EVIDENCE SUMMARY

A 2010 multicenter RCT with 445 women (mean age 49.8 years) compared PFMT, pessary use, and combined treatment.¹ Investigators used the Patient Global Impression of Improvement and the stress incontinence subscale of the Pelvic Floor Distress Inventory to measure patient satisfaction and urinary incontinence symptoms.

At 3 months, equivalent numbers of women using PFMT and a pessary (49% and 40%, respectively; P=.09) reported they were “much better” or “very much better.” More women in the PFMT cohort than women using a pessary reported resolution of incontinence symptoms at 3 months (49% vs 33%; P=.006), and satisfaction with treatment (75% vs 63%; P=.02), but these differences disappeared at 12 months. Combination therapy wasn’t superior to PFMT alone.

Pelvic floor muscle training improves symptoms, especially with perseverance

A 2011 Cochrane review that compared women receiving PFMT with a control group (observed but not treated) found that PFMT moderately improved prolapse symptoms and severity, especially following 6 months of supervised intervention.² Investigators evalu-ated 4 trials, (N=857), including 3 with fewer than 25 women per arm.

Three studies found that PFMT improved symptom severity and manometric measures. Although the authors couldn’t pool the data because of different symptom scoring instruments, typical improvements ranged from 20% to 30%. Two trials found that PFMT increased the chance of improvement in POP stage by 17% (pooled data, relative risk=.83; 95% confidence interval [CI], .71-.96). PFMT also improved urinary outcomes (approximately 30% reduction in urinary frequency and stress incontinence symptoms) in 2 of 3 trials and improved bowel symptoms in one trial (approximately 25% to 30% reduction).

Pessaries also relieve symptoms

A 2013 Cochrane Review seeking to determine the effectiveness of pessaries in POP, identified one RCT (crossover, 3 month, multicenter, United States) that compared symptom relief and change in life impact over baseline for 134 women (parous, mean age 61 years, range 30-89 years) with POP stage II or greater who were treated with ring with support or Gellhorn pessaries.³ Sixty percent of patients who completed the study (the dropout rate was 37%) reported symptom relief with both types of pessary. Outcomes were measured by multiple questionnaires and Likert scales.

Patients reported improved symptoms on both the Pelvic Organ Prolapse Distress Inventory (POPDI) and Pelvic Organ Prolapse Impact Questionnaire (POPIQ) scales (P<.05 for difference from baseline on each scale, actual scores not reported). The ring with support and Gellhorn pessaries didn’t produce different scores on either scale (POPDI, P=.99; POPIQ, P=.29).

Untreated mild prolapse postmenopause usually doesn’t progress and may regress

A cohort of 412 postmenopausal women (ages ≥50 years) with POP who were observed, but not treated, found that mild POP was unlikely to progress and sometimes improved spontaneously.⁴ Over a mean follow-up of 5.7 years, few women with grade 1 POP (prolapsed pelvic organs remaining within the vagina) progressed to grade 2 or 3 (probability of progression for women with cystoceles=.095, 95% CI, .07-.13; women with rectoceles=.135, 95% CI, .09-.19; and women with uterine prolapse=.019, 95% CI, .0005-.099).

Pelvic floor muscle training and pessaries are equally effective in treating symptoms of pelvic organ prolapse; combining them offers no added benefit.

Some women with grade 1 POP regressed to grade 0 (probability of regression for women with cystoceles=.235, 95% CI, .19- .28; women with rectoceles=.22, 95% CI, .16-.28; and women with uterine prolapse=.48, 95% CI, 0.34-.62). Women with grades 2 and 3 POP were less likely to regress to grade 0 (probability of regression for women with cystoceles=.093, 95% CI, .05-.14; women with rectoceles=.033, 95% CI, .011-.075; and women with uterine prolapse=0, 95% CI, 0-.37).

One flaw of this study was that the women received hormone replacement therapy, which the investigators didn’t evaluate independently. However, a 2010 Cochrane review (2 small trials, one meta-analysis) found insufficient data to determine whether hormone replacement therapy alters POP.⁵

RECOMMENDATIONS

The American College of Obstetricians and Gynecologists Practice Bulletin on POP recommends the following:⁶

• Pessaries can be fitted in most women with prolapse, regardless of prolapse stage (equivalent to grade) or site of predominant prolapse.
• Pessary use should be considered before surgical intervention in women with symptomatic prolapse.
• Women with prolapse who are asymptomatic or mildly symptomatic can be observed at regular intervals, unless new bothersome symptoms develop.

EVIDENCE SUMMARY

A 2010 multicenter RCT with 445 women (mean age 49.8 years) compared PFMT, pessary use, and combined treatment.¹ Investigators used the Patient Global Impression of Improvement and the stress incontinence subscale of the Pelvic Floor Distress Inventory to measure patient satisfaction and urinary incontinence symptoms.

At 3 months, equivalent numbers of women using PFMT and a pessary (49% and 40%, respectively; P=.09) reported they were “much better” or “very much better.” More women in the PFMT cohort than women using a pessary reported resolution of incontinence symptoms at 3 months (49% vs 33%; P=.006), and satisfaction with treatment (75% vs 63%; P=.02), but these differences disappeared at 12 months. Combination therapy wasn’t superior to PFMT alone.

Pelvic floor muscle training improves symptoms, especially with perseverance

A 2011 Cochrane review that compared women receiving PFMT with a control group (observed but not treated) found that PFMT moderately improved prolapse symptoms and severity, especially following 6 months of supervised intervention.² Investigators evalu-ated 4 trials, (N=857), including 3 with fewer than 25 women per arm.

Three studies found that PFMT improved symptom severity and manometric measures. Although the authors couldn’t pool the data because of different symptom scoring instruments, typical improvements ranged from 20% to 30%. Two trials found that PFMT increased the chance of improvement in POP stage by 17% (pooled data, relative risk=.83; 95% confidence interval [CI], .71-.96). PFMT also improved urinary outcomes (approximately 30% reduction in urinary frequency and stress incontinence symptoms) in 2 of 3 trials and improved bowel symptoms in one trial (approximately 25% to 30% reduction).

Pessaries also relieve symptoms

A 2013 Cochrane Review seeking to determine the effectiveness of pessaries in POP, identified one RCT (crossover, 3 month, multicenter, United States) that compared symptom relief and change in life impact over baseline for 134 women (parous, mean age 61 years, range 30-89 years) with POP stage II or greater who were treated with ring with support or Gellhorn pessaries.³ Sixty percent of patients who completed the study (the dropout rate was 37%) reported symptom relief with both types of pessary. Outcomes were measured by multiple questionnaires and Likert scales.

Patients reported improved symptoms on both the Pelvic Organ Prolapse Distress Inventory (POPDI) and Pelvic Organ Prolapse Impact Questionnaire (POPIQ) scales (P<.05 for difference from baseline on each scale, actual scores not reported). The ring with support and Gellhorn pessaries didn’t produce different scores on either scale (POPDI, P=.99; POPIQ, P=.29).

Untreated mild prolapse postmenopause usually doesn’t progress and may regress

A cohort of 412 postmenopausal women (ages ≥50 years) with POP who were observed, but not treated, found that mild POP was unlikely to progress and sometimes improved spontaneously.⁴ Over a mean follow-up of 5.7 years, few women with grade 1 POP (prolapsed pelvic organs remaining within the vagina) progressed to grade 2 or 3 (probability of progression for women with cystoceles=.095, 95% CI, .07-.13; women with rectoceles=.135, 95% CI, .09-.19; and women with uterine prolapse=.019, 95% CI, .0005-.099).

Pelvic floor muscle training and pessaries are equally effective in treating symptoms of pelvic organ prolapse; combining them offers no added benefit.

Some women with grade 1 POP regressed to grade 0 (probability of regression for women with cystoceles=.235, 95% CI, .19- .28; women with rectoceles=.22, 95% CI, .16-.28; and women with uterine prolapse=.48, 95% CI, 0.34-.62). Women with grades 2 and 3 POP were less likely to regress to grade 0 (probability of regression for women with cystoceles=.093, 95% CI, .05-.14; women with rectoceles=.033, 95% CI, .011-.075; and women with uterine prolapse=0, 95% CI, 0-.37).

One flaw of this study was that the women received hormone replacement therapy, which the investigators didn’t evaluate independently. However, a 2010 Cochrane review (2 small trials, one meta-analysis) found insufficient data to determine whether hormone replacement therapy alters POP.⁵

RECOMMENDATIONS

The American College of Obstetricians and Gynecologists Practice Bulletin on POP recommends the following:⁶

• Pessaries can be fitted in most women with prolapse, regardless of prolapse stage (equivalent to grade) or site of predominant prolapse.
• Pessary use should be considered before surgical intervention in women with symptomatic prolapse.
• Women with prolapse who are asymptomatic or mildly symptomatic can be observed at regular intervals, unless new bothersome symptoms develop.

EVIDENCE SUMMARY

A 2010 multicenter RCT with 445 women (mean age 49.8 years) compared PFMT, pessary use, and combined treatment.¹ Investigators used the Patient Global Impression of Improvement and the stress incontinence subscale of the Pelvic Floor Distress Inventory to measure patient satisfaction and urinary incontinence symptoms.

At 3 months, equivalent numbers of women using PFMT and a pessary (49% and 40%, respectively; P=.09) reported they were “much better” or “very much better.” More women in the PFMT cohort than women using a pessary reported resolution of incontinence symptoms at 3 months (49% vs 33%; P=.006), and satisfaction with treatment (75% vs 63%; P=.02), but these differences disappeared at 12 months. Combination therapy wasn’t superior to PFMT alone.

Pelvic floor muscle training improves symptoms, especially with perseverance

A 2011 Cochrane review that compared women receiving PFMT with a control group (observed but not treated) found that PFMT moderately improved prolapse symptoms and severity, especially following 6 months of supervised intervention.² Investigators evalu-ated 4 trials, (N=857), including 3 with fewer than 25 women per arm.

Three studies found that PFMT improved symptom severity and manometric measures. Although the authors couldn’t pool the data because of different symptom scoring instruments, typical improvements ranged from 20% to 30%. Two trials found that PFMT increased the chance of improvement in POP stage by 17% (pooled data, relative risk=.83; 95% confidence interval [CI], .71-.96). PFMT also improved urinary outcomes (approximately 30% reduction in urinary frequency and stress incontinence symptoms) in 2 of 3 trials and improved bowel symptoms in one trial (approximately 25% to 30% reduction).

Pessaries also relieve symptoms

A 2013 Cochrane Review seeking to determine the effectiveness of pessaries in POP, identified one RCT (crossover, 3 month, multicenter, United States) that compared symptom relief and change in life impact over baseline for 134 women (parous, mean age 61 years, range 30-89 years) with POP stage II or greater who were treated with ring with support or Gellhorn pessaries.³ Sixty percent of patients who completed the study (the dropout rate was 37%) reported symptom relief with both types of pessary. Outcomes were measured by multiple questionnaires and Likert scales.

Patients reported improved symptoms on both the Pelvic Organ Prolapse Distress Inventory (POPDI) and Pelvic Organ Prolapse Impact Questionnaire (POPIQ) scales (P<.05 for difference from baseline on each scale, actual scores not reported). The ring with support and Gellhorn pessaries didn’t produce different scores on either scale (POPDI, P=.99; POPIQ, P=.29).

Untreated mild prolapse postmenopause usually doesn’t progress and may regress

A cohort of 412 postmenopausal women (ages ≥50 years) with POP who were observed, but not treated, found that mild POP was unlikely to progress and sometimes improved spontaneously.⁴ Over a mean follow-up of 5.7 years, few women with grade 1 POP (prolapsed pelvic organs remaining within the vagina) progressed to grade 2 or 3 (probability of progression for women with cystoceles=.095, 95% CI, .07-.13; women with rectoceles=.135, 95% CI, .09-.19; and women with uterine prolapse=.019, 95% CI, .0005-.099).

Pelvic floor muscle training and pessaries are equally effective in treating symptoms of pelvic organ prolapse; combining them offers no added benefit.

Some women with grade 1 POP regressed to grade 0 (probability of regression for women with cystoceles=.235, 95% CI, .19- .28; women with rectoceles=.22, 95% CI, .16-.28; and women with uterine prolapse=.48, 95% CI, 0.34-.62). Women with grades 2 and 3 POP were less likely to regress to grade 0 (probability of regression for women with cystoceles=.093, 95% CI, .05-.14; women with rectoceles=.033, 95% CI, .011-.075; and women with uterine prolapse=0, 95% CI, 0-.37).

One flaw of this study was that the women received hormone replacement therapy, which the investigators didn’t evaluate independently. However, a 2010 Cochrane review (2 small trials, one meta-analysis) found insufficient data to determine whether hormone replacement therapy alters POP.⁵

RECOMMENDATIONS

The American College of Obstetricians and Gynecologists Practice Bulletin on POP recommends the following:⁶

• Pessaries can be fitted in most women with prolapse, regardless of prolapse stage (equivalent to grade) or site of predominant prolapse.
• Pessary use should be considered before surgical intervention in women with symptomatic prolapse.
• Women with prolapse who are asymptomatic or mildly symptomatic can be observed at regular intervals, unless new bothersome symptoms develop.

Dr. Scheurer

The U.S. Department of Health and Human Services (HHS) is putting forth stricter interventions and penalties aimed at curbing acts of careless billing by physicians it refers to as “recalcitrant providers.” Webster’s defines recalcitrant as “obstinately defiant of authority or restraint…difficult to manage or operate.” According to Medicare, these “recalcitrants” are providers who routinely and repeatedly overcharge for services billed through Medicare, despite proper training on how to bill appropriately for these services.¹

Medicare has long battled the issue of finding and curbing overcharging and overpayment. CMS estimates that such defiance accounts for up to $6 billion a year in unnecessary Medicare costs, which makes up about 10% of all physician fee payments, given the fact that total Medicare Part B payments are about $65 billion a year.²

Medicare has systems in place to prevent, detect, and/or mitigate improper payments, whether they result from mistakes or from intentional fraud. In 2011, CMS’ Center for Program Integrity implemented sophisticated technology, called the Fraud Prevention System (FPS), which uses predictive analytics to detect provider irregularities warranting further inspection. According to their 2012 report, the FPS generated 536 new investigations, assisted in providing additional information for 511 active investigations, and initiated thousands of verification interviews of beneficiaries and providers to validate the legitimate receipt of services and items. The center estimates that in the first year of this program, FPS prevented about $115 million in payments.³

So what is Medicare’s response to providers who are identified as outliers? For overpayments from mistakes, CMS generally aims to recover the overpayments and educate the providers. Tactics range from educational letters and phone calls to on-site reviews and “prepayment medical reviews.” For fraud, on the other hand, Medicare (obviously) pursues more disciplinary sanctions, including criminal or civil penalties.

