Helping hospitalized geriatric patients maintain an appropriate sleep-wake cycle can be a challenge. Older patients’ circadian rhythm may be affected by several factors—eg, obstructive sleep apnea and restless leg syndrome—that contribute to disrupted sleep and daytime fatigue. Some patients may have dementing illnesses that could dysregulate sleep. Many older patients experience delirium during hospitalization, of which sleep-wake cycle disturbances are a hallmark. Finally, geriatric patients’ natural sleep pattern often does not mimic a hospital’s typical schedule.

Sleep medication side effects

Medications used to promote sleep can cause side effects in geriatric patients. Benzodiazepine use by older adults is discouraged because these medications could cause falls or contribute to delirium. Non-benzodiazepine hypnotics such as zolpidem, zaleplon, and eszopiclone pose a similar risk. Medications containing diphenhydramine predispose patients to deliriogenic effects via their anticholinergic properties. Tricyclic antidepressants carry risks, such as delirium secondary to anticholinergic effects, orthostatic hypotension, falls from α-1 blockade, and cardiac arrythmias.

Atypical antipsychotics sometimes are used off-label to help initiate sleep, but they carry a “black-box” warning regarding sudden death from cardiovascular events in geriatric patients with dementia. Hydroxyzine and trazodone also are associated with side effects such as orthostatic hypotension and daytime sedation, and are not always effective.

Melatonin is a hormone secreted by the pineal gland in response to darkness, under the control of the suprachiasmatic nucleus (SCN), and is thought to promote sleep via synchronizing effects on the SCN.¹ Melatonin is available as an over-the-counter dietary supplement and via prescription in dosages of 1 or 3 mg. The typical effective dose is 3 to 9 mg.¹ Patients should take melatonin in the mid-evening, ideally between 7 pm and 8 pm, and effects become evident after a few days. Side effects are rare; the most common are headache and nausea. Daytime sedation and vivid dreams also have been reported. Melatonin can be used safely in conjunction with other sleep aids and its major drug-drug interactions involve enhancing the effects of other sedatives.²

We have found melatonin to be effective for treating sleep disturbances in older hospitalized patients. Its effectiveness may stem from the high incidence of dysregulated or calcified pineal glands in geriatric patients, which leads to a marked reduction in melatonin secretion.³ Recent evidence also suggests melatonin may reduce the incidence of delirium in older adults, and it has been proposed as a delirium treatment in post-operative and intensive care unit settings.⁴

Disclosure

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

Helping hospitalized geriatric patients maintain an appropriate sleep-wake cycle can be a challenge. Older patients’ circadian rhythm may be affected by several factors—eg, obstructive sleep apnea and restless leg syndrome—that contribute to disrupted sleep and daytime fatigue. Some patients may have dementing illnesses that could dysregulate sleep. Many older patients experience delirium during hospitalization, of which sleep-wake cycle disturbances are a hallmark. Finally, geriatric patients’ natural sleep pattern often does not mimic a hospital’s typical schedule.

Sleep medication side effects

Medications used to promote sleep can cause side effects in geriatric patients. Benzodiazepine use by older adults is discouraged because these medications could cause falls or contribute to delirium. Non-benzodiazepine hypnotics such as zolpidem, zaleplon, and eszopiclone pose a similar risk. Medications containing diphenhydramine predispose patients to deliriogenic effects via their anticholinergic properties. Tricyclic antidepressants carry risks, such as delirium secondary to anticholinergic effects, orthostatic hypotension, falls from α-1 blockade, and cardiac arrythmias.

Atypical antipsychotics sometimes are used off-label to help initiate sleep, but they carry a “black-box” warning regarding sudden death from cardiovascular events in geriatric patients with dementia. Hydroxyzine and trazodone also are associated with side effects such as orthostatic hypotension and daytime sedation, and are not always effective.

Melatonin is a hormone secreted by the pineal gland in response to darkness, under the control of the suprachiasmatic nucleus (SCN), and is thought to promote sleep via synchronizing effects on the SCN.¹ Melatonin is available as an over-the-counter dietary supplement and via prescription in dosages of 1 or 3 mg. The typical effective dose is 3 to 9 mg.¹ Patients should take melatonin in the mid-evening, ideally between 7 pm and 8 pm, and effects become evident after a few days. Side effects are rare; the most common are headache and nausea. Daytime sedation and vivid dreams also have been reported. Melatonin can be used safely in conjunction with other sleep aids and its major drug-drug interactions involve enhancing the effects of other sedatives.²

We have found melatonin to be effective for treating sleep disturbances in older hospitalized patients. Its effectiveness may stem from the high incidence of dysregulated or calcified pineal glands in geriatric patients, which leads to a marked reduction in melatonin secretion.³ Recent evidence also suggests melatonin may reduce the incidence of delirium in older adults, and it has been proposed as a delirium treatment in post-operative and intensive care unit settings.⁴

Disclosure

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

Helping hospitalized geriatric patients maintain an appropriate sleep-wake cycle can be a challenge. Older patients’ circadian rhythm may be affected by several factors—eg, obstructive sleep apnea and restless leg syndrome—that contribute to disrupted sleep and daytime fatigue. Some patients may have dementing illnesses that could dysregulate sleep. Many older patients experience delirium during hospitalization, of which sleep-wake cycle disturbances are a hallmark. Finally, geriatric patients’ natural sleep pattern often does not mimic a hospital’s typical schedule.

Sleep medication side effects

Medications used to promote sleep can cause side effects in geriatric patients. Benzodiazepine use by older adults is discouraged because these medications could cause falls or contribute to delirium. Non-benzodiazepine hypnotics such as zolpidem, zaleplon, and eszopiclone pose a similar risk. Medications containing diphenhydramine predispose patients to deliriogenic effects via their anticholinergic properties. Tricyclic antidepressants carry risks, such as delirium secondary to anticholinergic effects, orthostatic hypotension, falls from α-1 blockade, and cardiac arrythmias.

Atypical antipsychotics sometimes are used off-label to help initiate sleep, but they carry a “black-box” warning regarding sudden death from cardiovascular events in geriatric patients with dementia. Hydroxyzine and trazodone also are associated with side effects such as orthostatic hypotension and daytime sedation, and are not always effective.

Melatonin is a hormone secreted by the pineal gland in response to darkness, under the control of the suprachiasmatic nucleus (SCN), and is thought to promote sleep via synchronizing effects on the SCN.¹ Melatonin is available as an over-the-counter dietary supplement and via prescription in dosages of 1 or 3 mg. The typical effective dose is 3 to 9 mg.¹ Patients should take melatonin in the mid-evening, ideally between 7 pm and 8 pm, and effects become evident after a few days. Side effects are rare; the most common are headache and nausea. Daytime sedation and vivid dreams also have been reported. Melatonin can be used safely in conjunction with other sleep aids and its major drug-drug interactions involve enhancing the effects of other sedatives.²

We have found melatonin to be effective for treating sleep disturbances in older hospitalized patients. Its effectiveness may stem from the high incidence of dysregulated or calcified pineal glands in geriatric patients, which leads to a marked reduction in melatonin secretion.³ Recent evidence also suggests melatonin may reduce the incidence of delirium in older adults, and it has been proposed as a delirium treatment in post-operative and intensive care unit settings.⁴

Disclosure

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

Since the discovery of chlordiazepoxide in the 1950s, benzodiazepines have revolutionized the treatment of anxiety and insomnia, largely because of their improved safety profile compared with barbiturates, formerly the preferred sedative-hypnotic.¹ In addition to their anxiolytic and sedative-hypnotic effects, benzodiazepines exhibit anterograde amnesia, anticonvulsant, and muscle relaxant properties.¹ Psychiatrists use benzodiazepines to treat anxiety and sleep disorders, acute agitation, alcohol withdrawal, catatonia, and psychotropic side effects such as akathisia. This article highlights the evidence for using benzodiazepines in anxiety and other disorders and why they generally should not be used for obsessive-compulsive disorder and posttraumatic stress disorder (Box 1).

Box 1

Pharmacokinetic properties

Most benzodiazepines are considered to have similar efficacy; therefore, selection is based on pharmacokinetic considerations. Table 1 compares the indication, onset, and half-life of 12 commonly used benzodiazepines.^2-6 Although Table 1 lists approximate equivalent doses, studies report inconsistent data. These are approximations only and should not be used independently to make therapy decisions.

Table 1

Oral benzodiazepines: Indications, onset, half-life, and equivalent doses

A diverse range of indications

Alcohol withdrawal. Benzodiazepines are the treatment of choice for alcohol withdrawal syndrome, particularly to prevent seizures.⁷ Research supports symptom-triggered therapy using the revised Clinical Institute Withdrawal Assessment for Alcohol. Benzodiazepines reduce CNS sympathetic hyperactivity to mitigate withdrawal from alcohol by decreasing tachycardia, tremor, insomnia, agitation, and anxiety. Furthermore, these agents provide prophylaxis against serious sequelae such as seizures and delirium.

Insomnia. The American Academy of Sleep Medicine considers benzodiazepine receptor agonists (BzRAs, which include benzodiazepines and non-benzodiazepines) and ramelteon first-line pharmacotherapy for primary insomnia.⁸ However, pharmacologic treatment should be short-term. Agents with short to intermediate half-lives and rapid onset, such as triazolam, can aid sleep initiation. Those with longer half-lives, such as temazepam, could address sleep maintenance. If a patient does not respond to the initial agent, try another medication within the same class, because patients may respond differently. Use lower starting doses in geriatric patients.⁹ Closely monitor for adverse effects, rebound insomnia, and potential abuse or tolerance. Identify comorbid conditions and medications that may impair sleep, and address them accordingly.

Psychological and behavioral treatments given over 4 to 8 weeks can yield stable sleep improvements for up to 2 years. If available, these interventions may be considered first-line for treating insomnia because of their lasting effects compared with BzRAs.¹⁰

Generalized anxiety disorder (GAD). Benzodiazepines effectively treat GAD because they work quickly and are well tolerated. However, there are better first-line treatment options when considering efficacy studies and dependence and tolerance concerns. One effect-size comparison of 21 double-blind, placebo-controlled trials showed that the efficacy of selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and pregabalin are comparable to benzodiazepines.¹¹ Benzodiazepines can be used in the first 2 to 3 weeks after initiating antidepressants to alleviate and prevent worsening of anxiety that may occur at the start of antidepressant therapy. Recent treatment guidelines recommend benzodiazepines as a second-line treatment or for treatment-resistant GAD in patients who do not have a substance abuse history.^12,13

Panic disorder. Efficacy of benzodiazepines for panic disorder is comparable to SSRIs, SNRIs, and tricyclic antidepressants (TCAs). SSRIs and SNRIs are considered first-line treatments for panic disorder because of their favorable side effect profile.¹⁴ In practice, benzodiazepines often are combined with SSRIs, SNRIs, or TCAs. A randomized controlled trial demonstrated that paroxetine and clonazepam (mean dose 1.6 mg/d at 5 weeks) resulted in a more rapid response compared with paroxetine alone, although this difference lasted only a few weeks.¹⁵ Furthermore, this study suggested that brief treatment with clonazepam followed by a taper is as effective as sustained treatment with paroxetine and clonazepam.¹⁵

There is a lack of high-quality data on combining cognitive-behavioral therapy (CBT) and benzodiazepines for panic disorder, although a Cochrane Review found that adding a benzodiazepine to CBT did not lead to a significant difference in response compared with psychotherapy alone.¹⁶ A recent randomized controlled trial demonstrated that tapering benzodiazepines combined with CBT was associated with successful discontinuation of the drug and prevented return of panic symptoms.¹⁷

Social anxiety. A meta-analysis found that for treating social anxiety, benzodiazepines have better efficacy than SSRIs, monoamine oxidase inhibitors, and anticonvulsants.¹⁸ Longer-acting benzodiazepines may be more effective than shorter-acting agents. One study of patients with social anxiety showed a 38% response rate for alprazolam vs 20% for placebo over 12 weeks, and a similar 10-week study demonstrated a 73% recovery rate with clonazepam vs 22% for placebo.¹⁹ In addition, studies have observed that patients can be maintained on clonazepam for up to 2 years without symptom relapse and will tolerate slow-taper discontinuation.^18,20 Sedation and drowsiness can be lessened by limiting clonazepam doses to 2 to 3 mg/d.

Akathisia and tremor. Akathisia, a syndrome of motor restlessness and inner turmoil, is associated with antipsychotics but can occur with SSRIs. Reducing the dosage or switching to another, usually less potent agent often can relieve akathisia. When these remedies are not tenable, consider benzodiazepines along with other medications—including beta blockers and anticholinergic agents—with demonstrated efficacy in reducing akathisia symptoms. Lorazepam, diazepam, and clonazepam have demonstrated efficacy for relieving akathisia in comparison studies with placebo, propranolol, and diphenhydramine.^21,22

Drug-induced postural tremor can occur with several psychotropics, including lithium, valproic acid, antidepressants, and antipsychotics. A tremor is considered mild if a patient can drink a glass of water with 1 hand without spilling and severe if holding a glass with 2 hands is difficult. Propranolol is most commonly prescribed for these tremors, but alprazolam and clonazepam have demonstrated efficacy, either as monotherapy or coadministered with a beta blocker.²³

Acute agitation. Agitated patients often have acute psychosis and/or mania or dyscontrol secondary to axis II disorders.²⁴ Patients may be paranoid, hostile, disruptive, and combative. Rapidly initiating medication can prevent the need for more restrictive measures, such as seclusion or restraint. Antipsychotics—especially high-potency agents such as haloperidol—and benzodiazepines, as monotherapy or in combination, are a mainstay treatment. Although treatment protocols favor atypical antipsychotics over typical antipsychotics, benzodiazepines are a viable option because of their anxiolytic and sedative effects. Advantages of benzodiazepine monotherapy include decreased extrapyramidal symptoms, greater patient acceptance/preference, and increased sedation compared with antipsychotics. Lorazepam, 1 to 2 mg intramuscularly (IM) or orally, is well tolerated because of its favorable drug-drug interaction profile and lack of significant cardiac side effects. Benzodiazepines can cause respiratory depression in patients with chronic lung disease and additive sedation secondary to opiates, other sedatives/hypnotics, or alcohol. Behavioral disinhibition is rare and is associated with preexisting CNS pathology or mental retardation.²⁵ The IM olanzapine package insert warns against coadministering IM lorazepam because of additive cardiorespiratory depressive effects and excessive somnolence.²⁶

Catatonia. The characteristic symptoms of catatonia are immobility, negativism, muteness, and failure to eat or drink. Benzodiazepines improve these symptoms in approximately 70% to 80% of catatonic patients with affective disorders. Response rates are lower in catatonia in patients with schizophrenia.²⁷ If catatonia in a patient with psychosis is missed, giving antipsychotics before benzodiazepines may worsen catatonic symptoms or precipitate neuroleptic malignant syndrome in some cases. When you suspect a patient has catatonia, start with lorazepam, 1 to 2 mg IV or IM, and examine the patient for diminishing catatonic signs within 1 to 2 hours. If catatonia signs lessen, begin regularly scheduled lorazepam, with dosing varying by age—be more cautious in geriatric patients—and symptom severity. Titrate benzodiazepines for stuporous patients more slowly (eg, 1 mg 3 times a day as a starting dose) than for excited catatonic patients. Lorazepam can be increased gradually as tolerated; it is not unusual for patients to require up to 8 to 12 mg/d. Electroconvulsive therapy (ECT) is the treatment of choice when catatonic patients respond poorly or partially to high-dose benzodiazepines.^28,29

Benzodiazepine reversal for ECT

Benzodiazepines have anticonvulsant properties that may interfere with the therapeutic efficacy of ECT.³⁰ A multi-center study demonstrated that lorazepam (up to 4 mg/d as needed) in the 48 hours before the first ECT session was not associated with effects on seizure threshold or duration; however, larger lorazepam dosages were associated with briefer EEG seizure duration.³¹ Some patients may not tolerate withholding or tapering benzodiazepines in preparation for ECT. Studies investigating flumazenil for pre-ECT benzodiazepine reversal are lacking. One retrospective analysis showed that flumazenil administration immediately before and after ECT resulted in adequate seizures with no difference in clinical outcome compared with patients who were not receiving benzodiazepines or flumazenil.³²

Tapering benzodiazepines

Slow discontinuation of benzodiazepines is recommended to avoid withdrawal symptoms, such as rebound anxiety, agitation, insomnia, or seizures, particularly when use exceeds 8 weeks. The onset of withdrawal symptoms varies, depending on the medication used. Withdrawal symptoms may appear in 1 to 2 days for agents with shorter half-lives, but may not appear until 3 to 7 days for agents with longer half-lives.³³Table 2 lists recommended durations for tapering benzodiazepines.^33,34 In general, decrease the total daily dose by 25% the first week, another 25% the second week, then 10% a week until discontinuation. When benzodiazepine use exceeds 1 year, a slower taper is recommended; for example, decrease 10% every 1 to 2 weeks. When 20% of the dosage remains, begin a 5% dose reduction every 2 to 4 weeks. Monitor patients for withdrawal symptoms or symptom exacerbation. If either occur, consider maintaining the current benzodiazepine dose or increasing the dose for 1 to 2 weeks or longer, if necessary, then continue to taper at a slower rate.³⁴

Table 2

Recommendations for tapering benzodiazepines

Risks of benzodiazepine use

For most indications, benzodiazepine therapy should be short-term.³⁵ Use exceeding 2 to 4 weeks increases the risk for dependence and withdrawal. Tell patients to avoid alcohol while taking a benzodiazepine because this combination is potentially lethal. Benzodiazepines are commonly abused and abuse can lead to unintentional drug overdose. Benzodiazepines accounted for 37% of unintentional drug overdose deaths in West Virginia in 2006; in 46% of these cases, benzodiazepines were used for nonmedical purposes. Clinicians can help reduce the risk of diversion by limiting prescriptions to 30 days with no refills.³⁶

Older patients taking benzodiazepines are at increased risk of falls and hip fractures.³⁷ Lorazepam, oxazepam, and temazepam—agents with shorter half-lives that are not greatly affected by pharmacokinetic changes associated with aging—are preferred for these patients.³⁴ Patients with dementia or other CNS-compromising conditions may become confused or delirious with regular benzodiazepine dosing. Educate patients to whom you prescribe benzodiazepines about the importance of gauging their level of sedation before driving or engaging in other tasks for which sedation could compromise their safety. Benzodiazepine use during pregnancy requires a careful discussion of risks and benefits (Box 2).³⁸

Box 2

Related Resources

• Substance Abuse and Mental Health Services Administration. www.samhsa.gov.
• National Institute on Drug Abuse resources for medical and health professionals. www.drugabuse.gov/medical-health-professionals.
• American Academy of Sleep Medicine. www.aasmnet.org.

Drug Brand Names

• Alprazolam • Xanax
• Chlordiazepoxide • Librium, Limbitrol
• Clonazepam • Klonopin
• Clorazepate • Tranxene
• Diazepam • Valium
• Diphenhydramine • Benadryl, others
• Estazolam • ProSom
• Flumazenil • Romazicon
• Flurazepam • Dalmane
• Haloperidol • Haldol
• Lithium • Lithobid
• Lorazepam • Ativan
• Olanzapine • Zyprexa
• Oxazepam • Serax
• Paroxetine • Paxil
• Pregabalin • Lyrica
• Propranolol • Inderal, InnoPran XL, others
• Quazepam • Doral
• Ramelteon • Rozerem
• Sertraline • Zoloft
• Temazepam • Restoril
• Triazolam • Halcion
• Valproic acid • Depakene, Stavzor, others

Disclosures

Drs. Bostwick and Yasugi report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Casher is a speaker for AstraZeneca and Sunovion Pharmaceuticals.

Since the discovery of chlordiazepoxide in the 1950s, benzodiazepines have revolutionized the treatment of anxiety and insomnia, largely because of their improved safety profile compared with barbiturates, formerly the preferred sedative-hypnotic.¹ In addition to their anxiolytic and sedative-hypnotic effects, benzodiazepines exhibit anterograde amnesia, anticonvulsant, and muscle relaxant properties.¹ Psychiatrists use benzodiazepines to treat anxiety and sleep disorders, acute agitation, alcohol withdrawal, catatonia, and psychotropic side effects such as akathisia. This article highlights the evidence for using benzodiazepines in anxiety and other disorders and why they generally should not be used for obsessive-compulsive disorder and posttraumatic stress disorder (Box 1).

Box 1

Pharmacokinetic properties

Most benzodiazepines are considered to have similar efficacy; therefore, selection is based on pharmacokinetic considerations. Table 1 compares the indication, onset, and half-life of 12 commonly used benzodiazepines.^2-6 Although Table 1 lists approximate equivalent doses, studies report inconsistent data. These are approximations only and should not be used independently to make therapy decisions.

Table 1

Oral benzodiazepines: Indications, onset, half-life, and equivalent doses

A diverse range of indications

Alcohol withdrawal. Benzodiazepines are the treatment of choice for alcohol withdrawal syndrome, particularly to prevent seizures.⁷ Research supports symptom-triggered therapy using the revised Clinical Institute Withdrawal Assessment for Alcohol. Benzodiazepines reduce CNS sympathetic hyperactivity to mitigate withdrawal from alcohol by decreasing tachycardia, tremor, insomnia, agitation, and anxiety. Furthermore, these agents provide prophylaxis against serious sequelae such as seizures and delirium.

Insomnia. The American Academy of Sleep Medicine considers benzodiazepine receptor agonists (BzRAs, which include benzodiazepines and non-benzodiazepines) and ramelteon first-line pharmacotherapy for primary insomnia.⁸ However, pharmacologic treatment should be short-term. Agents with short to intermediate half-lives and rapid onset, such as triazolam, can aid sleep initiation. Those with longer half-lives, such as temazepam, could address sleep maintenance. If a patient does not respond to the initial agent, try another medication within the same class, because patients may respond differently. Use lower starting doses in geriatric patients.⁹ Closely monitor for adverse effects, rebound insomnia, and potential abuse or tolerance. Identify comorbid conditions and medications that may impair sleep, and address them accordingly.

Psychological and behavioral treatments given over 4 to 8 weeks can yield stable sleep improvements for up to 2 years. If available, these interventions may be considered first-line for treating insomnia because of their lasting effects compared with BzRAs.¹⁰

Generalized anxiety disorder (GAD). Benzodiazepines effectively treat GAD because they work quickly and are well tolerated. However, there are better first-line treatment options when considering efficacy studies and dependence and tolerance concerns. One effect-size comparison of 21 double-blind, placebo-controlled trials showed that the efficacy of selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and pregabalin are comparable to benzodiazepines.¹¹ Benzodiazepines can be used in the first 2 to 3 weeks after initiating antidepressants to alleviate and prevent worsening of anxiety that may occur at the start of antidepressant therapy. Recent treatment guidelines recommend benzodiazepines as a second-line treatment or for treatment-resistant GAD in patients who do not have a substance abuse history.^12,13

Panic disorder. Efficacy of benzodiazepines for panic disorder is comparable to SSRIs, SNRIs, and tricyclic antidepressants (TCAs). SSRIs and SNRIs are considered first-line treatments for panic disorder because of their favorable side effect profile.¹⁴ In practice, benzodiazepines often are combined with SSRIs, SNRIs, or TCAs. A randomized controlled trial demonstrated that paroxetine and clonazepam (mean dose 1.6 mg/d at 5 weeks) resulted in a more rapid response compared with paroxetine alone, although this difference lasted only a few weeks.¹⁵ Furthermore, this study suggested that brief treatment with clonazepam followed by a taper is as effective as sustained treatment with paroxetine and clonazepam.¹⁵

There is a lack of high-quality data on combining cognitive-behavioral therapy (CBT) and benzodiazepines for panic disorder, although a Cochrane Review found that adding a benzodiazepine to CBT did not lead to a significant difference in response compared with psychotherapy alone.¹⁶ A recent randomized controlled trial demonstrated that tapering benzodiazepines combined with CBT was associated with successful discontinuation of the drug and prevented return of panic symptoms.¹⁷

Social anxiety. A meta-analysis found that for treating social anxiety, benzodiazepines have better efficacy than SSRIs, monoamine oxidase inhibitors, and anticonvulsants.¹⁸ Longer-acting benzodiazepines may be more effective than shorter-acting agents. One study of patients with social anxiety showed a 38% response rate for alprazolam vs 20% for placebo over 12 weeks, and a similar 10-week study demonstrated a 73% recovery rate with clonazepam vs 22% for placebo.¹⁹ In addition, studies have observed that patients can be maintained on clonazepam for up to 2 years without symptom relapse and will tolerate slow-taper discontinuation.^18,20 Sedation and drowsiness can be lessened by limiting clonazepam doses to 2 to 3 mg/d.

