Would a colonoscopy have made a difference? ... Suicide blamed on failure to diagnose bipolar disorder

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Would a colonoscopy have made a difference? ... Suicide blamed on failure to diagnose bipolar disorder

Would a colonoscopy have made a difference?

ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.

The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.

The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.

A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.

Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.

The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.

An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.

PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.

THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.

VERDICT $4.65 million Massachusetts verdict.

COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.

Suicide blamed on failure to diagnose bipolar disorder

A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.

PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.

THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.

VERDICT $175,000 Michigan settlement.

COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.

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Would a colonoscopy have made a difference?

ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.

The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.

The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.

A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.

Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.

The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.

An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.

PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.

THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.

VERDICT $4.65 million Massachusetts verdict.

COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.

Suicide blamed on failure to diagnose bipolar disorder

A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.

PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.

THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.

VERDICT $175,000 Michigan settlement.

COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.

Would a colonoscopy have made a difference?

ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.

The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.

The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.

A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.

Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.

The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.

An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.

PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.

THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.

VERDICT $4.65 million Massachusetts verdict.

COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.

Suicide blamed on failure to diagnose bipolar disorder

A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.

PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.

THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.

VERDICT $175,000 Michigan settlement.

COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.

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Traumatic brain injury: Pharmacotherapy options for cognitive deficits

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Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.

With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.

TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.

Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4

TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7

Table 1

Psychiatric symptoms: Common among TBI patients

Psychiatric symptomIncidence
Aggression30%
Anxiety10% to 70%
Apathy10%
Cognitive impairment25% to 70%
Depression25% to 50%
Mania1% to 10%
Psychosis3% to 8%
TBI: traumatic brain injury
Source: Adapted from reference 2

Table 2

Classifying severity of traumatic brain injury

SeverityGCS scoreLOC durationPTA*
Mild13 to 15<30 minutes<1 hour
Moderate9 to 121 to 24 hours1 to 24 hours
Severe<8>24 hours>24 hours
*Includes loss of memory immediately before or after the accident
GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia
Source: Reference 5

Cognitive dysfunction and TBI

Cognitive dysfunction can be split into 3 categories:

  • executive function
  • memory
  • processing speed.

The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5

Off-label pharmacotherapy

There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8

Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.

 

 

Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10

Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11

Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8

Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11

Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.

Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23

The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26

Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27

Table 3

Recommended treatments for mild TBI-related cognitive deficits

DeficitFirst-line medicationSide effectsContraindicationsOther treatments
MemoryDonepezil (5 to 10 mg/d)Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexiaHypersensitivity to donepezil or piperidine derivativesRivastigmine, galantamine, physostigmine, CDP-choline
Speed of processingMethylphenidate (0.3 mg/kg twice daily)Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritabilityHypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 daysDextroamphetamine
Executive functionAmantadine (200 to 400 mg/d)CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexiaHypersensitivity to amantadineBromocriptine, pramipexole, carbidopa/levodopa
CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor
Source: Reference 8

Nonpharmacologic treatments

In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6

 

 

CASE CONTINUED: Improvement with stimulants

Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.

Related Resource

  • Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.

Drug Brand Names

  • Amantadine • Symadine, Symmetrel
  • Bromocriptine • Parlodel
  • Carbidopa/levodopa • Sinemet
  • Dextroamphetamine • Dexedrine
  • Donepezil • Aricept
  • Galantamine • Razadyne
  • Methylphenidate • Ritalin, Methylin, others
  • Physostigmine • Antilirium
  • Pramipexole • Mirapex
  • Rivastigmine • Exelon
  • Sertraline • Zoloft
  • Tacrine • Cognex

Disclosures

Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.

Dr. McCarron is a speaker for Eli Lilly and Company.

References

1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.

2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.

3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.

4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.

5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.

6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.

7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.

8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.

9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.

10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.

11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.

12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.

13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.

14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.

15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.

16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.

17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.

18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.

19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.

20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.

20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.

22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.

23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.

24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.

25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.

26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.

27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.

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Robert M. McCarron, DO
Training Director, Internal Medicine/Psychiatry Residency, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California, Davis Sacramento, CA

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Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.

With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.

TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.

Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4

TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7

Table 1

Psychiatric symptoms: Common among TBI patients

Psychiatric symptomIncidence
Aggression30%
Anxiety10% to 70%
Apathy10%
Cognitive impairment25% to 70%
Depression25% to 50%
Mania1% to 10%
Psychosis3% to 8%
TBI: traumatic brain injury
Source: Adapted from reference 2

Table 2

Classifying severity of traumatic brain injury

SeverityGCS scoreLOC durationPTA*
Mild13 to 15<30 minutes<1 hour
Moderate9 to 121 to 24 hours1 to 24 hours
Severe<8>24 hours>24 hours
*Includes loss of memory immediately before or after the accident
GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia
Source: Reference 5

Cognitive dysfunction and TBI

Cognitive dysfunction can be split into 3 categories:

  • executive function
  • memory
  • processing speed.

The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5

Off-label pharmacotherapy

There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8

Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.

 

 

Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10

Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11

Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8

Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11

Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.

Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23

The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26

Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27

Table 3

Recommended treatments for mild TBI-related cognitive deficits

DeficitFirst-line medicationSide effectsContraindicationsOther treatments
MemoryDonepezil (5 to 10 mg/d)Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexiaHypersensitivity to donepezil or piperidine derivativesRivastigmine, galantamine, physostigmine, CDP-choline
Speed of processingMethylphenidate (0.3 mg/kg twice daily)Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritabilityHypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 daysDextroamphetamine
Executive functionAmantadine (200 to 400 mg/d)CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexiaHypersensitivity to amantadineBromocriptine, pramipexole, carbidopa/levodopa
CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor
Source: Reference 8

Nonpharmacologic treatments

In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6

 

 

CASE CONTINUED: Improvement with stimulants

Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.

Related Resource

  • Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.

Drug Brand Names

  • Amantadine • Symadine, Symmetrel
  • Bromocriptine • Parlodel
  • Carbidopa/levodopa • Sinemet
  • Dextroamphetamine • Dexedrine
  • Donepezil • Aricept
  • Galantamine • Razadyne
  • Methylphenidate • Ritalin, Methylin, others
  • Physostigmine • Antilirium
  • Pramipexole • Mirapex
  • Rivastigmine • Exelon
  • Sertraline • Zoloft
  • Tacrine • Cognex

Disclosures

Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.

Dr. McCarron is a speaker for Eli Lilly and Company.

Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.

With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.

TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.

Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4

TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7

Table 1

Psychiatric symptoms: Common among TBI patients

Psychiatric symptomIncidence
Aggression30%
Anxiety10% to 70%
Apathy10%
Cognitive impairment25% to 70%
Depression25% to 50%
Mania1% to 10%
Psychosis3% to 8%
TBI: traumatic brain injury
Source: Adapted from reference 2

Table 2

Classifying severity of traumatic brain injury

SeverityGCS scoreLOC durationPTA*
Mild13 to 15<30 minutes<1 hour
Moderate9 to 121 to 24 hours1 to 24 hours
Severe<8>24 hours>24 hours
*Includes loss of memory immediately before or after the accident
GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia
Source: Reference 5

Cognitive dysfunction and TBI

Cognitive dysfunction can be split into 3 categories:

  • executive function
  • memory
  • processing speed.

The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5

Off-label pharmacotherapy

There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8

Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.

 

 

Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10

Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11

Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8

Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11

Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.

Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23

The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26

Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27

Table 3

Recommended treatments for mild TBI-related cognitive deficits

DeficitFirst-line medicationSide effectsContraindicationsOther treatments
MemoryDonepezil (5 to 10 mg/d)Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexiaHypersensitivity to donepezil or piperidine derivativesRivastigmine, galantamine, physostigmine, CDP-choline
Speed of processingMethylphenidate (0.3 mg/kg twice daily)Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritabilityHypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 daysDextroamphetamine
Executive functionAmantadine (200 to 400 mg/d)CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexiaHypersensitivity to amantadineBromocriptine, pramipexole, carbidopa/levodopa
CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor
Source: Reference 8

Nonpharmacologic treatments

In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6

 

 

CASE CONTINUED: Improvement with stimulants

Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.

Related Resource

  • Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.

Drug Brand Names

  • Amantadine • Symadine, Symmetrel
  • Bromocriptine • Parlodel
  • Carbidopa/levodopa • Sinemet
  • Dextroamphetamine • Dexedrine
  • Donepezil • Aricept
  • Galantamine • Razadyne
  • Methylphenidate • Ritalin, Methylin, others
  • Physostigmine • Antilirium
  • Pramipexole • Mirapex
  • Rivastigmine • Exelon
  • Sertraline • Zoloft
  • Tacrine • Cognex

Disclosures

Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.

Dr. McCarron is a speaker for Eli Lilly and Company.

References

1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.

2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.

3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.

4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.

5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.

6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.

7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.

8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.

9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.

10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.

11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.

12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.

13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.

14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.

15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.

16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.

17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.

18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.

19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.

20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.

20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.

22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.

23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.

24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.

25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.

26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.

27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.

References

1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.

2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.

3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.

4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.

5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.

6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.

7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.

8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.

9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.

10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.

11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.

12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.

13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.

14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.

15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.

16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.

17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.

18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.

19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.

20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.

20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.

22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.

23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.

24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.

25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.

26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.

