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Drugs help pass more ureteral stones
Prescribe tamsulosin (typically 0.4 mg daily) or nifedipine (typically 30 mg daily) for patients with lower ureteral calculi, to speed stone passage and to avoid surgical intervention
Strength of recommendation
A: Meta-analysis of randomized controlled trials
Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007; 50:552-563.1
ILLUSTRATIVE CASE
A 52-year-old man presents to your office for follow-up 2 days after he was seen in the ED and diagnosed with a distal ureteral calculus, his first. His pain is reasonably well controlled, but he has not yet passed the stone. Is there anything you can do to help him pass the stone?
Yes. Patients who are candidates for observation should be offered a trial of “medical expulsive therapy” using an α-antagonist or a calcium channel blocker. Until now, medical therapy for kidney stones consisted of pain relief only.
The ordeal of a first stone is all too common—the lifetime prevalence of kidney stones is 5.2%—and the probability of recurrence is about 50%.2,3
NHANES data show increasing prevalence between the periods 1976-1980 and 1988-1996.3 One fifth to one third of kidney stones require surgical intervention.4 In a cohort of 245 patients presenting to an ED in Canada, 50 (20%) required further procedures, including lithotripsy. Stones ≥ 6 mm in size were much less likely to pass (OR=10.7, 95% CI 4.6-24.8).5 The burden on the healthcare system is significant; there are approximately 2 million out-patient visits annually for this problem, and diagnosis and treatment costs about $2 billion annually.6
Watch and wait
The standard approach is a period of watchful waiting and pain control, with urgent urological referral for patients with evidence of upper urinary tract infection, high grade obstruction, inadequate pain or nausea control, or insufficient renal reserve.2,4 Most patients treated with watchful waiting pass their stone within 4 weeks. Any stones that don’t pass within 8 weeks are unlikely to pass spontaneously.2,7
Medical therapy has been proposed for decades
Medications that relax ureteral smooth muscle to help pass ureteral stones have been proposed for decades.8 Prior to 2000, however, only 1 randomized controlled trial (RCT) of medical therapy for ureteral stones had been published.9 A subsequent meta-analysis found 9 studies and showed that medical therapy did increase the chances that a stone would pass.10 The Singh meta-analysis found 13 subsequently published studies and nearly tripled the number of patients evaluated.
STUDY SUMMARY: A well-done meta-analysis
This meta-analysis is based on 16 studies of α-antagonists (most used tamsulosin) and 9 studies of nifedipine, a calcium channel blocker.1 The studies were identified by a comprehensive search strategy that included Medline, EMBASE, and the Cochrane Controlled Trials Register from January 1980 to January 2007. The authors included all randomized trials or controlled clinical trials of medical therapy for adults with acute ureteral colic.
The authors assessed the studies for quality using the Jadad scale, a validated scale of study quality. Higher scores represent better quality, including better documentation of randomization, blinding, and follow-up. The authors specified their planned sensitivity analyses, and used the random effects model to synthesize the results, which tends to provide a more conservative estimate of the effect.
In other words, this was a very well done meta-analysis.
Twenty-two studies met the inclusion criteria: 13 of α-antagonists, 6 of nifedipine, and 3 of both. In 13 of the 16 studies of α-antagonists, tamsulosin (Flomax) was the study drug. The results from the terazosin (Hytrin) and doxazosin (Cardura) studies were included with the tamsulosin studies. The Jadad quality scores of the 22 studies were fairly low, with a median of 2 (range of 0 to 3) on the 5-point scale. The most common deduction was because the study was not double-blinded.
Medical therapy makes sense
“Therapy using either α-antagonists or calcium channel blockers augments the stone expulsion rate compared to standard therapy for moderately sized distal ureteral stones.” 1 CT showing distal ureteral stone
α-Antagonist studies
These 16 studies enrolled 1235 patients with distal ureteral stones. Mean stone size ranged from 4.3 to 7.8 mm. α-Antagonists improved the stone expulsion rate (RR= 1.59, 95% CI 1.44-1.75; NNT=3.3).
The mean time to expulsion of the stone ranged from 2.7 to 14.2 days and duration of therapy ranged from 1 to 7 weeks. In the 9 trials that reported the time to stone expulsion, the stone came out between 2 and 6 days earlier than the control groups.
Adverse effects were reported in 4% of patients receiving the active medication; most were mild.
Nifedipine studies
There were 686 patients in the 9 trials of nifedipine. The mean stone size was 3.9 to 12.8 mm. Some studies included stones in the more proximal as well as the distal ureter.
Nifedipine treatment increased the rate of stone expulsion (RR=1.5, 95% CI 1.34-1.68; NNT=3.9). Time to stone expulsion was shorter in 7 of the 9 studies.
Adverse effects were reported in 15% of the patients. Most of these were mild— nausea, vomiting, asthenia, and dyspepsia.
WHAT’S NEW: Strong evidence for use of medical therapy
The new findings from the Singh meta-analysis reviewed in this PURL supports physicians who have already adopted this practice and should encourage usage by those who have not yet done so.
Inpatients in academic medical centers
There is a growing trend to use tamsulosin to facilitate passage of ureteral stones. The University Health System Consortium (www.uhc.org) has complete clinical data on inpatients with ureteral stones, from 64 academic medical centers and teaching hospitals, between 2003 and 2007. We used this database to analyze trends in the use of tamsulosin in 4300 inpatients with ureteral stones (ICD 9 code 5921).
In 2003, only 3.3% of patients with a discharge diagnosis of ureteral stone received tamsulosin. In 2007, 34.1% of patients with ureteral stones discharged from these hospitals received tamsulosin, with similar rates of use when stratified by the specialty of the attending physician at discharge (family medicine, emergency medicine, internal medicine, urology) (FIGURE 1). We noted a wide range in the rate of adoption of this practice among academic medical centers: 48% in the centers with the highest rate of usage and 4.4% in the centers with the lowest rate.
FIGURE 1
% of inpatients in academic medical centers who received tamsulosin for ureteral stones, by year
Source: Unpublished data from the University Health System Consortium
Outpatients from a sample of US practices
The use of tamsulosin or nifedipine in outpatient practice was infrequent even 2 or 3 years ago. We used the National Ambulatory Medical Care Survey data (www.cdc.gov/nchs/about/major/ahcd/ahcd1.htm) from 2004 and 2005 (the most recent available), which provides a sample of all US outpatient practices. Only 7% of an estimated 1,345,000 patients diagnosed with ureteral stones were prescribed either tamsulosin or nifedipine, and urologists cared for most of those.
These unpublished data show that physicians in academic medical centers are increasingly adopting the practice of using tamsulosin or nifedipine for expulsion of ureteral stones, that urologists appear to be the first to begin using these medications in outpatients several years ago, and that this practice is being adopted actively in selected academic medical centers.
CAVEATS: Is either drug better? Too little data to tell
Our conclusion is that the strengths of this meta-analysis outweigh the weaknesses, the findings across studies are consistent, and the use of smooth-muscle relaxants for this indication makes sense from a mechanistic point of view.
The quality of a meta-analysis is only as good as the quality of the included studies, and, in this case, the overall quality of studies was not uniformly high. Median Jadad score, a summary measure of study quality, was 2, and the highest score was 3 (of a maximum of 5). The most common problem was lack of blinding, which can be critical in studies with subjective outcomes such as pain. We doubt that the lack of blinding led to any significant misclassification of outcome in this study, however.
Patients either passed the stone or they didn’t, or had a surgical intervention or not. It is reassuring that, when the best quality studies (Jadad score= 3) were analyzed separately, the results were equally good.
There have not been sufficient head-to-head trials to know if one is better than the other. We prefer α-antagonists because of the lower apparent side-effect profile. Our analysis of the UHC data shows that most of the physicians who are using medical therapy are using tamsulosin primarily for this diagnosis.
The majority of the patients in the studies included in the meta-analysis had been referred to a urologist. This raises the possibility that this treatment may not be as effective in patients with less severe symptoms for whom urological consultation is not necessary.
CHALLENGES TO IMPLEMENTATION: This change should be easy to put into practice
Tamsulosin is the best studied of the drugs, but also the most expensive. Based on the estimated number need to treat (NNT) of between 3 and 4 to prevent a surgical intervention and an estimated cost of around $90 for 1 month (www. drugstore.com, February 16, 2008), tamsulosin seems like a good investment to avoid surgical intervention.
The evidence for the other α-antagonists is consistent with that of tamsulosin, but there are fewer data, so it is not clear that the other agents will work as well.
Many people with renal colic are diagnosed and treated in the emergency department; they may not see their family physician until some time after the stone is diagnosed. It is unclear what effect this delay might have on medication effectiveness.
Neither tamsulosin nor nifedipine have an FDA indication for ureterolithiasis. However, they are prescribed commonly, and most physicians are familiar with their use and adverse-effect profiles.
Drugs used in the meta-analysis studies
α-Antagonists
Tamsulosin (Flomax)
Terazosin (Hytrin)
Doxazosin (Cardura)
Calcium channel blockers
Nifedipine (Adalat, Nifedical, Procardia)
Acknowledgement
We acknowledge Sofia Medvedev, PhD of the University HealthSystem Consortium (UHC) in Oak Brook, IL for analysis of the UHC Clinical Database and the National Ambulatory Medical Care Survey data.
PURLs methodology
This study was selected and evaluated using FPIN’s Priority Updates from the Research Literature (PURL) Surveillance System methodology. The criteria and findings leading to the selection of this study as a PURL can be accessed at www.jfponline.com/purls.
1. Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007;50:552-563.
2. Teichman JM. Clinical practice. Acute renal colic from ureteral calculus. N Engl J Med. 2004;350:684-693.
3. Stamatelou KK, Francis ME, Jones CA, Nyberg LM. Curhan GC. Time trends in reported prevalence of kidney stones in the United States: 1976-1994. Kidney International. 2003;63:1817-1823.
4. American Urological Association. Clinical Guidelines: Ureteral Calculi. Last updated 2007. Available at: http://www.auanet.org/guidelines/uretcal07.cfm. Accessed February 11, 2008.
5. Papa L, Stiell IG, Wells GA, Ball I, Battram E, Mahoney JE. Predicting intervention in renal colic patients after emergency department evaluation. Can J Emerg Med. 2005;7:78-86.
6. Pearle MS, Calhoun EA, Curhan GC. Urologic Diseases of America Project. Urologic diseases in America project: urolithiasis. J Urol. 2005;173:848-857.
7. Morse RM, Resnick MI. Ureteral calculi: natural history and treatment in an era of advanced technology. J Urol. 1991;145:263-265.
8. Peters HJ, Eckstein W. Possible pharmacological means of treating renal colic. Urol Res. 1975;3:55-59.
9. Borghi L, Meschi T, Amato F, Novarini A, Giannini A, Quarantelli C, et al. Nifedipine and methylpredniso-lone in facilitating ureteral stone passage: a randomized, double-blind, placebo-controlled study. J Urol. 1994;152:1095-1098.
10. Hollingsworth JM, Rogers MA, Kaufman SR, Bradford TJ, Saint S, Wei JT, et al. Medical therapy to facilitate urinary stone passage: a meta-analysis. Lancet. 2006;368:1171-1179.
Prescribe tamsulosin (typically 0.4 mg daily) or nifedipine (typically 30 mg daily) for patients with lower ureteral calculi, to speed stone passage and to avoid surgical intervention
Strength of recommendation
A: Meta-analysis of randomized controlled trials
Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007; 50:552-563.1
ILLUSTRATIVE CASE
A 52-year-old man presents to your office for follow-up 2 days after he was seen in the ED and diagnosed with a distal ureteral calculus, his first. His pain is reasonably well controlled, but he has not yet passed the stone. Is there anything you can do to help him pass the stone?
Yes. Patients who are candidates for observation should be offered a trial of “medical expulsive therapy” using an α-antagonist or a calcium channel blocker. Until now, medical therapy for kidney stones consisted of pain relief only.
The ordeal of a first stone is all too common—the lifetime prevalence of kidney stones is 5.2%—and the probability of recurrence is about 50%.2,3
NHANES data show increasing prevalence between the periods 1976-1980 and 1988-1996.3 One fifth to one third of kidney stones require surgical intervention.4 In a cohort of 245 patients presenting to an ED in Canada, 50 (20%) required further procedures, including lithotripsy. Stones ≥ 6 mm in size were much less likely to pass (OR=10.7, 95% CI 4.6-24.8).5 The burden on the healthcare system is significant; there are approximately 2 million out-patient visits annually for this problem, and diagnosis and treatment costs about $2 billion annually.6
Watch and wait
The standard approach is a period of watchful waiting and pain control, with urgent urological referral for patients with evidence of upper urinary tract infection, high grade obstruction, inadequate pain or nausea control, or insufficient renal reserve.2,4 Most patients treated with watchful waiting pass their stone within 4 weeks. Any stones that don’t pass within 8 weeks are unlikely to pass spontaneously.2,7
Medical therapy has been proposed for decades
Medications that relax ureteral smooth muscle to help pass ureteral stones have been proposed for decades.8 Prior to 2000, however, only 1 randomized controlled trial (RCT) of medical therapy for ureteral stones had been published.9 A subsequent meta-analysis found 9 studies and showed that medical therapy did increase the chances that a stone would pass.10 The Singh meta-analysis found 13 subsequently published studies and nearly tripled the number of patients evaluated.
STUDY SUMMARY: A well-done meta-analysis
This meta-analysis is based on 16 studies of α-antagonists (most used tamsulosin) and 9 studies of nifedipine, a calcium channel blocker.1 The studies were identified by a comprehensive search strategy that included Medline, EMBASE, and the Cochrane Controlled Trials Register from January 1980 to January 2007. The authors included all randomized trials or controlled clinical trials of medical therapy for adults with acute ureteral colic.
The authors assessed the studies for quality using the Jadad scale, a validated scale of study quality. Higher scores represent better quality, including better documentation of randomization, blinding, and follow-up. The authors specified their planned sensitivity analyses, and used the random effects model to synthesize the results, which tends to provide a more conservative estimate of the effect.
In other words, this was a very well done meta-analysis.
Twenty-two studies met the inclusion criteria: 13 of α-antagonists, 6 of nifedipine, and 3 of both. In 13 of the 16 studies of α-antagonists, tamsulosin (Flomax) was the study drug. The results from the terazosin (Hytrin) and doxazosin (Cardura) studies were included with the tamsulosin studies. The Jadad quality scores of the 22 studies were fairly low, with a median of 2 (range of 0 to 3) on the 5-point scale. The most common deduction was because the study was not double-blinded.
Medical therapy makes sense
“Therapy using either α-antagonists or calcium channel blockers augments the stone expulsion rate compared to standard therapy for moderately sized distal ureteral stones.” 1 CT showing distal ureteral stone
α-Antagonist studies
These 16 studies enrolled 1235 patients with distal ureteral stones. Mean stone size ranged from 4.3 to 7.8 mm. α-Antagonists improved the stone expulsion rate (RR= 1.59, 95% CI 1.44-1.75; NNT=3.3).
The mean time to expulsion of the stone ranged from 2.7 to 14.2 days and duration of therapy ranged from 1 to 7 weeks. In the 9 trials that reported the time to stone expulsion, the stone came out between 2 and 6 days earlier than the control groups.
Adverse effects were reported in 4% of patients receiving the active medication; most were mild.
Nifedipine studies
There were 686 patients in the 9 trials of nifedipine. The mean stone size was 3.9 to 12.8 mm. Some studies included stones in the more proximal as well as the distal ureter.
Nifedipine treatment increased the rate of stone expulsion (RR=1.5, 95% CI 1.34-1.68; NNT=3.9). Time to stone expulsion was shorter in 7 of the 9 studies.
Adverse effects were reported in 15% of the patients. Most of these were mild— nausea, vomiting, asthenia, and dyspepsia.
WHAT’S NEW: Strong evidence for use of medical therapy
The new findings from the Singh meta-analysis reviewed in this PURL supports physicians who have already adopted this practice and should encourage usage by those who have not yet done so.
Inpatients in academic medical centers
There is a growing trend to use tamsulosin to facilitate passage of ureteral stones. The University Health System Consortium (www.uhc.org) has complete clinical data on inpatients with ureteral stones, from 64 academic medical centers and teaching hospitals, between 2003 and 2007. We used this database to analyze trends in the use of tamsulosin in 4300 inpatients with ureteral stones (ICD 9 code 5921).
In 2003, only 3.3% of patients with a discharge diagnosis of ureteral stone received tamsulosin. In 2007, 34.1% of patients with ureteral stones discharged from these hospitals received tamsulosin, with similar rates of use when stratified by the specialty of the attending physician at discharge (family medicine, emergency medicine, internal medicine, urology) (FIGURE 1). We noted a wide range in the rate of adoption of this practice among academic medical centers: 48% in the centers with the highest rate of usage and 4.4% in the centers with the lowest rate.
FIGURE 1
% of inpatients in academic medical centers who received tamsulosin for ureteral stones, by year
Source: Unpublished data from the University Health System Consortium
Outpatients from a sample of US practices
The use of tamsulosin or nifedipine in outpatient practice was infrequent even 2 or 3 years ago. We used the National Ambulatory Medical Care Survey data (www.cdc.gov/nchs/about/major/ahcd/ahcd1.htm) from 2004 and 2005 (the most recent available), which provides a sample of all US outpatient practices. Only 7% of an estimated 1,345,000 patients diagnosed with ureteral stones were prescribed either tamsulosin or nifedipine, and urologists cared for most of those.
These unpublished data show that physicians in academic medical centers are increasingly adopting the practice of using tamsulosin or nifedipine for expulsion of ureteral stones, that urologists appear to be the first to begin using these medications in outpatients several years ago, and that this practice is being adopted actively in selected academic medical centers.
CAVEATS: Is either drug better? Too little data to tell
Our conclusion is that the strengths of this meta-analysis outweigh the weaknesses, the findings across studies are consistent, and the use of smooth-muscle relaxants for this indication makes sense from a mechanistic point of view.
The quality of a meta-analysis is only as good as the quality of the included studies, and, in this case, the overall quality of studies was not uniformly high. Median Jadad score, a summary measure of study quality, was 2, and the highest score was 3 (of a maximum of 5). The most common problem was lack of blinding, which can be critical in studies with subjective outcomes such as pain. We doubt that the lack of blinding led to any significant misclassification of outcome in this study, however.
Patients either passed the stone or they didn’t, or had a surgical intervention or not. It is reassuring that, when the best quality studies (Jadad score= 3) were analyzed separately, the results were equally good.
There have not been sufficient head-to-head trials to know if one is better than the other. We prefer α-antagonists because of the lower apparent side-effect profile. Our analysis of the UHC data shows that most of the physicians who are using medical therapy are using tamsulosin primarily for this diagnosis.
The majority of the patients in the studies included in the meta-analysis had been referred to a urologist. This raises the possibility that this treatment may not be as effective in patients with less severe symptoms for whom urological consultation is not necessary.
CHALLENGES TO IMPLEMENTATION: This change should be easy to put into practice
Tamsulosin is the best studied of the drugs, but also the most expensive. Based on the estimated number need to treat (NNT) of between 3 and 4 to prevent a surgical intervention and an estimated cost of around $90 for 1 month (www. drugstore.com, February 16, 2008), tamsulosin seems like a good investment to avoid surgical intervention.
The evidence for the other α-antagonists is consistent with that of tamsulosin, but there are fewer data, so it is not clear that the other agents will work as well.
Many people with renal colic are diagnosed and treated in the emergency department; they may not see their family physician until some time after the stone is diagnosed. It is unclear what effect this delay might have on medication effectiveness.
Neither tamsulosin nor nifedipine have an FDA indication for ureterolithiasis. However, they are prescribed commonly, and most physicians are familiar with their use and adverse-effect profiles.
Drugs used in the meta-analysis studies
α-Antagonists
Tamsulosin (Flomax)
Terazosin (Hytrin)
Doxazosin (Cardura)
Calcium channel blockers
Nifedipine (Adalat, Nifedical, Procardia)
Acknowledgement
We acknowledge Sofia Medvedev, PhD of the University HealthSystem Consortium (UHC) in Oak Brook, IL for analysis of the UHC Clinical Database and the National Ambulatory Medical Care Survey data.
PURLs methodology
This study was selected and evaluated using FPIN’s Priority Updates from the Research Literature (PURL) Surveillance System methodology. The criteria and findings leading to the selection of this study as a PURL can be accessed at www.jfponline.com/purls.
Prescribe tamsulosin (typically 0.4 mg daily) or nifedipine (typically 30 mg daily) for patients with lower ureteral calculi, to speed stone passage and to avoid surgical intervention
Strength of recommendation
A: Meta-analysis of randomized controlled trials
Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007; 50:552-563.1
ILLUSTRATIVE CASE
A 52-year-old man presents to your office for follow-up 2 days after he was seen in the ED and diagnosed with a distal ureteral calculus, his first. His pain is reasonably well controlled, but he has not yet passed the stone. Is there anything you can do to help him pass the stone?
