instruments.

As reported above, combination therapy did not prove to be superior to single-modality intervention. And although behavioral therapy was superior to a pessary at 3 months, by 12 months the modalities were roughly equivalent, and only about half of patients were still using the prescribed therapy: pessary (45%) or pelvic floor exercises (57%).

This is not a real-world study

Most women who have stress incontinence and who select nonsurgical therapy choose only one option—pelvic floor exercises (if very motivated), a vaginal pessary or other device (if not so motivated), or another conservative option such as radiofrequency therapy (if even less motivated). In this study, women enrolled in behavioral therapy paid four visits (at roughly 2-week intervals) to approved “interventionists,” who instructed them in the technique for pelvic floor exercise and explained other skills and strategies to prevent urge and stress incontinence.

Many women find it difficult to attend the four to eight physiotherapy sessions that are necessary for behavioral intervention and are unwilling to devote 1 year to a therapy that they don’t find effective early on. (Physiotherapy is effective but requires a motivated patient.) Other women dislike inserting a vaginal device on a regular basis. ²

What’s more, very safe minimally invasive slings are available that offer more definitive therapy to patients who have stress incontinence. That said, a sling procedure should not be undertaken lightly. Patient selection should be based on preoperative testing, including an assessment of urethral function, for the transobturator sling.³ A retropubic sling requires a greater degree of expertise to tension appropriately but is suitable for a wider range of severity, including intrinsic sphincteric deficiency. The role of single-incision slings is unclear.

Bottom line: individualize care

The authors’ concluding statements are right on the money: “Individualization of care should continue to be the cornerstone of our approach to [stress incontinent] patients.” These women have several effective options available. We should help them make an educated choice based on symptom severity, lifestyle, and willingness to enroll in self-help intervention versus surgical therapy.

[email protected]

Ask about fever duration during your history taking. The main question is how to define “persistent.” If the fever lasts fewer than 5 days and everything else looks fine, most of the time the child will have whatever illness is going around.

If the fever lasts closer to 10 days, and especially if new symptoms appear, it could be a complication of what is going around. Obviously, once you go beyond 10 days, it is a more significant clinical situation. Then we are in the “fever of unknown origin” (FUO) range, which may require a subspecialist evaluation. The current official definition of FUO is fever lasting greater than 3 weeks with no diagnosis after reasonable outpatient or inpatient evaluation. Shorter episodes of unexplained fever are referred to as “fever without a source.” Most of these will resolve spontaneously or evolve into more easily recognized conditions, usually infections.

The best way to proceed really depends on the presentation. The initial evaluation always includes a careful history, physical examination, and screening labs as needed. Start a more thorough evaluation or refer when things are not adding up. How sick does the child look? Are there atypical findings? Remember your training about the typical course of strep throat, mono, or bronchitis—if you see a significant deviation, evaluate the child more thoroughly. Always ask: Do I have a reasonable working diagnosis that I am comfortable with?

Fever is a common symptom and most often is a feature of a routine viral infection. The bigger concern is a serious condition, such as a bloodstream infection; this child needs to get to the emergency room right away. A child with an unusual rash, especially with petechiae and purpura, would need an immediate referral.

Kawasaki disease is another major concern. If you suspect Kawasaki disease, the child needs to be evaluated by a subspecialist. The diagnosis is based on a fever lasting at least 4 or 5 days and associated findings, such as a rash, red strawberry tongue, or very red lips. The patient will need immediate treatment, ideally within 10 days, to minimize the risk for cardiac and coronary inflammation.

Helpful tests include a complete blood count, sedimentation rate, and C-reactive protein assay. Serum chemistries including liver function tests also may be useful. I do a urinalysis and a urine culture because urinary tract infections are common and a common cause of fever. Blood cultures should be considered.

These screening tests can be reassuring. When the clinical evaluation is benign, the white blood cell count is 5,000 cells/mcL with a normal differential; then you can tell the parent to come back in a few days for follow-up. In contrast, if a child with a persistent fever has a white count of 30,000, you really have to be more careful—it could be a sinus infection, pneumonia, or bacteremia. The other extreme, a child with a white blood count of 1,000, also requires more careful evaluation.

The pace of evaluation depends on how ill the child is, any associated findings, and whether one has a diagnosis or not. Time is your ally when the child is not very ill; watchful waiting will often reveal the nature of the problem.

It is important to take a good travel history. We saw a child with malaria last year, and the key to recognition was the history of a recent return from Ghana. Also ask about animal exposures and if anyone else at home is sick. Those can be important clinical clues for diagnosis of a child with prolonged fever.

Consider the time of year. A test that is not useful, but is often obtained, is a Lyme disease test. Lyme is rarely a cause of prolonged fever, especially in winter. Also, sometimes an extensive evaluation for autoimmune disease is performed too early in the diagnostic process. If you do an initial evaluation and do not have a diagnosis, and the fever persists, then you can move on to secondary and tertiary evaluations, such as you would with an FUO. Also, tests for mono are ordered way too often. The diagnosis of mono depends on more than a prolonged fever, and there are some very specific associated features, such as tonsils that look awful, large cervical nodes, and a palpable spleen.

Make sure the fever is real. Sometimes we see a child who reports persistent fever but is afebrile during each clinical visit. In this case, ask the parents how they take the child's temperature. Do they use a thermometer strip, or do they just touch the child and say the child feels warm? There should be some documentation of a persistent fever before you embark on additional, expensive evaluation.

Occasionally I have a child come to see me who is referred with say, 25 days of fever. Does the child really have one prolonged fever? It is more likely two different episodes—a child has illness No. 1, then a break, followed by illness No. 2. Use the history and clinical findings to distinguish between these two scenarios.

