The bedtime solution

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The bedtime solution

CASE: Refractory depression

Ms. W, age 38, is brought to the emergency department after her son finds her unresponsive and calls 911. Suffering from worsening depression, she wrote a note telling her children goodbye, and overdosed on zolpidem from an old prescription and her daughter’s opioids. After being evaluated and medically cleared in the emergency department, Ms. W was admitted to the psychiatric unit.

Ms. W has a history of recurrent major depressive disorder that developed after she was sexually abused by a relative as a teen. She also has bulimia nervosa, alcohol dependence, and posttraumatic stress disorder. She was hospitalized twice for depression and suicidality but had not previously attempted suicide. In the mid-to-late 1990s, she had trials of paroxetine, clomipramine, lithium, and bupropion.

She was seen regularly in our outpatient psychiatry clinic for medication management and supportive psychotherapy. Since being followed in our clinic starting in early 2005, she has had the following medication trials:

  • fluoxetine, citalopram, venlafaxine XR, and duloxetine for depression
  • atomoxetine, buspirone, liothyronine, risperidone, and aripiprazole for antidepressant augmentation
  • lorazepam, clonazepam, and gabapentin for anxiety
  • zolpidem and trazodone for insomnia
  • nortriptyline for migraine headache prophylaxis.

Some medications were not tolerated, primarily because of increased anxiety. Those that were tolerated were adequate trials in terms of dose titration and length. High-dose fluoxetine (80 mg/d) augmented by risperidone (0.375 to 0.5 mg/d) produced the most reliable and significant improvement.

Ms. W had 2 courses of electroconvulsive therapy (ECT) totaling 30 treatments—most recently in 2007—that resulted in significant memory loss with limited benefit. Premenstrual worsening of depression and suicidality were noted. In collaboration with her gynecologist, Ms. W was treated with a 3-month trial of leuprolide to suppress her ovarian axis, which was helpful. In 2008 she underwent bilateral oophorectomy. She has not had symptoms of mood elevation or psychosis. Family history includes schizophrenia, depression, anxiety, and alcoholism.

In the months before hospitalization, Ms. W had been increasingly depressed and intermittently suicidal, although she did not endorse a specific plan or intention to harm herself because she was concerned about the impact suicide would have on her children. Weight gain with risperidone had reactivated body image issues, so Ms. W stopped taking this medication 2 weeks before hospitalization. Her depression became worse, and she began using her husband’s hydrocodone/acetaminophen prescription.

The authors’ observations

Approximately 40% of patients with major depression fail to respond to an initial antidepressant trial.1 An additional 50% of these patients will be treatment-resistant to a subsequent antidepressant.1 Patients may be progressively less likely to respond to additional medication trials.2

One of the most rapid-acting and effective treatments for unipolar and bipolar depression is sleep deprivation. Wirz-Justice et al3 found total or partial sleep deprivation during the second half of the night induced rapid depression remission. Response rates range from 40% to 60% over hours to days.4 Sleep deprivation also can reduce suicidality in patients with seasonal depression.5 This treatment has not been widely employed, however, because up to 80% of patients who undergo sleep deprivation experience rapid and significant depressive relapse.4

Sleep deprivation usually is well tolerated. Potential side effects include:

  • headache
  • gastrointestinal upset
  • fatigue
  • cognitive impairment.

Less often, patients report worsening of depressive symptoms and, rarely, suicidal ideation or psychosis.4 Mania or hypomania are potential complications of sleep loss for patients with bipolar or unipolar depression. In a review, Oliwenstein6 suggested that rates of total sleep deprivation-induced mania are likely to be similar to or less than those reported for antidepressants. Because sleep deprivation can induce seizures, this therapy is contraindicated for patients with epilepsy or those at risk for seizures.4

Researchers have successfully explored strategies to reduce the rate of depressive relapse after sleep deprivation, including coadministering light therapy, antidepressants, lithium (particularly for bipolar depression), and sleep-phase advance.4 Sleep-phase advance involves shifting the sleep-wake schedule to a very early sleep time and wake-up time (such as 5 PM to midnight) for 1 day, and then pushing back this schedule by 1 or 2 hours each day until the patient is returned to a “normal” sleep schedule (such as 10 PM to 5 AM). Researchers have demonstrated that sleep-phase advance can have antidepressant effects.7

TREATMENT: Sleep manipulation

Ms. W is continued on fluoxetine, 80 mg/d. We opt for a trial of partial sleep deprivation and sleep-phase advance for Ms. W because of the severity of her depression, her multiple ineffective or poorly tolerated medication trials, and limited benefit from ECT. This treatment involves instituting partial sleep deprivation the first night and subsequently advancing her sleep phase over the next several days (Table 1).

 

 

Although she is sleepy the morning after partial sleep deprivation, Ms. W reports a marked improvement in her mood, decline in hopelessness, and absence of suicidal ideation. She continues the sleep-phase advance protocol for the next 3 nights and participates in cognitive-behavioral therapy groups and ward activities. Psychiatric unit staff support her continued wakefulness during sleep manipulation. Because Ms. W had previously responded to antidepressant augmentation with an atypical antipsychotic we add aripiprazole and titrate the dosage to 7.5 mg/d. We also continue fluoxetine, 80 mg/d, and add trazodone, 100 mg at bedtime, and hydroxyzine, 25 mg as needed.

Table 1

Ms. W’s chronotherapy protocol: Hours permitted for sleep*

Day number
 12345
Sleep deprivation9 PM to2 AM    
Sleep-phase advance 5 PM to midnight7 PM to 2 AM9 PM to 4 AM10 PM to 5 AM
*Treatment was implemented while Ms. W was hospitalized

The authors’ observations

Chronotherapy incorporates manipulations of the sleep/wake cycle such as sleep deprivation and dark or light therapy. It may use combinations of interventions to generate and sustain a response in patients with depression. In a 4-week pilot study, Moscovici et al8 employed a regimen of late partial sleep deprivation, light, and sleep-phase advance to generate and maintain an anti depressant response in 12 patients. Benedetti et al9 used a similar regimen plus lithium to successfully treat bipolar depression and sleep-phase advance to continue that response in 50% of patients for 3 months.

Circadian rhythms affect the function of serotonin (5-HT), norepinephrine, and dopamine.9,10 In a manner similar to antidepressant medications, sleep deprivation may up-regulate or otherwise alter these neurotransmitters’ function. In animals, sleep deprivation increases serotonin function.11 Several hypothetical mechanisms of action for sleep deprivation and other types of chronotherapies have been suggested (Table 2).11-14

Chronotherapies may affect function in brain pathways, as demonstrated by neuroimaging with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). Depression has been associated with increased or decreased brain activity measured by PET or fMRI in regions of the limbic cortex (cingulate and anterior cingulate) and frontal cortex.12

Wu et al13 examined patients treated for depression with medication and total sleep deprivation therapy. Response to treatment was associated with increased function in the cingulate, anterior cingulate, and medial prefrontal cortex as measured by PET. In contrast, mood improvement was associated with reduced baseline activity in the left medial prefrontal cortex, left frontal pole, and right lateral prefrontal cortex.

Researchers have noted the convergence of sleep-wake rhythms and abnormalities seen in depression and the subsequent link with improved sleep-wake cycles related to depression remission. Bunney and Potkin14 note the powerful effect of zeitgebers—environmental agents that reset the body’s internal clock. They suggested that sleep deprivation may affect the function of “master clock” genes involved in controlling the biological clock. These effects on the suprachiasmatic nucleus hypothalamic pacemaker may improve mood by altering control of genetic expression through chromatin remodeling of this master clock circuit.

Certain factors may increase the likelihood that a patient may respond to chronotherapy (Table 3).9,15-17

Table 2

Sleep deprivation for depression: Possible mechanisms

MechanismComponents
Alterations to neurotransmitter functionSerotonin, norepinephrine, dopamine11
Alterations to endogenous circadian pacemaker functionIncreased gene expression14
Changes in perfusion/activity of brain regionsAnterior cingulate, frontal cortex regions12,13

Table 3

Factors that suggest a patient might respond to chronotherapy

Diurnal mood variation15
Endogenous depression including insomnia and anorexia16
Abnormal dexamethasone suppression17
High motivation for treatment
Bipolar depression (possibly)9

OUTCOME: Lasting improvement

Ms. W’s mood improvement is sustained during her week-long hospitalization. At discharge she is hopeful about the future and does not have thoughts of suicide.

At subsequent outpatient visits up to 4 months after discharge, her depressive symptoms remain improved. Patient Health Questionnaire scores indicate mild depression, but Ms. W is not suicidal. She maintains a sleep schedule of 10 PM to 6:30 AM and undergoes 10,000 lux bright light therapy, which she began shortly after discharge, for 30 minutes every morning. She works more productively in psychotherapy, focusing on her eating disorder and anxiety.

Related resource

  • Wu JC, Kelsoe JR, Schachat C, et al. Rapid and sustained antidepressant response with sleep deprivation and chronotherapy in bipolar disorder. Biol Psychiatry. 2009; 66(3): 298-301.

Drug brand names

  • Aripiprazole • Abilify
  • Atomoxetine • Strattera
  • Bupropion • Wellbutrin
  • Buspirone • BuSpar
  • Citalopram • Celexa
  • Clomipramine • Anafranil
  • Clonazepam • Klonopin
  • Duloxetine • Cymbalta
  • Fluoxetine • Prozac
  • Gabapentin • Neurontin
  • Hydrocodone/APAP • Vicodin
  • Hydroxyzine • Atarax, Vistaril
  • Leuprolide • Lupron
  • Liothyronine • Cytomel
  • Lithium • Eskalith, Lithobid
  • Lorazepam • Ativan
  • Nortriptyline • Aventyl
  • Paroxetine • Paxil
  • Risperidone • Risperdal, Risperdal Consta
  • Trazodone • Desyrel
  • Venlafaxine XR • Effexor XR
  • Zolpidem • Ambien
 

 

Disclosures

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

References

1. AHCPR Depression Guideline Panel. Clinical practice guideline number 5. Depression in primary care. Volume 2: Treatment of major depression. Rockville, MD: Agency for Health Care Policy and Research, Public Health Services, U.S. Department of Health and Human Services; 1993. AHCPR publication 93-0550.

2. Fava M, Rush JA, Wisniewski SR, et al. A comparison of mirtazapine and nortriptyline following two consecutive failed medication treatments for depressed outpatients: a STAR*D report. Am J Psychiatry. 2006;163(7):1161-1172.

3. Wirz-Justice A, Benedetti F, Berger M. Chronotherapeutics (light and wake therapy) in affective disorders. Psychol Med. 2005;35(7):939-944.

4. Giedke H, Schwärzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev. 2002;6(5):361-377.

5. Lam RW, Tam EM, Shiah IS, et al. Effects of light therapy on suicidal ideation in patients with winter depression. J Clin Psychiatry. 2000;61(1):30-32.

6. Oliwenstein L. Lifting moods by losing sleep: an adjunct therapy for treating depression. Alternative and Complementary Therapies. 2006;12(2):66-70.