27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.

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Genetic Evaluation of Children

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Genetic Evaluation of Children

Genetic testing has entered a new era in the past few years. Our ability to perform DNA-based tests and identify an individual's susceptibility to cancer, heart disease, diabetes, and so many other conditions is beginning to have a major impact on our practice of medicine.

Experts predict – thanks to advances in technology we already have – that in a few years we will be able to screen during the newborn period and identify every mutation and polymorphism present. This screening will permit us to predict a child's “medical life” through identification of individual susceptibilities to disease likely to develop during his or her lifetime. Although still in its infancy, this technology would revolutionize pediatrics from a field in which we wait for the child to develop symptoms and signs of disease and then react with medication and other treatments, to one where we can predict disease. This will give us the opportunity to help our patients in a whole new way: to prevent the symptoms and signs from arising in the first place.

With the good comes the bad, as with any new technology. For example, interpretation of results with this advanced testing will require special expertise in genetics and genomics. Unfortunately, interpretation of genetic findings often is not as “black and white” as diagnosis of anemia based on serum hemoglobin and hematocrit levels. Genetic test results often include polymorphisms, and most of these variations of normal are benign and not associated with disease. Subspecialist consultation may be needed to make these important distinctions.

General pediatricians play an essential role in interpretation of newborn screening tests. Fortunately, results are normal for the majority of children and no further follow-up is indicated. However, if an abnormality is detected, referral to a specialist is warranted to facilitate an early intervention that, in some cases, can make a difference in the long-term health of the child. You also can refer families who request consultation with a geneticist to discuss recurrence risk in future progeny and for additional genetic testing, as indicated.

Beyond standard newborn genetic screening, the role of the pediatrician is somewhat limited regarding the screening and testing for specific genetic disorders. However, there are situations in which the pediatrician should feel comfortable in ordering and interpreting genetic tests.

For example, testing in children with intellectual disabilities and autism spectrum disorder has become standard. As tier 1 testing in such children, I usually order a microarray-based comparative genomic hybridization (array CGH), a test that has largely replaced high-resolution chromosome analysis in this population. I also perform DNA testing for fragile X syndrome, the most common inherited cause of intellectual disabilities. Because the results of this testing will be normal in 80%–90% of these children, I encourage pediatricians to order these tests themselves. I then make myself available if genetic evaluation reveals an abnormality.

Another factor to consider is the recent direct-to-consumer marketing of genetic testing that expands standard newborn screening or uses genetic markers to predict susceptibility to specific conditions. These tests often require the family, with or without the assistance of the pediatrician, to send a sample of DNA to a reference lab. The lab returns the results directly to the family. Again, the laboratory results are difficult to interpret, and you may be called on to provide guidance. Sometimes interpretation is straightforward, but in other cases it can be tricky, and if you are uncomfortable you might want to refer them to a medical geneticist or genetic counselor.

When you refer a child to a geneticist, include all results of your previous testing, those performed by other specialists, and newborn screening. Genetic tests performed on the mother during the pregnancy (for example, amniocentesis, chorionic villus sampling, sonograms, and/or biochemical screening tests) also are important. Provide any imaging findings, including MRIs or CT scans.

Proceed cautiously when counseling families regarding results of genetic testing. It can be trickier than you might think. For example, results of a test for a single gene disorder might uncover a previously unknown change in the child's DNA. The finding could be a benign polymorphism that has no clinical consequences or it could be a pathogenic mutation responsible for the child's signs and symptoms.

Simply informing the family about this finding is inadequate. To be certain, the parents need to be tested. If one or both of them has the same genetic change, the polymorphism might be benign. In contrast, if neither parent has the mutation, the child's test result might reflect a spontaneous genetic change and increase the likelihood you have discovered the cause of the clinical condition.

 

 

In general, there are three categories of children who may require genetic testing. First, there are those children who have multiple congenital anomalies or dysmorphic features. These findings could be caused by chromosome abnormalities, single gene mutations, or teratogenic agents. In these children, in order to ensure that the appropriate tests are ordered, a genetic consultation is important.

A second group of children who may require genetic testing are those in whom deviation from typical development or “normal” growth parameters occur during the first few years of life. Such children may have chromosome abnormalities, single gene mutations, and/or an underlying metabolic disorder. Keep in mind seizures, developmental regression, failure to thrive, and respiratory disturbances can bolster the likelihood of a genetic or metabolic etiology.

Before ordering any genetic testing, it is essential to take a complete patient and family history and to perform a complete physical exam. Children with a family history of a first- or second-degree family member with a genetic disorder also might benefit from genetic evaluation, comprising the third group. For example, even before symptoms are present, testing a child who has a brother with Duchenne muscular dystrophy or a relative with cystic fibrosis may prove life saving if it uncovers a similar diagnosis.

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Genetic testing has entered a new era in the past few years. Our ability to perform DNA-based tests and identify an individual's susceptibility to cancer, heart disease, diabetes, and so many other conditions is beginning to have a major impact on our practice of medicine.

Experts predict – thanks to advances in technology we already have – that in a few years we will be able to screen during the newborn period and identify every mutation and polymorphism present. This screening will permit us to predict a child's “medical life” through identification of individual susceptibilities to disease likely to develop during his or her lifetime. Although still in its infancy, this technology would revolutionize pediatrics from a field in which we wait for the child to develop symptoms and signs of disease and then react with medication and other treatments, to one where we can predict disease. This will give us the opportunity to help our patients in a whole new way: to prevent the symptoms and signs from arising in the first place.

With the good comes the bad, as with any new technology. For example, interpretation of results with this advanced testing will require special expertise in genetics and genomics. Unfortunately, interpretation of genetic findings often is not as “black and white” as diagnosis of anemia based on serum hemoglobin and hematocrit levels. Genetic test results often include polymorphisms, and most of these variations of normal are benign and not associated with disease. Subspecialist consultation may be needed to make these important distinctions.

General pediatricians play an essential role in interpretation of newborn screening tests. Fortunately, results are normal for the majority of children and no further follow-up is indicated. However, if an abnormality is detected, referral to a specialist is warranted to facilitate an early intervention that, in some cases, can make a difference in the long-term health of the child. You also can refer families who request consultation with a geneticist to discuss recurrence risk in future progeny and for additional genetic testing, as indicated.

Beyond standard newborn genetic screening, the role of the pediatrician is somewhat limited regarding the screening and testing for specific genetic disorders. However, there are situations in which the pediatrician should feel comfortable in ordering and interpreting genetic tests.

For example, testing in children with intellectual disabilities and autism spectrum disorder has become standard. As tier 1 testing in such children, I usually order a microarray-based comparative genomic hybridization (array CGH), a test that has largely replaced high-resolution chromosome analysis in this population. I also perform DNA testing for fragile X syndrome, the most common inherited cause of intellectual disabilities. Because the results of this testing will be normal in 80%–90% of these children, I encourage pediatricians to order these tests themselves. I then make myself available if genetic evaluation reveals an abnormality.

Another factor to consider is the recent direct-to-consumer marketing of genetic testing that expands standard newborn screening or uses genetic markers to predict susceptibility to specific conditions. These tests often require the family, with or without the assistance of the pediatrician, to send a sample of DNA to a reference lab. The lab returns the results directly to the family. Again, the laboratory results are difficult to interpret, and you may be called on to provide guidance. Sometimes interpretation is straightforward, but in other cases it can be tricky, and if you are uncomfortable you might want to refer them to a medical geneticist or genetic counselor.

When you refer a child to a geneticist, include all results of your previous testing, those performed by other specialists, and newborn screening. Genetic tests performed on the mother during the pregnancy (for example, amniocentesis, chorionic villus sampling, sonograms, and/or biochemical screening tests) also are important. Provide any imaging findings, including MRIs or CT scans.

Proceed cautiously when counseling families regarding results of genetic testing. It can be trickier than you might think. For example, results of a test for a single gene disorder might uncover a previously unknown change in the child's DNA. The finding could be a benign polymorphism that has no clinical consequences or it could be a pathogenic mutation responsible for the child's signs and symptoms.

Simply informing the family about this finding is inadequate. To be certain, the parents need to be tested. If one or both of them has the same genetic change, the polymorphism might be benign. In contrast, if neither parent has the mutation, the child's test result might reflect a spontaneous genetic change and increase the likelihood you have discovered the cause of the clinical condition.

 

 

In general, there are three categories of children who may require genetic testing. First, there are those children who have multiple congenital anomalies or dysmorphic features. These findings could be caused by chromosome abnormalities, single gene mutations, or teratogenic agents. In these children, in order to ensure that the appropriate tests are ordered, a genetic consultation is important.

A second group of children who may require genetic testing are those in whom deviation from typical development or “normal” growth parameters occur during the first few years of life. Such children may have chromosome abnormalities, single gene mutations, and/or an underlying metabolic disorder. Keep in mind seizures, developmental regression, failure to thrive, and respiratory disturbances can bolster the likelihood of a genetic or metabolic etiology.

Before ordering any genetic testing, it is essential to take a complete patient and family history and to perform a complete physical exam. Children with a family history of a first- or second-degree family member with a genetic disorder also might benefit from genetic evaluation, comprising the third group. For example, even before symptoms are present, testing a child who has a brother with Duchenne muscular dystrophy or a relative with cystic fibrosis may prove life saving if it uncovers a similar diagnosis.