[email protected]

Ask about fever duration during your history taking. The main question is how to define “persistent.” If the fever lasts fewer than 5 days and everything else looks fine, most of the time the child will have whatever illness is going around.

If the fever lasts closer to 10 days, and especially if new symptoms appear, it could be a complication of what is going around. Obviously, once you go beyond 10 days, it is a more significant clinical situation. Then we are in the “fever of unknown origin” (FUO) range, which may require a subspecialist evaluation. The current official definition of FUO is fever lasting greater than 3 weeks with no diagnosis after reasonable outpatient or inpatient evaluation. Shorter episodes of unexplained fever are referred to as “fever without a source.” Most of these will resolve spontaneously or evolve into more easily recognized conditions, usually infections.

The best way to proceed really depends on the presentation. The initial evaluation always includes a careful history, physical examination, and screening labs as needed. Start a more thorough evaluation or refer when things are not adding up. How sick does the child look? Are there atypical findings? Remember your training about the typical course of strep throat, mono, or bronchitis—if you see a significant deviation, evaluate the child more thoroughly. Always ask: Do I have a reasonable working diagnosis that I am comfortable with?

Fever is a common symptom and most often is a feature of a routine viral infection. The bigger concern is a serious condition, such as a bloodstream infection; this child needs to get to the emergency room right away. A child with an unusual rash, especially with petechiae and purpura, would need an immediate referral.

Kawasaki disease is another major concern. If you suspect Kawasaki disease, the child needs to be evaluated by a subspecialist. The diagnosis is based on a fever lasting at least 4 or 5 days and associated findings, such as a rash, red strawberry tongue, or very red lips. The patient will need immediate treatment, ideally within 10 days, to minimize the risk for cardiac and coronary inflammation.

Helpful tests include a complete blood count, sedimentation rate, and C-reactive protein assay. Serum chemistries including liver function tests also may be useful. I do a urinalysis and a urine culture because urinary tract infections are common and a common cause of fever. Blood cultures should be considered.

These screening tests can be reassuring. When the clinical evaluation is benign, the white blood cell count is 5,000 cells/mcL with a normal differential; then you can tell the parent to come back in a few days for follow-up. In contrast, if a child with a persistent fever has a white count of 30,000, you really have to be more careful—it could be a sinus infection, pneumonia, or bacteremia. The other extreme, a child with a white blood count of 1,000, also requires more careful evaluation.

The pace of evaluation depends on how ill the child is, any associated findings, and whether one has a diagnosis or not. Time is your ally when the child is not very ill; watchful waiting will often reveal the nature of the problem.

It is important to take a good travel history. We saw a child with malaria last year, and the key to recognition was the history of a recent return from Ghana. Also ask about animal exposures and if anyone else at home is sick. Those can be important clinical clues for diagnosis of a child with prolonged fever.

Consider the time of year. A test that is not useful, but is often obtained, is a Lyme disease test. Lyme is rarely a cause of prolonged fever, especially in winter. Also, sometimes an extensive evaluation for autoimmune disease is performed too early in the diagnostic process. If you do an initial evaluation and do not have a diagnosis, and the fever persists, then you can move on to secondary and tertiary evaluations, such as you would with an FUO. Also, tests for mono are ordered way too often. The diagnosis of mono depends on more than a prolonged fever, and there are some very specific associated features, such as tonsils that look awful, large cervical nodes, and a palpable spleen.

Make sure the fever is real. Sometimes we see a child who reports persistent fever but is afebrile during each clinical visit. In this case, ask the parents how they take the child's temperature. Do they use a thermometer strip, or do they just touch the child and say the child feels warm? There should be some documentation of a persistent fever before you embark on additional, expensive evaluation.

Occasionally I have a child come to see me who is referred with say, 25 days of fever. Does the child really have one prolonged fever? It is more likely two different episodes—a child has illness No. 1, then a break, followed by illness No. 2. Use the history and clinical findings to distinguish between these two scenarios.

[email protected]

Ask about fever duration during your history taking. The main question is how to define “persistent.” If the fever lasts fewer than 5 days and everything else looks fine, most of the time the child will have whatever illness is going around.

If the fever lasts closer to 10 days, and especially if new symptoms appear, it could be a complication of what is going around. Obviously, once you go beyond 10 days, it is a more significant clinical situation. Then we are in the “fever of unknown origin” (FUO) range, which may require a subspecialist evaluation. The current official definition of FUO is fever lasting greater than 3 weeks with no diagnosis after reasonable outpatient or inpatient evaluation. Shorter episodes of unexplained fever are referred to as “fever without a source.” Most of these will resolve spontaneously or evolve into more easily recognized conditions, usually infections.

The best way to proceed really depends on the presentation. The initial evaluation always includes a careful history, physical examination, and screening labs as needed. Start a more thorough evaluation or refer when things are not adding up. How sick does the child look? Are there atypical findings? Remember your training about the typical course of strep throat, mono, or bronchitis—if you see a significant deviation, evaluate the child more thoroughly. Always ask: Do I have a reasonable working diagnosis that I am comfortable with?

Fever is a common symptom and most often is a feature of a routine viral infection. The bigger concern is a serious condition, such as a bloodstream infection; this child needs to get to the emergency room right away. A child with an unusual rash, especially with petechiae and purpura, would need an immediate referral.

Kawasaki disease is another major concern. If you suspect Kawasaki disease, the child needs to be evaluated by a subspecialist. The diagnosis is based on a fever lasting at least 4 or 5 days and associated findings, such as a rash, red strawberry tongue, or very red lips. The patient will need immediate treatment, ideally within 10 days, to minimize the risk for cardiac and coronary inflammation.

