Mrs. J, age 75, has moderate Alzheimer’s dementia and lives at home with her husband. Since her Alzheimer’s disease (AD) diagnosis 2 years ago, Mrs. J generally has been cooperative and not physically aggressive, but has experienced occasional depressive symptoms. However, Mr. J reports that recently his wife is becoming increasingly confused and agitated and wanders the house at night. His efforts to calm and coax her back to bed often lead to increased agitation and yelling. On 1 occasion Mrs. J pushed her husband. Mr. J is concerned that if these behaviors continue he may not be able to care for her at home. Mr. J read online that antipsychotics might reduce aggressive behavior, but is concerned about the increased risk of mortality and stroke with these medications.

Mrs. J receives donepezil, 10 mg/d, sertra-line, 50 mg/d, and extended-release oxybutynin, 10 mg/d. Her over-the-counter (OTC) medications include acetaminophen, 650 mg as needed for pain, ranitidine, 150 mg/d, and docusate sodium, 100 mg/d. Several nights last week, Mr. J gave his wife an unknown OTC sleep medication, hoping it would stop her nighttime wandering, but it did not help. Physical examination, laboratory testing, and urine culture are all normal.

Most dementia patients experience neuropsychiatric disturbances, especially at later stages, that often lead to caregiver distress and nursing home placement. Although these symptoms may signal progressing dementia, environmental factors, medical conditions, and medications may worsen functioning and should be considered in the assessment.¹

Mrs. J has no medical problems that were identified as possible triggers for her behavior. Mr. J’s interference with his wife’s wandering could have increased her agitation, but he is gentle toward her and she has become agitated with no apparent trigger. “Sundowning” and poor sleep also may be involved, as sleep deprivation can lead to delirium and worsen cognitive deficits and behavioral problems.¹ Depression also should be considered.¹ Finally, Mrs. J is taking several medications with anticholinergic properties—oxybutynin, ranitidine, and an unknown OTC sleep medication, which likely contains diphenhydramine or doxylamine—that might contribute to her agitation.

Patients with dementia are highly sensitive to the cognitive and psychiatric adverse effects of anticholinergic medications. In studies of patients with mild or moderate Alzheimer’s dementia who received the potent anticholinergic scopolamine, adverse effects included:

• memory impairment
• restlessness
• disjointed speech
• motor incoordination
• drowsiness
• euphoria
• agitation
• hallucinations
• hostility.

Many of these effects worsened with increasing doses.^2,3 Age-matched controls experienced less severe memory impairment and no behavioral symptoms, which suggests that dementia-related damage to the cholinergic system leads to increased sensitivity to anticholinergics.

A cross-sectional study of 230 patients with AD identified anticholinergic use as a risk factor for psychosis (odds ratio 2.13, 95% confidence interval, 1.03 to 4.43), after adjusting for age and cognition.⁴ Among patients receiving 2 or 3 anticholinergics, 69% had psychotic symptoms compared with 48% of those receiving 1 anticholinergic and 32% of those receiving no anticholinergics.⁴ Anticholinergic overdoses can cause psychotic symptoms and delirium. A subtle presentation of delirium from prescribed anticholinergics may be confused with worsening dementia.¹ The sum of the evidence suggests that drugs with anticholinergic effects can contribute to agitation and psychosis in dementia.

When to discontinue

When diagnosing dementia it is important to address other potential causes of cognitive impairment, including medications. Approximately one-third of patients with dementia receive anticholinergic drugs, which suggests that providers often do not recognize the potential for harm with these medications.⁵ After patients receive acetylcholinesterase inhibitors (AChEIs)—which are used to enhance cognition in dementia patients—increased anticholinergic use may follow, often to treat adverse effects of AChEIs.⁵ This may negate the benefits of AChEIs and pose risk of further harm from the anticholinergics.^1,5 Although any time is a good time to discontinue an inessential anticholinergic in a patient with dementia, providers might consider screening for these drugs at the initial diagnosis, after initiating a cholinesterase inhibitor or increasing a dose, or if the patient develops psychotic or behavioral symptoms.

For Mrs. J, ranitidine and oxybutynin likely were used to treat gastrointestinal complaints and urinary frequency, which are known adverse effects of AChEIs. Many OTC preparations for insomnia, respiratory symptoms, and allergies contain older, anticholinergic antihistamines. Advise caregivers of dementia patients about possible adverse effects of OTC medications to prevent anticholinergic exposure. The Table provides a partial list of medications thought to have clinically significant anticholinergic effects.

‘Pharmacologic debridement’ refers to tapering and discontinuing medications that are no longer necessary or appropriate. Prescribers often are hesitant to discontinue medications prescribed by other clinicians and may assume that a medication used long term has been tolerated and helpful. However, as patients age—particularly if they develop dementia—their ability to tolerate a medication can change. Patients with dementia also may have difficulty attributing adverse experiences to medications and communicating these effects to providers. Some medical providers may not recognize adverse psychiatric and cognitive effects of the nonpsychiatric medications they prescribe because they do not have sufficient dementia expertise. Consulting with these providers may help determine the risk-benefit considerations of these medications.

Generally, anticholinergics should be discontinued if they are not essential to a patient’s health or if safer non-anticholinergic alternatives are available.⁵ Tapering may be necessary to prevent adverse effects from cholinergic rebound if a potent anticholinergic has been used chronically.⁵ The first step in addressing Mrs. J’s agitation is to discontinue the anticholinergic medications and monitor her symptoms. This pharmacologic debridement may avert the use of antipsychotics, which carry serious risks for dementia patients.¹

Table
Drugs with clinically significant anticholinergic effects*

Related Resources

• Cancelli I, Beltrame M, D’Anna L, et al. Drugs with anticholinergic properties: a potential risk factor for psychosis onset in Alzheimer’s disease? Expert Opin Drug Saf. 2009;8(5):549-557.
• Meeks TW, Jeste DV. Beyond the black box: what is the role for antipsychotics in dementia? Current Psychiatry. 2008;7(6): 50-65.
• Centers for Education and Research on Therapeutics. Anticholinergic pocket reference card. www.chainonline.org/home/content_images/Anticholinergic%20Pocket%20Card%20CLR%203_12_10.pdf.

Drug Brand Names

• Amitriptyline • Elavil
• Atropine • Sal-Tropine
• Azelastine nasal spray • Astelin
• Belladonna alkaloids • Donnatal
• Benztropine • Cogentin
• Brompheniramine • Dimetane
• Carbamazepine • Carbatrol, Tegretol, others
• Carbinoxamine • Palgic
• Chlorpheniramine • Chlor-Trimeton
• Chlorpromazine • Thorazine
• Cimetidine • Tagamet
• Clemastine • Tavist
• Clidinium • Quarzan
• Clomipramine • Anafranil
• Clozapine • Clozaril
• Cyclobenzaprine • Flexeril
• Cyproheptadine • Periactin
• Darifenacin • Enablex
• Desipramine • Norpramin
• Dexbrompheniramine • Drixoral
• Dexchlorpheniramine • Polaramine
• Dicyclomine • Bentyl
• Dimenhydrinate • Dramamine
• Diphenhydramine • Benadryl, Sominex, others
• Docusate Sodium • Colace
• Donepezil • Aricept
• Doxepin • Adapin
• Doxylamine • Aldex, Unisom, others
• Flavoxate • Urispas
• Glycopyrrolate • Robinul
• Hydroxyzine • Atarax
• Hyoscyamine • Cystospaz, Levbid
• Imipramine • Tofranil
• Ipratropium • Atrovent
• Loxapine • Loxitane
• Meclizine • Antivert
• Meperidine • Demerol
• Mepyramine • Anthisan
• Methscopolamine • Pamine
• Molindone • Moban
• Nortriptyline • Aventyl
• Olanzapine • Zyprexa
• Olopatadine nasal spray • Patanase
• Orphenadrine • Norflex
• Oxybutynin extended-release • Ditropan XL
• Paroxetine • Paxil
• Phenyltoloxamine • Dologesic, Durayin, others
• Pimozide • Orap
• Prochlorperazine • Compazine
• Procyclidine • Kemadrin
• Promethazine • Phenergan
• Propanthelin • Pro-Banthine
• Protriptyline • Vivactil
• Quetiapine • Seroquel
• Ranitidine • Zantac
• Scopolamine • Scopace
• Sertraline • Zoloft
• Solifenacin • VESIcare
• Thioridazine • Mellaril
• Tiotropium • Spiriva
• Tolterodine • Detrol
• Trihexyphenidyl • Artane
• Trimethobenzamide • Tigan
• Trimipramine • Surmontil
• Triprolidine • Actifed
• Trospium • Sanctura

Acknowledgements

This work was supported by an Agency for Healthcare Research and Quality (AHRQ) Centers for Education and Research on Therapeutics cooperative agreement #5 U18 HSO16094.

Disclosure

Dr. Carnahan receives grant/research support from the Agency for Healthcare Research and Quality.

Mrs. J, age 75, has moderate Alzheimer’s dementia and lives at home with her husband. Since her Alzheimer’s disease (AD) diagnosis 2 years ago, Mrs. J generally has been cooperative and not physically aggressive, but has experienced occasional depressive symptoms. However, Mr. J reports that recently his wife is becoming increasingly confused and agitated and wanders the house at night. His efforts to calm and coax her back to bed often lead to increased agitation and yelling. On 1 occasion Mrs. J pushed her husband. Mr. J is concerned that if these behaviors continue he may not be able to care for her at home. Mr. J read online that antipsychotics might reduce aggressive behavior, but is concerned about the increased risk of mortality and stroke with these medications.

Mrs. J receives donepezil, 10 mg/d, sertra-line, 50 mg/d, and extended-release oxybutynin, 10 mg/d. Her over-the-counter (OTC) medications include acetaminophen, 650 mg as needed for pain, ranitidine, 150 mg/d, and docusate sodium, 100 mg/d. Several nights last week, Mr. J gave his wife an unknown OTC sleep medication, hoping it would stop her nighttime wandering, but it did not help. Physical examination, laboratory testing, and urine culture are all normal.

Most dementia patients experience neuropsychiatric disturbances, especially at later stages, that often lead to caregiver distress and nursing home placement. Although these symptoms may signal progressing dementia, environmental factors, medical conditions, and medications may worsen functioning and should be considered in the assessment.¹

Mrs. J has no medical problems that were identified as possible triggers for her behavior. Mr. J’s interference with his wife’s wandering could have increased her agitation, but he is gentle toward her and she has become agitated with no apparent trigger. “Sundowning” and poor sleep also may be involved, as sleep deprivation can lead to delirium and worsen cognitive deficits and behavioral problems.¹ Depression also should be considered.¹ Finally, Mrs. J is taking several medications with anticholinergic properties—oxybutynin, ranitidine, and an unknown OTC sleep medication, which likely contains diphenhydramine or doxylamine—that might contribute to her agitation.

Patients with dementia are highly sensitive to the cognitive and psychiatric adverse effects of anticholinergic medications. In studies of patients with mild or moderate Alzheimer’s dementia who received the potent anticholinergic scopolamine, adverse effects included:

• memory impairment
• restlessness
• disjointed speech
• motor incoordination
• drowsiness
• euphoria
• agitation
• hallucinations
• hostility.

Many of these effects worsened with increasing doses.^2,3 Age-matched controls experienced less severe memory impairment and no behavioral symptoms, which suggests that dementia-related damage to the cholinergic system leads to increased sensitivity to anticholinergics.

A cross-sectional study of 230 patients with AD identified anticholinergic use as a risk factor for psychosis (odds ratio 2.13, 95% confidence interval, 1.03 to 4.43), after adjusting for age and cognition.⁴ Among patients receiving 2 or 3 anticholinergics, 69% had psychotic symptoms compared with 48% of those receiving 1 anticholinergic and 32% of those receiving no anticholinergics.⁴ Anticholinergic overdoses can cause psychotic symptoms and delirium. A subtle presentation of delirium from prescribed anticholinergics may be confused with worsening dementia.¹ The sum of the evidence suggests that drugs with anticholinergic effects can contribute to agitation and psychosis in dementia.

When to discontinue

When diagnosing dementia it is important to address other potential causes of cognitive impairment, including medications. Approximately one-third of patients with dementia receive anticholinergic drugs, which suggests that providers often do not recognize the potential for harm with these medications.⁵ After patients receive acetylcholinesterase inhibitors (AChEIs)—which are used to enhance cognition in dementia patients—increased anticholinergic use may follow, often to treat adverse effects of AChEIs.⁵ This may negate the benefits of AChEIs and pose risk of further harm from the anticholinergics.^1,5 Although any time is a good time to discontinue an inessential anticholinergic in a patient with dementia, providers might consider screening for these drugs at the initial diagnosis, after initiating a cholinesterase inhibitor or increasing a dose, or if the patient develops psychotic or behavioral symptoms.

For Mrs. J, ranitidine and oxybutynin likely were used to treat gastrointestinal complaints and urinary frequency, which are known adverse effects of AChEIs. Many OTC preparations for insomnia, respiratory symptoms, and allergies contain older, anticholinergic antihistamines. Advise caregivers of dementia patients about possible adverse effects of OTC medications to prevent anticholinergic exposure. The Table provides a partial list of medications thought to have clinically significant anticholinergic effects.

‘Pharmacologic debridement’ refers to tapering and discontinuing medications that are no longer necessary or appropriate. Prescribers often are hesitant to discontinue medications prescribed by other clinicians and may assume that a medication used long term has been tolerated and helpful. However, as patients age—particularly if they develop dementia—their ability to tolerate a medication can change. Patients with dementia also may have difficulty attributing adverse experiences to medications and communicating these effects to providers. Some medical providers may not recognize adverse psychiatric and cognitive effects of the nonpsychiatric medications they prescribe because they do not have sufficient dementia expertise. Consulting with these providers may help determine the risk-benefit considerations of these medications.