7. Wehr TA, Wirz-Justice A, Goodwin FK, et al. Phase advance of the circadian sleep-wake cycle as an antidepressant. Science. 1979;206(4419):710-713.

8. Moscovici L, Kotler M. A multistage chronobiologic intervention for the treatment of depression: a pilot study. J Affect Disord. 2009;116(3):201-217.

9. Benedetti F, Colombo C, Barbini B, et al. Morning sunlight reduces length of hospitalization in bipolar depression. J Affect Disord. 2001;62(3):221-223.

10. Benedetti F, Barbini B, Colombo C, et al. Chronotherapeutics in a psychiatric ward. Sleep Med Rev. 2007;11(6):509-522.

11. Lopez-Rodriguez F, Wilson CL, Maidment NT, et al. Total sleep deprivation increases extracellular serotonin in the rat hippocampus. Neuroscience. 2003;121(2):523-530.

12. Mayberg HS. Defining the neural circuitry of depression: toward a new nosology with therapeutic implications. Biol Psychiatry. 2007;61(6):729-730.

13. Wu JC, Gillin JC, Buchsbaum MS, et al. Sleep deprivation PET correlations of Hamilton symptom improvement ratings with changes in relative glucose metabolism in patients with depression. J Affect Disord. 2008;107(1-3):181-186.

14. Bunney JN, Potkin SG. Circadian abnormalities, molecular clock genes and chronobiological treatments in depression. Br Med Bull. 2008;86:23-32.

15. Benedetti F, Barbini B, Lucca A, et al. Sleep deprivation hastens the antidepressant action of fluoxetine. Eur Arch Psychiatry Clin Neurosci. 1997;247(2):100-103.

16. Vogel GW, Thurmond A, Gibbons P, et al. REM sleep reduction effects on depression syndromes. Arch Gen Psychiatry. 1975;32(6):765-777.

17. King D, Dowdy S, Jack R, et al. The dexamethasone suppression test as a predictor of sleep deprivation antidepressant effect. Psychiatry Res. 1982;7(1):93-99.

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Dr. Levy is assistant professor and Dr. McLaren is acting assistant professor, department of psychiatry, University of Washington, Seattle, WA.

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CASE: Refractory depression

Ms. W, age 38, is brought to the emergency department after her son finds her unresponsive and calls 911. Suffering from worsening depression, she wrote a note telling her children goodbye, and overdosed on zolpidem from an old prescription and her daughter’s opioids. After being evaluated and medically cleared in the emergency department, Ms. W was admitted to the psychiatric unit.

Ms. W has a history of recurrent major depressive disorder that developed after she was sexually abused by a relative as a teen. She also has bulimia nervosa, alcohol dependence, and posttraumatic stress disorder. She was hospitalized twice for depression and suicidality but had not previously attempted suicide. In the mid-to-late 1990s, she had trials of paroxetine, clomipramine, lithium, and bupropion.

She was seen regularly in our outpatient psychiatry clinic for medication management and supportive psychotherapy. Since being followed in our clinic starting in early 2005, she has had the following medication trials:

  • fluoxetine, citalopram, venlafaxine XR, and duloxetine for depression
  • atomoxetine, buspirone, liothyronine, risperidone, and aripiprazole for antidepressant augmentation
  • lorazepam, clonazepam, and gabapentin for anxiety
  • zolpidem and trazodone for insomnia
  • nortriptyline for migraine headache prophylaxis.

Some medications were not tolerated, primarily because of increased anxiety. Those that were tolerated were adequate trials in terms of dose titration and length. High-dose fluoxetine (80 mg/d) augmented by risperidone (0.375 to 0.5 mg/d) produced the most reliable and significant improvement.

Ms. W had 2 courses of electroconvulsive therapy (ECT) totaling 30 treatments—most recently in 2007—that resulted in significant memory loss with limited benefit. Premenstrual worsening of depression and suicidality were noted. In collaboration with her gynecologist, Ms. W was treated with a 3-month trial of leuprolide to suppress her ovarian axis, which was helpful. In 2008 she underwent bilateral oophorectomy. She has not had symptoms of mood elevation or psychosis. Family history includes schizophrenia, depression, anxiety, and alcoholism.

In the months before hospitalization, Ms. W had been increasingly depressed and intermittently suicidal, although she did not endorse a specific plan or intention to harm herself because she was concerned about the impact suicide would have on her children. Weight gain with risperidone had reactivated body image issues, so Ms. W stopped taking this medication 2 weeks before hospitalization. Her depression became worse, and she began using her husband’s hydrocodone/acetaminophen prescription.

The authors’ observations

Approximately 40% of patients with major depression fail to respond to an initial antidepressant trial.1 An additional 50% of these patients will be treatment-resistant to a subsequent antidepressant.1 Patients may be progressively less likely to respond to additional medication trials.2

One of the most rapid-acting and effective treatments for unipolar and bipolar depression is sleep deprivation. Wirz-Justice et al3 found total or partial sleep deprivation during the second half of the night induced rapid depression remission. Response rates range from 40% to 60% over hours to days.4 Sleep deprivation also can reduce suicidality in patients with seasonal depression.5 This treatment has not been widely employed, however, because up to 80% of patients who undergo sleep deprivation experience rapid and significant depressive relapse.4

Sleep deprivation usually is well tolerated. Potential side effects include:

  • headache
  • gastrointestinal upset
  • fatigue
  • cognitive impairment.

Less often, patients report worsening of depressive symptoms and, rarely, suicidal ideation or psychosis.4 Mania or hypomania are potential complications of sleep loss for patients with bipolar or unipolar depression. In a review, Oliwenstein6 suggested that rates of total sleep deprivation-induced mania are likely to be similar to or less than those reported for antidepressants. Because sleep deprivation can induce seizures, this therapy is contraindicated for patients with epilepsy or those at risk for seizures.4

Researchers have successfully explored strategies to reduce the rate of depressive relapse after sleep deprivation, including coadministering light therapy, antidepressants, lithium (particularly for bipolar depression), and sleep-phase advance.4 Sleep-phase advance involves shifting the sleep-wake schedule to a very early sleep time and wake-up time (such as 5 PM to midnight) for 1 day, and then pushing back this schedule by 1 or 2 hours each day until the patient is returned to a “normal” sleep schedule (such as 10 PM to 5 AM). Researchers have demonstrated that sleep-phase advance can have antidepressant effects.7

TREATMENT: Sleep manipulation

Ms. W is continued on fluoxetine, 80 mg/d. We opt for a trial of partial sleep deprivation and sleep-phase advance for Ms. W because of the severity of her depression, her multiple ineffective or poorly tolerated medication trials, and limited benefit from ECT. This treatment involves instituting partial sleep deprivation the first night and subsequently advancing her sleep phase over the next several days (Table 1).

 

 

Although she is sleepy the morning after partial sleep deprivation, Ms. W reports a marked improvement in her mood, decline in hopelessness, and absence of suicidal ideation. She continues the sleep-phase advance protocol for the next 3 nights and participates in cognitive-behavioral therapy groups and ward activities. Psychiatric unit staff support her continued wakefulness during sleep manipulation. Because Ms. W had previously responded to antidepressant augmentation with an atypical antipsychotic we add aripiprazole and titrate the dosage to 7.5 mg/d. We also continue fluoxetine, 80 mg/d, and add trazodone, 100 mg at bedtime, and hydroxyzine, 25 mg as needed.

Table 1

Ms. W’s chronotherapy protocol: Hours permitted for sleep*

Day number
 12345
Sleep deprivation9 PM to2 AM    
Sleep-phase advance 5 PM to midnight7 PM to 2 AM9 PM to 4 AM10 PM to 5 AM
*Treatment was implemented while Ms. W was hospitalized

The authors’ observations

Chronotherapy incorporates manipulations of the sleep/wake cycle such as sleep deprivation and dark or light therapy. It may use combinations of interventions to generate and sustain a response in patients with depression. In a 4-week pilot study, Moscovici et al8 employed a regimen of late partial sleep deprivation, light, and sleep-phase advance to generate and maintain an anti depressant response in 12 patients. Benedetti et al9 used a similar regimen plus lithium to successfully treat bipolar depression and sleep-phase advance to continue that response in 50% of patients for 3 months.

Circadian rhythms affect the function of serotonin (5-HT), norepinephrine, and dopamine.9,10 In a manner similar to antidepressant medications, sleep deprivation may up-regulate or otherwise alter these neurotransmitters’ function. In animals, sleep deprivation increases serotonin function.11 Several hypothetical mechanisms of action for sleep deprivation and other types of chronotherapies have been suggested (Table 2).11-14

Chronotherapies may affect function in brain pathways, as demonstrated by neuroimaging with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). Depression has been associated with increased or decreased brain activity measured by PET or fMRI in regions of the limbic cortex (cingulate and anterior cingulate) and frontal cortex.12

Wu et al13 examined patients treated for depression with medication and total sleep deprivation therapy. Response to treatment was associated with increased function in the cingulate, anterior cingulate, and medial prefrontal cortex as measured by PET. In contrast, mood improvement was associated with reduced baseline activity in the left medial prefrontal cortex, left frontal pole, and right lateral prefrontal cortex.

Researchers have noted the convergence of sleep-wake rhythms and abnormalities seen in depression and the subsequent link with improved sleep-wake cycles related to depression remission. Bunney and Potkin14 note the powerful effect of zeitgebers—environmental agents that reset the body’s internal clock. They suggested that sleep deprivation may affect the function of “master clock” genes involved in controlling the biological clock. These effects on the suprachiasmatic nucleus hypothalamic pacemaker may improve mood by altering control of genetic expression through chromatin remodeling of this master clock circuit.

Certain factors may increase the likelihood that a patient may respond to chronotherapy (Table 3).9,15-17

Table 2

Sleep deprivation for depression: Possible mechanisms

MechanismComponents
Alterations to neurotransmitter functionSerotonin, norepinephrine, dopamine11
Alterations to endogenous circadian pacemaker functionIncreased gene expression14
Changes in perfusion/activity of brain regionsAnterior cingulate, frontal cortex regions12,13

Table 3

Factors that suggest a patient might respond to chronotherapy

Diurnal mood variation15
Endogenous depression including insomnia and anorexia16
Abnormal dexamethasone suppression17
High motivation for treatment
Bipolar depression (possibly)9

OUTCOME: Lasting improvement

Ms. W’s mood improvement is sustained during her week-long hospitalization. At discharge she is hopeful about the future and does not have thoughts of suicide.

At subsequent outpatient visits up to 4 months after discharge, her depressive symptoms remain improved. Patient Health Questionnaire scores indicate mild depression, but Ms. W is not suicidal. She maintains a sleep schedule of 10 PM to 6:30 AM and undergoes 10,000 lux bright light therapy, which she began shortly after discharge, for 30 minutes every morning. She works more productively in psychotherapy, focusing on her eating disorder and anxiety.

Related resource

  • Wu JC, Kelsoe JR, Schachat C, et al. Rapid and sustained antidepressant response with sleep deprivation and chronotherapy in bipolar disorder. Biol Psychiatry. 2009; 66(3): 298-301.