Helpful tests include a complete blood count, sedimentation rate, and C-reactive protein assay. Serum chemistries including liver function tests also may be useful. I do a urinalysis and a urine culture because urinary tract infections are common and a common cause of fever. Blood cultures should be considered.

These screening tests can be reassuring. When the clinical evaluation is benign, the white blood cell count is 5,000 cells/mcL with a normal differential; then you can tell the parent to come back in a few days for follow-up. In contrast, if a child with a persistent fever has a white count of 30,000, you really have to be more careful—it could be a sinus infection, pneumonia, or bacteremia. The other extreme, a child with a white blood count of 1,000, also requires more careful evaluation.

The pace of evaluation depends on how ill the child is, any associated findings, and whether one has a diagnosis or not. Time is your ally when the child is not very ill; watchful waiting will often reveal the nature of the problem.

It is important to take a good travel history. We saw a child with malaria last year, and the key to recognition was the history of a recent return from Ghana. Also ask about animal exposures and if anyone else at home is sick. Those can be important clinical clues for diagnosis of a child with prolonged fever.

Consider the time of year. A test that is not useful, but is often obtained, is a Lyme disease test. Lyme is rarely a cause of prolonged fever, especially in winter. Also, sometimes an extensive evaluation for autoimmune disease is performed too early in the diagnostic process. If you do an initial evaluation and do not have a diagnosis, and the fever persists, then you can move on to secondary and tertiary evaluations, such as you would with an FUO. Also, tests for mono are ordered way too often. The diagnosis of mono depends on more than a prolonged fever, and there are some very specific associated features, such as tonsils that look awful, large cervical nodes, and a palpable spleen.

Make sure the fever is real. Sometimes we see a child who reports persistent fever but is afebrile during each clinical visit. In this case, ask the parents how they take the child's temperature. Do they use a thermometer strip, or do they just touch the child and say the child feels warm? There should be some documentation of a persistent fever before you embark on additional, expensive evaluation.

Occasionally I have a child come to see me who is referred with say, 25 days of fever. Does the child really have one prolonged fever? It is more likely two different episodes—a child has illness No. 1, then a break, followed by illness No. 2. Use the history and clinical findings to distinguish between these two scenarios.

A supplement to Skin & Allergy News. This supplement was sponsored by Ferndale Laboratories Inc.

• Copay Reduction
• Patient Rebate Programs
• Prescription Abandonment Rates
• Importance of Communication between Providers and their Patients

Faculty/Faculty Disclosure

Joseph S. Eastern, MD
Clinical Associate Professor of Dermatology
Seton Hall UniversitySchool of GraduateMedical Education
South Orange, NJ

Dr. Eastern has a consulting agreement with Abbott Laboratories, Amgen, Inc., Aqua Pharmaceuticals, LLC, Graceway Pharmaceuticals, LLC, Medicis Pharmaceutical Corporation, Promius Pharma, LLC, Stiefel Laboratories, Inc., Quinnova Pharmaceuticals, Inc., and Warner Chilcott; and is a stockholder of Medicis.

Copyright (C) 2010 Elsevier Inc.

To view the supplement, click the image above.

A supplement to Skin & Allergy News. This supplement was sponsored by Ferndale Laboratories Inc.

• Copay Reduction
• Patient Rebate Programs
• Prescription Abandonment Rates
• Importance of Communication between Providers and their Patients

Faculty/Faculty Disclosure

Joseph S. Eastern, MD
Clinical Associate Professor of Dermatology
Seton Hall UniversitySchool of GraduateMedical Education
South Orange, NJ

Dr. Eastern has a consulting agreement with Abbott Laboratories, Amgen, Inc., Aqua Pharmaceuticals, LLC, Graceway Pharmaceuticals, LLC, Medicis Pharmaceutical Corporation, Promius Pharma, LLC, Stiefel Laboratories, Inc., Quinnova Pharmaceuticals, Inc., and Warner Chilcott; and is a stockholder of Medicis.

Copyright (C) 2010 Elsevier Inc.

To view the supplement, click the image above.

A supplement to Skin & Allergy News. This supplement was sponsored by Ferndale Laboratories Inc.

• Copay Reduction
• Patient Rebate Programs
• Prescription Abandonment Rates
• Importance of Communication between Providers and their Patients

Faculty/Faculty Disclosure

Joseph S. Eastern, MD
Clinical Associate Professor of Dermatology
Seton Hall UniversitySchool of GraduateMedical Education
South Orange, NJ

Dr. Eastern has a consulting agreement with Abbott Laboratories, Amgen, Inc., Aqua Pharmaceuticals, LLC, Graceway Pharmaceuticals, LLC, Medicis Pharmaceutical Corporation, Promius Pharma, LLC, Stiefel Laboratories, Inc., Quinnova Pharmaceuticals, Inc., and Warner Chilcott; and is a stockholder of Medicis.

Copyright (C) 2010 Elsevier Inc.

To view the supplement, click the image above.

Click here to listen to the audio file.

Click here to listen to the audio file.

Click here to listen to the audio file.

Hospitalist Melissa Bartick, MD, MSc, became interested in breastfeeding some 10 years ago, as she was preparing for her first child. Her interest leaped to the national stage this month when several news outlets cited a study on which she is co-author and has implications for hospitalists treating lactating mothers.

"The Burden of Suboptimal Breastfeeding in the United States: A Pediatric Cost Analysis” reported that if 90% of U.S. families fell in line with doctors’ recommendations to breastfeed newborns for six months, the country “would save $13 billion a year and prevent an excess 911 deaths, nearly all of which would be infants” (DOI: 10.1542/peds.2009-1616).