Generally, anticholinergics should be discontinued if they are not essential to a patient’s health or if safer non-anticholinergic alternatives are available.⁵ Tapering may be necessary to prevent adverse effects from cholinergic rebound if a potent anticholinergic has been used chronically.⁵ The first step in addressing Mrs. J’s agitation is to discontinue the anticholinergic medications and monitor her symptoms. This pharmacologic debridement may avert the use of antipsychotics, which carry serious risks for dementia patients.¹

Table
Drugs with clinically significant anticholinergic effects*

Related Resources

• Cancelli I, Beltrame M, D’Anna L, et al. Drugs with anticholinergic properties: a potential risk factor for psychosis onset in Alzheimer’s disease? Expert Opin Drug Saf. 2009;8(5):549-557.
• Meeks TW, Jeste DV. Beyond the black box: what is the role for antipsychotics in dementia? Current Psychiatry. 2008;7(6): 50-65.
• Centers for Education and Research on Therapeutics. Anticholinergic pocket reference card. www.chainonline.org/home/content_images/Anticholinergic%20Pocket%20Card%20CLR%203_12_10.pdf.

Drug Brand Names

• Amitriptyline • Elavil
• Atropine • Sal-Tropine
• Azelastine nasal spray • Astelin
• Belladonna alkaloids • Donnatal
• Benztropine • Cogentin
• Brompheniramine • Dimetane
• Carbamazepine • Carbatrol, Tegretol, others
• Carbinoxamine • Palgic
• Chlorpheniramine • Chlor-Trimeton
• Chlorpromazine • Thorazine
• Cimetidine • Tagamet
• Clemastine • Tavist
• Clidinium • Quarzan
• Clomipramine • Anafranil
• Clozapine • Clozaril
• Cyclobenzaprine • Flexeril
• Cyproheptadine • Periactin
• Darifenacin • Enablex
• Desipramine • Norpramin
• Dexbrompheniramine • Drixoral
• Dexchlorpheniramine • Polaramine
• Dicyclomine • Bentyl
• Dimenhydrinate • Dramamine
• Diphenhydramine • Benadryl, Sominex, others
• Docusate Sodium • Colace
• Donepezil • Aricept
• Doxepin • Adapin
• Doxylamine • Aldex, Unisom, others
• Flavoxate • Urispas
• Glycopyrrolate • Robinul
• Hydroxyzine • Atarax
• Hyoscyamine • Cystospaz, Levbid
• Imipramine • Tofranil
• Ipratropium • Atrovent
• Loxapine • Loxitane
• Meclizine • Antivert
• Meperidine • Demerol
• Mepyramine • Anthisan
• Methscopolamine • Pamine
• Molindone • Moban
• Nortriptyline • Aventyl
• Olanzapine • Zyprexa
• Olopatadine nasal spray • Patanase
• Orphenadrine • Norflex
• Oxybutynin extended-release • Ditropan XL
• Paroxetine • Paxil
• Phenyltoloxamine • Dologesic, Durayin, others
• Pimozide • Orap
• Prochlorperazine • Compazine
• Procyclidine • Kemadrin
• Promethazine • Phenergan
• Propanthelin • Pro-Banthine
• Protriptyline • Vivactil
• Quetiapine • Seroquel
• Ranitidine • Zantac
• Scopolamine • Scopace
• Sertraline • Zoloft
• Solifenacin • VESIcare
• Thioridazine • Mellaril
• Tiotropium • Spiriva
• Tolterodine • Detrol
• Trihexyphenidyl • Artane
• Trimethobenzamide • Tigan
• Trimipramine • Surmontil
• Triprolidine • Actifed
• Trospium • Sanctura

Acknowledgements

This work was supported by an Agency for Healthcare Research and Quality (AHRQ) Centers for Education and Research on Therapeutics cooperative agreement #5 U18 HSO16094.

Disclosure

Dr. Carnahan receives grant/research support from the Agency for Healthcare Research and Quality.

Mrs. J, age 75, has moderate Alzheimer’s dementia and lives at home with her husband. Since her Alzheimer’s disease (AD) diagnosis 2 years ago, Mrs. J generally has been cooperative and not physically aggressive, but has experienced occasional depressive symptoms. However, Mr. J reports that recently his wife is becoming increasingly confused and agitated and wanders the house at night. His efforts to calm and coax her back to bed often lead to increased agitation and yelling. On 1 occasion Mrs. J pushed her husband. Mr. J is concerned that if these behaviors continue he may not be able to care for her at home. Mr. J read online that antipsychotics might reduce aggressive behavior, but is concerned about the increased risk of mortality and stroke with these medications.

Mrs. J receives donepezil, 10 mg/d, sertra-line, 50 mg/d, and extended-release oxybutynin, 10 mg/d. Her over-the-counter (OTC) medications include acetaminophen, 650 mg as needed for pain, ranitidine, 150 mg/d, and docusate sodium, 100 mg/d. Several nights last week, Mr. J gave his wife an unknown OTC sleep medication, hoping it would stop her nighttime wandering, but it did not help. Physical examination, laboratory testing, and urine culture are all normal.

Most dementia patients experience neuropsychiatric disturbances, especially at later stages, that often lead to caregiver distress and nursing home placement. Although these symptoms may signal progressing dementia, environmental factors, medical conditions, and medications may worsen functioning and should be considered in the assessment.¹

Mrs. J has no medical problems that were identified as possible triggers for her behavior. Mr. J’s interference with his wife’s wandering could have increased her agitation, but he is gentle toward her and she has become agitated with no apparent trigger. “Sundowning” and poor sleep also may be involved, as sleep deprivation can lead to delirium and worsen cognitive deficits and behavioral problems.¹ Depression also should be considered.¹ Finally, Mrs. J is taking several medications with anticholinergic properties—oxybutynin, ranitidine, and an unknown OTC sleep medication, which likely contains diphenhydramine or doxylamine—that might contribute to her agitation.

Patients with dementia are highly sensitive to the cognitive and psychiatric adverse effects of anticholinergic medications. In studies of patients with mild or moderate Alzheimer’s dementia who received the potent anticholinergic scopolamine, adverse effects included:

• memory impairment
• restlessness
• disjointed speech
• motor incoordination
• drowsiness
• euphoria
• agitation
• hallucinations
• hostility.

Many of these effects worsened with increasing doses.^2,3 Age-matched controls experienced less severe memory impairment and no behavioral symptoms, which suggests that dementia-related damage to the cholinergic system leads to increased sensitivity to anticholinergics.

A cross-sectional study of 230 patients with AD identified anticholinergic use as a risk factor for psychosis (odds ratio 2.13, 95% confidence interval, 1.03 to 4.43), after adjusting for age and cognition.⁴ Among patients receiving 2 or 3 anticholinergics, 69% had psychotic symptoms compared with 48% of those receiving 1 anticholinergic and 32% of those receiving no anticholinergics.⁴ Anticholinergic overdoses can cause psychotic symptoms and delirium. A subtle presentation of delirium from prescribed anticholinergics may be confused with worsening dementia.¹ The sum of the evidence suggests that drugs with anticholinergic effects can contribute to agitation and psychosis in dementia.

When to discontinue

When diagnosing dementia it is important to address other potential causes of cognitive impairment, including medications. Approximately one-third of patients with dementia receive anticholinergic drugs, which suggests that providers often do not recognize the potential for harm with these medications.⁵ After patients receive acetylcholinesterase inhibitors (AChEIs)—which are used to enhance cognition in dementia patients—increased anticholinergic use may follow, often to treat adverse effects of AChEIs.⁵ This may negate the benefits of AChEIs and pose risk of further harm from the anticholinergics.^1,5 Although any time is a good time to discontinue an inessential anticholinergic in a patient with dementia, providers might consider screening for these drugs at the initial diagnosis, after initiating a cholinesterase inhibitor or increasing a dose, or if the patient develops psychotic or behavioral symptoms.

For Mrs. J, ranitidine and oxybutynin likely were used to treat gastrointestinal complaints and urinary frequency, which are known adverse effects of AChEIs. Many OTC preparations for insomnia, respiratory symptoms, and allergies contain older, anticholinergic antihistamines. Advise caregivers of dementia patients about possible adverse effects of OTC medications to prevent anticholinergic exposure. The Table provides a partial list of medications thought to have clinically significant anticholinergic effects.

‘Pharmacologic debridement’ refers to tapering and discontinuing medications that are no longer necessary or appropriate. Prescribers often are hesitant to discontinue medications prescribed by other clinicians and may assume that a medication used long term has been tolerated and helpful. However, as patients age—particularly if they develop dementia—their ability to tolerate a medication can change. Patients with dementia also may have difficulty attributing adverse experiences to medications and communicating these effects to providers. Some medical providers may not recognize adverse psychiatric and cognitive effects of the nonpsychiatric medications they prescribe because they do not have sufficient dementia expertise. Consulting with these providers may help determine the risk-benefit considerations of these medications.

Generally, anticholinergics should be discontinued if they are not essential to a patient’s health or if safer non-anticholinergic alternatives are available.⁵ Tapering may be necessary to prevent adverse effects from cholinergic rebound if a potent anticholinergic has been used chronically.⁵ The first step in addressing Mrs. J’s agitation is to discontinue the anticholinergic medications and monitor her symptoms. This pharmacologic debridement may avert the use of antipsychotics, which carry serious risks for dementia patients.¹

Table
Drugs with clinically significant anticholinergic effects*

Related Resources

• Cancelli I, Beltrame M, D’Anna L, et al. Drugs with anticholinergic properties: a potential risk factor for psychosis onset in Alzheimer’s disease? Expert Opin Drug Saf. 2009;8(5):549-557.
• Meeks TW, Jeste DV. Beyond the black box: what is the role for antipsychotics in dementia? Current Psychiatry. 2008;7(6): 50-65.
• Centers for Education and Research on Therapeutics. Anticholinergic pocket reference card. www.chainonline.org/home/content_images/Anticholinergic%20Pocket%20Card%20CLR%203_12_10.pdf.

Drug Brand Names

• Amitriptyline • Elavil
• Atropine • Sal-Tropine
• Azelastine nasal spray • Astelin
• Belladonna alkaloids • Donnatal
• Benztropine • Cogentin
• Brompheniramine • Dimetane
• Carbamazepine • Carbatrol, Tegretol, others
• Carbinoxamine • Palgic
• Chlorpheniramine • Chlor-Trimeton
• Chlorpromazine • Thorazine
• Cimetidine • Tagamet
• Clemastine • Tavist
• Clidinium • Quarzan
• Clomipramine • Anafranil
• Clozapine • Clozaril
• Cyclobenzaprine • Flexeril
• Cyproheptadine • Periactin
• Darifenacin • Enablex
• Desipramine • Norpramin
• Dexbrompheniramine • Drixoral
• Dexchlorpheniramine • Polaramine
• Dicyclomine • Bentyl
• Dimenhydrinate • Dramamine
• Diphenhydramine • Benadryl, Sominex, others
• Docusate Sodium • Colace
• Donepezil • Aricept
• Doxepin • Adapin
• Doxylamine • Aldex, Unisom, others
• Flavoxate • Urispas
• Glycopyrrolate • Robinul
• Hydroxyzine • Atarax
• Hyoscyamine • Cystospaz, Levbid
• Imipramine • Tofranil
• Ipratropium • Atrovent
• Loxapine • Loxitane
• Meclizine • Antivert
• Meperidine • Demerol
• Mepyramine • Anthisan
• Methscopolamine • Pamine
• Molindone • Moban
• Nortriptyline • Aventyl
• Olanzapine • Zyprexa
• Olopatadine nasal spray • Patanase
• Orphenadrine • Norflex
• Oxybutynin extended-release • Ditropan XL
• Paroxetine • Paxil
• Phenyltoloxamine • Dologesic, Durayin, others
• Pimozide • Orap
• Prochlorperazine • Compazine
• Procyclidine • Kemadrin
• Promethazine • Phenergan
• Propanthelin • Pro-Banthine
• Protriptyline • Vivactil
• Quetiapine • Seroquel
• Ranitidine • Zantac
• Scopolamine • Scopace
• Sertraline • Zoloft
• Solifenacin • VESIcare
• Thioridazine • Mellaril
• Tiotropium • Spiriva
• Tolterodine • Detrol
• Trihexyphenidyl • Artane
• Trimethobenzamide • Tigan
• Trimipramine • Surmontil
• Triprolidine • Actifed
• Trospium • Sanctura

Acknowledgements

This work was supported by an Agency for Healthcare Research and Quality (AHRQ) Centers for Education and Research on Therapeutics cooperative agreement #5 U18 HSO16094.

Disclosure

Dr. Carnahan receives grant/research support from the Agency for Healthcare Research and Quality.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/treating-insomnia-in-women.html#comments

Ms. A, age 44, reports a 3-month history of forgetfulness, difficulty concentrating, and insomnia. She says she can fall asleep but wakes up multiple times during the night and feels tired during the day. She has no history of a mood or anxiety disorder or medications that might be responsible for her symptoms.

Before her current insomnia began, Ms. A could sleep for 7 to 8 hours at night. Her husband suffers from obstructive sleep apnea (OSA), and his snoring occasionally would awaken her, but she slept well overall. Ms. A cannot identify anything that could be causing her sleep complaints. She states “The weird thing is that sometimes I am not sure if I’m cold or hot” and “I sometimes wake up drenched in sweat.” She also reports recent changes in the timing of her otherwise regular menstrual flow.