Genetic testing has entered a new era in the past few years. Our ability to perform DNA-based tests and identify an individual's susceptibility to cancer, heart disease, diabetes, and so many other conditions is beginning to have a major impact on our practice of medicine.

Experts predict – thanks to advances in technology we already have – that in a few years we will be able to screen during the newborn period and identify every mutation and polymorphism present. This screening will permit us to predict a child's “medical life” through identification of individual susceptibilities to disease likely to develop during his or her lifetime. Although still in its infancy, this technology would revolutionize pediatrics from a field in which we wait for the child to develop symptoms and signs of disease and then react with medication and other treatments, to one where we can predict disease. This will give us the opportunity to help our patients in a whole new way: to prevent the symptoms and signs from arising in the first place.

With the good comes the bad, as with any new technology. For example, interpretation of results with this advanced testing will require special expertise in genetics and genomics. Unfortunately, interpretation of genetic findings often is not as “black and white” as diagnosis of anemia based on serum hemoglobin and hematocrit levels. Genetic test results often include polymorphisms, and most of these variations of normal are benign and not associated with disease. Subspecialist consultation may be needed to make these important distinctions.

General pediatricians play an essential role in interpretation of newborn screening tests. Fortunately, results are normal for the majority of children and no further follow-up is indicated. However, if an abnormality is detected, referral to a specialist is warranted to facilitate an early intervention that, in some cases, can make a difference in the long-term health of the child. You also can refer families who request consultation with a geneticist to discuss recurrence risk in future progeny and for additional genetic testing, as indicated.

Beyond standard newborn genetic screening, the role of the pediatrician is somewhat limited regarding the screening and testing for specific genetic disorders. However, there are situations in which the pediatrician should feel comfortable in ordering and interpreting genetic tests.

For example, testing in children with intellectual disabilities and autism spectrum disorder has become standard. As tier 1 testing in such children, I usually order a microarray-based comparative genomic hybridization (array CGH), a test that has largely replaced high-resolution chromosome analysis in this population. I also perform DNA testing for fragile X syndrome, the most common inherited cause of intellectual disabilities. Because the results of this testing will be normal in 80%–90% of these children, I encourage pediatricians to order these tests themselves. I then make myself available if genetic evaluation reveals an abnormality.

Another factor to consider is the recent direct-to-consumer marketing of genetic testing that expands standard newborn screening or uses genetic markers to predict susceptibility to specific conditions. These tests often require the family, with or without the assistance of the pediatrician, to send a sample of DNA to a reference lab. The lab returns the results directly to the family. Again, the laboratory results are difficult to interpret, and you may be called on to provide guidance. Sometimes interpretation is straightforward, but in other cases it can be tricky, and if you are uncomfortable you might want to refer them to a medical geneticist or genetic counselor.

When you refer a child to a geneticist, include all results of your previous testing, those performed by other specialists, and newborn screening. Genetic tests performed on the mother during the pregnancy (for example, amniocentesis, chorionic villus sampling, sonograms, and/or biochemical screening tests) also are important. Provide any imaging findings, including MRIs or CT scans.

Proceed cautiously when counseling families regarding results of genetic testing. It can be trickier than you might think. For example, results of a test for a single gene disorder might uncover a previously unknown change in the child's DNA. The finding could be a benign polymorphism that has no clinical consequences or it could be a pathogenic mutation responsible for the child's signs and symptoms.

Simply informing the family about this finding is inadequate. To be certain, the parents need to be tested. If one or both of them has the same genetic change, the polymorphism might be benign. In contrast, if neither parent has the mutation, the child's test result might reflect a spontaneous genetic change and increase the likelihood you have discovered the cause of the clinical condition.

 

 

In general, there are three categories of children who may require genetic testing. First, there are those children who have multiple congenital anomalies or dysmorphic features. These findings could be caused by chromosome abnormalities, single gene mutations, or teratogenic agents. In these children, in order to ensure that the appropriate tests are ordered, a genetic consultation is important.

A second group of children who may require genetic testing are those in whom deviation from typical development or “normal” growth parameters occur during the first few years of life. Such children may have chromosome abnormalities, single gene mutations, and/or an underlying metabolic disorder. Keep in mind seizures, developmental regression, failure to thrive, and respiratory disturbances can bolster the likelihood of a genetic or metabolic etiology.

Before ordering any genetic testing, it is essential to take a complete patient and family history and to perform a complete physical exam. Children with a family history of a first- or second-degree family member with a genetic disorder also might benefit from genetic evaluation, comprising the third group. For example, even before symptoms are present, testing a child who has a brother with Duchenne muscular dystrophy or a relative with cystic fibrosis may prove life saving if it uncovers a similar diagnosis.

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Helping Children With PTSD

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Different forms of trauma can cause posttraumatic stress disorder in children, whether from an objective event like a car crash or sports injury to trauma involving loved ones, such as domestic violence, abuse, or neglect.

Pediatricians can help by routinely screening for dysfunction and by asking questions at annual well-child visits. Overt symptoms include fear related to the trauma such as avoiding the traumatic setting or activity. Less specific symptoms include anxiety, avoidance, social isolation, depression, and low self-esteem.

If a standard screen such as the Pediatric Symptom Checklist or another instrument reveals psychosocial dysfunction, you have to determine the cause of dysfunction, and PTSD should certainly be considered.

Is there family discord leading to violence in the home? If you suspect PTSD, ask a child what happened and why he or she thinks it happened. Determine if the child is blaming himself or herself in any way. Is the child grieving following a permanent injury and/or loss of a loved one? How have the parents discussed any traumatic event with the child? Do the parents feel traumatized by the child's experience?

If PTSD is a possibility, ask if the child is experiencing flashbacks, intrusive thoughts, and/or any related anxiety.

Some symptoms are expected after a traumatic event or following cancer or critical care treatment experienced as traumatic. Most children and adolescents overcome the fear of riding in a car or playing the sport that resulted in the trauma.

However, symptoms that persist for a month or more, with avoidance and associated anxiety, are core to the diagnosis of PTSD. The anxiety can build and be self-reinforcing so as to interfere with daily functioning. At this point, consider referral to a mental health specialist, preferably one with some experience in PTSD treatment. A specialist can help the patient overcome his or her anxiety and return to functioning through cognitive and behavioral techniques such as reframing the events, dealing with any guilt, and staged exposure to the anxiety.

If one of your patients experienced a car crash or other major trauma, you will likely know about it, already be treating the child, and should be planning to monitor them for signs of PTSD. In contrast, detection of subtle PTSD is more challenging, particularly if the trauma is unknown or occurred years ago. Trauma related to domestic violence or sexual abuse first requires consideration of this possibility and then gentle, empathic, and persistent questioning.

Triggers for reliving/reexperiencing the trauma also can be straightforward. For example, a child who gets into a car with a similar interior design years after a crash can immediately experience and emotionally return to the trauma. Other triggers are less obvious, such as a teenage girl who was held down and forced to have sex against her will, who later feels constrained by tight clothing and immediately relives the fear and anguish.

Like many presentations in pediatrics, management of PTSD depends on the developmental stage of the child, including his or her cognitive abilities and emotional state. For example, infants or toddlers might not be able to make much sense of what is happening when they witness domestic violence. Terror, fear, and confusion are their most likely reactions.

School-age children aged 5–8 years would not fully understand either, but they will try to make some sense of the domestic violence. Assuming no one reassures them otherwise, they also may feel that something they did sparked or contributed to the violence. For example, if they overhear arguments around issues in the family and hear their name mentioned, they may quickly assume that they are the cause of the domestic violence. This can lead to feelings of guilt, self-criticism, and unworthiness.

Adolescents will experience some of the same reactions as younger children. They will still experience shock, even if they are better equipped to conceptualize the domestic violence. Some will feel powerless because they cannot end the strife, particularly at a time when they are supposed to have more control over the real world. Teens might feel they have not lived up to expectations and perceive some blame. Others may choose to flee, find support through friends, and/or may deal with their feelings using substances.

Act when you encounter a patient who feels very guilty about parental fighting or who justifies abuse because he feels worthless or was told repeatedly he was a bad child. Help him realize he was not responsible for the conflict and that no one deserves abuse. Discuss other, more realistic possibilities for the family paradigm.

 

 

These are not easy conversations. Some pediatricians will feel comfortable working at this depth, others will prefer to refer.

Healing from PTSD related to family violence, sexual abuse, or criminal activity is a several-step process. As one's sense of guilt diminishes, other emotions such as anger at not being better protected or valued need to be addressed. Finally, there needs to be some grieving for what was lacking and some acceptance of what was possible. This is not a simple process; however, it is worthwhile because if their PTSD remains untreated, there is a greater likelihood they will continue to relive traumatic memories as adults.

There is some controversy as to whether talking through the traumatic event over and over truly helps. Some clinicians feel that a certain amount of supportive discussion in a calm way makes sense, especially early. But solely repeating the details of the event may re-traumatize the child and intensify negative feelings, especially if the memories are very vivid.

Cognitive and behavioral approaches can help the child reframe their trauma. An example is exposure therapy, where the child is carefully reexposed to the trauma in stages while they learn to reframe and diminish the intensity of the experience. Often, ideas about the trauma come out that can be examined objectively to try to lessen some of those traumatic feelings.