Drug brand names

  • Aripiprazole • Abilify
  • Atomoxetine • Strattera
  • Bupropion • Wellbutrin
  • Buspirone • BuSpar
  • Citalopram • Celexa
  • Clomipramine • Anafranil
  • Clonazepam • Klonopin
  • Duloxetine • Cymbalta
  • Fluoxetine • Prozac
  • Gabapentin • Neurontin
  • Hydrocodone/APAP • Vicodin
  • Hydroxyzine • Atarax, Vistaril
  • Leuprolide • Lupron
  • Liothyronine • Cytomel
  • Lithium • Eskalith, Lithobid
  • Lorazepam • Ativan
  • Nortriptyline • Aventyl
  • Paroxetine • Paxil
  • Risperidone • Risperdal, Risperdal Consta
  • Trazodone • Desyrel
  • Venlafaxine XR • Effexor XR
  • Zolpidem • Ambien
 

 

Disclosures

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

CASE: Refractory depression

Ms. W, age 38, is brought to the emergency department after her son finds her unresponsive and calls 911. Suffering from worsening depression, she wrote a note telling her children goodbye, and overdosed on zolpidem from an old prescription and her daughter’s opioids. After being evaluated and medically cleared in the emergency department, Ms. W was admitted to the psychiatric unit.

Ms. W has a history of recurrent major depressive disorder that developed after she was sexually abused by a relative as a teen. She also has bulimia nervosa, alcohol dependence, and posttraumatic stress disorder. She was hospitalized twice for depression and suicidality but had not previously attempted suicide. In the mid-to-late 1990s, she had trials of paroxetine, clomipramine, lithium, and bupropion.

She was seen regularly in our outpatient psychiatry clinic for medication management and supportive psychotherapy. Since being followed in our clinic starting in early 2005, she has had the following medication trials:

  • fluoxetine, citalopram, venlafaxine XR, and duloxetine for depression
  • atomoxetine, buspirone, liothyronine, risperidone, and aripiprazole for antidepressant augmentation
  • lorazepam, clonazepam, and gabapentin for anxiety
  • zolpidem and trazodone for insomnia
  • nortriptyline for migraine headache prophylaxis.

Some medications were not tolerated, primarily because of increased anxiety. Those that were tolerated were adequate trials in terms of dose titration and length. High-dose fluoxetine (80 mg/d) augmented by risperidone (0.375 to 0.5 mg/d) produced the most reliable and significant improvement.

Ms. W had 2 courses of electroconvulsive therapy (ECT) totaling 30 treatments—most recently in 2007—that resulted in significant memory loss with limited benefit. Premenstrual worsening of depression and suicidality were noted. In collaboration with her gynecologist, Ms. W was treated with a 3-month trial of leuprolide to suppress her ovarian axis, which was helpful. In 2008 she underwent bilateral oophorectomy. She has not had symptoms of mood elevation or psychosis. Family history includes schizophrenia, depression, anxiety, and alcoholism.

In the months before hospitalization, Ms. W had been increasingly depressed and intermittently suicidal, although she did not endorse a specific plan or intention to harm herself because she was concerned about the impact suicide would have on her children. Weight gain with risperidone had reactivated body image issues, so Ms. W stopped taking this medication 2 weeks before hospitalization. Her depression became worse, and she began using her husband’s hydrocodone/acetaminophen prescription.

The authors’ observations

Approximately 40% of patients with major depression fail to respond to an initial antidepressant trial.1 An additional 50% of these patients will be treatment-resistant to a subsequent antidepressant.1 Patients may be progressively less likely to respond to additional medication trials.2

One of the most rapid-acting and effective treatments for unipolar and bipolar depression is sleep deprivation. Wirz-Justice et al3 found total or partial sleep deprivation during the second half of the night induced rapid depression remission. Response rates range from 40% to 60% over hours to days.4 Sleep deprivation also can reduce suicidality in patients with seasonal depression.5 This treatment has not been widely employed, however, because up to 80% of patients who undergo sleep deprivation experience rapid and significant depressive relapse.4

Sleep deprivation usually is well tolerated. Potential side effects include:

  • headache
  • gastrointestinal upset
  • fatigue
  • cognitive impairment.

Less often, patients report worsening of depressive symptoms and, rarely, suicidal ideation or psychosis.4 Mania or hypomania are potential complications of sleep loss for patients with bipolar or unipolar depression. In a review, Oliwenstein6 suggested that rates of total sleep deprivation-induced mania are likely to be similar to or less than those reported for antidepressants. Because sleep deprivation can induce seizures, this therapy is contraindicated for patients with epilepsy or those at risk for seizures.4

Researchers have successfully explored strategies to reduce the rate of depressive relapse after sleep deprivation, including coadministering light therapy, antidepressants, lithium (particularly for bipolar depression), and sleep-phase advance.4 Sleep-phase advance involves shifting the sleep-wake schedule to a very early sleep time and wake-up time (such as 5 PM to midnight) for 1 day, and then pushing back this schedule by 1 or 2 hours each day until the patient is returned to a “normal” sleep schedule (such as 10 PM to 5 AM). Researchers have demonstrated that sleep-phase advance can have antidepressant effects.7

TREATMENT: Sleep manipulation

Ms. W is continued on fluoxetine, 80 mg/d. We opt for a trial of partial sleep deprivation and sleep-phase advance for Ms. W because of the severity of her depression, her multiple ineffective or poorly tolerated medication trials, and limited benefit from ECT. This treatment involves instituting partial sleep deprivation the first night and subsequently advancing her sleep phase over the next several days (Table 1).

 

 

Although she is sleepy the morning after partial sleep deprivation, Ms. W reports a marked improvement in her mood, decline in hopelessness, and absence of suicidal ideation. She continues the sleep-phase advance protocol for the next 3 nights and participates in cognitive-behavioral therapy groups and ward activities. Psychiatric unit staff support her continued wakefulness during sleep manipulation. Because Ms. W had previously responded to antidepressant augmentation with an atypical antipsychotic we add aripiprazole and titrate the dosage to 7.5 mg/d. We also continue fluoxetine, 80 mg/d, and add trazodone, 100 mg at bedtime, and hydroxyzine, 25 mg as needed.

Table 1

Ms. W’s chronotherapy protocol: Hours permitted for sleep*

Day number
 12345
Sleep deprivation9 PM to2 AM    
Sleep-phase advance 5 PM to midnight7 PM to 2 AM9 PM to 4 AM10 PM to 5 AM
*Treatment was implemented while Ms. W was hospitalized

The authors’ observations

Chronotherapy incorporates manipulations of the sleep/wake cycle such as sleep deprivation and dark or light therapy. It may use combinations of interventions to generate and sustain a response in patients with depression. In a 4-week pilot study, Moscovici et al8 employed a regimen of late partial sleep deprivation, light, and sleep-phase advance to generate and maintain an anti depressant response in 12 patients. Benedetti et al9 used a similar regimen plus lithium to successfully treat bipolar depression and sleep-phase advance to continue that response in 50% of patients for 3 months.

Circadian rhythms affect the function of serotonin (5-HT), norepinephrine, and dopamine.9,10 In a manner similar to antidepressant medications, sleep deprivation may up-regulate or otherwise alter these neurotransmitters’ function. In animals, sleep deprivation increases serotonin function.11 Several hypothetical mechanisms of action for sleep deprivation and other types of chronotherapies have been suggested (Table 2).11-14

Chronotherapies may affect function in brain pathways, as demonstrated by neuroimaging with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). Depression has been associated with increased or decreased brain activity measured by PET or fMRI in regions of the limbic cortex (cingulate and anterior cingulate) and frontal cortex.12

Wu et al13 examined patients treated for depression with medication and total sleep deprivation therapy. Response to treatment was associated with increased function in the cingulate, anterior cingulate, and medial prefrontal cortex as measured by PET. In contrast, mood improvement was associated with reduced baseline activity in the left medial prefrontal cortex, left frontal pole, and right lateral prefrontal cortex.

Researchers have noted the convergence of sleep-wake rhythms and abnormalities seen in depression and the subsequent link with improved sleep-wake cycles related to depression remission. Bunney and Potkin14 note the powerful effect of zeitgebers—environmental agents that reset the body’s internal clock. They suggested that sleep deprivation may affect the function of “master clock” genes involved in controlling the biological clock. These effects on the suprachiasmatic nucleus hypothalamic pacemaker may improve mood by altering control of genetic expression through chromatin remodeling of this master clock circuit.

Certain factors may increase the likelihood that a patient may respond to chronotherapy (Table 3).9,15-17

Table 2

Sleep deprivation for depression: Possible mechanisms

MechanismComponents
Alterations to neurotransmitter functionSerotonin, norepinephrine, dopamine11
Alterations to endogenous circadian pacemaker functionIncreased gene expression14
Changes in perfusion/activity of brain regionsAnterior cingulate, frontal cortex regions12,13

Table 3

Factors that suggest a patient might respond to chronotherapy

Diurnal mood variation15
Endogenous depression including insomnia and anorexia16
Abnormal dexamethasone suppression17
High motivation for treatment
Bipolar depression (possibly)9

OUTCOME: Lasting improvement

Ms. W’s mood improvement is sustained during her week-long hospitalization. At discharge she is hopeful about the future and does not have thoughts of suicide.

At subsequent outpatient visits up to 4 months after discharge, her depressive symptoms remain improved. Patient Health Questionnaire scores indicate mild depression, but Ms. W is not suicidal. She maintains a sleep schedule of 10 PM to 6:30 AM and undergoes 10,000 lux bright light therapy, which she began shortly after discharge, for 30 minutes every morning. She works more productively in psychotherapy, focusing on her eating disorder and anxiety.

Related resource

  • Wu JC, Kelsoe JR, Schachat C, et al. Rapid and sustained antidepressant response with sleep deprivation and chronotherapy in bipolar disorder. Biol Psychiatry. 2009; 66(3): 298-301.

Drug brand names

  • Aripiprazole • Abilify
  • Atomoxetine • Strattera
  • Bupropion • Wellbutrin
  • Buspirone • BuSpar
  • Citalopram • Celexa
  • Clomipramine • Anafranil
  • Clonazepam • Klonopin
  • Duloxetine • Cymbalta
  • Fluoxetine • Prozac
  • Gabapentin • Neurontin
  • Hydrocodone/APAP • Vicodin
  • Hydroxyzine • Atarax, Vistaril
  • Leuprolide • Lupron
  • Liothyronine • Cytomel
  • Lithium • Eskalith, Lithobid
  • Lorazepam • Ativan
  • Nortriptyline • Aventyl
  • Paroxetine • Paxil
  • Risperidone • Risperdal, Risperdal Consta
  • Trazodone • Desyrel
  • Venlafaxine XR • Effexor XR
  • Zolpidem • Ambien
 

 

Disclosures

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

References

1. AHCPR Depression Guideline Panel. Clinical practice guideline number 5. Depression in primary care. Volume 2: Treatment of major depression. Rockville, MD: Agency for Health Care Policy and Research, Public Health Services, U.S. Department of Health and Human Services; 1993. AHCPR publication 93-0550.

2. Fava M, Rush JA, Wisniewski SR, et al. A comparison of mirtazapine and nortriptyline following two consecutive failed medication treatments for depressed outpatients: a STAR*D report. Am J Psychiatry. 2006;163(7):1161-1172.