While breastfeeding isn’t a topic often mentioned by HM leaders, Dr. Bartick, a hospitalist at Cambridge Health Alliance in suburban Boston, points to its ties to preventing obesity, cardiovascular disease, and myocardial infarction (MI) incidences as reasons for hospitalists to keep a keener eye on the issue.

“Breastfeeding affects all kinds of diseases that we as hospitalists see every day,” Dr. Bartick adds. “It makes sense to study it.”

Dr. Bartick pushes physicians to think more about keeping lactating mothers and their infants connected during admissions. She also recommends increased usage of LactMed, a National Library of Medicine-sponsored database of drugs to which breastfeeding mothers might be exposed. Too many physicians, hospitalists included, will simply stop breastfeeding for hospitalized women just to stay on the safe side when a bit of research could eliminate complications.

“It’s important to be familiar with the physiology around lactation,” Dr. Bartick says. “It’s important to keep it going uninterrupted even if a woman is in the hospital. ... It’s not going an extra mile. It’s 20 seconds on the computer to go to LactMed.”

Hospitalist Melissa Bartick, MD, MSc, became interested in breastfeeding some 10 years ago, as she was preparing for her first child. Her interest leaped to the national stage this month when several news outlets cited a study on which she is co-author and has implications for hospitalists treating lactating mothers.

"The Burden of Suboptimal Breastfeeding in the United States: A Pediatric Cost Analysis” reported that if 90% of U.S. families fell in line with doctors’ recommendations to breastfeed newborns for six months, the country “would save $13 billion a year and prevent an excess 911 deaths, nearly all of which would be infants” (DOI: 10.1542/peds.2009-1616).

While breastfeeding isn’t a topic often mentioned by HM leaders, Dr. Bartick, a hospitalist at Cambridge Health Alliance in suburban Boston, points to its ties to preventing obesity, cardiovascular disease, and myocardial infarction (MI) incidences as reasons for hospitalists to keep a keener eye on the issue.

“Breastfeeding affects all kinds of diseases that we as hospitalists see every day,” Dr. Bartick adds. “It makes sense to study it.”

Dr. Bartick pushes physicians to think more about keeping lactating mothers and their infants connected during admissions. She also recommends increased usage of LactMed, a National Library of Medicine-sponsored database of drugs to which breastfeeding mothers might be exposed. Too many physicians, hospitalists included, will simply stop breastfeeding for hospitalized women just to stay on the safe side when a bit of research could eliminate complications.

“It’s important to be familiar with the physiology around lactation,” Dr. Bartick says. “It’s important to keep it going uninterrupted even if a woman is in the hospital. ... It’s not going an extra mile. It’s 20 seconds on the computer to go to LactMed.”

Hospitalist Melissa Bartick, MD, MSc, became interested in breastfeeding some 10 years ago, as she was preparing for her first child. Her interest leaped to the national stage this month when several news outlets cited a study on which she is co-author and has implications for hospitalists treating lactating mothers.

"The Burden of Suboptimal Breastfeeding in the United States: A Pediatric Cost Analysis” reported that if 90% of U.S. families fell in line with doctors’ recommendations to breastfeed newborns for six months, the country “would save $13 billion a year and prevent an excess 911 deaths, nearly all of which would be infants” (DOI: 10.1542/peds.2009-1616).

While breastfeeding isn’t a topic often mentioned by HM leaders, Dr. Bartick, a hospitalist at Cambridge Health Alliance in suburban Boston, points to its ties to preventing obesity, cardiovascular disease, and myocardial infarction (MI) incidences as reasons for hospitalists to keep a keener eye on the issue.

“Breastfeeding affects all kinds of diseases that we as hospitalists see every day,” Dr. Bartick adds. “It makes sense to study it.”

Dr. Bartick pushes physicians to think more about keeping lactating mothers and their infants connected during admissions. She also recommends increased usage of LactMed, a National Library of Medicine-sponsored database of drugs to which breastfeeding mothers might be exposed. Too many physicians, hospitalists included, will simply stop breastfeeding for hospitalized women just to stay on the safe side when a bit of research could eliminate complications.

“It’s important to be familiar with the physiology around lactation,” Dr. Bartick says. “It’s important to keep it going uninterrupted even if a woman is in the hospital. ... It’s not going an extra mile. It’s 20 seconds on the computer to go to LactMed.”

Clinical question:Among older adults, what risk factors predict adverse events following syncope?

Background: Older adults with syncope are hospitalized regularly, although little data exist to substantiate such practice. These hospitalizations consume significant health resources and could have low diagnostic and therapeutic yields. Risk-assessment tools might help EDs identify low-risk patients eligible for early discharge versus high-risk patients requiring further monitoring.

Study design: Retrospective study of administrative data.

Setting: Regional managed-care system.

Synopsis: This retrospective study of 2,584 patients (age ≥60 years) across three EDs identified risk factors for 30-day adverse events following near-syncope or syncope. Compared with prior studies, the study enrolled larger numbers of patients and was the first to specifically study older adults. Adverse events included arrhythmia, myocardial infarction (MI), stroke, and pulmonary embolism (PE).

Using multivariable logistic regression, the study identified six easily obtainable predictors of increased risk (age >90 years, male sex, arrhythmia, triage SBP>160 mm Hg, abnormal ECG, and abnormal troponin I) and one predictor of decreased risk (near-syncope). Using the seven predictors, a simple risk score for 30-day adverse events was created to stratify patients into low (2.5%), intermediate (6.3%), and high-risk (20%) groups.

Of note, the risk score categorized 31% of participants as low-risk, and the authors suggest that such patients might be eligible for brief observation or discharge from the ED. However, the authors also point out the score must be externally validated and prospectively evaluated, particularly in non-managed-care settings.