Exposure therapy also can incorporate gradual steps to help the child overcome their fear. If a person survived a plane crash, the first step might be to take him or her to the airport, then to board an airplane without taking off, and so forth. This approach reintroduces the trauma without eliciting a full response. You don't want the brain to go on “red alert” again. In a state of hyperarousal, reliving the trauma may do more harm than good.

The terrified moments that children experience during a traumatic sequence tend to get burned into their memories much more strongly than everyday events. A school-age child might remember nothing about an uneventful trip in the car, but if a traumatic accident happens, often she remembers almost every detail. She recalls descriptive elements of what happened as well as the emotional fright or anguish very vividly.

Sometimes vivid, traumatic memories will enter your patient's mind spontaneously without him knowing why. In other cases, there are triggers. Sometimes these flashbacks arise shortly following trauma and sometimes they take years.

Pediatricians can do their patients and families a service if they are aware of PTSD either after an overt event like a car accident or by considering trauma in an anxious or dysfunctional child.

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Different forms of trauma can cause posttraumatic stress disorder in children, whether from an objective event like a car crash or sports injury to trauma involving loved ones, such as domestic violence, abuse, or neglect.

Pediatricians can help by routinely screening for dysfunction and by asking questions at annual well-child visits. Overt symptoms include fear related to the trauma such as avoiding the traumatic setting or activity. Less specific symptoms include anxiety, avoidance, social isolation, depression, and low self-esteem.

If a standard screen such as the Pediatric Symptom Checklist or another instrument reveals psychosocial dysfunction, you have to determine the cause of dysfunction, and PTSD should certainly be considered.

Is there family discord leading to violence in the home? If you suspect PTSD, ask a child what happened and why he or she thinks it happened. Determine if the child is blaming himself or herself in any way. Is the child grieving following a permanent injury and/or loss of a loved one? How have the parents discussed any traumatic event with the child? Do the parents feel traumatized by the child's experience?

If PTSD is a possibility, ask if the child is experiencing flashbacks, intrusive thoughts, and/or any related anxiety.

Some symptoms are expected after a traumatic event or following cancer or critical care treatment experienced as traumatic. Most children and adolescents overcome the fear of riding in a car or playing the sport that resulted in the trauma.

However, symptoms that persist for a month or more, with avoidance and associated anxiety, are core to the diagnosis of PTSD. The anxiety can build and be self-reinforcing so as to interfere with daily functioning. At this point, consider referral to a mental health specialist, preferably one with some experience in PTSD treatment. A specialist can help the patient overcome his or her anxiety and return to functioning through cognitive and behavioral techniques such as reframing the events, dealing with any guilt, and staged exposure to the anxiety.

If one of your patients experienced a car crash or other major trauma, you will likely know about it, already be treating the child, and should be planning to monitor them for signs of PTSD. In contrast, detection of subtle PTSD is more challenging, particularly if the trauma is unknown or occurred years ago. Trauma related to domestic violence or sexual abuse first requires consideration of this possibility and then gentle, empathic, and persistent questioning.

Triggers for reliving/reexperiencing the trauma also can be straightforward. For example, a child who gets into a car with a similar interior design years after a crash can immediately experience and emotionally return to the trauma. Other triggers are less obvious, such as a teenage girl who was held down and forced to have sex against her will, who later feels constrained by tight clothing and immediately relives the fear and anguish.

Like many presentations in pediatrics, management of PTSD depends on the developmental stage of the child, including his or her cognitive abilities and emotional state. For example, infants or toddlers might not be able to make much sense of what is happening when they witness domestic violence. Terror, fear, and confusion are their most likely reactions.

School-age children aged 5–8 years would not fully understand either, but they will try to make some sense of the domestic violence. Assuming no one reassures them otherwise, they also may feel that something they did sparked or contributed to the violence. For example, if they overhear arguments around issues in the family and hear their name mentioned, they may quickly assume that they are the cause of the domestic violence. This can lead to feelings of guilt, self-criticism, and unworthiness.

Adolescents will experience some of the same reactions as younger children. They will still experience shock, even if they are better equipped to conceptualize the domestic violence. Some will feel powerless because they cannot end the strife, particularly at a time when they are supposed to have more control over the real world. Teens might feel they have not lived up to expectations and perceive some blame. Others may choose to flee, find support through friends, and/or may deal with their feelings using substances.

Act when you encounter a patient who feels very guilty about parental fighting or who justifies abuse because he feels worthless or was told repeatedly he was a bad child. Help him realize he was not responsible for the conflict and that no one deserves abuse. Discuss other, more realistic possibilities for the family paradigm.

 

 

These are not easy conversations. Some pediatricians will feel comfortable working at this depth, others will prefer to refer.

Healing from PTSD related to family violence, sexual abuse, or criminal activity is a several-step process. As one's sense of guilt diminishes, other emotions such as anger at not being better protected or valued need to be addressed. Finally, there needs to be some grieving for what was lacking and some acceptance of what was possible. This is not a simple process; however, it is worthwhile because if their PTSD remains untreated, there is a greater likelihood they will continue to relive traumatic memories as adults.

There is some controversy as to whether talking through the traumatic event over and over truly helps. Some clinicians feel that a certain amount of supportive discussion in a calm way makes sense, especially early. But solely repeating the details of the event may re-traumatize the child and intensify negative feelings, especially if the memories are very vivid.

Cognitive and behavioral approaches can help the child reframe their trauma. An example is exposure therapy, where the child is carefully reexposed to the trauma in stages while they learn to reframe and diminish the intensity of the experience. Often, ideas about the trauma come out that can be examined objectively to try to lessen some of those traumatic feelings.

Exposure therapy also can incorporate gradual steps to help the child overcome their fear. If a person survived a plane crash, the first step might be to take him or her to the airport, then to board an airplane without taking off, and so forth. This approach reintroduces the trauma without eliciting a full response. You don't want the brain to go on “red alert” again. In a state of hyperarousal, reliving the trauma may do more harm than good.

The terrified moments that children experience during a traumatic sequence tend to get burned into their memories much more strongly than everyday events. A school-age child might remember nothing about an uneventful trip in the car, but if a traumatic accident happens, often she remembers almost every detail. She recalls descriptive elements of what happened as well as the emotional fright or anguish very vividly.

Sometimes vivid, traumatic memories will enter your patient's mind spontaneously without him knowing why. In other cases, there are triggers. Sometimes these flashbacks arise shortly following trauma and sometimes they take years.

Pediatricians can do their patients and families a service if they are aware of PTSD either after an overt event like a car accident or by considering trauma in an anxious or dysfunctional child.

 

[email protected]

Different forms of trauma can cause posttraumatic stress disorder in children, whether from an objective event like a car crash or sports injury to trauma involving loved ones, such as domestic violence, abuse, or neglect.

Pediatricians can help by routinely screening for dysfunction and by asking questions at annual well-child visits. Overt symptoms include fear related to the trauma such as avoiding the traumatic setting or activity. Less specific symptoms include anxiety, avoidance, social isolation, depression, and low self-esteem.

If a standard screen such as the Pediatric Symptom Checklist or another instrument reveals psychosocial dysfunction, you have to determine the cause of dysfunction, and PTSD should certainly be considered.

Is there family discord leading to violence in the home? If you suspect PTSD, ask a child what happened and why he or she thinks it happened. Determine if the child is blaming himself or herself in any way. Is the child grieving following a permanent injury and/or loss of a loved one? How have the parents discussed any traumatic event with the child? Do the parents feel traumatized by the child's experience?

If PTSD is a possibility, ask if the child is experiencing flashbacks, intrusive thoughts, and/or any related anxiety.

Some symptoms are expected after a traumatic event or following cancer or critical care treatment experienced as traumatic. Most children and adolescents overcome the fear of riding in a car or playing the sport that resulted in the trauma.

However, symptoms that persist for a month or more, with avoidance and associated anxiety, are core to the diagnosis of PTSD. The anxiety can build and be self-reinforcing so as to interfere with daily functioning. At this point, consider referral to a mental health specialist, preferably one with some experience in PTSD treatment. A specialist can help the patient overcome his or her anxiety and return to functioning through cognitive and behavioral techniques such as reframing the events, dealing with any guilt, and staged exposure to the anxiety.

If one of your patients experienced a car crash or other major trauma, you will likely know about it, already be treating the child, and should be planning to monitor them for signs of PTSD. In contrast, detection of subtle PTSD is more challenging, particularly if the trauma is unknown or occurred years ago. Trauma related to domestic violence or sexual abuse first requires consideration of this possibility and then gentle, empathic, and persistent questioning.

Triggers for reliving/reexperiencing the trauma also can be straightforward. For example, a child who gets into a car with a similar interior design years after a crash can immediately experience and emotionally return to the trauma. Other triggers are less obvious, such as a teenage girl who was held down and forced to have sex against her will, who later feels constrained by tight clothing and immediately relives the fear and anguish.

Like many presentations in pediatrics, management of PTSD depends on the developmental stage of the child, including his or her cognitive abilities and emotional state. For example, infants or toddlers might not be able to make much sense of what is happening when they witness domestic violence. Terror, fear, and confusion are their most likely reactions.