Akathisia and tremor. Akathisia, a syndrome of motor restlessness and inner turmoil, is associated with antipsychotics but can occur with SSRIs. Reducing the dosage or switching to another, usually less potent agent often can relieve akathisia. When these remedies are not tenable, consider benzodiazepines along with other medications—including beta blockers and anticholinergic agents—with demonstrated efficacy in reducing akathisia symptoms. Lorazepam, diazepam, and clonazepam have demonstrated efficacy for relieving akathisia in comparison studies with placebo, propranolol, and diphenhydramine.^21,22

Drug-induced postural tremor can occur with several psychotropics, including lithium, valproic acid, antidepressants, and antipsychotics. A tremor is considered mild if a patient can drink a glass of water with 1 hand without spilling and severe if holding a glass with 2 hands is difficult. Propranolol is most commonly prescribed for these tremors, but alprazolam and clonazepam have demonstrated efficacy, either as monotherapy or coadministered with a beta blocker.²³

Acute agitation. Agitated patients often have acute psychosis and/or mania or dyscontrol secondary to axis II disorders.²⁴ Patients may be paranoid, hostile, disruptive, and combative. Rapidly initiating medication can prevent the need for more restrictive measures, such as seclusion or restraint. Antipsychotics—especially high-potency agents such as haloperidol—and benzodiazepines, as monotherapy or in combination, are a mainstay treatment. Although treatment protocols favor atypical antipsychotics over typical antipsychotics, benzodiazepines are a viable option because of their anxiolytic and sedative effects. Advantages of benzodiazepine monotherapy include decreased extrapyramidal symptoms, greater patient acceptance/preference, and increased sedation compared with antipsychotics. Lorazepam, 1 to 2 mg intramuscularly (IM) or orally, is well tolerated because of its favorable drug-drug interaction profile and lack of significant cardiac side effects. Benzodiazepines can cause respiratory depression in patients with chronic lung disease and additive sedation secondary to opiates, other sedatives/hypnotics, or alcohol. Behavioral disinhibition is rare and is associated with preexisting CNS pathology or mental retardation.²⁵ The IM olanzapine package insert warns against coadministering IM lorazepam because of additive cardiorespiratory depressive effects and excessive somnolence.²⁶

Catatonia. The characteristic symptoms of catatonia are immobility, negativism, muteness, and failure to eat or drink. Benzodiazepines improve these symptoms in approximately 70% to 80% of catatonic patients with affective disorders. Response rates are lower in catatonia in patients with schizophrenia.²⁷ If catatonia in a patient with psychosis is missed, giving antipsychotics before benzodiazepines may worsen catatonic symptoms or precipitate neuroleptic malignant syndrome in some cases. When you suspect a patient has catatonia, start with lorazepam, 1 to 2 mg IV or IM, and examine the patient for diminishing catatonic signs within 1 to 2 hours. If catatonia signs lessen, begin regularly scheduled lorazepam, with dosing varying by age—be more cautious in geriatric patients—and symptom severity. Titrate benzodiazepines for stuporous patients more slowly (eg, 1 mg 3 times a day as a starting dose) than for excited catatonic patients. Lorazepam can be increased gradually as tolerated; it is not unusual for patients to require up to 8 to 12 mg/d. Electroconvulsive therapy (ECT) is the treatment of choice when catatonic patients respond poorly or partially to high-dose benzodiazepines.^28,29

Benzodiazepine reversal for ECT

Benzodiazepines have anticonvulsant properties that may interfere with the therapeutic efficacy of ECT.³⁰ A multi-center study demonstrated that lorazepam (up to 4 mg/d as needed) in the 48 hours before the first ECT session was not associated with effects on seizure threshold or duration; however, larger lorazepam dosages were associated with briefer EEG seizure duration.³¹ Some patients may not tolerate withholding or tapering benzodiazepines in preparation for ECT. Studies investigating flumazenil for pre-ECT benzodiazepine reversal are lacking. One retrospective analysis showed that flumazenil administration immediately before and after ECT resulted in adequate seizures with no difference in clinical outcome compared with patients who were not receiving benzodiazepines or flumazenil.³²

Tapering benzodiazepines

Slow discontinuation of benzodiazepines is recommended to avoid withdrawal symptoms, such as rebound anxiety, agitation, insomnia, or seizures, particularly when use exceeds 8 weeks. The onset of withdrawal symptoms varies, depending on the medication used. Withdrawal symptoms may appear in 1 to 2 days for agents with shorter half-lives, but may not appear until 3 to 7 days for agents with longer half-lives.³³Table 2 lists recommended durations for tapering benzodiazepines.^33,34 In general, decrease the total daily dose by 25% the first week, another 25% the second week, then 10% a week until discontinuation. When benzodiazepine use exceeds 1 year, a slower taper is recommended; for example, decrease 10% every 1 to 2 weeks. When 20% of the dosage remains, begin a 5% dose reduction every 2 to 4 weeks. Monitor patients for withdrawal symptoms or symptom exacerbation. If either occur, consider maintaining the current benzodiazepine dose or increasing the dose for 1 to 2 weeks or longer, if necessary, then continue to taper at a slower rate.³⁴

Table 2

Recommendations for tapering benzodiazepines

Risks of benzodiazepine use

For most indications, benzodiazepine therapy should be short-term.³⁵ Use exceeding 2 to 4 weeks increases the risk for dependence and withdrawal. Tell patients to avoid alcohol while taking a benzodiazepine because this combination is potentially lethal. Benzodiazepines are commonly abused and abuse can lead to unintentional drug overdose. Benzodiazepines accounted for 37% of unintentional drug overdose deaths in West Virginia in 2006; in 46% of these cases, benzodiazepines were used for nonmedical purposes. Clinicians can help reduce the risk of diversion by limiting prescriptions to 30 days with no refills.³⁶

Older patients taking benzodiazepines are at increased risk of falls and hip fractures.³⁷ Lorazepam, oxazepam, and temazepam—agents with shorter half-lives that are not greatly affected by pharmacokinetic changes associated with aging—are preferred for these patients.³⁴ Patients with dementia or other CNS-compromising conditions may become confused or delirious with regular benzodiazepine dosing. Educate patients to whom you prescribe benzodiazepines about the importance of gauging their level of sedation before driving or engaging in other tasks for which sedation could compromise their safety. Benzodiazepine use during pregnancy requires a careful discussion of risks and benefits (Box 2).³⁸

Box 2

Related Resources

• Substance Abuse and Mental Health Services Administration. www.samhsa.gov.
• National Institute on Drug Abuse resources for medical and health professionals. www.drugabuse.gov/medical-health-professionals.
• American Academy of Sleep Medicine. www.aasmnet.org.

Drug Brand Names

• Alprazolam • Xanax
• Chlordiazepoxide • Librium, Limbitrol
• Clonazepam • Klonopin
• Clorazepate • Tranxene
• Diazepam • Valium
• Diphenhydramine • Benadryl, others
• Estazolam • ProSom
• Flumazenil • Romazicon
• Flurazepam • Dalmane
• Haloperidol • Haldol
• Lithium • Lithobid
• Lorazepam • Ativan
• Olanzapine • Zyprexa
• Oxazepam • Serax
• Paroxetine • Paxil
• Pregabalin • Lyrica
• Propranolol • Inderal, InnoPran XL, others
• Quazepam • Doral
• Ramelteon • Rozerem
• Sertraline • Zoloft
• Temazepam • Restoril
• Triazolam • Halcion
• Valproic acid • Depakene, Stavzor, others

Disclosures

Drs. Bostwick and Yasugi report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Casher is a speaker for AstraZeneca and Sunovion Pharmaceuticals.

Since the discovery of chlordiazepoxide in the 1950s, benzodiazepines have revolutionized the treatment of anxiety and insomnia, largely because of their improved safety profile compared with barbiturates, formerly the preferred sedative-hypnotic.¹ In addition to their anxiolytic and sedative-hypnotic effects, benzodiazepines exhibit anterograde amnesia, anticonvulsant, and muscle relaxant properties.¹ Psychiatrists use benzodiazepines to treat anxiety and sleep disorders, acute agitation, alcohol withdrawal, catatonia, and psychotropic side effects such as akathisia. This article highlights the evidence for using benzodiazepines in anxiety and other disorders and why they generally should not be used for obsessive-compulsive disorder and posttraumatic stress disorder (Box 1).

Box 1

Pharmacokinetic properties

Most benzodiazepines are considered to have similar efficacy; therefore, selection is based on pharmacokinetic considerations. Table 1 compares the indication, onset, and half-life of 12 commonly used benzodiazepines.^2-6 Although Table 1 lists approximate equivalent doses, studies report inconsistent data. These are approximations only and should not be used independently to make therapy decisions.

Table 1

Oral benzodiazepines: Indications, onset, half-life, and equivalent doses

A diverse range of indications

Alcohol withdrawal. Benzodiazepines are the treatment of choice for alcohol withdrawal syndrome, particularly to prevent seizures.⁷ Research supports symptom-triggered therapy using the revised Clinical Institute Withdrawal Assessment for Alcohol. Benzodiazepines reduce CNS sympathetic hyperactivity to mitigate withdrawal from alcohol by decreasing tachycardia, tremor, insomnia, agitation, and anxiety. Furthermore, these agents provide prophylaxis against serious sequelae such as seizures and delirium.

Insomnia. The American Academy of Sleep Medicine considers benzodiazepine receptor agonists (BzRAs, which include benzodiazepines and non-benzodiazepines) and ramelteon first-line pharmacotherapy for primary insomnia.⁸ However, pharmacologic treatment should be short-term. Agents with short to intermediate half-lives and rapid onset, such as triazolam, can aid sleep initiation. Those with longer half-lives, such as temazepam, could address sleep maintenance. If a patient does not respond to the initial agent, try another medication within the same class, because patients may respond differently. Use lower starting doses in geriatric patients.⁹ Closely monitor for adverse effects, rebound insomnia, and potential abuse or tolerance. Identify comorbid conditions and medications that may impair sleep, and address them accordingly.

Psychological and behavioral treatments given over 4 to 8 weeks can yield stable sleep improvements for up to 2 years. If available, these interventions may be considered first-line for treating insomnia because of their lasting effects compared with BzRAs.¹⁰

Generalized anxiety disorder (GAD). Benzodiazepines effectively treat GAD because they work quickly and are well tolerated. However, there are better first-line treatment options when considering efficacy studies and dependence and tolerance concerns. One effect-size comparison of 21 double-blind, placebo-controlled trials showed that the efficacy of selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and pregabalin are comparable to benzodiazepines.¹¹ Benzodiazepines can be used in the first 2 to 3 weeks after initiating antidepressants to alleviate and prevent worsening of anxiety that may occur at the start of antidepressant therapy. Recent treatment guidelines recommend benzodiazepines as a second-line treatment or for treatment-resistant GAD in patients who do not have a substance abuse history.^12,13

Panic disorder. Efficacy of benzodiazepines for panic disorder is comparable to SSRIs, SNRIs, and tricyclic antidepressants (TCAs). SSRIs and SNRIs are considered first-line treatments for panic disorder because of their favorable side effect profile.¹⁴ In practice, benzodiazepines often are combined with SSRIs, SNRIs, or TCAs. A randomized controlled trial demonstrated that paroxetine and clonazepam (mean dose 1.6 mg/d at 5 weeks) resulted in a more rapid response compared with paroxetine alone, although this difference lasted only a few weeks.¹⁵ Furthermore, this study suggested that brief treatment with clonazepam followed by a taper is as effective as sustained treatment with paroxetine and clonazepam.¹⁵

There is a lack of high-quality data on combining cognitive-behavioral therapy (CBT) and benzodiazepines for panic disorder, although a Cochrane Review found that adding a benzodiazepine to CBT did not lead to a significant difference in response compared with psychotherapy alone.¹⁶ A recent randomized controlled trial demonstrated that tapering benzodiazepines combined with CBT was associated with successful discontinuation of the drug and prevented return of panic symptoms.¹⁷

Social anxiety. A meta-analysis found that for treating social anxiety, benzodiazepines have better efficacy than SSRIs, monoamine oxidase inhibitors, and anticonvulsants.¹⁸ Longer-acting benzodiazepines may be more effective than shorter-acting agents. One study of patients with social anxiety showed a 38% response rate for alprazolam vs 20% for placebo over 12 weeks, and a similar 10-week study demonstrated a 73% recovery rate with clonazepam vs 22% for placebo.¹⁹ In addition, studies have observed that patients can be maintained on clonazepam for up to 2 years without symptom relapse and will tolerate slow-taper discontinuation.^18,20 Sedation and drowsiness can be lessened by limiting clonazepam doses to 2 to 3 mg/d.

Akathisia and tremor. Akathisia, a syndrome of motor restlessness and inner turmoil, is associated with antipsychotics but can occur with SSRIs. Reducing the dosage or switching to another, usually less potent agent often can relieve akathisia. When these remedies are not tenable, consider benzodiazepines along with other medications—including beta blockers and anticholinergic agents—with demonstrated efficacy in reducing akathisia symptoms. Lorazepam, diazepam, and clonazepam have demonstrated efficacy for relieving akathisia in comparison studies with placebo, propranolol, and diphenhydramine.^21,22

Drug-induced postural tremor can occur with several psychotropics, including lithium, valproic acid, antidepressants, and antipsychotics. A tremor is considered mild if a patient can drink a glass of water with 1 hand without spilling and severe if holding a glass with 2 hands is difficult. Propranolol is most commonly prescribed for these tremors, but alprazolam and clonazepam have demonstrated efficacy, either as monotherapy or coadministered with a beta blocker.²³

Acute agitation. Agitated patients often have acute psychosis and/or mania or dyscontrol secondary to axis II disorders.²⁴ Patients may be paranoid, hostile, disruptive, and combative. Rapidly initiating medication can prevent the need for more restrictive measures, such as seclusion or restraint. Antipsychotics—especially high-potency agents such as haloperidol—and benzodiazepines, as monotherapy or in combination, are a mainstay treatment. Although treatment protocols favor atypical antipsychotics over typical antipsychotics, benzodiazepines are a viable option because of their anxiolytic and sedative effects. Advantages of benzodiazepine monotherapy include decreased extrapyramidal symptoms, greater patient acceptance/preference, and increased sedation compared with antipsychotics. Lorazepam, 1 to 2 mg intramuscularly (IM) or orally, is well tolerated because of its favorable drug-drug interaction profile and lack of significant cardiac side effects. Benzodiazepines can cause respiratory depression in patients with chronic lung disease and additive sedation secondary to opiates, other sedatives/hypnotics, or alcohol. Behavioral disinhibition is rare and is associated with preexisting CNS pathology or mental retardation.²⁵ The IM olanzapine package insert warns against coadministering IM lorazepam because of additive cardiorespiratory depressive effects and excessive somnolence.²⁶

Catatonia. The characteristic symptoms of catatonia are immobility, negativism, muteness, and failure to eat or drink. Benzodiazepines improve these symptoms in approximately 70% to 80% of catatonic patients with affective disorders. Response rates are lower in catatonia in patients with schizophrenia.²⁷ If catatonia in a patient with psychosis is missed, giving antipsychotics before benzodiazepines may worsen catatonic symptoms or precipitate neuroleptic malignant syndrome in some cases. When you suspect a patient has catatonia, start with lorazepam, 1 to 2 mg IV or IM, and examine the patient for diminishing catatonic signs within 1 to 2 hours. If catatonia signs lessen, begin regularly scheduled lorazepam, with dosing varying by age—be more cautious in geriatric patients—and symptom severity. Titrate benzodiazepines for stuporous patients more slowly (eg, 1 mg 3 times a day as a starting dose) than for excited catatonic patients. Lorazepam can be increased gradually as tolerated; it is not unusual for patients to require up to 8 to 12 mg/d. Electroconvulsive therapy (ECT) is the treatment of choice when catatonic patients respond poorly or partially to high-dose benzodiazepines.^28,29

Benzodiazepine reversal for ECT

Benzodiazepines have anticonvulsant properties that may interfere with the therapeutic efficacy of ECT.³⁰ A multi-center study demonstrated that lorazepam (up to 4 mg/d as needed) in the 48 hours before the first ECT session was not associated with effects on seizure threshold or duration; however, larger lorazepam dosages were associated with briefer EEG seizure duration.³¹ Some patients may not tolerate withholding or tapering benzodiazepines in preparation for ECT. Studies investigating flumazenil for pre-ECT benzodiazepine reversal are lacking. One retrospective analysis showed that flumazenil administration immediately before and after ECT resulted in adequate seizures with no difference in clinical outcome compared with patients who were not receiving benzodiazepines or flumazenil.³²

Tapering benzodiazepines

Slow discontinuation of benzodiazepines is recommended to avoid withdrawal symptoms, such as rebound anxiety, agitation, insomnia, or seizures, particularly when use exceeds 8 weeks. The onset of withdrawal symptoms varies, depending on the medication used. Withdrawal symptoms may appear in 1 to 2 days for agents with shorter half-lives, but may not appear until 3 to 7 days for agents with longer half-lives.³³Table 2 lists recommended durations for tapering benzodiazepines.^33,34 In general, decrease the total daily dose by 25% the first week, another 25% the second week, then 10% a week until discontinuation. When benzodiazepine use exceeds 1 year, a slower taper is recommended; for example, decrease 10% every 1 to 2 weeks. When 20% of the dosage remains, begin a 5% dose reduction every 2 to 4 weeks. Monitor patients for withdrawal symptoms or symptom exacerbation. If either occur, consider maintaining the current benzodiazepine dose or increasing the dose for 1 to 2 weeks or longer, if necessary, then continue to taper at a slower rate.³⁴

Table 2

Recommendations for tapering benzodiazepines

Risks of benzodiazepine use

For most indications, benzodiazepine therapy should be short-term.³⁵ Use exceeding 2 to 4 weeks increases the risk for dependence and withdrawal. Tell patients to avoid alcohol while taking a benzodiazepine because this combination is potentially lethal. Benzodiazepines are commonly abused and abuse can lead to unintentional drug overdose. Benzodiazepines accounted for 37% of unintentional drug overdose deaths in West Virginia in 2006; in 46% of these cases, benzodiazepines were used for nonmedical purposes. Clinicians can help reduce the risk of diversion by limiting prescriptions to 30 days with no refills.³⁶

Older patients taking benzodiazepines are at increased risk of falls and hip fractures.³⁷ Lorazepam, oxazepam, and temazepam—agents with shorter half-lives that are not greatly affected by pharmacokinetic changes associated with aging—are preferred for these patients.³⁴ Patients with dementia or other CNS-compromising conditions may become confused or delirious with regular benzodiazepine dosing. Educate patients to whom you prescribe benzodiazepines about the importance of gauging their level of sedation before driving or engaging in other tasks for which sedation could compromise their safety. Benzodiazepine use during pregnancy requires a careful discussion of risks and benefits (Box 2).³⁸

Box 2

Related Resources

• Substance Abuse and Mental Health Services Administration. www.samhsa.gov.
• National Institute on Drug Abuse resources for medical and health professionals. www.drugabuse.gov/medical-health-professionals.
• American Academy of Sleep Medicine. www.aasmnet.org.

Drug Brand Names

• Alprazolam • Xanax
• Chlordiazepoxide • Librium, Limbitrol
• Clonazepam • Klonopin
• Clorazepate • Tranxene
• Diazepam • Valium
• Diphenhydramine • Benadryl, others
• Estazolam • ProSom
• Flumazenil • Romazicon
• Flurazepam • Dalmane
• Haloperidol • Haldol
• Lithium • Lithobid
• Lorazepam • Ativan
• Olanzapine • Zyprexa
• Oxazepam • Serax
• Paroxetine • Paxil
• Pregabalin • Lyrica
• Propranolol • Inderal, InnoPran XL, others
• Quazepam • Doral
• Ramelteon • Rozerem
• Sertraline • Zoloft
• Temazepam • Restoril
• Triazolam • Halcion
• Valproic acid • Depakene, Stavzor, others

Disclosures

Drs. Bostwick and Yasugi report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Casher is a speaker for AstraZeneca and Sunovion Pharmaceuticals.

Bedside visit comes too late

A 22-YEAR-OLD MAN underwent a liver biopsy after being admitted to the hospital a week earlier with fever, chills, diarrhea, and general malaise. A number of specialists had seen him in the hospital because of abnormal laboratory studies, increasing fever, and a maculopapular rash over his trunk and face.

After the biopsy, the patient was dizzy and diaphoretic. His attending physician ordered hemoglobin and hematocrit levels, which were lower than earlier that day. Repeat testing showed a further decrease, prompting the physician to order 2 units of red blood cells.

Typing and cross-matching delayed the transfusion for several hours. Before it could be started, the patient was found unresponsive. When the attending physician came to the bedside, the patient had no palpable pulse. A code was called, but resuscitation efforts failed.

An autopsy found a small hole in the liver and 3500 mL of blood in the peritoneal cavity, as well as hepatitis with zonal and submassive necrosis, hemoperitoneum, and hypertrophy of the heart. An HIV test performed before the biopsy eventually came back positive.

PLAINTIFF’S CLAIM The attending physician and nurses were negligent in failing to respond to signs and symptoms of internal bleeding, including falling hematocrit and hemoglobin levels. The attending physician, who was at the hospital when the patient’s condition deteriorated, should have gone to the bedside and taken steps to prevent his death.

THE DEFENSE The patient had been stable overnight; a bedside exam was unnecessary.

VERDICT $1,815,658 Texas verdict.

COMMENT Considering the many demands on clinicians’ time, it’s easy to postpone a face-to-face evaluation of a patient after a procedure. In this case, such a delay cost more than $1.8 million. A laboratory test or nurses’ notes are sometimes inadequate substitutes for a physician’s evaluation.

Failure to investigate suspicious symptoms ends badly

A MAN WITH SIGNS AND SYMPTOMS SUGGESTIVE OF AORTIC ANEURYSM/DISSECTION—including chest pain, pericardial effusion, aortic regurgitation, and aortic dilatation—saw his physician, but the doctor didn’t order any tests, such as computed tomography (CT) with contrast, magnetic resonance imaging (MRI), or transesophageal echocardiogram (TEE).

Two weeks later, the 43-year-old patient returned to the physician, who noted left ventricular hypertrophy with pericardial effusion and mild aortic loop dilatation. Once again, the doctor didn’t order tests to rule out aneurysm/dissection.

Three weeks after the second office visit, the patient collapsed and was taken by ambulance to a hospital, where he was pronounced dead. An autopsy indicated that the cause of death was cardiac tamponade resulting from an undiagnosed aortic dissection.

PLAINTIFF’S CLAIM The physician should have ordered a CT scan with contrast, an MRI, or a TEE, any of which would have confirmed an aortic aneurysm/dissection, mandating immediate admission to a hospital for surgery.

THE DEFENSE No information about the defense is available.

VERDICT $1 million Maryland settlement.

COMMENT Although many common conditions will resolve spontaneously, it’s hard to imagine temporizing in a patient with chest pain and presumed aortic dissection.

Unrecognized spinal infection leads to paralysis

A 355-LB MAN WITH DIABETES AND SPINAL DISC DISEASE experienced a sharp pain between his shoulder blades after playing golf, followed by constant back pain radiating to his chest. He went to the emergency department (ED) the next day and was admitted to the hospital to rule out a heart attack.

During a week in the hospital, the patient was seen by several doctors and diagnosed with pneumonia and excessive myoglobin levels. A computed tomography (CT) scan of the thorax and abdomen showing fluid buildup in the lining around the lungs led to the pneumonia diagnosis. No definitive spinal view was available, however, because of a mixup between a secretary and a radiology technician.

When the patient saw the hospital attending physician (at the family practice group where she was a partner) after discharge from the hospital, he complained of shooting pain down his spine. The doctor prescribed muscle relaxants. Soon afterward, the patient developed difficulty walking and reported no bowel movements for 13 days.

Almost 2 weeks after discharge from the hospital, the patient broke his ankle. He told the paramedics who responded that he felt numb from his nipples to his feet. He was taken to a community hospital, where a doctor ordered another CT scan. The radiologist who read the scan failed to identify the serious spinal infection it indicated.

The patient was transferred back to the original hospital. No doctor saw him for 8 hours after transfer, by which time he was paralyzed from the chest down.

PLAINTIFF’S CLAIM The fluid buildup on the first CT scan was caused not by pneumonia but by an infection in the spinal discs that had spread to the vertebrae and surrounding tissue.

THE DEFENSE The attending physician denied at trial that the patient had told her about the shooting pains down his spine during the posthospitalization visit.

VERDICT $4.75 million Illinois verdict, preceded by more than $2.7 million in settlements with some of the doctors involved and the community hospital.

COMMENT Careful follow-up of ED visits and coordinated care are essential to avoid large verdicts such as this one.

Bedside visit comes too late

A 22-YEAR-OLD MAN underwent a liver biopsy after being admitted to the hospital a week earlier with fever, chills, diarrhea, and general malaise. A number of specialists had seen him in the hospital because of abnormal laboratory studies, increasing fever, and a maculopapular rash over his trunk and face.

After the biopsy, the patient was dizzy and diaphoretic. His attending physician ordered hemoglobin and hematocrit levels, which were lower than earlier that day. Repeat testing showed a further decrease, prompting the physician to order 2 units of red blood cells.

Typing and cross-matching delayed the transfusion for several hours. Before it could be started, the patient was found unresponsive. When the attending physician came to the bedside, the patient had no palpable pulse. A code was called, but resuscitation efforts failed.

An autopsy found a small hole in the liver and 3500 mL of blood in the peritoneal cavity, as well as hepatitis with zonal and submassive necrosis, hemoperitoneum, and hypertrophy of the heart. An HIV test performed before the biopsy eventually came back positive.

PLAINTIFF’S CLAIM The attending physician and nurses were negligent in failing to respond to signs and symptoms of internal bleeding, including falling hematocrit and hemoglobin levels. The attending physician, who was at the hospital when the patient’s condition deteriorated, should have gone to the bedside and taken steps to prevent his death.

THE DEFENSE The patient had been stable overnight; a bedside exam was unnecessary.

VERDICT $1,815,658 Texas verdict.

COMMENT Considering the many demands on clinicians’ time, it’s easy to postpone a face-to-face evaluation of a patient after a procedure. In this case, such a delay cost more than $1.8 million. A laboratory test or nurses’ notes are sometimes inadequate substitutes for a physician’s evaluation.

Failure to investigate suspicious symptoms ends badly

A MAN WITH SIGNS AND SYMPTOMS SUGGESTIVE OF AORTIC ANEURYSM/DISSECTION—including chest pain, pericardial effusion, aortic regurgitation, and aortic dilatation—saw his physician, but the doctor didn’t order any tests, such as computed tomography (CT) with contrast, magnetic resonance imaging (MRI), or transesophageal echocardiogram (TEE).

Two weeks later, the 43-year-old patient returned to the physician, who noted left ventricular hypertrophy with pericardial effusion and mild aortic loop dilatation. Once again, the doctor didn’t order tests to rule out aneurysm/dissection.