Bottom line: This risk score could be useful in stratifying the risk of serious post-syncopal events, but it needs to be externally validated before it can be adopted in clinical decision-making.

Reference: Sun BC, Derose SF, Liang LJ, et al. Predictors of 30-day serious events in older patients with syncope. Ann Emerg Med. 2009;54(6):769-778.e1-5.

Reviewed for TH Ewire by Glen Kim, MD, MPH, hospitalist, Brigham and Women’s Hospital and Harvard Medical School, Boston

For more HM-related literature reviews, check out our website archive.

Clinical question:Among older adults, what risk factors predict adverse events following syncope?

Background: Older adults with syncope are hospitalized regularly, although little data exist to substantiate such practice. These hospitalizations consume significant health resources and could have low diagnostic and therapeutic yields. Risk-assessment tools might help EDs identify low-risk patients eligible for early discharge versus high-risk patients requiring further monitoring.

Study design: Retrospective study of administrative data.

Setting: Regional managed-care system.

Synopsis: This retrospective study of 2,584 patients (age ≥60 years) across three EDs identified risk factors for 30-day adverse events following near-syncope or syncope. Compared with prior studies, the study enrolled larger numbers of patients and was the first to specifically study older adults. Adverse events included arrhythmia, myocardial infarction (MI), stroke, and pulmonary embolism (PE).

Using multivariable logistic regression, the study identified six easily obtainable predictors of increased risk (age >90 years, male sex, arrhythmia, triage SBP>160 mm Hg, abnormal ECG, and abnormal troponin I) and one predictor of decreased risk (near-syncope). Using the seven predictors, a simple risk score for 30-day adverse events was created to stratify patients into low (2.5%), intermediate (6.3%), and high-risk (20%) groups.

Of note, the risk score categorized 31% of participants as low-risk, and the authors suggest that such patients might be eligible for brief observation or discharge from the ED. However, the authors also point out the score must be externally validated and prospectively evaluated, particularly in non-managed-care settings.

Bottom line: This risk score could be useful in stratifying the risk of serious post-syncopal events, but it needs to be externally validated before it can be adopted in clinical decision-making.

Reference: Sun BC, Derose SF, Liang LJ, et al. Predictors of 30-day serious events in older patients with syncope. Ann Emerg Med. 2009;54(6):769-778.e1-5.

Reviewed for TH Ewire by Glen Kim, MD, MPH, hospitalist, Brigham and Women’s Hospital and Harvard Medical School, Boston

For more HM-related literature reviews, check out our website archive.

Clinical question:Among older adults, what risk factors predict adverse events following syncope?

Background: Older adults with syncope are hospitalized regularly, although little data exist to substantiate such practice. These hospitalizations consume significant health resources and could have low diagnostic and therapeutic yields. Risk-assessment tools might help EDs identify low-risk patients eligible for early discharge versus high-risk patients requiring further monitoring.

Study design: Retrospective study of administrative data.

Setting: Regional managed-care system.

Synopsis: This retrospective study of 2,584 patients (age ≥60 years) across three EDs identified risk factors for 30-day adverse events following near-syncope or syncope. Compared with prior studies, the study enrolled larger numbers of patients and was the first to specifically study older adults. Adverse events included arrhythmia, myocardial infarction (MI), stroke, and pulmonary embolism (PE).

Using multivariable logistic regression, the study identified six easily obtainable predictors of increased risk (age >90 years, male sex, arrhythmia, triage SBP>160 mm Hg, abnormal ECG, and abnormal troponin I) and one predictor of decreased risk (near-syncope). Using the seven predictors, a simple risk score for 30-day adverse events was created to stratify patients into low (2.5%), intermediate (6.3%), and high-risk (20%) groups.

Of note, the risk score categorized 31% of participants as low-risk, and the authors suggest that such patients might be eligible for brief observation or discharge from the ED. However, the authors also point out the score must be externally validated and prospectively evaluated, particularly in non-managed-care settings.

Bottom line: This risk score could be useful in stratifying the risk of serious post-syncopal events, but it needs to be externally validated before it can be adopted in clinical decision-making.

Reference: Sun BC, Derose SF, Liang LJ, et al. Predictors of 30-day serious events in older patients with syncope. Ann Emerg Med. 2009;54(6):769-778.e1-5.

Reviewed for TH Ewire by Glen Kim, MD, MPH, hospitalist, Brigham and Women’s Hospital and Harvard Medical School, Boston

For more HM-related literature reviews, check out our website archive.

Janet Nagamine, MD, SFHM, a hospitalist at Kaiser Permanente Medical Center in Santa Clara, Calif., has an affinity for patient safety and the West Coast.

“I’m a California girl through and through. Any sunshine or beach works for me,” says the new SHM board member, a former assistant chief of quality and former patient safety officer. “I see quality and safety as part of my clinical care. I started out saying I don’t like the way my glucoses are documented in these charts, and so I started creating graphs to help physicians understand the information better.”

Dr. Nagamine didn’t start her career as a hospitalist: She was an ICU nurse for 23 years. She also didn’t jump onto the quality-improvement (QI) bandwagon until she became a hospitalist 10 years ago. A charter SHM member, she has been a member of the Healthcare Quality and Patient Safety Committee since 2002, serving as chair the past three years.

“I began [my quality career] by addressing the obstacles that get in the way of caring for patients,” Dr. Nagamine says. “And back then, there was no shortage of opportunity to make things better.”

So it’s no surprise her professional passion will be at the forefront of her service to SHM’s board and members. “What is exciting is that we’ve really raised the bar the past five to 10 years,” she says. “We have a ways to go, but HM really is front and center to the solutions.”