School-age children aged 5–8 years would not fully understand either, but they will try to make some sense of the domestic violence. Assuming no one reassures them otherwise, they also may feel that something they did sparked or contributed to the violence. For example, if they overhear arguments around issues in the family and hear their name mentioned, they may quickly assume that they are the cause of the domestic violence. This can lead to feelings of guilt, self-criticism, and unworthiness.

Adolescents will experience some of the same reactions as younger children. They will still experience shock, even if they are better equipped to conceptualize the domestic violence. Some will feel powerless because they cannot end the strife, particularly at a time when they are supposed to have more control over the real world. Teens might feel they have not lived up to expectations and perceive some blame. Others may choose to flee, find support through friends, and/or may deal with their feelings using substances.

Act when you encounter a patient who feels very guilty about parental fighting or who justifies abuse because he feels worthless or was told repeatedly he was a bad child. Help him realize he was not responsible for the conflict and that no one deserves abuse. Discuss other, more realistic possibilities for the family paradigm.

 

 

These are not easy conversations. Some pediatricians will feel comfortable working at this depth, others will prefer to refer.

Healing from PTSD related to family violence, sexual abuse, or criminal activity is a several-step process. As one's sense of guilt diminishes, other emotions such as anger at not being better protected or valued need to be addressed. Finally, there needs to be some grieving for what was lacking and some acceptance of what was possible. This is not a simple process; however, it is worthwhile because if their PTSD remains untreated, there is a greater likelihood they will continue to relive traumatic memories as adults.

There is some controversy as to whether talking through the traumatic event over and over truly helps. Some clinicians feel that a certain amount of supportive discussion in a calm way makes sense, especially early. But solely repeating the details of the event may re-traumatize the child and intensify negative feelings, especially if the memories are very vivid.

Cognitive and behavioral approaches can help the child reframe their trauma. An example is exposure therapy, where the child is carefully reexposed to the trauma in stages while they learn to reframe and diminish the intensity of the experience. Often, ideas about the trauma come out that can be examined objectively to try to lessen some of those traumatic feelings.

Exposure therapy also can incorporate gradual steps to help the child overcome their fear. If a person survived a plane crash, the first step might be to take him or her to the airport, then to board an airplane without taking off, and so forth. This approach reintroduces the trauma without eliciting a full response. You don't want the brain to go on “red alert” again. In a state of hyperarousal, reliving the trauma may do more harm than good.

The terrified moments that children experience during a traumatic sequence tend to get burned into their memories much more strongly than everyday events. A school-age child might remember nothing about an uneventful trip in the car, but if a traumatic accident happens, often she remembers almost every detail. She recalls descriptive elements of what happened as well as the emotional fright or anguish very vividly.

Sometimes vivid, traumatic memories will enter your patient's mind spontaneously without him knowing why. In other cases, there are triggers. Sometimes these flashbacks arise shortly following trauma and sometimes they take years.

Pediatricians can do their patients and families a service if they are aware of PTSD either after an overt event like a car accident or by considering trauma in an anxious or dysfunctional child.

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FDA warns of possible link between breast implants and ALCL

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FDA warns of possible link between breast implants and ALCL

The Food and Drug Administration (FDA), after a review of reported cases of anaplastic large-cell lymphoma (ALCL), warns that there may be a link between silicone and saline breast implants and the rare cancer.

People with breast implants “may have a very small but significant risk of ALCL in the scar capsule adjacent to the implant,” according to the agency.

The FDA based its announcement on a review of literature published between January 1997 and May 2010 that identified 34 unique cases of ALCL in women with either type of breast implant.

William Maisel, MD, chief scientist and deputy director for science in the FDA’s Center for Devices and Radiological Health, said, “We need more data and are asking that healthcare professionals tell us about any confirmed cases they identify.”

Of the 34 unique ALCL cases reviewed, 24 had silicone and 7 had saline implants; 3 implants did not have the type specified. The women ranged in age from 28 to 87 years, with a median age of 51 years.

ALCL occurred in 19 women who received implants for aesthetic augmentation, 11 for reconstruction, and 4 had no reason recorded for the implant.

The women developed ALCL in a median of 8 years from time of implant, ranging from 1 year to 23 years. Most of the patients were diagnosed because they had implant-related symptoms, such as seromas, capsular contractures, or peri-implant masses that needed implant revision surgery.

Physicians found lymphoma cells in the seroma surrounding the implant, in the fibrous capsule, or within a peri-implant mass in all of the ALCL cases.

According to the FDA report, CD30 status was positive in all 29 of the cases that included this information, which is consistent with an ALCL diagnosis. ALCL cases in the rest of the body can be either ALK-positive or ALK-negative. The 26 reports of ALCL in women with breast implants that included ALK status were all ALK-negative.

The FDA recommends that physicians consider an ALCL diagnosis if patients present with capsular contracture or masses adjacent to the breast implant. Physicians should report all confirmed cases of ALCL in people with breast implants to Medwatch.

The FDA does not recommend removing breast implants in patients without symptoms, which include pain, lumps, swelllng, or asymmetry that develop after the surgical site is fully healed. The agency plans to update its review of silicone breast implants in spring 2011.

ALCL occurs in about 1 in 500,000 women each year in the United States, according to the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In the breast, ALCL occurs in approximately 3 in 100,000,000 women annually in the US.

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The Food and Drug Administration (FDA), after a review of reported cases of anaplastic large-cell lymphoma (ALCL), warns that there may be a link between silicone and saline breast implants and the rare cancer.

People with breast implants “may have a very small but significant risk of ALCL in the scar capsule adjacent to the implant,” according to the agency.

The FDA based its announcement on a review of literature published between January 1997 and May 2010 that identified 34 unique cases of ALCL in women with either type of breast implant.

William Maisel, MD, chief scientist and deputy director for science in the FDA’s Center for Devices and Radiological Health, said, “We need more data and are asking that healthcare professionals tell us about any confirmed cases they identify.”

Of the 34 unique ALCL cases reviewed, 24 had silicone and 7 had saline implants; 3 implants did not have the type specified. The women ranged in age from 28 to 87 years, with a median age of 51 years.

ALCL occurred in 19 women who received implants for aesthetic augmentation, 11 for reconstruction, and 4 had no reason recorded for the implant.

The women developed ALCL in a median of 8 years from time of implant, ranging from 1 year to 23 years. Most of the patients were diagnosed because they had implant-related symptoms, such as seromas, capsular contractures, or peri-implant masses that needed implant revision surgery.

Physicians found lymphoma cells in the seroma surrounding the implant, in the fibrous capsule, or within a peri-implant mass in all of the ALCL cases.

According to the FDA report, CD30 status was positive in all 29 of the cases that included this information, which is consistent with an ALCL diagnosis. ALCL cases in the rest of the body can be either ALK-positive or ALK-negative. The 26 reports of ALCL in women with breast implants that included ALK status were all ALK-negative.

The FDA recommends that physicians consider an ALCL diagnosis if patients present with capsular contracture or masses adjacent to the breast implant. Physicians should report all confirmed cases of ALCL in people with breast implants to Medwatch.

The FDA does not recommend removing breast implants in patients without symptoms, which include pain, lumps, swelllng, or asymmetry that develop after the surgical site is fully healed. The agency plans to update its review of silicone breast implants in spring 2011.

ALCL occurs in about 1 in 500,000 women each year in the United States, according to the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In the breast, ALCL occurs in approximately 3 in 100,000,000 women annually in the US.

The Food and Drug Administration (FDA), after a review of reported cases of anaplastic large-cell lymphoma (ALCL), warns that there may be a link between silicone and saline breast implants and the rare cancer.

People with breast implants “may have a very small but significant risk of ALCL in the scar capsule adjacent to the implant,” according to the agency.

The FDA based its announcement on a review of literature published between January 1997 and May 2010 that identified 34 unique cases of ALCL in women with either type of breast implant.

William Maisel, MD, chief scientist and deputy director for science in the FDA’s Center for Devices and Radiological Health, said, “We need more data and are asking that healthcare professionals tell us about any confirmed cases they identify.”

Of the 34 unique ALCL cases reviewed, 24 had silicone and 7 had saline implants; 3 implants did not have the type specified. The women ranged in age from 28 to 87 years, with a median age of 51 years.

ALCL occurred in 19 women who received implants for aesthetic augmentation, 11 for reconstruction, and 4 had no reason recorded for the implant.

The women developed ALCL in a median of 8 years from time of implant, ranging from 1 year to 23 years. Most of the patients were diagnosed because they had implant-related symptoms, such as seromas, capsular contractures, or peri-implant masses that needed implant revision surgery.

Physicians found lymphoma cells in the seroma surrounding the implant, in the fibrous capsule, or within a peri-implant mass in all of the ALCL cases.

According to the FDA report, CD30 status was positive in all 29 of the cases that included this information, which is consistent with an ALCL diagnosis. ALCL cases in the rest of the body can be either ALK-positive or ALK-negative. The 26 reports of ALCL in women with breast implants that included ALK status were all ALK-negative.

The FDA recommends that physicians consider an ALCL diagnosis if patients present with capsular contracture or masses adjacent to the breast implant. Physicians should report all confirmed cases of ALCL in people with breast implants to Medwatch.

The FDA does not recommend removing breast implants in patients without symptoms, which include pain, lumps, swelllng, or asymmetry that develop after the surgical site is fully healed. The agency plans to update its review of silicone breast implants in spring 2011.