Yes. Patients who are candidates for observation should be offered a trial of “medical expulsive therapy” using an α-antagonist or a calcium channel blocker. Until now, medical therapy for kidney stones consisted of pain relief only.
The ordeal of a first stone is all too common—the lifetime prevalence of kidney stones is 5.2%—and the probability of recurrence is about 50%.2,3
NHANES data show increasing prevalence between the periods 1976-1980 and 1988-1996.3 One fifth to one third of kidney stones require surgical intervention.4 In a cohort of 245 patients presenting to an ED in Canada, 50 (20%) required further procedures, including lithotripsy. Stones ≥ 6 mm in size were much less likely to pass (OR=10.7, 95% CI 4.6-24.8).5 The burden on the healthcare system is significant; there are approximately 2 million out-patient visits annually for this problem, and diagnosis and treatment costs about $2 billion annually.6
Watch and wait
The standard approach is a period of watchful waiting and pain control, with urgent urological referral for patients with evidence of upper urinary tract infection, high grade obstruction, inadequate pain or nausea control, or insufficient renal reserve.2,4 Most patients treated with watchful waiting pass their stone within 4 weeks. Any stones that don’t pass within 8 weeks are unlikely to pass spontaneously.2,7
Medical therapy has been proposed for decades
Medications that relax ureteral smooth muscle to help pass ureteral stones have been proposed for decades.8 Prior to 2000, however, only 1 randomized controlled trial (RCT) of medical therapy for ureteral stones had been published.9 A subsequent meta-analysis found 9 studies and showed that medical therapy did increase the chances that a stone would pass.10 The Singh meta-analysis found 13 subsequently published studies and nearly tripled the number of patients evaluated.
STUDY SUMMARY: A well-done meta-analysis
This meta-analysis is based on 16 studies of α-antagonists (most used tamsulosin) and 9 studies of nifedipine, a calcium channel blocker.1 The studies were identified by a comprehensive search strategy that included Medline, EMBASE, and the Cochrane Controlled Trials Register from January 1980 to January 2007. The authors included all randomized trials or controlled clinical trials of medical therapy for adults with acute ureteral colic.
The authors assessed the studies for quality using the Jadad scale, a validated scale of study quality. Higher scores represent better quality, including better documentation of randomization, blinding, and follow-up. The authors specified their planned sensitivity analyses, and used the random effects model to synthesize the results, which tends to provide a more conservative estimate of the effect.
In other words, this was a very well done meta-analysis.
Twenty-two studies met the inclusion criteria: 13 of α-antagonists, 6 of nifedipine, and 3 of both. In 13 of the 16 studies of α-antagonists, tamsulosin (Flomax) was the study drug. The results from the terazosin (Hytrin) and doxazosin (Cardura) studies were included with the tamsulosin studies. The Jadad quality scores of the 22 studies were fairly low, with a median of 2 (range of 0 to 3) on the 5-point scale. The most common deduction was because the study was not double-blinded.
Medical therapy makes sense
“Therapy using either α-antagonists or calcium channel blockers augments the stone expulsion rate compared to standard therapy for moderately sized distal ureteral stones.” 1 CT showing distal ureteral stone
α-Antagonist studies
These 16 studies enrolled 1235 patients with distal ureteral stones. Mean stone size ranged from 4.3 to 7.8 mm. α-Antagonists improved the stone expulsion rate (RR= 1.59, 95% CI 1.44-1.75; NNT=3.3).
The mean time to expulsion of the stone ranged from 2.7 to 14.2 days and duration of therapy ranged from 1 to 7 weeks. In the 9 trials that reported the time to stone expulsion, the stone came out between 2 and 6 days earlier than the control groups.
Adverse effects were reported in 4% of patients receiving the active medication; most were mild.
Nifedipine studies
There were 686 patients in the 9 trials of nifedipine. The mean stone size was 3.9 to 12.8 mm. Some studies included stones in the more proximal as well as the distal ureter.
Nifedipine treatment increased the rate of stone expulsion (RR=1.5, 95% CI 1.34-1.68; NNT=3.9). Time to stone expulsion was shorter in 7 of the 9 studies.
Adverse effects were reported in 15% of the patients. Most of these were mild— nausea, vomiting, asthenia, and dyspepsia.
WHAT’S NEW: Strong evidence for use of medical therapy
The new findings from the Singh meta-analysis reviewed in this PURL supports physicians who have already adopted this practice and should encourage usage by those who have not yet done so.
Inpatients in academic medical centers
There is a growing trend to use tamsulosin to facilitate passage of ureteral stones. The University Health System Consortium (www.uhc.org) has complete clinical data on inpatients with ureteral stones, from 64 academic medical centers and teaching hospitals, between 2003 and 2007. We used this database to analyze trends in the use of tamsulosin in 4300 inpatients with ureteral stones (ICD 9 code 5921).
In 2003, only 3.3% of patients with a discharge diagnosis of ureteral stone received tamsulosin. In 2007, 34.1% of patients with ureteral stones discharged from these hospitals received tamsulosin, with similar rates of use when stratified by the specialty of the attending physician at discharge (family medicine, emergency medicine, internal medicine, urology) (FIGURE 1). We noted a wide range in the rate of adoption of this practice among academic medical centers: 48% in the centers with the highest rate of usage and 4.4% in the centers with the lowest rate.
FIGURE 1
% of inpatients in academic medical centers who received tamsulosin for ureteral stones, by year
Source: Unpublished data from the University Health System Consortium
Outpatients from a sample of US practices
The use of tamsulosin or nifedipine in outpatient practice was infrequent even 2 or 3 years ago. We used the National Ambulatory Medical Care Survey data (www.cdc.gov/nchs/about/major/ahcd/ahcd1.htm) from 2004 and 2005 (the most recent available), which provides a sample of all US outpatient practices. Only 7% of an estimated 1,345,000 patients diagnosed with ureteral stones were prescribed either tamsulosin or nifedipine, and urologists cared for most of those.
These unpublished data show that physicians in academic medical centers are increasingly adopting the practice of using tamsulosin or nifedipine for expulsion of ureteral stones, that urologists appear to be the first to begin using these medications in outpatients several years ago, and that this practice is being adopted actively in selected academic medical centers.
CAVEATS: Is either drug better? Too little data to tell
Our conclusion is that the strengths of this meta-analysis outweigh the weaknesses, the findings across studies are consistent, and the use of smooth-muscle relaxants for this indication makes sense from a mechanistic point of view.
The quality of a meta-analysis is only as good as the quality of the included studies, and, in this case, the overall quality of studies was not uniformly high. Median Jadad score, a summary measure of study quality, was 2, and the highest score was 3 (of a maximum of 5). The most common problem was lack of blinding, which can be critical in studies with subjective outcomes such as pain. We doubt that the lack of blinding led to any significant misclassification of outcome in this study, however.
Patients either passed the stone or they didn’t, or had a surgical intervention or not. It is reassuring that, when the best quality studies (Jadad score= 3) were analyzed separately, the results were equally good.
There have not been sufficient head-to-head trials to know if one is better than the other. We prefer α-antagonists because of the lower apparent side-effect profile. Our analysis of the UHC data shows that most of the physicians who are using medical therapy are using tamsulosin primarily for this diagnosis.
The majority of the patients in the studies included in the meta-analysis had been referred to a urologist. This raises the possibility that this treatment may not be as effective in patients with less severe symptoms for whom urological consultation is not necessary.
CHALLENGES TO IMPLEMENTATION: This change should be easy to put into practice
Tamsulosin is the best studied of the drugs, but also the most expensive. Based on the estimated number need to treat (NNT) of between 3 and 4 to prevent a surgical intervention and an estimated cost of around $90 for 1 month (www. drugstore.com, February 16, 2008), tamsulosin seems like a good investment to avoid surgical intervention.
The evidence for the other α-antagonists is consistent with that of tamsulosin, but there are fewer data, so it is not clear that the other agents will work as well.
Many people with renal colic are diagnosed and treated in the emergency department; they may not see their family physician until some time after the stone is diagnosed. It is unclear what effect this delay might have on medication effectiveness.
Neither tamsulosin nor nifedipine have an FDA indication for ureterolithiasis. However, they are prescribed commonly, and most physicians are familiar with their use and adverse-effect profiles.
Drugs used in the meta-analysis studies
α-Antagonists
Tamsulosin (Flomax)
Terazosin (Hytrin)
Doxazosin (Cardura)
Calcium channel blockers
Nifedipine (Adalat, Nifedical, Procardia)
Acknowledgement
We acknowledge Sofia Medvedev, PhD of the University HealthSystem Consortium (UHC) in Oak Brook, IL for analysis of the UHC Clinical Database and the National Ambulatory Medical Care Survey data.
PURLs methodology
This study was selected and evaluated using FPIN’s Priority Updates from the Research Literature (PURL) Surveillance System methodology. The criteria and findings leading to the selection of this study as a PURL can be accessed at www.jfponline.com/purls.
1. Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007;50:552-563.
2. Teichman JM. Clinical practice. Acute renal colic from ureteral calculus. N Engl J Med. 2004;350:684-693.
3. Stamatelou KK, Francis ME, Jones CA, Nyberg LM. Curhan GC. Time trends in reported prevalence of kidney stones in the United States: 1976-1994. Kidney International. 2003;63:1817-1823.
4. American Urological Association. Clinical Guidelines: Ureteral Calculi. Last updated 2007. Available at: http://www.auanet.org/guidelines/uretcal07.cfm. Accessed February 11, 2008.
5. Papa L, Stiell IG, Wells GA, Ball I, Battram E, Mahoney JE. Predicting intervention in renal colic patients after emergency department evaluation. Can J Emerg Med. 2005;7:78-86.
6. Pearle MS, Calhoun EA, Curhan GC. Urologic Diseases of America Project. Urologic diseases in America project: urolithiasis. J Urol. 2005;173:848-857.
7. Morse RM, Resnick MI. Ureteral calculi: natural history and treatment in an era of advanced technology. J Urol. 1991;145:263-265.
8. Peters HJ, Eckstein W. Possible pharmacological means of treating renal colic. Urol Res. 1975;3:55-59.
9. Borghi L, Meschi T, Amato F, Novarini A, Giannini A, Quarantelli C, et al. Nifedipine and methylpredniso-lone in facilitating ureteral stone passage: a randomized, double-blind, placebo-controlled study. J Urol. 1994;152:1095-1098.
10. Hollingsworth JM, Rogers MA, Kaufman SR, Bradford TJ, Saint S, Wei JT, et al. Medical therapy to facilitate urinary stone passage: a meta-analysis. Lancet. 2006;368:1171-1179.
1. Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007;50:552-563.
2. Teichman JM. Clinical practice. Acute renal colic from ureteral calculus. N Engl J Med. 2004;350:684-693.
3. Stamatelou KK, Francis ME, Jones CA, Nyberg LM. Curhan GC. Time trends in reported prevalence of kidney stones in the United States: 1976-1994. Kidney International. 2003;63:1817-1823.
4. American Urological Association. Clinical Guidelines: Ureteral Calculi. Last updated 2007. Available at: http://www.auanet.org/guidelines/uretcal07.cfm. Accessed February 11, 2008.
5. Papa L, Stiell IG, Wells GA, Ball I, Battram E, Mahoney JE. Predicting intervention in renal colic patients after emergency department evaluation. Can J Emerg Med. 2005;7:78-86.
6. Pearle MS, Calhoun EA, Curhan GC. Urologic Diseases of America Project. Urologic diseases in America project: urolithiasis. J Urol. 2005;173:848-857.
7. Morse RM, Resnick MI. Ureteral calculi: natural history and treatment in an era of advanced technology. J Urol. 1991;145:263-265.
8. Peters HJ, Eckstein W. Possible pharmacological means of treating renal colic. Urol Res. 1975;3:55-59.
9. Borghi L, Meschi T, Amato F, Novarini A, Giannini A, Quarantelli C, et al. Nifedipine and methylpredniso-lone in facilitating ureteral stone passage: a randomized, double-blind, placebo-controlled study. J Urol. 1994;152:1095-1098.
10. Hollingsworth JM, Rogers MA, Kaufman SR, Bradford TJ, Saint S, Wei JT, et al. Medical therapy to facilitate urinary stone passage: a meta-analysis. Lancet. 2006;368:1171-1179.
Copyright © 2008 The Family Physicians Inquiries Network.
All rights reserved.
MEASLES HITS HOME: Sobering lessons from 2 travel-related outbreaks
Inform concerned parents about the safety and effectiveness of vaccines.
2 doses of measles-containing vaccine are 99% effective.
Those exposed who are not immune should be vaccinated or offered immune globulin if the vaccine is contraindicated.
Contraindications
- Primary immune deficiency diseases of T-cell functions
- Acquired immune deficiency from leukemia, lymphoma, or generalized malignancy
- Therapy with corticosteroids: 2 mg/kg prednisone >2 weeks
- Previous anaphylactic reaction to measles vaccine, gelatin, or neomycins
- Pregnancy
Measles is still a threat. Endemic transmission of measles no longer occurs in the United States (or any of the Americas), yet this highly infectious disease is still a threat from importation by visitors from other countries and from US residents who have traveled abroad. Two recent outbreaks (described at left) illustrate these risks.
3 infants too young to be vaccinated contracted measles in their doctor’s office in San Diego, in January 2008. (An infant with measles rash [above] is for illustration only, and does not depict any of the 3.)
What the CDC discovered
The 2 outbreaks of import-linked measles brought home—literally—the sobering facts about vulnerability among US residents. The CDC report 1,2 of its investigation observed:
US travelers can be exposed almost anywhere, developed countries included. The California outbreak started with a visit to Switzerland.
Measles spreads rapidly in susceptible subgroups, unless effective control strategies are used. In California, on 2 consecutive days, 5 school children and 4 children in a doctor’s office were infected; all were unvaccinated.
People not considered at risk can contract measles. Although 2 doses of vaccine are 99% effective, vaccinated individuals, such as the college students, can contract measles. Likewise, people born before 1957 may not be immune, in contrast to the general definition of immunity (see Measles Basics. Case in point: the airline passenger, born in 1954.
Disease can be severe. The 40-year-old salesperson (no documented vaccination) was hospitalized with seizure, 105ºF fever, and pneumonia. One of the infants was hospitalized due to dehydration.
People in routine contact with travelers entering the United States can be exposed to measles—like the airline worker.
CALIFORNIA - A February 22 early-release CDC report1 linked 12 measles cases in California to an unvaccinated 7-year-old boy infected while traveling in Europe with his family in January. He was taken to his pediatrician after onset of rash, and to the emergency department the next day, because of high fever and generalized rash. No isolation precautions were used in the office or hospital.
The boy’s 2 siblings, 5 children at his school, and 4 children at the doctor’s office while he was there contracted measles (3 of whom were infants <12 months of age).
Nearly 10% of the children at the index case’s school were unvaccinated because of personal belief exemptions.
PENNSYLVANIA, MICHIGAN, TEXAS - A young boy from Japan participated in an international sporting event and attended a related sales event in Pennsylvania last August. He was infectious when he left Japan and as he traveled in the United States.
The CDC2 linked a total of 6 additional cases of measles in US-born residents to the index case: another young person from Japan who watched the sporting event; a 53-year-old airline passenger and a 25-year-old airline worker in Michigan; and a corporate sales representative who had met the index patient at the sales event and subsequently made sales visits to Houston-area colleges, where 2 college roommates became infected.
Viral genotyping supported a single chain of transmission, and genetic sequencing linked 6 of the 7 cases.
Take-home lessons for family physicians
Include measles in the differential diagnosis of patients who have fever and rash, especially if they have traveled to another country within the past 3 to 4 weeks. Any patient who meets the definition of measles (fever 101ºF or higher; rash; and at least 1 of the 3 Cs—cough, coryza, conjunctivitis) should be immediately reported to the local health department. The health department will provide instructions for collecting laboratory samples for confirmation; instructions on patient isolation; and assistance with notification and disease control measures for exposed individuals.
Immunize patients and staff. These recurring cases of imported measles underscore the importance of maintaining a high level of immunity. Outbreaks can happen even where immunity is 90% to 95%. When vaccination rates dip below 90%, sustained outbreaks can occur.6
Ensure that staff and patients are all immunized against vaccine-preventable diseases, and inform concerned parents about the safety and effectiveness of vaccines. Parents who refuse to have their children vaccinated place their children at risk and contribute to higher community risk. Communities that have higher rates of non-adherence to vaccine recommendations are more likely to have outbreaks.7,8
Use strict infection control in the office. The recent outbreak in California where 4 children were infected in their physician’s office reinforces the need for strict infection-control practices. Do not allow patients with rash and fever to remain in a common waiting area. Move them to an examination room, preferably an airborne infection isolation room. Keep the door to the examination room closed, and be sure that all health care personnel who come in contact with such patients are immune. Do not use triage rooms for 2 hours after the patient suspected of having measles leaves. Do not send these patients to other health care facilities, such as laboratories, unless infection control measures can be adhered to at those locations. Guidelines on infection control practices in health care settings are available.9,10
Quick response
Quick control of these outbreaks shows the value of the public health infrastructure. Disease surveillance and outbreak response is vital to the public health system, and its value is frequently under-appreciated by physicians and the public.
Fewer than 100 cases of measles occur in the United States each year, and virtually all are linked to imported cases.3 Before vaccine was introduced in 1963, 3 to 4 million cases per year occurred, and caused, on average, 450 deaths, 1000 chronic disabilities, and 28,000 hospitalizations.1 Success in controlling measles is due largely to high levels of coverage with 2 doses of measles-containing vaccine and public health surveillance and disease control.
Measles virus is highly infectious and is spread by airborne droplets and direct contact with nose and throat secretions. The incubation is 7 to 18 days.
Measles begins with fever, cough, coryza, conjunctivitis, and whitish spots on the buccal mucosa (Koplick spots).4 Rash appears on the 3rd to 7th day and lasts 4 to 7 days. It begins on the face but soon becomes generalized. An infected person is contagious from 5 days before the rash until 4 days after the rash appears. The diagnosis of measles can be confirrmed by serum measles IGM, which occurs within 3 days of rash, or a rise in measles IGG between acute and 2-week convalescent serum titers.
Complications: pneumonia (5%), otitis media (10%), and encephalitis 1/1000). Death rates: 1 to 2/1000, varying greatly based on age and nutrition; more severe in the very young and the malnourished. Worldwide, about 500,000 children die from measles each year.5
Immunity is defined as:
- 2 vaccine doses at least 1 month apart, both given after the 1st birthday,
- born before 1957,
- serological evidence, or
- history of physician-diagnosed measles.
1. CDC. Outbreak of measles—San Diego, California, January-February 2008. MMWR. 2008;57:Early Release February 22, 2008.-
2. CDC. Multistate measles outbreak associated with an international youth sporting event—Pennsylvania, Michigan, and Texas, August-September 2007. MMWR. 2008;57:169-173.
3. CDC. Measles—United States, 2005. MMWR. 2006;55:1348-1351.
4. Measles. In: Heyman DL. Control of Communicable Diseases Manual. 18th ed. Washington, DC: American Public Health Association.
5. CDC. Parents’ guide to childhood immunizations. Available at: http://www.cdc.gov/vaccines/vpd-vac/measles/downloads/pg_why_vacc_measles.pdf. Accessed March 17, 2008.
6. Richard JL, Masserey-Spicher V, Santibanez S, Mankertz A. Measles outbreak in Switzerland. Available at: http://www.eurosurveillance.org/edition/v13n08/080221_1.asp. Accessed March 17. 2008.
7. Salmon DA, Haber M, Gangarosa EJ, et al. Health consequences of religious and philosophical exemptions from immunization laws; individual and societal risk of measles. JAMA. 1999;282:47-53
8. Feikin DR, Lezotte DC, Hamman RF, et al. Individual and community risks of measles and pertussis associated with personal exemptions to immunization. JAMA. 2008;284:3145-3150.
9. Siegel JD, Rhinehart E, Jackson M, Chiarello L. Health care infection control practices advisory committee, 2007.Guideline for isolation precautions: preventing transmission of infectious agents in health care settings. Am J Infect Control. 2007;35(suppl 2):S65-164.
10. Campos-Outcalt D. Infection control in outpatient settings. J Fam Pract. 2004;53:485-488.
Inform concerned parents about the safety and effectiveness of vaccines.
2 doses of measles-containing vaccine are 99% effective.
Those exposed who are not immune should be vaccinated or offered immune globulin if the vaccine is contraindicated.
Contraindications
- Primary immune deficiency diseases of T-cell functions
- Acquired immune deficiency from leukemia, lymphoma, or generalized malignancy
- Therapy with corticosteroids: 2 mg/kg prednisone >2 weeks
- Previous anaphylactic reaction to measles vaccine, gelatin, or neomycins
- Pregnancy
Measles is still a threat. Endemic transmission of measles no longer occurs in the United States (or any of the Americas), yet this highly infectious disease is still a threat from importation by visitors from other countries and from US residents who have traveled abroad. Two recent outbreaks (described at left) illustrate these risks.
3 infants too young to be vaccinated contracted measles in their doctor’s office in San Diego, in January 2008. (An infant with measles rash [above] is for illustration only, and does not depict any of the 3.)