Three weeks after the second office visit, the patient collapsed and was taken by ambulance to a hospital, where he was pronounced dead. An autopsy indicated that the cause of death was cardiac tamponade resulting from an undiagnosed aortic dissection.

PLAINTIFF’S CLAIM The physician should have ordered a CT scan with contrast, an MRI, or a TEE, any of which would have confirmed an aortic aneurysm/dissection, mandating immediate admission to a hospital for surgery.

THE DEFENSE No information about the defense is available.

VERDICT $1 million Maryland settlement.

COMMENT Although many common conditions will resolve spontaneously, it’s hard to imagine temporizing in a patient with chest pain and presumed aortic dissection.

Unrecognized spinal infection leads to paralysis

A 355-LB MAN WITH DIABETES AND SPINAL DISC DISEASE experienced a sharp pain between his shoulder blades after playing golf, followed by constant back pain radiating to his chest. He went to the emergency department (ED) the next day and was admitted to the hospital to rule out a heart attack.

During a week in the hospital, the patient was seen by several doctors and diagnosed with pneumonia and excessive myoglobin levels. A computed tomography (CT) scan of the thorax and abdomen showing fluid buildup in the lining around the lungs led to the pneumonia diagnosis. No definitive spinal view was available, however, because of a mixup between a secretary and a radiology technician.

When the patient saw the hospital attending physician (at the family practice group where she was a partner) after discharge from the hospital, he complained of shooting pain down his spine. The doctor prescribed muscle relaxants. Soon afterward, the patient developed difficulty walking and reported no bowel movements for 13 days.

Almost 2 weeks after discharge from the hospital, the patient broke his ankle. He told the paramedics who responded that he felt numb from his nipples to his feet. He was taken to a community hospital, where a doctor ordered another CT scan. The radiologist who read the scan failed to identify the serious spinal infection it indicated.

The patient was transferred back to the original hospital. No doctor saw him for 8 hours after transfer, by which time he was paralyzed from the chest down.

PLAINTIFF’S CLAIM The fluid buildup on the first CT scan was caused not by pneumonia but by an infection in the spinal discs that had spread to the vertebrae and surrounding tissue.

THE DEFENSE The attending physician denied at trial that the patient had told her about the shooting pains down his spine during the posthospitalization visit.

VERDICT $4.75 million Illinois verdict, preceded by more than $2.7 million in settlements with some of the doctors involved and the community hospital.

COMMENT Careful follow-up of ED visits and coordinated care are essential to avoid large verdicts such as this one.

Bedside visit comes too late

A 22-YEAR-OLD MAN underwent a liver biopsy after being admitted to the hospital a week earlier with fever, chills, diarrhea, and general malaise. A number of specialists had seen him in the hospital because of abnormal laboratory studies, increasing fever, and a maculopapular rash over his trunk and face.

After the biopsy, the patient was dizzy and diaphoretic. His attending physician ordered hemoglobin and hematocrit levels, which were lower than earlier that day. Repeat testing showed a further decrease, prompting the physician to order 2 units of red blood cells.

Typing and cross-matching delayed the transfusion for several hours. Before it could be started, the patient was found unresponsive. When the attending physician came to the bedside, the patient had no palpable pulse. A code was called, but resuscitation efforts failed.

An autopsy found a small hole in the liver and 3500 mL of blood in the peritoneal cavity, as well as hepatitis with zonal and submassive necrosis, hemoperitoneum, and hypertrophy of the heart. An HIV test performed before the biopsy eventually came back positive.

PLAINTIFF’S CLAIM The attending physician and nurses were negligent in failing to respond to signs and symptoms of internal bleeding, including falling hematocrit and hemoglobin levels. The attending physician, who was at the hospital when the patient’s condition deteriorated, should have gone to the bedside and taken steps to prevent his death.

THE DEFENSE The patient had been stable overnight; a bedside exam was unnecessary.

VERDICT $1,815,658 Texas verdict.

COMMENT Considering the many demands on clinicians’ time, it’s easy to postpone a face-to-face evaluation of a patient after a procedure. In this case, such a delay cost more than $1.8 million. A laboratory test or nurses’ notes are sometimes inadequate substitutes for a physician’s evaluation.

Failure to investigate suspicious symptoms ends badly

A MAN WITH SIGNS AND SYMPTOMS SUGGESTIVE OF AORTIC ANEURYSM/DISSECTION—including chest pain, pericardial effusion, aortic regurgitation, and aortic dilatation—saw his physician, but the doctor didn’t order any tests, such as computed tomography (CT) with contrast, magnetic resonance imaging (MRI), or transesophageal echocardiogram (TEE).

Two weeks later, the 43-year-old patient returned to the physician, who noted left ventricular hypertrophy with pericardial effusion and mild aortic loop dilatation. Once again, the doctor didn’t order tests to rule out aneurysm/dissection.

Three weeks after the second office visit, the patient collapsed and was taken by ambulance to a hospital, where he was pronounced dead. An autopsy indicated that the cause of death was cardiac tamponade resulting from an undiagnosed aortic dissection.

PLAINTIFF’S CLAIM The physician should have ordered a CT scan with contrast, an MRI, or a TEE, any of which would have confirmed an aortic aneurysm/dissection, mandating immediate admission to a hospital for surgery.

THE DEFENSE No information about the defense is available.

VERDICT $1 million Maryland settlement.

COMMENT Although many common conditions will resolve spontaneously, it’s hard to imagine temporizing in a patient with chest pain and presumed aortic dissection.

Unrecognized spinal infection leads to paralysis

A 355-LB MAN WITH DIABETES AND SPINAL DISC DISEASE experienced a sharp pain between his shoulder blades after playing golf, followed by constant back pain radiating to his chest. He went to the emergency department (ED) the next day and was admitted to the hospital to rule out a heart attack.

During a week in the hospital, the patient was seen by several doctors and diagnosed with pneumonia and excessive myoglobin levels. A computed tomography (CT) scan of the thorax and abdomen showing fluid buildup in the lining around the lungs led to the pneumonia diagnosis. No definitive spinal view was available, however, because of a mixup between a secretary and a radiology technician.

When the patient saw the hospital attending physician (at the family practice group where she was a partner) after discharge from the hospital, he complained of shooting pain down his spine. The doctor prescribed muscle relaxants. Soon afterward, the patient developed difficulty walking and reported no bowel movements for 13 days.

Almost 2 weeks after discharge from the hospital, the patient broke his ankle. He told the paramedics who responded that he felt numb from his nipples to his feet. He was taken to a community hospital, where a doctor ordered another CT scan. The radiologist who read the scan failed to identify the serious spinal infection it indicated.

The patient was transferred back to the original hospital. No doctor saw him for 8 hours after transfer, by which time he was paralyzed from the chest down.

PLAINTIFF’S CLAIM The fluid buildup on the first CT scan was caused not by pneumonia but by an infection in the spinal discs that had spread to the vertebrae and surrounding tissue.

THE DEFENSE The attending physician denied at trial that the patient had told her about the shooting pains down his spine during the posthospitalization visit.

VERDICT $4.75 million Illinois verdict, preceded by more than $2.7 million in settlements with some of the doctors involved and the community hospital.

COMMENT Careful follow-up of ED visits and coordinated care are essential to avoid large verdicts such as this one.

ILLUSTRATIVE CASE

A 25-year-old woman who has been your patient for several years has intermittent bouts of abdominal pain, constipation, gas, and bloating. You believe she can benefit from treatment for IBS. What should you recommend?

IBS is the most common functional disorder of the gastrointestinal (GI) tract, affecting approximately 15% of the US population² and accounting for annual health care costs of roughly $30 billion.³ The primary symptoms are bloating, gas, and abdominal pain that often improves immediately after a bowel movement. Patients may have intermittent diarrhea and constipation, as well.

IBS may be related to “brain-gut dysfunction”
The etiology of IBS is unclear, but many agree that a combination of abnormal GI motility, visceral hypersensitivity, and “brain-gut dysfunction”—the inability of the brain to send signals that turn down pain produced in the GI tract—are contributing factors. Although IBS is not life threatening, it has a significant personal, social, and psychological impact. Despite its high prevalence and impact, only a limited number of large studies have assessed the effectiveness of various treatments.

STUDY SUMMARY: Antispasmodics, antidepressants offer relief—fiber does not

The Cochrane review included 56 randomized controlled trials (RCTs) comparing the efficacy of bulking agents (fiber supplements), anti-spasmodics, or antidepressants with placebo for the treatment of IBS. Twelve RCTs (n=621) focused on bulking agents, 29 (n=2333) on antispasmodics, and 15 (n=922) on antidepressants. Inclusion criteria included age (>12 years) and an IBS diagnosis. The outcomes analyzed were improvement in abdominal pain, global health assessments, and IBS symptom scores. Adverse effects were not evaluated.

Bulking agents. In studies ranging from 4 to 16 weeks, bulking agents were found to have no significant effect on abdominal pain (4 studies; standardized mean difference [SMD], 0.03; 95% confidence interval [CI], -0.34 to 0.40; P=.87) or global functioning (11 studies; risk ratio [RR]=1.11; 95% CI, 0.91-1.35; P=.32). Nor was there an improvement in IBS symptom score (3 studies; SMD=0.00; 95% CI, -0.43 to 0.43; P=1.00).

Antispasmodics. Assessed in RCTs ranging from one week to 6 months, antispasmodics significantly improved abdominal pain (RR=1.3; 95% CI, 1.1-1.55; P<.001; number needed to treat [NNT]=7); global functioning (RR=1.5; 95% CI, 1.2-1.8; P<.0001; NNT=5), and IBS symptom score (RR=1.9; 95% CI, 1.3-2.8; P<.01; NNT=3). Ten different antispasmodic agents were studied; in subgroup analyses, 5 of them— cimetropium/dicyclomine, peppermint oil, pinaverium, and trimebutine—were found to have statistically significant benefits.

Antidepressants. In studies of both tricyclics and selective serotonin reuptake inhibitors (SSRIs), antidepressants were found to have a significant effect on improving abdominal pain (RR=1.5; 95% CI, 1.0-2.1; P<.03; NNT=5), global functioning (RR=1.6; 95% CI, 1.2-2; P<.001; NNT=4), and IBS symptom score (RR=2.0; 95% CI, 1.3-3.0; P<.001; NNT=4). Subgroup analyses found statistically significant benefits in global functioning for SSRIs, and in abdominal pain and symptom scores for tricyclics.

WHAT’S NEW: More evidence against fiber for IBS symptoms

This Cochrane review confirms earlier findings—that both antispasmodics and antidepressants are effective treatments for IBS, but bulking agents are not. This is an important finding because dietary fiber adjustment is still among the first recommendations made by leading organizations like the American Gastroenterological Association and the World Gastroenterology Organisation.^4,5

CAVEATS: Limitations of studies included in the meta-analysis

Adverse effects of antispasmodics and antidepressants, which may limit compliance and treatment efficacy, were not addressed by the Cochrane reviewers. The total number of participants in trials of bulking agents was much smaller than that of the other treatments, so it is possible that clinically meaningful improvements were missed due to inadequate statistical power. In addition, the duration of interventions was highly variable, ranging from one to 4 months for bulking agents and antidepressants and from one week to 6 months for antispasmodics.

It is also important to note that 8 of the 12 studies of bulking agents were conducted in GI clinics. (The settings in which the other 4 studies were conducted is unclear.) Given the possibility that patients referred to GI clinics have already tried and failed to respond to fiber (and thus, that those who do respond to fiber are not given referrals), it may be reasonable for family physicians to recommend a trial of bulking agents for patients with IBS and to monitor them for symptom improvement.

CHALLENGES TO IMPLEMENTATION: Patients may favor fiber

Patients with IBS may be reluctant to take antidepressants or antispasmodics, due to concern about adverse effects (eg, headache, insomnia, nervousness, dry mouth, and constipation) or because of a preference for what they see as a more “natural” remedy. It may be helpful to explain that while fiber may have some health benefits, such as lowering cholesterol,⁶ antispasmodics and antidepressants have been found to improve IBS symptoms but thus far, fiber has not.

Acknowledgement

The PURLs Surveillance System is 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 25-year-old woman who has been your patient for several years has intermittent bouts of abdominal pain, constipation, gas, and bloating. You believe she can benefit from treatment for IBS. What should you recommend?

IBS is the most common functional disorder of the gastrointestinal (GI) tract, affecting approximately 15% of the US population² and accounting for annual health care costs of roughly $30 billion.³ The primary symptoms are bloating, gas, and abdominal pain that often improves immediately after a bowel movement. Patients may have intermittent diarrhea and constipation, as well.

IBS may be related to “brain-gut dysfunction”
The etiology of IBS is unclear, but many agree that a combination of abnormal GI motility, visceral hypersensitivity, and “brain-gut dysfunction”—the inability of the brain to send signals that turn down pain produced in the GI tract—are contributing factors. Although IBS is not life threatening, it has a significant personal, social, and psychological impact. Despite its high prevalence and impact, only a limited number of large studies have assessed the effectiveness of various treatments.

STUDY SUMMARY: Antispasmodics, antidepressants offer relief—fiber does not

The Cochrane review included 56 randomized controlled trials (RCTs) comparing the efficacy of bulking agents (fiber supplements), anti-spasmodics, or antidepressants with placebo for the treatment of IBS. Twelve RCTs (n=621) focused on bulking agents, 29 (n=2333) on antispasmodics, and 15 (n=922) on antidepressants. Inclusion criteria included age (>12 years) and an IBS diagnosis. The outcomes analyzed were improvement in abdominal pain, global health assessments, and IBS symptom scores. Adverse effects were not evaluated.

Bulking agents. In studies ranging from 4 to 16 weeks, bulking agents were found to have no significant effect on abdominal pain (4 studies; standardized mean difference [SMD], 0.03; 95% confidence interval [CI], -0.34 to 0.40; P=.87) or global functioning (11 studies; risk ratio [RR]=1.11; 95% CI, 0.91-1.35; P=.32). Nor was there an improvement in IBS symptom score (3 studies; SMD=0.00; 95% CI, -0.43 to 0.43; P=1.00).

Antispasmodics. Assessed in RCTs ranging from one week to 6 months, antispasmodics significantly improved abdominal pain (RR=1.3; 95% CI, 1.1-1.55; P<.001; number needed to treat [NNT]=7); global functioning (RR=1.5; 95% CI, 1.2-1.8; P<.0001; NNT=5), and IBS symptom score (RR=1.9; 95% CI, 1.3-2.8; P<.01; NNT=3). Ten different antispasmodic agents were studied; in subgroup analyses, 5 of them— cimetropium/dicyclomine, peppermint oil, pinaverium, and trimebutine—were found to have statistically significant benefits.

Antidepressants. In studies of both tricyclics and selective serotonin reuptake inhibitors (SSRIs), antidepressants were found to have a significant effect on improving abdominal pain (RR=1.5; 95% CI, 1.0-2.1; P<.03; NNT=5), global functioning (RR=1.6; 95% CI, 1.2-2; P<.001; NNT=4), and IBS symptom score (RR=2.0; 95% CI, 1.3-3.0; P<.001; NNT=4). Subgroup analyses found statistically significant benefits in global functioning for SSRIs, and in abdominal pain and symptom scores for tricyclics.

WHAT’S NEW: More evidence against fiber for IBS symptoms

This Cochrane review confirms earlier findings—that both antispasmodics and antidepressants are effective treatments for IBS, but bulking agents are not. This is an important finding because dietary fiber adjustment is still among the first recommendations made by leading organizations like the American Gastroenterological Association and the World Gastroenterology Organisation.^4,5

CAVEATS: Limitations of studies included in the meta-analysis

Adverse effects of antispasmodics and antidepressants, which may limit compliance and treatment efficacy, were not addressed by the Cochrane reviewers. The total number of participants in trials of bulking agents was much smaller than that of the other treatments, so it is possible that clinically meaningful improvements were missed due to inadequate statistical power. In addition, the duration of interventions was highly variable, ranging from one to 4 months for bulking agents and antidepressants and from one week to 6 months for antispasmodics.

It is also important to note that 8 of the 12 studies of bulking agents were conducted in GI clinics. (The settings in which the other 4 studies were conducted is unclear.) Given the possibility that patients referred to GI clinics have already tried and failed to respond to fiber (and thus, that those who do respond to fiber are not given referrals), it may be reasonable for family physicians to recommend a trial of bulking agents for patients with IBS and to monitor them for symptom improvement.

CHALLENGES TO IMPLEMENTATION: Patients may favor fiber

Patients with IBS may be reluctant to take antidepressants or antispasmodics, due to concern about adverse effects (eg, headache, insomnia, nervousness, dry mouth, and constipation) or because of a preference for what they see as a more “natural” remedy. It may be helpful to explain that while fiber may have some health benefits, such as lowering cholesterol,⁶ antispasmodics and antidepressants have been found to improve IBS symptoms but thus far, fiber has not.

Acknowledgement

The PURLs Surveillance System is 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 25-year-old woman who has been your patient for several years has intermittent bouts of abdominal pain, constipation, gas, and bloating. You believe she can benefit from treatment for IBS. What should you recommend?

IBS is the most common functional disorder of the gastrointestinal (GI) tract, affecting approximately 15% of the US population² and accounting for annual health care costs of roughly $30 billion.³ The primary symptoms are bloating, gas, and abdominal pain that often improves immediately after a bowel movement. Patients may have intermittent diarrhea and constipation, as well.

IBS may be related to “brain-gut dysfunction”
The etiology of IBS is unclear, but many agree that a combination of abnormal GI motility, visceral hypersensitivity, and “brain-gut dysfunction”—the inability of the brain to send signals that turn down pain produced in the GI tract—are contributing factors. Although IBS is not life threatening, it has a significant personal, social, and psychological impact. Despite its high prevalence and impact, only a limited number of large studies have assessed the effectiveness of various treatments.

STUDY SUMMARY: Antispasmodics, antidepressants offer relief—fiber does not

The Cochrane review included 56 randomized controlled trials (RCTs) comparing the efficacy of bulking agents (fiber supplements), anti-spasmodics, or antidepressants with placebo for the treatment of IBS. Twelve RCTs (n=621) focused on bulking agents, 29 (n=2333) on antispasmodics, and 15 (n=922) on antidepressants. Inclusion criteria included age (>12 years) and an IBS diagnosis. The outcomes analyzed were improvement in abdominal pain, global health assessments, and IBS symptom scores. Adverse effects were not evaluated.

Bulking agents. In studies ranging from 4 to 16 weeks, bulking agents were found to have no significant effect on abdominal pain (4 studies; standardized mean difference [SMD], 0.03; 95% confidence interval [CI], -0.34 to 0.40; P=.87) or global functioning (11 studies; risk ratio [RR]=1.11; 95% CI, 0.91-1.35; P=.32). Nor was there an improvement in IBS symptom score (3 studies; SMD=0.00; 95% CI, -0.43 to 0.43; P=1.00).

Antispasmodics. Assessed in RCTs ranging from one week to 6 months, antispasmodics significantly improved abdominal pain (RR=1.3; 95% CI, 1.1-1.55; P<.001; number needed to treat [NNT]=7); global functioning (RR=1.5; 95% CI, 1.2-1.8; P<.0001; NNT=5), and IBS symptom score (RR=1.9; 95% CI, 1.3-2.8; P<.01; NNT=3). Ten different antispasmodic agents were studied; in subgroup analyses, 5 of them— cimetropium/dicyclomine, peppermint oil, pinaverium, and trimebutine—were found to have statistically significant benefits.

Antidepressants. In studies of both tricyclics and selective serotonin reuptake inhibitors (SSRIs), antidepressants were found to have a significant effect on improving abdominal pain (RR=1.5; 95% CI, 1.0-2.1; P<.03; NNT=5), global functioning (RR=1.6; 95% CI, 1.2-2; P<.001; NNT=4), and IBS symptom score (RR=2.0; 95% CI, 1.3-3.0; P<.001; NNT=4). Subgroup analyses found statistically significant benefits in global functioning for SSRIs, and in abdominal pain and symptom scores for tricyclics.

WHAT’S NEW: More evidence against fiber for IBS symptoms

This Cochrane review confirms earlier findings—that both antispasmodics and antidepressants are effective treatments for IBS, but bulking agents are not. This is an important finding because dietary fiber adjustment is still among the first recommendations made by leading organizations like the American Gastroenterological Association and the World Gastroenterology Organisation.^4,5

CAVEATS: Limitations of studies included in the meta-analysis

Adverse effects of antispasmodics and antidepressants, which may limit compliance and treatment efficacy, were not addressed by the Cochrane reviewers. The total number of participants in trials of bulking agents was much smaller than that of the other treatments, so it is possible that clinically meaningful improvements were missed due to inadequate statistical power. In addition, the duration of interventions was highly variable, ranging from one to 4 months for bulking agents and antidepressants and from one week to 6 months for antispasmodics.

It is also important to note that 8 of the 12 studies of bulking agents were conducted in GI clinics. (The settings in which the other 4 studies were conducted is unclear.) Given the possibility that patients referred to GI clinics have already tried and failed to respond to fiber (and thus, that those who do respond to fiber are not given referrals), it may be reasonable for family physicians to recommend a trial of bulking agents for patients with IBS and to monitor them for symptom improvement.

CHALLENGES TO IMPLEMENTATION: Patients may favor fiber

Patients with IBS may be reluctant to take antidepressants or antispasmodics, due to concern about adverse effects (eg, headache, insomnia, nervousness, dry mouth, and constipation) or because of a preference for what they see as a more “natural” remedy. It may be helpful to explain that while fiber may have some health benefits, such as lowering cholesterol,⁶ antispasmodics and antidepressants have been found to improve IBS symptoms but thus far, fiber has not.

Acknowledgement

The PURLs Surveillance System is 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.

A 31-year-old construction worker with a history of intermittent cocaine use was brought to the emergency department (ED) by the police. He was handcuffed and appeared confused and frightened. The patient’s wife had phoned the police after he began running through a field in pursuit of perceived invaders of their home. The wife reported that a few hours earlier, the patient had begun to hallucinate and had become very fearful after getting high.

His heart rate was 126, blood pressure 136/96 mm Hg, and temperature 99.6°F. During the initial exam, the patient became agitated, attempted to assault a nurse, and tried to leave the ED before being subdued. A urine screen for drugs was negative for cocaine. His creatine phosphokinase was 850 U/L, creatinine 2.32 mg/dL, and blood urea nitrogen 27 mg/dL.

The health care team learned that the drug he’d been snorting earlier that day—and the day before—was “bath salts.”

This patient was one of the 30 that we’ve seen at our university hospital over the past year.

Since early 2010, EDs, psychiatric facilities, and poison control centers have seen a surge in the number of patients abusing novel synthetic stimulants—cathinones—that had once been sold in convenience stores and tobacco shops and often labeled innocuously as “bath salts” or “plant food.” Sales have largely gone underground, sold by those trafficking in methamphetamine and cocaine. These products are also available for online purchase and may be sold under such provocative names as “Cloud Nine” or “Rave.”¹ In 2010, poison control centers received 304 calls related to the use of these substances; in 2011, the number was 6138.²

Cathinone: An emerging recreational drug

For centuries the peoples of East Africa and the Arabian Peninsula have used the leaves of the indigenous khat plant (Catha edulis) for its amphetamine-like properties.³ Its active ingredient, cathinone, is a central nervous system stimulant that inhibits dopamine reuptake.⁴ In 2005, extracts from the plant were imported to Israel as “Hagigat” and promoted as a stimulant or aphrodisiac. These products were banned by the Israeli government in 2008 following documented cases of cardiovascular and neurologic sequelae.⁵

The growing problem of synthetic cathinone analogs in the United States. In 2008, synthetic analogs of cathinone were first identified in an analysis of drugs seized in the United States from individuals suffering psychological reactions to their use.¹ Two such substances, 4-methylmethcathinone (mephedrone) and 3,4-methylenedioxypyrovalerone (MDPV), have since circulated worldwide, publicized by information on the Internet. Although the packets sold as “bath salts” clearly state that the contents are not for human consumption, Web sites promote the chemicals as “legal highs.”⁶

While these substances were being banned in many Western European countries, their use rapidly increased throughout the United States and elsewhere, often as an alternative to cocaine. Increases in the number of reports to poison control centers throughout the United States provide evidence of the increasing use of these drugs, despite legislation outlawing possession and sale in many states.⁷ In September 2011, the US Drug Enforcement Agency, using its emergency scheduling authority, made possession and sale of MDPV and mephedrone illegal throughout the United States.⁸

Who’s using bath salts? A review of calls to 2 poison control centers involving 236 patients over a 7-month period ending in February 2011 suggests that users of cathinones are primarily male (78%) and young (modal age 26).⁷ Many users of cathinones do not regularly use other drugs recreationally, and they believe the open sale of these substances implies low risk.⁷ However, one reported series from a hospital in Michigan indicated that 69% of users presenting to the ED had acknowledged past use of illicit drugs.⁹

What the drugs look like. Mephedrone and MDPV are supplied as white powders packaged in small packets of 500 mg and sell for about $25. Most users take the drug by nasal insufflation, although there is an alarming trend toward intravenous use.⁷ The intended effects in using these stimulants are improved attention and energy, as well as euphoria. Doses of about 25 mg produce these effects in most individuals and last for 2 to 3 hours, leading some users to compulsively re-dose to maintain the effects.

Use of bath salts leads to paranoid delusions, violent behavior

Both mephedrone and MDPV are strong inhibitors of dopamine reuptake in areas of the brain regulating reward and motivation.^10,11 With prolonged exposure, the resultant stimulant effect of dopamine in reward centers of the brain moves a user from recreational pleasure seeking to addictive use just to maintain normal function.¹² This transition occurs in a matter of days or weeks in some individuals, and we have seen multiple readmissions for paranoid psychotic reactions shortly after discharge from hospitalization.