3. Wirz-Justice A, Benedetti F, Berger M. Chronotherapeutics (light and wake therapy) in affective disorders. Psychol Med. 2005;35(7):939-944.

4. Giedke H, Schwärzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev. 2002;6(5):361-377.

5. Lam RW, Tam EM, Shiah IS, et al. Effects of light therapy on suicidal ideation in patients with winter depression. J Clin Psychiatry. 2000;61(1):30-32.

6. Oliwenstein L. Lifting moods by losing sleep: an adjunct therapy for treating depression. Alternative and Complementary Therapies. 2006;12(2):66-70.

7. Wehr TA, Wirz-Justice A, Goodwin FK, et al. Phase advance of the circadian sleep-wake cycle as an antidepressant. Science. 1979;206(4419):710-713.

8. Moscovici L, Kotler M. A multistage chronobiologic intervention for the treatment of depression: a pilot study. J Affect Disord. 2009;116(3):201-217.

9. Benedetti F, Colombo C, Barbini B, et al. Morning sunlight reduces length of hospitalization in bipolar depression. J Affect Disord. 2001;62(3):221-223.

10. Benedetti F, Barbini B, Colombo C, et al. Chronotherapeutics in a psychiatric ward. Sleep Med Rev. 2007;11(6):509-522.

11. Lopez-Rodriguez F, Wilson CL, Maidment NT, et al. Total sleep deprivation increases extracellular serotonin in the rat hippocampus. Neuroscience. 2003;121(2):523-530.

12. Mayberg HS. Defining the neural circuitry of depression: toward a new nosology with therapeutic implications. Biol Psychiatry. 2007;61(6):729-730.

13. Wu JC, Gillin JC, Buchsbaum MS, et al. Sleep deprivation PET correlations of Hamilton symptom improvement ratings with changes in relative glucose metabolism in patients with depression. J Affect Disord. 2008;107(1-3):181-186.

14. Bunney JN, Potkin SG. Circadian abnormalities, molecular clock genes and chronobiological treatments in depression. Br Med Bull. 2008;86:23-32.

15. Benedetti F, Barbini B, Lucca A, et al. Sleep deprivation hastens the antidepressant action of fluoxetine. Eur Arch Psychiatry Clin Neurosci. 1997;247(2):100-103.

16. Vogel GW, Thurmond A, Gibbons P, et al. REM sleep reduction effects on depression syndromes. Arch Gen Psychiatry. 1975;32(6):765-777.

17. King D, Dowdy S, Jack R, et al. The dexamethasone suppression test as a predictor of sleep deprivation antidepressant effect. Psychiatry Res. 1982;7(1):93-99.

References

1. AHCPR Depression Guideline Panel. Clinical practice guideline number 5. Depression in primary care. Volume 2: Treatment of major depression. Rockville, MD: Agency for Health Care Policy and Research, Public Health Services, U.S. Department of Health and Human Services; 1993. AHCPR publication 93-0550.

2. Fava M, Rush JA, Wisniewski SR, et al. A comparison of mirtazapine and nortriptyline following two consecutive failed medication treatments for depressed outpatients: a STAR*D report. Am J Psychiatry. 2006;163(7):1161-1172.

3. Wirz-Justice A, Benedetti F, Berger M. Chronotherapeutics (light and wake therapy) in affective disorders. Psychol Med. 2005;35(7):939-944.

4. Giedke H, Schwärzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev. 2002;6(5):361-377.

5. Lam RW, Tam EM, Shiah IS, et al. Effects of light therapy on suicidal ideation in patients with winter depression. J Clin Psychiatry. 2000;61(1):30-32.

6. Oliwenstein L. Lifting moods by losing sleep: an adjunct therapy for treating depression. Alternative and Complementary Therapies. 2006;12(2):66-70.

7. Wehr TA, Wirz-Justice A, Goodwin FK, et al. Phase advance of the circadian sleep-wake cycle as an antidepressant. Science. 1979;206(4419):710-713.

8. Moscovici L, Kotler M. A multistage chronobiologic intervention for the treatment of depression: a pilot study. J Affect Disord. 2009;116(3):201-217.

9. Benedetti F, Colombo C, Barbini B, et al. Morning sunlight reduces length of hospitalization in bipolar depression. J Affect Disord. 2001;62(3):221-223.

10. Benedetti F, Barbini B, Colombo C, et al. Chronotherapeutics in a psychiatric ward. Sleep Med Rev. 2007;11(6):509-522.

11. Lopez-Rodriguez F, Wilson CL, Maidment NT, et al. Total sleep deprivation increases extracellular serotonin in the rat hippocampus. Neuroscience. 2003;121(2):523-530.

12. Mayberg HS. Defining the neural circuitry of depression: toward a new nosology with therapeutic implications. Biol Psychiatry. 2007;61(6):729-730.

13. Wu JC, Gillin JC, Buchsbaum MS, et al. Sleep deprivation PET correlations of Hamilton symptom improvement ratings with changes in relative glucose metabolism in patients with depression. J Affect Disord. 2008;107(1-3):181-186.

14. Bunney JN, Potkin SG. Circadian abnormalities, molecular clock genes and chronobiological treatments in depression. Br Med Bull. 2008;86:23-32.

15. Benedetti F, Barbini B, Lucca A, et al. Sleep deprivation hastens the antidepressant action of fluoxetine. Eur Arch Psychiatry Clin Neurosci. 1997;247(2):100-103.

16. Vogel GW, Thurmond A, Gibbons P, et al. REM sleep reduction effects on depression syndromes. Arch Gen Psychiatry. 1975;32(6):765-777.

17. King D, Dowdy S, Jack R, et al. The dexamethasone suppression test as a predictor of sleep deprivation antidepressant effect. Psychiatry Res. 1982;7(1):93-99.

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When presented with an overweight child who has hypertension, collect a detailed history, including a 24-hour food-intake history.

Also assess the child's nutritional habits, such as number of fast-food items typically eaten per week and number of family dinners.

Ask about the fluids these children generally consume. For instance, do they drink any caloric beverages other than low-fat milk?

Take an exercise history. Inquire how many hours per day the child is exposed to television, video games, and other media.

Social interaction can be particularly important with an overweight child. Ask if the child has been teased or bullied at home, in school, or elsewhere in the community.

Next ask the parent(s) and patient what they know about high blood pressure. Also inquire about a family history of hypertension.

Confirm any elevation in the child's blood pressure during a physical examination. If the patient has severe hypertension, it is usually time to refer the child to a specialist.

If the child has hypertension for three consecutive monthly visits, further evaluation with blood work is appropriate. Order a complete metabolic panel, urinalysis, and fasting lipid panel. Urinalysis, for example, is useful as a screen for type 2 diabetes.

On a full review of systems, identify other morbidities associated with obesity and perform appropriate tests.

For instance, the child with daytime sleepiness and snoring may require a sleep study to identify obstructive sleep apnea.

In addition, if liver function tests are elevated, a pediatric ultrasound exam can identify a fatty liver.

You can also order an electrocardiogram to identify heart pathology and refer the child if the findings are abnormal.

Many families request thyroid testing for an overweight child. Full thyroid function tests are not cost effective and need not be done. A thyroid-stimulating hormone test should suffice.

As for behavioral counseling, at the Cleveland Clinic Children's Hospital, we recommend our “5 to GO!” messaging, in which children are told to eat 5-a-day fruits and veggies; give 4 compliments a day to anyone they encounter, including other kids, and get 4 compliments a day from anyone; consume 3 dairy products a day; engage in no more than 2 hours of media/TV time a day; drink 0 sugar-sweetened beverages, and go!

For teenagers, we aim for 4 dairy/calcium servings and 3 compliments a day (not that they need fewer compliments, but they do need more calcium than the under age 10 crowd).

The key is to follow patients monthly. Slow, steady change—with positive motivation tailored to each family—works better than trying to do everything at once.

Follow up, follow up, and follow up—with a lot of cheerleading!

Patient education is also essential. Help patients and their families figure out how to cook a no-added-salt diet, how to shop the periphery of a grocery store where the fresh produce is located, and how to build physical activity and exercise into the family's daily plan.

Consider a weight management program such as our Fit Youth Program. Patients and families who participate in this 12-week program at the Cleveland Clinic receive group counseling sessions led by a psychologist in combination with a pediatrician, a dietitian, and an exercise physiologist.

Multidisciplinary interventions such as this one can accomplish modest weight loss versus progression toward 30 pounds of weight gain per year, as occurs in many of our children who do not receive effective treatment.

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When presented with an overweight child who has hypertension, collect a detailed history, including a 24-hour food-intake history.

Also assess the child's nutritional habits, such as number of fast-food items typically eaten per week and number of family dinners.

Ask about the fluids these children generally consume. For instance, do they drink any caloric beverages other than low-fat milk?

Take an exercise history. Inquire how many hours per day the child is exposed to television, video games, and other media.

Social interaction can be particularly important with an overweight child. Ask if the child has been teased or bullied at home, in school, or elsewhere in the community.

Next ask the parent(s) and patient what they know about high blood pressure. Also inquire about a family history of hypertension.

Confirm any elevation in the child's blood pressure during a physical examination. If the patient has severe hypertension, it is usually time to refer the child to a specialist.

If the child has hypertension for three consecutive monthly visits, further evaluation with blood work is appropriate. Order a complete metabolic panel, urinalysis, and fasting lipid panel. Urinalysis, for example, is useful as a screen for type 2 diabetes.

On a full review of systems, identify other morbidities associated with obesity and perform appropriate tests.

For instance, the child with daytime sleepiness and snoring may require a sleep study to identify obstructive sleep apnea.

In addition, if liver function tests are elevated, a pediatric ultrasound exam can identify a fatty liver.

You can also order an electrocardiogram to identify heart pathology and refer the child if the findings are abnormal.

Many families request thyroid testing for an overweight child. Full thyroid function tests are not cost effective and need not be done. A thyroid-stimulating hormone test should suffice.

As for behavioral counseling, at the Cleveland Clinic Children's Hospital, we recommend our “5 to GO!” messaging, in which children are told to eat 5-a-day fruits and veggies; give 4 compliments a day to anyone they encounter, including other kids, and get 4 compliments a day from anyone; consume 3 dairy products a day; engage in no more than 2 hours of media/TV time a day; drink 0 sugar-sweetened beverages, and go!

For teenagers, we aim for 4 dairy/calcium servings and 3 compliments a day (not that they need fewer compliments, but they do need more calcium than the under age 10 crowd).

The key is to follow patients monthly. Slow, steady change—with positive motivation tailored to each family—works better than trying to do everything at once.

Follow up, follow up, and follow up—with a lot of cheerleading!

Patient education is also essential. Help patients and their families figure out how to cook a no-added-salt diet, how to shop the periphery of a grocery store where the fresh produce is located, and how to build physical activity and exercise into the family's daily plan.

Consider a weight management program such as our Fit Youth Program. Patients and families who participate in this 12-week program at the Cleveland Clinic receive group counseling sessions led by a psychologist in combination with a pediatrician, a dietitian, and an exercise physiologist.