What the CDC discovered
The 2 outbreaks of import-linked measles brought home—literally—the sobering facts about vulnerability among US residents. The CDC report 1,2 of its investigation observed:
US travelers can be exposed almost anywhere, developed countries included. The California outbreak started with a visit to Switzerland.
Measles spreads rapidly in susceptible subgroups, unless effective control strategies are used. In California, on 2 consecutive days, 5 school children and 4 children in a doctor’s office were infected; all were unvaccinated.
People not considered at risk can contract measles. Although 2 doses of vaccine are 99% effective, vaccinated individuals, such as the college students, can contract measles. Likewise, people born before 1957 may not be immune, in contrast to the general definition of immunity (see Measles Basics. Case in point: the airline passenger, born in 1954.
Disease can be severe. The 40-year-old salesperson (no documented vaccination) was hospitalized with seizure, 105ºF fever, and pneumonia. One of the infants was hospitalized due to dehydration.
People in routine contact with travelers entering the United States can be exposed to measles—like the airline worker.
CALIFORNIA - A February 22 early-release CDC report1 linked 12 measles cases in California to an unvaccinated 7-year-old boy infected while traveling in Europe with his family in January. He was taken to his pediatrician after onset of rash, and to the emergency department the next day, because of high fever and generalized rash. No isolation precautions were used in the office or hospital.
The boy’s 2 siblings, 5 children at his school, and 4 children at the doctor’s office while he was there contracted measles (3 of whom were infants <12 months of age).
Nearly 10% of the children at the index case’s school were unvaccinated because of personal belief exemptions.
PENNSYLVANIA, MICHIGAN, TEXAS - A young boy from Japan participated in an international sporting event and attended a related sales event in Pennsylvania last August. He was infectious when he left Japan and as he traveled in the United States.
The CDC2 linked a total of 6 additional cases of measles in US-born residents to the index case: another young person from Japan who watched the sporting event; a 53-year-old airline passenger and a 25-year-old airline worker in Michigan; and a corporate sales representative who had met the index patient at the sales event and subsequently made sales visits to Houston-area colleges, where 2 college roommates became infected.
Viral genotyping supported a single chain of transmission, and genetic sequencing linked 6 of the 7 cases.
Take-home lessons for family physicians
Include measles in the differential diagnosis of patients who have fever and rash, especially if they have traveled to another country within the past 3 to 4 weeks. Any patient who meets the definition of measles (fever 101ºF or higher; rash; and at least 1 of the 3 Cs—cough, coryza, conjunctivitis) should be immediately reported to the local health department. The health department will provide instructions for collecting laboratory samples for confirmation; instructions on patient isolation; and assistance with notification and disease control measures for exposed individuals.
Immunize patients and staff. These recurring cases of imported measles underscore the importance of maintaining a high level of immunity. Outbreaks can happen even where immunity is 90% to 95%. When vaccination rates dip below 90%, sustained outbreaks can occur.6
Ensure that staff and patients are all immunized against vaccine-preventable diseases, and inform concerned parents about the safety and effectiveness of vaccines. Parents who refuse to have their children vaccinated place their children at risk and contribute to higher community risk. Communities that have higher rates of non-adherence to vaccine recommendations are more likely to have outbreaks.7,8
Use strict infection control in the office. The recent outbreak in California where 4 children were infected in their physician’s office reinforces the need for strict infection-control practices. Do not allow patients with rash and fever to remain in a common waiting area. Move them to an examination room, preferably an airborne infection isolation room. Keep the door to the examination room closed, and be sure that all health care personnel who come in contact with such patients are immune. Do not use triage rooms for 2 hours after the patient suspected of having measles leaves. Do not send these patients to other health care facilities, such as laboratories, unless infection control measures can be adhered to at those locations. Guidelines on infection control practices in health care settings are available.9,10
Quick response
Quick control of these outbreaks shows the value of the public health infrastructure. Disease surveillance and outbreak response is vital to the public health system, and its value is frequently under-appreciated by physicians and the public.
Fewer than 100 cases of measles occur in the United States each year, and virtually all are linked to imported cases.3 Before vaccine was introduced in 1963, 3 to 4 million cases per year occurred, and caused, on average, 450 deaths, 1000 chronic disabilities, and 28,000 hospitalizations.1 Success in controlling measles is due largely to high levels of coverage with 2 doses of measles-containing vaccine and public health surveillance and disease control.
Measles virus is highly infectious and is spread by airborne droplets and direct contact with nose and throat secretions. The incubation is 7 to 18 days.
Measles begins with fever, cough, coryza, conjunctivitis, and whitish spots on the buccal mucosa (Koplick spots).4 Rash appears on the 3rd to 7th day and lasts 4 to 7 days. It begins on the face but soon becomes generalized. An infected person is contagious from 5 days before the rash until 4 days after the rash appears. The diagnosis of measles can be confirrmed by serum measles IGM, which occurs within 3 days of rash, or a rise in measles IGG between acute and 2-week convalescent serum titers.
Complications: pneumonia (5%), otitis media (10%), and encephalitis 1/1000). Death rates: 1 to 2/1000, varying greatly based on age and nutrition; more severe in the very young and the malnourished. Worldwide, about 500,000 children die from measles each year.5
Immunity is defined as:
- 2 vaccine doses at least 1 month apart, both given after the 1st birthday,
- born before 1957,
- serological evidence, or
- history of physician-diagnosed measles.
Inform concerned parents about the safety and effectiveness of vaccines.
2 doses of measles-containing vaccine are 99% effective.
Those exposed who are not immune should be vaccinated or offered immune globulin if the vaccine is contraindicated.
Contraindications
- Primary immune deficiency diseases of T-cell functions
- Acquired immune deficiency from leukemia, lymphoma, or generalized malignancy
- Therapy with corticosteroids: 2 mg/kg prednisone >2 weeks
- Previous anaphylactic reaction to measles vaccine, gelatin, or neomycins
- Pregnancy
Measles is still a threat. Endemic transmission of measles no longer occurs in the United States (or any of the Americas), yet this highly infectious disease is still a threat from importation by visitors from other countries and from US residents who have traveled abroad. Two recent outbreaks (described at left) illustrate these risks.
3 infants too young to be vaccinated contracted measles in their doctor’s office in San Diego, in January 2008. (An infant with measles rash [above] is for illustration only, and does not depict any of the 3.)
What the CDC discovered
The 2 outbreaks of import-linked measles brought home—literally—the sobering facts about vulnerability among US residents. The CDC report 1,2 of its investigation observed:
US travelers can be exposed almost anywhere, developed countries included. The California outbreak started with a visit to Switzerland.
Measles spreads rapidly in susceptible subgroups, unless effective control strategies are used. In California, on 2 consecutive days, 5 school children and 4 children in a doctor’s office were infected; all were unvaccinated.
People not considered at risk can contract measles. Although 2 doses of vaccine are 99% effective, vaccinated individuals, such as the college students, can contract measles. Likewise, people born before 1957 may not be immune, in contrast to the general definition of immunity (see Measles Basics. Case in point: the airline passenger, born in 1954.
Disease can be severe. The 40-year-old salesperson (no documented vaccination) was hospitalized with seizure, 105ºF fever, and pneumonia. One of the infants was hospitalized due to dehydration.
People in routine contact with travelers entering the United States can be exposed to measles—like the airline worker.
CALIFORNIA - A February 22 early-release CDC report1 linked 12 measles cases in California to an unvaccinated 7-year-old boy infected while traveling in Europe with his family in January. He was taken to his pediatrician after onset of rash, and to the emergency department the next day, because of high fever and generalized rash. No isolation precautions were used in the office or hospital.
The boy’s 2 siblings, 5 children at his school, and 4 children at the doctor’s office while he was there contracted measles (3 of whom were infants <12 months of age).
Nearly 10% of the children at the index case’s school were unvaccinated because of personal belief exemptions.
PENNSYLVANIA, MICHIGAN, TEXAS - A young boy from Japan participated in an international sporting event and attended a related sales event in Pennsylvania last August. He was infectious when he left Japan and as he traveled in the United States.
The CDC2 linked a total of 6 additional cases of measles in US-born residents to the index case: another young person from Japan who watched the sporting event; a 53-year-old airline passenger and a 25-year-old airline worker in Michigan; and a corporate sales representative who had met the index patient at the sales event and subsequently made sales visits to Houston-area colleges, where 2 college roommates became infected.
Viral genotyping supported a single chain of transmission, and genetic sequencing linked 6 of the 7 cases.
Take-home lessons for family physicians
Include measles in the differential diagnosis of patients who have fever and rash, especially if they have traveled to another country within the past 3 to 4 weeks. Any patient who meets the definition of measles (fever 101ºF or higher; rash; and at least 1 of the 3 Cs—cough, coryza, conjunctivitis) should be immediately reported to the local health department. The health department will provide instructions for collecting laboratory samples for confirmation; instructions on patient isolation; and assistance with notification and disease control measures for exposed individuals.
Immunize patients and staff. These recurring cases of imported measles underscore the importance of maintaining a high level of immunity. Outbreaks can happen even where immunity is 90% to 95%. When vaccination rates dip below 90%, sustained outbreaks can occur.6
Ensure that staff and patients are all immunized against vaccine-preventable diseases, and inform concerned parents about the safety and effectiveness of vaccines. Parents who refuse to have their children vaccinated place their children at risk and contribute to higher community risk. Communities that have higher rates of non-adherence to vaccine recommendations are more likely to have outbreaks.7,8
Use strict infection control in the office. The recent outbreak in California where 4 children were infected in their physician’s office reinforces the need for strict infection-control practices. Do not allow patients with rash and fever to remain in a common waiting area. Move them to an examination room, preferably an airborne infection isolation room. Keep the door to the examination room closed, and be sure that all health care personnel who come in contact with such patients are immune. Do not use triage rooms for 2 hours after the patient suspected of having measles leaves. Do not send these patients to other health care facilities, such as laboratories, unless infection control measures can be adhered to at those locations. Guidelines on infection control practices in health care settings are available.9,10
Quick response
Quick control of these outbreaks shows the value of the public health infrastructure. Disease surveillance and outbreak response is vital to the public health system, and its value is frequently under-appreciated by physicians and the public.
Fewer than 100 cases of measles occur in the United States each year, and virtually all are linked to imported cases.3 Before vaccine was introduced in 1963, 3 to 4 million cases per year occurred, and caused, on average, 450 deaths, 1000 chronic disabilities, and 28,000 hospitalizations.1 Success in controlling measles is due largely to high levels of coverage with 2 doses of measles-containing vaccine and public health surveillance and disease control.
Measles virus is highly infectious and is spread by airborne droplets and direct contact with nose and throat secretions. The incubation is 7 to 18 days.
Measles begins with fever, cough, coryza, conjunctivitis, and whitish spots on the buccal mucosa (Koplick spots).4 Rash appears on the 3rd to 7th day and lasts 4 to 7 days. It begins on the face but soon becomes generalized. An infected person is contagious from 5 days before the rash until 4 days after the rash appears. The diagnosis of measles can be confirrmed by serum measles IGM, which occurs within 3 days of rash, or a rise in measles IGG between acute and 2-week convalescent serum titers.
Complications: pneumonia (5%), otitis media (10%), and encephalitis 1/1000). Death rates: 1 to 2/1000, varying greatly based on age and nutrition; more severe in the very young and the malnourished. Worldwide, about 500,000 children die from measles each year.5
Immunity is defined as:
- 2 vaccine doses at least 1 month apart, both given after the 1st birthday,
- born before 1957,
- serological evidence, or
- history of physician-diagnosed measles.
1. CDC. Outbreak of measles—San Diego, California, January-February 2008. MMWR. 2008;57:Early Release February 22, 2008.-
2. CDC. Multistate measles outbreak associated with an international youth sporting event—Pennsylvania, Michigan, and Texas, August-September 2007. MMWR. 2008;57:169-173.
3. CDC. Measles—United States, 2005. MMWR. 2006;55:1348-1351.
4. Measles. In: Heyman DL. Control of Communicable Diseases Manual. 18th ed. Washington, DC: American Public Health Association.
5. CDC. Parents’ guide to childhood immunizations. Available at: http://www.cdc.gov/vaccines/vpd-vac/measles/downloads/pg_why_vacc_measles.pdf. Accessed March 17, 2008.
6. Richard JL, Masserey-Spicher V, Santibanez S, Mankertz A. Measles outbreak in Switzerland. Available at: http://www.eurosurveillance.org/edition/v13n08/080221_1.asp. Accessed March 17. 2008.
7. Salmon DA, Haber M, Gangarosa EJ, et al. Health consequences of religious and philosophical exemptions from immunization laws; individual and societal risk of measles. JAMA. 1999;282:47-53
8. Feikin DR, Lezotte DC, Hamman RF, et al. Individual and community risks of measles and pertussis associated with personal exemptions to immunization. JAMA. 2008;284:3145-3150.
9. Siegel JD, Rhinehart E, Jackson M, Chiarello L. Health care infection control practices advisory committee, 2007.Guideline for isolation precautions: preventing transmission of infectious agents in health care settings. Am J Infect Control. 2007;35(suppl 2):S65-164.
10. Campos-Outcalt D. Infection control in outpatient settings. J Fam Pract. 2004;53:485-488.
1. CDC. Outbreak of measles—San Diego, California, January-February 2008. MMWR. 2008;57:Early Release February 22, 2008.-
2. CDC. Multistate measles outbreak associated with an international youth sporting event—Pennsylvania, Michigan, and Texas, August-September 2007. MMWR. 2008;57:169-173.
3. CDC. Measles—United States, 2005. MMWR. 2006;55:1348-1351.
4. Measles. In: Heyman DL. Control of Communicable Diseases Manual. 18th ed. Washington, DC: American Public Health Association.
5. CDC. Parents’ guide to childhood immunizations. Available at: http://www.cdc.gov/vaccines/vpd-vac/measles/downloads/pg_why_vacc_measles.pdf. Accessed March 17, 2008.
6. Richard JL, Masserey-Spicher V, Santibanez S, Mankertz A. Measles outbreak in Switzerland. Available at: http://www.eurosurveillance.org/edition/v13n08/080221_1.asp. Accessed March 17. 2008.
7. Salmon DA, Haber M, Gangarosa EJ, et al. Health consequences of religious and philosophical exemptions from immunization laws; individual and societal risk of measles. JAMA. 1999;282:47-53
8. Feikin DR, Lezotte DC, Hamman RF, et al. Individual and community risks of measles and pertussis associated with personal exemptions to immunization. JAMA. 2008;284:3145-3150.
9. Siegel JD, Rhinehart E, Jackson M, Chiarello L. Health care infection control practices advisory committee, 2007.Guideline for isolation precautions: preventing transmission of infectious agents in health care settings. Am J Infect Control. 2007;35(suppl 2):S65-164.
10. Campos-Outcalt D. Infection control in outpatient settings. J Fam Pract. 2004;53:485-488.
Malpractice Minute
We give you facts of an actual malpractice case. Submit your verdict below and see how your colleagues voted.
Did the patient know the risks of risperidone?
THE PATIENT. A 53-year-old woman hospitalized for depression and suicidal thoughts was prescribed risperidone.
CASE FACTS. The patient developed excessive mouth and tongue movement—including pursed lips, protruding tongue, and biting the inside of her mouth—and uncontrollable urges to move her extremities. She was diagnosed with probable tardive dyskinesia (TD), and risperidone was tapered and discontinued.
THE PATIENT’S CLAIM. The psychiatrist failed to adequately monitor her and recognize early symptoms of TD and did not tell the patient to look for signs of TD.
THE DOCTOR’S DEFENSE. None
Submit your verdict and find out how the court ruled. Click on “Have more to say about this topic?” to comment.
Cases are selected by Current Psychiatry from Medical Malpractice Verdicts, Settlements & Experts, with permission of its editor, Lewis Laska of Nashville, TN (www.verdictslaska.com). Information may be incomplete in some instances, but these cases represent clinical situations that typically result in litigation.
We give you facts of an actual malpractice case. Submit your verdict below and see how your colleagues voted.
Did the patient know the risks of risperidone?
THE PATIENT. A 53-year-old woman hospitalized for depression and suicidal thoughts was prescribed risperidone.
CASE FACTS. The patient developed excessive mouth and tongue movement—including pursed lips, protruding tongue, and biting the inside of her mouth—and uncontrollable urges to move her extremities. She was diagnosed with probable tardive dyskinesia (TD), and risperidone was tapered and discontinued.
THE PATIENT’S CLAIM. The psychiatrist failed to adequately monitor her and recognize early symptoms of TD and did not tell the patient to look for signs of TD.
THE DOCTOR’S DEFENSE. None
Submit your verdict and find out how the court ruled. Click on “Have more to say about this topic?” to comment.
We give you facts of an actual malpractice case. Submit your verdict below and see how your colleagues voted.
Did the patient know the risks of risperidone?
THE PATIENT. A 53-year-old woman hospitalized for depression and suicidal thoughts was prescribed risperidone.
CASE FACTS. The patient developed excessive mouth and tongue movement—including pursed lips, protruding tongue, and biting the inside of her mouth—and uncontrollable urges to move her extremities. She was diagnosed with probable tardive dyskinesia (TD), and risperidone was tapered and discontinued.
THE PATIENT’S CLAIM. The psychiatrist failed to adequately monitor her and recognize early symptoms of TD and did not tell the patient to look for signs of TD.
THE DOCTOR’S DEFENSE. None
Submit your verdict and find out how the court ruled. Click on “Have more to say about this topic?” to comment.
Cases are selected by Current Psychiatry from Medical Malpractice Verdicts, Settlements & Experts, with permission of its editor, Lewis Laska of Nashville, TN (www.verdictslaska.com). Information may be incomplete in some instances, but these cases represent clinical situations that typically result in litigation.
Cases are selected by Current Psychiatry from Medical Malpractice Verdicts, Settlements & Experts, with permission of its editor, Lewis Laska of Nashville, TN (www.verdictslaska.com). Information may be incomplete in some instances, but these cases represent clinical situations that typically result in litigation.
Evaluate liability risks in prescribing
Dear Dr. Mossman,
I prescribed topiramate for Mr. B, a patient with no history of kidney stones. Many months later he developed back pain. During the medical workup for a possible kidney stone, Mr. B and I revisited the risk of kidney stones with topiramate, which we had discussed at the beginning of therapy. Mr. B was adamantly opposed to stopping topiramate, even if he had a kidney stone. Testing revealed that Mr. B did not have a stone, but I wasn’t sure how to proceed. I worried that I might be found liable if Mr. B stayed on topiramate and did develop a kidney stone.—Submitted by Dr. A
When a patient develops a medical problem from a drug you prescribed, it is natural to feel responsible—after all, your treatment caused the adverse event. But did you commit malpractice? To answer this, let’s review the concept of “medical negligence.”
Malpractice law applies legal principles of negligence to professional conduct.1 The elements of a negligence case (Table 1) can be summarized as “breach of duty causing damages.” Therefore, when you wonder whether possible harm to a patient might be considered malpractice, ask yourself, “Did I breach my professional duty?”
Physicians have a duty to practice within their specialty’s standard of care, and if they do this, they should not be held liable even if their treatments cause adverse effects. Each jurisdiction defines the standard of care differently, but the general expectation is “that physicians acting within the ambit of their professional work will exercise the skill, knowledge, and care normally possessed and exercised by other members of their profession…in the relevant medical community.”1
It’s impossible to describe all the skills, knowledge, and care a psychiatrist normally employs when prescribing a drug, but elements of good practice include reasonable efforts to:
- make an appropriate diagnosis
- offer appropriate treatment
- monitor effects of treatment.
Further, treatment should occur only when a patient gives informed consent. Let’s examine each of these elements as they apply to Dr. A and Mr. B.
- Submit your malpractice-related questions to Dr. Mossman at douglas.mossman@dowdenhealth.com.
- Include your name, address, and practice location. If your question is chosen for publication, your name can be withheld by request.
- All readers who submit questions will be included in quarterly drawings for a $50 gift certificate for Professional Risk Management Services, Inc’s online market-place of risk management publications and resources (www.prms.com).
Table 1
Elements of a successful negligence case
|
| Source: Reference 1 |
Appropriate assessment
Despite the availability of guidelines for psychiatric evaluation,2,3 it is tough to summarize everything psychiatrists do when assessing patients. But—focusing on Dr. A’s question—it is reasonable to ask: Did the psychiatric evaluation provide reasonably good evidence that Mr. B had a condition that topiramate might alleviate? Mr. B’s strong desire to keep taking the drug suggests that the answer is “yes.”
Dr. A also should consider potential interactions between topiramate and any other medications that Mr. B is taking. A prudent clinician must judge whether the potential benefit of topiramate for Mr. B outweighs the risk of adverse effects. If Mr. B actually had developed a kidney stone, Dr. A might seek a nephrologist’s advice about how to minimize the risk of recurrence.