One area in which Dr. Nagamine plans to be a driving force is SHM’s mentored implementation programs: Project BOOST, Glycemic Control, and VTE Prevention.

“We can all go to a seminar, take a course, but who do we turn to when we’re back in the trenches?” she says. “That’s the hard part. It helps to have someone who has been there before, made the mistakes before, to talk to. That can shave a couple years off the learning curve.”

Dr. Nagamine joins Eric Siegal, MD, SFHM, a critical-care fellow at the University of Wisconsin School of Medicine and Public Health in Madison, as the board’s newest members. Incumbent board members Joseph Ming Wah Li, MD, SFHM, assistant professor of medicine at Harvard Medical School and director of the hospital medicine division at Beth Israel Deaconess Medical Center in Boston, and Mahalakshmi K. Halasymani, MD, SFHM, vice president for quality and systems improvement at Saint Joseph Mercy Health System in Ann Arbor, Mich., were re-elected for three-year terms.

Janet Nagamine, MD, SFHM, a hospitalist at Kaiser Permanente Medical Center in Santa Clara, Calif., has an affinity for patient safety and the West Coast.

“I’m a California girl through and through. Any sunshine or beach works for me,” says the new SHM board member, a former assistant chief of quality and former patient safety officer. “I see quality and safety as part of my clinical care. I started out saying I don’t like the way my glucoses are documented in these charts, and so I started creating graphs to help physicians understand the information better.”

Dr. Nagamine didn’t start her career as a hospitalist: She was an ICU nurse for 23 years. She also didn’t jump onto the quality-improvement (QI) bandwagon until she became a hospitalist 10 years ago. A charter SHM member, she has been a member of the Healthcare Quality and Patient Safety Committee since 2002, serving as chair the past three years.

“I began [my quality career] by addressing the obstacles that get in the way of caring for patients,” Dr. Nagamine says. “And back then, there was no shortage of opportunity to make things better.”

So it’s no surprise her professional passion will be at the forefront of her service to SHM’s board and members. “What is exciting is that we’ve really raised the bar the past five to 10 years,” she says. “We have a ways to go, but HM really is front and center to the solutions.”

One area in which Dr. Nagamine plans to be a driving force is SHM’s mentored implementation programs: Project BOOST, Glycemic Control, and VTE Prevention.

“We can all go to a seminar, take a course, but who do we turn to when we’re back in the trenches?” she says. “That’s the hard part. It helps to have someone who has been there before, made the mistakes before, to talk to. That can shave a couple years off the learning curve.”

Dr. Nagamine joins Eric Siegal, MD, SFHM, a critical-care fellow at the University of Wisconsin School of Medicine and Public Health in Madison, as the board’s newest members. Incumbent board members Joseph Ming Wah Li, MD, SFHM, assistant professor of medicine at Harvard Medical School and director of the hospital medicine division at Beth Israel Deaconess Medical Center in Boston, and Mahalakshmi K. Halasymani, MD, SFHM, vice president for quality and systems improvement at Saint Joseph Mercy Health System in Ann Arbor, Mich., were re-elected for three-year terms.

Janet Nagamine, MD, SFHM, a hospitalist at Kaiser Permanente Medical Center in Santa Clara, Calif., has an affinity for patient safety and the West Coast.

“I’m a California girl through and through. Any sunshine or beach works for me,” says the new SHM board member, a former assistant chief of quality and former patient safety officer. “I see quality and safety as part of my clinical care. I started out saying I don’t like the way my glucoses are documented in these charts, and so I started creating graphs to help physicians understand the information better.”

Dr. Nagamine didn’t start her career as a hospitalist: She was an ICU nurse for 23 years. She also didn’t jump onto the quality-improvement (QI) bandwagon until she became a hospitalist 10 years ago. A charter SHM member, she has been a member of the Healthcare Quality and Patient Safety Committee since 2002, serving as chair the past three years.

“I began [my quality career] by addressing the obstacles that get in the way of caring for patients,” Dr. Nagamine says. “And back then, there was no shortage of opportunity to make things better.”

So it’s no surprise her professional passion will be at the forefront of her service to SHM’s board and members. “What is exciting is that we’ve really raised the bar the past five to 10 years,” she says. “We have a ways to go, but HM really is front and center to the solutions.”

One area in which Dr. Nagamine plans to be a driving force is SHM’s mentored implementation programs: Project BOOST, Glycemic Control, and VTE Prevention.

“We can all go to a seminar, take a course, but who do we turn to when we’re back in the trenches?” she says. “That’s the hard part. It helps to have someone who has been there before, made the mistakes before, to talk to. That can shave a couple years off the learning curve.”

Dr. Nagamine joins Eric Siegal, MD, SFHM, a critical-care fellow at the University of Wisconsin School of Medicine and Public Health in Madison, as the board’s newest members. Incumbent board members Joseph Ming Wah Li, MD, SFHM, assistant professor of medicine at Harvard Medical School and director of the hospital medicine division at Beth Israel Deaconess Medical Center in Boston, and Mahalakshmi K. Halasymani, MD, SFHM, vice president for quality and systems improvement at Saint Joseph Mercy Health System in Ann Arbor, Mich., were re-elected for three-year terms.

A review of 208 California hospitals shows the presence of hospitalists was associated with process improvements across three medical conditions—acute myocardial infarction (AMI), congestive heart failure (CHF), and pneumonia—but the specific role HM played in those results remains murky, according to a study in this month’s Journal of Hospital Medicine.