Ms. A attributes her memory problems to her poor sleep. A recent audit at her company held her responsible for several accounting errors, and Ms. A is worried that she might lose her job. She denies symptoms that would suggest major depression. You are unable to elicit a history of limb movements or excessive snoring.

Compared with men, women have a 1.3- to 1.8-fold greater risk for developing insomnia.^{Improve sleep with group CBT for insomnia,” Current Psychiatry, April 2009.) Pharmacotherapy during pregnancy and for breast-feeding mothers is guided by evaluating the risk/benefit ratio and safety considerations.}

Maintain a high index of suspicion for breathing-related sleep disorders, such as OSA,²¹ and RLS.²² Atypical presentations of OSA are common in pregnant or postpartum women; compared with men, women with OSA are more likely to report fatigue and less likely than to report sleepiness. Refer patients whom you think may have OSA for polysomnography.

If you suspect RLS, check for low ferritin and folate levels. Nutritional supplements may be necessary for women in high-risk groups, including those who are pregnant or have varicose veins, venous reflux, folate deficiency, uremia, diabetes, thyroid problems, peripheral neuropathy, Parkinson’s disease, or certain autoimmune disorders, such as Sjögren’s syndrome, celiac disease, and rheumatoid arthritis.²³ Advise these patients to avoid caffeine.

Although indicated for treating RLS, ropinirole and pramipexole are FDA Pregnancy Category C, which means animal studies have shown adverse effects on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite risks. Opioids, carbamazepine, or gabapentin may be safer for pregnant patients.²⁴

Insomnia during menopause

The prevalence of insomnia increases from 33% to 36% in premenopausal women to 44% to 61% in postmenopausal women.¹⁴ Hot flashes, comorbid mood disturbances, sleep-disordered breathing, and RLS contribute to increased insomnia risk in postmenopausal women (Table 3).^4,14,25,26

Treatment strategy. Always inquire about sleep in perimenopausal/postmenopausal women, even when her presenting complaint is related to menstrual cycle changes or vasomotor symptoms such as hot flashes.¹⁶ Assess patients for OSA, RLS, and mood, anxiety, and cognitive symptoms.²⁶ In addition to pharmacotherapy and behavioral therapy, treatment options include hormone replacement therapy (HRT) and herbal and dietary supplements (Table 4).^27-32

Table 3

Sleep difficulties during menopause: Differential diagnoses

Table 4

Treating insomnia in menopausal women

Comorbid psychiatric disorders

Women have a higher prevalence of psychiatric disorders such as major depressive disorder and anxiety disorders than men.¹ Women have a 10% to 25% lifetime risk of developing major depression. Three quarters of depressed patients experience insomnia.¹ Recent literature suggests insomnia is a risk factor for depression,³³ which emphasizes the need to screen women who present with sleep problems for depression and anxiety.

Five percent to 20% of women experience postpartum depression. Depression and insomnia are correlated to the rapid decline in estrogen and progesterone after delivery.³⁴

Treatment strategy. Insomnia is a common presenting symptom in patients with psychiatric conditions such as mood and anxiety disorders. Treating the underlying psychiatric disorder often alleviates sleeping difficulties. However, if the insomnia is disabling, treat the psychiatric disorder and insomnia concurrently.

CASE CONTINUED: Perimenopausal insomnia

Based on her history, you diagnose Ms. A with insomnia related to general medical condition (perimenopause). There are no indications to refer her for polysomnography. You educate Ms. A about sleep hygiene and recommend that she discuss her menstrual and physical complaints with her primary care physician or gynecologist. Ms. A is not interested in HRT because she has a strong family history of endometrial cancer. You reassure Ms. A and schedule a follow-up visit in 2 months to re-evaluate her insomnia.

Related resource

• Krahn LE. Perimenopausal depression? Ask how she’s sleeping. Current Psychiatry. 2005;4(6):39-53.

Drug brand names

• Carbamazepine • Carbatrol, Tegretol, others
• Escitalopram • Lexapro
• Eszopiclone • Lunesta
• Fluoxetine • Prozac
• Gabapentin • Neurontin, Gabarone
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Ramelteon • Rozerem
• Ropinirole • Requip
• Sertraline • Zoloft
• Trazodone • Desyrel
• Zolpidem • Ambien

Disclosure

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

Acknowledgements

The authors thank Dr. Namita Dhiman and Darrel E. Willoughby for their assistance with this article.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/treating-insomnia-in-women.html#comments

Ms. A, age 44, reports a 3-month history of forgetfulness, difficulty concentrating, and insomnia. She says she can fall asleep but wakes up multiple times during the night and feels tired during the day. She has no history of a mood or anxiety disorder or medications that might be responsible for her symptoms.

Before her current insomnia began, Ms. A could sleep for 7 to 8 hours at night. Her husband suffers from obstructive sleep apnea (OSA), and his snoring occasionally would awaken her, but she slept well overall. Ms. A cannot identify anything that could be causing her sleep complaints. She states “The weird thing is that sometimes I am not sure if I’m cold or hot” and “I sometimes wake up drenched in sweat.” She also reports recent changes in the timing of her otherwise regular menstrual flow.

Ms. A attributes her memory problems to her poor sleep. A recent audit at her company held her responsible for several accounting errors, and Ms. A is worried that she might lose her job. She denies symptoms that would suggest major depression. You are unable to elicit a history of limb movements or excessive snoring.

Compared with men, women have a 1.3- to 1.8-fold greater risk for developing insomnia.^{Improve sleep with group CBT for insomnia,” Current Psychiatry, April 2009.) Pharmacotherapy during pregnancy and for breast-feeding mothers is guided by evaluating the risk/benefit ratio and safety considerations.}

Maintain a high index of suspicion for breathing-related sleep disorders, such as OSA,²¹ and RLS.²² Atypical presentations of OSA are common in pregnant or postpartum women; compared with men, women with OSA are more likely to report fatigue and less likely than to report sleepiness. Refer patients whom you think may have OSA for polysomnography.

If you suspect RLS, check for low ferritin and folate levels. Nutritional supplements may be necessary for women in high-risk groups, including those who are pregnant or have varicose veins, venous reflux, folate deficiency, uremia, diabetes, thyroid problems, peripheral neuropathy, Parkinson’s disease, or certain autoimmune disorders, such as Sjögren’s syndrome, celiac disease, and rheumatoid arthritis.²³ Advise these patients to avoid caffeine.

Although indicated for treating RLS, ropinirole and pramipexole are FDA Pregnancy Category C, which means animal studies have shown adverse effects on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite risks. Opioids, carbamazepine, or gabapentin may be safer for pregnant patients.²⁴

Insomnia during menopause

The prevalence of insomnia increases from 33% to 36% in premenopausal women to 44% to 61% in postmenopausal women.¹⁴ Hot flashes, comorbid mood disturbances, sleep-disordered breathing, and RLS contribute to increased insomnia risk in postmenopausal women (Table 3).^4,14,25,26

Treatment strategy. Always inquire about sleep in perimenopausal/postmenopausal women, even when her presenting complaint is related to menstrual cycle changes or vasomotor symptoms such as hot flashes.¹⁶ Assess patients for OSA, RLS, and mood, anxiety, and cognitive symptoms.²⁶ In addition to pharmacotherapy and behavioral therapy, treatment options include hormone replacement therapy (HRT) and herbal and dietary supplements (Table 4).^27-32

Table 3

Sleep difficulties during menopause: Differential diagnoses

Table 4

Treating insomnia in menopausal women

Comorbid psychiatric disorders

Women have a higher prevalence of psychiatric disorders such as major depressive disorder and anxiety disorders than men.¹ Women have a 10% to 25% lifetime risk of developing major depression. Three quarters of depressed patients experience insomnia.¹ Recent literature suggests insomnia is a risk factor for depression,³³ which emphasizes the need to screen women who present with sleep problems for depression and anxiety.

Five percent to 20% of women experience postpartum depression. Depression and insomnia are correlated to the rapid decline in estrogen and progesterone after delivery.³⁴

Treatment strategy. Insomnia is a common presenting symptom in patients with psychiatric conditions such as mood and anxiety disorders. Treating the underlying psychiatric disorder often alleviates sleeping difficulties. However, if the insomnia is disabling, treat the psychiatric disorder and insomnia concurrently.

CASE CONTINUED: Perimenopausal insomnia

Based on her history, you diagnose Ms. A with insomnia related to general medical condition (perimenopause). There are no indications to refer her for polysomnography. You educate Ms. A about sleep hygiene and recommend that she discuss her menstrual and physical complaints with her primary care physician or gynecologist. Ms. A is not interested in HRT because she has a strong family history of endometrial cancer. You reassure Ms. A and schedule a follow-up visit in 2 months to re-evaluate her insomnia.

Related resource

• Krahn LE. Perimenopausal depression? Ask how she’s sleeping. Current Psychiatry. 2005;4(6):39-53.

Drug brand names

• Carbamazepine • Carbatrol, Tegretol, others
• Escitalopram • Lexapro
• Eszopiclone • Lunesta
• Fluoxetine • Prozac
• Gabapentin • Neurontin, Gabarone
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Ramelteon • Rozerem
• Ropinirole • Requip
• Sertraline • Zoloft
• Trazodone • Desyrel
• Zolpidem • Ambien

Disclosure

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

Acknowledgements

The authors thank Dr. Namita Dhiman and Darrel E. Willoughby for their assistance with this article.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/treating-insomnia-in-women.html#comments

Ms. A, age 44, reports a 3-month history of forgetfulness, difficulty concentrating, and insomnia. She says she can fall asleep but wakes up multiple times during the night and feels tired during the day. She has no history of a mood or anxiety disorder or medications that might be responsible for her symptoms.

Before her current insomnia began, Ms. A could sleep for 7 to 8 hours at night. Her husband suffers from obstructive sleep apnea (OSA), and his snoring occasionally would awaken her, but she slept well overall. Ms. A cannot identify anything that could be causing her sleep complaints. She states “The weird thing is that sometimes I am not sure if I’m cold or hot” and “I sometimes wake up drenched in sweat.” She also reports recent changes in the timing of her otherwise regular menstrual flow.

Ms. A attributes her memory problems to her poor sleep. A recent audit at her company held her responsible for several accounting errors, and Ms. A is worried that she might lose her job. She denies symptoms that would suggest major depression. You are unable to elicit a history of limb movements or excessive snoring.

Compared with men, women have a 1.3- to 1.8-fold greater risk for developing insomnia.^{Improve sleep with group CBT for insomnia,” Current Psychiatry, April 2009.) Pharmacotherapy during pregnancy and for breast-feeding mothers is guided by evaluating the risk/benefit ratio and safety considerations.}

Maintain a high index of suspicion for breathing-related sleep disorders, such as OSA,²¹ and RLS.²² Atypical presentations of OSA are common in pregnant or postpartum women; compared with men, women with OSA are more likely to report fatigue and less likely than to report sleepiness. Refer patients whom you think may have OSA for polysomnography.

If you suspect RLS, check for low ferritin and folate levels. Nutritional supplements may be necessary for women in high-risk groups, including those who are pregnant or have varicose veins, venous reflux, folate deficiency, uremia, diabetes, thyroid problems, peripheral neuropathy, Parkinson’s disease, or certain autoimmune disorders, such as Sjögren’s syndrome, celiac disease, and rheumatoid arthritis.²³ Advise these patients to avoid caffeine.

Although indicated for treating RLS, ropinirole and pramipexole are FDA Pregnancy Category C, which means animal studies have shown adverse effects on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite risks. Opioids, carbamazepine, or gabapentin may be safer for pregnant patients.²⁴

Insomnia during menopause

The prevalence of insomnia increases from 33% to 36% in premenopausal women to 44% to 61% in postmenopausal women.¹⁴ Hot flashes, comorbid mood disturbances, sleep-disordered breathing, and RLS contribute to increased insomnia risk in postmenopausal women (Table 3).^4,14,25,26

Treatment strategy. Always inquire about sleep in perimenopausal/postmenopausal women, even when her presenting complaint is related to menstrual cycle changes or vasomotor symptoms such as hot flashes.¹⁶ Assess patients for OSA, RLS, and mood, anxiety, and cognitive symptoms.²⁶ In addition to pharmacotherapy and behavioral therapy, treatment options include hormone replacement therapy (HRT) and herbal and dietary supplements (Table 4).^27-32

Table 3

Sleep difficulties during menopause: Differential diagnoses

Table 4

Treating insomnia in menopausal women

Comorbid psychiatric disorders

Women have a higher prevalence of psychiatric disorders such as major depressive disorder and anxiety disorders than men.¹ Women have a 10% to 25% lifetime risk of developing major depression. Three quarters of depressed patients experience insomnia.¹ Recent literature suggests insomnia is a risk factor for depression,³³ which emphasizes the need to screen women who present with sleep problems for depression and anxiety.

Five percent to 20% of women experience postpartum depression. Depression and insomnia are correlated to the rapid decline in estrogen and progesterone after delivery.³⁴

Treatment strategy. Insomnia is a common presenting symptom in patients with psychiatric conditions such as mood and anxiety disorders. Treating the underlying psychiatric disorder often alleviates sleeping difficulties. However, if the insomnia is disabling, treat the psychiatric disorder and insomnia concurrently.

CASE CONTINUED: Perimenopausal insomnia

Based on her history, you diagnose Ms. A with insomnia related to general medical condition (perimenopause). There are no indications to refer her for polysomnography. You educate Ms. A about sleep hygiene and recommend that she discuss her menstrual and physical complaints with her primary care physician or gynecologist. Ms. A is not interested in HRT because she has a strong family history of endometrial cancer. You reassure Ms. A and schedule a follow-up visit in 2 months to re-evaluate her insomnia.