A New Paradigm

Now CMS is stepping up its expectations of provider accountability, adding heftier penalties for infractions, including higher financial penalties and even expulsion from Medicare, Medicaid, and other federal programs. In addition to these disciplinary actions, the agency plans to utilize recently changed laws to maximize public transparency around provider billing practices.

As of March 2014, Medicare will be able to publicly report all federal payments that have been paid out to individual providers. Although it has not yet disclosed how or when these will be reported, CMS now has the authority, for the first time since 1979, to display this information publicly. The history on this topic is that a federal district judge in Florida in 1979 prohibited the disclosure of individual payments to physicians, based on the contention that such disclosure would be an invasion of physician privacy. This longstanding mandate, which was reversed in May 2012, now allows Medicare to weigh the risks and benefits of individual requests for information on charges/payments by individual physicians. According to a New York Times article, Medicare is now being pressured by advocacy groups (insurers, employers, consumers) to release as much of the data as possible, to aid in data dissection and analysis and prompt early identification of abusive providers.⁴

Understandably, many physician advocacy groups, such as the American Medical Association, are concerned that such unfiltered access to this raw data may lead to inaccurate and unnecessary conclusions about physician practice and billing patterns.

The good news is that the federal government currently estimates that the recalcitrant provider list comprises a relatively small group of providers, roughly 300 or so. Some of these providers have received up to $3 million in Medicare payments a year. They estimate that, overall, about 2% of total Medicare licensed providers charged 25% of total payments, and that the total volume of these high-charging outliers increased by 78% between the years 2008 to 2011. A 2009 audit found that more than half of these recalcitrants were internists; other “high offenders” were ophthalmology and radiation oncology.

The list of these particular high-outlier offenders will be turned over to the Office of the Inspector General (OIG) at HHS to impose the appropriate degree of penalty. Then the federal government will determine an appropriate process of “screening” for providers that may meet the criteria for penalties and will start with those at the highest levels of cumulative payments. The OIG acknowledges that high payments do not necessarily imply fraud or abuse but believes it is reasonable to start there when analyzing and investigating potential areas of fraud or abuse.

Transparency Is Coming

So, while it is not exactly clear when or how the data will be released, what is clear is that the federal government has been granted the authority to dissect and release the data as it sees fit, opening up a new era of transparency in pricing, cost, charges, billing, and payments.

This change should affect all types of providers that bill Medicare part B, including hospitalists and other physicians, as well as nurse practitioners and physical therapists.⁵ While this is likely to cause some degree of discomfort and generate many questions from the public, hospitalists should be willing to embrace such transparency and engage in the dialogue needed to help the lay public understand the data. Most hospitalists work in practices that routinely share their data about billing, at least among the group, if not with a larger audience.

This is just one of many examples of how transparency can and should identify those providers considered “recalcitrant” in a number of realms, including patient satisfaction, quality, utilization, or cost. And, similar to other publicly reported “metrics,” release of this data will likely generate more questions than answers in the short run. In the long run, we should all be prepared for the release of data that is coming, one that will usher us into a whole new era of transparency.

Dr. Scheurer is a hospitalist and chief quality officer at the Medical University of South Carolina in Charleston. She is physician editor of The Hospitalist. Email her at [email protected].

References

1. Department of Health and Human Services. Centers for Medicare and Medicaid Services. CMS Manual System. Pub 100-08 Medicare program integrity. December 13, 2013. Available at: https://www.cms.gov/Regulations-and-Guidance/Guidance/Transmittals/Downloads/R495PI.pdf. Accessed April 6, 2014.
2. Levinson DR. Department of Health and Human Services. Office of Inspector General. Reviews of clinicians associated with high cumulative payments could improve Medicare program integrity efforts. December 2013. Available at: http://oig.hhs.gov/oas/reports/region1/11100511.pdf. Accessed April 6, 2014.
3. Department of Health and Human Services. Centers for Medicare and Medicaid Services. Report to Congress: fraud prevention system—first implementation year, 2012. Available at: http://www.stopmedicarefraud.gov/fraud-rtc12142012.pdf. Accessed April 6, 2014.
4. Pear R. Doctors abusing Medicare face fines and expulsion. January 25, 2014. The New York Times website. Available at: http://www.nytimes.com/2014/01/26/us/doctors-abusing-medicare-to-face-fines.html. Accessed April 6, 2014.
5. Steinbrook R. Public disclosure of Medicare payments to individual physicians. The Journal of the American Medical Association website. April 2, 2014. Available at: http://jama.jamanetwork.com/article.aspx?articleID=1832217&utm_source=Silverchair%20Information%20Systems&utm_medium=email&utm_campaign=JAMA%3AOnlineFirst02%2F17%2F2014. Accessed April 6,

2014.

Dr. Scheurer

The U.S. Department of Health and Human Services (HHS) is putting forth stricter interventions and penalties aimed at curbing acts of careless billing by physicians it refers to as “recalcitrant providers.” Webster’s defines recalcitrant as “obstinately defiant of authority or restraint…difficult to manage or operate.” According to Medicare, these “recalcitrants” are providers who routinely and repeatedly overcharge for services billed through Medicare, despite proper training on how to bill appropriately for these services.¹

Medicare has long battled the issue of finding and curbing overcharging and overpayment. CMS estimates that such defiance accounts for up to $6 billion a year in unnecessary Medicare costs, which makes up about 10% of all physician fee payments, given the fact that total Medicare Part B payments are about $65 billion a year.²

Medicare has systems in place to prevent, detect, and/or mitigate improper payments, whether they result from mistakes or from intentional fraud. In 2011, CMS’ Center for Program Integrity implemented sophisticated technology, called the Fraud Prevention System (FPS), which uses predictive analytics to detect provider irregularities warranting further inspection. According to their 2012 report, the FPS generated 536 new investigations, assisted in providing additional information for 511 active investigations, and initiated thousands of verification interviews of beneficiaries and providers to validate the legitimate receipt of services and items. The center estimates that in the first year of this program, FPS prevented about $115 million in payments.³

So what is Medicare’s response to providers who are identified as outliers? For overpayments from mistakes, CMS generally aims to recover the overpayments and educate the providers. Tactics range from educational letters and phone calls to on-site reviews and “prepayment medical reviews.” For fraud, on the other hand, Medicare (obviously) pursues more disciplinary sanctions, including criminal or civil penalties.

A New Paradigm

Now CMS is stepping up its expectations of provider accountability, adding heftier penalties for infractions, including higher financial penalties and even expulsion from Medicare, Medicaid, and other federal programs. In addition to these disciplinary actions, the agency plans to utilize recently changed laws to maximize public transparency around provider billing practices.

As of March 2014, Medicare will be able to publicly report all federal payments that have been paid out to individual providers. Although it has not yet disclosed how or when these will be reported, CMS now has the authority, for the first time since 1979, to display this information publicly. The history on this topic is that a federal district judge in Florida in 1979 prohibited the disclosure of individual payments to physicians, based on the contention that such disclosure would be an invasion of physician privacy. This longstanding mandate, which was reversed in May 2012, now allows Medicare to weigh the risks and benefits of individual requests for information on charges/payments by individual physicians. According to a New York Times article, Medicare is now being pressured by advocacy groups (insurers, employers, consumers) to release as much of the data as possible, to aid in data dissection and analysis and prompt early identification of abusive providers.⁴

Understandably, many physician advocacy groups, such as the American Medical Association, are concerned that such unfiltered access to this raw data may lead to inaccurate and unnecessary conclusions about physician practice and billing patterns.

The good news is that the federal government currently estimates that the recalcitrant provider list comprises a relatively small group of providers, roughly 300 or so. Some of these providers have received up to $3 million in Medicare payments a year. They estimate that, overall, about 2% of total Medicare licensed providers charged 25% of total payments, and that the total volume of these high-charging outliers increased by 78% between the years 2008 to 2011. A 2009 audit found that more than half of these recalcitrants were internists; other “high offenders” were ophthalmology and radiation oncology.

The list of these particular high-outlier offenders will be turned over to the Office of the Inspector General (OIG) at HHS to impose the appropriate degree of penalty. Then the federal government will determine an appropriate process of “screening” for providers that may meet the criteria for penalties and will start with those at the highest levels of cumulative payments. The OIG acknowledges that high payments do not necessarily imply fraud or abuse but believes it is reasonable to start there when analyzing and investigating potential areas of fraud or abuse.

Transparency Is Coming

So, while it is not exactly clear when or how the data will be released, what is clear is that the federal government has been granted the authority to dissect and release the data as it sees fit, opening up a new era of transparency in pricing, cost, charges, billing, and payments.

This change should affect all types of providers that bill Medicare part B, including hospitalists and other physicians, as well as nurse practitioners and physical therapists.⁵ While this is likely to cause some degree of discomfort and generate many questions from the public, hospitalists should be willing to embrace such transparency and engage in the dialogue needed to help the lay public understand the data. Most hospitalists work in practices that routinely share their data about billing, at least among the group, if not with a larger audience.

This is just one of many examples of how transparency can and should identify those providers considered “recalcitrant” in a number of realms, including patient satisfaction, quality, utilization, or cost. And, similar to other publicly reported “metrics,” release of this data will likely generate more questions than answers in the short run. In the long run, we should all be prepared for the release of data that is coming, one that will usher us into a whole new era of transparency.

Dr. Scheurer is a hospitalist and chief quality officer at the Medical University of South Carolina in Charleston. She is physician editor of The Hospitalist. Email her at [email protected].

References

1. Department of Health and Human Services. Centers for Medicare and Medicaid Services. CMS Manual System. Pub 100-08 Medicare program integrity. December 13, 2013. Available at: https://www.cms.gov/Regulations-and-Guidance/Guidance/Transmittals/Downloads/R495PI.pdf. Accessed April 6, 2014.
2. Levinson DR. Department of Health and Human Services. Office of Inspector General. Reviews of clinicians associated with high cumulative payments could improve Medicare program integrity efforts. December 2013. Available at: http://oig.hhs.gov/oas/reports/region1/11100511.pdf. Accessed April 6, 2014.
3. Department of Health and Human Services. Centers for Medicare and Medicaid Services. Report to Congress: fraud prevention system—first implementation year, 2012. Available at: http://www.stopmedicarefraud.gov/fraud-rtc12142012.pdf. Accessed April 6, 2014.
4. Pear R. Doctors abusing Medicare face fines and expulsion. January 25, 2014. The New York Times website. Available at: http://www.nytimes.com/2014/01/26/us/doctors-abusing-medicare-to-face-fines.html. Accessed April 6, 2014.
5. Steinbrook R. Public disclosure of Medicare payments to individual physicians. The Journal of the American Medical Association website. April 2, 2014. Available at: http://jama.jamanetwork.com/article.aspx?articleID=1832217&utm_source=Silverchair%20Information%20Systems&utm_medium=email&utm_campaign=JAMA%3AOnlineFirst02%2F17%2F2014. Accessed April 6,

2014.

Dr. Scheurer

The U.S. Department of Health and Human Services (HHS) is putting forth stricter interventions and penalties aimed at curbing acts of careless billing by physicians it refers to as “recalcitrant providers.” Webster’s defines recalcitrant as “obstinately defiant of authority or restraint…difficult to manage or operate.” According to Medicare, these “recalcitrants” are providers who routinely and repeatedly overcharge for services billed through Medicare, despite proper training on how to bill appropriately for these services.¹

Medicare has long battled the issue of finding and curbing overcharging and overpayment. CMS estimates that such defiance accounts for up to $6 billion a year in unnecessary Medicare costs, which makes up about 10% of all physician fee payments, given the fact that total Medicare Part B payments are about $65 billion a year.²

Medicare has systems in place to prevent, detect, and/or mitigate improper payments, whether they result from mistakes or from intentional fraud. In 2011, CMS’ Center for Program Integrity implemented sophisticated technology, called the Fraud Prevention System (FPS), which uses predictive analytics to detect provider irregularities warranting further inspection. According to their 2012 report, the FPS generated 536 new investigations, assisted in providing additional information for 511 active investigations, and initiated thousands of verification interviews of beneficiaries and providers to validate the legitimate receipt of services and items. The center estimates that in the first year of this program, FPS prevented about $115 million in payments.³

So what is Medicare’s response to providers who are identified as outliers? For overpayments from mistakes, CMS generally aims to recover the overpayments and educate the providers. Tactics range from educational letters and phone calls to on-site reviews and “prepayment medical reviews.” For fraud, on the other hand, Medicare (obviously) pursues more disciplinary sanctions, including criminal or civil penalties.

A New Paradigm

Now CMS is stepping up its expectations of provider accountability, adding heftier penalties for infractions, including higher financial penalties and even expulsion from Medicare, Medicaid, and other federal programs. In addition to these disciplinary actions, the agency plans to utilize recently changed laws to maximize public transparency around provider billing practices.

As of March 2014, Medicare will be able to publicly report all federal payments that have been paid out to individual providers. Although it has not yet disclosed how or when these will be reported, CMS now has the authority, for the first time since 1979, to display this information publicly. The history on this topic is that a federal district judge in Florida in 1979 prohibited the disclosure of individual payments to physicians, based on the contention that such disclosure would be an invasion of physician privacy. This longstanding mandate, which was reversed in May 2012, now allows Medicare to weigh the risks and benefits of individual requests for information on charges/payments by individual physicians. According to a New York Times article, Medicare is now being pressured by advocacy groups (insurers, employers, consumers) to release as much of the data as possible, to aid in data dissection and analysis and prompt early identification of abusive providers.⁴

Understandably, many physician advocacy groups, such as the American Medical Association, are concerned that such unfiltered access to this raw data may lead to inaccurate and unnecessary conclusions about physician practice and billing patterns.

The good news is that the federal government currently estimates that the recalcitrant provider list comprises a relatively small group of providers, roughly 300 or so. Some of these providers have received up to $3 million in Medicare payments a year. They estimate that, overall, about 2% of total Medicare licensed providers charged 25% of total payments, and that the total volume of these high-charging outliers increased by 78% between the years 2008 to 2011. A 2009 audit found that more than half of these recalcitrants were internists; other “high offenders” were ophthalmology and radiation oncology.