Multiple serious complications of use have been described. The mainstream media have reported bizarre suicides and some homicides.^13,14 Our clinic has reported on a unique hallucinatory delirium after use of MDPV, resulting in paranoid delusions and violent behavior in response to vivid hallucinations.¹⁵ Other patients suffer prolonged anxiety and panic reactions or depressive symptoms with suicidal ideation.¹⁶

Cardiovascular and other sequelae
About half of patients presenting to hospital EDs have cardiovascular complications such as tachycardia, chest pain, and hypertension from the sympathomimetic effects of these agents.^9,16 There have also been reports of rhabdomyolysis and renal failure requiring intensive medical treatment.^7,9,16

Taken together, mental status changes and physiologic reactions are similar to the “excited delirium” attributed to cocaine, methamphetamine, phencyclidine (PCP), and methylenedioxymethamphetamine (Ecstasy), all drugs that act on central monoamines.^17–20 There have also been reports of death after the use of these drugs.²¹

Cathinones do not show up on routine drug screens
A routine urine screen for synthetic cathinones is not available, although a specific test arranged through commercial laboratories is available for cases when use is suspected. According to a written communication from A. Macher, MD, in 2011 (manuscript in preparation), urine drug screens for PCP using the immunoassay method may yield a false-positive result in the presence of MDPV. Simply asking patients whether they’ve been using these products often elicits an honest answer.

Treatment is largely supportive

Management guidance based on clinical trials is lacking. Cardiovascular complications require usual treatment.^9,16 Serious psychiatric reactions may necessitate hospitalization to assure patient safety, particularly with evidence suggesting the potential to act on paranoid delusions or suicidal ideation. Benzodiazepines may be needed to control agitation, and low-dose antipsychotics, such as risperidone 1 mg, can aid in treating hallucinations.^9,15

The hallucinatory psychosis seen with these substances is best characterized as a toxic delirium.¹⁵ Aggressive use of antipsychotic agents is not advised, given the risk of treatment-related morbidity in patients with a history of repeated stimulant use.²² Many patients presenting with acute delirium may require restraints. These procedures should be used with caution to minimize muscle tissue damage; patients should be monitored frequently for hyperthermia, dehydration, and rhabdomyolysis.¹⁶

Nothing is known about the long-term effects of these drugs, although substances with similar actions are associated with long-term cognitive and memory deficits after repeated use.⁴

CORRESPONDENCE Thomas M. Penders, MD, LFAPA, Department of Psychiatry, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC 27834; penderst@ecu.edu

A 31-year-old construction worker with a history of intermittent cocaine use was brought to the emergency department (ED) by the police. He was handcuffed and appeared confused and frightened. The patient’s wife had phoned the police after he began running through a field in pursuit of perceived invaders of their home. The wife reported that a few hours earlier, the patient had begun to hallucinate and had become very fearful after getting high.

His heart rate was 126, blood pressure 136/96 mm Hg, and temperature 99.6°F. During the initial exam, the patient became agitated, attempted to assault a nurse, and tried to leave the ED before being subdued. A urine screen for drugs was negative for cocaine. His creatine phosphokinase was 850 U/L, creatinine 2.32 mg/dL, and blood urea nitrogen 27 mg/dL.

The health care team learned that the drug he’d been snorting earlier that day—and the day before—was “bath salts.”

This patient was one of the 30 that we’ve seen at our university hospital over the past year.

Since early 2010, EDs, psychiatric facilities, and poison control centers have seen a surge in the number of patients abusing novel synthetic stimulants—cathinones—that had once been sold in convenience stores and tobacco shops and often labeled innocuously as “bath salts” or “plant food.” Sales have largely gone underground, sold by those trafficking in methamphetamine and cocaine. These products are also available for online purchase and may be sold under such provocative names as “Cloud Nine” or “Rave.”¹ In 2010, poison control centers received 304 calls related to the use of these substances; in 2011, the number was 6138.²

Cathinone: An emerging recreational drug

For centuries the peoples of East Africa and the Arabian Peninsula have used the leaves of the indigenous khat plant (Catha edulis) for its amphetamine-like properties.³ Its active ingredient, cathinone, is a central nervous system stimulant that inhibits dopamine reuptake.⁴ In 2005, extracts from the plant were imported to Israel as “Hagigat” and promoted as a stimulant or aphrodisiac. These products were banned by the Israeli government in 2008 following documented cases of cardiovascular and neurologic sequelae.⁵

The growing problem of synthetic cathinone analogs in the United States. In 2008, synthetic analogs of cathinone were first identified in an analysis of drugs seized in the United States from individuals suffering psychological reactions to their use.¹ Two such substances, 4-methylmethcathinone (mephedrone) and 3,4-methylenedioxypyrovalerone (MDPV), have since circulated worldwide, publicized by information on the Internet. Although the packets sold as “bath salts” clearly state that the contents are not for human consumption, Web sites promote the chemicals as “legal highs.”⁶

While these substances were being banned in many Western European countries, their use rapidly increased throughout the United States and elsewhere, often as an alternative to cocaine. Increases in the number of reports to poison control centers throughout the United States provide evidence of the increasing use of these drugs, despite legislation outlawing possession and sale in many states.⁷ In September 2011, the US Drug Enforcement Agency, using its emergency scheduling authority, made possession and sale of MDPV and mephedrone illegal throughout the United States.⁸

Who’s using bath salts? A review of calls to 2 poison control centers involving 236 patients over a 7-month period ending in February 2011 suggests that users of cathinones are primarily male (78%) and young (modal age 26).⁷ Many users of cathinones do not regularly use other drugs recreationally, and they believe the open sale of these substances implies low risk.⁷ However, one reported series from a hospital in Michigan indicated that 69% of users presenting to the ED had acknowledged past use of illicit drugs.⁹

What the drugs look like. Mephedrone and MDPV are supplied as white powders packaged in small packets of 500 mg and sell for about $25. Most users take the drug by nasal insufflation, although there is an alarming trend toward intravenous use.⁷ The intended effects in using these stimulants are improved attention and energy, as well as euphoria. Doses of about 25 mg produce these effects in most individuals and last for 2 to 3 hours, leading some users to compulsively re-dose to maintain the effects.

Use of bath salts leads to paranoid delusions, violent behavior

Both mephedrone and MDPV are strong inhibitors of dopamine reuptake in areas of the brain regulating reward and motivation.^10,11 With prolonged exposure, the resultant stimulant effect of dopamine in reward centers of the brain moves a user from recreational pleasure seeking to addictive use just to maintain normal function.¹² This transition occurs in a matter of days or weeks in some individuals, and we have seen multiple readmissions for paranoid psychotic reactions shortly after discharge from hospitalization.

Multiple serious complications of use have been described. The mainstream media have reported bizarre suicides and some homicides.^13,14 Our clinic has reported on a unique hallucinatory delirium after use of MDPV, resulting in paranoid delusions and violent behavior in response to vivid hallucinations.¹⁵ Other patients suffer prolonged anxiety and panic reactions or depressive symptoms with suicidal ideation.¹⁶

Cardiovascular and other sequelae
About half of patients presenting to hospital EDs have cardiovascular complications such as tachycardia, chest pain, and hypertension from the sympathomimetic effects of these agents.^9,16 There have also been reports of rhabdomyolysis and renal failure requiring intensive medical treatment.^7,9,16

Taken together, mental status changes and physiologic reactions are similar to the “excited delirium” attributed to cocaine, methamphetamine, phencyclidine (PCP), and methylenedioxymethamphetamine (Ecstasy), all drugs that act on central monoamines.^17–20 There have also been reports of death after the use of these drugs.²¹

Cathinones do not show up on routine drug screens
A routine urine screen for synthetic cathinones is not available, although a specific test arranged through commercial laboratories is available for cases when use is suspected. According to a written communication from A. Macher, MD, in 2011 (manuscript in preparation), urine drug screens for PCP using the immunoassay method may yield a false-positive result in the presence of MDPV. Simply asking patients whether they’ve been using these products often elicits an honest answer.

Treatment is largely supportive

Management guidance based on clinical trials is lacking. Cardiovascular complications require usual treatment.^9,16 Serious psychiatric reactions may necessitate hospitalization to assure patient safety, particularly with evidence suggesting the potential to act on paranoid delusions or suicidal ideation. Benzodiazepines may be needed to control agitation, and low-dose antipsychotics, such as risperidone 1 mg, can aid in treating hallucinations.^9,15

The hallucinatory psychosis seen with these substances is best characterized as a toxic delirium.¹⁵ Aggressive use of antipsychotic agents is not advised, given the risk of treatment-related morbidity in patients with a history of repeated stimulant use.²² Many patients presenting with acute delirium may require restraints. These procedures should be used with caution to minimize muscle tissue damage; patients should be monitored frequently for hyperthermia, dehydration, and rhabdomyolysis.¹⁶

Nothing is known about the long-term effects of these drugs, although substances with similar actions are associated with long-term cognitive and memory deficits after repeated use.⁴

CORRESPONDENCE Thomas M. Penders, MD, LFAPA, Department of Psychiatry, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC 27834; penderst@ecu.edu

A 31-year-old construction worker with a history of intermittent cocaine use was brought to the emergency department (ED) by the police. He was handcuffed and appeared confused and frightened. The patient’s wife had phoned the police after he began running through a field in pursuit of perceived invaders of their home. The wife reported that a few hours earlier, the patient had begun to hallucinate and had become very fearful after getting high.

His heart rate was 126, blood pressure 136/96 mm Hg, and temperature 99.6°F. During the initial exam, the patient became agitated, attempted to assault a nurse, and tried to leave the ED before being subdued. A urine screen for drugs was negative for cocaine. His creatine phosphokinase was 850 U/L, creatinine 2.32 mg/dL, and blood urea nitrogen 27 mg/dL.

The health care team learned that the drug he’d been snorting earlier that day—and the day before—was “bath salts.”

This patient was one of the 30 that we’ve seen at our university hospital over the past year.

Since early 2010, EDs, psychiatric facilities, and poison control centers have seen a surge in the number of patients abusing novel synthetic stimulants—cathinones—that had once been sold in convenience stores and tobacco shops and often labeled innocuously as “bath salts” or “plant food.” Sales have largely gone underground, sold by those trafficking in methamphetamine and cocaine. These products are also available for online purchase and may be sold under such provocative names as “Cloud Nine” or “Rave.”¹ In 2010, poison control centers received 304 calls related to the use of these substances; in 2011, the number was 6138.²

Cathinone: An emerging recreational drug

For centuries the peoples of East Africa and the Arabian Peninsula have used the leaves of the indigenous khat plant (Catha edulis) for its amphetamine-like properties.³ Its active ingredient, cathinone, is a central nervous system stimulant that inhibits dopamine reuptake.⁴ In 2005, extracts from the plant were imported to Israel as “Hagigat” and promoted as a stimulant or aphrodisiac. These products were banned by the Israeli government in 2008 following documented cases of cardiovascular and neurologic sequelae.⁵

The growing problem of synthetic cathinone analogs in the United States. In 2008, synthetic analogs of cathinone were first identified in an analysis of drugs seized in the United States from individuals suffering psychological reactions to their use.¹ Two such substances, 4-methylmethcathinone (mephedrone) and 3,4-methylenedioxypyrovalerone (MDPV), have since circulated worldwide, publicized by information on the Internet. Although the packets sold as “bath salts” clearly state that the contents are not for human consumption, Web sites promote the chemicals as “legal highs.”⁶

While these substances were being banned in many Western European countries, their use rapidly increased throughout the United States and elsewhere, often as an alternative to cocaine. Increases in the number of reports to poison control centers throughout the United States provide evidence of the increasing use of these drugs, despite legislation outlawing possession and sale in many states.⁷ In September 2011, the US Drug Enforcement Agency, using its emergency scheduling authority, made possession and sale of MDPV and mephedrone illegal throughout the United States.⁸

Who’s using bath salts? A review of calls to 2 poison control centers involving 236 patients over a 7-month period ending in February 2011 suggests that users of cathinones are primarily male (78%) and young (modal age 26).⁷ Many users of cathinones do not regularly use other drugs recreationally, and they believe the open sale of these substances implies low risk.⁷ However, one reported series from a hospital in Michigan indicated that 69% of users presenting to the ED had acknowledged past use of illicit drugs.⁹

What the drugs look like. Mephedrone and MDPV are supplied as white powders packaged in small packets of 500 mg and sell for about $25. Most users take the drug by nasal insufflation, although there is an alarming trend toward intravenous use.⁷ The intended effects in using these stimulants are improved attention and energy, as well as euphoria. Doses of about 25 mg produce these effects in most individuals and last for 2 to 3 hours, leading some users to compulsively re-dose to maintain the effects.

Use of bath salts leads to paranoid delusions, violent behavior

Both mephedrone and MDPV are strong inhibitors of dopamine reuptake in areas of the brain regulating reward and motivation.^10,11 With prolonged exposure, the resultant stimulant effect of dopamine in reward centers of the brain moves a user from recreational pleasure seeking to addictive use just to maintain normal function.¹² This transition occurs in a matter of days or weeks in some individuals, and we have seen multiple readmissions for paranoid psychotic reactions shortly after discharge from hospitalization.

Multiple serious complications of use have been described. The mainstream media have reported bizarre suicides and some homicides.^13,14 Our clinic has reported on a unique hallucinatory delirium after use of MDPV, resulting in paranoid delusions and violent behavior in response to vivid hallucinations.¹⁵ Other patients suffer prolonged anxiety and panic reactions or depressive symptoms with suicidal ideation.¹⁶

Cardiovascular and other sequelae
About half of patients presenting to hospital EDs have cardiovascular complications such as tachycardia, chest pain, and hypertension from the sympathomimetic effects of these agents.^9,16 There have also been reports of rhabdomyolysis and renal failure requiring intensive medical treatment.^7,9,16

Taken together, mental status changes and physiologic reactions are similar to the “excited delirium” attributed to cocaine, methamphetamine, phencyclidine (PCP), and methylenedioxymethamphetamine (Ecstasy), all drugs that act on central monoamines.^17–20 There have also been reports of death after the use of these drugs.²¹

Cathinones do not show up on routine drug screens
A routine urine screen for synthetic cathinones is not available, although a specific test arranged through commercial laboratories is available for cases when use is suspected. According to a written communication from A. Macher, MD, in 2011 (manuscript in preparation), urine drug screens for PCP using the immunoassay method may yield a false-positive result in the presence of MDPV. Simply asking patients whether they’ve been using these products often elicits an honest answer.

Treatment is largely supportive

Management guidance based on clinical trials is lacking. Cardiovascular complications require usual treatment.^9,16 Serious psychiatric reactions may necessitate hospitalization to assure patient safety, particularly with evidence suggesting the potential to act on paranoid delusions or suicidal ideation. Benzodiazepines may be needed to control agitation, and low-dose antipsychotics, such as risperidone 1 mg, can aid in treating hallucinations.^9,15

The hallucinatory psychosis seen with these substances is best characterized as a toxic delirium.¹⁵ Aggressive use of antipsychotic agents is not advised, given the risk of treatment-related morbidity in patients with a history of repeated stimulant use.²² Many patients presenting with acute delirium may require restraints. These procedures should be used with caution to minimize muscle tissue damage; patients should be monitored frequently for hyperthermia, dehydration, and rhabdomyolysis.¹⁶

Nothing is known about the long-term effects of these drugs, although substances with similar actions are associated with long-term cognitive and memory deficits after repeated use.⁴

CORRESPONDENCE Thomas M. Penders, MD, LFAPA, Department of Psychiatry, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC 27834; penderst@ecu.edu

Ankle sprain, one of the more common injuries that primary care physicians evaluate, is usually managed with conservative treatment. Not uncommonly, however, lateral ankle sprain is diagnosed without consideration of a broader differential diagnosis.

Contributing to the problem is the fact that the clinical presentation of some fractures and tendon injuries is similar to that of a routine sprain. In some cases, the mechanism of injury—sprains are usually caused by excessive inversion of the ankle on a plantar-flexed foot—is similar, as well. What’s more, radiographs are often omitted or misinterpreted.

In the pages that follow, we highlight 4 commonly misdiagnosed injuries: fifth metatarsal fractures, navicular fractures, talar dome lesions, and peroneal tendon injuries. These injuries should be included in the differential diagnosis of an acute ankle injury—or a subacute foot or ankle injury that fails to respond as expected. Prompt recognition and appropriate treatment result in optimal outcomes. When foot and ankle fractures and tendon injuries are misdiagnosed (or simply missed) and do not receive adequate treatment, long-term morbidity, including frequent reinjury and disability, may result.¹

Are x-rays needed? Turn to the Ottawa rules

Ankle sprains represent a disruption in a ligament supporting a joint, and result in pain, edema, and ecchymosis, and often affect a patient’s ability to bear weight. While uncomplicated sprains generally heal with conservative treatment, other common foot and ankle injuries may require a different approach.

The Ottawa foot and ankle rules are an evidence-based guide to the use of initial radiographs after acute ankle injury (TABLE 1).^2-4 Pain—near the malleoli (for the ankle) or in the midfoot—is the key criterion, but x-rays are recommended only if at least one other specified criterion is also met. With a sensitivity of nearly 100%, the rules have been shown to reliably exclude, and diagnose, ankle and midfoot fractures in children >5 years and adults.^2,5

Table 1
Ottawa ankle and foot rules^2-4

Fifth metatarsal fractures are easily missed

The mechanism of injury for a fifth metatarsal fracture is often similar to that of a lateral ankle sprain. In addition, isolated ankle radiographs may not adequately evaluate the fifth metatarsal, which increases the risk of misdiagnosis.⁶

3 types of fifth metatarsal fractures
Fifth metatarsal fractures involve one of the following:

1. an avulsion fracture, caused by the pull of the plantar aponeurosis and the peroneus brevis tendon at the tuberosity of the bone
2. a Jones fracture, at the base of the fourth and fifth metatarsal (FIGURE 1)
3. a shaft fracture, distal to the fifth metatarsal joint in the proximal diaphysis.^6-8

FIGURE 1
Jones fractures heal slowly

While avulsion fractures are generally the result of an inversion ankle injury, Jones fractures are usually caused by a large adductive force applied to the forefoot on a plantar-flexed ankle.⁶ Shaft fractures, also known as diaphyseal stress fractures, are overuse injuries from chronic overload, usually after a sudden increase in running or walking.⁹

Patients with fifth metatarsal fractures typically have tenderness with palpation over the area of injury, with edema and ecchymosis when the injury is acute. Evidence-based guidelines recommend x-rays of the foot, including anteroposterior (AP), lateral, and oblique views.^2-4 One study supports the use of an additional x-ray—an AP view of the ankle, including the base of the fifth metatarsal—if clinical suspicion is high and initial radiographs are negative or inconclusive.¹⁰

Shaft fractures may not be seen on x-rays in the first 3 weeks, but a periosteal reaction or linear lucency near the symptomatic area may be noticeable on radiographs taken at a later date.¹¹ If this overuse injury seems likely but does not show up on the initial x-rays, however, magnetic resonance imaging (MRI) or a technetium bone scan can reliably identify a stress fracture.⁹

How to treat, when to refer
Treatment of fifth metatarsal fractures range from conservative to surgical, depending on the type (and extent) of injury (TABLE 2).^1,5,6,12-14

TABLE 2

Nondisplaced avulsion fractures can be treated conservatively, with relative immobilization. In one prospective study, the use of a stiff-soled shoe, with weight-bearing as tolerated, was associated with excellent long-term outcomes.¹¹ Orthopedic referral for probable reduction and fixation is indicated for avulsion fractures that are comminuted or >2 mm displaced, or have >30% involvement of the cubometatarsal joint.^15,16

Jones fractures are known for prolonged healing and nonunion, as well as a high rate of complications. If the fracture is nondisplaced, start with conservative treatment, consisting of nonweight-bearing immobilization for 6 to 8 weeks, with additional immobilization dependent on radiographs. One randomized controlled trial of patients with Jones fractures showed a relatively high failure rate (44%) with casting; patients for whom casting was successful still had a median time to bony union of 15 weeks.¹⁷ Specialty consultation may be needed when there is fracture displacement, absence of bony union, or high clinical concern.^6,17

Is your patient an athlete? Surgical fixation is favored for injured athletes with Jones fractures because failure rates are lower and both clinical union and return to play are shorter.^18,19 In a case series involving 23 athletic patients with Jones fractures, the success rate for immediate surgical screw fixation approached 100% within 6 to 8 weeks.¹⁸

Nondisplaced shaft fractures may be treated conservatively, with 6 to 8 weeks of immobilization with a protective orthosis. An orthopedic referral is recommended for patients whose fractures have >3 mm displacement or >10 degree angulation.¹⁵

Navicular fractures are overuse injuries

The navicular is predisposed to stress injury because the central third of the bone is relatively avascular. In addition, the navicular is the area of greatest stress and impingement between the talus and cuneiform bones during repetitive foot strikes.^12,20 Navicular fractures occur predominantly in track and field athletes.¹²

Patients presenting with a navicular stress fracture often report a gradual onset of vague dorsal midfoot pain associated with their workout.¹⁷ Examination typically reveals tenderness on palpation over the dorsal aspect of the navicular; passive eversion and active inversion may be painful, but edema and ecchymosis are usually absent.²¹

When pain is elicited by palpation of the navicular, radiographs are recommended.^2,6 X-rays have a relatively low sensitivity (33%), however, for detecting acute navicular stress fractures. If initial radiographs are negative but there is a high clinical suspicion, advanced studies—with either MRI or a technetium bone scan—are recommended for a definitive diagnosis.^12,22 While both are highly sensitive for navicular stress fractures, MRI provides greater specificity and anatomic detail.²³

Most navicular fractures are nondisplaced
Nondisplaced navicular fractures can be treated conservatively, with nonweight-bearing immobilization for 6 to 8 weeks followed by progressive activity.²⁴ Prospective studies have found that conservative treatment has a high success rate, with athletes usually able to return to play within 6 months.^22,24,25 If tenderness remains after 6 to 8 weeks of immobilization, treatment choices are continued immobilization with no weight-bearing or orthopedic referral.²⁶

Referral is indicated for navicular fractures that are comminuted or displaced, or involve more than one bone cortex.²⁶ Surgical screw fixation may be recommended for navicular stress fractures in selected athletes because of its high success rate—and likelihood of an earlier return to play.²⁷

Talar injuries are characterized by persistent pain

Injuries to the talus commonly occur at the same time as ankle sprains and may cause persistent pain, even after the sprain has healed.²⁸ Evidence suggests that up to 90% of residual pain is related to an underlying cartilage injury.^29,30 Most talar injuries are associated with the disruption of the cartilage overlaying the talar dome, which may lead to osteochondritis dissecans.²⁹ Subtle talus fractures are also a concern after an acute ankle injury.

Osteochondral lesions are associated with a dull ankle pain deep in a location with a prior ankle injury; in some cases, the pain will become chronic.³¹ Physical exam findings typically include ankle joint effusion with localized tenderness around the joint.³¹

Ankle radiographs are insensitive for identifying osteochondral lesions, and MRI is recommended for evaluating suspected lesions.^29,31 Treatment varies, depending on symptoms and severity. Patients with minimal symptoms may be treated conservatively; however, high failure rates have been reported.³² Surgical treatment depends on the size and site of the lesion and the degree of cartilage injury, and surgical consultation is recommended.³¹

Fractures of the talar dome (FIGURE 2) may be either medial or lateral and are often the result of inversion ankle injuries.¹⁴ History and clinical findings vary depending on the type of fracture.

FIGURE 2
Talar dome injuries often result from inversion ankle injuries

As with osteochondral lesions, ankle radiographs may fail to identify talus fractures. Computed tomography (CT) should be used to evaluate acute fractures of the talus, as CT scan is better able to define displacement, size, and intra-articular involvement.³³ Talar fractures may be managed conservatively with immobilization and nonweight-bearing for 4 to 6 weeks, but specialty consultation should be considered.14,33

A tarsal coalition—an incomplete, congenital separation of the bones, occasionally involving the talus and the calcaneus—can also be a cause of persistent pain after a sprain.²⁸ Physical exam typically demonstrates decreased range of motion in the subtalar or transverse tarsal joint. Radiographs may identify the coalition, but MRI or CT scan provides optimal visualization. Immobilization for 6 weeks is the recommended initial treatment, but if that fails, surgical excision or fusion may be necessary.

Peroneal tendon injuries may cause ankle instability

Peroneal tendon injuries, which include strains, subluxation, dislocation, and tears of one or both of the peroneal tendons, are often caused by ankle inversion similar to that of an uncomplicated sprain. Subsequent ankle instability may result from untreated peroneal tendon injuries.³⁴ Peroneal tendon subluxation accounts for a very small number (0.3%-0.5%) of traumatic ankle injuries.³⁵

Peroneal tendon injuries often occur during sports that involve frequent lateral movement or cutting—eg, football, basketball, and soccer—and are often caused by sudden dorsiflexion of the inverted foot, with coincident contraction of the peroneal muscles.^36,37 This mechanism can disrupt the superior peroneal retinaculum, leading to recurrent subluxation or dislocation and subsequent ankle instability.^36,38 Chronic subluxation can also result in longitudinal tears of the peroneal tendons, especially of the peroneus brevis.^36,38,39

Patients with peroneal tendon injuries may report a “pop” at the time of injury. Pain is typically located posterior to the lateral malleolus, and recurrent subluxation is often described as a “snapping” around the lateral ankle during athletic activities.^37,38 Instability is common in patients with subacute or chronic peroneal tendon injuries, especially on uneven surfaces.³⁸

Acute peroneal tendon injuries cause posterolateral ankle pain, swelling, and weakness; exam findings include tenderness along the course of the peroneal tendons with associated edema.³⁷ Subluxation or dislocation of the peroneal brevis tendon may be confirmed by placing the foot in plantar flexion and inversion and asking the patient to forcibly dorsiflex and evert the injured ankle.