Multidisciplinary interventions such as this one can accomplish modest weight loss versus progression toward 30 pounds of weight gain per year, as occurs in many of our children who do not receive effective treatment.

pdnews@elsevier.com

When presented with an overweight child who has hypertension, collect a detailed history, including a 24-hour food-intake history.

Also assess the child's nutritional habits, such as number of fast-food items typically eaten per week and number of family dinners.

Ask about the fluids these children generally consume. For instance, do they drink any caloric beverages other than low-fat milk?

Take an exercise history. Inquire how many hours per day the child is exposed to television, video games, and other media.

Social interaction can be particularly important with an overweight child. Ask if the child has been teased or bullied at home, in school, or elsewhere in the community.

Next ask the parent(s) and patient what they know about high blood pressure. Also inquire about a family history of hypertension.

Confirm any elevation in the child's blood pressure during a physical examination. If the patient has severe hypertension, it is usually time to refer the child to a specialist.

If the child has hypertension for three consecutive monthly visits, further evaluation with blood work is appropriate. Order a complete metabolic panel, urinalysis, and fasting lipid panel. Urinalysis, for example, is useful as a screen for type 2 diabetes.

On a full review of systems, identify other morbidities associated with obesity and perform appropriate tests.

For instance, the child with daytime sleepiness and snoring may require a sleep study to identify obstructive sleep apnea.

In addition, if liver function tests are elevated, a pediatric ultrasound exam can identify a fatty liver.

You can also order an electrocardiogram to identify heart pathology and refer the child if the findings are abnormal.

Many families request thyroid testing for an overweight child. Full thyroid function tests are not cost effective and need not be done. A thyroid-stimulating hormone test should suffice.

As for behavioral counseling, at the Cleveland Clinic Children's Hospital, we recommend our “5 to GO!” messaging, in which children are told to eat 5-a-day fruits and veggies; give 4 compliments a day to anyone they encounter, including other kids, and get 4 compliments a day from anyone; consume 3 dairy products a day; engage in no more than 2 hours of media/TV time a day; drink 0 sugar-sweetened beverages, and go!

For teenagers, we aim for 4 dairy/calcium servings and 3 compliments a day (not that they need fewer compliments, but they do need more calcium than the under age 10 crowd).

The key is to follow patients monthly. Slow, steady change—with positive motivation tailored to each family—works better than trying to do everything at once.

Follow up, follow up, and follow up—with a lot of cheerleading!

Patient education is also essential. Help patients and their families figure out how to cook a no-added-salt diet, how to shop the periphery of a grocery store where the fresh produce is located, and how to build physical activity and exercise into the family's daily plan.

Consider a weight management program such as our Fit Youth Program. Patients and families who participate in this 12-week program at the Cleveland Clinic receive group counseling sessions led by a psychologist in combination with a pediatrician, a dietitian, and an exercise physiologist.

Multidisciplinary interventions such as this one can accomplish modest weight loss versus progression toward 30 pounds of weight gain per year, as occurs in many of our children who do not receive effective treatment.

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A hospitalist-led initiative to boost the implementation of glycemic controls has exceeded initial goals at an Alabama hospital, an early sign of success for the SHM-sponsored pilot program.

Steven C. Smith, MD, FHM, medical director of hospitalist services at Healthcare Authority for Medical West in Bessemer, Ala., says that after the Glycemic Control Mentored Implementation (GCMI) program was put in place earlier this year, his group set a two-week goal of 5% utilization of the program's evidence-based order set. He also set a three-month goal of 25% compliance with the order set.

"Much to my surprise, we achieved 16% utilization at two weeks," Dr. Smith says, adding that three-month data are still being tabulated. "The involvement by SHM is what made the difference. Being able to tell people on the medical staff that this is part of a national-level QI project, we're participating in something bigger—that made a big difference in getting people interested in the order set."

Representatives from several of the 30 pilot sites have reported similar success in the early stages of the yearlong project. Among other issues, the GCMI program tackles subcutaneous insulin protocols, transition from subcutaneous to infusion, care coordination, improving follow-up care, and hypoglycemia management.

Although institutions entered the program in April, Dr. Smith and his colleagues didn't begin their formal mentoring relationship until July. Since then, his HM group has stayed in touch with program mentors through teleconferences and direct e-mail exchanges. The service also has access to a data-aggregation system through the Yale Center for Medical Informatics, which encourages more attention and utilization of newly created order sets.

"We are in the process of collecting data from a period of about one year prior to our project and comparing that to data since the implementation of our order set," Dr. Smith says. The analysis "will allow us, and our mentor, to tailor our efforts to our particular institution in an ongoing fashion. The ongoing measures of our success with this project will include outcomes measures like length of stay, cost of stay, mortality and morbidity, ICU length of stay, ventilator days, and others."

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A hospitalist-led initiative to boost the implementation of glycemic controls has exceeded initial goals at an Alabama hospital, an early sign of success for the SHM-sponsored pilot program.

Steven C. Smith, MD, FHM, medical director of hospitalist services at Healthcare Authority for Medical West in Bessemer, Ala., says that after the Glycemic Control Mentored Implementation (GCMI) program was put in place earlier this year, his group set a two-week goal of 5% utilization of the program's evidence-based order set. He also set a three-month goal of 25% compliance with the order set.

"Much to my surprise, we achieved 16% utilization at two weeks," Dr. Smith says, adding that three-month data are still being tabulated. "The involvement by SHM is what made the difference. Being able to tell people on the medical staff that this is part of a national-level QI project, we're participating in something bigger—that made a big difference in getting people interested in the order set."

Representatives from several of the 30 pilot sites have reported similar success in the early stages of the yearlong project. Among other issues, the GCMI program tackles subcutaneous insulin protocols, transition from subcutaneous to infusion, care coordination, improving follow-up care, and hypoglycemia management.

Although institutions entered the program in April, Dr. Smith and his colleagues didn't begin their formal mentoring relationship until July. Since then, his HM group has stayed in touch with program mentors through teleconferences and direct e-mail exchanges. The service also has access to a data-aggregation system through the Yale Center for Medical Informatics, which encourages more attention and utilization of newly created order sets.

"We are in the process of collecting data from a period of about one year prior to our project and comparing that to data since the implementation of our order set," Dr. Smith says. The analysis "will allow us, and our mentor, to tailor our efforts to our particular institution in an ongoing fashion. The ongoing measures of our success with this project will include outcomes measures like length of stay, cost of stay, mortality and morbidity, ICU length of stay, ventilator days, and others."

A hospitalist-led initiative to boost the implementation of glycemic controls has exceeded initial goals at an Alabama hospital, an early sign of success for the SHM-sponsored pilot program.

Steven C. Smith, MD, FHM, medical director of hospitalist services at Healthcare Authority for Medical West in Bessemer, Ala., says that after the Glycemic Control Mentored Implementation (GCMI) program was put in place earlier this year, his group set a two-week goal of 5% utilization of the program's evidence-based order set. He also set a three-month goal of 25% compliance with the order set.

"Much to my surprise, we achieved 16% utilization at two weeks," Dr. Smith says, adding that three-month data are still being tabulated. "The involvement by SHM is what made the difference. Being able to tell people on the medical staff that this is part of a national-level QI project, we're participating in something bigger—that made a big difference in getting people interested in the order set."

Representatives from several of the 30 pilot sites have reported similar success in the early stages of the yearlong project. Among other issues, the GCMI program tackles subcutaneous insulin protocols, transition from subcutaneous to infusion, care coordination, improving follow-up care, and hypoglycemia management.

Although institutions entered the program in April, Dr. Smith and his colleagues didn't begin their formal mentoring relationship until July. Since then, his HM group has stayed in touch with program mentors through teleconferences and direct e-mail exchanges. The service also has access to a data-aggregation system through the Yale Center for Medical Informatics, which encourages more attention and utilization of newly created order sets.

"We are in the process of collecting data from a period of about one year prior to our project and comparing that to data since the implementation of our order set," Dr. Smith says. The analysis "will allow us, and our mentor, to tailor our efforts to our particular institution in an ongoing fashion. The ongoing measures of our success with this project will include outcomes measures like length of stay, cost of stay, mortality and morbidity, ICU length of stay, ventilator days, and others."

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Clinical question: What factors are associated with methicillin-resistant Staphylococcus aureus (MRSA) carriage at hospital discharge to home health care, prolonged MRSA colonization, and MRSA transmission to household contacts?

Background: Previous studies have reported prolonged colonization with hospital-acquired MRSA after discharge, as well as transmission of MRSA to household contacts. However, the rates and risk factors for MRSA carriage and transmission are unknown.

Study design: Multicenter prospective cohort.

Setting: Home-health-care system associated with 47 public teaching hospitals in France.

Synopsis: More than 1,500 hospitalized adult patients with planned discharge to home health care were screened for MRSA colonization, and 12.7% were MRSA-positive by nasal or skin lesion swab.

Factors independently associated with MRSA carriage at hospital discharge were chronic skin lesions, older age, longer duration of hospitalization, and neurologic and cardiovascular primary diagnoses.

Surveillance sampling for up to one year showed that approximately half of these patients had clearance of MRSA, with a median time to clearance of 282 days. Lack of self-sufficiency in daily activities was associated with persistent MRSA carriage.

Nineteen percent of household contacts acquired MRSA during the study period. Risks included older age and providing healthcare to the index patient.

Bottom line: Hospital-acquired MRSA colonization is prevalent at discharge to home health settings, is frequently prolonged, and commonly results in transmission to household contacts, particularly those providing healthcare to the index patient.

Citation: Lucet JC, Paoletti X, Demontpion C, et al. Carriage of methicillin-resistant Staphylococcus aureus in home care settings: prevalence, duration, and transmission to household members. Arch Intern Med. 2009;169(15):1372-1378.

Reviewed for TH eWire by Kelly Cunningham, MD, Elizabeth Rice, MD, Eduard Vasilevskis, MD, Joshua LaBrin, MD, Kelly Sopko, MD, Shelley Ellis, MD, MPH, and Sunil Kripalani, MD, MSc, Section of Hospital Medicine, Vanderbilt University, Nashville, Tenn.

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Clinical question: What factors are associated with methicillin-resistant Staphylococcus aureus (MRSA) carriage at hospital discharge to home health care, prolonged MRSA colonization, and MRSA transmission to household contacts?

Background: Previous studies have reported prolonged colonization with hospital-acquired MRSA after discharge, as well as transmission of MRSA to household contacts. However, the rates and risk factors for MRSA carriage and transmission are unknown.

Study design: Multicenter prospective cohort.

Setting: Home-health-care system associated with 47 public teaching hospitals in France.

Synopsis: More than 1,500 hospitalized adult patients with planned discharge to home health care were screened for MRSA colonization, and 12.7% were MRSA-positive by nasal or skin lesion swab.

Factors independently associated with MRSA carriage at hospital discharge were chronic skin lesions, older age, longer duration of hospitalization, and neurologic and cardiovascular primary diagnoses.

Surveillance sampling for up to one year showed that approximately half of these patients had clearance of MRSA, with a median time to clearance of 282 days. Lack of self-sufficiency in daily activities was associated with persistent MRSA carriage.