The list of these particular high-outlier offenders will be turned over to the Office of the Inspector General (OIG) at HHS to impose the appropriate degree of penalty. Then the federal government will determine an appropriate process of “screening” for providers that may meet the criteria for penalties and will start with those at the highest levels of cumulative payments. The OIG acknowledges that high payments do not necessarily imply fraud or abuse but believes it is reasonable to start there when analyzing and investigating potential areas of fraud or abuse.

Transparency Is Coming

So, while it is not exactly clear when or how the data will be released, what is clear is that the federal government has been granted the authority to dissect and release the data as it sees fit, opening up a new era of transparency in pricing, cost, charges, billing, and payments.

This change should affect all types of providers that bill Medicare part B, including hospitalists and other physicians, as well as nurse practitioners and physical therapists.⁵ While this is likely to cause some degree of discomfort and generate many questions from the public, hospitalists should be willing to embrace such transparency and engage in the dialogue needed to help the lay public understand the data. Most hospitalists work in practices that routinely share their data about billing, at least among the group, if not with a larger audience.

This is just one of many examples of how transparency can and should identify those providers considered “recalcitrant” in a number of realms, including patient satisfaction, quality, utilization, or cost. And, similar to other publicly reported “metrics,” release of this data will likely generate more questions than answers in the short run. In the long run, we should all be prepared for the release of data that is coming, one that will usher us into a whole new era of transparency.

Dr. Scheurer is a hospitalist and chief quality officer at the Medical University of South Carolina in Charleston. She is physician editor of The Hospitalist. Email her at [email protected].

References

1. Department of Health and Human Services. Centers for Medicare and Medicaid Services. CMS Manual System. Pub 100-08 Medicare program integrity. December 13, 2013. Available at: https://www.cms.gov/Regulations-and-Guidance/Guidance/Transmittals/Downloads/R495PI.pdf. Accessed April 6, 2014.
2. Levinson DR. Department of Health and Human Services. Office of Inspector General. Reviews of clinicians associated with high cumulative payments could improve Medicare program integrity efforts. December 2013. Available at: http://oig.hhs.gov/oas/reports/region1/11100511.pdf. Accessed April 6, 2014.
3. Department of Health and Human Services. Centers for Medicare and Medicaid Services. Report to Congress: fraud prevention system—first implementation year, 2012. Available at: http://www.stopmedicarefraud.gov/fraud-rtc12142012.pdf. Accessed April 6, 2014.
4. Pear R. Doctors abusing Medicare face fines and expulsion. January 25, 2014. The New York Times website. Available at: http://www.nytimes.com/2014/01/26/us/doctors-abusing-medicare-to-face-fines.html. Accessed April 6, 2014.
5. Steinbrook R. Public disclosure of Medicare payments to individual physicians. The Journal of the American Medical Association website. April 2, 2014. Available at: http://jama.jamanetwork.com/article.aspx?articleID=1832217&utm_source=Silverchair%20Information%20Systems&utm_medium=email&utm_campaign=JAMA%3AOnlineFirst02%2F17%2F2014. Accessed April 6,

2014.

Dr. Kealey

Hippocrates, Epidemics.“The Physician must be able to do good or to do no harm.”

This is part three of my ongoing series on the journey of hospital medicine and how we are poised for greater things yet. In part one, “Tinder and Spark,” macro changes in the American healthcare landscape pressured primary care physicians to get creative with new ways to practice, the most prominent result being the creation of hospitalist practices. Wachter and Goldman provided the spark that gave the field its name and cohesiveness. In part two, “Fuel,” the Baby Boomers shaped the field, setting the stage for the Generation X physicians who fueled HM’s early growth.

But the field might have stagnated there, the fire attenuated, if not for the rise of something new, something that stoked our growth to new heights.

Orlando, Fla., December 2006.

SHM President-Elect Rusty Holman, MD, MHM, was on stage representing hospitalists at the annual Institute for Healthcare Improvement (IHI) National Forum in front of more than 5,000 enthusiastic attendees representing every discipline of clinical care from hundreds of healthcare organizations across the country and internationally. This was a special event. Two years earlier, IHI President Don Berwick, MD, MPP, had launched an audacious campaign, called the 100,000 Lives Campaign, that aimed to prevent the deaths of 100,000 patients in our nation’s hospitals in the following 18 months, not by utilizing some great new technological advance but by changing the culture around safety and quality in our nation’s hospitals and enacting proven safety methods and processes.1 Out of this plan came widespread use of terms and programs that weren’t widely adopted then but are familiar to all of us now: rapid response teams, medicine reconciliation, surgical site infection prevention, and ventilator-acquired pneumonia.

That program estimated that it saved 122,000 lives.¹

IHI was looking to build on the safety and quality infrastructure that had been built up to make the 100,000 Lives Campaign a success and to launch an even bigger program. The 5 Million Lives Campaign’s goal was to reduce incidents of harm in five million patients over the next two years. For this campaign, IHI understood that success could only be achieved with partners. SHM and the field of hospital medicine, which had grown in size and influence, was seen as a critical and influential partner in achieving the goal of reducing harm in our nation’s hospitals. Thus, Dr. Holman was standing on that stage for SHM at the launch of the biggest safety and quality initiative in our nation’s history. SHM was among seven partner organizations, including the American Nurses Association, the Centers for Medicare and Medicaid Services (CMS), the American Heart Association, and the CDC. SHM was the only medical society represented. Pretty heady stuff for a field barely 10 years old. How did we get there? For that story, we need to go back a few years.

In 1984, Libby Zion, an 18-year-old college student, died from serotonin syndrome. A contributing factor was felt to be overworked residents not getting enough sleep. In his landmark 1990 article, “Human Factors in Hazardous Situations,” James Reason, PhD, introduced the world to some key concepts: active versus latent errors and the Swiss cheese model of errors.² These concepts influence our thinking to this day. In 1994, Betsy Lehman, a health reporter for the Boston Globe, died from a massive chemotherapy overdose. That same year Lucian Leape, MD, a Harvard pediatric surgeon, published his influential article in JAMA, “Errors in Medicine,” which called for a systems approach to improving patient safety.³

These key moments in safety and quality, all of which occurred in the years leading up to hospitalists gaining their identity, were but a prelude to the widespread patient safety and quality movement. Like our own social movement, “Patient Safety and Quality” was born with an influential publication. This was the 1999 release of the Institute of Medicine’s “To Err is Human,” a report that reiterated claims that up to 98,000 U.S. patients per year were dying from medical errors.⁴ It also supported Dr. Leape’s earlier work calling for systems changes. In 2001, the Institute of Medicine published a second report, “Crossing the Quality Chasm: A New Health System for the 21st Century,” which introduced the six aims for healthcare improvement: safe, timely, effective, efficient, equitable, and patient-centered.⁵

Before 1999, hospitalists were just getting their feet on the ground. Groups were experimenting with practice models and recruiting young talent, mostly with a pitch for a new way to practice with freedom to design their day and often an interesting work schedule.

After the publication of “To Err is Human” in 1999, changes in patient safety and quality began to accelerate. Taking one of the recommendations from “To Err is Human,” which suggested that employers should use their market power to improve quality and safety, the Leapfrog Group, a consortium of large employers, organized in 2000. Leapfrog began rewarding and recognizing hospitals that put accepted safety measures in place.⁶ Suddenly, hospital CEOs began to see tangible rewards for improving quality in their hospitals.

Here is where the hospitalist movement and the patient safety and quality movement began to intersect.

Shift to Quality and Safety

In 2001, the same year “Crossing the Quality Chasm” was published, Congress created the Center for Quality Improvement and Patient Safety within the Agency for Healthcare Research and Quality. Significant funding was suddenly available for quality and safety research, and a more organized reporting mechanism for quality would soon be available.

In 2002, the Joint Commission released its first set of National Patient Safety Goals. There were seven, and key goals for hospitalists included improving the effectiveness of communication among caregivers, reducing the risk of healthcare-acquired infections, and reconciling medications.

And, lastly, as if that weren’t enough activity in the patient safety and quality world, the Joint Commission and CMS released in 2003 the first joint, aligned set of core measures, with which we are all now very familiar, around acute myocardial infarction, congestive heart failure, and pneumonia.

Hospital executives were trying to get a handle on the meaning of this flurry of activity for their hospitals. It certainly meant new regulatory requirements. It probably meant greater visibility to the public around what happened behind the walls of their facilities. No doubt dollars on the line wouldn’t be too far behind. They needed help, and they needed it fast.

No longer were hospitalists a small group of young docs roaming the halls; now, instead of just taking care of one patient at a time, they were reaching the threshold of size—and even status in some organizations—where they could leverage their working knowledge of the system and presence on site to affect the various facets of quality now being measured and incented. Additionally, as the information technology (IT) revolution rolled out, hospitalists, mostly tech-savvy Gen X’ers, looked to ease the transition into the new world of EHRs, which promised to serve as a new base for improving quality.

As the C-suite continued making value calculations in their heads, they saw that, in addition to helping them manage the many facets of the transition of primary care and specialty teaching attendings out of the hospital, hospitalists could now be a powerful weapon in helping them stay competitive in the looming patient safety and quality revolution. They pulled out their checkbooks.

When SHM first started gathering data to explore this gap, we discovered that in 2003 the reported median support per FTE of an adult hospitalist in this country was $60,000.⁷ With an estimated 11,000 hospitalists in the country at that time, C-suite funders paid out over $600 million to help overcome the deficit between hospitalist professional billings and salary and benefits. By the time SHM partnered with IHI on the 5 Million Lives Campaign in 2006, the figure stood at well over $2 billion. The 2011 SHM/Medical Group Management Association survey data showed $139,090 support per FTE. With 31,000 U.S. hospitalists estimated at the time, that figure had doubled to over $4 billion in just five years’ time.

The new generation of doctors had come along in the late 1990s looking for a practice that fit their wants and needs. HM gave them what they were looking for: autonomy, the promise of work-life balance, and the ability to help patients in their most vulnerable time. The traditional E&M [evaluation and management]-based funding mechanisms simply weren’t designed to account for physicians who spend all of their time doing the critical cognitive and coordinating clinical work. To account for this, hospitals and medical groups, seeing the value to their organizations in this new specialty, anteed up to cover the difference. That gave us a great beginning.

But it was the convergence of the early hospitalist movement and the emergent patient safety and quality movement that created a synergy that propelled both movements forward. Boosted by the influx of funding directly and indirectly related to patient safety and quality, hospitalists grew in number from an estimated 5,000 physicians at the 1999 publication of “To Err is Human” to north of 40,000 today.

The synergy was evident when SHM President-Elect Dr. Holman, representing our fledgling specialty and society, faced that cheering throng in Orlando alongside Dr. Don Berwick, the face of the patient safety and quality movement.

But that’s not quite the end of the story.

To get us up to the present and on to our bright future, there will be a few more additions to the quality story and an all-new generation arriving on the scene to shake things up.

Dr. Kealey is SHM president and medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn.

References

1. Institute for Healthcare Improvement. Overview of the 100,000 Lives Campaign. Available at: http://www.ihi.org/Engage/Initiatives/Completed/5MillionLivesCampaign/Documents/Overview%20of%20the%20100K%20Campaign.pdf. Accessed July 6, 2014.
2. Broadbent DE, Reason J, Baddeley A, eds. Human Factors in Hazardous Situations: Proceedings of a Royal Society Discussion Meeting Held on 28 and 29 June 1989. Gloucestershire, England: Clarendon Press; 1990:475-484.
3. Leape LL. Error in medicine JAMA.1994;272(23):1851-1857.
4. Institute of Medicine. Kohn LT, Corrigan JM, Donaldson MS, eds. To Err Is Human: Building a Safer Health System. Washington, D.C.: The National Academy Press; 2000.
5. Institute of Medicine. Committee on Quality of Healthcare in America. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, D.C.: The National Academy Press; 2001.
6. The Leapfrog Group. About Leapfrog. Available at: http://www.leapfroggroup.org/about_leapfrog. Accessed July 6, 2014.
7. Society of Hospital Medicine. SHM’s State of Hospital Medicine Surveys 2003-2012. Available at: www.hospitalmedicine.org/survey. Accessed July 3, 2014.

Dr. Kealey

Hippocrates, Epidemics.“The Physician must be able to do good or to do no harm.”

This is part three of my ongoing series on the journey of hospital medicine and how we are poised for greater things yet. In part one, “Tinder and Spark,” macro changes in the American healthcare landscape pressured primary care physicians to get creative with new ways to practice, the most prominent result being the creation of hospitalist practices. Wachter and Goldman provided the spark that gave the field its name and cohesiveness. In part two, “Fuel,” the Baby Boomers shaped the field, setting the stage for the Generation X physicians who fueled HM’s early growth.

But the field might have stagnated there, the fire attenuated, if not for the rise of something new, something that stoked our growth to new heights.

Orlando, Fla., December 2006.

SHM President-Elect Rusty Holman, MD, MHM, was on stage representing hospitalists at the annual Institute for Healthcare Improvement (IHI) National Forum in front of more than 5,000 enthusiastic attendees representing every discipline of clinical care from hundreds of healthcare organizations across the country and internationally. This was a special event. Two years earlier, IHI President Don Berwick, MD, MPP, had launched an audacious campaign, called the 100,000 Lives Campaign, that aimed to prevent the deaths of 100,000 patients in our nation’s hospitals in the following 18 months, not by utilizing some great new technological advance but by changing the culture around safety and quality in our nation’s hospitals and enacting proven safety methods and processes.1 Out of this plan came widespread use of terms and programs that weren’t widely adopted then but are familiar to all of us now: rapid response teams, medicine reconciliation, surgical site infection prevention, and ventilator-acquired pneumonia.

That program estimated that it saved 122,000 lives.¹

IHI was looking to build on the safety and quality infrastructure that had been built up to make the 100,000 Lives Campaign a success and to launch an even bigger program. The 5 Million Lives Campaign’s goal was to reduce incidents of harm in five million patients over the next two years. For this campaign, IHI understood that success could only be achieved with partners. SHM and the field of hospital medicine, which had grown in size and influence, was seen as a critical and influential partner in achieving the goal of reducing harm in our nation’s hospitals. Thus, Dr. Holman was standing on that stage for SHM at the launch of the biggest safety and quality initiative in our nation’s history. SHM was among seven partner organizations, including the American Nurses Association, the Centers for Medicare and Medicaid Services (CMS), the American Heart Association, and the CDC. SHM was the only medical society represented. Pretty heady stuff for a field barely 10 years old. How did we get there? For that story, we need to go back a few years.