Appropriate treatment
Topiramate is FDA-approved only for treating seizures and for prophylaxis against migraine headaches. However, FDA approval limits only how pharmaceutical companies can promote a medication.4 Physicians may prescribe drugs for unapproved “off-label” uses, and doing so is accepted medical practice. Peer-reviewed publications support using topiramate to treat agitation,5 alcohol dependence,6 binge-eating disorder,7 and other conditions that psychiatrists often manage. A tendency to promote weight loss has made topiramate an attractive add-on medication for patients whose weight problems are causing other health difficulties.8
Assuming that Mr. B is taking topiramate for an off-label purpose, an appropriate question to ask is, “Does professional literature support use of topiramate in Mr. B’s circumstances?” Also, given everything known about Mr. B up to this point, is topiramate a good treatment choice?
Appropriate monitoring
As every clinician knows, medications can cause problems. Monitoring topiramate therapy involves periodic lab testing and assessment of effectiveness. Dr. A should feel reasonably sure that Mr. B—assisted by a family member or close friend, if necessary—can and will cooperate with monitoring requirements. Dr. A also should verify that Mr. B can grasp and follow instructions designed to avert complications—such as ample hydration to reduce risk of nephrolithiasis—and will promptly address problems if they occur.
Informed consent
Informed consent is especially important when a patient receives a treatment that has a known risk. Although the Physician’s Desk Reference does not list previous kidney stones as a contraindication to topiramate therapy, it urges caution under these circumstances.4 Therefore, if Dr. A wishes to prescribe topiramate for a patient with a history of kidney stone, the patient should meaningfully collaborate in the treatment decision.
Informed consent for treatment requires that patients not feel coerced by the doctor or setting and have the mental capacity or competence to give consent. Under the conceptualization developed by Appelbaum and Grisso,9 competent patients can:
- express a consistent choice
- understand medical information provided to them
- appreciate how this information applies to them and their condition
- reason logically about treatment.
What information should patients receive before giving consent? The legal standard varies, but in most U.S. jurisdictions, patients “are entitled to material information about the nature of any proposed medical procedure. For example, patients are entitled to information about the risks of the procedure, its necessity, and alternate procedures that might be preferable.”1 Topiramate’s manufacturer instructs physicians to question and warn patients about the risk of kidney stones—which Dr. A did in Mr. B’s case. When you prescribe a drug off-label, you may want to tell patients this, but explain why the drug is appropriate nonetheless.
Table 2
Evaluating a patient’s capacity to consent to treatment
| Is this patient able to? | Questions to ask |
|---|---|
| Express a clear treatment preference | What treatment have you chosen? |
| Understand basic information communicated by caregivers | Can you tell me in your own words about your condition and the treatment options I have told you about? |
| Appreciate his or her medical condition and how information about treatment applies | What do you think is wrong with your health now? Do you think you need some kind of treatment? What do you think treatment will do for you? |
| Reason logically when choosing treatment options | Why did you choose this treatment? Why is it better than your other treatment options? |
| Source: Adapted and reprinted with permission from Appelbaum PS. Assessment of patients’ competence to consent to treatment. N Engl J Med 2007;357:1834-40 | |
1. Dobbs DB. The law of torts. St. Paul, MN: West Group; 2000:269.
2. King RA. Practice parameters for the psychiatric assessment of children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(10 suppl):4S-20S.
3. American Psychiatric Association. Practice guideline for psychiatric evaluation of adults. Am J Psychiatry 1995;152(11 suppl):63-80.
4. Physicians’ Desk Reference. 62 ed. Montvale, NJ: Thomson Healthcare Inc.; 2007.
5. Guay DR. Newer antiepileptic drugs in the management of agitation/aggression in patients with dementia or developmental disability. Consult Pharm 2007;22:1004-34.
6. Johnson BA, Rosenthal N, Capece JA, et al. Topiramate for Alcoholism Advisory Board; Topiramate for Alcoholism Study Group. Topiramate for treating alcohol dependence: a randomized controlled trial. JAMA. 2007;298:1641-51.
7. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of binge eating disorder associated with obesity: a randomized, placebo-controlled trial. Am J Psychiatry 2003;160:255-61.
8. Kirov G, Tredget J. Add-on topiramate reduces weight in overweight patients with affective disorders: a clinical case series. BMC Psychiatry 2005;5(1):19.-
9. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med 1988;319:1635-8.
10. Appelbaum PS. Assessment of patients’ competence to consent to treatment. N Engl J Med 2007;357:1834-40.
Dear Dr. Mossman,
I prescribed topiramate for Mr. B, a patient with no history of kidney stones. Many months later he developed back pain. During the medical workup for a possible kidney stone, Mr. B and I revisited the risk of kidney stones with topiramate, which we had discussed at the beginning of therapy. Mr. B was adamantly opposed to stopping topiramate, even if he had a kidney stone. Testing revealed that Mr. B did not have a stone, but I wasn’t sure how to proceed. I worried that I might be found liable if Mr. B stayed on topiramate and did develop a kidney stone.—Submitted by Dr. A
When a patient develops a medical problem from a drug you prescribed, it is natural to feel responsible—after all, your treatment caused the adverse event. But did you commit malpractice? To answer this, let’s review the concept of “medical negligence.”
Malpractice law applies legal principles of negligence to professional conduct.1 The elements of a negligence case (Table 1) can be summarized as “breach of duty causing damages.” Therefore, when you wonder whether possible harm to a patient might be considered malpractice, ask yourself, “Did I breach my professional duty?”
Physicians have a duty to practice within their specialty’s standard of care, and if they do this, they should not be held liable even if their treatments cause adverse effects. Each jurisdiction defines the standard of care differently, but the general expectation is “that physicians acting within the ambit of their professional work will exercise the skill, knowledge, and care normally possessed and exercised by other members of their profession…in the relevant medical community.”1
It’s impossible to describe all the skills, knowledge, and care a psychiatrist normally employs when prescribing a drug, but elements of good practice include reasonable efforts to:
- make an appropriate diagnosis
- offer appropriate treatment
- monitor effects of treatment.
Further, treatment should occur only when a patient gives informed consent. Let’s examine each of these elements as they apply to Dr. A and Mr. B.
- Submit your malpractice-related questions to Dr. Mossman at douglas.mossman@dowdenhealth.com.
- Include your name, address, and practice location. If your question is chosen for publication, your name can be withheld by request.
- All readers who submit questions will be included in quarterly drawings for a $50 gift certificate for Professional Risk Management Services, Inc’s online market-place of risk management publications and resources (www.prms.com).
Table 1
Elements of a successful negligence case
|
| Source: Reference 1 |
Appropriate assessment
Despite the availability of guidelines for psychiatric evaluation,2,3 it is tough to summarize everything psychiatrists do when assessing patients. But—focusing on Dr. A’s question—it is reasonable to ask: Did the psychiatric evaluation provide reasonably good evidence that Mr. B had a condition that topiramate might alleviate? Mr. B’s strong desire to keep taking the drug suggests that the answer is “yes.”
Dr. A also should consider potential interactions between topiramate and any other medications that Mr. B is taking. A prudent clinician must judge whether the potential benefit of topiramate for Mr. B outweighs the risk of adverse effects. If Mr. B actually had developed a kidney stone, Dr. A might seek a nephrologist’s advice about how to minimize the risk of recurrence.
Appropriate treatment
Topiramate is FDA-approved only for treating seizures and for prophylaxis against migraine headaches. However, FDA approval limits only how pharmaceutical companies can promote a medication.4 Physicians may prescribe drugs for unapproved “off-label” uses, and doing so is accepted medical practice. Peer-reviewed publications support using topiramate to treat agitation,5 alcohol dependence,6 binge-eating disorder,7 and other conditions that psychiatrists often manage. A tendency to promote weight loss has made topiramate an attractive add-on medication for patients whose weight problems are causing other health difficulties.8
Assuming that Mr. B is taking topiramate for an off-label purpose, an appropriate question to ask is, “Does professional literature support use of topiramate in Mr. B’s circumstances?” Also, given everything known about Mr. B up to this point, is topiramate a good treatment choice?
Appropriate monitoring
As every clinician knows, medications can cause problems. Monitoring topiramate therapy involves periodic lab testing and assessment of effectiveness. Dr. A should feel reasonably sure that Mr. B—assisted by a family member or close friend, if necessary—can and will cooperate with monitoring requirements. Dr. A also should verify that Mr. B can grasp and follow instructions designed to avert complications—such as ample hydration to reduce risk of nephrolithiasis—and will promptly address problems if they occur.
Informed consent
Informed consent is especially important when a patient receives a treatment that has a known risk. Although the Physician’s Desk Reference does not list previous kidney stones as a contraindication to topiramate therapy, it urges caution under these circumstances.4 Therefore, if Dr. A wishes to prescribe topiramate for a patient with a history of kidney stone, the patient should meaningfully collaborate in the treatment decision.
Informed consent for treatment requires that patients not feel coerced by the doctor or setting and have the mental capacity or competence to give consent. Under the conceptualization developed by Appelbaum and Grisso,9 competent patients can:
- express a consistent choice
- understand medical information provided to them
- appreciate how this information applies to them and their condition
- reason logically about treatment.
What information should patients receive before giving consent? The legal standard varies, but in most U.S. jurisdictions, patients “are entitled to material information about the nature of any proposed medical procedure. For example, patients are entitled to information about the risks of the procedure, its necessity, and alternate procedures that might be preferable.”1 Topiramate’s manufacturer instructs physicians to question and warn patients about the risk of kidney stones—which Dr. A did in Mr. B’s case. When you prescribe a drug off-label, you may want to tell patients this, but explain why the drug is appropriate nonetheless.
Table 2
Evaluating a patient’s capacity to consent to treatment
| Is this patient able to? | Questions to ask |
|---|---|
| Express a clear treatment preference | What treatment have you chosen? |
| Understand basic information communicated by caregivers | Can you tell me in your own words about your condition and the treatment options I have told you about? |
| Appreciate his or her medical condition and how information about treatment applies | What do you think is wrong with your health now? Do you think you need some kind of treatment? What do you think treatment will do for you? |
| Reason logically when choosing treatment options | Why did you choose this treatment? Why is it better than your other treatment options? |
| Source: Adapted and reprinted with permission from Appelbaum PS. Assessment of patients’ competence to consent to treatment. N Engl J Med 2007;357:1834-40 | |
Dear Dr. Mossman,
I prescribed topiramate for Mr. B, a patient with no history of kidney stones. Many months later he developed back pain. During the medical workup for a possible kidney stone, Mr. B and I revisited the risk of kidney stones with topiramate, which we had discussed at the beginning of therapy. Mr. B was adamantly opposed to stopping topiramate, even if he had a kidney stone. Testing revealed that Mr. B did not have a stone, but I wasn’t sure how to proceed. I worried that I might be found liable if Mr. B stayed on topiramate and did develop a kidney stone.—Submitted by Dr. A
When a patient develops a medical problem from a drug you prescribed, it is natural to feel responsible—after all, your treatment caused the adverse event. But did you commit malpractice? To answer this, let’s review the concept of “medical negligence.”
Malpractice law applies legal principles of negligence to professional conduct.1 The elements of a negligence case (Table 1) can be summarized as “breach of duty causing damages.” Therefore, when you wonder whether possible harm to a patient might be considered malpractice, ask yourself, “Did I breach my professional duty?”
Physicians have a duty to practice within their specialty’s standard of care, and if they do this, they should not be held liable even if their treatments cause adverse effects. Each jurisdiction defines the standard of care differently, but the general expectation is “that physicians acting within the ambit of their professional work will exercise the skill, knowledge, and care normally possessed and exercised by other members of their profession…in the relevant medical community.”1
It’s impossible to describe all the skills, knowledge, and care a psychiatrist normally employs when prescribing a drug, but elements of good practice include reasonable efforts to:
- make an appropriate diagnosis
- offer appropriate treatment
- monitor effects of treatment.
Further, treatment should occur only when a patient gives informed consent. Let’s examine each of these elements as they apply to Dr. A and Mr. B.
- Submit your malpractice-related questions to Dr. Mossman at douglas.mossman@dowdenhealth.com.
- Include your name, address, and practice location. If your question is chosen for publication, your name can be withheld by request.
- All readers who submit questions will be included in quarterly drawings for a $50 gift certificate for Professional Risk Management Services, Inc’s online market-place of risk management publications and resources (www.prms.com).
Table 1
Elements of a successful negligence case
|
| Source: Reference 1 |
Appropriate assessment
Despite the availability of guidelines for psychiatric evaluation,2,3 it is tough to summarize everything psychiatrists do when assessing patients. But—focusing on Dr. A’s question—it is reasonable to ask: Did the psychiatric evaluation provide reasonably good evidence that Mr. B had a condition that topiramate might alleviate? Mr. B’s strong desire to keep taking the drug suggests that the answer is “yes.”
Dr. A also should consider potential interactions between topiramate and any other medications that Mr. B is taking. A prudent clinician must judge whether the potential benefit of topiramate for Mr. B outweighs the risk of adverse effects. If Mr. B actually had developed a kidney stone, Dr. A might seek a nephrologist’s advice about how to minimize the risk of recurrence.
Appropriate treatment
Topiramate is FDA-approved only for treating seizures and for prophylaxis against migraine headaches. However, FDA approval limits only how pharmaceutical companies can promote a medication.4 Physicians may prescribe drugs for unapproved “off-label” uses, and doing so is accepted medical practice. Peer-reviewed publications support using topiramate to treat agitation,5 alcohol dependence,6 binge-eating disorder,7 and other conditions that psychiatrists often manage. A tendency to promote weight loss has made topiramate an attractive add-on medication for patients whose weight problems are causing other health difficulties.8
Assuming that Mr. B is taking topiramate for an off-label purpose, an appropriate question to ask is, “Does professional literature support use of topiramate in Mr. B’s circumstances?” Also, given everything known about Mr. B up to this point, is topiramate a good treatment choice?
Appropriate monitoring
As every clinician knows, medications can cause problems. Monitoring topiramate therapy involves periodic lab testing and assessment of effectiveness. Dr. A should feel reasonably sure that Mr. B—assisted by a family member or close friend, if necessary—can and will cooperate with monitoring requirements. Dr. A also should verify that Mr. B can grasp and follow instructions designed to avert complications—such as ample hydration to reduce risk of nephrolithiasis—and will promptly address problems if they occur.
Informed consent
Informed consent is especially important when a patient receives a treatment that has a known risk. Although the Physician’s Desk Reference does not list previous kidney stones as a contraindication to topiramate therapy, it urges caution under these circumstances.4 Therefore, if Dr. A wishes to prescribe topiramate for a patient with a history of kidney stone, the patient should meaningfully collaborate in the treatment decision.
Informed consent for treatment requires that patients not feel coerced by the doctor or setting and have the mental capacity or competence to give consent. Under the conceptualization developed by Appelbaum and Grisso,9 competent patients can:
- express a consistent choice
- understand medical information provided to them
- appreciate how this information applies to them and their condition
- reason logically about treatment.
What information should patients receive before giving consent? The legal standard varies, but in most U.S. jurisdictions, patients “are entitled to material information about the nature of any proposed medical procedure. For example, patients are entitled to information about the risks of the procedure, its necessity, and alternate procedures that might be preferable.”1 Topiramate’s manufacturer instructs physicians to question and warn patients about the risk of kidney stones—which Dr. A did in Mr. B’s case. When you prescribe a drug off-label, you may want to tell patients this, but explain why the drug is appropriate nonetheless.
Table 2
Evaluating a patient’s capacity to consent to treatment
| Is this patient able to? | Questions to ask |
|---|---|
| Express a clear treatment preference | What treatment have you chosen? |
| Understand basic information communicated by caregivers | Can you tell me in your own words about your condition and the treatment options I have told you about? |
| Appreciate his or her medical condition and how information about treatment applies | What do you think is wrong with your health now? Do you think you need some kind of treatment? What do you think treatment will do for you? |
| Reason logically when choosing treatment options | Why did you choose this treatment? Why is it better than your other treatment options? |
| Source: Adapted and reprinted with permission from Appelbaum PS. Assessment of patients’ competence to consent to treatment. N Engl J Med 2007;357:1834-40 | |
1. Dobbs DB. The law of torts. St. Paul, MN: West Group; 2000:269.
2. King RA. Practice parameters for the psychiatric assessment of children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(10 suppl):4S-20S.
3. American Psychiatric Association. Practice guideline for psychiatric evaluation of adults. Am J Psychiatry 1995;152(11 suppl):63-80.
4. Physicians’ Desk Reference. 62 ed. Montvale, NJ: Thomson Healthcare Inc.; 2007.
5. Guay DR. Newer antiepileptic drugs in the management of agitation/aggression in patients with dementia or developmental disability. Consult Pharm 2007;22:1004-34.
6. Johnson BA, Rosenthal N, Capece JA, et al. Topiramate for Alcoholism Advisory Board; Topiramate for Alcoholism Study Group. Topiramate for treating alcohol dependence: a randomized controlled trial. JAMA. 2007;298:1641-51.
7. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of binge eating disorder associated with obesity: a randomized, placebo-controlled trial. Am J Psychiatry 2003;160:255-61.
8. Kirov G, Tredget J. Add-on topiramate reduces weight in overweight patients with affective disorders: a clinical case series. BMC Psychiatry 2005;5(1):19.-
9. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med 1988;319:1635-8.
10. Appelbaum PS. Assessment of patients’ competence to consent to treatment. N Engl J Med 2007;357:1834-40.
1. Dobbs DB. The law of torts. St. Paul, MN: West Group; 2000:269.
2. King RA. Practice parameters for the psychiatric assessment of children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(10 suppl):4S-20S.
3. American Psychiatric Association. Practice guideline for psychiatric evaluation of adults. Am J Psychiatry 1995;152(11 suppl):63-80.
4. Physicians’ Desk Reference. 62 ed. Montvale, NJ: Thomson Healthcare Inc.; 2007.
5. Guay DR. Newer antiepileptic drugs in the management of agitation/aggression in patients with dementia or developmental disability. Consult Pharm 2007;22:1004-34.
6. Johnson BA, Rosenthal N, Capece JA, et al. Topiramate for Alcoholism Advisory Board; Topiramate for Alcoholism Study Group. Topiramate for treating alcohol dependence: a randomized controlled trial. JAMA. 2007;298:1641-51.
7. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of binge eating disorder associated with obesity: a randomized, placebo-controlled trial. Am J Psychiatry 2003;160:255-61.
8. Kirov G, Tredget J. Add-on topiramate reduces weight in overweight patients with affective disorders: a clinical case series. BMC Psychiatry 2005;5(1):19.-
9. Appelbaum PS, Grisso T. Assessing patients’ capacities to consent to treatment. N Engl J Med 1988;319:1635-8.
10. Appelbaum PS. Assessment of patients’ competence to consent to treatment. N Engl J Med 2007;357:1834-40.
Heparin contaminant identified
The US Food and Drug Administration (FDA) has identified the structure and source of the contaminant found in lots of heparin.
The contaminant, which has been linked to severe allergic reactions and deaths, was found in crude lots of heparin at a Chinese processing plant. The substance has been identified as over-sulfated chondroitin sulfate.
Researchers initially had difficulty identifying the contaminant because it is so similar to heparin. Over-sulfated chondroitin sulfate has approximately the same molecular weight as heparin, and both materials belong to the class of molecules known as glucosaminoglycans (GAGs).
It is still unknown whether the over-sulfated chondroitin sulfate was a byproduct of the heparin production process or if it was intentionally added to the active pharmaceutical ingredient.
After learning about the source of the over-sulfated chondroitin sulfate, the FDA issued a border alert that requires all finished heparin, as well as heparin source material, to be tested before it is allowed into the US. Five heparin manufacturers, companies that supply most of the heparin used in this country, have agreed to conduct the tests.
Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said the agency would test heparin products made by companies that cannot conduct the testing themselves. Any product that is not tested or fails the tests will be destroyed.
Scientific Protein Laboratories is the company that supplied crude heparin from the Changzhou plant in China to the biopharmaceutical company Baxter. Scientific Protein Laboratories has said it is cooperating with the FDA, and the Changzhou plant is not currently producing heparin.
In addition to the new testing instituted at the US borders, the FDA said heparin testing is now being conducted worldwide. Germany and Japan are among the countries that have started testing.
Germany recalled heparin last week after a cluster of about 100 serious allergic reactions, including hypotension and anaphylaxis. Japan has also recalled heparin but has not reported any adverse events linked to heparin injections.
Both Scientific Protein Laboratories and Baxter have conducted massive voluntary recalls of heparin products. Since Baxter recalled all of its heparin vials, there have been no additional deaths.
Last week, the FDA received 785 reports of adverse events associated with heparin. Those reports included 46 deaths, but Dr Woodcock said only 19 were related to the allergic profile associated with the Baxter heparin.
Baxter has said it cannot confirm that heparin has caused any fatalities as a result of an allergic reaction. The company said there are 4 cases in which patients received Baxter heparin and suffered an allergic-type reaction to the drug.
Baxter also said there is not yet enough medical data available to draw a firm conclusion that the reaction caused death. In each of these cases, the patient had multiple underlying complex medical conditions. Three of the 4 patients had undergone, or were in the process of undergoing, invasive cardiac surgery.