Nineteen percent of household contacts acquired MRSA during the study period. Risks included older age and providing healthcare to the index patient.

Bottom line: Hospital-acquired MRSA colonization is prevalent at discharge to home health settings, is frequently prolonged, and commonly results in transmission to household contacts, particularly those providing healthcare to the index patient.

Citation: Lucet JC, Paoletti X, Demontpion C, et al. Carriage of methicillin-resistant Staphylococcus aureus in home care settings: prevalence, duration, and transmission to household members. Arch Intern Med. 2009;169(15):1372-1378.

Reviewed for TH eWire by Kelly Cunningham, MD, Elizabeth Rice, MD, Eduard Vasilevskis, MD, Joshua LaBrin, MD, Kelly Sopko, MD, Shelley Ellis, MD, MPH, and Sunil Kripalani, MD, MSc, Section of Hospital Medicine, Vanderbilt University, Nashville, Tenn.

Clinical question: What factors are associated with methicillin-resistant Staphylococcus aureus (MRSA) carriage at hospital discharge to home health care, prolonged MRSA colonization, and MRSA transmission to household contacts?

Background: Previous studies have reported prolonged colonization with hospital-acquired MRSA after discharge, as well as transmission of MRSA to household contacts. However, the rates and risk factors for MRSA carriage and transmission are unknown.

Study design: Multicenter prospective cohort.

Setting: Home-health-care system associated with 47 public teaching hospitals in France.

Synopsis: More than 1,500 hospitalized adult patients with planned discharge to home health care were screened for MRSA colonization, and 12.7% were MRSA-positive by nasal or skin lesion swab.

Factors independently associated with MRSA carriage at hospital discharge were chronic skin lesions, older age, longer duration of hospitalization, and neurologic and cardiovascular primary diagnoses.

Surveillance sampling for up to one year showed that approximately half of these patients had clearance of MRSA, with a median time to clearance of 282 days. Lack of self-sufficiency in daily activities was associated with persistent MRSA carriage.

Nineteen percent of household contacts acquired MRSA during the study period. Risks included older age and providing healthcare to the index patient.

Bottom line: Hospital-acquired MRSA colonization is prevalent at discharge to home health settings, is frequently prolonged, and commonly results in transmission to household contacts, particularly those providing healthcare to the index patient.

Citation: Lucet JC, Paoletti X, Demontpion C, et al. Carriage of methicillin-resistant Staphylococcus aureus in home care settings: prevalence, duration, and transmission to household members. Arch Intern Med. 2009;169(15):1372-1378.

Reviewed for TH eWire by Kelly Cunningham, MD, Elizabeth Rice, MD, Eduard Vasilevskis, MD, Joshua LaBrin, MD, Kelly Sopko, MD, Shelley Ellis, MD, MPH, and Sunil Kripalani, MD, MSc, Section of Hospital Medicine, Vanderbilt University, Nashville, Tenn.

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Communication, interdisciplinary approaches key to effective transitions

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Improving patient discharges and reducing preventable "bounce-back" readmissions will have increasing implications for hospitals’ bottom lines—especially if proposed Medicare payment bundling reforms are adopted by Congress. Discharge improvement also enhances a hospital’s reputation with patients and providers, says Neil Gupta, MD, a hospitalist at the University of California at San Francisco.

"I think we all recognize in our daily practice that there are things we can do better for patients at discharge," Dr. Gupta says. "It's sometimes hard to get the resources and motivation to do this. But we know it could really impact patient care and make it better."

Dr. Gupta's hospital is one of 24 participating in SHM's Project BOOST (Better Outcomes for Older Adults through Safe Transitions). The mentorship program is developing a consensus and resources for best practices in patient discharges. National data show that about one in five hospitalized Medicare patients are readmitted within 30 days. While some of these readmissions are appropriate, the sheer quantity of readmissions shows room for improvement, says Dr. Gupta's colleague, Arpana Vidyarthi, MD, a hospitalist and director of quality at UCSF. "In reality, no one in the United States is doing it very well," she says.

Drs. Gupta and Vidyarthi suggest focusing your HM group's communication with primary-care physicians (PCPs): Study whether the hospitalist's messages are getting through to the PCPs and ask for their feedback. Other targets should include identifying high-risk patients, reconciling medications, scheduling the patient's first outpatient visit prior to discharge, and confirming the patient's understanding of the discharge plan.

The first step is to form an interdisciplinary team that approaches discharges as a QI project, Dr. Gupta explains. "Building that team is huge," he says. "It adds a whole new perspective." At UCSF, the team meets monthly and includes hospitalists, PCPs, staff nurses and nursing supervisors, pharmacists, care managers, and patients.

For more information about Project BOOST, visit SHM's resource room.

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Improving patient discharges and reducing preventable "bounce-back" readmissions will have increasing implications for hospitals’ bottom lines—especially if proposed Medicare payment bundling reforms are adopted by Congress. Discharge improvement also enhances a hospital’s reputation with patients and providers, says Neil Gupta, MD, a hospitalist at the University of California at San Francisco.

"I think we all recognize in our daily practice that there are things we can do better for patients at discharge," Dr. Gupta says. "It's sometimes hard to get the resources and motivation to do this. But we know it could really impact patient care and make it better."

Dr. Gupta's hospital is one of 24 participating in SHM's Project BOOST (Better Outcomes for Older Adults through Safe Transitions). The mentorship program is developing a consensus and resources for best practices in patient discharges. National data show that about one in five hospitalized Medicare patients are readmitted within 30 days. While some of these readmissions are appropriate, the sheer quantity of readmissions shows room for improvement, says Dr. Gupta's colleague, Arpana Vidyarthi, MD, a hospitalist and director of quality at UCSF. "In reality, no one in the United States is doing it very well," she says.

Drs. Gupta and Vidyarthi suggest focusing your HM group's communication with primary-care physicians (PCPs): Study whether the hospitalist's messages are getting through to the PCPs and ask for their feedback. Other targets should include identifying high-risk patients, reconciling medications, scheduling the patient's first outpatient visit prior to discharge, and confirming the patient's understanding of the discharge plan.

The first step is to form an interdisciplinary team that approaches discharges as a QI project, Dr. Gupta explains. "Building that team is huge," he says. "It adds a whole new perspective." At UCSF, the team meets monthly and includes hospitalists, PCPs, staff nurses and nursing supervisors, pharmacists, care managers, and patients.

For more information about Project BOOST, visit SHM's resource room.

Improving patient discharges and reducing preventable "bounce-back" readmissions will have increasing implications for hospitals’ bottom lines—especially if proposed Medicare payment bundling reforms are adopted by Congress. Discharge improvement also enhances a hospital’s reputation with patients and providers, says Neil Gupta, MD, a hospitalist at the University of California at San Francisco.

"I think we all recognize in our daily practice that there are things we can do better for patients at discharge," Dr. Gupta says. "It's sometimes hard to get the resources and motivation to do this. But we know it could really impact patient care and make it better."

Dr. Gupta's hospital is one of 24 participating in SHM's Project BOOST (Better Outcomes for Older Adults through Safe Transitions). The mentorship program is developing a consensus and resources for best practices in patient discharges. National data show that about one in five hospitalized Medicare patients are readmitted within 30 days. While some of these readmissions are appropriate, the sheer quantity of readmissions shows room for improvement, says Dr. Gupta's colleague, Arpana Vidyarthi, MD, a hospitalist and director of quality at UCSF. "In reality, no one in the United States is doing it very well," she says.

Drs. Gupta and Vidyarthi suggest focusing your HM group's communication with primary-care physicians (PCPs): Study whether the hospitalist's messages are getting through to the PCPs and ask for their feedback. Other targets should include identifying high-risk patients, reconciling medications, scheduling the patient's first outpatient visit prior to discharge, and confirming the patient's understanding of the discharge plan.

The first step is to form an interdisciplinary team that approaches discharges as a QI project, Dr. Gupta explains. "Building that team is huge," he says. "It adds a whole new perspective." At UCSF, the team meets monthly and includes hospitalists, PCPs, staff nurses and nursing supervisors, pharmacists, care managers, and patients.

For more information about Project BOOST, visit SHM's resource room.

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Every six months, physicians and nurses from Geisinger Medical Center in Danville, Pa., travel to a rural area outside of Chiquimula, Guatemala, to care for people who live without access to modern medicine. Lice, tooth decay, poor eyesight, and asthma are common. Some of the locals suffer from more severe health issues, including parasitic infections, pneumonia, malnutrition, and malaria.

Joel L. Strohecker, DO, a family-medicine-trained hospitalist practicing at Lutheran Medical Center and St. Anthony Hospital in Denver, joined the Geisinger group in June. He recently spoke with TH eWire about his weeklong trip.

Question: About 70% of your patients were children. When did you really feel like you were able to help?

Answer: A couple of little kids who had asthma were brought back a couple days later and were so much better. And the joint injections you could do for the men who worked in the fields. Those were gratifying experiences because they immediately feel better. Then they bring their families the next day because we’ve done something good for them.

Q: You mentioned one memorable patient, a woman with a spinal cord injury. Tell me more about her.

A: She's someone that brought tears to my eyes. It had taken her a couple of hours to walk the trails to get there. She had fallen 20 years earlier and had never been able to really walk well since then. It was very obvious, just by her exam, that she had an upper cervical spinal cord injury. It was just so sad. I mean, what can you do? We gave her steroids, but she had diminished function in her legs.

Q: What was the most rewarding part of the trip?

A: The work was tiring and not necessarily uplifting at times, but I think the best part for me was when we would go back to Chiquimula every night. … We would all go back and play soccer. For me, that was probably the biggest treat and most enjoyable time of the trip. You weren't just a tourist; you were really embedded with the people.

For more information about volunteer opportunities in Guatemala, contact Dr. Strohecker at JoelStrohecker@hotmail.com.

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Every six months, physicians and nurses from Geisinger Medical Center in Danville, Pa., travel to a rural area outside of Chiquimula, Guatemala, to care for people who live without access to modern medicine. Lice, tooth decay, poor eyesight, and asthma are common. Some of the locals suffer from more severe health issues, including parasitic infections, pneumonia, malnutrition, and malaria.

Joel L. Strohecker, DO, a family-medicine-trained hospitalist practicing at Lutheran Medical Center and St. Anthony Hospital in Denver, joined the Geisinger group in June. He recently spoke with TH eWire about his weeklong trip.

Question: About 70% of your patients were children. When did you really feel like you were able to help?

Answer: A couple of little kids who had asthma were brought back a couple days later and were so much better. And the joint injections you could do for the men who worked in the fields. Those were gratifying experiences because they immediately feel better. Then they bring their families the next day because we’ve done something good for them.

Q: You mentioned one memorable patient, a woman with a spinal cord injury. Tell me more about her.

A: She's someone that brought tears to my eyes. It had taken her a couple of hours to walk the trails to get there. She had fallen 20 years earlier and had never been able to really walk well since then. It was very obvious, just by her exam, that she had an upper cervical spinal cord injury. It was just so sad. I mean, what can you do? We gave her steroids, but she had diminished function in her legs.

Q: What was the most rewarding part of the trip?