Plain radiographs are usually normal in an isolated injury to the peroneal tendons. A fracture of the posterolateral margin of the fibula is a rare finding but indicates disruption of the peroneal retinaculum.³⁶ MRI provides the best imaging for peroneal tendons and the stabilizing retinaculum, although a CT scan can provide detailed bony anatomy when subtle fractures are suspected or additional evaluation is needed.

Subluxation or dislocation indicate a need for surgery
Conservative management is recommended for peroneal tendon strains, but surgical treatment is increasingly recommended for subluxation or dislocation, especially if the problem is recurrent.^36,37 Conservative treatment consists of short-term immobilization with a walking boot or brace, followed by physical therapy to improve strength and motion. Surgical treatment of subluxation and dislocation by stabilizing the peroneal tendons within the peroneal groove has been shown to provide lasting stability and improvement.^37,38,40,41

CORRESPONDENCE Scott Hall, MD, University of Nevada-Reno, Brigham Building 316, Reno, NV 89557; shallmd@specialtyhealth.com

Ankle sprain, one of the more common injuries that primary care physicians evaluate, is usually managed with conservative treatment. Not uncommonly, however, lateral ankle sprain is diagnosed without consideration of a broader differential diagnosis.

Contributing to the problem is the fact that the clinical presentation of some fractures and tendon injuries is similar to that of a routine sprain. In some cases, the mechanism of injury—sprains are usually caused by excessive inversion of the ankle on a plantar-flexed foot—is similar, as well. What’s more, radiographs are often omitted or misinterpreted.

In the pages that follow, we highlight 4 commonly misdiagnosed injuries: fifth metatarsal fractures, navicular fractures, talar dome lesions, and peroneal tendon injuries. These injuries should be included in the differential diagnosis of an acute ankle injury—or a subacute foot or ankle injury that fails to respond as expected. Prompt recognition and appropriate treatment result in optimal outcomes. When foot and ankle fractures and tendon injuries are misdiagnosed (or simply missed) and do not receive adequate treatment, long-term morbidity, including frequent reinjury and disability, may result.¹

Are x-rays needed? Turn to the Ottawa rules

Ankle sprains represent a disruption in a ligament supporting a joint, and result in pain, edema, and ecchymosis, and often affect a patient’s ability to bear weight. While uncomplicated sprains generally heal with conservative treatment, other common foot and ankle injuries may require a different approach.

The Ottawa foot and ankle rules are an evidence-based guide to the use of initial radiographs after acute ankle injury (TABLE 1).^2-4 Pain—near the malleoli (for the ankle) or in the midfoot—is the key criterion, but x-rays are recommended only if at least one other specified criterion is also met. With a sensitivity of nearly 100%, the rules have been shown to reliably exclude, and diagnose, ankle and midfoot fractures in children >5 years and adults.^2,5

Table 1
Ottawa ankle and foot rules^2-4

Fifth metatarsal fractures are easily missed

The mechanism of injury for a fifth metatarsal fracture is often similar to that of a lateral ankle sprain. In addition, isolated ankle radiographs may not adequately evaluate the fifth metatarsal, which increases the risk of misdiagnosis.⁶

3 types of fifth metatarsal fractures
Fifth metatarsal fractures involve one of the following:

1. an avulsion fracture, caused by the pull of the plantar aponeurosis and the peroneus brevis tendon at the tuberosity of the bone
2. a Jones fracture, at the base of the fourth and fifth metatarsal (FIGURE 1)
3. a shaft fracture, distal to the fifth metatarsal joint in the proximal diaphysis.^6-8

FIGURE 1
Jones fractures heal slowly

While avulsion fractures are generally the result of an inversion ankle injury, Jones fractures are usually caused by a large adductive force applied to the forefoot on a plantar-flexed ankle.⁶ Shaft fractures, also known as diaphyseal stress fractures, are overuse injuries from chronic overload, usually after a sudden increase in running or walking.⁹

Patients with fifth metatarsal fractures typically have tenderness with palpation over the area of injury, with edema and ecchymosis when the injury is acute. Evidence-based guidelines recommend x-rays of the foot, including anteroposterior (AP), lateral, and oblique views.^2-4 One study supports the use of an additional x-ray—an AP view of the ankle, including the base of the fifth metatarsal—if clinical suspicion is high and initial radiographs are negative or inconclusive.¹⁰

Shaft fractures may not be seen on x-rays in the first 3 weeks, but a periosteal reaction or linear lucency near the symptomatic area may be noticeable on radiographs taken at a later date.¹¹ If this overuse injury seems likely but does not show up on the initial x-rays, however, magnetic resonance imaging (MRI) or a technetium bone scan can reliably identify a stress fracture.⁹

How to treat, when to refer
Treatment of fifth metatarsal fractures range from conservative to surgical, depending on the type (and extent) of injury (TABLE 2).^1,5,6,12-14

TABLE 2

Nondisplaced avulsion fractures can be treated conservatively, with relative immobilization. In one prospective study, the use of a stiff-soled shoe, with weight-bearing as tolerated, was associated with excellent long-term outcomes.¹¹ Orthopedic referral for probable reduction and fixation is indicated for avulsion fractures that are comminuted or >2 mm displaced, or have >30% involvement of the cubometatarsal joint.^15,16

Jones fractures are known for prolonged healing and nonunion, as well as a high rate of complications. If the fracture is nondisplaced, start with conservative treatment, consisting of nonweight-bearing immobilization for 6 to 8 weeks, with additional immobilization dependent on radiographs. One randomized controlled trial of patients with Jones fractures showed a relatively high failure rate (44%) with casting; patients for whom casting was successful still had a median time to bony union of 15 weeks.¹⁷ Specialty consultation may be needed when there is fracture displacement, absence of bony union, or high clinical concern.^6,17

Is your patient an athlete? Surgical fixation is favored for injured athletes with Jones fractures because failure rates are lower and both clinical union and return to play are shorter.^18,19 In a case series involving 23 athletic patients with Jones fractures, the success rate for immediate surgical screw fixation approached 100% within 6 to 8 weeks.¹⁸

Nondisplaced shaft fractures may be treated conservatively, with 6 to 8 weeks of immobilization with a protective orthosis. An orthopedic referral is recommended for patients whose fractures have >3 mm displacement or >10 degree angulation.¹⁵

Navicular fractures are overuse injuries

The navicular is predisposed to stress injury because the central third of the bone is relatively avascular. In addition, the navicular is the area of greatest stress and impingement between the talus and cuneiform bones during repetitive foot strikes.^12,20 Navicular fractures occur predominantly in track and field athletes.¹²

Patients presenting with a navicular stress fracture often report a gradual onset of vague dorsal midfoot pain associated with their workout.¹⁷ Examination typically reveals tenderness on palpation over the dorsal aspect of the navicular; passive eversion and active inversion may be painful, but edema and ecchymosis are usually absent.²¹

When pain is elicited by palpation of the navicular, radiographs are recommended.^2,6 X-rays have a relatively low sensitivity (33%), however, for detecting acute navicular stress fractures. If initial radiographs are negative but there is a high clinical suspicion, advanced studies—with either MRI or a technetium bone scan—are recommended for a definitive diagnosis.^12,22 While both are highly sensitive for navicular stress fractures, MRI provides greater specificity and anatomic detail.²³

Most navicular fractures are nondisplaced
Nondisplaced navicular fractures can be treated conservatively, with nonweight-bearing immobilization for 6 to 8 weeks followed by progressive activity.²⁴ Prospective studies have found that conservative treatment has a high success rate, with athletes usually able to return to play within 6 months.^22,24,25 If tenderness remains after 6 to 8 weeks of immobilization, treatment choices are continued immobilization with no weight-bearing or orthopedic referral.²⁶

Referral is indicated for navicular fractures that are comminuted or displaced, or involve more than one bone cortex.²⁶ Surgical screw fixation may be recommended for navicular stress fractures in selected athletes because of its high success rate—and likelihood of an earlier return to play.²⁷

Talar injuries are characterized by persistent pain

Injuries to the talus commonly occur at the same time as ankle sprains and may cause persistent pain, even after the sprain has healed.²⁸ Evidence suggests that up to 90% of residual pain is related to an underlying cartilage injury.^29,30 Most talar injuries are associated with the disruption of the cartilage overlaying the talar dome, which may lead to osteochondritis dissecans.²⁹ Subtle talus fractures are also a concern after an acute ankle injury.

Osteochondral lesions are associated with a dull ankle pain deep in a location with a prior ankle injury; in some cases, the pain will become chronic.³¹ Physical exam findings typically include ankle joint effusion with localized tenderness around the joint.³¹

Ankle radiographs are insensitive for identifying osteochondral lesions, and MRI is recommended for evaluating suspected lesions.^29,31 Treatment varies, depending on symptoms and severity. Patients with minimal symptoms may be treated conservatively; however, high failure rates have been reported.³² Surgical treatment depends on the size and site of the lesion and the degree of cartilage injury, and surgical consultation is recommended.³¹

Fractures of the talar dome (FIGURE 2) may be either medial or lateral and are often the result of inversion ankle injuries.¹⁴ History and clinical findings vary depending on the type of fracture.

FIGURE 2
Talar dome injuries often result from inversion ankle injuries

As with osteochondral lesions, ankle radiographs may fail to identify talus fractures. Computed tomography (CT) should be used to evaluate acute fractures of the talus, as CT scan is better able to define displacement, size, and intra-articular involvement.³³ Talar fractures may be managed conservatively with immobilization and nonweight-bearing for 4 to 6 weeks, but specialty consultation should be considered.14,33

A tarsal coalition—an incomplete, congenital separation of the bones, occasionally involving the talus and the calcaneus—can also be a cause of persistent pain after a sprain.²⁸ Physical exam typically demonstrates decreased range of motion in the subtalar or transverse tarsal joint. Radiographs may identify the coalition, but MRI or CT scan provides optimal visualization. Immobilization for 6 weeks is the recommended initial treatment, but if that fails, surgical excision or fusion may be necessary.

Peroneal tendon injuries may cause ankle instability

Peroneal tendon injuries, which include strains, subluxation, dislocation, and tears of one or both of the peroneal tendons, are often caused by ankle inversion similar to that of an uncomplicated sprain. Subsequent ankle instability may result from untreated peroneal tendon injuries.³⁴ Peroneal tendon subluxation accounts for a very small number (0.3%-0.5%) of traumatic ankle injuries.³⁵

Peroneal tendon injuries often occur during sports that involve frequent lateral movement or cutting—eg, football, basketball, and soccer—and are often caused by sudden dorsiflexion of the inverted foot, with coincident contraction of the peroneal muscles.^36,37 This mechanism can disrupt the superior peroneal retinaculum, leading to recurrent subluxation or dislocation and subsequent ankle instability.^36,38 Chronic subluxation can also result in longitudinal tears of the peroneal tendons, especially of the peroneus brevis.^36,38,39

Patients with peroneal tendon injuries may report a “pop” at the time of injury. Pain is typically located posterior to the lateral malleolus, and recurrent subluxation is often described as a “snapping” around the lateral ankle during athletic activities.^37,38 Instability is common in patients with subacute or chronic peroneal tendon injuries, especially on uneven surfaces.³⁸

Acute peroneal tendon injuries cause posterolateral ankle pain, swelling, and weakness; exam findings include tenderness along the course of the peroneal tendons with associated edema.³⁷ Subluxation or dislocation of the peroneal brevis tendon may be confirmed by placing the foot in plantar flexion and inversion and asking the patient to forcibly dorsiflex and evert the injured ankle.

Plain radiographs are usually normal in an isolated injury to the peroneal tendons. A fracture of the posterolateral margin of the fibula is a rare finding but indicates disruption of the peroneal retinaculum.³⁶ MRI provides the best imaging for peroneal tendons and the stabilizing retinaculum, although a CT scan can provide detailed bony anatomy when subtle fractures are suspected or additional evaluation is needed.

Subluxation or dislocation indicate a need for surgery
Conservative management is recommended for peroneal tendon strains, but surgical treatment is increasingly recommended for subluxation or dislocation, especially if the problem is recurrent.^36,37 Conservative treatment consists of short-term immobilization with a walking boot or brace, followed by physical therapy to improve strength and motion. Surgical treatment of subluxation and dislocation by stabilizing the peroneal tendons within the peroneal groove has been shown to provide lasting stability and improvement.^37,38,40,41

CORRESPONDENCE Scott Hall, MD, University of Nevada-Reno, Brigham Building 316, Reno, NV 89557; shallmd@specialtyhealth.com

Ankle sprain, one of the more common injuries that primary care physicians evaluate, is usually managed with conservative treatment. Not uncommonly, however, lateral ankle sprain is diagnosed without consideration of a broader differential diagnosis.

Contributing to the problem is the fact that the clinical presentation of some fractures and tendon injuries is similar to that of a routine sprain. In some cases, the mechanism of injury—sprains are usually caused by excessive inversion of the ankle on a plantar-flexed foot—is similar, as well. What’s more, radiographs are often omitted or misinterpreted.

In the pages that follow, we highlight 4 commonly misdiagnosed injuries: fifth metatarsal fractures, navicular fractures, talar dome lesions, and peroneal tendon injuries. These injuries should be included in the differential diagnosis of an acute ankle injury—or a subacute foot or ankle injury that fails to respond as expected. Prompt recognition and appropriate treatment result in optimal outcomes. When foot and ankle fractures and tendon injuries are misdiagnosed (or simply missed) and do not receive adequate treatment, long-term morbidity, including frequent reinjury and disability, may result.¹

Are x-rays needed? Turn to the Ottawa rules

Ankle sprains represent a disruption in a ligament supporting a joint, and result in pain, edema, and ecchymosis, and often affect a patient’s ability to bear weight. While uncomplicated sprains generally heal with conservative treatment, other common foot and ankle injuries may require a different approach.

The Ottawa foot and ankle rules are an evidence-based guide to the use of initial radiographs after acute ankle injury (TABLE 1).^2-4 Pain—near the malleoli (for the ankle) or in the midfoot—is the key criterion, but x-rays are recommended only if at least one other specified criterion is also met. With a sensitivity of nearly 100%, the rules have been shown to reliably exclude, and diagnose, ankle and midfoot fractures in children >5 years and adults.^2,5

Table 1
Ottawa ankle and foot rules^2-4

Fifth metatarsal fractures are easily missed

The mechanism of injury for a fifth metatarsal fracture is often similar to that of a lateral ankle sprain. In addition, isolated ankle radiographs may not adequately evaluate the fifth metatarsal, which increases the risk of misdiagnosis.⁶

3 types of fifth metatarsal fractures
Fifth metatarsal fractures involve one of the following:

1. an avulsion fracture, caused by the pull of the plantar aponeurosis and the peroneus brevis tendon at the tuberosity of the bone
2. a Jones fracture, at the base of the fourth and fifth metatarsal (FIGURE 1)
3. a shaft fracture, distal to the fifth metatarsal joint in the proximal diaphysis.^6-8

FIGURE 1
Jones fractures heal slowly

While avulsion fractures are generally the result of an inversion ankle injury, Jones fractures are usually caused by a large adductive force applied to the forefoot on a plantar-flexed ankle.⁶ Shaft fractures, also known as diaphyseal stress fractures, are overuse injuries from chronic overload, usually after a sudden increase in running or walking.⁹

Patients with fifth metatarsal fractures typically have tenderness with palpation over the area of injury, with edema and ecchymosis when the injury is acute. Evidence-based guidelines recommend x-rays of the foot, including anteroposterior (AP), lateral, and oblique views.^2-4 One study supports the use of an additional x-ray—an AP view of the ankle, including the base of the fifth metatarsal—if clinical suspicion is high and initial radiographs are negative or inconclusive.¹⁰

Shaft fractures may not be seen on x-rays in the first 3 weeks, but a periosteal reaction or linear lucency near the symptomatic area may be noticeable on radiographs taken at a later date.¹¹ If this overuse injury seems likely but does not show up on the initial x-rays, however, magnetic resonance imaging (MRI) or a technetium bone scan can reliably identify a stress fracture.⁹

How to treat, when to refer
Treatment of fifth metatarsal fractures range from conservative to surgical, depending on the type (and extent) of injury (TABLE 2).^1,5,6,12-14

TABLE 2

Nondisplaced avulsion fractures can be treated conservatively, with relative immobilization. In one prospective study, the use of a stiff-soled shoe, with weight-bearing as tolerated, was associated with excellent long-term outcomes.¹¹ Orthopedic referral for probable reduction and fixation is indicated for avulsion fractures that are comminuted or >2 mm displaced, or have >30% involvement of the cubometatarsal joint.^15,16

Jones fractures are known for prolonged healing and nonunion, as well as a high rate of complications. If the fracture is nondisplaced, start with conservative treatment, consisting of nonweight-bearing immobilization for 6 to 8 weeks, with additional immobilization dependent on radiographs. One randomized controlled trial of patients with Jones fractures showed a relatively high failure rate (44%) with casting; patients for whom casting was successful still had a median time to bony union of 15 weeks.¹⁷ Specialty consultation may be needed when there is fracture displacement, absence of bony union, or high clinical concern.^6,17

Is your patient an athlete? Surgical fixation is favored for injured athletes with Jones fractures because failure rates are lower and both clinical union and return to play are shorter.^18,19 In a case series involving 23 athletic patients with Jones fractures, the success rate for immediate surgical screw fixation approached 100% within 6 to 8 weeks.¹⁸

Nondisplaced shaft fractures may be treated conservatively, with 6 to 8 weeks of immobilization with a protective orthosis. An orthopedic referral is recommended for patients whose fractures have >3 mm displacement or >10 degree angulation.¹⁵

Navicular fractures are overuse injuries

The navicular is predisposed to stress injury because the central third of the bone is relatively avascular. In addition, the navicular is the area of greatest stress and impingement between the talus and cuneiform bones during repetitive foot strikes.^12,20 Navicular fractures occur predominantly in track and field athletes.¹²

Patients presenting with a navicular stress fracture often report a gradual onset of vague dorsal midfoot pain associated with their workout.¹⁷ Examination typically reveals tenderness on palpation over the dorsal aspect of the navicular; passive eversion and active inversion may be painful, but edema and ecchymosis are usually absent.²¹

When pain is elicited by palpation of the navicular, radiographs are recommended.^2,6 X-rays have a relatively low sensitivity (33%), however, for detecting acute navicular stress fractures. If initial radiographs are negative but there is a high clinical suspicion, advanced studies—with either MRI or a technetium bone scan—are recommended for a definitive diagnosis.^12,22 While both are highly sensitive for navicular stress fractures, MRI provides greater specificity and anatomic detail.²³

Most navicular fractures are nondisplaced
Nondisplaced navicular fractures can be treated conservatively, with nonweight-bearing immobilization for 6 to 8 weeks followed by progressive activity.²⁴ Prospective studies have found that conservative treatment has a high success rate, with athletes usually able to return to play within 6 months.^22,24,25 If tenderness remains after 6 to 8 weeks of immobilization, treatment choices are continued immobilization with no weight-bearing or orthopedic referral.²⁶

Referral is indicated for navicular fractures that are comminuted or displaced, or involve more than one bone cortex.²⁶ Surgical screw fixation may be recommended for navicular stress fractures in selected athletes because of its high success rate—and likelihood of an earlier return to play.²⁷

Talar injuries are characterized by persistent pain

Injuries to the talus commonly occur at the same time as ankle sprains and may cause persistent pain, even after the sprain has healed.²⁸ Evidence suggests that up to 90% of residual pain is related to an underlying cartilage injury.^29,30 Most talar injuries are associated with the disruption of the cartilage overlaying the talar dome, which may lead to osteochondritis dissecans.²⁹ Subtle talus fractures are also a concern after an acute ankle injury.

Osteochondral lesions are associated with a dull ankle pain deep in a location with a prior ankle injury; in some cases, the pain will become chronic.³¹ Physical exam findings typically include ankle joint effusion with localized tenderness around the joint.³¹

Ankle radiographs are insensitive for identifying osteochondral lesions, and MRI is recommended for evaluating suspected lesions.^29,31 Treatment varies, depending on symptoms and severity. Patients with minimal symptoms may be treated conservatively; however, high failure rates have been reported.³² Surgical treatment depends on the size and site of the lesion and the degree of cartilage injury, and surgical consultation is recommended.³¹

Fractures of the talar dome (FIGURE 2) may be either medial or lateral and are often the result of inversion ankle injuries.¹⁴ History and clinical findings vary depending on the type of fracture.

FIGURE 2
Talar dome injuries often result from inversion ankle injuries

As with osteochondral lesions, ankle radiographs may fail to identify talus fractures. Computed tomography (CT) should be used to evaluate acute fractures of the talus, as CT scan is better able to define displacement, size, and intra-articular involvement.³³ Talar fractures may be managed conservatively with immobilization and nonweight-bearing for 4 to 6 weeks, but specialty consultation should be considered.14,33

A tarsal coalition—an incomplete, congenital separation of the bones, occasionally involving the talus and the calcaneus—can also be a cause of persistent pain after a sprain.²⁸ Physical exam typically demonstrates decreased range of motion in the subtalar or transverse tarsal joint. Radiographs may identify the coalition, but MRI or CT scan provides optimal visualization. Immobilization for 6 weeks is the recommended initial treatment, but if that fails, surgical excision or fusion may be necessary.

Peroneal tendon injuries may cause ankle instability

Peroneal tendon injuries, which include strains, subluxation, dislocation, and tears of one or both of the peroneal tendons, are often caused by ankle inversion similar to that of an uncomplicated sprain. Subsequent ankle instability may result from untreated peroneal tendon injuries.³⁴ Peroneal tendon subluxation accounts for a very small number (0.3%-0.5%) of traumatic ankle injuries.³⁵

Peroneal tendon injuries often occur during sports that involve frequent lateral movement or cutting—eg, football, basketball, and soccer—and are often caused by sudden dorsiflexion of the inverted foot, with coincident contraction of the peroneal muscles.^36,37 This mechanism can disrupt the superior peroneal retinaculum, leading to recurrent subluxation or dislocation and subsequent ankle instability.^36,38 Chronic subluxation can also result in longitudinal tears of the peroneal tendons, especially of the peroneus brevis.^36,38,39

Patients with peroneal tendon injuries may report a “pop” at the time of injury. Pain is typically located posterior to the lateral malleolus, and recurrent subluxation is often described as a “snapping” around the lateral ankle during athletic activities.^37,38 Instability is common in patients with subacute or chronic peroneal tendon injuries, especially on uneven surfaces.³⁸

Acute peroneal tendon injuries cause posterolateral ankle pain, swelling, and weakness; exam findings include tenderness along the course of the peroneal tendons with associated edema.³⁷ Subluxation or dislocation of the peroneal brevis tendon may be confirmed by placing the foot in plantar flexion and inversion and asking the patient to forcibly dorsiflex and evert the injured ankle.

Plain radiographs are usually normal in an isolated injury to the peroneal tendons. A fracture of the posterolateral margin of the fibula is a rare finding but indicates disruption of the peroneal retinaculum.³⁶ MRI provides the best imaging for peroneal tendons and the stabilizing retinaculum, although a CT scan can provide detailed bony anatomy when subtle fractures are suspected or additional evaluation is needed.

Subluxation or dislocation indicate a need for surgery
Conservative management is recommended for peroneal tendon strains, but surgical treatment is increasingly recommended for subluxation or dislocation, especially if the problem is recurrent.^36,37 Conservative treatment consists of short-term immobilization with a walking boot or brace, followed by physical therapy to improve strength and motion. Surgical treatment of subluxation and dislocation by stabilizing the peroneal tendons within the peroneal groove has been shown to provide lasting stability and improvement.^37,38,40,41

CORRESPONDENCE Scott Hall, MD, University of Nevada-Reno, Brigham Building 316, Reno, NV 89557; shallmd@specialtyhealth.com

Objective: Although depression is prevalent among cancer patients, it remains underdiagnosed and undertreated. Quality of life is an important outcome in cancer patients and can be measured by questionnaires such as the Functional Assessment of Cancer Therapy-General version (FACT-G). The purpose of our study was to establish whether or not a group of items in FACT-G could be used as a screening tool for depression as well as for assessing quality of life.

Methods: A total of 62 chemotherapy patients (median age, 62 years [range, 22-81 years]; 55% women) completed Zung Self-Rating Depression Scale (ZSDS) and FACT-G questionnaires. Patients with ZSDS scores of 40 or more underwent clinical interviews for major depression. Pearson’s correlation was used to examine the relationship between the ZSDS and FACT-G scores. FACT-G score results were then analyzed to evaluate if subsets of the FACT-G can be used as a screening tool for major depression.

Results: In all, 30 of 62 patients (48%) had ZSDS scores less than 40 and were ruled out for major depression, and 30 of the 32 patients with ZSDS scores greater or equal to 40 participated in clinical interviews. Of those who were interviewed, 7 patients (23%) were confirmed to have major depression. Overall, the prevalence of major depression was 7 of 60 patients (12%; 95% CI: 5%-23%). The ZSDS and FACT-G scores had strong correlation (r   -0.75). The composite score of six statements in FACT-G were found to have sensitivity of 100% and specificity of 81% in predicting major depression, using a cut-off value of 12 (range, 0-24). The six statements were, I have a lack of energy; I feel sad; I feel nervous; I am able to enjoy life; I am sleeping well; and I am enjoying the things I usually do for fun.

Conclusions: The prevalence of major depression among all participants was 12%. The ZSDS score and FACT-G score had strong correlation; the subsets of FACT-G may be useful as a screening tool for depression.

*For a PDF of the full article, click on the link to the left of this introduction.

Objective: Although depression is prevalent among cancer patients, it remains underdiagnosed and undertreated. Quality of life is an important outcome in cancer patients and can be measured by questionnaires such as the Functional Assessment of Cancer Therapy-General version (FACT-G). The purpose of our study was to establish whether or not a group of items in FACT-G could be used as a screening tool for depression as well as for assessing quality of life.