The heparin saga began January 17 of this year, when Baxter recalled the first batch of heparin after receiving reports of the allergic reactions. Recalls of the drug have continued since that time.
The FDA released the news of the contaminant’s source March 14 and the discovery of its structure March 19. 
The US Food and Drug Administration (FDA) has identified the structure and source of the contaminant found in lots of heparin.
The contaminant, which has been linked to severe allergic reactions and deaths, was found in crude lots of heparin at a Chinese processing plant. The substance has been identified as over-sulfated chondroitin sulfate.
Researchers initially had difficulty identifying the contaminant because it is so similar to heparin. Over-sulfated chondroitin sulfate has approximately the same molecular weight as heparin, and both materials belong to the class of molecules known as glucosaminoglycans (GAGs).
It is still unknown whether the over-sulfated chondroitin sulfate was a byproduct of the heparin production process or if it was intentionally added to the active pharmaceutical ingredient.
After learning about the source of the over-sulfated chondroitin sulfate, the FDA issued a border alert that requires all finished heparin, as well as heparin source material, to be tested before it is allowed into the US. Five heparin manufacturers, companies that supply most of the heparin used in this country, have agreed to conduct the tests.
Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said the agency would test heparin products made by companies that cannot conduct the testing themselves. Any product that is not tested or fails the tests will be destroyed.
Scientific Protein Laboratories is the company that supplied crude heparin from the Changzhou plant in China to the biopharmaceutical company Baxter. Scientific Protein Laboratories has said it is cooperating with the FDA, and the Changzhou plant is not currently producing heparin.
In addition to the new testing instituted at the US borders, the FDA said heparin testing is now being conducted worldwide. Germany and Japan are among the countries that have started testing.
Germany recalled heparin last week after a cluster of about 100 serious allergic reactions, including hypotension and anaphylaxis. Japan has also recalled heparin but has not reported any adverse events linked to heparin injections.
Both Scientific Protein Laboratories and Baxter have conducted massive voluntary recalls of heparin products. Since Baxter recalled all of its heparin vials, there have been no additional deaths.
Last week, the FDA received 785 reports of adverse events associated with heparin. Those reports included 46 deaths, but Dr Woodcock said only 19 were related to the allergic profile associated with the Baxter heparin.
Baxter has said it cannot confirm that heparin has caused any fatalities as a result of an allergic reaction. The company said there are 4 cases in which patients received Baxter heparin and suffered an allergic-type reaction to the drug.
Baxter also said there is not yet enough medical data available to draw a firm conclusion that the reaction caused death. In each of these cases, the patient had multiple underlying complex medical conditions. Three of the 4 patients had undergone, or were in the process of undergoing, invasive cardiac surgery.
The heparin saga began January 17 of this year, when Baxter recalled the first batch of heparin after receiving reports of the allergic reactions. Recalls of the drug have continued since that time.
The FDA released the news of the contaminant’s source March 14 and the discovery of its structure March 19.
The US Food and Drug Administration (FDA) has identified the structure and source of the contaminant found in lots of heparin.
The contaminant, which has been linked to severe allergic reactions and deaths, was found in crude lots of heparin at a Chinese processing plant. The substance has been identified as over-sulfated chondroitin sulfate.
Researchers initially had difficulty identifying the contaminant because it is so similar to heparin. Over-sulfated chondroitin sulfate has approximately the same molecular weight as heparin, and both materials belong to the class of molecules known as glucosaminoglycans (GAGs).
It is still unknown whether the over-sulfated chondroitin sulfate was a byproduct of the heparin production process or if it was intentionally added to the active pharmaceutical ingredient.
After learning about the source of the over-sulfated chondroitin sulfate, the FDA issued a border alert that requires all finished heparin, as well as heparin source material, to be tested before it is allowed into the US. Five heparin manufacturers, companies that supply most of the heparin used in this country, have agreed to conduct the tests.
Janet Woodcock, MD, director of the FDA’s Center for Drug Evaluation and Research, said the agency would test heparin products made by companies that cannot conduct the testing themselves. Any product that is not tested or fails the tests will be destroyed.
Scientific Protein Laboratories is the company that supplied crude heparin from the Changzhou plant in China to the biopharmaceutical company Baxter. Scientific Protein Laboratories has said it is cooperating with the FDA, and the Changzhou plant is not currently producing heparin.
In addition to the new testing instituted at the US borders, the FDA said heparin testing is now being conducted worldwide. Germany and Japan are among the countries that have started testing.
Germany recalled heparin last week after a cluster of about 100 serious allergic reactions, including hypotension and anaphylaxis. Japan has also recalled heparin but has not reported any adverse events linked to heparin injections.
Both Scientific Protein Laboratories and Baxter have conducted massive voluntary recalls of heparin products. Since Baxter recalled all of its heparin vials, there have been no additional deaths.
Last week, the FDA received 785 reports of adverse events associated with heparin. Those reports included 46 deaths, but Dr Woodcock said only 19 were related to the allergic profile associated with the Baxter heparin.
Baxter has said it cannot confirm that heparin has caused any fatalities as a result of an allergic reaction. The company said there are 4 cases in which patients received Baxter heparin and suffered an allergic-type reaction to the drug.
Baxter also said there is not yet enough medical data available to draw a firm conclusion that the reaction caused death. In each of these cases, the patient had multiple underlying complex medical conditions. Three of the 4 patients had undergone, or were in the process of undergoing, invasive cardiac surgery.
The heparin saga began January 17 of this year, when Baxter recalled the first batch of heparin after receiving reports of the allergic reactions. Recalls of the drug have continued since that time.
The FDA released the news of the contaminant’s source March 14 and the discovery of its structure March 19.
Proceedings of the 2nd Heart-Brain Summit
Supplement Editor:
Marc S. Penn, MD, PhD
Contents*†
Introduction: Heart-brain medicine: Update 2007
Marc S. Penn, MD, PhD, and Earl E. Bakken, MD, HonC, (3) SciDHon
Depression in coronary artery disease: Does treatment help?
Peter A. Shapiro, MD
Case study in heart-brain interplay: A 53-year-old woman recovering from mitral valve repair
Thomas D. Callahan, IV, MD; Ubaid Khokhar, MD; Leo Pozuelo, MD; and James B. Young, MD
Emotional predictors and behavioral triggers of acute coronary syndrome
Karina W. Davidson, PhD
Impacts of depression and emotional distress on cardiac disease
Wei Jiang, MD
Inflammation as a link between brain injury and heart damage: The model of subarachnoid hemorrhage
Hazem Antar Mashaly, MD, and J. Javier Provencio, MD
Biofeedback: An overview in the context of heart-brain medicine
Michael G. McKee, PhD
Biofeedback therapy in cardiovascular disease: Rationale and research overview
Christine S. Moravec, PhD
Helping children and adults with hypnosis and biofeedback
Karen Olness, MD
Clinical hypnosis for reduction of atrial fibrillation after coronary artery bypass graft surgery
Roberto Novoa, MD, and Tracy Hammonds, BA
Depression and coronary heart disease: Association and implications for treatment
James A. Blumenthal, PhD
Cardiovascular autonomic dysfunction in patients with movement disorders
Benjamin L. Walter, MD
Deep brain stimulation: How does it work?
Jerrold L. Vitek, MD, PhD
Sudden unexpected death in epilepsy: Impact, mechanisms, and prevention
Lara Jehi, MD, and Imad M. Najm, MD
Evaluating brain function in patients with disorders of consciousness
Tristan Bekinschtein, PhD, and Facundo Manes, MD
Preconditioning paradigms and pathways in the brain
Karl B. Shpargel; Walid Jalabi, PhD; Yongming Jin; Alisher Dadabayev, MD; Marc S. Penn, MD, PhD,
and Bruce D. Trapp, PhD
Post-stroke exercise rehabilitation:What we know about retraining the motor system and how it may apply to retraining the heart
Andreas Luft, MD; Richard Macko, MD; Larry Forrester, PhD; Andrew Goldberg, MD; and Daniel F. Hanley, MD
Hippocampal volume change in the Alzheimer Disease Cholesterol-Lowering Treatment trial
D. Larry Sparks, PhD; Susan K. Lemieux, PhD; Marc W. Haut, PhD; Leslie C. Baxter, PhD; Sterling C. Johnson, PhD; Lisa M. Sparks, BS; Hemalatha Sampath, BSEE; Jean E. Lopez, RN; Marwan H. Sabbagh, MD; and Donald J. Connor, PhD
Heart-brain interactions in cardiac arrhythmias: Role of the autonomic nervous system
Douglas P. Zipes, MD
Insular Alzheimer disease pathology and the psychometric correlates of mortality
Donald R. Royall, MD
Poster abstracts
* These proceedings represent the large majority of presentations at the 2nd Heart-Brain Summit, but five Summit presentations were not able to be captured for publication here.
† Articles in these proceedings were either submitted as manuscripts by the Summit faculty or developed by the Cleveland Clinic Journal of Medicine staff from transcripts of audiotaped Summit presentations and then revised and approved by the Summit faculty.
Supplement Editor:
Marc S. Penn, MD, PhD
Contents*†
Introduction: Heart-brain medicine: Update 2007
Marc S. Penn, MD, PhD, and Earl E. Bakken, MD, HonC, (3) SciDHon
Depression in coronary artery disease: Does treatment help?
Peter A. Shapiro, MD
Case study in heart-brain interplay: A 53-year-old woman recovering from mitral valve repair
Thomas D. Callahan, IV, MD; Ubaid Khokhar, MD; Leo Pozuelo, MD; and James B. Young, MD
Emotional predictors and behavioral triggers of acute coronary syndrome
Karina W. Davidson, PhD
Impacts of depression and emotional distress on cardiac disease
Wei Jiang, MD
Inflammation as a link between brain injury and heart damage: The model of subarachnoid hemorrhage
Hazem Antar Mashaly, MD, and J. Javier Provencio, MD
Biofeedback: An overview in the context of heart-brain medicine
Michael G. McKee, PhD
Biofeedback therapy in cardiovascular disease: Rationale and research overview
Christine S. Moravec, PhD
Helping children and adults with hypnosis and biofeedback
Karen Olness, MD
Clinical hypnosis for reduction of atrial fibrillation after coronary artery bypass graft surgery
Roberto Novoa, MD, and Tracy Hammonds, BA
Depression and coronary heart disease: Association and implications for treatment
James A. Blumenthal, PhD
Cardiovascular autonomic dysfunction in patients with movement disorders
Benjamin L. Walter, MD
Deep brain stimulation: How does it work?
Jerrold L. Vitek, MD, PhD
Sudden unexpected death in epilepsy: Impact, mechanisms, and prevention
Lara Jehi, MD, and Imad M. Najm, MD
Evaluating brain function in patients with disorders of consciousness
Tristan Bekinschtein, PhD, and Facundo Manes, MD
Preconditioning paradigms and pathways in the brain
Karl B. Shpargel; Walid Jalabi, PhD; Yongming Jin; Alisher Dadabayev, MD; Marc S. Penn, MD, PhD,
and Bruce D. Trapp, PhD
Post-stroke exercise rehabilitation:What we know about retraining the motor system and how it may apply to retraining the heart
Andreas Luft, MD; Richard Macko, MD; Larry Forrester, PhD; Andrew Goldberg, MD; and Daniel F. Hanley, MD
Hippocampal volume change in the Alzheimer Disease Cholesterol-Lowering Treatment trial
D. Larry Sparks, PhD; Susan K. Lemieux, PhD; Marc W. Haut, PhD; Leslie C. Baxter, PhD; Sterling C. Johnson, PhD; Lisa M. Sparks, BS; Hemalatha Sampath, BSEE; Jean E. Lopez, RN; Marwan H. Sabbagh, MD; and Donald J. Connor, PhD
Heart-brain interactions in cardiac arrhythmias: Role of the autonomic nervous system
Douglas P. Zipes, MD
Insular Alzheimer disease pathology and the psychometric correlates of mortality
Donald R. Royall, MD
Poster abstracts
* These proceedings represent the large majority of presentations at the 2nd Heart-Brain Summit, but five Summit presentations were not able to be captured for publication here.
† Articles in these proceedings were either submitted as manuscripts by the Summit faculty or developed by the Cleveland Clinic Journal of Medicine staff from transcripts of audiotaped Summit presentations and then revised and approved by the Summit faculty.
Supplement Editor:
Marc S. Penn, MD, PhD
Contents*†
Introduction: Heart-brain medicine: Update 2007
Marc S. Penn, MD, PhD, and Earl E. Bakken, MD, HonC, (3) SciDHon
Depression in coronary artery disease: Does treatment help?
Peter A. Shapiro, MD
Case study in heart-brain interplay: A 53-year-old woman recovering from mitral valve repair
Thomas D. Callahan, IV, MD; Ubaid Khokhar, MD; Leo Pozuelo, MD; and James B. Young, MD
Emotional predictors and behavioral triggers of acute coronary syndrome
Karina W. Davidson, PhD
Impacts of depression and emotional distress on cardiac disease
Wei Jiang, MD
Inflammation as a link between brain injury and heart damage: The model of subarachnoid hemorrhage
Hazem Antar Mashaly, MD, and J. Javier Provencio, MD
Biofeedback: An overview in the context of heart-brain medicine
Michael G. McKee, PhD
Biofeedback therapy in cardiovascular disease: Rationale and research overview
Christine S. Moravec, PhD
Helping children and adults with hypnosis and biofeedback
Karen Olness, MD
Clinical hypnosis for reduction of atrial fibrillation after coronary artery bypass graft surgery
Roberto Novoa, MD, and Tracy Hammonds, BA
Depression and coronary heart disease: Association and implications for treatment
James A. Blumenthal, PhD
Cardiovascular autonomic dysfunction in patients with movement disorders
Benjamin L. Walter, MD
Deep brain stimulation: How does it work?
Jerrold L. Vitek, MD, PhD
Sudden unexpected death in epilepsy: Impact, mechanisms, and prevention
Lara Jehi, MD, and Imad M. Najm, MD
Evaluating brain function in patients with disorders of consciousness
Tristan Bekinschtein, PhD, and Facundo Manes, MD
Preconditioning paradigms and pathways in the brain
Karl B. Shpargel; Walid Jalabi, PhD; Yongming Jin; Alisher Dadabayev, MD; Marc S. Penn, MD, PhD,
and Bruce D. Trapp, PhD
Post-stroke exercise rehabilitation:What we know about retraining the motor system and how it may apply to retraining the heart
Andreas Luft, MD; Richard Macko, MD; Larry Forrester, PhD; Andrew Goldberg, MD; and Daniel F. Hanley, MD
Hippocampal volume change in the Alzheimer Disease Cholesterol-Lowering Treatment trial
D. Larry Sparks, PhD; Susan K. Lemieux, PhD; Marc W. Haut, PhD; Leslie C. Baxter, PhD; Sterling C. Johnson, PhD; Lisa M. Sparks, BS; Hemalatha Sampath, BSEE; Jean E. Lopez, RN; Marwan H. Sabbagh, MD; and Donald J. Connor, PhD
Heart-brain interactions in cardiac arrhythmias: Role of the autonomic nervous system
Douglas P. Zipes, MD
Insular Alzheimer disease pathology and the psychometric correlates of mortality
Donald R. Royall, MD
Poster abstracts
* These proceedings represent the large majority of presentations at the 2nd Heart-Brain Summit, but five Summit presentations were not able to be captured for publication here.
† Articles in these proceedings were either submitted as manuscripts by the Summit faculty or developed by the Cleveland Clinic Journal of Medicine staff from transcripts of audiotaped Summit presentations and then revised and approved by the Summit faculty.
Post-stroke exercise rehabilitation: What we know about retraining the motor system and how it may apply to retraining the heart
Ideally, rehabilitation following a stroke that leads to functional deficit will result in a rapid return to normal function. In the real world, however, a rapid improvement in function is rarely achieved. Between 80% and 90% of stroke survivors have a motor deficit, with impairments in walking being the most common motor deficits.1 Most stroke survivors have a diminished fitness reserve that is stable and resistant to routine rehabilitative interventions. Recent research has begun to assess the value of exercise and other modalities of training during this period of stability to improve function long after cessation of other therapeutic interventions. This article will review this research and provide insight into those issues in post-stroke rehabilitation that remain to be addressed and may affect heart and brain physiology.
STROKE REDUCES AEROBIC CAPACITY
At all ages, the fitness level of stroke survivors, as measured by maximum oxygen consumption, is reduced by approximately 50% below that of an age-matched normal population. In a study comparing peak oxygen consumption during treadmill walking between stroke survivors and age-matched sedentary controls, we found that the stroke participants had an approximately 50% lower level of peak fitness relative to the control subjects.2 During treadmill walking at self-selected speeds, the stroke volunteers used 75% of their functional capacity, compared with 27% for the age-matched healthy controls. Furthermore, compared with the controls, the stroke subjects demonstrated a poorer economy of gait that required greater oxygen consumption to sustain their self-selected walking speeds.
CLINICAL TRIALS OF POST-STROKE EXERCISE REHABILITATION
In light of the efficacy of treadmill exercise in cardiac rehabilitation, we are evaluating whether treadmill exercise can similarly improve fitness, endurance, and walking velocity in stroke survivors. We have completed 6 months of treadmill training in two separate cohorts that show highly consistent results in terms of improved walking abilities in hemiparetic stroke subjects.3,4 A third cohort is in progress to confirm these findings and examine the effects of intensity on the functional benefits5 and mechanisms6 underlying the effects of treadmill training.
Treadmill exercise results in functional benefits and improved glucose metabolism
The first cohort was a before-and-after comparison of stable stroke survivors who underwent a three-times-weekly treadmill exercise program for 6 months.3 Peak exercise capacity testing (VO2peak) revealed functional benefits with minimal cardiac and injury risk compared with baseline, demonstrating the feasibility and safety of treadmill exercise therapy in stroke-impaired adults.
Potential mechanisms for the benefits
These findings raise the question of whether these beneficial effects of treadmill exercise are attributable to muscle training effects, cardiopulmonary circulatory training effects, or perhaps neural mechanisms involving economy of gait movements and neuroplasticity of the motor system.
This question is being examined in our third cohort, now under investigation. This cohort will evaluate the effects of treadmill exercise on 32 chronically disabled stroke survivors in a single-center study design that is randomizing 64 subjects to 6 months of three-times-weekly treadmill training or conventional physiotherapy.6 Similar to our prior studies, subjects are randomized at least 6 months after their index stroke; this lengthy interval is deliberate because subjects are considered to be in a “plateau” phase of recovery, as they have previously completed rehabilitative therapy.
Activation will be measured in five prespecified “regions of interest”: the precentral gyrus, the postcentral gyrus, the supplementary motor area, the midbrain, and the cerebellum (anterior/posterior lobes). Difference activation maps of post-training minus pretraining fMRIs of paretic knee movement across all patients undergoing treadmill therapy will then be analyzed. The control group, which will receive dose-matched stretching activity from physical therapy, can be contrasted by comparing the patterns of pre/post differences in each region. This will allow for assessment of increased regional activation in the brain that should be specific to the treadmill training intervention. Furthermore, if a specifically localized regional activation difference is found, then individual fMRI and VO2 training responses (VO2peak, increase in walking speeds) can be correlated to further assess the relationship between regional activation and magnitude of functional response to the treadmill intervention.
DISCUSSION AND CONCLUSIONS
Central control of walking
Control of gait in animals is mediated by the cortex, brainstem/cerebellum,9,10 and spinal cord—the so-called cervical gait and lumbar gait pattern-generating areas of the spinal cord. In humans, cortical and spinal gait pattern areas are thought to be major regulatory centers of ambulation. Whether the cortical areas influence ambulatory recovery mediated by exercise training or whether the recruitment of spinal gait areas is needed to improve motor control after stroke is not known in humans. We will test the hypothesis that the recruitment of cortical and/or subcortical areas is relevant to some or all of the exercise-induced neuroplasticity response to treadmill rehabilitation. If a consistent pattern of brain regional activation is associated with an improvement in walking ability, this finding will suggest potential brain targets for neurally directed rehabilitation interventions. If brain targets for rehabilitation produce viable therapeutic improvement in walking and cardiocirculatory performance (such as VO2), this will be further evidence of heart-brain interactions.
Future research directions
Studies to date demonstrate that long-term treadmill exercise affects both the brain and cardiac physiology. This has holistic implications for the function of the whole person as well. Yet several pressing issues continue to confront researchers in post-stroke rehabilitation. One is the optimal therapeutic target and the intensity of the rehabilitative effort. Is this improvement solely a response of muscle and cardiac tissue to exercise, or is it possible that improved neuromotor control is a critical component to a major recovery of walking function? Furthermore, the most efficacious elements of rehabilitative therapy are not known. Should treadmill training be high- or low-intensity, and should it be accompanied by strength training, agility and flexibility activities, or other elements directed at reacquisition of finer degrees of gait-related motor training and neuropsychological input, as achieved by tai-chi or yoga? Another issue is the proper dose of rehabilitative therapy, which has barely been explored, although recent preliminary work suggests that the response is dose-dependent. Finally, predictors of response have not been established because the mechanisms of therapy and surrogate markers for early response are not well understood.