Related resource

• Krahn LE. Perimenopausal depression? Ask how she’s sleeping. Current Psychiatry. 2005;4(6):39-53.

Drug brand names

• Carbamazepine • Carbatrol, Tegretol, others
• Escitalopram • Lexapro
• Eszopiclone • Lunesta
• Fluoxetine • Prozac
• Gabapentin • Neurontin, Gabarone
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Ramelteon • Rozerem
• Ropinirole • Requip
• Sertraline • Zoloft
• Trazodone • Desyrel
• Zolpidem • Ambien

Disclosure

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

Acknowledgements

The authors thank Dr. Namita Dhiman and Darrel E. Willoughby for their assistance with this article.

A new, 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13), from Wyeth Pharmaceuticals was licensed by the US Food and Drug Administration (FDA) in February for use in all children ages 6 weeks to 59 months. The new vaccine was licensed for the prevention of invasive pneumococcal disease (pneumonia, meningitis, and bacteremia) and otitis media.¹ PCV13 is meant to replace the 7-valent PCV7 (Prevnar), and will offer protection against a wider array of pneumococcal serotypes.¹

Invasive pneumococcal disease in kids has diminished substantially

Soon after PCV7 was included in the routine child immunization schedule, the incidence of invasive pneumococcal disease (IPD) began to decline.^2-5 In 1 study, the annual rate of IPD among children younger than 5 years of age decreased from 98.7 cases/100,000 in 1998–1999 to 22.6 cases/100,000 in 2006-2007.³ This decline was due to a decrease in the rate of disease caused by the 7 vaccine serotypes, from 81.9 cases/100,000 to 0.4 cases/100,000.

However, during that same time period, the rate of IPD caused by nonvaccine serotypes increased from 16.8 cases/100,000 population to 22.1 cases/100,000.³ The percentage of IPD caused by nonvaccine serotypes rose from 20% to 90% among children younger than 5 years of age during that time period.³

Fewer cases in adults, as well
In addition to the decline of IPD in children, there has also been a decline in adults. In those older than age 65, the rate of IPD decreased from 60.1/100,000 to 38.2/100,000 between 1998 and 2007—most likely because routine use of the PCV7 vaccine in children has resulted in decreased carriage and transmission of infection from children to adults.³ As in children, the decline was due to a decreasing incidence of infection from PCV7 vaccine serotypes, from 33.7 cases/100,000 to 3.3 cases/100,000. At the same time, the rate of disease caused by nonvaccine serotypes increased from 26.4 cases/100,000 to 34.9 cases/100,000.³

Nonvaccine serotypes still cause concern
While the overall decline in IPD has been a public health success, the increase in incidence of disease caused by nonvaccine serotypes has been cause for concern. According to an analysis of 2007 data from the Centers for Disease Control and Prevention (CDC)’s Active Bacterial Core surveillance, 64% of IPD cases in children younger than 5 years of age in 2006-2007 were caused by serotypes 1, 3, 5, 6A, 7F, and 19A.⁶ Several of these replacement serotypes have high levels of resistance to penicillin and erythromycin. This trend is what led to the development of the PCV13, which adds these 6 to the 7 serotypes covered by Prevnar.

The dosing schedule is complicated

The recommended schedule for the older PCV7 vaccine has always been a challenge, because the number of doses depends on the age of the child when first vaccinated.^7,8 The introduction of PCV13 adds to the complexity, because many children will be in the midst of a PCV7 series when they make the transition to PCV13.

The Advisory Committee on Immunization Practices (ACIP) recommendations on how many doses of PCV13 a child should receive depend now on the age at which the first PCV vaccine was received (either PCV7 or PCV13), the number of doses of each received, and the presence or absence of high-risk medical conditions. These recommendations are summarized below and illustrated in TABLE 1 and TABLE 2.

TABLE 1
PCV13: Routine vaccination schedule

TABLE 2
In transition: From PCV7 to PCV13

For a child who started PCV7 on time and is in mid series, the recommendation is to simply finish the series with PCV13.

If a child has completed a series of PCV7, the recommendation is to give him or her 1 dose of PCV13 up to age 59 months. (If the child has a chronic underlying medical condition, this age is extended to 71 months.¹)

Infants between the ages of 1 and 6 months who have never received any PCV product should complete a series of PCV13 at 2, 4, 6, and 12 to 15 months—the same time line as the PCV7 series.

Children ages 7 to 59 months who have not been vaccinated with PCV7 or PCV13 previously should receive 1 to 3 doses of PCV13, depending on their age at the time when vaccination begins and whether underlying medical conditions are present (TABLE 3).

Healthy children ages 24 to 59 months without previous PCV vaccine should receive 1 dose of PCV13.

Children ages 24 to 71 months without previous PCV vaccine who have a chronic medical condition that increases their risk for pneumococcal disease should receive 2 doses of PCV13, 8 weeks apart.¹

TABLE 3
Underlying conditions that place kids at risk for pneumococcal disease

Recommendations for children at higher risk

Provisional recommendations from ACIP advise that children 2 through 18 years of age at increased risk for invasive pneumococcal disease should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ideally, the child should have received all of the recommended doses of PCV13 before the physician administers PPSV23, with a minimum interval of at least 8 weeks after the last dose of PCV13.

However, some children will have previously received PPSV23. They should also receive the recommended PCV13 doses. A second dose of PPSV23 is recommended 5 years after the first dose of PPSV23 for children who have sickle cell disease, or functional or anatomic asplenia, human immunodeficiency virus (HIV) infection, or other immunocompromising conditions. No more than 2 PPSV23 doses are recommended.⁹

The ACIP provisional recommendations also say that a single dose of PCV13 may be administered to children ages 6 to 18 years who are at increased risk for IPD because of sickle cell disease, HIV infection or other immunocompromising condition, cochlear implant, or cerebrospinal fluid leaks, regardless of whether they have previously received PCV7 or PPSV23.⁹ This, however, is an off-label recommendation.

The usual contraindications
PCV13 is contraindicated among individuals known to have a severe allergic reaction to any component of PCV13 or PCV7 or to any diphtheria toxoid-containing vaccine, because the pneumococcal antigens are conjugated to a diphtheria carrier protein.¹

A useful vaccine, with its share of challenges

The pneumococcal conjugate vaccine combats infections such as pneumococcal pneumonia and meningitis, which are potentially serious—even though their incidence is relatively low.

The vaccine’s high private-sector cost—reported by the manufacturer to the CDC as $435 for the full, 4-dose series of PCV13—can be a drawback for the family physician trying to keep a full array of vaccine products on hand.¹⁰ Eligible low-income and uninsured children can receive free vaccine under the federal Vaccines for Children Program, and providers who choose to enroll in the program can access free vaccines and may charge for the expense of administering them.¹¹

With this hurdle overcome, the remaining challenge for physicians will be to stay on top of the complicated dosing schedule.

A new, 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13), from Wyeth Pharmaceuticals was licensed by the US Food and Drug Administration (FDA) in February for use in all children ages 6 weeks to 59 months. The new vaccine was licensed for the prevention of invasive pneumococcal disease (pneumonia, meningitis, and bacteremia) and otitis media.¹ PCV13 is meant to replace the 7-valent PCV7 (Prevnar), and will offer protection against a wider array of pneumococcal serotypes.¹

Invasive pneumococcal disease in kids has diminished substantially

Soon after PCV7 was included in the routine child immunization schedule, the incidence of invasive pneumococcal disease (IPD) began to decline.^2-5 In 1 study, the annual rate of IPD among children younger than 5 years of age decreased from 98.7 cases/100,000 in 1998–1999 to 22.6 cases/100,000 in 2006-2007.³ This decline was due to a decrease in the rate of disease caused by the 7 vaccine serotypes, from 81.9 cases/100,000 to 0.4 cases/100,000.

However, during that same time period, the rate of IPD caused by nonvaccine serotypes increased from 16.8 cases/100,000 population to 22.1 cases/100,000.³ The percentage of IPD caused by nonvaccine serotypes rose from 20% to 90% among children younger than 5 years of age during that time period.³

Fewer cases in adults, as well
In addition to the decline of IPD in children, there has also been a decline in adults. In those older than age 65, the rate of IPD decreased from 60.1/100,000 to 38.2/100,000 between 1998 and 2007—most likely because routine use of the PCV7 vaccine in children has resulted in decreased carriage and transmission of infection from children to adults.³ As in children, the decline was due to a decreasing incidence of infection from PCV7 vaccine serotypes, from 33.7 cases/100,000 to 3.3 cases/100,000. At the same time, the rate of disease caused by nonvaccine serotypes increased from 26.4 cases/100,000 to 34.9 cases/100,000.³

Nonvaccine serotypes still cause concern
While the overall decline in IPD has been a public health success, the increase in incidence of disease caused by nonvaccine serotypes has been cause for concern. According to an analysis of 2007 data from the Centers for Disease Control and Prevention (CDC)’s Active Bacterial Core surveillance, 64% of IPD cases in children younger than 5 years of age in 2006-2007 were caused by serotypes 1, 3, 5, 6A, 7F, and 19A.⁶ Several of these replacement serotypes have high levels of resistance to penicillin and erythromycin. This trend is what led to the development of the PCV13, which adds these 6 to the 7 serotypes covered by Prevnar.

The dosing schedule is complicated

The recommended schedule for the older PCV7 vaccine has always been a challenge, because the number of doses depends on the age of the child when first vaccinated.^7,8 The introduction of PCV13 adds to the complexity, because many children will be in the midst of a PCV7 series when they make the transition to PCV13.

The Advisory Committee on Immunization Practices (ACIP) recommendations on how many doses of PCV13 a child should receive depend now on the age at which the first PCV vaccine was received (either PCV7 or PCV13), the number of doses of each received, and the presence or absence of high-risk medical conditions. These recommendations are summarized below and illustrated in TABLE 1 and TABLE 2.

TABLE 1
PCV13: Routine vaccination schedule

TABLE 2
In transition: From PCV7 to PCV13

For a child who started PCV7 on time and is in mid series, the recommendation is to simply finish the series with PCV13.

If a child has completed a series of PCV7, the recommendation is to give him or her 1 dose of PCV13 up to age 59 months. (If the child has a chronic underlying medical condition, this age is extended to 71 months.¹)

Infants between the ages of 1 and 6 months who have never received any PCV product should complete a series of PCV13 at 2, 4, 6, and 12 to 15 months—the same time line as the PCV7 series.

Children ages 7 to 59 months who have not been vaccinated with PCV7 or PCV13 previously should receive 1 to 3 doses of PCV13, depending on their age at the time when vaccination begins and whether underlying medical conditions are present (TABLE 3).

Healthy children ages 24 to 59 months without previous PCV vaccine should receive 1 dose of PCV13.

Children ages 24 to 71 months without previous PCV vaccine who have a chronic medical condition that increases their risk for pneumococcal disease should receive 2 doses of PCV13, 8 weeks apart.¹

TABLE 3
Underlying conditions that place kids at risk for pneumococcal disease

Recommendations for children at higher risk

Provisional recommendations from ACIP advise that children 2 through 18 years of age at increased risk for invasive pneumococcal disease should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ideally, the child should have received all of the recommended doses of PCV13 before the physician administers PPSV23, with a minimum interval of at least 8 weeks after the last dose of PCV13.

However, some children will have previously received PPSV23. They should also receive the recommended PCV13 doses. A second dose of PPSV23 is recommended 5 years after the first dose of PPSV23 for children who have sickle cell disease, or functional or anatomic asplenia, human immunodeficiency virus (HIV) infection, or other immunocompromising conditions. No more than 2 PPSV23 doses are recommended.⁹

The ACIP provisional recommendations also say that a single dose of PCV13 may be administered to children ages 6 to 18 years who are at increased risk for IPD because of sickle cell disease, HIV infection or other immunocompromising condition, cochlear implant, or cerebrospinal fluid leaks, regardless of whether they have previously received PCV7 or PPSV23.⁹ This, however, is an off-label recommendation.

The usual contraindications
PCV13 is contraindicated among individuals known to have a severe allergic reaction to any component of PCV13 or PCV7 or to any diphtheria toxoid-containing vaccine, because the pneumococcal antigens are conjugated to a diphtheria carrier protein.¹

A useful vaccine, with its share of challenges

The pneumococcal conjugate vaccine combats infections such as pneumococcal pneumonia and meningitis, which are potentially serious—even though their incidence is relatively low.

The vaccine’s high private-sector cost—reported by the manufacturer to the CDC as $435 for the full, 4-dose series of PCV13—can be a drawback for the family physician trying to keep a full array of vaccine products on hand.¹⁰ Eligible low-income and uninsured children can receive free vaccine under the federal Vaccines for Children Program, and providers who choose to enroll in the program can access free vaccines and may charge for the expense of administering them.¹¹

With this hurdle overcome, the remaining challenge for physicians will be to stay on top of the complicated dosing schedule.

A new, 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13), from Wyeth Pharmaceuticals was licensed by the US Food and Drug Administration (FDA) in February for use in all children ages 6 weeks to 59 months. The new vaccine was licensed for the prevention of invasive pneumococcal disease (pneumonia, meningitis, and bacteremia) and otitis media.¹ PCV13 is meant to replace the 7-valent PCV7 (Prevnar), and will offer protection against a wider array of pneumococcal serotypes.¹

Invasive pneumococcal disease in kids has diminished substantially

Soon after PCV7 was included in the routine child immunization schedule, the incidence of invasive pneumococcal disease (IPD) began to decline.^2-5 In 1 study, the annual rate of IPD among children younger than 5 years of age decreased from 98.7 cases/100,000 in 1998–1999 to 22.6 cases/100,000 in 2006-2007.³ This decline was due to a decrease in the rate of disease caused by the 7 vaccine serotypes, from 81.9 cases/100,000 to 0.4 cases/100,000.