Methods: A total of 62 chemotherapy patients (median age, 62 years [range, 22-81 years]; 55% women) completed Zung Self-Rating Depression Scale (ZSDS) and FACT-G questionnaires. Patients with ZSDS scores of 40 or more underwent clinical interviews for major depression. Pearson’s correlation was used to examine the relationship between the ZSDS and FACT-G scores. FACT-G score results were then analyzed to evaluate if subsets of the FACT-G can be used as a screening tool for major depression.

Results: In all, 30 of 62 patients (48%) had ZSDS scores less than 40 and were ruled out for major depression, and 30 of the 32 patients with ZSDS scores greater or equal to 40 participated in clinical interviews. Of those who were interviewed, 7 patients (23%) were confirmed to have major depression. Overall, the prevalence of major depression was 7 of 60 patients (12%; 95% CI: 5%-23%). The ZSDS and FACT-G scores had strong correlation (r   -0.75). The composite score of six statements in FACT-G were found to have sensitivity of 100% and specificity of 81% in predicting major depression, using a cut-off value of 12 (range, 0-24). The six statements were, I have a lack of energy; I feel sad; I feel nervous; I am able to enjoy life; I am sleeping well; and I am enjoying the things I usually do for fun.

Conclusions: The prevalence of major depression among all participants was 12%. The ZSDS score and FACT-G score had strong correlation; the subsets of FACT-G may be useful as a screening tool for depression.

*For a PDF of the full article, click on the link to the left of this introduction.

Objective: Although depression is prevalent among cancer patients, it remains underdiagnosed and undertreated. Quality of life is an important outcome in cancer patients and can be measured by questionnaires such as the Functional Assessment of Cancer Therapy-General version (FACT-G). The purpose of our study was to establish whether or not a group of items in FACT-G could be used as a screening tool for depression as well as for assessing quality of life.

Methods: A total of 62 chemotherapy patients (median age, 62 years [range, 22-81 years]; 55% women) completed Zung Self-Rating Depression Scale (ZSDS) and FACT-G questionnaires. Patients with ZSDS scores of 40 or more underwent clinical interviews for major depression. Pearson’s correlation was used to examine the relationship between the ZSDS and FACT-G scores. FACT-G score results were then analyzed to evaluate if subsets of the FACT-G can be used as a screening tool for major depression.

Results: In all, 30 of 62 patients (48%) had ZSDS scores less than 40 and were ruled out for major depression, and 30 of the 32 patients with ZSDS scores greater or equal to 40 participated in clinical interviews. Of those who were interviewed, 7 patients (23%) were confirmed to have major depression. Overall, the prevalence of major depression was 7 of 60 patients (12%; 95% CI: 5%-23%). The ZSDS and FACT-G scores had strong correlation (r   -0.75). The composite score of six statements in FACT-G were found to have sensitivity of 100% and specificity of 81% in predicting major depression, using a cut-off value of 12 (range, 0-24). The six statements were, I have a lack of energy; I feel sad; I feel nervous; I am able to enjoy life; I am sleeping well; and I am enjoying the things I usually do for fun.

Conclusions: The prevalence of major depression among all participants was 12%. The ZSDS score and FACT-G score had strong correlation; the subsets of FACT-G may be useful as a screening tool for depression.

*For a PDF of the full article, click on the link to the left of this introduction.

Several years into her hospitalist career, committee work had satisfied Sarita Satpathy, MD’s desire to positively impact patient care. Then she attended SHM’s Leadership Academy and was inspired to do more.

“I thought, ‘I want to do something and actually have a title where I can effect change,’” says Dr. Satpathy, now the hospitalist program medical director for Cogent HMG at Seton Medical Center in Daly City, Calif.

A year and a half after starting from scratch, Dr. Satpathy’s program has improved patient-care continuity, implemented 24/7 coverage, and earned buy-in from specialists, surgeons, and hospital leaders—most of whom are men.

“There aren’t as many female physician leaders, period,” says Dr. Satpathy, speaking of Seton Medical Center.

She could be talking about medicine in general.

Despite the fact that women have made up nearly half of all medical school graduates since 2005-2006 and make up 30% of the total physician population, only 16% of MD faculty at the full professor rank are female.^1,2,3 Just 11% and 13% of medical school permanent deans and department chairs are women, respectively.⁴

Beyond academia, results from surveys conducted by the American College of Healthcare Executives show that female healthcare executives are less likely to be CEOs and chief operating officers than their male counterparts. The results also indicate that the proportion of female CEOs remained fairly stable between surveys in 1990, 1995, 2000, and 2006; the proportion of female vice presidents actually decreased.⁵

This reality, experts say, undercuts America’s ability to remain at the leading edge of medical research, impedes women’s health improvements, and leaves fewer role models for future generations of physicians. In looking at why female physicians are underrepresented in leadership, key issues emerge, including unconscious bias, outdated work structures, lack of sponsorship, and conflict between the biological and professional time clocks. Although not all female doctors have faced these obstacles, many of them have and still do.

But opportunities are there—especially in HM—for female doctors to step into leadership roles. The onus is on women to seize them and on institutions to create a fertile environment for diverse leadership, physician leaders say.

Leadership Obstacles

Men often are associated with leadership by virtue of a phenomenon called unconscious bias, which posits that people identify certain genders with certain roles due to subconscious cues accumulated over time, says Hannah Valantine, MD, professor of medicine and senior associate dean for diversity and leadership at the Stanford

University School of Medicine in Palo Alto, Calif.

“These biases exist in all of us in the way we evaluate women and their work, in the way we evaluate them for leadership positions and when they’re in leadership positions, and in the thought processes that they have of their own qualifications and actions,” says Molly Carnes, MD, MS, a professor of medicine and industrial and systems engineering and co-director of the Women in Science and Engineering Leadership Institute at the University of Wisconsin at Madison.

click for large version

Bias also exists in how institutions write their job announcements, performance evaluations, and grant and award applications, Dr. Carnes explains. When such terms as “aggressive” and “risk-taking” are used, women are less likely to be seen as viable candidates, she says.

What often impedes female physicians from taking leadership roles are a lack of sponsorship and obsolete work structures that don’t reflect life in the 21st century.

“There is some thought out there that women nowadays are overmentored and undersponsored,” says Dr. Valantine, a cardiologist. “By ‘sponsored,’ we mean going that extra mile to make sure a woman is promoted into the next level of leadership and into the next level of opportunities. It’s the ‘old boys’ network,’ and, unfortunately for women, there isn’t an old girls’ network that’s as well-oiled.”

Work environments are largely designed for the single breadwinner, even though most households, including physicians, have two earners. As a result, women who seek work flexibility or work part time often are labeled as “not serious about their careers,” Dr. Valantine says. This label affects women, who begin to think they can’t pursue leadership roles because they’re working less than full time, says Rachel George, MD, MBA, CPE, FHM, chief operating officer of the West and North-Central regions and chief medical officer of the West region for Nashville, Tenn.-based Cogent HMG, the largest privately held HM and critical-care company in the nation with partnerships in more than 100 hospitals.

There’s an inherent conflict between the professional and biological time clocks in that when female hospitalists are trained, working for a few years, and ready to accept new challenges, they’re also starting families, says Kim Bell, MD, FACP, SFHM, regional medical director of the Pacific West region for Dallas-based EmCare, a company that provides outsourced physician services, including hospitalist care, in more than 500 hospitals in 40 states.

“Part of the problem is that we look at this as an all or none, that you have to be fully immersed in whatever leadership role it is, and be willing to give a tremendous amount of hours, but that’s really not true,” Dr. George says. “There are different levels of leadership. It’s OK to take it slow and do a little bit, whatever the reasoning may be.”

Dr. Carnes says many women who achieve leadership positions find themselves outside the behavioral norms assigned to women and, therefore, often confront negative reactions and perceptions that they’re disagreeable, arrogant, and superior-minded. Women sometimes get pushback from other women, too.

“When you talk to stay-at-home moms and part-time moms, I think they try and put the guilt trip on you all the time,” says Theresa Rohr-Kirchgraber, MD, board member of the American Women’s Medical Association and executive director of the National Center of Excellence in Women’s Health at Indiana University in Indianapolis.

That, in turn, often compounds the internal guilt many women feel, pitting their work and leadership goals against their responsibilities at home, she says. “There is still a big pull for women to be at home, and when you’re not, you feel guilty about it,” Dr. Rohr-Kirchgraber explains.

Good Things Don’t Come to Those Who Wait

Regardless of gender, those individuals who are known to get results, be proactive, and be part of a solution are the ones who gain the attention and, many times, have opportunities open up for advancement.

—Kay Cannon, MBA, MCC

Female hospitalists who aspire to lead must take the initiative, experts say.

“Regardless of gender, those individuals who are known to get results, be proactive, and be part of a solution are the ones who gain the attention and, many times, have opportunities open up for advancement,” says Kay Cannon, MBA, MCC, an executive leadership consultant and coach who teaches advanced courses at SHM’s Leadership Academy.

Cathleen Ammann, MD, can attest to that. A year after joining the then-fledgling hospitalist program at Wentworth-Douglass Hospital in Dover, N.H., Dr. Ammann thought she could lead it in a positive direction.

“With zero leadership experience, I went to our CMO, who was basically the administrator for our group, and said, ‘I think I could do a good job with this,’” she says. The CMO concurred, and in October 2006, Dr. Ammann took over the hospitalist program, which she continues to lead today. “They really took a chance with me, and I’m glad they did.”

Dr. Bell says HM, as a whole, has more leadership opportunities than there are trained, capable physicians to do the job—something female hospitalists can take advantage of. But it’s up to women to seize the opportunity, says Mary Jo Gorman, MD, MBA, MHM, who started her career as a hospitalist and is now CEO of Advanced ICU Care, a St. Louis-based firm that connects intensivists to hospital ICU patients via telemedicine.

“Every leadership position that I’ve been in, I got there because I was trying to solve a problem,” says Dr. Gorman, a past president of SHM. “The No. 1 mistake that women make is they don’t step up to volunteer to take responsibility for things; they expect somebody to notice their good work and ask them to lead. Culturally, that’s been shown not to be what happens and not very successful.”

The No. 1 mistake that women make is they don’t step up to volunteer to take responsibility for things; they expect somebody to notice their good work and ask them to lead. Culturally, that’s been shown not to be what happens and not very successful.

—Mary Jo Gorman, MD, MBA, MHM, CEO, Advanced ICU Care, St. Louis

Where There’s a Will, There’s a Way

Female hospitalists who are interested in leadership need to find an organization that values and encourages their employees to make meaningful contributions, Cannon says. Then they need to join projects and committees in order to develop some leadership qualities, Dr. Ammann says.

“Being involved in one or two committees initially that you strongly believe in, being active, voicing your opinion, and finding ways to find solutions─that’s where you get seen and known,” Dr. Satpathy says. “You actually gain credibility because it’s authentic.”

click for large version

The old adage “from small beginnings come great things” applies to leadership, Dr. Gorman says.

“If you can complete things regularly and successfully, if you can do that, then the next time you go to a slightly bigger project and then a bigger project and a bigger project, until you’re directing a couple hundred people,” she says.

It’s also important for female physicians to find multiple mentors, Dr. Valantine notes. “You may need a mentor that is within your own discipline who can help guide you about planning your career, writing a grant, doing a project. You might need someone else entirely different who will help you think about when is the right time for you to consider having a family, taking sabbatical, and just integrating your work with life,” she says.

Additionally, female hospitalists pursuing leadership roles must remember that every time they say “yes” to something, they’re saying “no” to something else, Cannon says.

“Too often what I see is women are so eager to please and they’re so driven to be their best, they end up saying ‘yes’ in their career. Then, all of a sudden, they arrive at a point and they say, ‘Something is really missing,’” she says. “If you can get ahead of that and think through things, it’s really going to help your planning.”

Dr. Valantine says female physicians should “take the long view” of leadership and pace themselves.

“Look at this along the entire career path and say, ‘I may not be able to do everything right now, but there might be periods of flexing up and flexing down in my career, and that’s fine,’” she says. “The important thing is to stay in it.”

Dr. Bell and others urge hospitalists who are motivated to lead to tell people in positions of authority that they’re interested; otherwise, they’re not going to be thought of when a position opens.

click for large version

Dr. Rohr-Kirchgarber has made appointments with deans, associate deans, and faculty affairs staff to introduce herself, explain her expertise, and find ways to use her skill sets in initiatives and committees that are important to the institution.

“Rather than waiting for three or four years for them to find out who I am and think about me for a committee, I need to get out there from Day One,” she says. “It’s proven to be successful.”

Drs. Ammann and Bell encourage hospitalists in community settings to approach their CMOs or other hospital administrators about their leadership aspirations. “And, of course, networking in a professional organization helps,” Dr. Satpathy says.

Meet Halfway

Female physicians can take the initiative and position themselves for leadership roles. They can acquire necessary skills by attending SHM’s Leadership Academy, management classes offered by the American College of Physicians and the American College of Physician Executives, and even adult education courses taught at business schools. But in order for them to be successful leaders, institutions must be invested in the effort.

Organizations can start by defining what they mean by “leadership.”

“‘Leader’ is actually a very abstract concept,” Dr. Carnes says. “But if you break it down into very specific activities, then I think you will get more women saying ‘yes.’ The first thing is getting women to see what leadership can allow them to do.”

There are different levels of leadership. It’s OK to take it slow and do a little bit, whatever the reasoning may be.

—Rachel George, MBA, MCC

Men—and women—also have to acknowledge they have unconscious biases, then work to change the cultural norms, she says.

“Smoking is a really good example,” Dr. Carnes explains. “It took multilevel intervention at the individual and institutional level to change the cultural norms for smoking. You have to have a clear statement by the institution endorsed by all the institutional leaders that this is an institutional priority.” Examples of priorities include eliminating male-gendered words from job announcements and performance evaluations, and ensuring a fair and open application process for leadership positions that allow female physicians to make a case for themselves, she says.

Institutions can implement structural elements to help women—and men—better manage their careers and assume leadership roles, Dr. Valantine says. These include tenure clock extension, extended maternity and family leave, short- and long-term sabbaticals, onsite childcare, and emergency backup childcare.(Read about how Stanford University’s School of Medicine encourages women to seek leadership positions at the-hospitalist.org.)

“When I give talks to women about leadership, I tell them about all the programs we’re doing. I say to them, ‘I hope that you will go out and ask for these programs to be set up in your institutions,” she says. “But, more importantly, I tell women, ‘You have a responsibility to remain standing. It’s going to be tough sometimes, but if you don’t remain standing, we won’t have the role models that we need. It’s going to be a vicious cycle. We just won’t advance and increase the numbers of women leaders.”

Lisa Ryan is a freelance writer based in New Jersey.

References

1. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Table 1. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/170248/data/2010_table1.pdf. Accessed March 2, 2012.
2. American Medical Association. Physician Characteristics and Distribution in the US. American Medical Association, 2012. 2012 ed. Chicago: American Medical Association Press; 2011.
3. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Table 4A. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/170254/data/2009_table04a.pdf. Accessed March 2, 2012.
4. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Figure 5. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/179458/data/2009_figure05.pdf. Accessed March 2, 2012.
5. American College of Healthcare Executives. A Comparison of the Career Attainments of Men and Women Healthcare Executives: 2006, Table 2. American College of Healthcare Executives website. Available at: http://www.ache.org/pubs/research/gender_study_full_report.pdf. Accessed March 2, 2012.

Several years into her hospitalist career, committee work had satisfied Sarita Satpathy, MD’s desire to positively impact patient care. Then she attended SHM’s Leadership Academy and was inspired to do more.

“I thought, ‘I want to do something and actually have a title where I can effect change,’” says Dr. Satpathy, now the hospitalist program medical director for Cogent HMG at Seton Medical Center in Daly City, Calif.

A year and a half after starting from scratch, Dr. Satpathy’s program has improved patient-care continuity, implemented 24/7 coverage, and earned buy-in from specialists, surgeons, and hospital leaders—most of whom are men.

“There aren’t as many female physician leaders, period,” says Dr. Satpathy, speaking of Seton Medical Center.

She could be talking about medicine in general.

Despite the fact that women have made up nearly half of all medical school graduates since 2005-2006 and make up 30% of the total physician population, only 16% of MD faculty at the full professor rank are female.^1,2,3 Just 11% and 13% of medical school permanent deans and department chairs are women, respectively.⁴

Beyond academia, results from surveys conducted by the American College of Healthcare Executives show that female healthcare executives are less likely to be CEOs and chief operating officers than their male counterparts. The results also indicate that the proportion of female CEOs remained fairly stable between surveys in 1990, 1995, 2000, and 2006; the proportion of female vice presidents actually decreased.⁵

This reality, experts say, undercuts America’s ability to remain at the leading edge of medical research, impedes women’s health improvements, and leaves fewer role models for future generations of physicians. In looking at why female physicians are underrepresented in leadership, key issues emerge, including unconscious bias, outdated work structures, lack of sponsorship, and conflict between the biological and professional time clocks. Although not all female doctors have faced these obstacles, many of them have and still do.

But opportunities are there—especially in HM—for female doctors to step into leadership roles. The onus is on women to seize them and on institutions to create a fertile environment for diverse leadership, physician leaders say.

Leadership Obstacles

Men often are associated with leadership by virtue of a phenomenon called unconscious bias, which posits that people identify certain genders with certain roles due to subconscious cues accumulated over time, says Hannah Valantine, MD, professor of medicine and senior associate dean for diversity and leadership at the Stanford

University School of Medicine in Palo Alto, Calif.

“These biases exist in all of us in the way we evaluate women and their work, in the way we evaluate them for leadership positions and when they’re in leadership positions, and in the thought processes that they have of their own qualifications and actions,” says Molly Carnes, MD, MS, a professor of medicine and industrial and systems engineering and co-director of the Women in Science and Engineering Leadership Institute at the University of Wisconsin at Madison.

click for large version

Bias also exists in how institutions write their job announcements, performance evaluations, and grant and award applications, Dr. Carnes explains. When such terms as “aggressive” and “risk-taking” are used, women are less likely to be seen as viable candidates, she says.

What often impedes female physicians from taking leadership roles are a lack of sponsorship and obsolete work structures that don’t reflect life in the 21st century.

“There is some thought out there that women nowadays are overmentored and undersponsored,” says Dr. Valantine, a cardiologist. “By ‘sponsored,’ we mean going that extra mile to make sure a woman is promoted into the next level of leadership and into the next level of opportunities. It’s the ‘old boys’ network,’ and, unfortunately for women, there isn’t an old girls’ network that’s as well-oiled.”

Work environments are largely designed for the single breadwinner, even though most households, including physicians, have two earners. As a result, women who seek work flexibility or work part time often are labeled as “not serious about their careers,” Dr. Valantine says. This label affects women, who begin to think they can’t pursue leadership roles because they’re working less than full time, says Rachel George, MD, MBA, CPE, FHM, chief operating officer of the West and North-Central regions and chief medical officer of the West region for Nashville, Tenn.-based Cogent HMG, the largest privately held HM and critical-care company in the nation with partnerships in more than 100 hospitals.

There’s an inherent conflict between the professional and biological time clocks in that when female hospitalists are trained, working for a few years, and ready to accept new challenges, they’re also starting families, says Kim Bell, MD, FACP, SFHM, regional medical director of the Pacific West region for Dallas-based EmCare, a company that provides outsourced physician services, including hospitalist care, in more than 500 hospitals in 40 states.

“Part of the problem is that we look at this as an all or none, that you have to be fully immersed in whatever leadership role it is, and be willing to give a tremendous amount of hours, but that’s really not true,” Dr. George says. “There are different levels of leadership. It’s OK to take it slow and do a little bit, whatever the reasoning may be.”

Dr. Carnes says many women who achieve leadership positions find themselves outside the behavioral norms assigned to women and, therefore, often confront negative reactions and perceptions that they’re disagreeable, arrogant, and superior-minded. Women sometimes get pushback from other women, too.

“When you talk to stay-at-home moms and part-time moms, I think they try and put the guilt trip on you all the time,” says Theresa Rohr-Kirchgraber, MD, board member of the American Women’s Medical Association and executive director of the National Center of Excellence in Women’s Health at Indiana University in Indianapolis.

That, in turn, often compounds the internal guilt many women feel, pitting their work and leadership goals against their responsibilities at home, she says. “There is still a big pull for women to be at home, and when you’re not, you feel guilty about it,” Dr. Rohr-Kirchgraber explains.

Good Things Don’t Come to Those Who Wait

Regardless of gender, those individuals who are known to get results, be proactive, and be part of a solution are the ones who gain the attention and, many times, have opportunities open up for advancement.

—Kay Cannon, MBA, MCC

Female hospitalists who aspire to lead must take the initiative, experts say.

“Regardless of gender, those individuals who are known to get results, be proactive, and be part of a solution are the ones who gain the attention and, many times, have opportunities open up for advancement,” says Kay Cannon, MBA, MCC, an executive leadership consultant and coach who teaches advanced courses at SHM’s Leadership Academy.

Cathleen Ammann, MD, can attest to that. A year after joining the then-fledgling hospitalist program at Wentworth-Douglass Hospital in Dover, N.H., Dr. Ammann thought she could lead it in a positive direction.

“With zero leadership experience, I went to our CMO, who was basically the administrator for our group, and said, ‘I think I could do a good job with this,’” she says. The CMO concurred, and in October 2006, Dr. Ammann took over the hospitalist program, which she continues to lead today. “They really took a chance with me, and I’m glad they did.”

Dr. Bell says HM, as a whole, has more leadership opportunities than there are trained, capable physicians to do the job—something female hospitalists can take advantage of. But it’s up to women to seize the opportunity, says Mary Jo Gorman, MD, MBA, MHM, who started her career as a hospitalist and is now CEO of Advanced ICU Care, a St. Louis-based firm that connects intensivists to hospital ICU patients via telemedicine.

“Every leadership position that I’ve been in, I got there because I was trying to solve a problem,” says Dr. Gorman, a past president of SHM. “The No. 1 mistake that women make is they don’t step up to volunteer to take responsibility for things; they expect somebody to notice their good work and ask them to lead. Culturally, that’s been shown not to be what happens and not very successful.”

The No. 1 mistake that women make is they don’t step up to volunteer to take responsibility for things; they expect somebody to notice their good work and ask them to lead. Culturally, that’s been shown not to be what happens and not very successful.

—Mary Jo Gorman, MD, MBA, MHM, CEO, Advanced ICU Care, St. Louis

Where There’s a Will, There’s a Way

Female hospitalists who are interested in leadership need to find an organization that values and encourages their employees to make meaningful contributions, Cannon says. Then they need to join projects and committees in order to develop some leadership qualities, Dr. Ammann says.

“Being involved in one or two committees initially that you strongly believe in, being active, voicing your opinion, and finding ways to find solutions─that’s where you get seen and known,” Dr. Satpathy says. “You actually gain credibility because it’s authentic.”

click for large version

The old adage “from small beginnings come great things” applies to leadership, Dr. Gorman says.

“If you can complete things regularly and successfully, if you can do that, then the next time you go to a slightly bigger project and then a bigger project and a bigger project, until you’re directing a couple hundred people,” she says.

It’s also important for female physicians to find multiple mentors, Dr. Valantine notes. “You may need a mentor that is within your own discipline who can help guide you about planning your career, writing a grant, doing a project. You might need someone else entirely different who will help you think about when is the right time for you to consider having a family, taking sabbatical, and just integrating your work with life,” she says.

Additionally, female hospitalists pursuing leadership roles must remember that every time they say “yes” to something, they’re saying “no” to something else, Cannon says.

“Too often what I see is women are so eager to please and they’re so driven to be their best, they end up saying ‘yes’ in their career. Then, all of a sudden, they arrive at a point and they say, ‘Something is really missing,’” she says. “If you can get ahead of that and think through things, it’s really going to help your planning.”

Dr. Valantine says female physicians should “take the long view” of leadership and pace themselves.

“Look at this along the entire career path and say, ‘I may not be able to do everything right now, but there might be periods of flexing up and flexing down in my career, and that’s fine,’” she says. “The important thing is to stay in it.”

Dr. Bell and others urge hospitalists who are motivated to lead to tell people in positions of authority that they’re interested; otherwise, they’re not going to be thought of when a position opens.

click for large version

Dr. Rohr-Kirchgarber has made appointments with deans, associate deans, and faculty affairs staff to introduce herself, explain her expertise, and find ways to use her skill sets in initiatives and committees that are important to the institution.

“Rather than waiting for three or four years for them to find out who I am and think about me for a committee, I need to get out there from Day One,” she says. “It’s proven to be successful.”

Drs. Ammann and Bell encourage hospitalists in community settings to approach their CMOs or other hospital administrators about their leadership aspirations. “And, of course, networking in a professional organization helps,” Dr. Satpathy says.

Meet Halfway

Female physicians can take the initiative and position themselves for leadership roles. They can acquire necessary skills by attending SHM’s Leadership Academy, management classes offered by the American College of Physicians and the American College of Physician Executives, and even adult education courses taught at business schools. But in order for them to be successful leaders, institutions must be invested in the effort.

Organizations can start by defining what they mean by “leadership.”

“‘Leader’ is actually a very abstract concept,” Dr. Carnes says. “But if you break it down into very specific activities, then I think you will get more women saying ‘yes.’ The first thing is getting women to see what leadership can allow them to do.”

There are different levels of leadership. It’s OK to take it slow and do a little bit, whatever the reasoning may be.

—Rachel George, MBA, MCC

Men—and women—also have to acknowledge they have unconscious biases, then work to change the cultural norms, she says.

“Smoking is a really good example,” Dr. Carnes explains. “It took multilevel intervention at the individual and institutional level to change the cultural norms for smoking. You have to have a clear statement by the institution endorsed by all the institutional leaders that this is an institutional priority.” Examples of priorities include eliminating male-gendered words from job announcements and performance evaluations, and ensuring a fair and open application process for leadership positions that allow female physicians to make a case for themselves, she says.