Our future research plans are to assess whether a better understanding of neural targets for rehabilitative treatment will be a fruitful avenue to improve recovery. Additionally, this plan will assess whether fMRI can serve as a surrogate marker of recovery by offering a noninvasive means to measure response to rehabilitation.
- Mayo NE, Wood-Dauphinee S, Ahmed S, et al. Disablement following stroke. Disabil Rehabil 1999; 21:258–268.
- Michael K, Macko RF. Ambulatory activity intensity profiles, fitness, and fatigue in chronic stroke. Top Stroke Rehabil 2007; 14:5–12.
- Macko RF, Smith GV, Dobrovolny CL, Sorkin JD, Goldberg AP, Silver KH. Treadmill training improves fitness reserve in chronic stroke patients. Arch Phys Med Rehabil 2001; 82:879–884.
- Macko RF, Ivey FM, Forrester LW, et al. Treadmill exercise rehabilitation improves ambulatory function and cardiovascular fitness in patients with chronic stroke. A randomized, controlled trial. Stroke 2005; 36:2206–2211.
- Ivey FM, Ryan AS, Hafer-Macko CE, Goldberg AP, Macko RF. Treadmill aerobic training improves glucose tolerance and indices of insulin sensitivity in disabled stroke survivors: a preliminary report. Stroke 2007; 38:2752–2758.
- Luft AR, Macko R, Forrester L, Villagra F, Hanley D. Subcortical reorganization induced by aerobic locomotor training in chronic stroke survivors [abstract]. Poster presented at: Annual Meeting of the Society for Neuroscience; November 15, 2005; Washington, DC.
- Luft AR, Smith GV, Forrester L, et al. Comparing brain activation associated with isolated upper and lower limb movement across corresponding joints. Hum Brain Mapping 2002; 17:131–140.
- Luft AR, Forrester L, Macko RF, et al. Brain activation of lower extremity movement in chronically impaired stroke survivors. Neuroimage 2005; 26:184–194.
- Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. I. The effects of bilateral pyramidal lesions. Brain 1968; 91:1–14.
- Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. II. The effects of lesions of the descending brain-stem pathways. Brain 1968; 91:15–36.
Ideally, rehabilitation following a stroke that leads to functional deficit will result in a rapid return to normal function. In the real world, however, a rapid improvement in function is rarely achieved. Between 80% and 90% of stroke survivors have a motor deficit, with impairments in walking being the most common motor deficits.1 Most stroke survivors have a diminished fitness reserve that is stable and resistant to routine rehabilitative interventions. Recent research has begun to assess the value of exercise and other modalities of training during this period of stability to improve function long after cessation of other therapeutic interventions. This article will review this research and provide insight into those issues in post-stroke rehabilitation that remain to be addressed and may affect heart and brain physiology.
STROKE REDUCES AEROBIC CAPACITY
At all ages, the fitness level of stroke survivors, as measured by maximum oxygen consumption, is reduced by approximately 50% below that of an age-matched normal population. In a study comparing peak oxygen consumption during treadmill walking between stroke survivors and age-matched sedentary controls, we found that the stroke participants had an approximately 50% lower level of peak fitness relative to the control subjects.2 During treadmill walking at self-selected speeds, the stroke volunteers used 75% of their functional capacity, compared with 27% for the age-matched healthy controls. Furthermore, compared with the controls, the stroke subjects demonstrated a poorer economy of gait that required greater oxygen consumption to sustain their self-selected walking speeds.
CLINICAL TRIALS OF POST-STROKE EXERCISE REHABILITATION
In light of the efficacy of treadmill exercise in cardiac rehabilitation, we are evaluating whether treadmill exercise can similarly improve fitness, endurance, and walking velocity in stroke survivors. We have completed 6 months of treadmill training in two separate cohorts that show highly consistent results in terms of improved walking abilities in hemiparetic stroke subjects.3,4 A third cohort is in progress to confirm these findings and examine the effects of intensity on the functional benefits5 and mechanisms6 underlying the effects of treadmill training.
Treadmill exercise results in functional benefits and improved glucose metabolism
The first cohort was a before-and-after comparison of stable stroke survivors who underwent a three-times-weekly treadmill exercise program for 6 months.3 Peak exercise capacity testing (VO2peak) revealed functional benefits with minimal cardiac and injury risk compared with baseline, demonstrating the feasibility and safety of treadmill exercise therapy in stroke-impaired adults.
Potential mechanisms for the benefits
These findings raise the question of whether these beneficial effects of treadmill exercise are attributable to muscle training effects, cardiopulmonary circulatory training effects, or perhaps neural mechanisms involving economy of gait movements and neuroplasticity of the motor system.
This question is being examined in our third cohort, now under investigation. This cohort will evaluate the effects of treadmill exercise on 32 chronically disabled stroke survivors in a single-center study design that is randomizing 64 subjects to 6 months of three-times-weekly treadmill training or conventional physiotherapy.6 Similar to our prior studies, subjects are randomized at least 6 months after their index stroke; this lengthy interval is deliberate because subjects are considered to be in a “plateau” phase of recovery, as they have previously completed rehabilitative therapy.
Activation will be measured in five prespecified “regions of interest”: the precentral gyrus, the postcentral gyrus, the supplementary motor area, the midbrain, and the cerebellum (anterior/posterior lobes). Difference activation maps of post-training minus pretraining fMRIs of paretic knee movement across all patients undergoing treadmill therapy will then be analyzed. The control group, which will receive dose-matched stretching activity from physical therapy, can be contrasted by comparing the patterns of pre/post differences in each region. This will allow for assessment of increased regional activation in the brain that should be specific to the treadmill training intervention. Furthermore, if a specifically localized regional activation difference is found, then individual fMRI and VO2 training responses (VO2peak, increase in walking speeds) can be correlated to further assess the relationship between regional activation and magnitude of functional response to the treadmill intervention.
DISCUSSION AND CONCLUSIONS
Central control of walking
Control of gait in animals is mediated by the cortex, brainstem/cerebellum,9,10 and spinal cord—the so-called cervical gait and lumbar gait pattern-generating areas of the spinal cord. In humans, cortical and spinal gait pattern areas are thought to be major regulatory centers of ambulation. Whether the cortical areas influence ambulatory recovery mediated by exercise training or whether the recruitment of spinal gait areas is needed to improve motor control after stroke is not known in humans. We will test the hypothesis that the recruitment of cortical and/or subcortical areas is relevant to some or all of the exercise-induced neuroplasticity response to treadmill rehabilitation. If a consistent pattern of brain regional activation is associated with an improvement in walking ability, this finding will suggest potential brain targets for neurally directed rehabilitation interventions. If brain targets for rehabilitation produce viable therapeutic improvement in walking and cardiocirculatory performance (such as VO2), this will be further evidence of heart-brain interactions.
Future research directions
Studies to date demonstrate that long-term treadmill exercise affects both the brain and cardiac physiology. This has holistic implications for the function of the whole person as well. Yet several pressing issues continue to confront researchers in post-stroke rehabilitation. One is the optimal therapeutic target and the intensity of the rehabilitative effort. Is this improvement solely a response of muscle and cardiac tissue to exercise, or is it possible that improved neuromotor control is a critical component to a major recovery of walking function? Furthermore, the most efficacious elements of rehabilitative therapy are not known. Should treadmill training be high- or low-intensity, and should it be accompanied by strength training, agility and flexibility activities, or other elements directed at reacquisition of finer degrees of gait-related motor training and neuropsychological input, as achieved by tai-chi or yoga? Another issue is the proper dose of rehabilitative therapy, which has barely been explored, although recent preliminary work suggests that the response is dose-dependent. Finally, predictors of response have not been established because the mechanisms of therapy and surrogate markers for early response are not well understood.
Our future research plans are to assess whether a better understanding of neural targets for rehabilitative treatment will be a fruitful avenue to improve recovery. Additionally, this plan will assess whether fMRI can serve as a surrogate marker of recovery by offering a noninvasive means to measure response to rehabilitation.
Ideally, rehabilitation following a stroke that leads to functional deficit will result in a rapid return to normal function. In the real world, however, a rapid improvement in function is rarely achieved. Between 80% and 90% of stroke survivors have a motor deficit, with impairments in walking being the most common motor deficits.1 Most stroke survivors have a diminished fitness reserve that is stable and resistant to routine rehabilitative interventions. Recent research has begun to assess the value of exercise and other modalities of training during this period of stability to improve function long after cessation of other therapeutic interventions. This article will review this research and provide insight into those issues in post-stroke rehabilitation that remain to be addressed and may affect heart and brain physiology.
STROKE REDUCES AEROBIC CAPACITY
At all ages, the fitness level of stroke survivors, as measured by maximum oxygen consumption, is reduced by approximately 50% below that of an age-matched normal population. In a study comparing peak oxygen consumption during treadmill walking between stroke survivors and age-matched sedentary controls, we found that the stroke participants had an approximately 50% lower level of peak fitness relative to the control subjects.2 During treadmill walking at self-selected speeds, the stroke volunteers used 75% of their functional capacity, compared with 27% for the age-matched healthy controls. Furthermore, compared with the controls, the stroke subjects demonstrated a poorer economy of gait that required greater oxygen consumption to sustain their self-selected walking speeds.
CLINICAL TRIALS OF POST-STROKE EXERCISE REHABILITATION
In light of the efficacy of treadmill exercise in cardiac rehabilitation, we are evaluating whether treadmill exercise can similarly improve fitness, endurance, and walking velocity in stroke survivors. We have completed 6 months of treadmill training in two separate cohorts that show highly consistent results in terms of improved walking abilities in hemiparetic stroke subjects.3,4 A third cohort is in progress to confirm these findings and examine the effects of intensity on the functional benefits5 and mechanisms6 underlying the effects of treadmill training.
Treadmill exercise results in functional benefits and improved glucose metabolism
The first cohort was a before-and-after comparison of stable stroke survivors who underwent a three-times-weekly treadmill exercise program for 6 months.3 Peak exercise capacity testing (VO2peak) revealed functional benefits with minimal cardiac and injury risk compared with baseline, demonstrating the feasibility and safety of treadmill exercise therapy in stroke-impaired adults.
Potential mechanisms for the benefits
These findings raise the question of whether these beneficial effects of treadmill exercise are attributable to muscle training effects, cardiopulmonary circulatory training effects, or perhaps neural mechanisms involving economy of gait movements and neuroplasticity of the motor system.
This question is being examined in our third cohort, now under investigation. This cohort will evaluate the effects of treadmill exercise on 32 chronically disabled stroke survivors in a single-center study design that is randomizing 64 subjects to 6 months of three-times-weekly treadmill training or conventional physiotherapy.6 Similar to our prior studies, subjects are randomized at least 6 months after their index stroke; this lengthy interval is deliberate because subjects are considered to be in a “plateau” phase of recovery, as they have previously completed rehabilitative therapy.
Activation will be measured in five prespecified “regions of interest”: the precentral gyrus, the postcentral gyrus, the supplementary motor area, the midbrain, and the cerebellum (anterior/posterior lobes). Difference activation maps of post-training minus pretraining fMRIs of paretic knee movement across all patients undergoing treadmill therapy will then be analyzed. The control group, which will receive dose-matched stretching activity from physical therapy, can be contrasted by comparing the patterns of pre/post differences in each region. This will allow for assessment of increased regional activation in the brain that should be specific to the treadmill training intervention. Furthermore, if a specifically localized regional activation difference is found, then individual fMRI and VO2 training responses (VO2peak, increase in walking speeds) can be correlated to further assess the relationship between regional activation and magnitude of functional response to the treadmill intervention.
DISCUSSION AND CONCLUSIONS
Central control of walking
Control of gait in animals is mediated by the cortex, brainstem/cerebellum,9,10 and spinal cord—the so-called cervical gait and lumbar gait pattern-generating areas of the spinal cord. In humans, cortical and spinal gait pattern areas are thought to be major regulatory centers of ambulation. Whether the cortical areas influence ambulatory recovery mediated by exercise training or whether the recruitment of spinal gait areas is needed to improve motor control after stroke is not known in humans. We will test the hypothesis that the recruitment of cortical and/or subcortical areas is relevant to some or all of the exercise-induced neuroplasticity response to treadmill rehabilitation. If a consistent pattern of brain regional activation is associated with an improvement in walking ability, this finding will suggest potential brain targets for neurally directed rehabilitation interventions. If brain targets for rehabilitation produce viable therapeutic improvement in walking and cardiocirculatory performance (such as VO2), this will be further evidence of heart-brain interactions.
Future research directions
Studies to date demonstrate that long-term treadmill exercise affects both the brain and cardiac physiology. This has holistic implications for the function of the whole person as well. Yet several pressing issues continue to confront researchers in post-stroke rehabilitation. One is the optimal therapeutic target and the intensity of the rehabilitative effort. Is this improvement solely a response of muscle and cardiac tissue to exercise, or is it possible that improved neuromotor control is a critical component to a major recovery of walking function? Furthermore, the most efficacious elements of rehabilitative therapy are not known. Should treadmill training be high- or low-intensity, and should it be accompanied by strength training, agility and flexibility activities, or other elements directed at reacquisition of finer degrees of gait-related motor training and neuropsychological input, as achieved by tai-chi or yoga? Another issue is the proper dose of rehabilitative therapy, which has barely been explored, although recent preliminary work suggests that the response is dose-dependent. Finally, predictors of response have not been established because the mechanisms of therapy and surrogate markers for early response are not well understood.
Our future research plans are to assess whether a better understanding of neural targets for rehabilitative treatment will be a fruitful avenue to improve recovery. Additionally, this plan will assess whether fMRI can serve as a surrogate marker of recovery by offering a noninvasive means to measure response to rehabilitation.
- Mayo NE, Wood-Dauphinee S, Ahmed S, et al. Disablement following stroke. Disabil Rehabil 1999; 21:258–268.
- Michael K, Macko RF. Ambulatory activity intensity profiles, fitness, and fatigue in chronic stroke. Top Stroke Rehabil 2007; 14:5–12.
- Macko RF, Smith GV, Dobrovolny CL, Sorkin JD, Goldberg AP, Silver KH. Treadmill training improves fitness reserve in chronic stroke patients. Arch Phys Med Rehabil 2001; 82:879–884.
- Macko RF, Ivey FM, Forrester LW, et al. Treadmill exercise rehabilitation improves ambulatory function and cardiovascular fitness in patients with chronic stroke. A randomized, controlled trial. Stroke 2005; 36:2206–2211.
- Ivey FM, Ryan AS, Hafer-Macko CE, Goldberg AP, Macko RF. Treadmill aerobic training improves glucose tolerance and indices of insulin sensitivity in disabled stroke survivors: a preliminary report. Stroke 2007; 38:2752–2758.
- Luft AR, Macko R, Forrester L, Villagra F, Hanley D. Subcortical reorganization induced by aerobic locomotor training in chronic stroke survivors [abstract]. Poster presented at: Annual Meeting of the Society for Neuroscience; November 15, 2005; Washington, DC.
- Luft AR, Smith GV, Forrester L, et al. Comparing brain activation associated with isolated upper and lower limb movement across corresponding joints. Hum Brain Mapping 2002; 17:131–140.
- Luft AR, Forrester L, Macko RF, et al. Brain activation of lower extremity movement in chronically impaired stroke survivors. Neuroimage 2005; 26:184–194.
- Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. I. The effects of bilateral pyramidal lesions. Brain 1968; 91:1–14.
- Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. II. The effects of lesions of the descending brain-stem pathways. Brain 1968; 91:15–36.
- Mayo NE, Wood-Dauphinee S, Ahmed S, et al. Disablement following stroke. Disabil Rehabil 1999; 21:258–268.
- Michael K, Macko RF. Ambulatory activity intensity profiles, fitness, and fatigue in chronic stroke. Top Stroke Rehabil 2007; 14:5–12.
- Macko RF, Smith GV, Dobrovolny CL, Sorkin JD, Goldberg AP, Silver KH. Treadmill training improves fitness reserve in chronic stroke patients. Arch Phys Med Rehabil 2001; 82:879–884.
- Macko RF, Ivey FM, Forrester LW, et al. Treadmill exercise rehabilitation improves ambulatory function and cardiovascular fitness in patients with chronic stroke. A randomized, controlled trial. Stroke 2005; 36:2206–2211.
- Ivey FM, Ryan AS, Hafer-Macko CE, Goldberg AP, Macko RF. Treadmill aerobic training improves glucose tolerance and indices of insulin sensitivity in disabled stroke survivors: a preliminary report. Stroke 2007; 38:2752–2758.
- Luft AR, Macko R, Forrester L, Villagra F, Hanley D. Subcortical reorganization induced by aerobic locomotor training in chronic stroke survivors [abstract]. Poster presented at: Annual Meeting of the Society for Neuroscience; November 15, 2005; Washington, DC.
- Luft AR, Smith GV, Forrester L, et al. Comparing brain activation associated with isolated upper and lower limb movement across corresponding joints. Hum Brain Mapping 2002; 17:131–140.
- Luft AR, Forrester L, Macko RF, et al. Brain activation of lower extremity movement in chronically impaired stroke survivors. Neuroimage 2005; 26:184–194.
- Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. I. The effects of bilateral pyramidal lesions. Brain 1968; 91:1–14.
- Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. II. The effects of lesions of the descending brain-stem pathways. Brain 1968; 91:15–36.
Team Approach
Team Approach
Question: We work with a large orthopedic group. We would like to propose a more formal structure to this. We are interested in building business and partnerships. Do you know of any articles or references to support hospitalists doing this, or any sources to show the orthopedic group we can and would improve outcomes and their work life and workload?
Julie Lepzinski, director,
hospitalist medicine group,
Michigan
Dr. Hospitalist responds: I commend you and your hospitalist group for taking the initiative to develop a relationship with your orthopedics colleagues. Many hospitalist groups are exploring such relationships with not only orthopedists but also with other surgical and medical subspecialists.
As you mentioned, the opportunity exists to improve your group’s income and improve orthopedist work life. More importantly, there is a real opportunity to improve the medical care of patients admitted to the hospital primarily with orthopedic problems.
There are published data from an academic medical center on a hospitalist-orthopedics co-management model. Huddleston, et al., studied the effect of such a co-management model on the care of patients after elective hip and knee arthroplasty at the Mayo Clinic.1 They found that “the co-management medical hospitalist-orthopedic team model reduced minor postoperative complication rates with no statistically significant difference in length of stay or cost. The nurses and surgeons strongly preferred the co-management hospitalist model.”
This study would seem to support your notion that orthopedists may prefer the involvement of hospitalists in the care of their patients. Hospitalist involvement reduced minor complications (urinary tract infections, fever, electrolyte abnormalities). However, investigators did not find that hospitalist co-management reduced major postoperative complications (death, myocardial infarction, renal failure requiring hemodialysis) or intermediate ones (heart failure, pulmonary embolus, ileus, pneumonia).
Mayo Clinic hospitalists also studied the impact of a hospitalist-orthopedist co-management model of the care on elderly patients admitted to their hospital with hip fracture.2 Phy, et al., found that, “In elderly patients with hip fracture, a hospitalist model decreased time to surgery, time from surgery to dismissal and length of stay without adversely affecting inpatient deaths or 30-day readmission rates.” This study demonstrated that hospitalist co-management can decrease hospital length of stay in this population of patients.
We should recognize the obvious limitations of these studies. They were done at a single large academic institution with a largely Caucasian population at the turn of the century (2000-2001), early in the hospitalist movement. The hospitalist movement has matured, with approximately 20,000 hospitalists in the country. I hope we will soon see more robust data coming from multicenter trials that include a more diverse population of patients as well as a mix of community and academic institutions.
Start an HMG?
Question: We own a medical clinic in Arizona and are thinking of starting a hospitalist group as a separate business entity. Are you aware of any recommended reading or articles on how to start one, if it’s profitable, and in what shape or form? And most important--regarding the current trends and projections--I wonder if the need has changed, as most hospitals reduce their number of vendors.
Shawn Toloui, president and owner,
1st Care Medical Clinic,
Phoenix, Ariz.
Dr. Hospitalist responds: These are the kind of questions people have been asking since the term “hospitalist” was coined in 1996. Over the past decade, we have seen an explosion in the number of hospitalists in the country. Few folks in the 1990s thought there would be 20,000 hospitalists today.
If I understand you correctly, you are concerned that because many hospitals are reducing their numbers of vendors, this may have an adverse effect on the need for hospitalists. Hospitals will engage in business relationships with hospitalists as long as the hospitalists can bring solutions to problems and fulfill needs. To understand this better, let’s examine the reasons the numbers of hospitalists have grown over the past decade.
Costs: When Medicare started paying hospitals based on diagnosis-related groups (DRGs) in the early ’80s, this forced hospitals to “manage” patients’ length of stay. The DRG system pays a fixed fee regardless of the length of stay but allows for an adjusted higher payment based on a hospital’s case mix index (a measure of how “sick” patients are in a given hospital).