However, during that same time period, the rate of IPD caused by nonvaccine serotypes increased from 16.8 cases/100,000 population to 22.1 cases/100,000.³ The percentage of IPD caused by nonvaccine serotypes rose from 20% to 90% among children younger than 5 years of age during that time period.³

Fewer cases in adults, as well
In addition to the decline of IPD in children, there has also been a decline in adults. In those older than age 65, the rate of IPD decreased from 60.1/100,000 to 38.2/100,000 between 1998 and 2007—most likely because routine use of the PCV7 vaccine in children has resulted in decreased carriage and transmission of infection from children to adults.³ As in children, the decline was due to a decreasing incidence of infection from PCV7 vaccine serotypes, from 33.7 cases/100,000 to 3.3 cases/100,000. At the same time, the rate of disease caused by nonvaccine serotypes increased from 26.4 cases/100,000 to 34.9 cases/100,000.³

Nonvaccine serotypes still cause concern
While the overall decline in IPD has been a public health success, the increase in incidence of disease caused by nonvaccine serotypes has been cause for concern. According to an analysis of 2007 data from the Centers for Disease Control and Prevention (CDC)’s Active Bacterial Core surveillance, 64% of IPD cases in children younger than 5 years of age in 2006-2007 were caused by serotypes 1, 3, 5, 6A, 7F, and 19A.⁶ Several of these replacement serotypes have high levels of resistance to penicillin and erythromycin. This trend is what led to the development of the PCV13, which adds these 6 to the 7 serotypes covered by Prevnar.

The dosing schedule is complicated

The recommended schedule for the older PCV7 vaccine has always been a challenge, because the number of doses depends on the age of the child when first vaccinated.^7,8 The introduction of PCV13 adds to the complexity, because many children will be in the midst of a PCV7 series when they make the transition to PCV13.

The Advisory Committee on Immunization Practices (ACIP) recommendations on how many doses of PCV13 a child should receive depend now on the age at which the first PCV vaccine was received (either PCV7 or PCV13), the number of doses of each received, and the presence or absence of high-risk medical conditions. These recommendations are summarized below and illustrated in TABLE 1 and TABLE 2.

TABLE 1
PCV13: Routine vaccination schedule

TABLE 2
In transition: From PCV7 to PCV13

For a child who started PCV7 on time and is in mid series, the recommendation is to simply finish the series with PCV13.

If a child has completed a series of PCV7, the recommendation is to give him or her 1 dose of PCV13 up to age 59 months. (If the child has a chronic underlying medical condition, this age is extended to 71 months.¹)

Infants between the ages of 1 and 6 months who have never received any PCV product should complete a series of PCV13 at 2, 4, 6, and 12 to 15 months—the same time line as the PCV7 series.

Children ages 7 to 59 months who have not been vaccinated with PCV7 or PCV13 previously should receive 1 to 3 doses of PCV13, depending on their age at the time when vaccination begins and whether underlying medical conditions are present (TABLE 3).

Healthy children ages 24 to 59 months without previous PCV vaccine should receive 1 dose of PCV13.

Children ages 24 to 71 months without previous PCV vaccine who have a chronic medical condition that increases their risk for pneumococcal disease should receive 2 doses of PCV13, 8 weeks apart.¹

TABLE 3
Underlying conditions that place kids at risk for pneumococcal disease

Recommendations for children at higher risk

Provisional recommendations from ACIP advise that children 2 through 18 years of age at increased risk for invasive pneumococcal disease should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ideally, the child should have received all of the recommended doses of PCV13 before the physician administers PPSV23, with a minimum interval of at least 8 weeks after the last dose of PCV13.

However, some children will have previously received PPSV23. They should also receive the recommended PCV13 doses. A second dose of PPSV23 is recommended 5 years after the first dose of PPSV23 for children who have sickle cell disease, or functional or anatomic asplenia, human immunodeficiency virus (HIV) infection, or other immunocompromising conditions. No more than 2 PPSV23 doses are recommended.⁹

The ACIP provisional recommendations also say that a single dose of PCV13 may be administered to children ages 6 to 18 years who are at increased risk for IPD because of sickle cell disease, HIV infection or other immunocompromising condition, cochlear implant, or cerebrospinal fluid leaks, regardless of whether they have previously received PCV7 or PPSV23.⁹ This, however, is an off-label recommendation.

The usual contraindications
PCV13 is contraindicated among individuals known to have a severe allergic reaction to any component of PCV13 or PCV7 or to any diphtheria toxoid-containing vaccine, because the pneumococcal antigens are conjugated to a diphtheria carrier protein.¹

A useful vaccine, with its share of challenges

The pneumococcal conjugate vaccine combats infections such as pneumococcal pneumonia and meningitis, which are potentially serious—even though their incidence is relatively low.

The vaccine’s high private-sector cost—reported by the manufacturer to the CDC as $435 for the full, 4-dose series of PCV13—can be a drawback for the family physician trying to keep a full array of vaccine products on hand.¹⁰ Eligible low-income and uninsured children can receive free vaccine under the federal Vaccines for Children Program, and providers who choose to enroll in the program can access free vaccines and may charge for the expense of administering them.¹¹

With this hurdle overcome, the remaining challenge for physicians will be to stay on top of the complicated dosing schedule.

How do the authors of “Do beta blockers cause depression?” (Medicine in Brief, Current Psychiatry, May 2010) feel about using propranolol augmentation for patients with anxiety who are already taking a selective serotonin reuptake inhibitor and a benzodiazepine? I often prescribe propranolol because it has a different mechanism of action—but I am curious if others would consider doing more of this, provided the patient is at low risk for suicidal thoughts and attempts.

Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ

The authors respond

In 1966 Drs. Granville-Grossman and Turner published a seminal article on propranolol for anxiety disorders.¹ Their study included 16 patients who used propranolol, 20 mg/d, which had a beneficial effect on anxiety by alleviating autonomically mediated symptoms. This article also provided evidence for a belief that beta blockers are beneficial in anxiety mainly because they reduce somatic symptoms, a finding that has been supported by review articles.^2,3 We found only 2 studies examining adjunctive use of propranolol.^4,5 In these studies, propranolol combined with alprazolam was found to be well tolerated and effectively reduced somatic anxiety symptoms. Based on available evidence, the addition of a beta blocker could benefit patients who continue to experience physical symptoms of anxiety despite being treated with psychotropics.

Andrew J. Muzyk, PharmD
Assistant professor
Campbell University School of Pharmacy
Clinical specialist in internal medicine/psychiatry
Department of pharmacy
Duke University Hospital

Jane Gagliardi, MD
Assistant professor of psychiatry and behavioral sciences
Assistant clinical professor of medicine
Duke University School of Medicine
Durham, NC

How do the authors of “Do beta blockers cause depression?” (Medicine in Brief, Current Psychiatry, May 2010) feel about using propranolol augmentation for patients with anxiety who are already taking a selective serotonin reuptake inhibitor and a benzodiazepine? I often prescribe propranolol because it has a different mechanism of action—but I am curious if others would consider doing more of this, provided the patient is at low risk for suicidal thoughts and attempts.

Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ

The authors respond

In 1966 Drs. Granville-Grossman and Turner published a seminal article on propranolol for anxiety disorders.¹ Their study included 16 patients who used propranolol, 20 mg/d, which had a beneficial effect on anxiety by alleviating autonomically mediated symptoms. This article also provided evidence for a belief that beta blockers are beneficial in anxiety mainly because they reduce somatic symptoms, a finding that has been supported by review articles.^2,3 We found only 2 studies examining adjunctive use of propranolol.^4,5 In these studies, propranolol combined with alprazolam was found to be well tolerated and effectively reduced somatic anxiety symptoms. Based on available evidence, the addition of a beta blocker could benefit patients who continue to experience physical symptoms of anxiety despite being treated with psychotropics.

Andrew J. Muzyk, PharmD
Assistant professor
Campbell University School of Pharmacy
Clinical specialist in internal medicine/psychiatry
Department of pharmacy
Duke University Hospital

Jane Gagliardi, MD
Assistant professor of psychiatry and behavioral sciences
Assistant clinical professor of medicine
Duke University School of Medicine
Durham, NC

How do the authors of “Do beta blockers cause depression?” (Medicine in Brief, Current Psychiatry, May 2010) feel about using propranolol augmentation for patients with anxiety who are already taking a selective serotonin reuptake inhibitor and a benzodiazepine? I often prescribe propranolol because it has a different mechanism of action—but I am curious if others would consider doing more of this, provided the patient is at low risk for suicidal thoughts and attempts.

Corey Yilmaz, MD
Adult and child psychiatrist
Buckeye, AZ

The authors respond

In 1966 Drs. Granville-Grossman and Turner published a seminal article on propranolol for anxiety disorders.¹ Their study included 16 patients who used propranolol, 20 mg/d, which had a beneficial effect on anxiety by alleviating autonomically mediated symptoms. This article also provided evidence for a belief that beta blockers are beneficial in anxiety mainly because they reduce somatic symptoms, a finding that has been supported by review articles.^2,3 We found only 2 studies examining adjunctive use of propranolol.^4,5 In these studies, propranolol combined with alprazolam was found to be well tolerated and effectively reduced somatic anxiety symptoms. Based on available evidence, the addition of a beta blocker could benefit patients who continue to experience physical symptoms of anxiety despite being treated with psychotropics.

Andrew J. Muzyk, PharmD
Assistant professor
Campbell University School of Pharmacy
Clinical specialist in internal medicine/psychiatry
Department of pharmacy
Duke University Hospital

Jane Gagliardi, MD
Assistant professor of psychiatry and behavioral sciences
Assistant clinical professor of medicine
Duke University School of Medicine
Durham, NC

[email protected]

Identification of children and adolescents with anxiety is important, so consider the diagnosis in your differential. Always think: Could this be anxiety?

Pediatricians are well trained to rule out medical or other causes of anxiety. Questions to ask include: Is the child hypoxic? Does the patient have hypothyroidism? Is the anxiety caused by stress or social factors, including sexual and/or physical abuse? Do the symptoms come from a general adjustment disorder from a major life change or event, such as a move or divorce?

Does the patient have a secret she is afraid to share with anyone else? A shy child, for example, may have something she is afraid to discuss that, together with stressors, can lead her into a true anxiety disorder.

Panic attacks, in particular, can be clinically challenging. Is the attack anxiety driven or caused by an underlying medical problem? We tend to minimize cardiac symptoms, for example, in some children because it is easier to say these symptoms are related only to anxiety. But we need due diligence to rule out any major cardiac or pulmonary etiologies.

When screening patients for anxiety disorders, child and adolescent psychiatrists use comprehensive instruments like the Screen for Child Anxiety-Related Emotional Disorders (SCARED). In a busy primary care setting, I would recommend that pediatricians use the SCARED tool. It is available at no cost and features separate rating scales that can be completed by the child and parent.

For a more comprehensive screening tool, use the Child Behavior Checklist (CBCL), the Child Symptom Inventory (CSI), or the Behavior Assessment Symptom for Children (BASC). Other screening instruments are available that are more disease specific, such as the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) for obsessive-compulsive disorder (OCD).

It is appropriate for pediatricians to manage the treatment of an anxious child or adolescent when the patient is stabilized and continues to improve with treatment. In this way, a child with anxiety is managed no differently than a patient with asthma or diabetes.

Some pediatricians refer a child with a suspected anxiety disorder for an initial evaluation by a mental health specialist such as a child and adolescent psychiatrist, followed by annual consultations. We are happy to consult with pediatricians. One challenge, however, is an overall workforce shortage of child and adolescent psychiatrists. The American Academy of Child & Adolescent Psychiatry offers an online map of the United States that shows the number of specialists per county (www.aacap.org/cs/physicians.AlliedProfessionals/workforce_issues

When is it appropriate for a pediatrician to initiate medication in this patient population? Any time it is indicated! And that really depends on the diagnosis: for OCD, yes; for PTSD, maybe; and for social phobias, probably not. Medication use also is based on symptom severity, especially in generalized anxiety disorder. If the child is not sleeping well or participating in activities of daily living, you have to get him or her stabilized first. The bulk of our treatment for anxiety disorders is psychotherapy, but the child is less likely to benefit from therapy if anxiety impedes the ability to participate in therapy.

Referral to a specialist is indicated when anxiety symptoms interfere with activities of daily living. School refusal is another scenario that warrants immediate referral. Some parents will allow anxious children to stay out of school, so try to determine the reason: Is the parent making it more comfortable for the child to stay at home? Or is the patient avoiding school because they are the target of teasing?

Copies of a recent physical examination, growth chart, and any laboratory work already ordered are helpful with a referral to a child and adolescent psychiatrist. In addition, a detailed clinical assessment facilitates management by a child and adolescent psychiatrist. In other words, it is helpful to get a note that states: “Referring Johnny to you. He was a developmentally normal 5-year-old until he nearly drowned in a pool last summer. He now refuses to sleep alone.” In contrast, a less helpful note might read: “Here is a 5-year-old named Johnny. Please assess.”

Unless you suspect a true organic etiology, such as an abnormal neurologic examination, avoid ordering routine imaging studies for a child with anxiety prior to referral. I am concerned about the risks of sedation for pediatric patients and risks associated with radiation exposure (with CT scans, for example).

Avoid excessive laboratory testing as well, unless there is a clear indication that results could rule out a suspected medical diagnosis.

[email protected]

Identification of children and adolescents with anxiety is important, so consider the diagnosis in your differential. Always think: Could this be anxiety?