In 1984, Libby Zion, an 18-year-old college student, died from serotonin syndrome. A contributing factor was felt to be overworked residents not getting enough sleep. In his landmark 1990 article, “Human Factors in Hazardous Situations,” James Reason, PhD, introduced the world to some key concepts: active versus latent errors and the Swiss cheese model of errors.² These concepts influence our thinking to this day. In 1994, Betsy Lehman, a health reporter for the Boston Globe, died from a massive chemotherapy overdose. That same year Lucian Leape, MD, a Harvard pediatric surgeon, published his influential article in JAMA, “Errors in Medicine,” which called for a systems approach to improving patient safety.³

These key moments in safety and quality, all of which occurred in the years leading up to hospitalists gaining their identity, were but a prelude to the widespread patient safety and quality movement. Like our own social movement, “Patient Safety and Quality” was born with an influential publication. This was the 1999 release of the Institute of Medicine’s “To Err is Human,” a report that reiterated claims that up to 98,000 U.S. patients per year were dying from medical errors.⁴ It also supported Dr. Leape’s earlier work calling for systems changes. In 2001, the Institute of Medicine published a second report, “Crossing the Quality Chasm: A New Health System for the 21st Century,” which introduced the six aims for healthcare improvement: safe, timely, effective, efficient, equitable, and patient-centered.⁵

Before 1999, hospitalists were just getting their feet on the ground. Groups were experimenting with practice models and recruiting young talent, mostly with a pitch for a new way to practice with freedom to design their day and often an interesting work schedule.

After the publication of “To Err is Human” in 1999, changes in patient safety and quality began to accelerate. Taking one of the recommendations from “To Err is Human,” which suggested that employers should use their market power to improve quality and safety, the Leapfrog Group, a consortium of large employers, organized in 2000. Leapfrog began rewarding and recognizing hospitals that put accepted safety measures in place.⁶ Suddenly, hospital CEOs began to see tangible rewards for improving quality in their hospitals.

Here is where the hospitalist movement and the patient safety and quality movement began to intersect.

Shift to Quality and Safety

In 2001, the same year “Crossing the Quality Chasm” was published, Congress created the Center for Quality Improvement and Patient Safety within the Agency for Healthcare Research and Quality. Significant funding was suddenly available for quality and safety research, and a more organized reporting mechanism for quality would soon be available.

In 2002, the Joint Commission released its first set of National Patient Safety Goals. There were seven, and key goals for hospitalists included improving the effectiveness of communication among caregivers, reducing the risk of healthcare-acquired infections, and reconciling medications.

And, lastly, as if that weren’t enough activity in the patient safety and quality world, the Joint Commission and CMS released in 2003 the first joint, aligned set of core measures, with which we are all now very familiar, around acute myocardial infarction, congestive heart failure, and pneumonia.

Hospital executives were trying to get a handle on the meaning of this flurry of activity for their hospitals. It certainly meant new regulatory requirements. It probably meant greater visibility to the public around what happened behind the walls of their facilities. No doubt dollars on the line wouldn’t be too far behind. They needed help, and they needed it fast.

No longer were hospitalists a small group of young docs roaming the halls; now, instead of just taking care of one patient at a time, they were reaching the threshold of size—and even status in some organizations—where they could leverage their working knowledge of the system and presence on site to affect the various facets of quality now being measured and incented. Additionally, as the information technology (IT) revolution rolled out, hospitalists, mostly tech-savvy Gen X’ers, looked to ease the transition into the new world of EHRs, which promised to serve as a new base for improving quality.

As the C-suite continued making value calculations in their heads, they saw that, in addition to helping them manage the many facets of the transition of primary care and specialty teaching attendings out of the hospital, hospitalists could now be a powerful weapon in helping them stay competitive in the looming patient safety and quality revolution. They pulled out their checkbooks.

When SHM first started gathering data to explore this gap, we discovered that in 2003 the reported median support per FTE of an adult hospitalist in this country was $60,000.⁷ With an estimated 11,000 hospitalists in the country at that time, C-suite funders paid out over $600 million to help overcome the deficit between hospitalist professional billings and salary and benefits. By the time SHM partnered with IHI on the 5 Million Lives Campaign in 2006, the figure stood at well over $2 billion. The 2011 SHM/Medical Group Management Association survey data showed $139,090 support per FTE. With 31,000 U.S. hospitalists estimated at the time, that figure had doubled to over $4 billion in just five years’ time.

The new generation of doctors had come along in the late 1990s looking for a practice that fit their wants and needs. HM gave them what they were looking for: autonomy, the promise of work-life balance, and the ability to help patients in their most vulnerable time. The traditional E&M [evaluation and management]-based funding mechanisms simply weren’t designed to account for physicians who spend all of their time doing the critical cognitive and coordinating clinical work. To account for this, hospitals and medical groups, seeing the value to their organizations in this new specialty, anteed up to cover the difference. That gave us a great beginning.

But it was the convergence of the early hospitalist movement and the emergent patient safety and quality movement that created a synergy that propelled both movements forward. Boosted by the influx of funding directly and indirectly related to patient safety and quality, hospitalists grew in number from an estimated 5,000 physicians at the 1999 publication of “To Err is Human” to north of 40,000 today.

The synergy was evident when SHM President-Elect Dr. Holman, representing our fledgling specialty and society, faced that cheering throng in Orlando alongside Dr. Don Berwick, the face of the patient safety and quality movement.

But that’s not quite the end of the story.

To get us up to the present and on to our bright future, there will be a few more additions to the quality story and an all-new generation arriving on the scene to shake things up.

Dr. Kealey is SHM president and medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn.

References

1. Institute for Healthcare Improvement. Overview of the 100,000 Lives Campaign. Available at: http://www.ihi.org/Engage/Initiatives/Completed/5MillionLivesCampaign/Documents/Overview%20of%20the%20100K%20Campaign.pdf. Accessed July 6, 2014.
2. Broadbent DE, Reason J, Baddeley A, eds. Human Factors in Hazardous Situations: Proceedings of a Royal Society Discussion Meeting Held on 28 and 29 June 1989. Gloucestershire, England: Clarendon Press; 1990:475-484.
3. Leape LL. Error in medicine JAMA.1994;272(23):1851-1857.
4. Institute of Medicine. Kohn LT, Corrigan JM, Donaldson MS, eds. To Err Is Human: Building a Safer Health System. Washington, D.C.: The National Academy Press; 2000.
5. Institute of Medicine. Committee on Quality of Healthcare in America. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, D.C.: The National Academy Press; 2001.
6. The Leapfrog Group. About Leapfrog. Available at: http://www.leapfroggroup.org/about_leapfrog. Accessed July 6, 2014.
7. Society of Hospital Medicine. SHM’s State of Hospital Medicine Surveys 2003-2012. Available at: www.hospitalmedicine.org/survey. Accessed July 3, 2014.

Dr. Kealey

Hippocrates, Epidemics.“The Physician must be able to do good or to do no harm.”

This is part three of my ongoing series on the journey of hospital medicine and how we are poised for greater things yet. In part one, “Tinder and Spark,” macro changes in the American healthcare landscape pressured primary care physicians to get creative with new ways to practice, the most prominent result being the creation of hospitalist practices. Wachter and Goldman provided the spark that gave the field its name and cohesiveness. In part two, “Fuel,” the Baby Boomers shaped the field, setting the stage for the Generation X physicians who fueled HM’s early growth.

But the field might have stagnated there, the fire attenuated, if not for the rise of something new, something that stoked our growth to new heights.

Orlando, Fla., December 2006.

SHM President-Elect Rusty Holman, MD, MHM, was on stage representing hospitalists at the annual Institute for Healthcare Improvement (IHI) National Forum in front of more than 5,000 enthusiastic attendees representing every discipline of clinical care from hundreds of healthcare organizations across the country and internationally. This was a special event. Two years earlier, IHI President Don Berwick, MD, MPP, had launched an audacious campaign, called the 100,000 Lives Campaign, that aimed to prevent the deaths of 100,000 patients in our nation’s hospitals in the following 18 months, not by utilizing some great new technological advance but by changing the culture around safety and quality in our nation’s hospitals and enacting proven safety methods and processes.1 Out of this plan came widespread use of terms and programs that weren’t widely adopted then but are familiar to all of us now: rapid response teams, medicine reconciliation, surgical site infection prevention, and ventilator-acquired pneumonia.

That program estimated that it saved 122,000 lives.¹

IHI was looking to build on the safety and quality infrastructure that had been built up to make the 100,000 Lives Campaign a success and to launch an even bigger program. The 5 Million Lives Campaign’s goal was to reduce incidents of harm in five million patients over the next two years. For this campaign, IHI understood that success could only be achieved with partners. SHM and the field of hospital medicine, which had grown in size and influence, was seen as a critical and influential partner in achieving the goal of reducing harm in our nation’s hospitals. Thus, Dr. Holman was standing on that stage for SHM at the launch of the biggest safety and quality initiative in our nation’s history. SHM was among seven partner organizations, including the American Nurses Association, the Centers for Medicare and Medicaid Services (CMS), the American Heart Association, and the CDC. SHM was the only medical society represented. Pretty heady stuff for a field barely 10 years old. How did we get there? For that story, we need to go back a few years.

In 1984, Libby Zion, an 18-year-old college student, died from serotonin syndrome. A contributing factor was felt to be overworked residents not getting enough sleep. In his landmark 1990 article, “Human Factors in Hazardous Situations,” James Reason, PhD, introduced the world to some key concepts: active versus latent errors and the Swiss cheese model of errors.² These concepts influence our thinking to this day. In 1994, Betsy Lehman, a health reporter for the Boston Globe, died from a massive chemotherapy overdose. That same year Lucian Leape, MD, a Harvard pediatric surgeon, published his influential article in JAMA, “Errors in Medicine,” which called for a systems approach to improving patient safety.³

These key moments in safety and quality, all of which occurred in the years leading up to hospitalists gaining their identity, were but a prelude to the widespread patient safety and quality movement. Like our own social movement, “Patient Safety and Quality” was born with an influential publication. This was the 1999 release of the Institute of Medicine’s “To Err is Human,” a report that reiterated claims that up to 98,000 U.S. patients per year were dying from medical errors.⁴ It also supported Dr. Leape’s earlier work calling for systems changes. In 2001, the Institute of Medicine published a second report, “Crossing the Quality Chasm: A New Health System for the 21st Century,” which introduced the six aims for healthcare improvement: safe, timely, effective, efficient, equitable, and patient-centered.⁵

Before 1999, hospitalists were just getting their feet on the ground. Groups were experimenting with practice models and recruiting young talent, mostly with a pitch for a new way to practice with freedom to design their day and often an interesting work schedule.

After the publication of “To Err is Human” in 1999, changes in patient safety and quality began to accelerate. Taking one of the recommendations from “To Err is Human,” which suggested that employers should use their market power to improve quality and safety, the Leapfrog Group, a consortium of large employers, organized in 2000. Leapfrog began rewarding and recognizing hospitals that put accepted safety measures in place.⁶ Suddenly, hospital CEOs began to see tangible rewards for improving quality in their hospitals.

Here is where the hospitalist movement and the patient safety and quality movement began to intersect.

Shift to Quality and Safety

In 2001, the same year “Crossing the Quality Chasm” was published, Congress created the Center for Quality Improvement and Patient Safety within the Agency for Healthcare Research and Quality. Significant funding was suddenly available for quality and safety research, and a more organized reporting mechanism for quality would soon be available.

In 2002, the Joint Commission released its first set of National Patient Safety Goals. There were seven, and key goals for hospitalists included improving the effectiveness of communication among caregivers, reducing the risk of healthcare-acquired infections, and reconciling medications.

And, lastly, as if that weren’t enough activity in the patient safety and quality world, the Joint Commission and CMS released in 2003 the first joint, aligned set of core measures, with which we are all now very familiar, around acute myocardial infarction, congestive heart failure, and pneumonia.

Hospital executives were trying to get a handle on the meaning of this flurry of activity for their hospitals. It certainly meant new regulatory requirements. It probably meant greater visibility to the public around what happened behind the walls of their facilities. No doubt dollars on the line wouldn’t be too far behind. They needed help, and they needed it fast.

No longer were hospitalists a small group of young docs roaming the halls; now, instead of just taking care of one patient at a time, they were reaching the threshold of size—and even status in some organizations—where they could leverage their working knowledge of the system and presence on site to affect the various facets of quality now being measured and incented. Additionally, as the information technology (IT) revolution rolled out, hospitalists, mostly tech-savvy Gen X’ers, looked to ease the transition into the new world of EHRs, which promised to serve as a new base for improving quality.

As the C-suite continued making value calculations in their heads, they saw that, in addition to helping them manage the many facets of the transition of primary care and specialty teaching attendings out of the hospital, hospitalists could now be a powerful weapon in helping them stay competitive in the looming patient safety and quality revolution. They pulled out their checkbooks.

When SHM first started gathering data to explore this gap, we discovered that in 2003 the reported median support per FTE of an adult hospitalist in this country was $60,000.⁷ With an estimated 11,000 hospitalists in the country at that time, C-suite funders paid out over $600 million to help overcome the deficit between hospitalist professional billings and salary and benefits. By the time SHM partnered with IHI on the 5 Million Lives Campaign in 2006, the figure stood at well over $2 billion. The 2011 SHM/Medical Group Management Association survey data showed $139,090 support per FTE. With 31,000 U.S. hospitalists estimated at the time, that figure had doubled to over $4 billion in just five years’ time.

The new generation of doctors had come along in the late 1990s looking for a practice that fit their wants and needs. HM gave them what they were looking for: autonomy, the promise of work-life balance, and the ability to help patients in their most vulnerable time. The traditional E&M [evaluation and management]-based funding mechanisms simply weren’t designed to account for physicians who spend all of their time doing the critical cognitive and coordinating clinical work. To account for this, hospitals and medical groups, seeing the value to their organizations in this new specialty, anteed up to cover the difference. That gave us a great beginning.

But it was the convergence of the early hospitalist movement and the emergent patient safety and quality movement that created a synergy that propelled both movements forward. Boosted by the influx of funding directly and indirectly related to patient safety and quality, hospitalists grew in number from an estimated 5,000 physicians at the 1999 publication of “To Err is Human” to north of 40,000 today.

The synergy was evident when SHM President-Elect Dr. Holman, representing our fledgling specialty and society, faced that cheering throng in Orlando alongside Dr. Don Berwick, the face of the patient safety and quality movement.

But that’s not quite the end of the story.

To get us up to the present and on to our bright future, there will be a few more additions to the quality story and an all-new generation arriving on the scene to shake things up.

Dr. Kealey is SHM president and medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn.