The review, "Cross-Sectional Analysis of Hospitalist Prevalence and Quality of Care in California (PDF)” (2010;5(4);200-207), found that in the 170 subject hospitals with HM programs, every 10% increase in the estimated percentage of patients admitted by hospitalists was associated with 0.5% fewer (P<0.001) missed quality opportunities for AMI at admission. In addition, hospitalists were associated with 0.6% (P<0.001), 0.5% (P=0.004), and 1.5% (P=0.006) fewer missed quality opportunities for AMI, CHF, and pneumonia assessed at discharge, respectively.

“You can’t really see anything that’s causative, but … hospitals with hospitalists versus those who were without were definitely different,” says lead author Eduard Vasilevskis, MD, assistant professor of medicine in the Section of Hospital Medicine at Vanderbilt University and the Tennessee Valley-Nashville VA Hospital. “But it’s unclear if it’s the hospitalists themselves who are doing the improvements in quality initiatives, or is it more a hospital willing to invest in quality and hospitalists are part of that but there other investments going on?”

Dr. Vasilevskis’ team measured 16 publicly reported quality measures but could draw no conclusions as to HM’s direct role in the quality improvements. He suggests the next step in HM research will be to bridge the gap between defining the presence of hospitalists and qualitatively defining their impacts on respective institutions. Along that line, Dr. Vasilevskis notes that only 38 of the 208 hospitals in the review did not have HM programs, a trend that in time would eliminate the ability to study hospital performance without taking hospitalist care into account.

“Ten years from now, this study couldn’t be done any longer,” he says. “Given the evidence we know so far on length of stay, readmissions … that’s probably a good thing.”

A review of 208 California hospitals shows the presence of hospitalists was associated with process improvements across three medical conditions—acute myocardial infarction (AMI), congestive heart failure (CHF), and pneumonia—but the specific role HM played in those results remains murky, according to a study in this month’s Journal of Hospital Medicine.

The review, "Cross-Sectional Analysis of Hospitalist Prevalence and Quality of Care in California (PDF)” (2010;5(4);200-207), found that in the 170 subject hospitals with HM programs, every 10% increase in the estimated percentage of patients admitted by hospitalists was associated with 0.5% fewer (P<0.001) missed quality opportunities for AMI at admission. In addition, hospitalists were associated with 0.6% (P<0.001), 0.5% (P=0.004), and 1.5% (P=0.006) fewer missed quality opportunities for AMI, CHF, and pneumonia assessed at discharge, respectively.

“You can’t really see anything that’s causative, but … hospitals with hospitalists versus those who were without were definitely different,” says lead author Eduard Vasilevskis, MD, assistant professor of medicine in the Section of Hospital Medicine at Vanderbilt University and the Tennessee Valley-Nashville VA Hospital. “But it’s unclear if it’s the hospitalists themselves who are doing the improvements in quality initiatives, or is it more a hospital willing to invest in quality and hospitalists are part of that but there other investments going on?”

Dr. Vasilevskis’ team measured 16 publicly reported quality measures but could draw no conclusions as to HM’s direct role in the quality improvements. He suggests the next step in HM research will be to bridge the gap between defining the presence of hospitalists and qualitatively defining their impacts on respective institutions. Along that line, Dr. Vasilevskis notes that only 38 of the 208 hospitals in the review did not have HM programs, a trend that in time would eliminate the ability to study hospital performance without taking hospitalist care into account.

“Ten years from now, this study couldn’t be done any longer,” he says. “Given the evidence we know so far on length of stay, readmissions … that’s probably a good thing.”

A review of 208 California hospitals shows the presence of hospitalists was associated with process improvements across three medical conditions—acute myocardial infarction (AMI), congestive heart failure (CHF), and pneumonia—but the specific role HM played in those results remains murky, according to a study in this month’s Journal of Hospital Medicine.

The review, "Cross-Sectional Analysis of Hospitalist Prevalence and Quality of Care in California (PDF)” (2010;5(4);200-207), found that in the 170 subject hospitals with HM programs, every 10% increase in the estimated percentage of patients admitted by hospitalists was associated with 0.5% fewer (P<0.001) missed quality opportunities for AMI at admission. In addition, hospitalists were associated with 0.6% (P<0.001), 0.5% (P=0.004), and 1.5% (P=0.006) fewer missed quality opportunities for AMI, CHF, and pneumonia assessed at discharge, respectively.

“You can’t really see anything that’s causative, but … hospitals with hospitalists versus those who were without were definitely different,” says lead author Eduard Vasilevskis, MD, assistant professor of medicine in the Section of Hospital Medicine at Vanderbilt University and the Tennessee Valley-Nashville VA Hospital. “But it’s unclear if it’s the hospitalists themselves who are doing the improvements in quality initiatives, or is it more a hospital willing to invest in quality and hospitalists are part of that but there other investments going on?”

Dr. Vasilevskis’ team measured 16 publicly reported quality measures but could draw no conclusions as to HM’s direct role in the quality improvements. He suggests the next step in HM research will be to bridge the gap between defining the presence of hospitalists and qualitatively defining their impacts on respective institutions. Along that line, Dr. Vasilevskis notes that only 38 of the 208 hospitals in the review did not have HM programs, a trend that in time would eliminate the ability to study hospital performance without taking hospitalist care into account.

“Ten years from now, this study couldn’t be done any longer,” he says. “Given the evidence we know so far on length of stay, readmissions … that’s probably a good thing.”

Eric Siegal, MD, SFHM, is not an SHM newbie. Since becoming a member in 1999, he has served on the awards and annual meeting committees, and he is the current chair of the Public Policy Committee. So when he learned he was elected to a three-year term as SHM’s newest board member, he says, he was excited about the opportunity to continue to work with “old friends.”

Dr. Siegal is a Critical Care Fellow at the University of Wisconsin School of Medicine and Public Health, and previously served as regional medical director for Brentwood, Tenn.-based Cogent Healthcare. TH eWire caught up with him just as he finished attending his first board meeting at HM10.