Institutions can implement structural elements to help women—and men—better manage their careers and assume leadership roles, Dr. Valantine says. These include tenure clock extension, extended maternity and family leave, short- and long-term sabbaticals, onsite childcare, and emergency backup childcare.(Read about how Stanford University’s School of Medicine encourages women to seek leadership positions at the-hospitalist.org.)

“When I give talks to women about leadership, I tell them about all the programs we’re doing. I say to them, ‘I hope that you will go out and ask for these programs to be set up in your institutions,” she says. “But, more importantly, I tell women, ‘You have a responsibility to remain standing. It’s going to be tough sometimes, but if you don’t remain standing, we won’t have the role models that we need. It’s going to be a vicious cycle. We just won’t advance and increase the numbers of women leaders.”

Lisa Ryan is a freelance writer based in New Jersey.

References

1. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Table 1. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/170248/data/2010_table1.pdf. Accessed March 2, 2012.
2. American Medical Association. Physician Characteristics and Distribution in the US. American Medical Association, 2012. 2012 ed. Chicago: American Medical Association Press; 2011.
3. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Table 4A. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/170254/data/2009_table04a.pdf. Accessed March 2, 2012.
4. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Figure 5. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/179458/data/2009_figure05.pdf. Accessed March 2, 2012.
5. American College of Healthcare Executives. A Comparison of the Career Attainments of Men and Women Healthcare Executives: 2006, Table 2. American College of Healthcare Executives website. Available at: http://www.ache.org/pubs/research/gender_study_full_report.pdf. Accessed March 2, 2012.

Several years into her hospitalist career, committee work had satisfied Sarita Satpathy, MD’s desire to positively impact patient care. Then she attended SHM’s Leadership Academy and was inspired to do more.

“I thought, ‘I want to do something and actually have a title where I can effect change,’” says Dr. Satpathy, now the hospitalist program medical director for Cogent HMG at Seton Medical Center in Daly City, Calif.

A year and a half after starting from scratch, Dr. Satpathy’s program has improved patient-care continuity, implemented 24/7 coverage, and earned buy-in from specialists, surgeons, and hospital leaders—most of whom are men.

“There aren’t as many female physician leaders, period,” says Dr. Satpathy, speaking of Seton Medical Center.

She could be talking about medicine in general.

Despite the fact that women have made up nearly half of all medical school graduates since 2005-2006 and make up 30% of the total physician population, only 16% of MD faculty at the full professor rank are female.^1,2,3 Just 11% and 13% of medical school permanent deans and department chairs are women, respectively.⁴

Beyond academia, results from surveys conducted by the American College of Healthcare Executives show that female healthcare executives are less likely to be CEOs and chief operating officers than their male counterparts. The results also indicate that the proportion of female CEOs remained fairly stable between surveys in 1990, 1995, 2000, and 2006; the proportion of female vice presidents actually decreased.⁵

This reality, experts say, undercuts America’s ability to remain at the leading edge of medical research, impedes women’s health improvements, and leaves fewer role models for future generations of physicians. In looking at why female physicians are underrepresented in leadership, key issues emerge, including unconscious bias, outdated work structures, lack of sponsorship, and conflict between the biological and professional time clocks. Although not all female doctors have faced these obstacles, many of them have and still do.

But opportunities are there—especially in HM—for female doctors to step into leadership roles. The onus is on women to seize them and on institutions to create a fertile environment for diverse leadership, physician leaders say.

Leadership Obstacles

Men often are associated with leadership by virtue of a phenomenon called unconscious bias, which posits that people identify certain genders with certain roles due to subconscious cues accumulated over time, says Hannah Valantine, MD, professor of medicine and senior associate dean for diversity and leadership at the Stanford

University School of Medicine in Palo Alto, Calif.

“These biases exist in all of us in the way we evaluate women and their work, in the way we evaluate them for leadership positions and when they’re in leadership positions, and in the thought processes that they have of their own qualifications and actions,” says Molly Carnes, MD, MS, a professor of medicine and industrial and systems engineering and co-director of the Women in Science and Engineering Leadership Institute at the University of Wisconsin at Madison.

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Bias also exists in how institutions write their job announcements, performance evaluations, and grant and award applications, Dr. Carnes explains. When such terms as “aggressive” and “risk-taking” are used, women are less likely to be seen as viable candidates, she says.

What often impedes female physicians from taking leadership roles are a lack of sponsorship and obsolete work structures that don’t reflect life in the 21st century.

“There is some thought out there that women nowadays are overmentored and undersponsored,” says Dr. Valantine, a cardiologist. “By ‘sponsored,’ we mean going that extra mile to make sure a woman is promoted into the next level of leadership and into the next level of opportunities. It’s the ‘old boys’ network,’ and, unfortunately for women, there isn’t an old girls’ network that’s as well-oiled.”

Work environments are largely designed for the single breadwinner, even though most households, including physicians, have two earners. As a result, women who seek work flexibility or work part time often are labeled as “not serious about their careers,” Dr. Valantine says. This label affects women, who begin to think they can’t pursue leadership roles because they’re working less than full time, says Rachel George, MD, MBA, CPE, FHM, chief operating officer of the West and North-Central regions and chief medical officer of the West region for Nashville, Tenn.-based Cogent HMG, the largest privately held HM and critical-care company in the nation with partnerships in more than 100 hospitals.

There’s an inherent conflict between the professional and biological time clocks in that when female hospitalists are trained, working for a few years, and ready to accept new challenges, they’re also starting families, says Kim Bell, MD, FACP, SFHM, regional medical director of the Pacific West region for Dallas-based EmCare, a company that provides outsourced physician services, including hospitalist care, in more than 500 hospitals in 40 states.

“Part of the problem is that we look at this as an all or none, that you have to be fully immersed in whatever leadership role it is, and be willing to give a tremendous amount of hours, but that’s really not true,” Dr. George says. “There are different levels of leadership. It’s OK to take it slow and do a little bit, whatever the reasoning may be.”

Dr. Carnes says many women who achieve leadership positions find themselves outside the behavioral norms assigned to women and, therefore, often confront negative reactions and perceptions that they’re disagreeable, arrogant, and superior-minded. Women sometimes get pushback from other women, too.

“When you talk to stay-at-home moms and part-time moms, I think they try and put the guilt trip on you all the time,” says Theresa Rohr-Kirchgraber, MD, board member of the American Women’s Medical Association and executive director of the National Center of Excellence in Women’s Health at Indiana University in Indianapolis.

That, in turn, often compounds the internal guilt many women feel, pitting their work and leadership goals against their responsibilities at home, she says. “There is still a big pull for women to be at home, and when you’re not, you feel guilty about it,” Dr. Rohr-Kirchgraber explains.

Good Things Don’t Come to Those Who Wait

Regardless of gender, those individuals who are known to get results, be proactive, and be part of a solution are the ones who gain the attention and, many times, have opportunities open up for advancement.

—Kay Cannon, MBA, MCC

Female hospitalists who aspire to lead must take the initiative, experts say.

“Regardless of gender, those individuals who are known to get results, be proactive, and be part of a solution are the ones who gain the attention and, many times, have opportunities open up for advancement,” says Kay Cannon, MBA, MCC, an executive leadership consultant and coach who teaches advanced courses at SHM’s Leadership Academy.

Cathleen Ammann, MD, can attest to that. A year after joining the then-fledgling hospitalist program at Wentworth-Douglass Hospital in Dover, N.H., Dr. Ammann thought she could lead it in a positive direction.

“With zero leadership experience, I went to our CMO, who was basically the administrator for our group, and said, ‘I think I could do a good job with this,’” she says. The CMO concurred, and in October 2006, Dr. Ammann took over the hospitalist program, which she continues to lead today. “They really took a chance with me, and I’m glad they did.”

Dr. Bell says HM, as a whole, has more leadership opportunities than there are trained, capable physicians to do the job—something female hospitalists can take advantage of. But it’s up to women to seize the opportunity, says Mary Jo Gorman, MD, MBA, MHM, who started her career as a hospitalist and is now CEO of Advanced ICU Care, a St. Louis-based firm that connects intensivists to hospital ICU patients via telemedicine.

“Every leadership position that I’ve been in, I got there because I was trying to solve a problem,” says Dr. Gorman, a past president of SHM. “The No. 1 mistake that women make is they don’t step up to volunteer to take responsibility for things; they expect somebody to notice their good work and ask them to lead. Culturally, that’s been shown not to be what happens and not very successful.”

The No. 1 mistake that women make is they don’t step up to volunteer to take responsibility for things; they expect somebody to notice their good work and ask them to lead. Culturally, that’s been shown not to be what happens and not very successful.

—Mary Jo Gorman, MD, MBA, MHM, CEO, Advanced ICU Care, St. Louis

Where There’s a Will, There’s a Way

Female hospitalists who are interested in leadership need to find an organization that values and encourages their employees to make meaningful contributions, Cannon says. Then they need to join projects and committees in order to develop some leadership qualities, Dr. Ammann says.

“Being involved in one or two committees initially that you strongly believe in, being active, voicing your opinion, and finding ways to find solutions─that’s where you get seen and known,” Dr. Satpathy says. “You actually gain credibility because it’s authentic.”

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The old adage “from small beginnings come great things” applies to leadership, Dr. Gorman says.

“If you can complete things regularly and successfully, if you can do that, then the next time you go to a slightly bigger project and then a bigger project and a bigger project, until you’re directing a couple hundred people,” she says.

It’s also important for female physicians to find multiple mentors, Dr. Valantine notes. “You may need a mentor that is within your own discipline who can help guide you about planning your career, writing a grant, doing a project. You might need someone else entirely different who will help you think about when is the right time for you to consider having a family, taking sabbatical, and just integrating your work with life,” she says.

Additionally, female hospitalists pursuing leadership roles must remember that every time they say “yes” to something, they’re saying “no” to something else, Cannon says.

“Too often what I see is women are so eager to please and they’re so driven to be their best, they end up saying ‘yes’ in their career. Then, all of a sudden, they arrive at a point and they say, ‘Something is really missing,’” she says. “If you can get ahead of that and think through things, it’s really going to help your planning.”

Dr. Valantine says female physicians should “take the long view” of leadership and pace themselves.

“Look at this along the entire career path and say, ‘I may not be able to do everything right now, but there might be periods of flexing up and flexing down in my career, and that’s fine,’” she says. “The important thing is to stay in it.”

Dr. Bell and others urge hospitalists who are motivated to lead to tell people in positions of authority that they’re interested; otherwise, they’re not going to be thought of when a position opens.

click for large version

Dr. Rohr-Kirchgarber has made appointments with deans, associate deans, and faculty affairs staff to introduce herself, explain her expertise, and find ways to use her skill sets in initiatives and committees that are important to the institution.

“Rather than waiting for three or four years for them to find out who I am and think about me for a committee, I need to get out there from Day One,” she says. “It’s proven to be successful.”

Drs. Ammann and Bell encourage hospitalists in community settings to approach their CMOs or other hospital administrators about their leadership aspirations. “And, of course, networking in a professional organization helps,” Dr. Satpathy says.

Meet Halfway

Female physicians can take the initiative and position themselves for leadership roles. They can acquire necessary skills by attending SHM’s Leadership Academy, management classes offered by the American College of Physicians and the American College of Physician Executives, and even adult education courses taught at business schools. But in order for them to be successful leaders, institutions must be invested in the effort.

Organizations can start by defining what they mean by “leadership.”

“‘Leader’ is actually a very abstract concept,” Dr. Carnes says. “But if you break it down into very specific activities, then I think you will get more women saying ‘yes.’ The first thing is getting women to see what leadership can allow them to do.”

There are different levels of leadership. It’s OK to take it slow and do a little bit, whatever the reasoning may be.

—Rachel George, MBA, MCC

Men—and women—also have to acknowledge they have unconscious biases, then work to change the cultural norms, she says.

“Smoking is a really good example,” Dr. Carnes explains. “It took multilevel intervention at the individual and institutional level to change the cultural norms for smoking. You have to have a clear statement by the institution endorsed by all the institutional leaders that this is an institutional priority.” Examples of priorities include eliminating male-gendered words from job announcements and performance evaluations, and ensuring a fair and open application process for leadership positions that allow female physicians to make a case for themselves, she says.

Institutions can implement structural elements to help women—and men—better manage their careers and assume leadership roles, Dr. Valantine says. These include tenure clock extension, extended maternity and family leave, short- and long-term sabbaticals, onsite childcare, and emergency backup childcare.(Read about how Stanford University’s School of Medicine encourages women to seek leadership positions at the-hospitalist.org.)

“When I give talks to women about leadership, I tell them about all the programs we’re doing. I say to them, ‘I hope that you will go out and ask for these programs to be set up in your institutions,” she says. “But, more importantly, I tell women, ‘You have a responsibility to remain standing. It’s going to be tough sometimes, but if you don’t remain standing, we won’t have the role models that we need. It’s going to be a vicious cycle. We just won’t advance and increase the numbers of women leaders.”

Lisa Ryan is a freelance writer based in New Jersey.

References

1. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Table 1. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/170248/data/2010_table1.pdf. Accessed March 2, 2012.
2. American Medical Association. Physician Characteristics and Distribution in the US. American Medical Association, 2012. 2012 ed. Chicago: American Medical Association Press; 2011.
3. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Table 4A. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/170254/data/2009_table04a.pdf. Accessed March 2, 2012.
4. Association of American Medical Colleges. Women in U.S. Academic Medicine: Statistics and Benchmarking Report 2009-2010, Figure 5. Association of American Medical Colleges website. Available at: https://www.aamc.org/download/179458/data/2009_figure05.pdf. Accessed March 2, 2012.
5. American College of Healthcare Executives. A Comparison of the Career Attainments of Men and Women Healthcare Executives: 2006, Table 2. American College of Healthcare Executives website. Available at: http://www.ache.org/pubs/research/gender_study_full_report.pdf. Accessed March 2, 2012.

The Hospitalist surveyed half a dozen infectious disease (ID) experts—some of whom also have experience as hospitalists—what they would tell a roomful of hospitalists who were curious about ID. Based on those discussions, we offer 10 tips that should help hospitalists treat their patients more effectively.

Hospitalists routinely care for patients with infections, or symptoms of infections, or suspected infections that might not even be infections at all. Many times, hospitalists have more than one treatment option. So which is the best to use? Is there a better option than the therapy that first comes to mind? What about that new antibiotic out there—is it really worth it?

All the while, hospitalists who want to practice conscientious medicine have to be careful they don’t overuse broad-spectrum antibiotics so that bugs’ resistance to the drugs is not speeded up unnecessarily.

In short, infectious diseases can be dicey terrain.

1. Prepare for the reality that the availability of new drugs is shrinking because of antibiotic resistance.

That grim fact might be cause for hospitalists to seek help from ID specialists at their hospitals, says John Bartlett, MD, professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore and founding director of the Center for Civilian Biodefense Strategies. The FDA has approved just two new drugs for major infections in the last five years, he says.

“The FDA faucet is really dry,” says Dr. Bartlett, a world-renowned speaker on ID topics and a frequent speaker at SHM annual meetings. “There are no new antibiotics to speak of, no new antibiotics for resistant bacteria. And there’s not likely to be any for several years. So [hospitalists] are going to find themselves painted in a corner, and they’ll probably have to ask for help.”

Leland Allen, MD, an infectious-disease specialist at Shelby Baptist Medical Center near Birmingham, Ala., who worked as a hospitalist for nine years, says hospitalists should not hesitate to seek assistance. “It’s never a burden to do a consult,” he says. “The reality is that it’s a lot less work if you consult early rather than waiting until the patient is sick.”

Dr. Bartlett says hospitalists should brush up on the use of colistin, a drug developed in 1959 that has been little used and requires careful dosing to avoid toxicity. “We’re finding more and more patients that that’s the only thing we’ve got for them,” he says.

If you’re going to practice 2012 medicine and infectious disease,you’ve got to know about the rapid movement in micro-biology. It’s very fast.

—John Bartlett, MD, professor of epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, founding director, Center for Civilian Biodefense Strategies

2. Familiarize yourself with new technologyfor identifying bugs.

“Mass spectrometers have been used for identifying microorganisms through a computerized database, and these units are just starting to become available to large health centers,” says Robert Orenstein, DO, associate professor of medicine in infectious diseases at the Mayo Clinic in Phoenix. “This allows you potentially to identify some of these microorganisms almost immediately—if they’re in the database, which is the key.”

Dr. Bartlett says it’s important for hospitalists to pay attention to the “dramatic changes” in the technology, including the emergence of the ppolymerase chain reaction (PCR) test.

“They have to be aware that there are methods that are very sophisticated and very sensitive and specific,” he says, adding that hospitalists have to keep up with what the methods can measure and what their limitations are.

“If you’re going to practice 2012 medicine and infectious disease, you’ve got to know about the rapid movement in microbiology,” he says. “It’s very fast.”

3. Beware the nuances of Staphylococcus aureus treatment.

James Pile, MD, FACP, SFHM, an ID specialist and interim director of hospital medicine at Case Western Reserve University/MetroHealth Medical Center in Cleveland, says an important tidbit regarding S. aureus is that when it’s isolated from blood culture, it should never be considered a contaminant; it’s the real thing.

“Any of us that have practiced for any length of time can certainly recite tales of bad outcomes when even transients. aureus bacteremia was ignored or considered a contaminant, and then patients many times were subsequently readmitted with serious complications,” he says.

He also notes that beta-lactam antibiotics continue to be the clear choice for serious methicillin-sensitive S. aureus (MSSA) infections. He says doctors should not give in to the temptation to treat these patients with vancomycin, as studies have shown better outcomes and lower mortality with beta-lactams.^1,2,3

Mass spectrometers have been used for identifying microorganisms through a computerized database, and these units are just starting to become available to large health centers.

—Robert Orenstein, DO, associate professor of medicinein infectious diseases, Mayo Clinic, Phoenix

As for methicillin-resistant. aureus (MRSA), vancomycin—long the “workhorse” in the fight against MRSA—might remain the best choice despite a series of newer, and more costly, drugs. The reason: a lack of persuasive data that show the new therapies are better, he notes.

Dr. Bartlett cautions that because of the growing resistance of MRSA, the rules for vancomycin use for MRSA are “totally new.”

“They have to know the rules,” he adds.

4. It’s important to continue to keep Clostridium difficile on your radar—it’s still a top threat.

Neil Gupta, MD, a former hospitalist who works as an epidemic intelligence service officer with Atlanta-based Centers for Disease Control and Prevention (CDC), emphasizes glove use and, if possible, immediately curtailing the use of other antibiotics for patients with suspected C. diff.

“Glove use has been proven to be one of the most effective measures at reducing transmission of C. diff,” he says, “and treatment for C. diff is less effective if a patient is on other antimicrobials.”

Dr. Orenstein says hospitalists should be familiar with the evidence-based guidelines for C. diff treatment—the use of metronidazole for mild to moderate cases, or vancomycin for severe cases.

“The practice that we see is all over the board,” Dr. Orenstein notes.

Dr. Pile offered another C. diff tip: If patients who are hospitalized or were recently hospitalized display an unexplained, marked elevation of their white blood cell count, it’s important to think about the possibility of a C. diff infection due to the organism’s predilection for causing striking leukocytosis. On occasion, this might precede, or occur in the absence of, diarrhea.

5. Take out unnecessary IV lines.

David Chansolme, MD, medical director of infection control for Integra Southwest Medical Center in Oklahoma City and a member of the Clinical Affairs Committee with the Infectious Diseases Society of America, explains that all too often the lines will be kept in during the transport of a patient to a skilled-nursing facility. It’s a practice that, he says, comes with a big risk.

“Leaving a line in just for blood draws is probably not OK,” Dr. Chansolme says. “Nowadays, you’re just seeing way too many of those infections.”

Patients headed for a skilled-nursing facility are at an especially high risk because there is such a high rate of multi-drug-resistant organisms, he says.

6. Be aware of urinary catheters, and use appropriate therapy for catheter-associated urinary tract infections (CAUTIs).

Physicians often are unaware when patients have urinary catheters, Dr. Gupta says, in part because they are frequently placed in the ED and documentation can be missing.

“It’s important to keep this on [hospitalists’] radar whenever they see a patient, so they can remember to remove these as soon as they can, when they’re no longer needed,” Dr. Gupta says, adding that timely removal can prevent an unnecessary risk of CAUTIs.

He also cautions that a third of antimicrobials used to treat CAUTIs are inappropriately aimed at treating asymptomatic bacteriuria, and hospitalists have to be sure that there truly is an infection.

7. A urine culture without a simultaneous urine analysis is practically worthless.

Once a catheter has been in for three or four days, most patients will have “all kinds of bacteria and fungus growing in their urine,” Dr. Allen says.

“A urinalysis lets you assess for the presence of pyuria or other signs of urinary tract inflammation,” he says. “That’s how you determine whether a germ growing in the urine is a colonizer or a true pathogen.”

8. Bactrim does not treat strep.

“If you have somebody that maybe has been in the hospital on vancomycin because they have cellulitis and are getting better and ready to go home, if you don’t know if that cellulitis is staph or strep, be careful about the agent that you choose to send them home on,” Dr. Chansolme says. “Make sure it has activity against Streptococcus.”

He frequently sees patients de-escalated to the wrong drug—trimethoprim/sulfamethoxazole (Bactrim).

“They’ll go home, and a couple days later they’ll be back because it was in fact a strep infection, not a staph infection,” he says. “If you’re not sure, it’s probably better to use something like doxycycline or clindamycin, or something along those lines, that will treat both.”

9. Be sure to take proper precautions when it comes to norovirus.

Winter is the time of year to be most concerned about norovirus outbreaks. It’s also important to realize it affects people of all ages, is especially common to closed or semi-closed communities (i.e. hospitals, long-term care facilities, cruise ships), and spreads very rapidly either by person-to-person transmission or contaminated food.

“It’s really important to understand that if a patient is suspected of having norovirus, that patient should be placed in contact precautions immediately, and preferably, when possible, in a single-occupancy room,” Dr. Gupta says. “If a healthcare provider becomes ill with sudden nausea, vomiting, or diarrhea, that’s consistent with possible norovirus. They should stay home for a minimum of 48 hours after symptom resolution before coming back to work.”

And because norovirus is so contagious, quick action has to be taken if such an outbreak is suspected.

“If there’s any concern at all in your facility,” he says, “get in touch with an infection prevention committee to make sue all appropriate measures are taken.”

10. Never swab a decubitus ulcer unless that ulcer is clearly infected.

Dr. Allen says it’s important to know that it doesn’t make sense to culture an ulcer that doesn’t have any signs of infection, such as pus or redness—although he sees it happen routinely.

“Just because a patient has a bedsore doesn’t mean it’s infected,” Dr. Allen says. “Usually, they’re not infected. But they’re going to have a dozen different germs growing in them.”

Culturing and treatment without signs of infection, he says, often leads to “inappropriate antibiotic use and probably increased length of stay."

Tom Collins is a freelance writer in South Florida

References

1. Kim SH, Kim KH, Kim HB, et al. Outcome of vancomycin treatment in patients with methicillin-susceptible Staphylococcus aureus bacteremia. Antimicrob Agents Chemother. 2008;52(1):192-197.
2. González C, Rubio M, Romero-Vivas J, González M, Picazo JJ.. Bacteremic pneumonia due to Staphylococcus aureus: A comparison of disease caused by methicillin-resistant and methicillin-susceptible organisms. Clin Infect Dis. 1999;29(5):1171-1177.
3. Stryjewski ME, Szczech LA, Benjamin DK Jr., et al. Use of vancomycin or first-generation cephalosporins for the treatment of hemodialysis-dependent patients with methicillin-susceptible Staphylococcus aureus bacteremia. Clin Infect Dis. 2007;44(2):190-196.

The Hospitalist surveyed half a dozen infectious disease (ID) experts—some of whom also have experience as hospitalists—what they would tell a roomful of hospitalists who were curious about ID. Based on those discussions, we offer 10 tips that should help hospitalists treat their patients more effectively.

Hospitalists routinely care for patients with infections, or symptoms of infections, or suspected infections that might not even be infections at all. Many times, hospitalists have more than one treatment option. So which is the best to use? Is there a better option than the therapy that first comes to mind? What about that new antibiotic out there—is it really worth it?

All the while, hospitalists who want to practice conscientious medicine have to be careful they don’t overuse broad-spectrum antibiotics so that bugs’ resistance to the drugs is not speeded up unnecessarily.

In short, infectious diseases can be dicey terrain.

1. Prepare for the reality that the availability of new drugs is shrinking because of antibiotic resistance.

That grim fact might be cause for hospitalists to seek help from ID specialists at their hospitals, says John Bartlett, MD, professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore and founding director of the Center for Civilian Biodefense Strategies. The FDA has approved just two new drugs for major infections in the last five years, he says.

“The FDA faucet is really dry,” says Dr. Bartlett, a world-renowned speaker on ID topics and a frequent speaker at SHM annual meetings. “There are no new antibiotics to speak of, no new antibiotics for resistant bacteria. And there’s not likely to be any for several years. So [hospitalists] are going to find themselves painted in a corner, and they’ll probably have to ask for help.”

Leland Allen, MD, an infectious-disease specialist at Shelby Baptist Medical Center near Birmingham, Ala., who worked as a hospitalist for nine years, says hospitalists should not hesitate to seek assistance. “It’s never a burden to do a consult,” he says. “The reality is that it’s a lot less work if you consult early rather than waiting until the patient is sick.”

Dr. Bartlett says hospitalists should brush up on the use of colistin, a drug developed in 1959 that has been little used and requires careful dosing to avoid toxicity. “We’re finding more and more patients that that’s the only thing we’ve got for them,” he says.

If you’re going to practice 2012 medicine and infectious disease,you’ve got to know about the rapid movement in micro-biology. It’s very fast.