Pediatricians are well trained to rule out medical or other causes of anxiety. Questions to ask include: Is the child hypoxic? Does the patient have hypothyroidism? Is the anxiety caused by stress or social factors, including sexual and/or physical abuse? Do the symptoms come from a general adjustment disorder from a major life change or event, such as a move or divorce?

Does the patient have a secret she is afraid to share with anyone else? A shy child, for example, may have something she is afraid to discuss that, together with stressors, can lead her into a true anxiety disorder.

Panic attacks, in particular, can be clinically challenging. Is the attack anxiety driven or caused by an underlying medical problem? We tend to minimize cardiac symptoms, for example, in some children because it is easier to say these symptoms are related only to anxiety. But we need due diligence to rule out any major cardiac or pulmonary etiologies.

When screening patients for anxiety disorders, child and adolescent psychiatrists use comprehensive instruments like the Screen for Child Anxiety-Related Emotional Disorders (SCARED). In a busy primary care setting, I would recommend that pediatricians use the SCARED tool. It is available at no cost and features separate rating scales that can be completed by the child and parent.

For a more comprehensive screening tool, use the Child Behavior Checklist (CBCL), the Child Symptom Inventory (CSI), or the Behavior Assessment Symptom for Children (BASC). Other screening instruments are available that are more disease specific, such as the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) for obsessive-compulsive disorder (OCD).

It is appropriate for pediatricians to manage the treatment of an anxious child or adolescent when the patient is stabilized and continues to improve with treatment. In this way, a child with anxiety is managed no differently than a patient with asthma or diabetes.

Some pediatricians refer a child with a suspected anxiety disorder for an initial evaluation by a mental health specialist such as a child and adolescent psychiatrist, followed by annual consultations. We are happy to consult with pediatricians. One challenge, however, is an overall workforce shortage of child and adolescent psychiatrists. The American Academy of Child & Adolescent Psychiatry offers an online map of the United States that shows the number of specialists per county (www.aacap.org/cs/physicians.AlliedProfessionals/workforce_issues

When is it appropriate for a pediatrician to initiate medication in this patient population? Any time it is indicated! And that really depends on the diagnosis: for OCD, yes; for PTSD, maybe; and for social phobias, probably not. Medication use also is based on symptom severity, especially in generalized anxiety disorder. If the child is not sleeping well or participating in activities of daily living, you have to get him or her stabilized first. The bulk of our treatment for anxiety disorders is psychotherapy, but the child is less likely to benefit from therapy if anxiety impedes the ability to participate in therapy.

Referral to a specialist is indicated when anxiety symptoms interfere with activities of daily living. School refusal is another scenario that warrants immediate referral. Some parents will allow anxious children to stay out of school, so try to determine the reason: Is the parent making it more comfortable for the child to stay at home? Or is the patient avoiding school because they are the target of teasing?

Copies of a recent physical examination, growth chart, and any laboratory work already ordered are helpful with a referral to a child and adolescent psychiatrist. In addition, a detailed clinical assessment facilitates management by a child and adolescent psychiatrist. In other words, it is helpful to get a note that states: “Referring Johnny to you. He was a developmentally normal 5-year-old until he nearly drowned in a pool last summer. He now refuses to sleep alone.” In contrast, a less helpful note might read: “Here is a 5-year-old named Johnny. Please assess.”

Unless you suspect a true organic etiology, such as an abnormal neurologic examination, avoid ordering routine imaging studies for a child with anxiety prior to referral. I am concerned about the risks of sedation for pediatric patients and risks associated with radiation exposure (with CT scans, for example).

Avoid excessive laboratory testing as well, unless there is a clear indication that results could rule out a suspected medical diagnosis.

[email protected]

Identification of children and adolescents with anxiety is important, so consider the diagnosis in your differential. Always think: Could this be anxiety?

Pediatricians are well trained to rule out medical or other causes of anxiety. Questions to ask include: Is the child hypoxic? Does the patient have hypothyroidism? Is the anxiety caused by stress or social factors, including sexual and/or physical abuse? Do the symptoms come from a general adjustment disorder from a major life change or event, such as a move or divorce?

Does the patient have a secret she is afraid to share with anyone else? A shy child, for example, may have something she is afraid to discuss that, together with stressors, can lead her into a true anxiety disorder.

Panic attacks, in particular, can be clinically challenging. Is the attack anxiety driven or caused by an underlying medical problem? We tend to minimize cardiac symptoms, for example, in some children because it is easier to say these symptoms are related only to anxiety. But we need due diligence to rule out any major cardiac or pulmonary etiologies.

When screening patients for anxiety disorders, child and adolescent psychiatrists use comprehensive instruments like the Screen for Child Anxiety-Related Emotional Disorders (SCARED). In a busy primary care setting, I would recommend that pediatricians use the SCARED tool. It is available at no cost and features separate rating scales that can be completed by the child and parent.

For a more comprehensive screening tool, use the Child Behavior Checklist (CBCL), the Child Symptom Inventory (CSI), or the Behavior Assessment Symptom for Children (BASC). Other screening instruments are available that are more disease specific, such as the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS) for obsessive-compulsive disorder (OCD).

It is appropriate for pediatricians to manage the treatment of an anxious child or adolescent when the patient is stabilized and continues to improve with treatment. In this way, a child with anxiety is managed no differently than a patient with asthma or diabetes.

Some pediatricians refer a child with a suspected anxiety disorder for an initial evaluation by a mental health specialist such as a child and adolescent psychiatrist, followed by annual consultations. We are happy to consult with pediatricians. One challenge, however, is an overall workforce shortage of child and adolescent psychiatrists. The American Academy of Child & Adolescent Psychiatry offers an online map of the United States that shows the number of specialists per county (www.aacap.org/cs/physicians.AlliedProfessionals/workforce_issues

When is it appropriate for a pediatrician to initiate medication in this patient population? Any time it is indicated! And that really depends on the diagnosis: for OCD, yes; for PTSD, maybe; and for social phobias, probably not. Medication use also is based on symptom severity, especially in generalized anxiety disorder. If the child is not sleeping well or participating in activities of daily living, you have to get him or her stabilized first. The bulk of our treatment for anxiety disorders is psychotherapy, but the child is less likely to benefit from therapy if anxiety impedes the ability to participate in therapy.

Referral to a specialist is indicated when anxiety symptoms interfere with activities of daily living. School refusal is another scenario that warrants immediate referral. Some parents will allow anxious children to stay out of school, so try to determine the reason: Is the parent making it more comfortable for the child to stay at home? Or is the patient avoiding school because they are the target of teasing?

Copies of a recent physical examination, growth chart, and any laboratory work already ordered are helpful with a referral to a child and adolescent psychiatrist. In addition, a detailed clinical assessment facilitates management by a child and adolescent psychiatrist. In other words, it is helpful to get a note that states: “Referring Johnny to you. He was a developmentally normal 5-year-old until he nearly drowned in a pool last summer. He now refuses to sleep alone.” In contrast, a less helpful note might read: “Here is a 5-year-old named Johnny. Please assess.”

Unless you suspect a true organic etiology, such as an abnormal neurologic examination, avoid ordering routine imaging studies for a child with anxiety prior to referral. I am concerned about the risks of sedation for pediatric patients and risks associated with radiation exposure (with CT scans, for example).

Avoid excessive laboratory testing as well, unless there is a clear indication that results could rule out a suspected medical diagnosis.

www.CHADIS.com[email protected]

From Cane and Abel to Linus and Lucy, Wally and the Beaver to Bart and Lisa Simpson, sibling rivalry is the stuff of legend and comedy. But when it presents as a source of serious concern for parents during pediatric office visits, it's usually no laughing matter for them.

Research suggests that 64% of school-age siblings fight “sometimes or often”—a figure likely matched in magnitude if not muscle by younger siblings as well.

Sibling rivalry is so common, in fact, that we may tend to think back to our own sibling spats, or those of our kids, roll our eyes and offer the “they'll grow out of it” platitude.

But in truth, sibling wars can have consequences. While injuries are rare in most sibling disputes, in 25% of child abuse cases a sibling has been involved in victimization (usually in concert with adults).

Serious sibling conflict tremendously compromises quality of life for children, and for their parents as well. We know that marriages suffer in households with high levels of sibling discord, with the issue a common flashpoint for disagreements between parents about how to respond. Children exposed to serious sibling conflict in middle childhood appear to suffer higher levels of anxiety, depression, and delinquent behavior in early adolescence. Down the road, people carry the grudges of sibling difficulties for decades, undermining bonds that might otherwise be a significant source of support in our increasingly fragmented society.

So sibling struggles are worthy of our time and thoughtfulness, and addressing them productively will build trust in your relationship with parents and perhaps bring some semblance of peace to their households.

The first response to a parent's frustration over sibling quarrels should be to listen with respect. Their pain is often significant as they describe the battles unfolding among children they hold precious. Patiently listening to the details of sibling encounters also can help you sort out whether the issues they're describing fall into the normal range or may signify more serious individual or relational issues that deserve attention.

Assuming it's the former, I think it helps to remind parents of how common sibling rivalry is, and more importantly, why it occurs. Annoying as they may be, fracases actually serve a number of important biological functions. Watch any nature documentary featuring lions lounging under a tree on the savannah, and what are the cubs doing? Attacking, defending, tumbling, and biting, growling all the while.

In kids, like cubs, important social skills arise from the sibling relationship, even when the dust flies. Siblings teach each other to giggle and laugh, bait and switch, sneak and chase, parry and defend. From each other, they learn which jokes fly and which land with a thud, how to toss out an insult and absorb one tossed their way.

Siblings also learn how to pull their punches, practicing evolutionarily useful conflict skills while stopping short of inflicting serious harm.

The question remains, how does a family foster productive resilience-building sibling interactions while preserving affectionate connections and at least a modicum of household calm?

Like so many things in life, household chaos is associated with unhealthy levels of sibling conflict, according to research by psychologist Judy Dunn, the author of “Sisters and Brothers” (Cambridge: Harvard University Press, 1985), “Separate Lives: Why Siblings Are So Different” (New York: Basic Books, 1992), and “From One Child to Two” (New York: Ballantine Books, 1995).

Corporal punishment in the family makes rivalry worse as well.

Individual temperaments, the presence of a child with special needs, and family structure (children of opposite sexes) also have been found to play roles in sibling relationships, but spacing of children makes less of a difference than most people think. In general, children spaced more than 4 years apart have less conflict, but they also spend less time together and have less of an integrated relationship than closely spaced siblings do.

When looking at underlying dynamics, research points to the perception of favoritism by the parents as the main contributing factor. Importantly, the children's impressions of favoritism are not always accurate, but they are such an important driver of sibling conflict that they deserve consideration.

I suggest to parents that they make a special effort to provide roughly equal “alone” time with each child. When one child's needs really do require inordinate attention—as in the case of homework time for a child with learning disabilities—they need to be up front about that reality, and say, “If you need something special, I will be there for you, too.” Remind the child who feels slighted about exceptional times when all the focus was on them: during assembly of the science fair project, or when they learned to ride a bike, for example.

Acknowledge jealousy as a real and understandable emotion, but one that must be handled within limits and household rules.

Parents will do well to practice prevention with siblings, reinforcing cooperation in general and any specific examples of good deeds performed on behalf of each other with acknowledgment or even rewards if the rivalry is serious.

Advise parents to be sensitive to situations, like boredom, that lend themselves to sibling disputes, and to intervene with distractions. Promote cooperative projects and noncompetitive games: building a fort or puzzle, playing in the sprinkler, or making breakfast as a family, instead of games with winners and losers.

When board games are necessarily competitive, make it a practice to turn the board around every fourth move to minimize age-related inequities. Even out the teams in driveway basketball as well.

Once children are old enough to participate, family meetings are an excellent forum in which to air grievances. Again, ground rules apply; everyone gets to be heard. No interrupting. Solutions can be brainstormed and tried out, to be reviewed at the next regularly scheduled session.

A stepwise approach to dealing with actual sibling disputes also helps bring order to the chaos that feeds sibling wars. Parents may want to read the popular if optimistically titled book by Adele Faber and Irene Mazlish, “Siblings Without Rivalry” (New York: HarperCollins Publishing, 2004).

Essentially, their basic plan is to teach parents to ignore whatever can be ignored, thus avoiding a self-feeding loop of inadvertent reinforcement of the conflicts.

Situations that are a bit too much to ignore should be handled dispassionately. The parent may want to ask, “Is this a real fight or a play fight?” If it's a play fight but noisy, they might want to suggest a new venue—in the basement or outdoors.

If it's a real fight, encourage parents to simply describe the situation they see. “It looks like you both want to play with the truck, and it's hard to decide how to work it out.” Follow this with an affirming statement like, “I'm sure you can figure out a solution.”

If things are even more volatile—maybe someone has hit or pinched—parents should intervene, but in an unbiased manner and with the least amount of punishment that makes sense. They need to emphasize that hitting is never acceptable, but not take sides. A useful mantra for parents: “Don't try to judge who started it. You can never tell.”

Depending on the situation, both children may need to be sent to a room away from the toy to make a plan for resolution. The toy may need to be put in time out. Both kids may need to be put in time out for the same amount of time, with duration based on the younger child's age. Each child may need to take on an individual chore card, or even chores requiring the effort of both kids.

Whatever the solution, it should be brief.

Counsel parents that rivalry is part of sibling interaction: a challenge best met through prevention, structured responses, and reliance on family rules.

Remind them of the fleeting nature of sibling spats—don't they hear the kids giggling 15 minutes later?—and the permanence of warm, mutually respectful, sibling bonds through a lifetime.

www.CHADIS.com[email protected]

From Cane and Abel to Linus and Lucy, Wally and the Beaver to Bart and Lisa Simpson, sibling rivalry is the stuff of legend and comedy. But when it presents as a source of serious concern for parents during pediatric office visits, it's usually no laughing matter for them.