References

1. Institute for Healthcare Improvement. Overview of the 100,000 Lives Campaign. Available at: http://www.ihi.org/Engage/Initiatives/Completed/5MillionLivesCampaign/Documents/Overview%20of%20the%20100K%20Campaign.pdf. Accessed July 6, 2014.
2. Broadbent DE, Reason J, Baddeley A, eds. Human Factors in Hazardous Situations: Proceedings of a Royal Society Discussion Meeting Held on 28 and 29 June 1989. Gloucestershire, England: Clarendon Press; 1990:475-484.
3. Leape LL. Error in medicine JAMA.1994;272(23):1851-1857.
4. Institute of Medicine. Kohn LT, Corrigan JM, Donaldson MS, eds. To Err Is Human: Building a Safer Health System. Washington, D.C.: The National Academy Press; 2000.
5. Institute of Medicine. Committee on Quality of Healthcare in America. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, D.C.: The National Academy Press; 2001.
6. The Leapfrog Group. About Leapfrog. Available at: http://www.leapfroggroup.org/about_leapfrog. Accessed July 6, 2014.
7. Society of Hospital Medicine. SHM’s State of Hospital Medicine Surveys 2003-2012. Available at: www.hospitalmedicine.org/survey. Accessed July 3, 2014.

Dr. Fedderson

Growing up in America’s heartland, Julie Fedderson, MD, realized at an early age that something wasn’t right with the U.S. healthcare system. Her grandmother, a “headstrong” immigrant from the Czech Republic, died of colon cancer when Dr. Fedderson was young, and that experience—watching a loved one “reduced to tears” trying to navigate a complicated and impersonal healthcare system in rural Nebraska—made her realize “how important having dedicated physicians is.”

“It may sound naïve, but I really wanted to help people,” says Dr. Fedderson, who grew up and went to high school in a small town two hours from an urban center. She eventually attended college in what she saw as the big city—Lincoln, Nebraska. After attending the University of Nebraska, Dr. Fedderson went to medical school at the University of Nebraska Medical School (UNMC) in Omaha. She did her residency at Baylor College of Medicine in Houston, then returned to Nebraska.

Since 2003, she has worked as a hospitalist and is currently an assistant professor in the department of internal medicine at the UNMC. Her story, practicing as a “traditional” internist for several years before making the switch to HM, is similar to many in hospital medicine.

“I wanted to make an impact on the seamless transition of in-house care to outpatient care,” says one of the newest members of Team Hospitalist, the volunteer editorial advisory board of The Hospitalist. “The two are so intricately intertwined, yet so siloed, and many times the patient—who is the least capable of navigating our complex systems—is the one who is left with the responsibility to do it. I wanted to improve that.”

Dr. Fedderson

Dr. Fedderson is working toward her master’s degree from the University of Colorado’s Executive MBA Program. She is the resident supervisor for UNMC’s Physicians Midtown Clinic, serves as the Nebraska Medical Center’s enterprise chief quality and outcomes officer, and is on the board of directors of Nebraska Health Partners. She is also a member of the department of internal medicine’s executive committee.

Question: What do you like most about working as a hospitalist?

Answer: The ability to implement rapid change of process in a controlled environment.

Q: What do you dislike most?

A: The regulatory ties placed on hospitals that may not be quality oriented [and] the difficulty of handling the outpatient care of uninsured or underinsured patients.

Q: What’s the best advice you ever received?

A: For life: Shut up and listen. From one of my attendings during my residency: Piss, pus, and hostility all must come out eventually.

Q: What’s the biggest change you’ve seen in hospital medicine in your career?

A: The shift to technology as a basis of care. When done well, it is phenomenal. When done without appropriate thought, it can be disastrous for patients and providers alike.

Q: Why is it important for you, as a hospitalist group leader, to continue seeing patients?

A: How do you implement change if you have no skin in the game? I stay current and see patients to see the system work firsthand and to provide innovative—but practical—solutions.

Q: Outside of patient care, what are your career interests?

A: I am currently our new chief quality and outcomes officer at The Nebraska Medical Center Enterprise. I am also involved as a physician champion for our electronic health record [EHR] implementation and in clinical documentation improvement at all levels.

Q: What is your biggest professional challenge?

A: There are a lot of daunting things coming from entities that don’t necessarily have a patient’s best interests at heart. Keeping sane doing the “regulatory” quality while still providing good quality care is a challenge. Sometimes it feels like a game—but obviously a game with serious consequences.

Q: What is your biggest professional reward?

A: Frankly, [it is] when one of my colleagues relates to me a success story with a new process or plan. I hear so many of my medical friends so dissatisfied with healthcare’s trajectory—they’re burned out, telling their kids to not go into medicine. When I see someone get that spark back for their career and their reason for choosing it, that makes me feel fantastic.

Q: When you aren’t working, what is important to you?

A: I have two boys, and they hung the moon. We hang out as much as possible. I am also into physical fitness, so I try to run, do yoga, and hike as much as I can.

Q: Where do you see yourself in 10 years?

A: I would like to continue to be a chief quality officer, potentially for an entire healthcare system.

Q: If you weren’t a doctor, what would you be doing right now?

A: Writing romance novels.

Q: What’s the best book you’ve read recently? Why?

A: “Mountains Beyond Mountains” by Tracy Kidder. It’s about Dr. Paul Farmer’s work in Haiti. Really exemplifies that one person can change lives.

Q: How many Apple products (phones, iPods, tablets, iTunes, etc.) do you interface with in a given week?

A: I’ve been infiltrated with Apples. My iPhone seldom leaves my hand. I use an iPad for notes and to chart. I run three miles a day with my iPod. I own two Macs.

Q: What’s next in your Netflix queue?

A: I have a six- and a seven-year-old, so anything with animation. Last great movie I saw was “Silver Linings Playbook.”

Richard Quinn is a freelance writer in New Jersey.

Dr. Fedderson

Growing up in America’s heartland, Julie Fedderson, MD, realized at an early age that something wasn’t right with the U.S. healthcare system. Her grandmother, a “headstrong” immigrant from the Czech Republic, died of colon cancer when Dr. Fedderson was young, and that experience—watching a loved one “reduced to tears” trying to navigate a complicated and impersonal healthcare system in rural Nebraska—made her realize “how important having dedicated physicians is.”

“It may sound naïve, but I really wanted to help people,” says Dr. Fedderson, who grew up and went to high school in a small town two hours from an urban center. She eventually attended college in what she saw as the big city—Lincoln, Nebraska. After attending the University of Nebraska, Dr. Fedderson went to medical school at the University of Nebraska Medical School (UNMC) in Omaha. She did her residency at Baylor College of Medicine in Houston, then returned to Nebraska.

Since 2003, she has worked as a hospitalist and is currently an assistant professor in the department of internal medicine at the UNMC. Her story, practicing as a “traditional” internist for several years before making the switch to HM, is similar to many in hospital medicine.

“I wanted to make an impact on the seamless transition of in-house care to outpatient care,” says one of the newest members of Team Hospitalist, the volunteer editorial advisory board of The Hospitalist. “The two are so intricately intertwined, yet so siloed, and many times the patient—who is the least capable of navigating our complex systems—is the one who is left with the responsibility to do it. I wanted to improve that.”

Dr. Fedderson

Dr. Fedderson is working toward her master’s degree from the University of Colorado’s Executive MBA Program. She is the resident supervisor for UNMC’s Physicians Midtown Clinic, serves as the Nebraska Medical Center’s enterprise chief quality and outcomes officer, and is on the board of directors of Nebraska Health Partners. She is also a member of the department of internal medicine’s executive committee.

Question: What do you like most about working as a hospitalist?

Answer: The ability to implement rapid change of process in a controlled environment.

Q: What do you dislike most?

A: The regulatory ties placed on hospitals that may not be quality oriented [and] the difficulty of handling the outpatient care of uninsured or underinsured patients.

Q: What’s the best advice you ever received?

A: For life: Shut up and listen. From one of my attendings during my residency: Piss, pus, and hostility all must come out eventually.

Q: What’s the biggest change you’ve seen in hospital medicine in your career?

A: The shift to technology as a basis of care. When done well, it is phenomenal. When done without appropriate thought, it can be disastrous for patients and providers alike.

Q: Why is it important for you, as a hospitalist group leader, to continue seeing patients?

A: How do you implement change if you have no skin in the game? I stay current and see patients to see the system work firsthand and to provide innovative—but practical—solutions.

Q: Outside of patient care, what are your career interests?

A: I am currently our new chief quality and outcomes officer at The Nebraska Medical Center Enterprise. I am also involved as a physician champion for our electronic health record [EHR] implementation and in clinical documentation improvement at all levels.

Q: What is your biggest professional challenge?

A: There are a lot of daunting things coming from entities that don’t necessarily have a patient’s best interests at heart. Keeping sane doing the “regulatory” quality while still providing good quality care is a challenge. Sometimes it feels like a game—but obviously a game with serious consequences.

Q: What is your biggest professional reward?

A: Frankly, [it is] when one of my colleagues relates to me a success story with a new process or plan. I hear so many of my medical friends so dissatisfied with healthcare’s trajectory—they’re burned out, telling their kids to not go into medicine. When I see someone get that spark back for their career and their reason for choosing it, that makes me feel fantastic.

Q: When you aren’t working, what is important to you?

A: I have two boys, and they hung the moon. We hang out as much as possible. I am also into physical fitness, so I try to run, do yoga, and hike as much as I can.

Q: Where do you see yourself in 10 years?

A: I would like to continue to be a chief quality officer, potentially for an entire healthcare system.

Q: If you weren’t a doctor, what would you be doing right now?

A: Writing romance novels.

Q: What’s the best book you’ve read recently? Why?

A: “Mountains Beyond Mountains” by Tracy Kidder. It’s about Dr. Paul Farmer’s work in Haiti. Really exemplifies that one person can change lives.

Q: How many Apple products (phones, iPods, tablets, iTunes, etc.) do you interface with in a given week?

A: I’ve been infiltrated with Apples. My iPhone seldom leaves my hand. I use an iPad for notes and to chart. I run three miles a day with my iPod. I own two Macs.

Q: What’s next in your Netflix queue?

A: I have a six- and a seven-year-old, so anything with animation. Last great movie I saw was “Silver Linings Playbook.”

Richard Quinn is a freelance writer in New Jersey.

Dr. Fedderson

Growing up in America’s heartland, Julie Fedderson, MD, realized at an early age that something wasn’t right with the U.S. healthcare system. Her grandmother, a “headstrong” immigrant from the Czech Republic, died of colon cancer when Dr. Fedderson was young, and that experience—watching a loved one “reduced to tears” trying to navigate a complicated and impersonal healthcare system in rural Nebraska—made her realize “how important having dedicated physicians is.”

“It may sound naïve, but I really wanted to help people,” says Dr. Fedderson, who grew up and went to high school in a small town two hours from an urban center. She eventually attended college in what she saw as the big city—Lincoln, Nebraska. After attending the University of Nebraska, Dr. Fedderson went to medical school at the University of Nebraska Medical School (UNMC) in Omaha. She did her residency at Baylor College of Medicine in Houston, then returned to Nebraska.

Since 2003, she has worked as a hospitalist and is currently an assistant professor in the department of internal medicine at the UNMC. Her story, practicing as a “traditional” internist for several years before making the switch to HM, is similar to many in hospital medicine.

“I wanted to make an impact on the seamless transition of in-house care to outpatient care,” says one of the newest members of Team Hospitalist, the volunteer editorial advisory board of The Hospitalist. “The two are so intricately intertwined, yet so siloed, and many times the patient—who is the least capable of navigating our complex systems—is the one who is left with the responsibility to do it. I wanted to improve that.”

Dr. Fedderson

Dr. Fedderson is working toward her master’s degree from the University of Colorado’s Executive MBA Program. She is the resident supervisor for UNMC’s Physicians Midtown Clinic, serves as the Nebraska Medical Center’s enterprise chief quality and outcomes officer, and is on the board of directors of Nebraska Health Partners. She is also a member of the department of internal medicine’s executive committee.

Question: What do you like most about working as a hospitalist?

Answer: The ability to implement rapid change of process in a controlled environment.

Q: What do you dislike most?

A: The regulatory ties placed on hospitals that may not be quality oriented [and] the difficulty of handling the outpatient care of uninsured or underinsured patients.

Q: What’s the best advice you ever received?

A: For life: Shut up and listen. From one of my attendings during my residency: Piss, pus, and hostility all must come out eventually.

Q: What’s the biggest change you’ve seen in hospital medicine in your career?

A: The shift to technology as a basis of care. When done well, it is phenomenal. When done without appropriate thought, it can be disastrous for patients and providers alike.

Q: Why is it important for you, as a hospitalist group leader, to continue seeing patients?

A: How do you implement change if you have no skin in the game? I stay current and see patients to see the system work firsthand and to provide innovative—but practical—solutions.

Q: Outside of patient care, what are your career interests?

A: I am currently our new chief quality and outcomes officer at The Nebraska Medical Center Enterprise. I am also involved as a physician champion for our electronic health record [EHR] implementation and in clinical documentation improvement at all levels.

Q: What is your biggest professional challenge?

A: There are a lot of daunting things coming from entities that don’t necessarily have a patient’s best interests at heart. Keeping sane doing the “regulatory” quality while still providing good quality care is a challenge. Sometimes it feels like a game—but obviously a game with serious consequences.

Q: What is your biggest professional reward?

A: Frankly, [it is] when one of my colleagues relates to me a success story with a new process or plan. I hear so many of my medical friends so dissatisfied with healthcare’s trajectory—they’re burned out, telling their kids to not go into medicine. When I see someone get that spark back for their career and their reason for choosing it, that makes me feel fantastic.

Q: When you aren’t working, what is important to you?

A: I have two boys, and they hung the moon. We hang out as much as possible. I am also into physical fitness, so I try to run, do yoga, and hike as much as I can.

Q: Where do you see yourself in 10 years?

A: I would like to continue to be a chief quality officer, potentially for an entire healthcare system.

Q: If you weren’t a doctor, what would you be doing right now?

A: Writing romance novels.

Q: What’s the best book you’ve read recently? Why?

A: “Mountains Beyond Mountains” by Tracy Kidder. It’s about Dr. Paul Farmer’s work in Haiti. Really exemplifies that one person can change lives.

Q: How many Apple products (phones, iPods, tablets, iTunes, etc.) do you interface with in a given week?

A: I’ve been infiltrated with Apples. My iPhone seldom leaves my hand. I use an iPad for notes and to chart. I run three miles a day with my iPod. I own two Macs.

Q: What’s next in your Netflix queue?

A: I have a six- and a seven-year-old, so anything with animation. Last great movie I saw was “Silver Linings Playbook.”