This reimbursement system encourages hospitals to take care of ill patients but also to “manage” their length of stay. It is difficult for doctors to manage any hospitalized patients from outpatient offices, let alone sick patients. Hospitals and payers found that hospitalists are able to manage sick patients and reduce costs, mostly by being available to admit, manage, and discharge patients in a timely manner. This increased throughput of patients also allows hospitals to put another patient in a bed sooner, bringing additional revenue.
Quality: By serendipity, the hospitalist movement coincided with the quality movement. Hospitalists have helped reduce variations in care by working locally to develop and implement clinical-care pathways. Hospitalists have also served as partners for hospitals to achieve compliance with payer quality mandates.
For example, in 2003, Medicare began requiring hospitals to report a handful of diagnosis-based quality measures it called the Core Measures. The number of measures continues to grow. In 2007, Medicare tied hospital reimbursement to performance on the Core Measures. I hear from hospital administrators that they find it easier to educate and work with a small group of hospitalists, rather than a large medical staff, to achieve optimal results on these measures.
Satisfaction: The exodus of primary care physicians (PCPs) from the hospital has fueled much of the growth in hospital medicine. PCPs have found it increasingly difficult to care for hospitalized patients while juggling the demands of a busy outpatient practice. In hospitalists, nurses have found a physician partner who is available physically to work with them in the care of acutely ill patients.
PCPs and nurses have been very satisfied with the hospitalist model of care. Although provider satisfaction is important, satisfaction in healthcare begins and ends with patients. Despite the discontinuity of care of meeting a new provider during hospitalization, patients have been satisfied with hospitalist care. Patients view hospitalists as providers available to provide for their acute needs while also communicating with the patients’ outpatient providers to understand their long-term needs.
I expect the number of hospitalists to grow over the next decade, albeit at a slower pace as most programs begin to fill their available positions. SHM believes the numbers of hospitalists will grow to 40,000.
There are a number of resources that can help you understand how to develop, manage, and grow a hospitalist program. I suggest you visit the “Practice Resources” section of the SHM Web site at www.hospitalmedicine.org. In particular, I recommend the “Best Practices in Managing a Hospital Medicine Program,” held twice a year. The spring program is held in conjunction with the SHM Annual Meeting in San Diego, April 3-5. The fall program is held in conjunction with the University of California, San Francisco’s “Management of the Hospitalized Patient” course in San Francisco. Also, the book Hospitalists: A Guide to Building and Sustaining a Successful Program by SHM Senior Vice President Joe Miller and SHM cofounders John Nelson, MD, and Winthrop F. Whitcomb, MD, is a must read for anybody looking to build a hospitalist program. TH
References
- Huddleston JM, Long KH, Naessens JM, Vanness DJ, Larson D, Trousdale R, Plevak M, et al. Medical and surgical comanagement after elective hip and knee arthroplasty. Ann Intern Med. 2004 July 6;141(1):28-38.
- Phy MP, Vanness DJ, Melton JL, Hallong K, Schleck C, Larson DR, Huddleston PM. et al. Effects of a hospitalist model on elderly patients with hip fracture. Arch Intern Med. 2005;165:796-801.
Team Approach
Question: We work with a large orthopedic group. We would like to propose a more formal structure to this. We are interested in building business and partnerships. Do you know of any articles or references to support hospitalists doing this, or any sources to show the orthopedic group we can and would improve outcomes and their work life and workload?
Julie Lepzinski, director,
hospitalist medicine group,
Michigan
Dr. Hospitalist responds: I commend you and your hospitalist group for taking the initiative to develop a relationship with your orthopedics colleagues. Many hospitalist groups are exploring such relationships with not only orthopedists but also with other surgical and medical subspecialists.
As you mentioned, the opportunity exists to improve your group’s income and improve orthopedist work life. More importantly, there is a real opportunity to improve the medical care of patients admitted to the hospital primarily with orthopedic problems.
There are published data from an academic medical center on a hospitalist-orthopedics co-management model. Huddleston, et al., studied the effect of such a co-management model on the care of patients after elective hip and knee arthroplasty at the Mayo Clinic.1 They found that “the co-management medical hospitalist-orthopedic team model reduced minor postoperative complication rates with no statistically significant difference in length of stay or cost. The nurses and surgeons strongly preferred the co-management hospitalist model.”
This study would seem to support your notion that orthopedists may prefer the involvement of hospitalists in the care of their patients. Hospitalist involvement reduced minor complications (urinary tract infections, fever, electrolyte abnormalities). However, investigators did not find that hospitalist co-management reduced major postoperative complications (death, myocardial infarction, renal failure requiring hemodialysis) or intermediate ones (heart failure, pulmonary embolus, ileus, pneumonia).
Mayo Clinic hospitalists also studied the impact of a hospitalist-orthopedist co-management model of the care on elderly patients admitted to their hospital with hip fracture.2 Phy, et al., found that, “In elderly patients with hip fracture, a hospitalist model decreased time to surgery, time from surgery to dismissal and length of stay without adversely affecting inpatient deaths or 30-day readmission rates.” This study demonstrated that hospitalist co-management can decrease hospital length of stay in this population of patients.
We should recognize the obvious limitations of these studies. They were done at a single large academic institution with a largely Caucasian population at the turn of the century (2000-2001), early in the hospitalist movement. The hospitalist movement has matured, with approximately 20,000 hospitalists in the country. I hope we will soon see more robust data coming from multicenter trials that include a more diverse population of patients as well as a mix of community and academic institutions.
Start an HMG?
Question: We own a medical clinic in Arizona and are thinking of starting a hospitalist group as a separate business entity. Are you aware of any recommended reading or articles on how to start one, if it’s profitable, and in what shape or form? And most important--regarding the current trends and projections--I wonder if the need has changed, as most hospitals reduce their number of vendors.
Shawn Toloui, president and owner,
1st Care Medical Clinic,
Phoenix, Ariz.
Dr. Hospitalist responds: These are the kind of questions people have been asking since the term “hospitalist” was coined in 1996. Over the past decade, we have seen an explosion in the number of hospitalists in the country. Few folks in the 1990s thought there would be 20,000 hospitalists today.
If I understand you correctly, you are concerned that because many hospitals are reducing their numbers of vendors, this may have an adverse effect on the need for hospitalists. Hospitals will engage in business relationships with hospitalists as long as the hospitalists can bring solutions to problems and fulfill needs. To understand this better, let’s examine the reasons the numbers of hospitalists have grown over the past decade.
Costs: When Medicare started paying hospitals based on diagnosis-related groups (DRGs) in the early ’80s, this forced hospitals to “manage” patients’ length of stay. The DRG system pays a fixed fee regardless of the length of stay but allows for an adjusted higher payment based on a hospital’s case mix index (a measure of how “sick” patients are in a given hospital).
This reimbursement system encourages hospitals to take care of ill patients but also to “manage” their length of stay. It is difficult for doctors to manage any hospitalized patients from outpatient offices, let alone sick patients. Hospitals and payers found that hospitalists are able to manage sick patients and reduce costs, mostly by being available to admit, manage, and discharge patients in a timely manner. This increased throughput of patients also allows hospitals to put another patient in a bed sooner, bringing additional revenue.
Quality: By serendipity, the hospitalist movement coincided with the quality movement. Hospitalists have helped reduce variations in care by working locally to develop and implement clinical-care pathways. Hospitalists have also served as partners for hospitals to achieve compliance with payer quality mandates.
For example, in 2003, Medicare began requiring hospitals to report a handful of diagnosis-based quality measures it called the Core Measures. The number of measures continues to grow. In 2007, Medicare tied hospital reimbursement to performance on the Core Measures. I hear from hospital administrators that they find it easier to educate and work with a small group of hospitalists, rather than a large medical staff, to achieve optimal results on these measures.
Satisfaction: The exodus of primary care physicians (PCPs) from the hospital has fueled much of the growth in hospital medicine. PCPs have found it increasingly difficult to care for hospitalized patients while juggling the demands of a busy outpatient practice. In hospitalists, nurses have found a physician partner who is available physically to work with them in the care of acutely ill patients.
PCPs and nurses have been very satisfied with the hospitalist model of care. Although provider satisfaction is important, satisfaction in healthcare begins and ends with patients. Despite the discontinuity of care of meeting a new provider during hospitalization, patients have been satisfied with hospitalist care. Patients view hospitalists as providers available to provide for their acute needs while also communicating with the patients’ outpatient providers to understand their long-term needs.
I expect the number of hospitalists to grow over the next decade, albeit at a slower pace as most programs begin to fill their available positions. SHM believes the numbers of hospitalists will grow to 40,000.
There are a number of resources that can help you understand how to develop, manage, and grow a hospitalist program. I suggest you visit the “Practice Resources” section of the SHM Web site at www.hospitalmedicine.org. In particular, I recommend the “Best Practices in Managing a Hospital Medicine Program,” held twice a year. The spring program is held in conjunction with the SHM Annual Meeting in San Diego, April 3-5. The fall program is held in conjunction with the University of California, San Francisco’s “Management of the Hospitalized Patient” course in San Francisco. Also, the book Hospitalists: A Guide to Building and Sustaining a Successful Program by SHM Senior Vice President Joe Miller and SHM cofounders John Nelson, MD, and Winthrop F. Whitcomb, MD, is a must read for anybody looking to build a hospitalist program. TH
References
- Huddleston JM, Long KH, Naessens JM, Vanness DJ, Larson D, Trousdale R, Plevak M, et al. Medical and surgical comanagement after elective hip and knee arthroplasty. Ann Intern Med. 2004 July 6;141(1):28-38.
- Phy MP, Vanness DJ, Melton JL, Hallong K, Schleck C, Larson DR, Huddleston PM. et al. Effects of a hospitalist model on elderly patients with hip fracture. Arch Intern Med. 2005;165:796-801.
Team Approach
Question: We work with a large orthopedic group. We would like to propose a more formal structure to this. We are interested in building business and partnerships. Do you know of any articles or references to support hospitalists doing this, or any sources to show the orthopedic group we can and would improve outcomes and their work life and workload?
Julie Lepzinski, director,
hospitalist medicine group,
Michigan
Dr. Hospitalist responds: I commend you and your hospitalist group for taking the initiative to develop a relationship with your orthopedics colleagues. Many hospitalist groups are exploring such relationships with not only orthopedists but also with other surgical and medical subspecialists.
As you mentioned, the opportunity exists to improve your group’s income and improve orthopedist work life. More importantly, there is a real opportunity to improve the medical care of patients admitted to the hospital primarily with orthopedic problems.
There are published data from an academic medical center on a hospitalist-orthopedics co-management model. Huddleston, et al., studied the effect of such a co-management model on the care of patients after elective hip and knee arthroplasty at the Mayo Clinic.1 They found that “the co-management medical hospitalist-orthopedic team model reduced minor postoperative complication rates with no statistically significant difference in length of stay or cost. The nurses and surgeons strongly preferred the co-management hospitalist model.”
This study would seem to support your notion that orthopedists may prefer the involvement of hospitalists in the care of their patients. Hospitalist involvement reduced minor complications (urinary tract infections, fever, electrolyte abnormalities). However, investigators did not find that hospitalist co-management reduced major postoperative complications (death, myocardial infarction, renal failure requiring hemodialysis) or intermediate ones (heart failure, pulmonary embolus, ileus, pneumonia).
Mayo Clinic hospitalists also studied the impact of a hospitalist-orthopedist co-management model of the care on elderly patients admitted to their hospital with hip fracture.2 Phy, et al., found that, “In elderly patients with hip fracture, a hospitalist model decreased time to surgery, time from surgery to dismissal and length of stay without adversely affecting inpatient deaths or 30-day readmission rates.” This study demonstrated that hospitalist co-management can decrease hospital length of stay in this population of patients.
We should recognize the obvious limitations of these studies. They were done at a single large academic institution with a largely Caucasian population at the turn of the century (2000-2001), early in the hospitalist movement. The hospitalist movement has matured, with approximately 20,000 hospitalists in the country. I hope we will soon see more robust data coming from multicenter trials that include a more diverse population of patients as well as a mix of community and academic institutions.
Start an HMG?
Question: We own a medical clinic in Arizona and are thinking of starting a hospitalist group as a separate business entity. Are you aware of any recommended reading or articles on how to start one, if it’s profitable, and in what shape or form? And most important--regarding the current trends and projections--I wonder if the need has changed, as most hospitals reduce their number of vendors.
Shawn Toloui, president and owner,
1st Care Medical Clinic,
Phoenix, Ariz.
Dr. Hospitalist responds: These are the kind of questions people have been asking since the term “hospitalist” was coined in 1996. Over the past decade, we have seen an explosion in the number of hospitalists in the country. Few folks in the 1990s thought there would be 20,000 hospitalists today.
If I understand you correctly, you are concerned that because many hospitals are reducing their numbers of vendors, this may have an adverse effect on the need for hospitalists. Hospitals will engage in business relationships with hospitalists as long as the hospitalists can bring solutions to problems and fulfill needs. To understand this better, let’s examine the reasons the numbers of hospitalists have grown over the past decade.
Costs: When Medicare started paying hospitals based on diagnosis-related groups (DRGs) in the early ’80s, this forced hospitals to “manage” patients’ length of stay. The DRG system pays a fixed fee regardless of the length of stay but allows for an adjusted higher payment based on a hospital’s case mix index (a measure of how “sick” patients are in a given hospital).
This reimbursement system encourages hospitals to take care of ill patients but also to “manage” their length of stay. It is difficult for doctors to manage any hospitalized patients from outpatient offices, let alone sick patients. Hospitals and payers found that hospitalists are able to manage sick patients and reduce costs, mostly by being available to admit, manage, and discharge patients in a timely manner. This increased throughput of patients also allows hospitals to put another patient in a bed sooner, bringing additional revenue.
Quality: By serendipity, the hospitalist movement coincided with the quality movement. Hospitalists have helped reduce variations in care by working locally to develop and implement clinical-care pathways. Hospitalists have also served as partners for hospitals to achieve compliance with payer quality mandates.
For example, in 2003, Medicare began requiring hospitals to report a handful of diagnosis-based quality measures it called the Core Measures. The number of measures continues to grow. In 2007, Medicare tied hospital reimbursement to performance on the Core Measures. I hear from hospital administrators that they find it easier to educate and work with a small group of hospitalists, rather than a large medical staff, to achieve optimal results on these measures.
Satisfaction: The exodus of primary care physicians (PCPs) from the hospital has fueled much of the growth in hospital medicine. PCPs have found it increasingly difficult to care for hospitalized patients while juggling the demands of a busy outpatient practice. In hospitalists, nurses have found a physician partner who is available physically to work with them in the care of acutely ill patients.
PCPs and nurses have been very satisfied with the hospitalist model of care. Although provider satisfaction is important, satisfaction in healthcare begins and ends with patients. Despite the discontinuity of care of meeting a new provider during hospitalization, patients have been satisfied with hospitalist care. Patients view hospitalists as providers available to provide for their acute needs while also communicating with the patients’ outpatient providers to understand their long-term needs.
I expect the number of hospitalists to grow over the next decade, albeit at a slower pace as most programs begin to fill their available positions. SHM believes the numbers of hospitalists will grow to 40,000.
There are a number of resources that can help you understand how to develop, manage, and grow a hospitalist program. I suggest you visit the “Practice Resources” section of the SHM Web site at www.hospitalmedicine.org. In particular, I recommend the “Best Practices in Managing a Hospital Medicine Program,” held twice a year. The spring program is held in conjunction with the SHM Annual Meeting in San Diego, April 3-5. The fall program is held in conjunction with the University of California, San Francisco’s “Management of the Hospitalized Patient” course in San Francisco. Also, the book Hospitalists: A Guide to Building and Sustaining a Successful Program by SHM Senior Vice President Joe Miller and SHM cofounders John Nelson, MD, and Winthrop F. Whitcomb, MD, is a must read for anybody looking to build a hospitalist program. TH
References
- Huddleston JM, Long KH, Naessens JM, Vanness DJ, Larson D, Trousdale R, Plevak M, et al. Medical and surgical comanagement after elective hip and knee arthroplasty. Ann Intern Med. 2004 July 6;141(1):28-38.
- Phy MP, Vanness DJ, Melton JL, Hallong K, Schleck C, Larson DR, Huddleston PM. et al. Effects of a hospitalist model on elderly patients with hip fracture. Arch Intern Med. 2005;165:796-801.
Nocturnal Economics
In my previous column, I reviewed different strategies for providing hospitalist practice night coverage based on the size of the group (February 2008, p. 61). I suggested that dedicated nocturnists are a valuable though expensive asset that any practice larger than about six to eight full-time equivalents (FTE) should consider.
This month, I offer additional thoughts about compensation for nocturnists. I’ll demonstrate why adding dedicated night coverage—in which the doctor working at night doesn’t work during the daytime hours the day before or after the night shift—may not increase practice workload significantly.
What follows is adapted from a new book I co-wrote with Joe Miller, senior vice president of SHM, and Win Whitcomb, MD, a hospitalist at Mercy Medical Center in Springfield, Mass., and co-founder of SHM.1
Compensation
If all hospitalists provide an equal amount of night coverage in rotation (e.g., each member of a four-person group works 61 nights annually), it’s not necessary to adjust the compensation scheme to reflect night work. A night-shift differential in this situation will not influence a doctor’s annual income relative to that of his partner hospitalists.
However, if the hospitalist program seeks more flexibility, it may be advisable to pay more for a night of work than a day of work. Under this scheme, hospitalists may trade day and night work among themselves, leading to enhanced satisfaction. For example, Dr. McCartney is willing to work some of Dr. Lennon’s nights because of the income benefit. Dr. Lennon may or may not work some of Dr. McCartney’s days in return.
If the practice has one or more dedicated nocturnists, they will need to realize some benefit to working only nights. This benefit can take many forms:
- The night hospitalist works less often than day doctors (e.g., day doctors work 220 days annually, night doctors work 182);
- The night hospitalist has a lighter patient load (e.g., a night hospitalist in a small practice typically sleeps three to six hours per night shift while the day doctors typically work a busy eight-to-12-hour shift);
- The night doctor earns more than the day doctors; or
- The night doctor has a higher priority in time-off scheduling.
It is common to combine these benefits. For example a night hospitalist might work less often than day doctors, have a lighter patient load, and earn the same annual income. Anecdotal experience shows that having more income or fewer workdays than day doctors is valued more than a reduced patient load.
For most practices, compensating hospitalists based significantly or entirely on their production can be a good idea but might be problematic for a night doctor. It could lead the night doctor to encourage marginal admissions, some of whom would need to be discharged by the daytime hospitalists hours later. In effect, the night hospitalist could say: “I’ll admit anyone I can get my hands on because my income will increase. I’ll leave it for the day doctors to sort out what to do with all these patients tomorrow.”
An Example
A traditional system of night call (such as pager call from home while also working days) is usually cheaper than dedicated night shifts. And while there are many benefits to having dedicated night shifts, increased patient capacity may not be one of them. Consider the following example:
- On any given day, a five-FTE hospitalist practice has three doctors working, one of whom will be on-call that night by pager;
- That will mean 219 worked days per year for each doctor, one-third of which (73) will be on-call. Each hospitalist gets 146 days off per year;
- The practice decides to switch to dedicated night shifts in which the doctors do not work the day before or after a night shift. The practice wants to retain the 146 days off for each hospitalist. This new coverage arrangement is equivalent to adding 365 shifts annually (one for each night); and
- This will require an additional 1.67 FTE hospitalists (1.67 hospitalists at 219 shifts/year=365).
In this example, by switching from on-call coverage to on-site coverage, the practice increased from five FTEs to 6.67 FTEs. If the daytime work was already enough to keep all three doctors busy, adding 1.67 FTEs for dedicated night shifts may not increase practice productivity or revenue significantly. The practice looks much less productive per FTE (6.67 FTEs are now seeing the volume previously handled by five FTEs) and much costlier.
Changing from traditional night call to dedicated night coverage can be expensive because it may require adding staff yet doesn’t usually increase practice capacity significantly. But it offers other benefits such as those listed in Table 1 (see p. TK). Some practices find they must provide dedicated night coverage to recruit hospitalists. Other institutions choose to support it believing it leads to more timely, efficient, higher-quality care. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. He is also part of the faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Reference
- Miller J, Nelson J, Whitcomb W. Hospitalists: A Guide to Building and Sustaining a Successful Program. Chicago:Health Administration Press;2007:149-150.
In my previous column, I reviewed different strategies for providing hospitalist practice night coverage based on the size of the group (February 2008, p. 61). I suggested that dedicated nocturnists are a valuable though expensive asset that any practice larger than about six to eight full-time equivalents (FTE) should consider.
This month, I offer additional thoughts about compensation for nocturnists. I’ll demonstrate why adding dedicated night coverage—in which the doctor working at night doesn’t work during the daytime hours the day before or after the night shift—may not increase practice workload significantly.