—John Bartlett, MD, professor of epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, founding director, Center for Civilian Biodefense Strategies

2. Familiarize yourself with new technologyfor identifying bugs.

“Mass spectrometers have been used for identifying microorganisms through a computerized database, and these units are just starting to become available to large health centers,” says Robert Orenstein, DO, associate professor of medicine in infectious diseases at the Mayo Clinic in Phoenix. “This allows you potentially to identify some of these microorganisms almost immediately—if they’re in the database, which is the key.”

Dr. Bartlett says it’s important for hospitalists to pay attention to the “dramatic changes” in the technology, including the emergence of the ppolymerase chain reaction (PCR) test.

“They have to be aware that there are methods that are very sophisticated and very sensitive and specific,” he says, adding that hospitalists have to keep up with what the methods can measure and what their limitations are.

“If you’re going to practice 2012 medicine and infectious disease, you’ve got to know about the rapid movement in microbiology,” he says. “It’s very fast.”

3. Beware the nuances of Staphylococcus aureus treatment.

James Pile, MD, FACP, SFHM, an ID specialist and interim director of hospital medicine at Case Western Reserve University/MetroHealth Medical Center in Cleveland, says an important tidbit regarding S. aureus is that when it’s isolated from blood culture, it should never be considered a contaminant; it’s the real thing.

“Any of us that have practiced for any length of time can certainly recite tales of bad outcomes when even transients. aureus bacteremia was ignored or considered a contaminant, and then patients many times were subsequently readmitted with serious complications,” he says.

He also notes that beta-lactam antibiotics continue to be the clear choice for serious methicillin-sensitive S. aureus (MSSA) infections. He says doctors should not give in to the temptation to treat these patients with vancomycin, as studies have shown better outcomes and lower mortality with beta-lactams.^1,2,3

Mass spectrometers have been used for identifying microorganisms through a computerized database, and these units are just starting to become available to large health centers.

—Robert Orenstein, DO, associate professor of medicinein infectious diseases, Mayo Clinic, Phoenix

As for methicillin-resistant. aureus (MRSA), vancomycin—long the “workhorse” in the fight against MRSA—might remain the best choice despite a series of newer, and more costly, drugs. The reason: a lack of persuasive data that show the new therapies are better, he notes.

Dr. Bartlett cautions that because of the growing resistance of MRSA, the rules for vancomycin use for MRSA are “totally new.”

“They have to know the rules,” he adds.

4. It’s important to continue to keep Clostridium difficile on your radar—it’s still a top threat.

Neil Gupta, MD, a former hospitalist who works as an epidemic intelligence service officer with Atlanta-based Centers for Disease Control and Prevention (CDC), emphasizes glove use and, if possible, immediately curtailing the use of other antibiotics for patients with suspected C. diff.

“Glove use has been proven to be one of the most effective measures at reducing transmission of C. diff,” he says, “and treatment for C. diff is less effective if a patient is on other antimicrobials.”

Dr. Orenstein says hospitalists should be familiar with the evidence-based guidelines for C. diff treatment—the use of metronidazole for mild to moderate cases, or vancomycin for severe cases.

“The practice that we see is all over the board,” Dr. Orenstein notes.

Dr. Pile offered another C. diff tip: If patients who are hospitalized or were recently hospitalized display an unexplained, marked elevation of their white blood cell count, it’s important to think about the possibility of a C. diff infection due to the organism’s predilection for causing striking leukocytosis. On occasion, this might precede, or occur in the absence of, diarrhea.

5. Take out unnecessary IV lines.

David Chansolme, MD, medical director of infection control for Integra Southwest Medical Center in Oklahoma City and a member of the Clinical Affairs Committee with the Infectious Diseases Society of America, explains that all too often the lines will be kept in during the transport of a patient to a skilled-nursing facility. It’s a practice that, he says, comes with a big risk.

“Leaving a line in just for blood draws is probably not OK,” Dr. Chansolme says. “Nowadays, you’re just seeing way too many of those infections.”

Patients headed for a skilled-nursing facility are at an especially high risk because there is such a high rate of multi-drug-resistant organisms, he says.

6. Be aware of urinary catheters, and use appropriate therapy for catheter-associated urinary tract infections (CAUTIs).

Physicians often are unaware when patients have urinary catheters, Dr. Gupta says, in part because they are frequently placed in the ED and documentation can be missing.

“It’s important to keep this on [hospitalists’] radar whenever they see a patient, so they can remember to remove these as soon as they can, when they’re no longer needed,” Dr. Gupta says, adding that timely removal can prevent an unnecessary risk of CAUTIs.

He also cautions that a third of antimicrobials used to treat CAUTIs are inappropriately aimed at treating asymptomatic bacteriuria, and hospitalists have to be sure that there truly is an infection.

7. A urine culture without a simultaneous urine analysis is practically worthless.

Once a catheter has been in for three or four days, most patients will have “all kinds of bacteria and fungus growing in their urine,” Dr. Allen says.

“A urinalysis lets you assess for the presence of pyuria or other signs of urinary tract inflammation,” he says. “That’s how you determine whether a germ growing in the urine is a colonizer or a true pathogen.”

8. Bactrim does not treat strep.

“If you have somebody that maybe has been in the hospital on vancomycin because they have cellulitis and are getting better and ready to go home, if you don’t know if that cellulitis is staph or strep, be careful about the agent that you choose to send them home on,” Dr. Chansolme says. “Make sure it has activity against Streptococcus.”

He frequently sees patients de-escalated to the wrong drug—trimethoprim/sulfamethoxazole (Bactrim).

“They’ll go home, and a couple days later they’ll be back because it was in fact a strep infection, not a staph infection,” he says. “If you’re not sure, it’s probably better to use something like doxycycline or clindamycin, or something along those lines, that will treat both.”

9. Be sure to take proper precautions when it comes to norovirus.

Winter is the time of year to be most concerned about norovirus outbreaks. It’s also important to realize it affects people of all ages, is especially common to closed or semi-closed communities (i.e. hospitals, long-term care facilities, cruise ships), and spreads very rapidly either by person-to-person transmission or contaminated food.

“It’s really important to understand that if a patient is suspected of having norovirus, that patient should be placed in contact precautions immediately, and preferably, when possible, in a single-occupancy room,” Dr. Gupta says. “If a healthcare provider becomes ill with sudden nausea, vomiting, or diarrhea, that’s consistent with possible norovirus. They should stay home for a minimum of 48 hours after symptom resolution before coming back to work.”

And because norovirus is so contagious, quick action has to be taken if such an outbreak is suspected.

“If there’s any concern at all in your facility,” he says, “get in touch with an infection prevention committee to make sue all appropriate measures are taken.”

10. Never swab a decubitus ulcer unless that ulcer is clearly infected.

Dr. Allen says it’s important to know that it doesn’t make sense to culture an ulcer that doesn’t have any signs of infection, such as pus or redness—although he sees it happen routinely.

“Just because a patient has a bedsore doesn’t mean it’s infected,” Dr. Allen says. “Usually, they’re not infected. But they’re going to have a dozen different germs growing in them.”

Culturing and treatment without signs of infection, he says, often leads to “inappropriate antibiotic use and probably increased length of stay."

Tom Collins is a freelance writer in South Florida

References

1. Kim SH, Kim KH, Kim HB, et al. Outcome of vancomycin treatment in patients with methicillin-susceptible Staphylococcus aureus bacteremia. Antimicrob Agents Chemother. 2008;52(1):192-197.
2. González C, Rubio M, Romero-Vivas J, González M, Picazo JJ.. Bacteremic pneumonia due to Staphylococcus aureus: A comparison of disease caused by methicillin-resistant and methicillin-susceptible organisms. Clin Infect Dis. 1999;29(5):1171-1177.
3. Stryjewski ME, Szczech LA, Benjamin DK Jr., et al. Use of vancomycin or first-generation cephalosporins for the treatment of hemodialysis-dependent patients with methicillin-susceptible Staphylococcus aureus bacteremia. Clin Infect Dis. 2007;44(2):190-196.

The Hospitalist surveyed half a dozen infectious disease (ID) experts—some of whom also have experience as hospitalists—what they would tell a roomful of hospitalists who were curious about ID. Based on those discussions, we offer 10 tips that should help hospitalists treat their patients more effectively.

Hospitalists routinely care for patients with infections, or symptoms of infections, or suspected infections that might not even be infections at all. Many times, hospitalists have more than one treatment option. So which is the best to use? Is there a better option than the therapy that first comes to mind? What about that new antibiotic out there—is it really worth it?

All the while, hospitalists who want to practice conscientious medicine have to be careful they don’t overuse broad-spectrum antibiotics so that bugs’ resistance to the drugs is not speeded up unnecessarily.

In short, infectious diseases can be dicey terrain.

1. Prepare for the reality that the availability of new drugs is shrinking because of antibiotic resistance.

That grim fact might be cause for hospitalists to seek help from ID specialists at their hospitals, says John Bartlett, MD, professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore and founding director of the Center for Civilian Biodefense Strategies. The FDA has approved just two new drugs for major infections in the last five years, he says.

“The FDA faucet is really dry,” says Dr. Bartlett, a world-renowned speaker on ID topics and a frequent speaker at SHM annual meetings. “There are no new antibiotics to speak of, no new antibiotics for resistant bacteria. And there’s not likely to be any for several years. So [hospitalists] are going to find themselves painted in a corner, and they’ll probably have to ask for help.”

Leland Allen, MD, an infectious-disease specialist at Shelby Baptist Medical Center near Birmingham, Ala., who worked as a hospitalist for nine years, says hospitalists should not hesitate to seek assistance. “It’s never a burden to do a consult,” he says. “The reality is that it’s a lot less work if you consult early rather than waiting until the patient is sick.”

Dr. Bartlett says hospitalists should brush up on the use of colistin, a drug developed in 1959 that has been little used and requires careful dosing to avoid toxicity. “We’re finding more and more patients that that’s the only thing we’ve got for them,” he says.

If you’re going to practice 2012 medicine and infectious disease,you’ve got to know about the rapid movement in micro-biology. It’s very fast.

—John Bartlett, MD, professor of epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, founding director, Center for Civilian Biodefense Strategies

2. Familiarize yourself with new technologyfor identifying bugs.

“Mass spectrometers have been used for identifying microorganisms through a computerized database, and these units are just starting to become available to large health centers,” says Robert Orenstein, DO, associate professor of medicine in infectious diseases at the Mayo Clinic in Phoenix. “This allows you potentially to identify some of these microorganisms almost immediately—if they’re in the database, which is the key.”

Dr. Bartlett says it’s important for hospitalists to pay attention to the “dramatic changes” in the technology, including the emergence of the ppolymerase chain reaction (PCR) test.

“They have to be aware that there are methods that are very sophisticated and very sensitive and specific,” he says, adding that hospitalists have to keep up with what the methods can measure and what their limitations are.

“If you’re going to practice 2012 medicine and infectious disease, you’ve got to know about the rapid movement in microbiology,” he says. “It’s very fast.”

3. Beware the nuances of Staphylococcus aureus treatment.

James Pile, MD, FACP, SFHM, an ID specialist and interim director of hospital medicine at Case Western Reserve University/MetroHealth Medical Center in Cleveland, says an important tidbit regarding S. aureus is that when it’s isolated from blood culture, it should never be considered a contaminant; it’s the real thing.

“Any of us that have practiced for any length of time can certainly recite tales of bad outcomes when even transients. aureus bacteremia was ignored or considered a contaminant, and then patients many times were subsequently readmitted with serious complications,” he says.

He also notes that beta-lactam antibiotics continue to be the clear choice for serious methicillin-sensitive S. aureus (MSSA) infections. He says doctors should not give in to the temptation to treat these patients with vancomycin, as studies have shown better outcomes and lower mortality with beta-lactams.^1,2,3

Mass spectrometers have been used for identifying microorganisms through a computerized database, and these units are just starting to become available to large health centers.

—Robert Orenstein, DO, associate professor of medicinein infectious diseases, Mayo Clinic, Phoenix

As for methicillin-resistant. aureus (MRSA), vancomycin—long the “workhorse” in the fight against MRSA—might remain the best choice despite a series of newer, and more costly, drugs. The reason: a lack of persuasive data that show the new therapies are better, he notes.

Dr. Bartlett cautions that because of the growing resistance of MRSA, the rules for vancomycin use for MRSA are “totally new.”

“They have to know the rules,” he adds.

4. It’s important to continue to keep Clostridium difficile on your radar—it’s still a top threat.

Neil Gupta, MD, a former hospitalist who works as an epidemic intelligence service officer with Atlanta-based Centers for Disease Control and Prevention (CDC), emphasizes glove use and, if possible, immediately curtailing the use of other antibiotics for patients with suspected C. diff.

“Glove use has been proven to be one of the most effective measures at reducing transmission of C. diff,” he says, “and treatment for C. diff is less effective if a patient is on other antimicrobials.”

Dr. Orenstein says hospitalists should be familiar with the evidence-based guidelines for C. diff treatment—the use of metronidazole for mild to moderate cases, or vancomycin for severe cases.

“The practice that we see is all over the board,” Dr. Orenstein notes.

Dr. Pile offered another C. diff tip: If patients who are hospitalized or were recently hospitalized display an unexplained, marked elevation of their white blood cell count, it’s important to think about the possibility of a C. diff infection due to the organism’s predilection for causing striking leukocytosis. On occasion, this might precede, or occur in the absence of, diarrhea.

5. Take out unnecessary IV lines.

David Chansolme, MD, medical director of infection control for Integra Southwest Medical Center in Oklahoma City and a member of the Clinical Affairs Committee with the Infectious Diseases Society of America, explains that all too often the lines will be kept in during the transport of a patient to a skilled-nursing facility. It’s a practice that, he says, comes with a big risk.

“Leaving a line in just for blood draws is probably not OK,” Dr. Chansolme says. “Nowadays, you’re just seeing way too many of those infections.”

Patients headed for a skilled-nursing facility are at an especially high risk because there is such a high rate of multi-drug-resistant organisms, he says.

6. Be aware of urinary catheters, and use appropriate therapy for catheter-associated urinary tract infections (CAUTIs).

Physicians often are unaware when patients have urinary catheters, Dr. Gupta says, in part because they are frequently placed in the ED and documentation can be missing.

“It’s important to keep this on [hospitalists’] radar whenever they see a patient, so they can remember to remove these as soon as they can, when they’re no longer needed,” Dr. Gupta says, adding that timely removal can prevent an unnecessary risk of CAUTIs.

He also cautions that a third of antimicrobials used to treat CAUTIs are inappropriately aimed at treating asymptomatic bacteriuria, and hospitalists have to be sure that there truly is an infection.

7. A urine culture without a simultaneous urine analysis is practically worthless.

Once a catheter has been in for three or four days, most patients will have “all kinds of bacteria and fungus growing in their urine,” Dr. Allen says.

“A urinalysis lets you assess for the presence of pyuria or other signs of urinary tract inflammation,” he says. “That’s how you determine whether a germ growing in the urine is a colonizer or a true pathogen.”

8. Bactrim does not treat strep.

“If you have somebody that maybe has been in the hospital on vancomycin because they have cellulitis and are getting better and ready to go home, if you don’t know if that cellulitis is staph or strep, be careful about the agent that you choose to send them home on,” Dr. Chansolme says. “Make sure it has activity against Streptococcus.”

He frequently sees patients de-escalated to the wrong drug—trimethoprim/sulfamethoxazole (Bactrim).

“They’ll go home, and a couple days later they’ll be back because it was in fact a strep infection, not a staph infection,” he says. “If you’re not sure, it’s probably better to use something like doxycycline or clindamycin, or something along those lines, that will treat both.”

9. Be sure to take proper precautions when it comes to norovirus.

Winter is the time of year to be most concerned about norovirus outbreaks. It’s also important to realize it affects people of all ages, is especially common to closed or semi-closed communities (i.e. hospitals, long-term care facilities, cruise ships), and spreads very rapidly either by person-to-person transmission or contaminated food.

“It’s really important to understand that if a patient is suspected of having norovirus, that patient should be placed in contact precautions immediately, and preferably, when possible, in a single-occupancy room,” Dr. Gupta says. “If a healthcare provider becomes ill with sudden nausea, vomiting, or diarrhea, that’s consistent with possible norovirus. They should stay home for a minimum of 48 hours after symptom resolution before coming back to work.”

And because norovirus is so contagious, quick action has to be taken if such an outbreak is suspected.

“If there’s any concern at all in your facility,” he says, “get in touch with an infection prevention committee to make sue all appropriate measures are taken.”

10. Never swab a decubitus ulcer unless that ulcer is clearly infected.

Dr. Allen says it’s important to know that it doesn’t make sense to culture an ulcer that doesn’t have any signs of infection, such as pus or redness—although he sees it happen routinely.

“Just because a patient has a bedsore doesn’t mean it’s infected,” Dr. Allen says. “Usually, they’re not infected. But they’re going to have a dozen different germs growing in them.”

Culturing and treatment without signs of infection, he says, often leads to “inappropriate antibiotic use and probably increased length of stay."

Tom Collins is a freelance writer in South Florida

References

1. Kim SH, Kim KH, Kim HB, et al. Outcome of vancomycin treatment in patients with methicillin-susceptible Staphylococcus aureus bacteremia. Antimicrob Agents Chemother. 2008;52(1):192-197.
2. González C, Rubio M, Romero-Vivas J, González M, Picazo JJ.. Bacteremic pneumonia due to Staphylococcus aureus: A comparison of disease caused by methicillin-resistant and methicillin-susceptible organisms. Clin Infect Dis. 1999;29(5):1171-1177.
3. Stryjewski ME, Szczech LA, Benjamin DK Jr., et al. Use of vancomycin or first-generation cephalosporins for the treatment of hemodialysis-dependent patients with methicillin-susceptible Staphylococcus aureus bacteremia. Clin Infect Dis. 2007;44(2):190-196.

We’re going to celebrate in San Diego with everybody, but once the [annual] meeting is over, we’re going to roll up our sleeves. There’s a heck of a lot more work to get done.

—Joseph Ming-Wah Li, MD, SFHM, SHM president

Hospitalist Jordan Messler, MD, SFHM, has experienced SHM’s mentored-implementation program as both mentee and mentor. So when he heard that the mentored-implementation model was named the winner of the 2011 John M. Eisenberg Innovation in Patient Safety and Quality at the National Level Award, he knew it was well-earned.

“The biggest aspect of these programs has been the collegiality and the learning from others,” says Dr. Messler, medical director at Morton Plant Hospital in Clearwater, Fla. “That’s really the core of this. We’ve all felt that we’re out on an island and we’re all building these projects from the ground up. We all probably at one point in a meeting say, ‘Someone else must have solved this.’ ... These mentored-implementation programs say, ‘Yes, of course other folks have solved this.’”

SHM is the first professional society to earn the award, bestowed by the National Quality Forum (NQF) and The Joint Commission. The model has helped propel SHM’s Glycemic Control Mentored Implementation (GCMI) Program, Project BOOST (Better Outcomes for Older Adults through Safe Transitions), and the VTE Prevention Collaborative. Mentors have been put in place in more than 300 hospitals in the U.S. and Canada, according to an announcement.

“There are significant congratulations [due] to the profession and all the people at the society who have done all the work on this,” says SHM president Joseph Ming-Wah Li, MD, SFHM. “Part of what we’ve been saying all along is that quality is important. In terms of teaching quality—it’s a real team effort.”

NQF president and chief executive Janet Corrigan, PhD, MBA, says that one of the hallmarks of SHM’s program is its ability to be applied to different quality initiatives. Corrigan adds that while a professional society had never previously won the national award, SHM’s execution in creating, implementing, and providing follow-up resources helped differentiate the construct.

“We want to shed light on the kinds of things that are working and encourage others to emulate them, to build on them, and to reinvent them in new and even better ways,” Corrigan says. “It is a whole process of quality improvement.”

Dr. Li says the honor is a milestone for SHM, but the society must not rest on its laurels because it “hit a home run.” Instead, the society should use the momentum of the award to push for and apply for more QI programs. The more successful programs the society and its members launch and successfully implement, the more HM as a field will be considered a leader in quality improvement, he adds.

“We’re an absolute infant compared to many other medical organizations and other medical societies,” Dr. Li says. “Hospitalists and SHM should be very proud that NQF and The Joint Commission chose to bestow this award onto SHM. But at the end of the day, we at SHM also recognize that this is an award. We’re going to celebrate in San Diego with everybody, but once the [annual] meeting is over, we’re going to roll up our sleeves. There’s a heck of a lot more work to get done.”

Richard Quinn is a freelance writer based in New Jersey.

We’re going to celebrate in San Diego with everybody, but once the [annual] meeting is over, we’re going to roll up our sleeves. There’s a heck of a lot more work to get done.

—Joseph Ming-Wah Li, MD, SFHM, SHM president

Hospitalist Jordan Messler, MD, SFHM, has experienced SHM’s mentored-implementation program as both mentee and mentor. So when he heard that the mentored-implementation model was named the winner of the 2011 John M. Eisenberg Innovation in Patient Safety and Quality at the National Level Award, he knew it was well-earned.

“The biggest aspect of these programs has been the collegiality and the learning from others,” says Dr. Messler, medical director at Morton Plant Hospital in Clearwater, Fla. “That’s really the core of this. We’ve all felt that we’re out on an island and we’re all building these projects from the ground up. We all probably at one point in a meeting say, ‘Someone else must have solved this.’ ... These mentored-implementation programs say, ‘Yes, of course other folks have solved this.’”

SHM is the first professional society to earn the award, bestowed by the National Quality Forum (NQF) and The Joint Commission. The model has helped propel SHM’s Glycemic Control Mentored Implementation (GCMI) Program, Project BOOST (Better Outcomes for Older Adults through Safe Transitions), and the VTE Prevention Collaborative. Mentors have been put in place in more than 300 hospitals in the U.S. and Canada, according to an announcement.

“There are significant congratulations [due] to the profession and all the people at the society who have done all the work on this,” says SHM president Joseph Ming-Wah Li, MD, SFHM. “Part of what we’ve been saying all along is that quality is important. In terms of teaching quality—it’s a real team effort.”

NQF president and chief executive Janet Corrigan, PhD, MBA, says that one of the hallmarks of SHM’s program is its ability to be applied to different quality initiatives. Corrigan adds that while a professional society had never previously won the national award, SHM’s execution in creating, implementing, and providing follow-up resources helped differentiate the construct.

“We want to shed light on the kinds of things that are working and encourage others to emulate them, to build on them, and to reinvent them in new and even better ways,” Corrigan says. “It is a whole process of quality improvement.”

Dr. Li says the honor is a milestone for SHM, but the society must not rest on its laurels because it “hit a home run.” Instead, the society should use the momentum of the award to push for and apply for more QI programs. The more successful programs the society and its members launch and successfully implement, the more HM as a field will be considered a leader in quality improvement, he adds.

“We’re an absolute infant compared to many other medical organizations and other medical societies,” Dr. Li says. “Hospitalists and SHM should be very proud that NQF and The Joint Commission chose to bestow this award onto SHM. But at the end of the day, we at SHM also recognize that this is an award. We’re going to celebrate in San Diego with everybody, but once the [annual] meeting is over, we’re going to roll up our sleeves. There’s a heck of a lot more work to get done.”

Richard Quinn is a freelance writer based in New Jersey.

We’re going to celebrate in San Diego with everybody, but once the [annual] meeting is over, we’re going to roll up our sleeves. There’s a heck of a lot more work to get done.

—Joseph Ming-Wah Li, MD, SFHM, SHM president

Hospitalist Jordan Messler, MD, SFHM, has experienced SHM’s mentored-implementation program as both mentee and mentor. So when he heard that the mentored-implementation model was named the winner of the 2011 John M. Eisenberg Innovation in Patient Safety and Quality at the National Level Award, he knew it was well-earned.

“The biggest aspect of these programs has been the collegiality and the learning from others,” says Dr. Messler, medical director at Morton Plant Hospital in Clearwater, Fla. “That’s really the core of this. We’ve all felt that we’re out on an island and we’re all building these projects from the ground up. We all probably at one point in a meeting say, ‘Someone else must have solved this.’ ... These mentored-implementation programs say, ‘Yes, of course other folks have solved this.’”

SHM is the first professional society to earn the award, bestowed by the National Quality Forum (NQF) and The Joint Commission. The model has helped propel SHM’s Glycemic Control Mentored Implementation (GCMI) Program, Project BOOST (Better Outcomes for Older Adults through Safe Transitions), and the VTE Prevention Collaborative. Mentors have been put in place in more than 300 hospitals in the U.S. and Canada, according to an announcement.

“There are significant congratulations [due] to the profession and all the people at the society who have done all the work on this,” says SHM president Joseph Ming-Wah Li, MD, SFHM. “Part of what we’ve been saying all along is that quality is important. In terms of teaching quality—it’s a real team effort.”

NQF president and chief executive Janet Corrigan, PhD, MBA, says that one of the hallmarks of SHM’s program is its ability to be applied to different quality initiatives. Corrigan adds that while a professional society had never previously won the national award, SHM’s execution in creating, implementing, and providing follow-up resources helped differentiate the construct.

“We want to shed light on the kinds of things that are working and encourage others to emulate them, to build on them, and to reinvent them in new and even better ways,” Corrigan says. “It is a whole process of quality improvement.”

Dr. Li says the honor is a milestone for SHM, but the society must not rest on its laurels because it “hit a home run.” Instead, the society should use the momentum of the award to push for and apply for more QI programs. The more successful programs the society and its members launch and successfully implement, the more HM as a field will be considered a leader in quality improvement, he adds.

“We’re an absolute infant compared to many other medical organizations and other medical societies,” Dr. Li says. “Hospitalists and SHM should be very proud that NQF and The Joint Commission chose to bestow this award onto SHM. But at the end of the day, we at SHM also recognize that this is an award. We’re going to celebrate in San Diego with everybody, but once the [annual] meeting is over, we’re going to roll up our sleeves. There’s a heck of a lot more work to get done.”

Richard Quinn is a freelance writer based in New Jersey.