Research suggests that 64% of school-age siblings fight “sometimes or often”—a figure likely matched in magnitude if not muscle by younger siblings as well.

Sibling rivalry is so common, in fact, that we may tend to think back to our own sibling spats, or those of our kids, roll our eyes and offer the “they'll grow out of it” platitude.

But in truth, sibling wars can have consequences. While injuries are rare in most sibling disputes, in 25% of child abuse cases a sibling has been involved in victimization (usually in concert with adults).

Serious sibling conflict tremendously compromises quality of life for children, and for their parents as well. We know that marriages suffer in households with high levels of sibling discord, with the issue a common flashpoint for disagreements between parents about how to respond. Children exposed to serious sibling conflict in middle childhood appear to suffer higher levels of anxiety, depression, and delinquent behavior in early adolescence. Down the road, people carry the grudges of sibling difficulties for decades, undermining bonds that might otherwise be a significant source of support in our increasingly fragmented society.

So sibling struggles are worthy of our time and thoughtfulness, and addressing them productively will build trust in your relationship with parents and perhaps bring some semblance of peace to their households.

The first response to a parent's frustration over sibling quarrels should be to listen with respect. Their pain is often significant as they describe the battles unfolding among children they hold precious. Patiently listening to the details of sibling encounters also can help you sort out whether the issues they're describing fall into the normal range or may signify more serious individual or relational issues that deserve attention.

Assuming it's the former, I think it helps to remind parents of how common sibling rivalry is, and more importantly, why it occurs. Annoying as they may be, fracases actually serve a number of important biological functions. Watch any nature documentary featuring lions lounging under a tree on the savannah, and what are the cubs doing? Attacking, defending, tumbling, and biting, growling all the while.

In kids, like cubs, important social skills arise from the sibling relationship, even when the dust flies. Siblings teach each other to giggle and laugh, bait and switch, sneak and chase, parry and defend. From each other, they learn which jokes fly and which land with a thud, how to toss out an insult and absorb one tossed their way.

Siblings also learn how to pull their punches, practicing evolutionarily useful conflict skills while stopping short of inflicting serious harm.

The question remains, how does a family foster productive resilience-building sibling interactions while preserving affectionate connections and at least a modicum of household calm?

Like so many things in life, household chaos is associated with unhealthy levels of sibling conflict, according to research by psychologist Judy Dunn, the author of “Sisters and Brothers” (Cambridge: Harvard University Press, 1985), “Separate Lives: Why Siblings Are So Different” (New York: Basic Books, 1992), and “From One Child to Two” (New York: Ballantine Books, 1995).

Corporal punishment in the family makes rivalry worse as well.

Individual temperaments, the presence of a child with special needs, and family structure (children of opposite sexes) also have been found to play roles in sibling relationships, but spacing of children makes less of a difference than most people think. In general, children spaced more than 4 years apart have less conflict, but they also spend less time together and have less of an integrated relationship than closely spaced siblings do.

When looking at underlying dynamics, research points to the perception of favoritism by the parents as the main contributing factor. Importantly, the children's impressions of favoritism are not always accurate, but they are such an important driver of sibling conflict that they deserve consideration.

I suggest to parents that they make a special effort to provide roughly equal “alone” time with each child. When one child's needs really do require inordinate attention—as in the case of homework time for a child with learning disabilities—they need to be up front about that reality, and say, “If you need something special, I will be there for you, too.” Remind the child who feels slighted about exceptional times when all the focus was on them: during assembly of the science fair project, or when they learned to ride a bike, for example.

Acknowledge jealousy as a real and understandable emotion, but one that must be handled within limits and household rules.

Parents will do well to practice prevention with siblings, reinforcing cooperation in general and any specific examples of good deeds performed on behalf of each other with acknowledgment or even rewards if the rivalry is serious.

Advise parents to be sensitive to situations, like boredom, that lend themselves to sibling disputes, and to intervene with distractions. Promote cooperative projects and noncompetitive games: building a fort or puzzle, playing in the sprinkler, or making breakfast as a family, instead of games with winners and losers.

When board games are necessarily competitive, make it a practice to turn the board around every fourth move to minimize age-related inequities. Even out the teams in driveway basketball as well.

Once children are old enough to participate, family meetings are an excellent forum in which to air grievances. Again, ground rules apply; everyone gets to be heard. No interrupting. Solutions can be brainstormed and tried out, to be reviewed at the next regularly scheduled session.

A stepwise approach to dealing with actual sibling disputes also helps bring order to the chaos that feeds sibling wars. Parents may want to read the popular if optimistically titled book by Adele Faber and Irene Mazlish, “Siblings Without Rivalry” (New York: HarperCollins Publishing, 2004).

Essentially, their basic plan is to teach parents to ignore whatever can be ignored, thus avoiding a self-feeding loop of inadvertent reinforcement of the conflicts.

Situations that are a bit too much to ignore should be handled dispassionately. The parent may want to ask, “Is this a real fight or a play fight?” If it's a play fight but noisy, they might want to suggest a new venue—in the basement or outdoors.

If it's a real fight, encourage parents to simply describe the situation they see. “It looks like you both want to play with the truck, and it's hard to decide how to work it out.” Follow this with an affirming statement like, “I'm sure you can figure out a solution.”

If things are even more volatile—maybe someone has hit or pinched—parents should intervene, but in an unbiased manner and with the least amount of punishment that makes sense. They need to emphasize that hitting is never acceptable, but not take sides. A useful mantra for parents: “Don't try to judge who started it. You can never tell.”

Depending on the situation, both children may need to be sent to a room away from the toy to make a plan for resolution. The toy may need to be put in time out. Both kids may need to be put in time out for the same amount of time, with duration based on the younger child's age. Each child may need to take on an individual chore card, or even chores requiring the effort of both kids.

Whatever the solution, it should be brief.

Counsel parents that rivalry is part of sibling interaction: a challenge best met through prevention, structured responses, and reliance on family rules.

Remind them of the fleeting nature of sibling spats—don't they hear the kids giggling 15 minutes later?—and the permanence of warm, mutually respectful, sibling bonds through a lifetime.

www.CHADIS.com[email protected]

From Cane and Abel to Linus and Lucy, Wally and the Beaver to Bart and Lisa Simpson, sibling rivalry is the stuff of legend and comedy. But when it presents as a source of serious concern for parents during pediatric office visits, it's usually no laughing matter for them.

Research suggests that 64% of school-age siblings fight “sometimes or often”—a figure likely matched in magnitude if not muscle by younger siblings as well.

Sibling rivalry is so common, in fact, that we may tend to think back to our own sibling spats, or those of our kids, roll our eyes and offer the “they'll grow out of it” platitude.

But in truth, sibling wars can have consequences. While injuries are rare in most sibling disputes, in 25% of child abuse cases a sibling has been involved in victimization (usually in concert with adults).

Serious sibling conflict tremendously compromises quality of life for children, and for their parents as well. We know that marriages suffer in households with high levels of sibling discord, with the issue a common flashpoint for disagreements between parents about how to respond. Children exposed to serious sibling conflict in middle childhood appear to suffer higher levels of anxiety, depression, and delinquent behavior in early adolescence. Down the road, people carry the grudges of sibling difficulties for decades, undermining bonds that might otherwise be a significant source of support in our increasingly fragmented society.

So sibling struggles are worthy of our time and thoughtfulness, and addressing them productively will build trust in your relationship with parents and perhaps bring some semblance of peace to their households.

The first response to a parent's frustration over sibling quarrels should be to listen with respect. Their pain is often significant as they describe the battles unfolding among children they hold precious. Patiently listening to the details of sibling encounters also can help you sort out whether the issues they're describing fall into the normal range or may signify more serious individual or relational issues that deserve attention.

Assuming it's the former, I think it helps to remind parents of how common sibling rivalry is, and more importantly, why it occurs. Annoying as they may be, fracases actually serve a number of important biological functions. Watch any nature documentary featuring lions lounging under a tree on the savannah, and what are the cubs doing? Attacking, defending, tumbling, and biting, growling all the while.

In kids, like cubs, important social skills arise from the sibling relationship, even when the dust flies. Siblings teach each other to giggle and laugh, bait and switch, sneak and chase, parry and defend. From each other, they learn which jokes fly and which land with a thud, how to toss out an insult and absorb one tossed their way.

Siblings also learn how to pull their punches, practicing evolutionarily useful conflict skills while stopping short of inflicting serious harm.

The question remains, how does a family foster productive resilience-building sibling interactions while preserving affectionate connections and at least a modicum of household calm?

Like so many things in life, household chaos is associated with unhealthy levels of sibling conflict, according to research by psychologist Judy Dunn, the author of “Sisters and Brothers” (Cambridge: Harvard University Press, 1985), “Separate Lives: Why Siblings Are So Different” (New York: Basic Books, 1992), and “From One Child to Two” (New York: Ballantine Books, 1995).

Corporal punishment in the family makes rivalry worse as well.

Individual temperaments, the presence of a child with special needs, and family structure (children of opposite sexes) also have been found to play roles in sibling relationships, but spacing of children makes less of a difference than most people think. In general, children spaced more than 4 years apart have less conflict, but they also spend less time together and have less of an integrated relationship than closely spaced siblings do.

When looking at underlying dynamics, research points to the perception of favoritism by the parents as the main contributing factor. Importantly, the children's impressions of favoritism are not always accurate, but they are such an important driver of sibling conflict that they deserve consideration.

I suggest to parents that they make a special effort to provide roughly equal “alone” time with each child. When one child's needs really do require inordinate attention—as in the case of homework time for a child with learning disabilities—they need to be up front about that reality, and say, “If you need something special, I will be there for you, too.” Remind the child who feels slighted about exceptional times when all the focus was on them: during assembly of the science fair project, or when they learned to ride a bike, for example.

Acknowledge jealousy as a real and understandable emotion, but one that must be handled within limits and household rules.

Parents will do well to practice prevention with siblings, reinforcing cooperation in general and any specific examples of good deeds performed on behalf of each other with acknowledgment or even rewards if the rivalry is serious.

Advise parents to be sensitive to situations, like boredom, that lend themselves to sibling disputes, and to intervene with distractions. Promote cooperative projects and noncompetitive games: building a fort or puzzle, playing in the sprinkler, or making breakfast as a family, instead of games with winners and losers.

When board games are necessarily competitive, make it a practice to turn the board around every fourth move to minimize age-related inequities. Even out the teams in driveway basketball as well.

Once children are old enough to participate, family meetings are an excellent forum in which to air grievances. Again, ground rules apply; everyone gets to be heard. No interrupting. Solutions can be brainstormed and tried out, to be reviewed at the next regularly scheduled session.

A stepwise approach to dealing with actual sibling disputes also helps bring order to the chaos that feeds sibling wars. Parents may want to read the popular if optimistically titled book by Adele Faber and Irene Mazlish, “Siblings Without Rivalry” (New York: HarperCollins Publishing, 2004).

Essentially, their basic plan is to teach parents to ignore whatever can be ignored, thus avoiding a self-feeding loop of inadvertent reinforcement of the conflicts.

Situations that are a bit too much to ignore should be handled dispassionately. The parent may want to ask, “Is this a real fight or a play fight?” If it's a play fight but noisy, they might want to suggest a new venue—in the basement or outdoors.

If it's a real fight, encourage parents to simply describe the situation they see. “It looks like you both want to play with the truck, and it's hard to decide how to work it out.” Follow this with an affirming statement like, “I'm sure you can figure out a solution.”

If things are even more volatile—maybe someone has hit or pinched—parents should intervene, but in an unbiased manner and with the least amount of punishment that makes sense. They need to emphasize that hitting is never acceptable, but not take sides. A useful mantra for parents: “Don't try to judge who started it. You can never tell.”

Depending on the situation, both children may need to be sent to a room away from the toy to make a plan for resolution. The toy may need to be put in time out. Both kids may need to be put in time out for the same amount of time, with duration based on the younger child's age. Each child may need to take on an individual chore card, or even chores requiring the effort of both kids.

Whatever the solution, it should be brief.

Counsel parents that rivalry is part of sibling interaction: a challenge best met through prevention, structured responses, and reliance on family rules.

Remind them of the fleeting nature of sibling spats—don't they hear the kids giggling 15 minutes later?—and the permanence of warm, mutually respectful, sibling bonds through a lifetime.

New hospitalist compensation and productivity information is available via the 2010 Physician Compensation and Production Survey Report, the Medical Group Management Association’s (MGMA) annual survey. However, HM leaders are urging restraint to group directors and individual hospitalists pining for the latest industry benchmarks.

“We want to be careful not to read too much into trends at this point. This is a new set of data,” says William “Tex” Landis, MD, FHM, medical director of Wellspan Hospitalists in York, Pa., and chair of SHM’s Practice Analysis Committee. “I think the trending might be beneficial, but I think it should be done with great caution.”

The report, which surveyed 4,211 hospitalists from 443 groups, shows median hospitalist compensation at $215,000 annually. That’s an increase of about $20,000 per year compared with SHM’s 2007-2008 survey data.

The report also shows the median number of work RVUs at 4,107 per hospitalist per year.

SHM, which collaborated on the survey with MGMA, will release a more detailed compensation and productivity report in September. That report replaces SHM’s biannual survey, and will break down such hospitalist-specific data as night coverage, financial support, and staffing models.

The MGMA survey adds new layers of detail, as compared with past SHM surveys. In addition to mean and median values, the MGMA report breaks down production and compensation values to 25th-, 75th-, and 90th-percentile ranges. “It provides a lot more ways to cut the data than [SHM] has traditionally done,” says Leslie Flores, SHM senior advisor of practice management.