What unique perspective do you bring to the board?

I think I have a pretty varied experience. I ran both community and academic hospitalist programs. And I obviously have the policy bent, which, with all that is going with healthcare policy reform, I think it will be important to have someone on the board who has a fair degree of fluency with that. Although I will also say that two other board members come from the policy committee, so I’m by no means alone.

What kind of issues do you look forward to getting involved in?

The two areas that interest me most are healthcare policy and how hospitalists are going to interface with the critical-care environment. We know there is a large percentage, if not a majority, of hospitalists practicing critical-care medicine, some of whom may be appropriately trained to do so and others who are not. I think there are opportunities to figure out how hospitalists can and should participate in the critical care of patients. Hopefully, we can pair up with critical-care societies to figure out how we’re going to address the massive and growing shortage of critical-care physicians in the U.S.

Where do you see SHM in 10 years?

I would like to see us recognized as part of the solution to making healthcare better. We have worked very hard up to now to demonstrate to legislators, insurers, and people in the quality world that SHM [that] although we do advocate for members, we also advocate for healthcare reform. I think, unfortunately, that many professional societies start and end primarily with what is in the best financial interest of their membership. We have gone to great lengths not to be that: to be seen as an organization that is part of the solution to healthcare, not part of the problem. … I would hope that in 10 years that would not only be widely accepted throughout the healthcare community, but that when Congress or [the Centers for Medicaid and Medicare Services] looks around and thinks about who are the people who they can work with to make things better, hospital medicine is at the top of the list.

Eric Siegal, MD, SFHM, is not an SHM newbie. Since becoming a member in 1999, he has served on the awards and annual meeting committees, and he is the current chair of the Public Policy Committee. So when he learned he was elected to a three-year term as SHM’s newest board member, he says, he was excited about the opportunity to continue to work with “old friends.”

Dr. Siegal is a Critical Care Fellow at the University of Wisconsin School of Medicine and Public Health, and previously served as regional medical director for Brentwood, Tenn.-based Cogent Healthcare. TH eWire caught up with him just as he finished attending his first board meeting at HM10.

What unique perspective do you bring to the board?

I think I have a pretty varied experience. I ran both community and academic hospitalist programs. And I obviously have the policy bent, which, with all that is going with healthcare policy reform, I think it will be important to have someone on the board who has a fair degree of fluency with that. Although I will also say that two other board members come from the policy committee, so I’m by no means alone.

What kind of issues do you look forward to getting involved in?

The two areas that interest me most are healthcare policy and how hospitalists are going to interface with the critical-care environment. We know there is a large percentage, if not a majority, of hospitalists practicing critical-care medicine, some of whom may be appropriately trained to do so and others who are not. I think there are opportunities to figure out how hospitalists can and should participate in the critical care of patients. Hopefully, we can pair up with critical-care societies to figure out how we’re going to address the massive and growing shortage of critical-care physicians in the U.S.

Where do you see SHM in 10 years?

I would like to see us recognized as part of the solution to making healthcare better. We have worked very hard up to now to demonstrate to legislators, insurers, and people in the quality world that SHM [that] although we do advocate for members, we also advocate for healthcare reform. I think, unfortunately, that many professional societies start and end primarily with what is in the best financial interest of their membership. We have gone to great lengths not to be that: to be seen as an organization that is part of the solution to healthcare, not part of the problem. … I would hope that in 10 years that would not only be widely accepted throughout the healthcare community, but that when Congress or [the Centers for Medicaid and Medicare Services] looks around and thinks about who are the people who they can work with to make things better, hospital medicine is at the top of the list.

Eric Siegal, MD, SFHM, is not an SHM newbie. Since becoming a member in 1999, he has served on the awards and annual meeting committees, and he is the current chair of the Public Policy Committee. So when he learned he was elected to a three-year term as SHM’s newest board member, he says, he was excited about the opportunity to continue to work with “old friends.”

Dr. Siegal is a Critical Care Fellow at the University of Wisconsin School of Medicine and Public Health, and previously served as regional medical director for Brentwood, Tenn.-based Cogent Healthcare. TH eWire caught up with him just as he finished attending his first board meeting at HM10.

What unique perspective do you bring to the board?

I think I have a pretty varied experience. I ran both community and academic hospitalist programs. And I obviously have the policy bent, which, with all that is going with healthcare policy reform, I think it will be important to have someone on the board who has a fair degree of fluency with that. Although I will also say that two other board members come from the policy committee, so I’m by no means alone.

What kind of issues do you look forward to getting involved in?

The two areas that interest me most are healthcare policy and how hospitalists are going to interface with the critical-care environment. We know there is a large percentage, if not a majority, of hospitalists practicing critical-care medicine, some of whom may be appropriately trained to do so and others who are not. I think there are opportunities to figure out how hospitalists can and should participate in the critical care of patients. Hopefully, we can pair up with critical-care societies to figure out how we’re going to address the massive and growing shortage of critical-care physicians in the U.S.

Where do you see SHM in 10 years?

I would like to see us recognized as part of the solution to making healthcare better. We have worked very hard up to now to demonstrate to legislators, insurers, and people in the quality world that SHM [that] although we do advocate for members, we also advocate for healthcare reform. I think, unfortunately, that many professional societies start and end primarily with what is in the best financial interest of their membership. We have gone to great lengths not to be that: to be seen as an organization that is part of the solution to healthcare, not part of the problem. … I would hope that in 10 years that would not only be widely accepted throughout the healthcare community, but that when Congress or [the Centers for Medicaid and Medicare Services] looks around and thinks about who are the people who they can work with to make things better, hospital medicine is at the top of the list.