Richard Quinn is a freelance writer in New Jersey.

Since 2008, the American Community Survey, conducted by the U.S. Census Bureau, has queried respondents regarding deafness or hearing difficulties. According to these data, about 3.5% of the U.S. population has serious difficulty hearing. Other estimates vary, putting the number higher, especially those that include the numbers of elderly who experience hearing difficulties.

People who are deaf and hard of hearing (DHoH) work in diverse areas of the healthcare field, according to Samuel Atcherson, PhD, associate professor of audiology at the University of Arkansas in Little Rock and registry co-chair for the Association of Medical Professionals with Hearing Losses (www.amphl.org). AMPHL does not have statistics to report on the numbers of DHoH individuals practicing in medical occupations, but Dr. Atcherson noted that, as of 2011, there were 55 physicians, 41 nurses, and eight physician assistants in the membership.

Dr. Moreland and co-authors recently published a national survey that queried deaf physicians and trainees on a variety of subjects (e.g. career satisfaction, satisfaction with education, workplace accommodations). Due to the Rehabilitation Act of 1973 and the Americans with Disabilities Act of 1990, more people with hearing impairments are entering healthcare professions. Technological advances, such as electronic stethoscopes, also contribute to this surge.

The authors found that DHoH physicians and trainees responding to their survey were satisfied with multimodal employment and educational accommodations. Based on these results, they surmise, there might be an opportunity to recruit these individuals and further reach the underserved DHoH patient population.

—Gretchen Henkel

Since 2008, the American Community Survey, conducted by the U.S. Census Bureau, has queried respondents regarding deafness or hearing difficulties. According to these data, about 3.5% of the U.S. population has serious difficulty hearing. Other estimates vary, putting the number higher, especially those that include the numbers of elderly who experience hearing difficulties.

People who are deaf and hard of hearing (DHoH) work in diverse areas of the healthcare field, according to Samuel Atcherson, PhD, associate professor of audiology at the University of Arkansas in Little Rock and registry co-chair for the Association of Medical Professionals with Hearing Losses (www.amphl.org). AMPHL does not have statistics to report on the numbers of DHoH individuals practicing in medical occupations, but Dr. Atcherson noted that, as of 2011, there were 55 physicians, 41 nurses, and eight physician assistants in the membership.

Dr. Moreland and co-authors recently published a national survey that queried deaf physicians and trainees on a variety of subjects (e.g. career satisfaction, satisfaction with education, workplace accommodations). Due to the Rehabilitation Act of 1973 and the Americans with Disabilities Act of 1990, more people with hearing impairments are entering healthcare professions. Technological advances, such as electronic stethoscopes, also contribute to this surge.

The authors found that DHoH physicians and trainees responding to their survey were satisfied with multimodal employment and educational accommodations. Based on these results, they surmise, there might be an opportunity to recruit these individuals and further reach the underserved DHoH patient population.

—Gretchen Henkel

Since 2008, the American Community Survey, conducted by the U.S. Census Bureau, has queried respondents regarding deafness or hearing difficulties. According to these data, about 3.5% of the U.S. population has serious difficulty hearing. Other estimates vary, putting the number higher, especially those that include the numbers of elderly who experience hearing difficulties.

People who are deaf and hard of hearing (DHoH) work in diverse areas of the healthcare field, according to Samuel Atcherson, PhD, associate professor of audiology at the University of Arkansas in Little Rock and registry co-chair for the Association of Medical Professionals with Hearing Losses (www.amphl.org). AMPHL does not have statistics to report on the numbers of DHoH individuals practicing in medical occupations, but Dr. Atcherson noted that, as of 2011, there were 55 physicians, 41 nurses, and eight physician assistants in the membership.

Dr. Moreland and co-authors recently published a national survey that queried deaf physicians and trainees on a variety of subjects (e.g. career satisfaction, satisfaction with education, workplace accommodations). Due to the Rehabilitation Act of 1973 and the Americans with Disabilities Act of 1990, more people with hearing impairments are entering healthcare professions. Technological advances, such as electronic stethoscopes, also contribute to this surge.

The authors found that DHoH physicians and trainees responding to their survey were satisfied with multimodal employment and educational accommodations. Based on these results, they surmise, there might be an opportunity to recruit these individuals and further reach the underserved DHoH patient population.

—Gretchen Henkel

click for large version

Case

A 67-year-old male patient who has depression and is on sertraline presents with increasing confusion over the past week. Initial plasma sodium is 109 mEq/L. On exam, he weighs 70 kg and is euvolemic. His urine osmolarity (Uosm) is 800 mosm/L with a urine sodium (UNa) of 40 mEq/L. He is somnolent but awakens to sternal rub. How should this patient’s hyponatremia be evaluated and managed?

Overview

Hyponatremia, a disorder of excess total body water in relation to sodium, occurs in up to 42% of hospitalized patients.^1,2 Regardless of the cause, hyponatremia is usually associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or with the appropriate elevation of antidiuretic hormone (ADH), known as hypovolemia. ADH is produced in the hypothalamus and released in the posterior pituitary in response to increasing plasma osmolarity (pOSM) or effective circulating volume depletion. ADH acts in the cortical collecting duct to increase the number of luminal aquaporin channels, increasing water reabsorption and decreasing plasma osmolarity. When hyponatremia is severe, the movement of water into cells causes cellular brain swelling, and clinical symptoms progress from malaise, headache, and nausea to obtundation, seizures, or respiratory arrest (see Figure 1). Even mild, chronic hyponatremia (120-131 mEq/L) is associated with an increased risk of falls due to mild gait and attention impairment.³

Evaluation

Step 1: Plasma osmolarity

The first step in diagnosing the cause of hyponatremia and treating it is to measure pOSM. The majority of patients with hyponatremia have hypoosmolar hyponatremia and therefore have a low pOSM; however, patients may have normal or high osmolarity. Hyponatremia with normal osmolarity can be caused by pseudohyponatremia (i.e., hyperglycemia, paraproteinemia, hyperlipidemia), severe renal failure, ingestion of excess alcohol, or post-transurethral resection of prostate or bladder.

Hyponatremia with high pOSM occurs as a result of elevated levels of an extra solute in the plasma that does not readily enter cells. This draws water into the extracellular fluid and lowers the sodium concentration. This will most commonly result from hyperglycemia or infusion of mannitol.

Step 2: Assess volume status with physical exam, urine sodium (UNa)

The majority of patients with hyponatremia will have low pOSM. These patients should be categorized by volume status: hypovolemic, euvolemic, or hypervolemic (see Figure 2). On exam, hypervolemia is usually evident, and the cause of hypervolemic hyponatremia is usually elicited from a patient’s history; however, differentiating between hypovolemic and euvolemic hyponatremia by history and physical exam can be difficult, because examination findings are neither sensitive nor specific.⁴ UNa should always be evaluated, especially when differentiating between hypovolemic and euvolemic. This was illustrated in a study of 58 non-edematous patients with hyponatremia. Investigators determined which patients had hypovolemic hyponatremia based on their response to saline infusion. Of the patients identified as hypovolemic using physical exam, only 47% responded to saline. In contrast, a spot UNa of less than 30 mEq/L was 80% sensitive and 100% specific for saline responsiveness.⁵ Although the majority of hypovolemic hyponatremia patients will have a low UNa, the following causes of hypovolemic hyponatremia can result in high UNa: diuretics, adrenal insufficiency, salt-wasting nephropathy, and cerebral salt-wasting.

A low serum uric acid can also be useful in differentiating hypovolemic and euvolemic hyponatremia, which is most commonly caused by SIADH. In SIADH, there is urinary wasting of uric acid, which leads to low serum uric acid. In a study of 105 patients with lung cancer, a serum uric acid of less than 4 mg/dL was 75% sensitive and 89% specific for SIADH.⁶

click for large version

Step 3: Urine osmolarity

After determining volume status, the physician should determine if there is excess ADH by measuring Uosm. Under normal conditions, hyponatremia should suppress ADH secretion and allow the kidney to excrete water by diluting the urine to less than 100 mosm/L. If Uosm is less than 100 mosm/L, then the kidneys are responding appropriately and can only persist in the following situations: The patient is drinking large volumes of water (e.g. primary polydipsia), there is insufficient solute to excrete free water (e.g. beer potomania, “tea and toast” diet), or the patient has a different set point for ADH suppression (i.e., reset osmostat). After determining volume status, UNa, and Uosm, the physician will have narrowed the cause of hyponatremia significantly (see Figure 2). Of note, when SIADH is diagnosed, it is important to look for and reverse causes (see Figure 3).

click for large version

click for large version

Treatment

Severe symptomatic hyponatremia

In patients with severe neurologic symptoms, physicians must balance the need to reduce symptoms quickly with the dangers of overly rapid correction. After its use in marathon runners, several experts have endorsed the following regimen to reduce symptoms rapidly: an intravenous bolus of 100 mL of 3% saline is given and repeated if symptoms persist after 10 minutes.7,8 Once symptoms improve, the basal rate can be calculated using the equation below, but the rate of sodium correction in 24 hours with this regimen should not exceed 6 to 8 mEq/L in 24 hours or 12 to 14 mEq/L in 48 hours.^9,10 This is based on several case studies showing that there were no cases of central pontine myelinolysis (CPM) if correction rates were less than 10 mEq/L over 24 hours.^11,12

It is important to remember that this is only a rough guide, because the equation assumes the entire infusate is retained and there is no sodium or water output. The best way to avoid overly rapid correction is to check serum sodium every two hours and monitor urine output closely. If the patient is making large volumes of urine, serum sodium may be rising too quickly. If the patient corrects too rapidly, it may be possible to avoid CPM by re-lowering the sodium.13 This can be accomplished by giving desmopressin to slow urinary free water loss while simultaneously giving hypotonic fluids.

Asymptomatic or mildly symptomatic hyponatremia

Hypovolemic hyponatremia: Treatment of hypovolemic hyponatremia is aimed at correcting volume status, the underlying problem that drives ADH secretion. The body will always choose to preserve volume over osmolarity. In most cases, normal saline (NS) should be used to restore intravascular volume, and the rate of infusion can be calculated using the same equation as above. Once volume is replete, ADH release will cease. Patients will be in danger of overly rapid correction of serum sodium, so fluids should be switched to hypotonic solutions, such as ½ NS.

Euvolemic Hyponatremia: Euvolemic hyponatremia, typically caused by SIADH, is characterized by a high Uosm (>100 mosm/L) and a high UNa (>30 mEq/L). All patients require free water restriction, and fluid intake should be at least 500 mL below a patient’s urine output, usually one liter or less. If this is ineffective, salt tabs can be given. Salt tabs will increase the solute load, necessitating an increase in urine output. Patients should be given approximately nine grams of salt tabs in three divided doses (equivalent to 1 L of NS). Patients with highly concentrated urine (Uosm >500 mosm/L) will not respond as well to the salt load, because the kidneys will continue to excrete much of the sodium in a concentrated urine. In such patients, a loop diuretic can be used to help excrete free water, because it decreases the Uosm to about ½ NS (154 mOsm/L). One possible regimen is 20-40 mg of oral furosemide two to three times daily.

Hypervolemic Hyponatremia: Hypervolemic hyponatremia is caused by congestive heart failure (CHF), cirrhosis, or nephrotic syndrome. In all cases, there is excess ADH as a result of the carotid baroreceptors sensing a decrease in effective circulation volume. In the case of CHF and cirrhosis, the degree of hyponatremia is a marker of disease severity, but there is no data to show that correction of hyponatremia improves outcomes. Fluid restriction is the cornerstone of therapy, but if the patient’s volume status is not optimized, then loop diuretics may improve hyponatremia through excretion of diluted urine. In addition, angiotensin-converting enzyme inhibitors can improve hyponatremia in CHF by reducing ADH levels and improving cardiac output via afterload reduction.

There has been recent interest in the use of vasopressin V2 receptor antagonists or “vaptans.” The SALT 1 and 2 trials, which included patients with CHF and cirrhosis, showed that they are effective in increasing serum sodium and improving mental function in the short term. But there are concerns about hepatotoxicity, overly rapid correction of serum sodium, lack of mortality benefit, and cost.¹⁴ The latest American Heart Association CHF guidelines recommend (class IIb) vaptans in patients with “hyponatremia that may be causing cognitive symptoms when standard measures have failed.”¹⁵ Tolvaptan, in particular, should not be used in cirrhotic patients due to concerns of hepatotoxicity.

Outcome of the Case

Because of the high UNa and Uosm and the use of a selective serotonin reuptake inhibitor (SSRI), the treating physician suspects the patient has SIADH. Given the severe symptoms, he is given 100 mL of 3% hypertonic saline and experiences improvement in his lethargy. Repeat sodium is 112 mEq/L. Using the equation above, a basal rate is calculated:

Change in serum sodium from 1 L of 3% saline= 514 mEq/L -112 mEq/L = 9.4 mEq 43 L

Because the goal correction rate is 6-8 mEq/L in 24 hours and the sodium has already increased by three, the physician elects to increase the sodium by 5 mEq/L for a total of 8 mEq/L for 24 hours:

5.0 mEq x 1000 ml = 532 ml of 3% saline ÷ 24 hours = 22 mL/hr. 9.4 mEq

Serum sodium is checked every two hours. The following day, the sodium is 115 mEq/L and the patient is fully alert. The hypertonic saline is stopped and the patient is maintained on free water restriction. Some 72 hours later, the sodium is 124 mEq/L.

Dr. Chang is co-director of the medicine-geriatrics clerkship, director of education in the division of hospital medicine, and assistant professor in the department of medicine at Mount Sinai Medical Center in New York City. Dr. Madeira is clinical instructor in the department of general internal medicine at the NYU School of Medicine and a hospitalist at the VA NY Harbor Healthcare System.