A: The work was tiring and not necessarily uplifting at times, but I think the best part for me was when we would go back to Chiquimula every night. … We would all go back and play soccer. For me, that was probably the biggest treat and most enjoyable time of the trip. You weren't just a tourist; you were really embedded with the people.

For more information about volunteer opportunities in Guatemala, contact Dr. Strohecker at JoelStrohecker@hotmail.com.

Every six months, physicians and nurses from Geisinger Medical Center in Danville, Pa., travel to a rural area outside of Chiquimula, Guatemala, to care for people who live without access to modern medicine. Lice, tooth decay, poor eyesight, and asthma are common. Some of the locals suffer from more severe health issues, including parasitic infections, pneumonia, malnutrition, and malaria.

Joel L. Strohecker, DO, a family-medicine-trained hospitalist practicing at Lutheran Medical Center and St. Anthony Hospital in Denver, joined the Geisinger group in June. He recently spoke with TH eWire about his weeklong trip.

Question: About 70% of your patients were children. When did you really feel like you were able to help?

Answer: A couple of little kids who had asthma were brought back a couple days later and were so much better. And the joint injections you could do for the men who worked in the fields. Those were gratifying experiences because they immediately feel better. Then they bring their families the next day because we’ve done something good for them.

Q: You mentioned one memorable patient, a woman with a spinal cord injury. Tell me more about her.

A: She's someone that brought tears to my eyes. It had taken her a couple of hours to walk the trails to get there. She had fallen 20 years earlier and had never been able to really walk well since then. It was very obvious, just by her exam, that she had an upper cervical spinal cord injury. It was just so sad. I mean, what can you do? We gave her steroids, but she had diminished function in her legs.

Q: What was the most rewarding part of the trip?

A: The work was tiring and not necessarily uplifting at times, but I think the best part for me was when we would go back to Chiquimula every night. … We would all go back and play soccer. For me, that was probably the biggest treat and most enjoyable time of the trip. You weren't just a tourist; you were really embedded with the people.

For more information about volunteer opportunities in Guatemala, contact Dr. Strohecker at JoelStrohecker@hotmail.com.

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Medicare Cuts Could Hit HM Hard

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The final 2010 Medicare physician fee schedule presents a mixed bag for hospitalists. As officials from the Centers for Medicare and Medicaid Services (CMS) warned, the update carries a hefty 21.2% fee schedule cut. Congressional action to avert that cut is expected, though wrangling over healthcare reform may force a stopgap measure to prevent the cuts from taking effect Jan. 1.

In a statement, Jonathan Blum, director of the CMS Center for Medicare Management, said the Obama administration is committed to repealing the sustainable growth rate formula that resulted in the substantial cut. In the meantime, he said, CMS is finalizing its proposal to drop physician-administered drugs from the definition of "physician services," which is used to formulate future fee updates. SHM has strongly supported both efforts and is calling on members to contact their legislators before a Nov. 16 vote.

Another huge change for hospitalists: The use of consultation codes has been discontinued, with the exception of codes related to telemedicine. In their place, healthcare providers must bill under initial hospital care, initial nursing facility care, or initial office visits. All transfers of care, for example, will now require billing under an initial visit code rather than a subsequent visit code. Consultation documentation requirements will no longer apply, though initial codes could be valued somewhat lower than similar consultation codes despite proposed adjustments to the relative value units (RVUs). Although bad for traditional consultations, some analysts see the net change as good for the comanagement of patients.

To help smooth the transition to this new coding system, SHM will be hosting a webinar, "Hot Topics in Evaluation and Management Coding," on Dec. 2.

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The final 2010 Medicare physician fee schedule presents a mixed bag for hospitalists. As officials from the Centers for Medicare and Medicaid Services (CMS) warned, the update carries a hefty 21.2% fee schedule cut. Congressional action to avert that cut is expected, though wrangling over healthcare reform may force a stopgap measure to prevent the cuts from taking effect Jan. 1.

In a statement, Jonathan Blum, director of the CMS Center for Medicare Management, said the Obama administration is committed to repealing the sustainable growth rate formula that resulted in the substantial cut. In the meantime, he said, CMS is finalizing its proposal to drop physician-administered drugs from the definition of "physician services," which is used to formulate future fee updates. SHM has strongly supported both efforts and is calling on members to contact their legislators before a Nov. 16 vote.

Another huge change for hospitalists: The use of consultation codes has been discontinued, with the exception of codes related to telemedicine. In their place, healthcare providers must bill under initial hospital care, initial nursing facility care, or initial office visits. All transfers of care, for example, will now require billing under an initial visit code rather than a subsequent visit code. Consultation documentation requirements will no longer apply, though initial codes could be valued somewhat lower than similar consultation codes despite proposed adjustments to the relative value units (RVUs). Although bad for traditional consultations, some analysts see the net change as good for the comanagement of patients.

To help smooth the transition to this new coding system, SHM will be hosting a webinar, "Hot Topics in Evaluation and Management Coding," on Dec. 2.

The final 2010 Medicare physician fee schedule presents a mixed bag for hospitalists. As officials from the Centers for Medicare and Medicaid Services (CMS) warned, the update carries a hefty 21.2% fee schedule cut. Congressional action to avert that cut is expected, though wrangling over healthcare reform may force a stopgap measure to prevent the cuts from taking effect Jan. 1.

In a statement, Jonathan Blum, director of the CMS Center for Medicare Management, said the Obama administration is committed to repealing the sustainable growth rate formula that resulted in the substantial cut. In the meantime, he said, CMS is finalizing its proposal to drop physician-administered drugs from the definition of "physician services," which is used to formulate future fee updates. SHM has strongly supported both efforts and is calling on members to contact their legislators before a Nov. 16 vote.

Another huge change for hospitalists: The use of consultation codes has been discontinued, with the exception of codes related to telemedicine. In their place, healthcare providers must bill under initial hospital care, initial nursing facility care, or initial office visits. All transfers of care, for example, will now require billing under an initial visit code rather than a subsequent visit code. Consultation documentation requirements will no longer apply, though initial codes could be valued somewhat lower than similar consultation codes despite proposed adjustments to the relative value units (RVUs). Although bad for traditional consultations, some analysts see the net change as good for the comanagement of patients.

To help smooth the transition to this new coding system, SHM will be hosting a webinar, "Hot Topics in Evaluation and Management Coding," on Dec. 2.

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Academics Energized

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Frank Marquez, MD, wasn't told he was going to the Academic Hospitalist Academy (AHA) until a couple of days before the start of the four-day training program in Atlanta. Short notice aside, Dr. Marquez was elated he was able to attend.

"There are a lot of practical tips. For me, the biggest thing is the academy has shown me that I have to stop being passive and start being proactive. I need to take an active role, serve on committees," says Dr. Marquez, a third-year academic hospitalist at St. Joseph's Hospital and Medical Center in Phoenix. "I think that's going to help my career."

Dr. Marquez, who leads a five-person team of residents, interns, and medical students, was one of nearly 80 early-career physicians—the average attendee had two years of HM experience—who attended AHA. The inaugural event was co-sponsored by SHM, the Society of General Internal Medicine and the Associate Chiefs of General Internal Medicine. The program featured top-flight HM faculty, but Dr. Marquez especially enjoyed the emphasis on small-group workshops and interactive teaching.

"When we first took our jobs as hospitalists, no one took the time to explain to us how to be an effective leader, mentor people, implement change," he says. "Here you have an opportunity to learn that and to participate. It’s not a lecture; it’s not intimidating. You can speak up."

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Frank Marquez, MD, wasn't told he was going to the Academic Hospitalist Academy (AHA) until a couple of days before the start of the four-day training program in Atlanta. Short notice aside, Dr. Marquez was elated he was able to attend.

"There are a lot of practical tips. For me, the biggest thing is the academy has shown me that I have to stop being passive and start being proactive. I need to take an active role, serve on committees," says Dr. Marquez, a third-year academic hospitalist at St. Joseph's Hospital and Medical Center in Phoenix. "I think that's going to help my career."

Dr. Marquez, who leads a five-person team of residents, interns, and medical students, was one of nearly 80 early-career physicians—the average attendee had two years of HM experience—who attended AHA. The inaugural event was co-sponsored by SHM, the Society of General Internal Medicine and the Associate Chiefs of General Internal Medicine. The program featured top-flight HM faculty, but Dr. Marquez especially enjoyed the emphasis on small-group workshops and interactive teaching.

"When we first took our jobs as hospitalists, no one took the time to explain to us how to be an effective leader, mentor people, implement change," he says. "Here you have an opportunity to learn that and to participate. It’s not a lecture; it’s not intimidating. You can speak up."

Frank Marquez, MD, wasn't told he was going to the Academic Hospitalist Academy (AHA) until a couple of days before the start of the four-day training program in Atlanta. Short notice aside, Dr. Marquez was elated he was able to attend.

"There are a lot of practical tips. For me, the biggest thing is the academy has shown me that I have to stop being passive and start being proactive. I need to take an active role, serve on committees," says Dr. Marquez, a third-year academic hospitalist at St. Joseph's Hospital and Medical Center in Phoenix. "I think that's going to help my career."

Dr. Marquez, who leads a five-person team of residents, interns, and medical students, was one of nearly 80 early-career physicians—the average attendee had two years of HM experience—who attended AHA. The inaugural event was co-sponsored by SHM, the Society of General Internal Medicine and the Associate Chiefs of General Internal Medicine. The program featured top-flight HM faculty, but Dr. Marquez especially enjoyed the emphasis on small-group workshops and interactive teaching.

"When we first took our jobs as hospitalists, no one took the time to explain to us how to be an effective leader, mentor people, implement change," he says. "Here you have an opportunity to learn that and to participate. It’s not a lecture; it’s not intimidating. You can speak up."

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    Courtesy Dr. Donna Marti

Diagnosis: Contact Dermatitis to Paraphenylenediamine

The patient’s mother reported blisters, erythema, and scabbing in the area of the tattoo. Six months later, the patient underwent paraphenylenediamine patch testing and exhibited a reaction.

The patient was treated with mild topical steroids and a 4-day prednisone course prior to presentation. A week of clobetasol ointment improved the pruritus and erythema.

Henna is a green powdered extract derived from the leaves of the Lawsonia alba plant. The active ingredient is lawsone. Middle Eastern and Indian cultures use the extract to dye the hair, skin, and nails. Contact with the skin for an extended period of time yields a brownish orange pigment. In Western countries, Henna tattoos have gained popularity as a temporary alternative to ink tattoos.

Henna may be used in its pure form, however, paraphenylenediamine (PPD) is often added to darken the pigment, expedite drying time, and improve design accuracy. PPD is an allergen found in hair dyes and photographic film processing. It is a potent T-cell stimulator, and its efficacy is directly related to concentration and duration of exposure. Patch tests among individuals with henna contact dermatitis are negative to pure henna powder but react strongly to PPD, which has lead to the assumption that PPD is the main allergen in henna paste.

Henna tattoo inks have been found to have PPD concentrations as high as 15%-30%, and, often, the inks are in contact with the skin for several days after application. The hypersensitivity can sensitize individuals to PPD-containing substances such as dark hair dyes and dark clothing. Cross reaction may cause hypersensitivity to natural rubber latex, azo dyes, thiurams, PABA sunscreen, para-aminosalicylic acid, and benzocaine.