ALCL occurs in about 1 in 500,000 women each year in the United States, according to the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute. In the breast, ALCL occurs in approximately 3 in 100,000,000 women annually in the US.

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When Opportunity Knocks

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News that domestic spending on healthcare grew at the lowest rate in recorded history could be viewed as trouble for HM leaders negotiating new contracts—or it could be the chance for a new generation of hospitalists to prove their worth.

"This is an opportunity for people who can do good clinical integration. … You can have gainsharing and actually still make physicians win financially but still deliver the right care for patients," says Steven Deitelzweig, MD, MMM, SFHM, chair of SHM's Practice Management Committee and chair of hospital medicine for Ochsner Health System in New Orleans.

According to the report "Recession Contributes To Slowest Annual Rate Of Increase In Health Spending In Five Decades" (doi:10.1377/hlthaff.2010.1032), healthcare spending in 2009 grew just 4%, to $2.5 trillion, the lowest growth rate since the federal government began tracking the data 50 years ago.

The impact of a record slowing in healthcare spending is particularly germane to HM group negotiators, considering they find themselves in talks at a unique time, according to an article in this month’s issue of The Hospitalist. Industry participants say that between stimulus money for quality reforms, the worst economic downturn since the Great Depression, and healthcare reform, hospitals have to do the proverbial more with less.

Dr. Deitelzweig urges hospitalists to promote their quality initiatives and take charge of processes that can save their institutions money. A hospital administration that saves money by eliminating unnecessary procedures and smoothing transitions of care, for example, can argue it deserves a piece of those savings, he says.

"The pie will be shrinking," he adds. "But that doesn't mean you can't figure a way to provide the right care in a less expensive way."

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News that domestic spending on healthcare grew at the lowest rate in recorded history could be viewed as trouble for HM leaders negotiating new contracts—or it could be the chance for a new generation of hospitalists to prove their worth.

"This is an opportunity for people who can do good clinical integration. … You can have gainsharing and actually still make physicians win financially but still deliver the right care for patients," says Steven Deitelzweig, MD, MMM, SFHM, chair of SHM's Practice Management Committee and chair of hospital medicine for Ochsner Health System in New Orleans.

According to the report "Recession Contributes To Slowest Annual Rate Of Increase In Health Spending In Five Decades" (doi:10.1377/hlthaff.2010.1032), healthcare spending in 2009 grew just 4%, to $2.5 trillion, the lowest growth rate since the federal government began tracking the data 50 years ago.

The impact of a record slowing in healthcare spending is particularly germane to HM group negotiators, considering they find themselves in talks at a unique time, according to an article in this month’s issue of The Hospitalist. Industry participants say that between stimulus money for quality reforms, the worst economic downturn since the Great Depression, and healthcare reform, hospitals have to do the proverbial more with less.

Dr. Deitelzweig urges hospitalists to promote their quality initiatives and take charge of processes that can save their institutions money. A hospital administration that saves money by eliminating unnecessary procedures and smoothing transitions of care, for example, can argue it deserves a piece of those savings, he says.

"The pie will be shrinking," he adds. "But that doesn't mean you can't figure a way to provide the right care in a less expensive way."

News that domestic spending on healthcare grew at the lowest rate in recorded history could be viewed as trouble for HM leaders negotiating new contracts—or it could be the chance for a new generation of hospitalists to prove their worth.

"This is an opportunity for people who can do good clinical integration. … You can have gainsharing and actually still make physicians win financially but still deliver the right care for patients," says Steven Deitelzweig, MD, MMM, SFHM, chair of SHM's Practice Management Committee and chair of hospital medicine for Ochsner Health System in New Orleans.

According to the report "Recession Contributes To Slowest Annual Rate Of Increase In Health Spending In Five Decades" (doi:10.1377/hlthaff.2010.1032), healthcare spending in 2009 grew just 4%, to $2.5 trillion, the lowest growth rate since the federal government began tracking the data 50 years ago.

The impact of a record slowing in healthcare spending is particularly germane to HM group negotiators, considering they find themselves in talks at a unique time, according to an article in this month’s issue of The Hospitalist. Industry participants say that between stimulus money for quality reforms, the worst economic downturn since the Great Depression, and healthcare reform, hospitals have to do the proverbial more with less.

Dr. Deitelzweig urges hospitalists to promote their quality initiatives and take charge of processes that can save their institutions money. A hospital administration that saves money by eliminating unnecessary procedures and smoothing transitions of care, for example, can argue it deserves a piece of those savings, he says.

"The pie will be shrinking," he adds. "But that doesn't mean you can't figure a way to provide the right care in a less expensive way."

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A Perfect Fit

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Sally Bullock, MD, medical director of the hospitalist program at Middle Tennessee Medical Center (MTMC) in Murfreesboro, Tenn., received the hospital’s 2011 Physician of the Year award at its annual Physician Christmas Reception in December. The award is voted on by hospital staff, and this is the first time it was given to a hospitalist.

“I’ve been here on staff for 26 years, mostly in private practice as an internist,” Dr. Bullock says. “Visiting the hospital was always a favorite part of my practice. In fact, I did not use hospitalists to care for my patients.”

However, family demands and time pressures of the practice led her to leave it for the flexibility of multiple part-time medical jobs, including HM shifts. In November of 2007, after repeated requests from Andy Brown, MD, MTMC's vice president of medical affairs, she accepted the hospitalist leadership position.

"I encouraged Dr. Bullock to take on this role because she genuinely cares about her patients. Sally is an excellent clinician and communicator who also leads by example," Dr. Brown says. "I knew that physicians would recognize these qualities and want to be part of the program."

The hospitalist program at MTMC started in 1999 with six physicians but experienced contraction in 2006. Under Dr. Bullock's leadership, it has grown to 22 physicians, with more expansion expected this year.

"I just jumped on it, and we got busy recruiting," Dr. Bullock says, adding that the award from her peers at MTMC reflects both her longevity in the medical community and appreciation for "taking the hospitalist program where it needs to be."

Currently, her position includes hospitalist shifts, both scheduled and fill-in, squeezing in administrative duties, and mentoring other physicians. "I'm sort of the program's surge protector," she says.

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Sally Bullock, MD, medical director of the hospitalist program at Middle Tennessee Medical Center (MTMC) in Murfreesboro, Tenn., received the hospital’s 2011 Physician of the Year award at its annual Physician Christmas Reception in December. The award is voted on by hospital staff, and this is the first time it was given to a hospitalist.

“I’ve been here on staff for 26 years, mostly in private practice as an internist,” Dr. Bullock says. “Visiting the hospital was always a favorite part of my practice. In fact, I did not use hospitalists to care for my patients.”

However, family demands and time pressures of the practice led her to leave it for the flexibility of multiple part-time medical jobs, including HM shifts. In November of 2007, after repeated requests from Andy Brown, MD, MTMC's vice president of medical affairs, she accepted the hospitalist leadership position.

"I encouraged Dr. Bullock to take on this role because she genuinely cares about her patients. Sally is an excellent clinician and communicator who also leads by example," Dr. Brown says. "I knew that physicians would recognize these qualities and want to be part of the program."

The hospitalist program at MTMC started in 1999 with six physicians but experienced contraction in 2006. Under Dr. Bullock's leadership, it has grown to 22 physicians, with more expansion expected this year.

"I just jumped on it, and we got busy recruiting," Dr. Bullock says, adding that the award from her peers at MTMC reflects both her longevity in the medical community and appreciation for "taking the hospitalist program where it needs to be."

Currently, her position includes hospitalist shifts, both scheduled and fill-in, squeezing in administrative duties, and mentoring other physicians. "I'm sort of the program's surge protector," she says.

Sally Bullock, MD, medical director of the hospitalist program at Middle Tennessee Medical Center (MTMC) in Murfreesboro, Tenn., received the hospital’s 2011 Physician of the Year award at its annual Physician Christmas Reception in December. The award is voted on by hospital staff, and this is the first time it was given to a hospitalist.

“I’ve been here on staff for 26 years, mostly in private practice as an internist,” Dr. Bullock says. “Visiting the hospital was always a favorite part of my practice. In fact, I did not use hospitalists to care for my patients.”

However, family demands and time pressures of the practice led her to leave it for the flexibility of multiple part-time medical jobs, including HM shifts. In November of 2007, after repeated requests from Andy Brown, MD, MTMC's vice president of medical affairs, she accepted the hospitalist leadership position.

"I encouraged Dr. Bullock to take on this role because she genuinely cares about her patients. Sally is an excellent clinician and communicator who also leads by example," Dr. Brown says. "I knew that physicians would recognize these qualities and want to be part of the program."

The hospitalist program at MTMC started in 1999 with six physicians but experienced contraction in 2006. Under Dr. Bullock's leadership, it has grown to 22 physicians, with more expansion expected this year.

"I just jumped on it, and we got busy recruiting," Dr. Bullock says, adding that the award from her peers at MTMC reflects both her longevity in the medical community and appreciation for "taking the hospitalist program where it needs to be."

Currently, her position includes hospitalist shifts, both scheduled and fill-in, squeezing in administrative duties, and mentoring other physicians. "I'm sort of the program's surge protector," she says.

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Why I like ham

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Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary

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Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary

Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary Why I like ham, by Gary

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A New Year’s Resolution to Crack Down on Opioids?