References

1. Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatraemia in hospitalized patients: Treatment-related risk factors and inadequate management. Nephrol Dial Transplant. 2006;21(1):70-76.
2. Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta. 2003;337(1-2):169-172.
3. Renneboog B, Musch W, Vandemergel X, Manto MU, Decaux G. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Am J Med. 2006;119(1):71.e1-8.
4. McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination: Is this patient hypovolemic? JAMA. 1999;281(11):1022-1029.
5. Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med. 1987;83(5):905-908.
6. Passamonte PM. Hypouricemia, inappropriate secretion of antidiuretic hormone, and small cell carcinoma of the lung. Arch Intern Med. 1984;144(8):1569-1570.
7. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-42.
8. Rogers IR, Hook G, Stuempfle KJ, Hoffman MD, Hew-Butler, T. An intervention study of oral versus intravenous hypertonic saline administration in ultramarathon runners with exercise-associated hyponatremia: a preliminary randomized trial. Clin J Sport Med. 2011;21(3):200-203.
9. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581-1589.
10. Tzamaloukas AH, Malhotra D, Rosen BH, Raj DS, Murata GH, Shapiro JI. Principles of management of severe hyponatremia. J Am Heart Assoc. 2013;2(1):e005199.
11. Sterns RH. Severe symptomatic hyponatremia: Treatment and outcome. A study of 64 cases. Ann Intern Med. 1987;107(5):656-664.
12. Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore). 1993;72(6):359-373.
13. Soupart A, Penninckx R, Crenier L, Stenuit A, Perier O, Decaux G. Prevention of brain demyelination in rats after excessive correction of chronic hyponatremia by serum sodium lowering. Kidney Int. 1994;45(1):193-200.
14. Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355(20):2099-2112.
15. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147-239.

click for large version

Case

A 67-year-old male patient who has depression and is on sertraline presents with increasing confusion over the past week. Initial plasma sodium is 109 mEq/L. On exam, he weighs 70 kg and is euvolemic. His urine osmolarity (Uosm) is 800 mosm/L with a urine sodium (UNa) of 40 mEq/L. He is somnolent but awakens to sternal rub. How should this patient’s hyponatremia be evaluated and managed?

Overview

Hyponatremia, a disorder of excess total body water in relation to sodium, occurs in up to 42% of hospitalized patients.^1,2 Regardless of the cause, hyponatremia is usually associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or with the appropriate elevation of antidiuretic hormone (ADH), known as hypovolemia. ADH is produced in the hypothalamus and released in the posterior pituitary in response to increasing plasma osmolarity (pOSM) or effective circulating volume depletion. ADH acts in the cortical collecting duct to increase the number of luminal aquaporin channels, increasing water reabsorption and decreasing plasma osmolarity. When hyponatremia is severe, the movement of water into cells causes cellular brain swelling, and clinical symptoms progress from malaise, headache, and nausea to obtundation, seizures, or respiratory arrest (see Figure 1). Even mild, chronic hyponatremia (120-131 mEq/L) is associated with an increased risk of falls due to mild gait and attention impairment.³

Evaluation

Step 1: Plasma osmolarity

The first step in diagnosing the cause of hyponatremia and treating it is to measure pOSM. The majority of patients with hyponatremia have hypoosmolar hyponatremia and therefore have a low pOSM; however, patients may have normal or high osmolarity. Hyponatremia with normal osmolarity can be caused by pseudohyponatremia (i.e., hyperglycemia, paraproteinemia, hyperlipidemia), severe renal failure, ingestion of excess alcohol, or post-transurethral resection of prostate or bladder.

Hyponatremia with high pOSM occurs as a result of elevated levels of an extra solute in the plasma that does not readily enter cells. This draws water into the extracellular fluid and lowers the sodium concentration. This will most commonly result from hyperglycemia or infusion of mannitol.

Step 2: Assess volume status with physical exam, urine sodium (UNa)

The majority of patients with hyponatremia will have low pOSM. These patients should be categorized by volume status: hypovolemic, euvolemic, or hypervolemic (see Figure 2). On exam, hypervolemia is usually evident, and the cause of hypervolemic hyponatremia is usually elicited from a patient’s history; however, differentiating between hypovolemic and euvolemic hyponatremia by history and physical exam can be difficult, because examination findings are neither sensitive nor specific.⁴ UNa should always be evaluated, especially when differentiating between hypovolemic and euvolemic. This was illustrated in a study of 58 non-edematous patients with hyponatremia. Investigators determined which patients had hypovolemic hyponatremia based on their response to saline infusion. Of the patients identified as hypovolemic using physical exam, only 47% responded to saline. In contrast, a spot UNa of less than 30 mEq/L was 80% sensitive and 100% specific for saline responsiveness.⁵ Although the majority of hypovolemic hyponatremia patients will have a low UNa, the following causes of hypovolemic hyponatremia can result in high UNa: diuretics, adrenal insufficiency, salt-wasting nephropathy, and cerebral salt-wasting.

A low serum uric acid can also be useful in differentiating hypovolemic and euvolemic hyponatremia, which is most commonly caused by SIADH. In SIADH, there is urinary wasting of uric acid, which leads to low serum uric acid. In a study of 105 patients with lung cancer, a serum uric acid of less than 4 mg/dL was 75% sensitive and 89% specific for SIADH.⁶

click for large version

Step 3: Urine osmolarity

After determining volume status, the physician should determine if there is excess ADH by measuring Uosm. Under normal conditions, hyponatremia should suppress ADH secretion and allow the kidney to excrete water by diluting the urine to less than 100 mosm/L. If Uosm is less than 100 mosm/L, then the kidneys are responding appropriately and can only persist in the following situations: The patient is drinking large volumes of water (e.g. primary polydipsia), there is insufficient solute to excrete free water (e.g. beer potomania, “tea and toast” diet), or the patient has a different set point for ADH suppression (i.e., reset osmostat). After determining volume status, UNa, and Uosm, the physician will have narrowed the cause of hyponatremia significantly (see Figure 2). Of note, when SIADH is diagnosed, it is important to look for and reverse causes (see Figure 3).

click for large version

click for large version

Treatment

Severe symptomatic hyponatremia

In patients with severe neurologic symptoms, physicians must balance the need to reduce symptoms quickly with the dangers of overly rapid correction. After its use in marathon runners, several experts have endorsed the following regimen to reduce symptoms rapidly: an intravenous bolus of 100 mL of 3% saline is given and repeated if symptoms persist after 10 minutes.7,8 Once symptoms improve, the basal rate can be calculated using the equation below, but the rate of sodium correction in 24 hours with this regimen should not exceed 6 to 8 mEq/L in 24 hours or 12 to 14 mEq/L in 48 hours.^9,10 This is based on several case studies showing that there were no cases of central pontine myelinolysis (CPM) if correction rates were less than 10 mEq/L over 24 hours.^11,12

It is important to remember that this is only a rough guide, because the equation assumes the entire infusate is retained and there is no sodium or water output. The best way to avoid overly rapid correction is to check serum sodium every two hours and monitor urine output closely. If the patient is making large volumes of urine, serum sodium may be rising too quickly. If the patient corrects too rapidly, it may be possible to avoid CPM by re-lowering the sodium.13 This can be accomplished by giving desmopressin to slow urinary free water loss while simultaneously giving hypotonic fluids.

Asymptomatic or mildly symptomatic hyponatremia

Hypovolemic hyponatremia: Treatment of hypovolemic hyponatremia is aimed at correcting volume status, the underlying problem that drives ADH secretion. The body will always choose to preserve volume over osmolarity. In most cases, normal saline (NS) should be used to restore intravascular volume, and the rate of infusion can be calculated using the same equation as above. Once volume is replete, ADH release will cease. Patients will be in danger of overly rapid correction of serum sodium, so fluids should be switched to hypotonic solutions, such as ½ NS.

Euvolemic Hyponatremia: Euvolemic hyponatremia, typically caused by SIADH, is characterized by a high Uosm (>100 mosm/L) and a high UNa (>30 mEq/L). All patients require free water restriction, and fluid intake should be at least 500 mL below a patient’s urine output, usually one liter or less. If this is ineffective, salt tabs can be given. Salt tabs will increase the solute load, necessitating an increase in urine output. Patients should be given approximately nine grams of salt tabs in three divided doses (equivalent to 1 L of NS). Patients with highly concentrated urine (Uosm >500 mosm/L) will not respond as well to the salt load, because the kidneys will continue to excrete much of the sodium in a concentrated urine. In such patients, a loop diuretic can be used to help excrete free water, because it decreases the Uosm to about ½ NS (154 mOsm/L). One possible regimen is 20-40 mg of oral furosemide two to three times daily.

Hypervolemic Hyponatremia: Hypervolemic hyponatremia is caused by congestive heart failure (CHF), cirrhosis, or nephrotic syndrome. In all cases, there is excess ADH as a result of the carotid baroreceptors sensing a decrease in effective circulation volume. In the case of CHF and cirrhosis, the degree of hyponatremia is a marker of disease severity, but there is no data to show that correction of hyponatremia improves outcomes. Fluid restriction is the cornerstone of therapy, but if the patient’s volume status is not optimized, then loop diuretics may improve hyponatremia through excretion of diluted urine. In addition, angiotensin-converting enzyme inhibitors can improve hyponatremia in CHF by reducing ADH levels and improving cardiac output via afterload reduction.

There has been recent interest in the use of vasopressin V2 receptor antagonists or “vaptans.” The SALT 1 and 2 trials, which included patients with CHF and cirrhosis, showed that they are effective in increasing serum sodium and improving mental function in the short term. But there are concerns about hepatotoxicity, overly rapid correction of serum sodium, lack of mortality benefit, and cost.¹⁴ The latest American Heart Association CHF guidelines recommend (class IIb) vaptans in patients with “hyponatremia that may be causing cognitive symptoms when standard measures have failed.”¹⁵ Tolvaptan, in particular, should not be used in cirrhotic patients due to concerns of hepatotoxicity.

Outcome of the Case

Because of the high UNa and Uosm and the use of a selective serotonin reuptake inhibitor (SSRI), the treating physician suspects the patient has SIADH. Given the severe symptoms, he is given 100 mL of 3% hypertonic saline and experiences improvement in his lethargy. Repeat sodium is 112 mEq/L. Using the equation above, a basal rate is calculated:

Change in serum sodium from 1 L of 3% saline= 514 mEq/L -112 mEq/L = 9.4 mEq 43 L

Because the goal correction rate is 6-8 mEq/L in 24 hours and the sodium has already increased by three, the physician elects to increase the sodium by 5 mEq/L for a total of 8 mEq/L for 24 hours:

5.0 mEq x 1000 ml = 532 ml of 3% saline ÷ 24 hours = 22 mL/hr. 9.4 mEq

Serum sodium is checked every two hours. The following day, the sodium is 115 mEq/L and the patient is fully alert. The hypertonic saline is stopped and the patient is maintained on free water restriction. Some 72 hours later, the sodium is 124 mEq/L.

Dr. Chang is co-director of the medicine-geriatrics clerkship, director of education in the division of hospital medicine, and assistant professor in the department of medicine at Mount Sinai Medical Center in New York City. Dr. Madeira is clinical instructor in the department of general internal medicine at the NYU School of Medicine and a hospitalist at the VA NY Harbor Healthcare System.

References

1. Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatraemia in hospitalized patients: Treatment-related risk factors and inadequate management. Nephrol Dial Transplant. 2006;21(1):70-76.
2. Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta. 2003;337(1-2):169-172.
3. Renneboog B, Musch W, Vandemergel X, Manto MU, Decaux G. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Am J Med. 2006;119(1):71.e1-8.
4. McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination: Is this patient hypovolemic? JAMA. 1999;281(11):1022-1029.
5. Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med. 1987;83(5):905-908.
6. Passamonte PM. Hypouricemia, inappropriate secretion of antidiuretic hormone, and small cell carcinoma of the lung. Arch Intern Med. 1984;144(8):1569-1570.
7. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-42.
8. Rogers IR, Hook G, Stuempfle KJ, Hoffman MD, Hew-Butler, T. An intervention study of oral versus intravenous hypertonic saline administration in ultramarathon runners with exercise-associated hyponatremia: a preliminary randomized trial. Clin J Sport Med. 2011;21(3):200-203.
9. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581-1589.
10. Tzamaloukas AH, Malhotra D, Rosen BH, Raj DS, Murata GH, Shapiro JI. Principles of management of severe hyponatremia. J Am Heart Assoc. 2013;2(1):e005199.
11. Sterns RH. Severe symptomatic hyponatremia: Treatment and outcome. A study of 64 cases. Ann Intern Med. 1987;107(5):656-664.
12. Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore). 1993;72(6):359-373.
13. Soupart A, Penninckx R, Crenier L, Stenuit A, Perier O, Decaux G. Prevention of brain demyelination in rats after excessive correction of chronic hyponatremia by serum sodium lowering. Kidney Int. 1994;45(1):193-200.
14. Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355(20):2099-2112.
15. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147-239.

click for large version

Case

A 67-year-old male patient who has depression and is on sertraline presents with increasing confusion over the past week. Initial plasma sodium is 109 mEq/L. On exam, he weighs 70 kg and is euvolemic. His urine osmolarity (Uosm) is 800 mosm/L with a urine sodium (UNa) of 40 mEq/L. He is somnolent but awakens to sternal rub. How should this patient’s hyponatremia be evaluated and managed?

Overview

Hyponatremia, a disorder of excess total body water in relation to sodium, occurs in up to 42% of hospitalized patients.^1,2 Regardless of the cause, hyponatremia is usually associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or with the appropriate elevation of antidiuretic hormone (ADH), known as hypovolemia. ADH is produced in the hypothalamus and released in the posterior pituitary in response to increasing plasma osmolarity (pOSM) or effective circulating volume depletion. ADH acts in the cortical collecting duct to increase the number of luminal aquaporin channels, increasing water reabsorption and decreasing plasma osmolarity. When hyponatremia is severe, the movement of water into cells causes cellular brain swelling, and clinical symptoms progress from malaise, headache, and nausea to obtundation, seizures, or respiratory arrest (see Figure 1). Even mild, chronic hyponatremia (120-131 mEq/L) is associated with an increased risk of falls due to mild gait and attention impairment.³

Evaluation

Step 1: Plasma osmolarity

The first step in diagnosing the cause of hyponatremia and treating it is to measure pOSM. The majority of patients with hyponatremia have hypoosmolar hyponatremia and therefore have a low pOSM; however, patients may have normal or high osmolarity. Hyponatremia with normal osmolarity can be caused by pseudohyponatremia (i.e., hyperglycemia, paraproteinemia, hyperlipidemia), severe renal failure, ingestion of excess alcohol, or post-transurethral resection of prostate or bladder.

Hyponatremia with high pOSM occurs as a result of elevated levels of an extra solute in the plasma that does not readily enter cells. This draws water into the extracellular fluid and lowers the sodium concentration. This will most commonly result from hyperglycemia or infusion of mannitol.