The initial inflammatory response may present as erythematous, eczematous, pruritic, or papulovesicular eruption in the area or boundary of the original design. Edema, anaphylaxis, and collapse are less common manifestations. The inflammation can result in scarring, keloid formation, and permanent, post-inflammatory pigment changes.

As demonstrated in my patient, hypopigmentation occurs more frequently in children than adults. Therapy includes protection of the blistered area, antihistamines, treatment of infection, and aggressive topical corticosteroid therapy.

This case was first presented at Maryland Derm, at the University of Maryland School of Medicine in Baltimore, by Dr. Martin, Dr. Vera David, and Dr. Anthony Gaspari.

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    Courtesy Dr. Donna Marti

Diagnosis: Contact Dermatitis to Paraphenylenediamine

The patient’s mother reported blisters, erythema, and scabbing in the area of the tattoo. Six months later, the patient underwent paraphenylenediamine patch testing and exhibited a reaction.

The patient was treated with mild topical steroids and a 4-day prednisone course prior to presentation. A week of clobetasol ointment improved the pruritus and erythema.

Henna is a green powdered extract derived from the leaves of the Lawsonia alba plant. The active ingredient is lawsone. Middle Eastern and Indian cultures use the extract to dye the hair, skin, and nails. Contact with the skin for an extended period of time yields a brownish orange pigment. In Western countries, Henna tattoos have gained popularity as a temporary alternative to ink tattoos.

Henna may be used in its pure form, however, paraphenylenediamine (PPD) is often added to darken the pigment, expedite drying time, and improve design accuracy. PPD is an allergen found in hair dyes and photographic film processing. It is a potent T-cell stimulator, and its efficacy is directly related to concentration and duration of exposure. Patch tests among individuals with henna contact dermatitis are negative to pure henna powder but react strongly to PPD, which has lead to the assumption that PPD is the main allergen in henna paste.

Henna tattoo inks have been found to have PPD concentrations as high as 15%-30%, and, often, the inks are in contact with the skin for several days after application. The hypersensitivity can sensitize individuals to PPD-containing substances such as dark hair dyes and dark clothing. Cross reaction may cause hypersensitivity to natural rubber latex, azo dyes, thiurams, PABA sunscreen, para-aminosalicylic acid, and benzocaine.

The initial inflammatory response may present as erythematous, eczematous, pruritic, or papulovesicular eruption in the area or boundary of the original design. Edema, anaphylaxis, and collapse are less common manifestations. The inflammation can result in scarring, keloid formation, and permanent, post-inflammatory pigment changes.

As demonstrated in my patient, hypopigmentation occurs more frequently in children than adults. Therapy includes protection of the blistered area, antihistamines, treatment of infection, and aggressive topical corticosteroid therapy.

This case was first presented at Maryland Derm, at the University of Maryland School of Medicine in Baltimore, by Dr. Martin, Dr. Vera David, and Dr. Anthony Gaspari.

    Courtesy Dr. Donna Marti

Diagnosis: Contact Dermatitis to Paraphenylenediamine

The patient’s mother reported blisters, erythema, and scabbing in the area of the tattoo. Six months later, the patient underwent paraphenylenediamine patch testing and exhibited a reaction.

The patient was treated with mild topical steroids and a 4-day prednisone course prior to presentation. A week of clobetasol ointment improved the pruritus and erythema.

Henna is a green powdered extract derived from the leaves of the Lawsonia alba plant. The active ingredient is lawsone. Middle Eastern and Indian cultures use the extract to dye the hair, skin, and nails. Contact with the skin for an extended period of time yields a brownish orange pigment. In Western countries, Henna tattoos have gained popularity as a temporary alternative to ink tattoos.

Henna may be used in its pure form, however, paraphenylenediamine (PPD) is often added to darken the pigment, expedite drying time, and improve design accuracy. PPD is an allergen found in hair dyes and photographic film processing. It is a potent T-cell stimulator, and its efficacy is directly related to concentration and duration of exposure. Patch tests among individuals with henna contact dermatitis are negative to pure henna powder but react strongly to PPD, which has lead to the assumption that PPD is the main allergen in henna paste.

Henna tattoo inks have been found to have PPD concentrations as high as 15%-30%, and, often, the inks are in contact with the skin for several days after application. The hypersensitivity can sensitize individuals to PPD-containing substances such as dark hair dyes and dark clothing. Cross reaction may cause hypersensitivity to natural rubber latex, azo dyes, thiurams, PABA sunscreen, para-aminosalicylic acid, and benzocaine.

The initial inflammatory response may present as erythematous, eczematous, pruritic, or papulovesicular eruption in the area or boundary of the original design. Edema, anaphylaxis, and collapse are less common manifestations. The inflammation can result in scarring, keloid formation, and permanent, post-inflammatory pigment changes.

As demonstrated in my patient, hypopigmentation occurs more frequently in children than adults. Therapy includes protection of the blistered area, antihistamines, treatment of infection, and aggressive topical corticosteroid therapy.

This case was first presented at Maryland Derm, at the University of Maryland School of Medicine in Baltimore, by Dr. Martin, Dr. Vera David, and Dr. Anthony Gaspari.

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VTE Prophylaxis Compliance Lacking

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Only one in six medical discharges receives venous thromboembolism (VTE) prophylaxis that conforms to the seventh American College of Chest Physicians (ACCP) guidelines, according to a report in the Journal of Hospital Medicine.

The study reported that, overall, 65.9% of medical discharges and 77.7% of surgical discharges received at least one order for VTE prophylaxis during hospitalization. However, when ACCP guidelines for type, dose, and duration are overlaid on the same data set, the percentage of "appropriate prophylaxis" dropped to 16.4% for medical discharges and 12.7% for surgical discharges (JHM 2009;doi 10.1002/jhm.526).

"If we're going to be in the business of healthcare safety and quality … that's not good enough," says lead investigator Alpesh Amin, MD, MBA, FHM, FACP, professor and chairman of the Department of Medicine and executive director of the hospitalist program at the University of California at Irvine. "We're only doing it appropriately [part] of the time."

Dr. Amin has turned VTE research into an area of focus, and is in San Diego today presenting two additional VTE studies at CHEST 2009. One study, "Analysis of Inpatient and Outpatient Venous Thromboembolism Prophylaxis Patterns in U.S. Critical Care Patients," found that of 1,279 discharges analyzed, only 4% continued prophylaxis. The other study, "VTE Prophylaxis Across the Continuum of Care in U.S. Medical and Surgical Patients at Risk of Venous Thromboembolism," reported nearly 90% of patients received no outpatient prophylaxis.

All three studies were supported by Sanofi-Aventis U.S. Inc. The CHEST 2009 presentations have not been published yet. Dr. Amin says the studies show hospitalists can take charge of VTE orders to assure treatment is delivered in line with approved protocols.

"The idea of these studies was to say, 'We've got these national recommendations; how well are we actually doing?' " Dr. Amin says. "You can do something, but you ought to do it according to national guidelines."

For more information on the essential elements of VTE prevention and performance improvement, visit SHM's VTE Resource Room.

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Only one in six medical discharges receives venous thromboembolism (VTE) prophylaxis that conforms to the seventh American College of Chest Physicians (ACCP) guidelines, according to a report in the Journal of Hospital Medicine.

The study reported that, overall, 65.9% of medical discharges and 77.7% of surgical discharges received at least one order for VTE prophylaxis during hospitalization. However, when ACCP guidelines for type, dose, and duration are overlaid on the same data set, the percentage of "appropriate prophylaxis" dropped to 16.4% for medical discharges and 12.7% for surgical discharges (JHM 2009;doi 10.1002/jhm.526).

"If we're going to be in the business of healthcare safety and quality … that's not good enough," says lead investigator Alpesh Amin, MD, MBA, FHM, FACP, professor and chairman of the Department of Medicine and executive director of the hospitalist program at the University of California at Irvine. "We're only doing it appropriately [part] of the time."

Dr. Amin has turned VTE research into an area of focus, and is in San Diego today presenting two additional VTE studies at CHEST 2009. One study, "Analysis of Inpatient and Outpatient Venous Thromboembolism Prophylaxis Patterns in U.S. Critical Care Patients," found that of 1,279 discharges analyzed, only 4% continued prophylaxis. The other study, "VTE Prophylaxis Across the Continuum of Care in U.S. Medical and Surgical Patients at Risk of Venous Thromboembolism," reported nearly 90% of patients received no outpatient prophylaxis.

All three studies were supported by Sanofi-Aventis U.S. Inc. The CHEST 2009 presentations have not been published yet. Dr. Amin says the studies show hospitalists can take charge of VTE orders to assure treatment is delivered in line with approved protocols.

"The idea of these studies was to say, 'We've got these national recommendations; how well are we actually doing?' " Dr. Amin says. "You can do something, but you ought to do it according to national guidelines."

For more information on the essential elements of VTE prevention and performance improvement, visit SHM's VTE Resource Room.

Only one in six medical discharges receives venous thromboembolism (VTE) prophylaxis that conforms to the seventh American College of Chest Physicians (ACCP) guidelines, according to a report in the Journal of Hospital Medicine.

The study reported that, overall, 65.9% of medical discharges and 77.7% of surgical discharges received at least one order for VTE prophylaxis during hospitalization. However, when ACCP guidelines for type, dose, and duration are overlaid on the same data set, the percentage of "appropriate prophylaxis" dropped to 16.4% for medical discharges and 12.7% for surgical discharges (JHM 2009;doi 10.1002/jhm.526).

"If we're going to be in the business of healthcare safety and quality … that's not good enough," says lead investigator Alpesh Amin, MD, MBA, FHM, FACP, professor and chairman of the Department of Medicine and executive director of the hospitalist program at the University of California at Irvine. "We're only doing it appropriately [part] of the time."

Dr. Amin has turned VTE research into an area of focus, and is in San Diego today presenting two additional VTE studies at CHEST 2009. One study, "Analysis of Inpatient and Outpatient Venous Thromboembolism Prophylaxis Patterns in U.S. Critical Care Patients," found that of 1,279 discharges analyzed, only 4% continued prophylaxis. The other study, "VTE Prophylaxis Across the Continuum of Care in U.S. Medical and Surgical Patients at Risk of Venous Thromboembolism," reported nearly 90% of patients received no outpatient prophylaxis.

All three studies were supported by Sanofi-Aventis U.S. Inc. The CHEST 2009 presentations have not been published yet. Dr. Amin says the studies show hospitalists can take charge of VTE orders to assure treatment is delivered in line with approved protocols.

"The idea of these studies was to say, 'We've got these national recommendations; how well are we actually doing?' " Dr. Amin says. "You can do something, but you ought to do it according to national guidelines."

For more information on the essential elements of VTE prevention and performance improvement, visit SHM's VTE Resource Room.

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The Hospitalist - 2009(11)
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The Hospitalist - 2009(11)
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VTE Prophylaxis Compliance Lacking
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VTE Prophylaxis Compliance Lacking
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