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Sometime early this year, after two years of controversy, the FDA might finally release its revised proposal for more stringent regulations on opioid pain relievers. The following are the key questions—and answers—surrounding new regulations, as well as a look at other recent FDA actions, including increased scrutiny of diabetes and obesity drugs due to heart concerns.

Question: What’s the latest on the FDA release of new regulations for prescription opioids?

Answer: First, the back story: The controversy concerns the creation of a Risk Evaluation and Mitigation Strategy (REMS) for opioid analgesics amid a troubling boom in prescription drug abuse, addiction, and overdose, and an accompanying spike in deaths from opioid overdoses. Under a 2007 law, the FDA can require drug and medical device manufacturers to adopt a REMS to ensure that the benefits outweigh the risks of continued use and that patients are adequately informed. In this case, the strategy could impact how nearly 4 million patients receive long-acting and extended-release opioids annually, according to FDA statistics.

In February 2009, the FDA sent a letter to manufacturers of opioid pain relievers, proposing a classwide REMS that would require certification by a physician or pharmacist and restrict distribution of the drugs, among other provisions. In response, many healthcare providers and medical organizations warned of an increased regulatory burden that would negatively impact patients. Among the concerns: fewer primary-care physicians (PCPs) willing to manage patients with chronic pain, reduced access to medically necessary drugs in underserved communities, undermedicated cancer patients, and increased use of other drugs with less stringent oversight.

In response, the FDA dropped its proposal for a prescriber accreditation program and another for a patient registry. But an FDA advisory panel soundly rejected a revised REMS proposal in July, by a vote of 25-10. The panel criticized the new plans as being too lax, lacking a formal requirement f

or physician training or verification of that training, and failing to address immediate-release opioid formulations. The FDA is now drafting newly revised REMS plans, with an anticipated release date of early this year.

Q: What will the new REMS likely include?

A: Based on the criticisms of FDA panelists in July, the revised REMS could mandate a training requirement for all prescribers. The program would likely be created by the FDA and not by the drug industry, as had first been proposed (many doctors have agreed that a centralized, standardized program would be far preferable to dealing with programs set up independently by drug manufacturers). The strategy also might govern immediate-release opioids, in addition to extended-release and long-acting formulations. The FDA could propose linking doctor education to an existing Drug Enforcement Administration registration, but that would require congressional approval.

Q: What was the outcome of safety deliberations over the diabetes drug rosiglitazone (Avandia)?

A: After several years of concern over a heightened risk of heart attacks and other heart problems among patients taking rosiglitazone for type 2 diabetes mellitus, the FDA sharply restricted its availability in September and required the manufacturer, GlaxoSmithKline, to submit a REMS. When implemented, the REMS will limit new prescriptions to patients who cannot achieve glycemic control with other medications and decide not to take the alternative (pioglitazone) for medical reasons.1 Other diabetes drugs have faced similar scrutiny: In October, the FDA rejected an extended-release form of the diabetes drug exenatide (Bydureon) due to safety concerns, citing the need for more studies from manufacturer Eli Lilly about its effect on heart rate.

Q: What’s the upshot of recent FDA actions on weight-loss drugs and supplements?

A: The FDA also cracked down on weight-loss formulations in 2010, declining to approve several new drugs, overseeing the withdrawal of Abbott Laboratory’s Meridia in October, and announcing a December recall of capsules marketed online as Fruta Planta. Safety concerns over the latter two were linked to sibutramine, a drug that is “known to increase blood pressure and/or pulse rate in some patients and may present a serious risk for patients with a history of coronary artery disease, congestive heart failure, arrhythmias or stroke,” according to the FDA. Additionally, the drug can interact “in life-threatening ways” with other medications, reinforcing the idea that hospitalists and other doctors should delve into patients’ recent history of weight-loss drug or supplement use.

 

 

The FDA gave 21 drugs the go-ahead in 2010, down from 25 cleared in 2009 and 24 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients.

Q: What should we expect from the FDA in the next year?

A: Analysts will be keeping an eye on the number of new drugs approved in 2011 to discern any new trends. As reported by The Wall Street Journal and other publications, the FDA gave 21 drugs the go-ahead in 2010, down from 26 cleared in 2009 and 25 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients. Of course, the lower number also could reflect a continued dry spell in the pipelines of many pharmaceutical companies. On the flipside, consumer watchdogs have expressed optimism that the FDA might be devoting more attention to safety. In November, for example, the FDA oversaw the pulling of popular painkiller propoxyphene (marketed as Darvon and Darvocet) after evidence accumulated that the medication can cause potentially fatal heart damage and rhythm abnormalities.

Bryn Nelson is a freelance medical writer based in Seattle.

References

1. Woodcock J, Sharfstein JM, Hamburg M. Regulatory action on rosiglitazone by the U.S. Food and Drug Administration. N Engl J Med. 2010;363(16):1489-1491.

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Sometime early this year, after two years of controversy, the FDA might finally release its revised proposal for more stringent regulations on opioid pain relievers. The following are the key questions—and answers—surrounding new regulations, as well as a look at other recent FDA actions, including increased scrutiny of diabetes and obesity drugs due to heart concerns.

Question: What’s the latest on the FDA release of new regulations for prescription opioids?

Answer: First, the back story: The controversy concerns the creation of a Risk Evaluation and Mitigation Strategy (REMS) for opioid analgesics amid a troubling boom in prescription drug abuse, addiction, and overdose, and an accompanying spike in deaths from opioid overdoses. Under a 2007 law, the FDA can require drug and medical device manufacturers to adopt a REMS to ensure that the benefits outweigh the risks of continued use and that patients are adequately informed. In this case, the strategy could impact how nearly 4 million patients receive long-acting and extended-release opioids annually, according to FDA statistics.

In February 2009, the FDA sent a letter to manufacturers of opioid pain relievers, proposing a classwide REMS that would require certification by a physician or pharmacist and restrict distribution of the drugs, among other provisions. In response, many healthcare providers and medical organizations warned of an increased regulatory burden that would negatively impact patients. Among the concerns: fewer primary-care physicians (PCPs) willing to manage patients with chronic pain, reduced access to medically necessary drugs in underserved communities, undermedicated cancer patients, and increased use of other drugs with less stringent oversight.

In response, the FDA dropped its proposal for a prescriber accreditation program and another for a patient registry. But an FDA advisory panel soundly rejected a revised REMS proposal in July, by a vote of 25-10. The panel criticized the new plans as being too lax, lacking a formal requirement f

or physician training or verification of that training, and failing to address immediate-release opioid formulations. The FDA is now drafting newly revised REMS plans, with an anticipated release date of early this year.

Q: What will the new REMS likely include?

A: Based on the criticisms of FDA panelists in July, the revised REMS could mandate a training requirement for all prescribers. The program would likely be created by the FDA and not by the drug industry, as had first been proposed (many doctors have agreed that a centralized, standardized program would be far preferable to dealing with programs set up independently by drug manufacturers). The strategy also might govern immediate-release opioids, in addition to extended-release and long-acting formulations. The FDA could propose linking doctor education to an existing Drug Enforcement Administration registration, but that would require congressional approval.

Q: What was the outcome of safety deliberations over the diabetes drug rosiglitazone (Avandia)?

A: After several years of concern over a heightened risk of heart attacks and other heart problems among patients taking rosiglitazone for type 2 diabetes mellitus, the FDA sharply restricted its availability in September and required the manufacturer, GlaxoSmithKline, to submit a REMS. When implemented, the REMS will limit new prescriptions to patients who cannot achieve glycemic control with other medications and decide not to take the alternative (pioglitazone) for medical reasons.1 Other diabetes drugs have faced similar scrutiny: In October, the FDA rejected an extended-release form of the diabetes drug exenatide (Bydureon) due to safety concerns, citing the need for more studies from manufacturer Eli Lilly about its effect on heart rate.

Q: What’s the upshot of recent FDA actions on weight-loss drugs and supplements?

A: The FDA also cracked down on weight-loss formulations in 2010, declining to approve several new drugs, overseeing the withdrawal of Abbott Laboratory’s Meridia in October, and announcing a December recall of capsules marketed online as Fruta Planta. Safety concerns over the latter two were linked to sibutramine, a drug that is “known to increase blood pressure and/or pulse rate in some patients and may present a serious risk for patients with a history of coronary artery disease, congestive heart failure, arrhythmias or stroke,” according to the FDA. Additionally, the drug can interact “in life-threatening ways” with other medications, reinforcing the idea that hospitalists and other doctors should delve into patients’ recent history of weight-loss drug or supplement use.

 

 

The FDA gave 21 drugs the go-ahead in 2010, down from 25 cleared in 2009 and 24 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients.

Q: What should we expect from the FDA in the next year?

A: Analysts will be keeping an eye on the number of new drugs approved in 2011 to discern any new trends. As reported by The Wall Street Journal and other publications, the FDA gave 21 drugs the go-ahead in 2010, down from 26 cleared in 2009 and 25 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients. Of course, the lower number also could reflect a continued dry spell in the pipelines of many pharmaceutical companies. On the flipside, consumer watchdogs have expressed optimism that the FDA might be devoting more attention to safety. In November, for example, the FDA oversaw the pulling of popular painkiller propoxyphene (marketed as Darvon and Darvocet) after evidence accumulated that the medication can cause potentially fatal heart damage and rhythm abnormalities.