Although he warns of taking the MGMA survey information too literally, Dr. Landis knows his peers are anxiously awaiting the new numbers. “It provides the best possible data to help with optimal decision-making, especially as it pertains to resourcing hospitalist programs,” he says. “What will be more important, however, will be what next year’s numbers show; then, we will be comparing like with like.”

New hospitalist compensation and productivity information is available via the 2010 Physician Compensation and Production Survey Report, the Medical Group Management Association’s (MGMA) annual survey. However, HM leaders are urging restraint to group directors and individual hospitalists pining for the latest industry benchmarks.

“We want to be careful not to read too much into trends at this point. This is a new set of data,” says William “Tex” Landis, MD, FHM, medical director of Wellspan Hospitalists in York, Pa., and chair of SHM’s Practice Analysis Committee. “I think the trending might be beneficial, but I think it should be done with great caution.”

The report, which surveyed 4,211 hospitalists from 443 groups, shows median hospitalist compensation at $215,000 annually. That’s an increase of about $20,000 per year compared with SHM’s 2007-2008 survey data.

The report also shows the median number of work RVUs at 4,107 per hospitalist per year.

SHM, which collaborated on the survey with MGMA, will release a more detailed compensation and productivity report in September. That report replaces SHM’s biannual survey, and will break down such hospitalist-specific data as night coverage, financial support, and staffing models.

The MGMA survey adds new layers of detail, as compared with past SHM surveys. In addition to mean and median values, the MGMA report breaks down production and compensation values to 25th-, 75th-, and 90th-percentile ranges. “It provides a lot more ways to cut the data than [SHM] has traditionally done,” says Leslie Flores, SHM senior advisor of practice management.

Although he warns of taking the MGMA survey information too literally, Dr. Landis knows his peers are anxiously awaiting the new numbers. “It provides the best possible data to help with optimal decision-making, especially as it pertains to resourcing hospitalist programs,” he says. “What will be more important, however, will be what next year’s numbers show; then, we will be comparing like with like.”

New hospitalist compensation and productivity information is available via the 2010 Physician Compensation and Production Survey Report, the Medical Group Management Association’s (MGMA) annual survey. However, HM leaders are urging restraint to group directors and individual hospitalists pining for the latest industry benchmarks.

“We want to be careful not to read too much into trends at this point. This is a new set of data,” says William “Tex” Landis, MD, FHM, medical director of Wellspan Hospitalists in York, Pa., and chair of SHM’s Practice Analysis Committee. “I think the trending might be beneficial, but I think it should be done with great caution.”

The report, which surveyed 4,211 hospitalists from 443 groups, shows median hospitalist compensation at $215,000 annually. That’s an increase of about $20,000 per year compared with SHM’s 2007-2008 survey data.

The report also shows the median number of work RVUs at 4,107 per hospitalist per year.

SHM, which collaborated on the survey with MGMA, will release a more detailed compensation and productivity report in September. That report replaces SHM’s biannual survey, and will break down such hospitalist-specific data as night coverage, financial support, and staffing models.

The MGMA survey adds new layers of detail, as compared with past SHM surveys. In addition to mean and median values, the MGMA report breaks down production and compensation values to 25th-, 75th-, and 90th-percentile ranges. “It provides a lot more ways to cut the data than [SHM] has traditionally done,” says Leslie Flores, SHM senior advisor of practice management.

Although he warns of taking the MGMA survey information too literally, Dr. Landis knows his peers are anxiously awaiting the new numbers. “It provides the best possible data to help with optimal decision-making, especially as it pertains to resourcing hospitalist programs,” he says. “What will be more important, however, will be what next year’s numbers show; then, we will be comparing like with like.”

Let the debate formally begin.

Proposed regulations (PDF) from the Accreditation Council for Graduate Medical Education (ACGME) that limit first-year residents to 16 hours of duty will be seen either as an awakening or an abomination to educational leaders, according to the incoming president of the Association of Program Directors in Internal Medicine (APDIM).

“The draft ... will be welcomed by programs wishing to manage fatigue and will be seen as a threat by programs who have not yet accepted the need to reform graduate medical education,” says Ethan Fried, who takes over as APDIM president July 1.

The new changes come as no shock to academic hospitalists who have been waiting for the prescribed five-year update to the landmark 2003 duty-hour standards, especially after the recommendations published in the Institute of Medicine’s 2008 report “Resident Duty Hours: Enhancing Sleep, Supervision and Safety.” If approved, the new regulations will likely take effect in July 2011.

The data points of the rules will be debated thoroughly between now and then, but Dr. Fried views the recommendations as more than just tweaks to the existing infrastructure governing residency programs. He sees the suggestions as a sea change, particularly allowances for added duty time for second- and third-year residents, as well as situational exceptions that allow residents to work longer to ensure continuity of care.

“The draft turns the old concept of professionalism 180 degrees by telling residents that sleep deprivation is no longer a lifestyle choice,” adds Dr. Fried, MD, MS, FACP, assistant professor of clinical medicine at Columbia University, vice chair for education in the Department of Medicine and director of Graduate Medical Education at St. Luke's-Roosevelt in New York City. “Residents must explicitly believe that it is their personal responsibility to work rested and free of fatigue in most cases. Furthermore, the draft makes explicit the rare but real situation in which the care of an individual patient supersedes the duty hour restrictions.”

In an editorial, members of the ACGME Duty Hour Task Force also argue that their recommendations should be viewed as more than a singular recommendation on how many hours young doctors can work (10.1056/NEJMsb1005800).

“Although much of the debate has focused on establishing appropriate limits on resident hours,” the authors wrote, “the task force recognized that ensuring patient safety and providing an excellent teaching environment entail more than setting these limits.”

Let the debate formally begin.

Proposed regulations (PDF) from the Accreditation Council for Graduate Medical Education (ACGME) that limit first-year residents to 16 hours of duty will be seen either as an awakening or an abomination to educational leaders, according to the incoming president of the Association of Program Directors in Internal Medicine (APDIM).

“The draft ... will be welcomed by programs wishing to manage fatigue and will be seen as a threat by programs who have not yet accepted the need to reform graduate medical education,” says Ethan Fried, who takes over as APDIM president July 1.

The new changes come as no shock to academic hospitalists who have been waiting for the prescribed five-year update to the landmark 2003 duty-hour standards, especially after the recommendations published in the Institute of Medicine’s 2008 report “Resident Duty Hours: Enhancing Sleep, Supervision and Safety.” If approved, the new regulations will likely take effect in July 2011.

The data points of the rules will be debated thoroughly between now and then, but Dr. Fried views the recommendations as more than just tweaks to the existing infrastructure governing residency programs. He sees the suggestions as a sea change, particularly allowances for added duty time for second- and third-year residents, as well as situational exceptions that allow residents to work longer to ensure continuity of care.

“The draft turns the old concept of professionalism 180 degrees by telling residents that sleep deprivation is no longer a lifestyle choice,” adds Dr. Fried, MD, MS, FACP, assistant professor of clinical medicine at Columbia University, vice chair for education in the Department of Medicine and director of Graduate Medical Education at St. Luke's-Roosevelt in New York City. “Residents must explicitly believe that it is their personal responsibility to work rested and free of fatigue in most cases. Furthermore, the draft makes explicit the rare but real situation in which the care of an individual patient supersedes the duty hour restrictions.”

In an editorial, members of the ACGME Duty Hour Task Force also argue that their recommendations should be viewed as more than a singular recommendation on how many hours young doctors can work (10.1056/NEJMsb1005800).

“Although much of the debate has focused on establishing appropriate limits on resident hours,” the authors wrote, “the task force recognized that ensuring patient safety and providing an excellent teaching environment entail more than setting these limits.”

Let the debate formally begin.

Proposed regulations (PDF) from the Accreditation Council for Graduate Medical Education (ACGME) that limit first-year residents to 16 hours of duty will be seen either as an awakening or an abomination to educational leaders, according to the incoming president of the Association of Program Directors in Internal Medicine (APDIM).

“The draft ... will be welcomed by programs wishing to manage fatigue and will be seen as a threat by programs who have not yet accepted the need to reform graduate medical education,” says Ethan Fried, who takes over as APDIM president July 1.

The new changes come as no shock to academic hospitalists who have been waiting for the prescribed five-year update to the landmark 2003 duty-hour standards, especially after the recommendations published in the Institute of Medicine’s 2008 report “Resident Duty Hours: Enhancing Sleep, Supervision and Safety.” If approved, the new regulations will likely take effect in July 2011.

The data points of the rules will be debated thoroughly between now and then, but Dr. Fried views the recommendations as more than just tweaks to the existing infrastructure governing residency programs. He sees the suggestions as a sea change, particularly allowances for added duty time for second- and third-year residents, as well as situational exceptions that allow residents to work longer to ensure continuity of care.

“The draft turns the old concept of professionalism 180 degrees by telling residents that sleep deprivation is no longer a lifestyle choice,” adds Dr. Fried, MD, MS, FACP, assistant professor of clinical medicine at Columbia University, vice chair for education in the Department of Medicine and director of Graduate Medical Education at St. Luke's-Roosevelt in New York City. “Residents must explicitly believe that it is their personal responsibility to work rested and free of fatigue in most cases. Furthermore, the draft makes explicit the rare but real situation in which the care of an individual patient supersedes the duty hour restrictions.”

In an editorial, members of the ACGME Duty Hour Task Force also argue that their recommendations should be viewed as more than a singular recommendation on how many hours young doctors can work (10.1056/NEJMsb1005800).

“Although much of the debate has focused on establishing appropriate limits on resident hours,” the authors wrote, “the task force recognized that ensuring patient safety and providing an excellent teaching environment entail more than setting these limits.”

A new study that shows time and money could be saved by standardizing billing practices will likely find a supportive audience from HM groups and their business staffs, one hospitalist program executive says.

James Kodjababian, chief revenue officer and vice president of management services for Sound Physicians in Tacoma, Wash., says his firm is large enough that it has put in place systems and information technology (IT) to navigate the complex billing infrastructure that varies from carrier to carrier. But he thinks smaller HM groups likely struggle to deal with the labyrinthine codes and regulations that different insurance companies use.

“It’s like translating 43 different languages to consolidate it and manage it,” he says.

His sentiment is buttressed by “Saving Billions of Dollars—and Physician’s Time—By Streamlining Billing Practices,” which reported that standardized payment rules and claim forms “would translate into $7 million of savings annually in physician and clinical services” (doi: 10.1377/hlthaff.2009.0075). The study in Health Affairs also reported that four hours of physician time and five of support staff time could be saved each week.

Kodjababian acknowledges that to achieve such industrywide standardization, insurance companies would have to invest funding and man-hours. However, he says, the data that could be culled from an improved system would prove beneficial both to carriers and physicians.

“It’s time and money, but at the end of the day, you create a much better information set for people to benefit from,” Kodjababian says. “Right now, it’s very difficult to compare notes. If everybody is processing the same way, you can start to run statistics. You can start to see in a more macro perspective what things we should be doing.”

A new study that shows time and money could be saved by standardizing billing practices will likely find a supportive audience from HM groups and their business staffs, one hospitalist program executive says.

James Kodjababian, chief revenue officer and vice president of management services for Sound Physicians in Tacoma, Wash., says his firm is large enough that it has put in place systems and information technology (IT) to navigate the complex billing infrastructure that varies from carrier to carrier. But he thinks smaller HM groups likely struggle to deal with the labyrinthine codes and regulations that different insurance companies use.

“It’s like translating 43 different languages to consolidate it and manage it,” he says.

His sentiment is buttressed by “Saving Billions of Dollars—and Physician’s Time—By Streamlining Billing Practices,” which reported that standardized payment rules and claim forms “would translate into $7 million of savings annually in physician and clinical services” (doi: 10.1377/hlthaff.2009.0075). The study in Health Affairs also reported that four hours of physician time and five of support staff time could be saved each week.

Kodjababian acknowledges that to achieve such industrywide standardization, insurance companies would have to invest funding and man-hours. However, he says, the data that could be culled from an improved system would prove beneficial both to carriers and physicians.

“It’s time and money, but at the end of the day, you create a much better information set for people to benefit from,” Kodjababian says. “Right now, it’s very difficult to compare notes. If everybody is processing the same way, you can start to run statistics. You can start to see in a more macro perspective what things we should be doing.”

A new study that shows time and money could be saved by standardizing billing practices will likely find a supportive audience from HM groups and their business staffs, one hospitalist program executive says.

James Kodjababian, chief revenue officer and vice president of management services for Sound Physicians in Tacoma, Wash., says his firm is large enough that it has put in place systems and information technology (IT) to navigate the complex billing infrastructure that varies from carrier to carrier. But he thinks smaller HM groups likely struggle to deal with the labyrinthine codes and regulations that different insurance companies use.

“It’s like translating 43 different languages to consolidate it and manage it,” he says.

His sentiment is buttressed by “Saving Billions of Dollars—and Physician’s Time—By Streamlining Billing Practices,” which reported that standardized payment rules and claim forms “would translate into $7 million of savings annually in physician and clinical services” (doi: 10.1377/hlthaff.2009.0075). The study in Health Affairs also reported that four hours of physician time and five of support staff time could be saved each week.

Kodjababian acknowledges that to achieve such industrywide standardization, insurance companies would have to invest funding and man-hours. However, he says, the data that could be culled from an improved system would prove beneficial both to carriers and physicians.

“It’s time and money, but at the end of the day, you create a much better information set for people to benefit from,” Kodjababian says. “Right now, it’s very difficult to compare notes. If everybody is processing the same way, you can start to run statistics. You can start to see in a more macro perspective what things we should be doing.”