What follows is adapted from a new book I co-wrote with Joe Miller, senior vice president of SHM, and Win Whitcomb, MD, a hospitalist at Mercy Medical Center in Springfield, Mass., and co-founder of SHM.1
Compensation
If all hospitalists provide an equal amount of night coverage in rotation (e.g., each member of a four-person group works 61 nights annually), it’s not necessary to adjust the compensation scheme to reflect night work. A night-shift differential in this situation will not influence a doctor’s annual income relative to that of his partner hospitalists.
However, if the hospitalist program seeks more flexibility, it may be advisable to pay more for a night of work than a day of work. Under this scheme, hospitalists may trade day and night work among themselves, leading to enhanced satisfaction. For example, Dr. McCartney is willing to work some of Dr. Lennon’s nights because of the income benefit. Dr. Lennon may or may not work some of Dr. McCartney’s days in return.
If the practice has one or more dedicated nocturnists, they will need to realize some benefit to working only nights. This benefit can take many forms:
- The night hospitalist works less often than day doctors (e.g., day doctors work 220 days annually, night doctors work 182);
- The night hospitalist has a lighter patient load (e.g., a night hospitalist in a small practice typically sleeps three to six hours per night shift while the day doctors typically work a busy eight-to-12-hour shift);
- The night doctor earns more than the day doctors; or
- The night doctor has a higher priority in time-off scheduling.
It is common to combine these benefits. For example a night hospitalist might work less often than day doctors, have a lighter patient load, and earn the same annual income. Anecdotal experience shows that having more income or fewer workdays than day doctors is valued more than a reduced patient load.
For most practices, compensating hospitalists based significantly or entirely on their production can be a good idea but might be problematic for a night doctor. It could lead the night doctor to encourage marginal admissions, some of whom would need to be discharged by the daytime hospitalists hours later. In effect, the night hospitalist could say: “I’ll admit anyone I can get my hands on because my income will increase. I’ll leave it for the day doctors to sort out what to do with all these patients tomorrow.”
An Example
A traditional system of night call (such as pager call from home while also working days) is usually cheaper than dedicated night shifts. And while there are many benefits to having dedicated night shifts, increased patient capacity may not be one of them. Consider the following example:
- On any given day, a five-FTE hospitalist practice has three doctors working, one of whom will be on-call that night by pager;
- That will mean 219 worked days per year for each doctor, one-third of which (73) will be on-call. Each hospitalist gets 146 days off per year;
- The practice decides to switch to dedicated night shifts in which the doctors do not work the day before or after a night shift. The practice wants to retain the 146 days off for each hospitalist. This new coverage arrangement is equivalent to adding 365 shifts annually (one for each night); and
- This will require an additional 1.67 FTE hospitalists (1.67 hospitalists at 219 shifts/year=365).
In this example, by switching from on-call coverage to on-site coverage, the practice increased from five FTEs to 6.67 FTEs. If the daytime work was already enough to keep all three doctors busy, adding 1.67 FTEs for dedicated night shifts may not increase practice productivity or revenue significantly. The practice looks much less productive per FTE (6.67 FTEs are now seeing the volume previously handled by five FTEs) and much costlier.
Changing from traditional night call to dedicated night coverage can be expensive because it may require adding staff yet doesn’t usually increase practice capacity significantly. But it offers other benefits such as those listed in Table 1 (see p. TK). Some practices find they must provide dedicated night coverage to recruit hospitalists. Other institutions choose to support it believing it leads to more timely, efficient, higher-quality care. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. He is also part of the faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Reference
- Miller J, Nelson J, Whitcomb W. Hospitalists: A Guide to Building and Sustaining a Successful Program. Chicago:Health Administration Press;2007:149-150.
In my previous column, I reviewed different strategies for providing hospitalist practice night coverage based on the size of the group (February 2008, p. 61). I suggested that dedicated nocturnists are a valuable though expensive asset that any practice larger than about six to eight full-time equivalents (FTE) should consider.
This month, I offer additional thoughts about compensation for nocturnists. I’ll demonstrate why adding dedicated night coverage—in which the doctor working at night doesn’t work during the daytime hours the day before or after the night shift—may not increase practice workload significantly.
What follows is adapted from a new book I co-wrote with Joe Miller, senior vice president of SHM, and Win Whitcomb, MD, a hospitalist at Mercy Medical Center in Springfield, Mass., and co-founder of SHM.1
Compensation
If all hospitalists provide an equal amount of night coverage in rotation (e.g., each member of a four-person group works 61 nights annually), it’s not necessary to adjust the compensation scheme to reflect night work. A night-shift differential in this situation will not influence a doctor’s annual income relative to that of his partner hospitalists.
However, if the hospitalist program seeks more flexibility, it may be advisable to pay more for a night of work than a day of work. Under this scheme, hospitalists may trade day and night work among themselves, leading to enhanced satisfaction. For example, Dr. McCartney is willing to work some of Dr. Lennon’s nights because of the income benefit. Dr. Lennon may or may not work some of Dr. McCartney’s days in return.
If the practice has one or more dedicated nocturnists, they will need to realize some benefit to working only nights. This benefit can take many forms:
- The night hospitalist works less often than day doctors (e.g., day doctors work 220 days annually, night doctors work 182);
- The night hospitalist has a lighter patient load (e.g., a night hospitalist in a small practice typically sleeps three to six hours per night shift while the day doctors typically work a busy eight-to-12-hour shift);
- The night doctor earns more than the day doctors; or
- The night doctor has a higher priority in time-off scheduling.
It is common to combine these benefits. For example a night hospitalist might work less often than day doctors, have a lighter patient load, and earn the same annual income. Anecdotal experience shows that having more income or fewer workdays than day doctors is valued more than a reduced patient load.
For most practices, compensating hospitalists based significantly or entirely on their production can be a good idea but might be problematic for a night doctor. It could lead the night doctor to encourage marginal admissions, some of whom would need to be discharged by the daytime hospitalists hours later. In effect, the night hospitalist could say: “I’ll admit anyone I can get my hands on because my income will increase. I’ll leave it for the day doctors to sort out what to do with all these patients tomorrow.”
An Example
A traditional system of night call (such as pager call from home while also working days) is usually cheaper than dedicated night shifts. And while there are many benefits to having dedicated night shifts, increased patient capacity may not be one of them. Consider the following example:
- On any given day, a five-FTE hospitalist practice has three doctors working, one of whom will be on-call that night by pager;
- That will mean 219 worked days per year for each doctor, one-third of which (73) will be on-call. Each hospitalist gets 146 days off per year;
- The practice decides to switch to dedicated night shifts in which the doctors do not work the day before or after a night shift. The practice wants to retain the 146 days off for each hospitalist. This new coverage arrangement is equivalent to adding 365 shifts annually (one for each night); and
- This will require an additional 1.67 FTE hospitalists (1.67 hospitalists at 219 shifts/year=365).
In this example, by switching from on-call coverage to on-site coverage, the practice increased from five FTEs to 6.67 FTEs. If the daytime work was already enough to keep all three doctors busy, adding 1.67 FTEs for dedicated night shifts may not increase practice productivity or revenue significantly. The practice looks much less productive per FTE (6.67 FTEs are now seeing the volume previously handled by five FTEs) and much costlier.
Changing from traditional night call to dedicated night coverage can be expensive because it may require adding staff yet doesn’t usually increase practice capacity significantly. But it offers other benefits such as those listed in Table 1 (see p. TK). Some practices find they must provide dedicated night coverage to recruit hospitalists. Other institutions choose to support it believing it leads to more timely, efficient, higher-quality care. TH
Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. He is also part of the faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.
Reference
- Miller J, Nelson J, Whitcomb W. Hospitalists: A Guide to Building and Sustaining a Successful Program. Chicago:Health Administration Press;2007:149-150.
Lessons of the Deposed
Recently I served as an expert witness in two cases; in each a hospitalist was being sued. While I can’t share details of these confidential cases, I can share my insights using a couple of hypothetical cases that illustrate the key lessons I learned:
- A 75-year-old woman was admitted by orthopedics after a fall requiring hip fracture repair. A hospitalist automatically saw her per the standing agreement. The hospitalist adjusted her diabetes regimen and held her aspirin because of bleeding. On the evening prior to discharge she developed right lower-extremity pain. The on-call orthopedist ordered a lower-extremity ultrasound from home.
The patient felt better the next morning and was discharged with hospitalist recommendations to increase her basal insulin, restart her aspirin, and follow up with her primary care provider (PCP). Three days later the patient presented in respiratory extremis and died in the emergency department. Post-mortem chart review noted a sonographic venous thrombosis in the right femoral vein that went unnoticed during her hospital stay.
- A 58-year-old woman was admitted after an uncomplicated appendectomy. On post-op day two, the surgeon asked the hospitalist to see the patient for a depressed mood. The hospitalist recommended starting an antidepressant and following up with her PCP after discharge. She also noted that the patient had right lower-extremity pain and swelling and recommended an ultrasound for workup of a deep venous thrombosis (DVT). The hospitalist did not see the patient again, and the ultrasound was not completed. Two days after discharge, the patient died at home after complaining of chest pain. Post-mortem autopsy revealed massive pulmonary embolism.
Two difficult cases, indeed. And I learned plenty from them:
Lesson one: Most lawsuits do not stem from deficiencies of medical knowledge.
In both cases, the hospitalists’ clinical reasoning was sound. In the first he was unaware of the patient’s overnight symptoms, which were not documented in the chart because the patient was not seen by the on-call orthopedist—a major systems error and lack of professionalism. This was compounded by a system that did not alert providers that an ultrasound was ordered or read as abnormal.
In the second case, the hospitalist got it right and made the correct recommendation—but the surgeon didn’t follow through.
Lesson two: Clarify your role—consultant or co-manager.
The differences between consultant and co-manager are subtle but crucial.
A consult is a request to answer a specific question: “Is this patient depressed, and how would you manage this problem?” This results in a detailed, focused appraisal of that issue, culminating in a note listing recommendations for further evaluation and management. It is the primary team’s responsibility to follow up on recommendations as they deem appropriate.
With this decision-making capacity, the primary team accepts near-full clinical and medical legal responsibility. As long as the consultant does due diligence and makes sound recommendations, it is unlikely he/she will be successfully sued for a bad outcome if the recommendations are not followed.
However, the hospitalist movement has changed this landscape considerably. We often function in a co-management model with our consulting colleagues, each of us caring for the issues within our respective scope of expertise.
This paradigm demands a level of responsibility sharing and communication that differs significantly from the traditional consultative model.
Knowing which model you are functioning under and who is responsible for which problems can be tricky. In the first case, who owned the decision-making for the patient’s DVT work-up?
The orthopedist may assume his role is focused on the care of the hip fracture surgery, while all else is the hospitalist’s purview. The hospitalist may assume DVT is a complication of the hip fracture surgery and is the orthopedist’s responsibility.
The second case seems easier as the hospitalist was clearly functioning as a consultant and therefore his obligation ends with his recommendation to further evaluate for DVT.
Or does it?
Lesson three: Communication is imperative.
The role we are functioning in—consultant versus co-manager—is not always intuitive. This perplexity can be further exacerbated by poor communication.
In both cases the hospitalists’ role was not established up front. Further, the hospitalists and their colleagues never spoke directly about the case or the management decisions.
In the second case the surgeon saw the recommendation but presumed the hospitalist would write the order for the ultrasound because they were co-managing the patient. He argued that he is not expert in the care of DVT and could not determine if the recommendation was sound. He assumed the hospitalist would appropriately evaluate this situation and complete the work-up if warranted. Because the hospitalist did not, the surgeon assumed the hospitalist was no longer concerned about DVT.
The hospitalist countered that she was specifically consulted to answer a question about depression. The recommendations regarding the swollen calf were also done in a consultative fashion, and the decision to obtain the ultrasound would fall to the surgeon.
The hospitalist argued that because the surgeon did not consult her again for this specific issue, she assumed he was comfortable evaluating and managing DVT.
This foray into the legal system reminded me that our patients trust we will give them the best care. When system and communication inadequacies get in the way of this, we can get sued—but our patients can lose their lives. TH
Dr. Glasheen is associate professor of medicine at the University of Colorado at Denver, where he serves as director of the Hospital Medicine Program and the Hospitalist Training Program, and as associate program director of the Internal Medicine Residency Program.
Recently I served as an expert witness in two cases; in each a hospitalist was being sued. While I can’t share details of these confidential cases, I can share my insights using a couple of hypothetical cases that illustrate the key lessons I learned:
- A 75-year-old woman was admitted by orthopedics after a fall requiring hip fracture repair. A hospitalist automatically saw her per the standing agreement. The hospitalist adjusted her diabetes regimen and held her aspirin because of bleeding. On the evening prior to discharge she developed right lower-extremity pain. The on-call orthopedist ordered a lower-extremity ultrasound from home.
The patient felt better the next morning and was discharged with hospitalist recommendations to increase her basal insulin, restart her aspirin, and follow up with her primary care provider (PCP). Three days later the patient presented in respiratory extremis and died in the emergency department. Post-mortem chart review noted a sonographic venous thrombosis in the right femoral vein that went unnoticed during her hospital stay.
- A 58-year-old woman was admitted after an uncomplicated appendectomy. On post-op day two, the surgeon asked the hospitalist to see the patient for a depressed mood. The hospitalist recommended starting an antidepressant and following up with her PCP after discharge. She also noted that the patient had right lower-extremity pain and swelling and recommended an ultrasound for workup of a deep venous thrombosis (DVT). The hospitalist did not see the patient again, and the ultrasound was not completed. Two days after discharge, the patient died at home after complaining of chest pain. Post-mortem autopsy revealed massive pulmonary embolism.
Two difficult cases, indeed. And I learned plenty from them:
Lesson one: Most lawsuits do not stem from deficiencies of medical knowledge.
In both cases, the hospitalists’ clinical reasoning was sound. In the first he was unaware of the patient’s overnight symptoms, which were not documented in the chart because the patient was not seen by the on-call orthopedist—a major systems error and lack of professionalism. This was compounded by a system that did not alert providers that an ultrasound was ordered or read as abnormal.
In the second case, the hospitalist got it right and made the correct recommendation—but the surgeon didn’t follow through.
Lesson two: Clarify your role—consultant or co-manager.
The differences between consultant and co-manager are subtle but crucial.
A consult is a request to answer a specific question: “Is this patient depressed, and how would you manage this problem?” This results in a detailed, focused appraisal of that issue, culminating in a note listing recommendations for further evaluation and management. It is the primary team’s responsibility to follow up on recommendations as they deem appropriate.
With this decision-making capacity, the primary team accepts near-full clinical and medical legal responsibility. As long as the consultant does due diligence and makes sound recommendations, it is unlikely he/she will be successfully sued for a bad outcome if the recommendations are not followed.
However, the hospitalist movement has changed this landscape considerably. We often function in a co-management model with our consulting colleagues, each of us caring for the issues within our respective scope of expertise.
This paradigm demands a level of responsibility sharing and communication that differs significantly from the traditional consultative model.
Knowing which model you are functioning under and who is responsible for which problems can be tricky. In the first case, who owned the decision-making for the patient’s DVT work-up?
The orthopedist may assume his role is focused on the care of the hip fracture surgery, while all else is the hospitalist’s purview. The hospitalist may assume DVT is a complication of the hip fracture surgery and is the orthopedist’s responsibility.
The second case seems easier as the hospitalist was clearly functioning as a consultant and therefore his obligation ends with his recommendation to further evaluate for DVT.
Or does it?
Lesson three: Communication is imperative.
The role we are functioning in—consultant versus co-manager—is not always intuitive. This perplexity can be further exacerbated by poor communication.
In both cases the hospitalists’ role was not established up front. Further, the hospitalists and their colleagues never spoke directly about the case or the management decisions.
In the second case the surgeon saw the recommendation but presumed the hospitalist would write the order for the ultrasound because they were co-managing the patient. He argued that he is not expert in the care of DVT and could not determine if the recommendation was sound. He assumed the hospitalist would appropriately evaluate this situation and complete the work-up if warranted. Because the hospitalist did not, the surgeon assumed the hospitalist was no longer concerned about DVT.
The hospitalist countered that she was specifically consulted to answer a question about depression. The recommendations regarding the swollen calf were also done in a consultative fashion, and the decision to obtain the ultrasound would fall to the surgeon.
The hospitalist argued that because the surgeon did not consult her again for this specific issue, she assumed he was comfortable evaluating and managing DVT.
This foray into the legal system reminded me that our patients trust we will give them the best care. When system and communication inadequacies get in the way of this, we can get sued—but our patients can lose their lives. TH
Dr. Glasheen is associate professor of medicine at the University of Colorado at Denver, where he serves as director of the Hospital Medicine Program and the Hospitalist Training Program, and as associate program director of the Internal Medicine Residency Program.
Recently I served as an expert witness in two cases; in each a hospitalist was being sued. While I can’t share details of these confidential cases, I can share my insights using a couple of hypothetical cases that illustrate the key lessons I learned:
- A 75-year-old woman was admitted by orthopedics after a fall requiring hip fracture repair. A hospitalist automatically saw her per the standing agreement. The hospitalist adjusted her diabetes regimen and held her aspirin because of bleeding. On the evening prior to discharge she developed right lower-extremity pain. The on-call orthopedist ordered a lower-extremity ultrasound from home.
The patient felt better the next morning and was discharged with hospitalist recommendations to increase her basal insulin, restart her aspirin, and follow up with her primary care provider (PCP). Three days later the patient presented in respiratory extremis and died in the emergency department. Post-mortem chart review noted a sonographic venous thrombosis in the right femoral vein that went unnoticed during her hospital stay.
- A 58-year-old woman was admitted after an uncomplicated appendectomy. On post-op day two, the surgeon asked the hospitalist to see the patient for a depressed mood. The hospitalist recommended starting an antidepressant and following up with her PCP after discharge. She also noted that the patient had right lower-extremity pain and swelling and recommended an ultrasound for workup of a deep venous thrombosis (DVT). The hospitalist did not see the patient again, and the ultrasound was not completed. Two days after discharge, the patient died at home after complaining of chest pain. Post-mortem autopsy revealed massive pulmonary embolism.
Two difficult cases, indeed. And I learned plenty from them:
Lesson one: Most lawsuits do not stem from deficiencies of medical knowledge.
In both cases, the hospitalists’ clinical reasoning was sound. In the first he was unaware of the patient’s overnight symptoms, which were not documented in the chart because the patient was not seen by the on-call orthopedist—a major systems error and lack of professionalism. This was compounded by a system that did not alert providers that an ultrasound was ordered or read as abnormal.
In the second case, the hospitalist got it right and made the correct recommendation—but the surgeon didn’t follow through.
Lesson two: Clarify your role—consultant or co-manager.
The differences between consultant and co-manager are subtle but crucial.
A consult is a request to answer a specific question: “Is this patient depressed, and how would you manage this problem?” This results in a detailed, focused appraisal of that issue, culminating in a note listing recommendations for further evaluation and management. It is the primary team’s responsibility to follow up on recommendations as they deem appropriate.
With this decision-making capacity, the primary team accepts near-full clinical and medical legal responsibility. As long as the consultant does due diligence and makes sound recommendations, it is unlikely he/she will be successfully sued for a bad outcome if the recommendations are not followed.
However, the hospitalist movement has changed this landscape considerably. We often function in a co-management model with our consulting colleagues, each of us caring for the issues within our respective scope of expertise.
This paradigm demands a level of responsibility sharing and communication that differs significantly from the traditional consultative model.
Knowing which model you are functioning under and who is responsible for which problems can be tricky. In the first case, who owned the decision-making for the patient’s DVT work-up?
The orthopedist may assume his role is focused on the care of the hip fracture surgery, while all else is the hospitalist’s purview. The hospitalist may assume DVT is a complication of the hip fracture surgery and is the orthopedist’s responsibility.
The second case seems easier as the hospitalist was clearly functioning as a consultant and therefore his obligation ends with his recommendation to further evaluate for DVT.
Or does it?
Lesson three: Communication is imperative.
The role we are functioning in—consultant versus co-manager—is not always intuitive. This perplexity can be further exacerbated by poor communication.
In both cases the hospitalists’ role was not established up front. Further, the hospitalists and their colleagues never spoke directly about the case or the management decisions.
In the second case the surgeon saw the recommendation but presumed the hospitalist would write the order for the ultrasound because they were co-managing the patient. He argued that he is not expert in the care of DVT and could not determine if the recommendation was sound. He assumed the hospitalist would appropriately evaluate this situation and complete the work-up if warranted. Because the hospitalist did not, the surgeon assumed the hospitalist was no longer concerned about DVT.
The hospitalist countered that she was specifically consulted to answer a question about depression. The recommendations regarding the swollen calf were also done in a consultative fashion, and the decision to obtain the ultrasound would fall to the surgeon.
The hospitalist argued that because the surgeon did not consult her again for this specific issue, she assumed he was comfortable evaluating and managing DVT.
This foray into the legal system reminded me that our patients trust we will give them the best care. When system and communication inadequacies get in the way of this, we can get sued—but our patients can lose their lives. TH
Dr. Glasheen is associate professor of medicine at the University of Colorado at Denver, where he serves as director of the Hospital Medicine Program and the Hospitalist Training Program, and as associate program director of the Internal Medicine Residency Program.