Bryn Nelson is a freelance medical writer based in Seattle.

References

1. Woodcock J, Sharfstein JM, Hamburg M. Regulatory action on rosiglitazone by the U.S. Food and Drug Administration. N Engl J Med. 2010;363(16):1489-1491.

Sometime early this year, after two years of controversy, the FDA might finally release its revised proposal for more stringent regulations on opioid pain relievers. The following are the key questions—and answers—surrounding new regulations, as well as a look at other recent FDA actions, including increased scrutiny of diabetes and obesity drugs due to heart concerns.

Question: What’s the latest on the FDA release of new regulations for prescription opioids?

Answer: First, the back story: The controversy concerns the creation of a Risk Evaluation and Mitigation Strategy (REMS) for opioid analgesics amid a troubling boom in prescription drug abuse, addiction, and overdose, and an accompanying spike in deaths from opioid overdoses. Under a 2007 law, the FDA can require drug and medical device manufacturers to adopt a REMS to ensure that the benefits outweigh the risks of continued use and that patients are adequately informed. In this case, the strategy could impact how nearly 4 million patients receive long-acting and extended-release opioids annually, according to FDA statistics.

In February 2009, the FDA sent a letter to manufacturers of opioid pain relievers, proposing a classwide REMS that would require certification by a physician or pharmacist and restrict distribution of the drugs, among other provisions. In response, many healthcare providers and medical organizations warned of an increased regulatory burden that would negatively impact patients. Among the concerns: fewer primary-care physicians (PCPs) willing to manage patients with chronic pain, reduced access to medically necessary drugs in underserved communities, undermedicated cancer patients, and increased use of other drugs with less stringent oversight.

In response, the FDA dropped its proposal for a prescriber accreditation program and another for a patient registry. But an FDA advisory panel soundly rejected a revised REMS proposal in July, by a vote of 25-10. The panel criticized the new plans as being too lax, lacking a formal requirement f

or physician training or verification of that training, and failing to address immediate-release opioid formulations. The FDA is now drafting newly revised REMS plans, with an anticipated release date of early this year.

Q: What will the new REMS likely include?

A: Based on the criticisms of FDA panelists in July, the revised REMS could mandate a training requirement for all prescribers. The program would likely be created by the FDA and not by the drug industry, as had first been proposed (many doctors have agreed that a centralized, standardized program would be far preferable to dealing with programs set up independently by drug manufacturers). The strategy also might govern immediate-release opioids, in addition to extended-release and long-acting formulations. The FDA could propose linking doctor education to an existing Drug Enforcement Administration registration, but that would require congressional approval.

Q: What was the outcome of safety deliberations over the diabetes drug rosiglitazone (Avandia)?

A: After several years of concern over a heightened risk of heart attacks and other heart problems among patients taking rosiglitazone for type 2 diabetes mellitus, the FDA sharply restricted its availability in September and required the manufacturer, GlaxoSmithKline, to submit a REMS. When implemented, the REMS will limit new prescriptions to patients who cannot achieve glycemic control with other medications and decide not to take the alternative (pioglitazone) for medical reasons.1 Other diabetes drugs have faced similar scrutiny: In October, the FDA rejected an extended-release form of the diabetes drug exenatide (Bydureon) due to safety concerns, citing the need for more studies from manufacturer Eli Lilly about its effect on heart rate.

Q: What’s the upshot of recent FDA actions on weight-loss drugs and supplements?

A: The FDA also cracked down on weight-loss formulations in 2010, declining to approve several new drugs, overseeing the withdrawal of Abbott Laboratory’s Meridia in October, and announcing a December recall of capsules marketed online as Fruta Planta. Safety concerns over the latter two were linked to sibutramine, a drug that is “known to increase blood pressure and/or pulse rate in some patients and may present a serious risk for patients with a history of coronary artery disease, congestive heart failure, arrhythmias or stroke,” according to the FDA. Additionally, the drug can interact “in life-threatening ways” with other medications, reinforcing the idea that hospitalists and other doctors should delve into patients’ recent history of weight-loss drug or supplement use.

 

 

The FDA gave 21 drugs the go-ahead in 2010, down from 25 cleared in 2009 and 24 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients.

Q: What should we expect from the FDA in the next year?

A: Analysts will be keeping an eye on the number of new drugs approved in 2011 to discern any new trends. As reported by The Wall Street Journal and other publications, the FDA gave 21 drugs the go-ahead in 2010, down from 26 cleared in 2009 and 25 approved in 2008. The dip has concerned some drug industry representatives, who warn that an overly cautious approach could lead to more delays in new drugs reaching patients. Of course, the lower number also could reflect a continued dry spell in the pipelines of many pharmaceutical companies. On the flipside, consumer watchdogs have expressed optimism that the FDA might be devoting more attention to safety. In November, for example, the FDA oversaw the pulling of popular painkiller propoxyphene (marketed as Darvon and Darvocet) after evidence accumulated that the medication can cause potentially fatal heart damage and rhythm abnormalities.

Bryn Nelson is a freelance medical writer based in Seattle.

References

1. Woodcock J, Sharfstein JM, Hamburg M. Regulatory action on rosiglitazone by the U.S. Food and Drug Administration. N Engl J Med. 2010;363(16):1489-1491.

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Hospitalist Mentoring Lacking, Survey Shows

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Academic HM group leaders are concerned about the lack of mentorship their physicians receive and often feel viewed as a clinical service, not a pedagogical program, according to a report in this month's Journal of Hospital Medicine.

The cross-sectional e-mail survey of 57 leaders found that respondents agree a lack of mentorship is a worry for both clinician-educator faculty (75%) and research faculty (58%). Six in 10 of those surveyed say their departments of medicine view them through more of a clinical lens, with that number rising to nearly 8 in 10 when the perceived views of other departments are taken into account.

"The division chiefs, the section chiefs have to pay attention to mentoring; they have to pay attention to faculty development, they have to really understand the needs of their people," says study coauthor Rebecca Harrison, MD, FACP, a hospitalist at Oregon Health & Science University in Portland, Ore.

The report is based on a 2007 survey. Dr. Harrison says that as budgets became "more dire" during the economic downturn, academic HM leaders likely grew more frustrated by a perceived lack of resources committed to them.

She suggests that academic leaders look more to the negotiating tactics of their private-physician counterparts, who seek to leverage their involvement in quality programs and their return on investment when pushing for more support, respect, or resources.

Dr. Harrison adds that given that recruitment costs can range up to $400,000 for clinician-educator faculty, hospital executives "need to see the big picture. Hospital medicine is here to say. It's to their advantage; it behooves them not to avoid investing in sustainability."

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Academic HM group leaders are concerned about the lack of mentorship their physicians receive and often feel viewed as a clinical service, not a pedagogical program, according to a report in this month's Journal of Hospital Medicine.

The cross-sectional e-mail survey of 57 leaders found that respondents agree a lack of mentorship is a worry for both clinician-educator faculty (75%) and research faculty (58%). Six in 10 of those surveyed say their departments of medicine view them through more of a clinical lens, with that number rising to nearly 8 in 10 when the perceived views of other departments are taken into account.

"The division chiefs, the section chiefs have to pay attention to mentoring; they have to pay attention to faculty development, they have to really understand the needs of their people," says study coauthor Rebecca Harrison, MD, FACP, a hospitalist at Oregon Health & Science University in Portland, Ore.

The report is based on a 2007 survey. Dr. Harrison says that as budgets became "more dire" during the economic downturn, academic HM leaders likely grew more frustrated by a perceived lack of resources committed to them.

She suggests that academic leaders look more to the negotiating tactics of their private-physician counterparts, who seek to leverage their involvement in quality programs and their return on investment when pushing for more support, respect, or resources.

Dr. Harrison adds that given that recruitment costs can range up to $400,000 for clinician-educator faculty, hospital executives "need to see the big picture. Hospital medicine is here to say. It's to their advantage; it behooves them not to avoid investing in sustainability."

Academic HM group leaders are concerned about the lack of mentorship their physicians receive and often feel viewed as a clinical service, not a pedagogical program, according to a report in this month's Journal of Hospital Medicine.

The cross-sectional e-mail survey of 57 leaders found that respondents agree a lack of mentorship is a worry for both clinician-educator faculty (75%) and research faculty (58%). Six in 10 of those surveyed say their departments of medicine view them through more of a clinical lens, with that number rising to nearly 8 in 10 when the perceived views of other departments are taken into account.

"The division chiefs, the section chiefs have to pay attention to mentoring; they have to pay attention to faculty development, they have to really understand the needs of their people," says study coauthor Rebecca Harrison, MD, FACP, a hospitalist at Oregon Health & Science University in Portland, Ore.

The report is based on a 2007 survey. Dr. Harrison says that as budgets became "more dire" during the economic downturn, academic HM leaders likely grew more frustrated by a perceived lack of resources committed to them.

She suggests that academic leaders look more to the negotiating tactics of their private-physician counterparts, who seek to leverage their involvement in quality programs and their return on investment when pushing for more support, respect, or resources.

Dr. Harrison adds that given that recruitment costs can range up to $400,000 for clinician-educator faculty, hospital executives "need to see the big picture. Hospital medicine is here to say. It's to their advantage; it behooves them not to avoid investing in sustainability."

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