Step 2: Assess volume status with physical exam, urine sodium (UNa)

The majority of patients with hyponatremia will have low pOSM. These patients should be categorized by volume status: hypovolemic, euvolemic, or hypervolemic (see Figure 2). On exam, hypervolemia is usually evident, and the cause of hypervolemic hyponatremia is usually elicited from a patient’s history; however, differentiating between hypovolemic and euvolemic hyponatremia by history and physical exam can be difficult, because examination findings are neither sensitive nor specific.⁴ UNa should always be evaluated, especially when differentiating between hypovolemic and euvolemic. This was illustrated in a study of 58 non-edematous patients with hyponatremia. Investigators determined which patients had hypovolemic hyponatremia based on their response to saline infusion. Of the patients identified as hypovolemic using physical exam, only 47% responded to saline. In contrast, a spot UNa of less than 30 mEq/L was 80% sensitive and 100% specific for saline responsiveness.⁵ Although the majority of hypovolemic hyponatremia patients will have a low UNa, the following causes of hypovolemic hyponatremia can result in high UNa: diuretics, adrenal insufficiency, salt-wasting nephropathy, and cerebral salt-wasting.

A low serum uric acid can also be useful in differentiating hypovolemic and euvolemic hyponatremia, which is most commonly caused by SIADH. In SIADH, there is urinary wasting of uric acid, which leads to low serum uric acid. In a study of 105 patients with lung cancer, a serum uric acid of less than 4 mg/dL was 75% sensitive and 89% specific for SIADH.⁶

click for large version

Step 3: Urine osmolarity

After determining volume status, the physician should determine if there is excess ADH by measuring Uosm. Under normal conditions, hyponatremia should suppress ADH secretion and allow the kidney to excrete water by diluting the urine to less than 100 mosm/L. If Uosm is less than 100 mosm/L, then the kidneys are responding appropriately and can only persist in the following situations: The patient is drinking large volumes of water (e.g. primary polydipsia), there is insufficient solute to excrete free water (e.g. beer potomania, “tea and toast” diet), or the patient has a different set point for ADH suppression (i.e., reset osmostat). After determining volume status, UNa, and Uosm, the physician will have narrowed the cause of hyponatremia significantly (see Figure 2). Of note, when SIADH is diagnosed, it is important to look for and reverse causes (see Figure 3).

click for large version

click for large version

Treatment

Severe symptomatic hyponatremia

In patients with severe neurologic symptoms, physicians must balance the need to reduce symptoms quickly with the dangers of overly rapid correction. After its use in marathon runners, several experts have endorsed the following regimen to reduce symptoms rapidly: an intravenous bolus of 100 mL of 3% saline is given and repeated if symptoms persist after 10 minutes.7,8 Once symptoms improve, the basal rate can be calculated using the equation below, but the rate of sodium correction in 24 hours with this regimen should not exceed 6 to 8 mEq/L in 24 hours or 12 to 14 mEq/L in 48 hours.^9,10 This is based on several case studies showing that there were no cases of central pontine myelinolysis (CPM) if correction rates were less than 10 mEq/L over 24 hours.^11,12

It is important to remember that this is only a rough guide, because the equation assumes the entire infusate is retained and there is no sodium or water output. The best way to avoid overly rapid correction is to check serum sodium every two hours and monitor urine output closely. If the patient is making large volumes of urine, serum sodium may be rising too quickly. If the patient corrects too rapidly, it may be possible to avoid CPM by re-lowering the sodium.13 This can be accomplished by giving desmopressin to slow urinary free water loss while simultaneously giving hypotonic fluids.

Asymptomatic or mildly symptomatic hyponatremia

Hypovolemic hyponatremia: Treatment of hypovolemic hyponatremia is aimed at correcting volume status, the underlying problem that drives ADH secretion. The body will always choose to preserve volume over osmolarity. In most cases, normal saline (NS) should be used to restore intravascular volume, and the rate of infusion can be calculated using the same equation as above. Once volume is replete, ADH release will cease. Patients will be in danger of overly rapid correction of serum sodium, so fluids should be switched to hypotonic solutions, such as ½ NS.

Euvolemic Hyponatremia: Euvolemic hyponatremia, typically caused by SIADH, is characterized by a high Uosm (>100 mosm/L) and a high UNa (>30 mEq/L). All patients require free water restriction, and fluid intake should be at least 500 mL below a patient’s urine output, usually one liter or less. If this is ineffective, salt tabs can be given. Salt tabs will increase the solute load, necessitating an increase in urine output. Patients should be given approximately nine grams of salt tabs in three divided doses (equivalent to 1 L of NS). Patients with highly concentrated urine (Uosm >500 mosm/L) will not respond as well to the salt load, because the kidneys will continue to excrete much of the sodium in a concentrated urine. In such patients, a loop diuretic can be used to help excrete free water, because it decreases the Uosm to about ½ NS (154 mOsm/L). One possible regimen is 20-40 mg of oral furosemide two to three times daily.

Hypervolemic Hyponatremia: Hypervolemic hyponatremia is caused by congestive heart failure (CHF), cirrhosis, or nephrotic syndrome. In all cases, there is excess ADH as a result of the carotid baroreceptors sensing a decrease in effective circulation volume. In the case of CHF and cirrhosis, the degree of hyponatremia is a marker of disease severity, but there is no data to show that correction of hyponatremia improves outcomes. Fluid restriction is the cornerstone of therapy, but if the patient’s volume status is not optimized, then loop diuretics may improve hyponatremia through excretion of diluted urine. In addition, angiotensin-converting enzyme inhibitors can improve hyponatremia in CHF by reducing ADH levels and improving cardiac output via afterload reduction.

There has been recent interest in the use of vasopressin V2 receptor antagonists or “vaptans.” The SALT 1 and 2 trials, which included patients with CHF and cirrhosis, showed that they are effective in increasing serum sodium and improving mental function in the short term. But there are concerns about hepatotoxicity, overly rapid correction of serum sodium, lack of mortality benefit, and cost.¹⁴ The latest American Heart Association CHF guidelines recommend (class IIb) vaptans in patients with “hyponatremia that may be causing cognitive symptoms when standard measures have failed.”¹⁵ Tolvaptan, in particular, should not be used in cirrhotic patients due to concerns of hepatotoxicity.

Outcome of the Case

Because of the high UNa and Uosm and the use of a selective serotonin reuptake inhibitor (SSRI), the treating physician suspects the patient has SIADH. Given the severe symptoms, he is given 100 mL of 3% hypertonic saline and experiences improvement in his lethargy. Repeat sodium is 112 mEq/L. Using the equation above, a basal rate is calculated:

Change in serum sodium from 1 L of 3% saline= 514 mEq/L -112 mEq/L = 9.4 mEq 43 L

Because the goal correction rate is 6-8 mEq/L in 24 hours and the sodium has already increased by three, the physician elects to increase the sodium by 5 mEq/L for a total of 8 mEq/L for 24 hours:

5.0 mEq x 1000 ml = 532 ml of 3% saline ÷ 24 hours = 22 mL/hr. 9.4 mEq

Serum sodium is checked every two hours. The following day, the sodium is 115 mEq/L and the patient is fully alert. The hypertonic saline is stopped and the patient is maintained on free water restriction. Some 72 hours later, the sodium is 124 mEq/L.

Dr. Chang is co-director of the medicine-geriatrics clerkship, director of education in the division of hospital medicine, and assistant professor in the department of medicine at Mount Sinai Medical Center in New York City. Dr. Madeira is clinical instructor in the department of general internal medicine at the NYU School of Medicine and a hospitalist at the VA NY Harbor Healthcare System.

References

1. Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatraemia in hospitalized patients: Treatment-related risk factors and inadequate management. Nephrol Dial Transplant. 2006;21(1):70-76.
2. Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta. 2003;337(1-2):169-172.
3. Renneboog B, Musch W, Vandemergel X, Manto MU, Decaux G. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Am J Med. 2006;119(1):71.e1-8.
4. McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination: Is this patient hypovolemic? JAMA. 1999;281(11):1022-1029.
5. Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med. 1987;83(5):905-908.
6. Passamonte PM. Hypouricemia, inappropriate secretion of antidiuretic hormone, and small cell carcinoma of the lung. Arch Intern Med. 1984;144(8):1569-1570.
7. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-42.
8. Rogers IR, Hook G, Stuempfle KJ, Hoffman MD, Hew-Butler, T. An intervention study of oral versus intravenous hypertonic saline administration in ultramarathon runners with exercise-associated hyponatremia: a preliminary randomized trial. Clin J Sport Med. 2011;21(3):200-203.
9. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581-1589.
10. Tzamaloukas AH, Malhotra D, Rosen BH, Raj DS, Murata GH, Shapiro JI. Principles of management of severe hyponatremia. J Am Heart Assoc. 2013;2(1):e005199.
11. Sterns RH. Severe symptomatic hyponatremia: Treatment and outcome. A study of 64 cases. Ann Intern Med. 1987;107(5):656-664.
12. Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore). 1993;72(6):359-373.
13. Soupart A, Penninckx R, Crenier L, Stenuit A, Perier O, Decaux G. Prevention of brain demyelination in rats after excessive correction of chronic hyponatremia by serum sodium lowering. Kidney Int. 1994;45(1):193-200.
14. Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355(20):2099-2112.
15. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147-239.

Clinical question: Which risk factors are key in the development of nonleg deep vein thromboses (NLDVTs) and what are the expected clinical sequelae from these events?

Background: Critically ill patients are at increased risk of venous thrombosis. Despite adherence to recommended daily thromboprophylaxis, many patients will develop a venous thrombosis in a vein other than the lower extremity. The association between NLDVT and pulmonary embolism (PE) or death is less clearly identified.

Study design: The PROphylaxis for ThromboEmbolism in Critical Care Trial (PROTECT), a multicenter, randomized, blinded, and concealed prospective cohort study occurring between May 2006 and June 2010.

Setting: Sixty-seven international secondary and tertiary care ICUs in both academic and community settings.

Synopsis: Researchers enrolled 3,746 ICU patients in a randomized controlled trial of dalteparin vs. standard heparin for thromboprophylaxis. Of these patients, 84 (2.2%) developed a NLDVT. These thromboses were more likely to be deep and located proximally.

Risk factors were assessed using five selected variables: APACHE [acute physiology and chronic health evaluation], BMI, malignancy, and treatment with vasopressors or statins. Outside of indwelling upper extremity central venous catheters, cancer was the only independent predictor of NLDVT.

Compared to patients without any VTE, those with NLDVT were more likely to develop PE (14.9% vs. 1.9%) and have longer ICU stays (19 vs. nine days). On average, one in seven patients with NLDVT developed PE during their hospital stay. Despite the association with PE, NLDVT was not associated with an increased ICU mortality in an adjusted model.

However, the PROTECT trial may have been underpowered to detect a difference. Additional limitations of the study included a relatively small total number of NLDVTs and a lack of standardized screening protocols for both NLDVT and PE.

Bottom line: Despite universal heparin thromboprophylaxis, many medical-surgical critically ill patients may develop NLDVT, placing them at higher risk for longer ICU stays and PE.

Citation: Lamontagne F, McIntyre L, Dodek P, et al. Nonleg venous thrombosis in critically ill adults: a nested prospective cohort study. JAMA Intern Med. 2014;174(5):689-696.

Clinical question: Which risk factors are key in the development of nonleg deep vein thromboses (NLDVTs) and what are the expected clinical sequelae from these events?

Background: Critically ill patients are at increased risk of venous thrombosis. Despite adherence to recommended daily thromboprophylaxis, many patients will develop a venous thrombosis in a vein other than the lower extremity. The association between NLDVT and pulmonary embolism (PE) or death is less clearly identified.

Study design: The PROphylaxis for ThromboEmbolism in Critical Care Trial (PROTECT), a multicenter, randomized, blinded, and concealed prospective cohort study occurring between May 2006 and June 2010.

Setting: Sixty-seven international secondary and tertiary care ICUs in both academic and community settings.

Synopsis: Researchers enrolled 3,746 ICU patients in a randomized controlled trial of dalteparin vs. standard heparin for thromboprophylaxis. Of these patients, 84 (2.2%) developed a NLDVT. These thromboses were more likely to be deep and located proximally.

Risk factors were assessed using five selected variables: APACHE [acute physiology and chronic health evaluation], BMI, malignancy, and treatment with vasopressors or statins. Outside of indwelling upper extremity central venous catheters, cancer was the only independent predictor of NLDVT.

Compared to patients without any VTE, those with NLDVT were more likely to develop PE (14.9% vs. 1.9%) and have longer ICU stays (19 vs. nine days). On average, one in seven patients with NLDVT developed PE during their hospital stay. Despite the association with PE, NLDVT was not associated with an increased ICU mortality in an adjusted model.

However, the PROTECT trial may have been underpowered to detect a difference. Additional limitations of the study included a relatively small total number of NLDVTs and a lack of standardized screening protocols for both NLDVT and PE.

Bottom line: Despite universal heparin thromboprophylaxis, many medical-surgical critically ill patients may develop NLDVT, placing them at higher risk for longer ICU stays and PE.

Citation: Lamontagne F, McIntyre L, Dodek P, et al. Nonleg venous thrombosis in critically ill adults: a nested prospective cohort study. JAMA Intern Med. 2014;174(5):689-696.

Clinical question: Which risk factors are key in the development of nonleg deep vein thromboses (NLDVTs) and what are the expected clinical sequelae from these events?

Background: Critically ill patients are at increased risk of venous thrombosis. Despite adherence to recommended daily thromboprophylaxis, many patients will develop a venous thrombosis in a vein other than the lower extremity. The association between NLDVT and pulmonary embolism (PE) or death is less clearly identified.

Study design: The PROphylaxis for ThromboEmbolism in Critical Care Trial (PROTECT), a multicenter, randomized, blinded, and concealed prospective cohort study occurring between May 2006 and June 2010.

Setting: Sixty-seven international secondary and tertiary care ICUs in both academic and community settings.

Synopsis: Researchers enrolled 3,746 ICU patients in a randomized controlled trial of dalteparin vs. standard heparin for thromboprophylaxis. Of these patients, 84 (2.2%) developed a NLDVT. These thromboses were more likely to be deep and located proximally.

Risk factors were assessed using five selected variables: APACHE [acute physiology and chronic health evaluation], BMI, malignancy, and treatment with vasopressors or statins. Outside of indwelling upper extremity central venous catheters, cancer was the only independent predictor of NLDVT.

Compared to patients without any VTE, those with NLDVT were more likely to develop PE (14.9% vs. 1.9%) and have longer ICU stays (19 vs. nine days). On average, one in seven patients with NLDVT developed PE during their hospital stay. Despite the association with PE, NLDVT was not associated with an increased ICU mortality in an adjusted model.

However, the PROTECT trial may have been underpowered to detect a difference. Additional limitations of the study included a relatively small total number of NLDVTs and a lack of standardized screening protocols for both NLDVT and PE.

Bottom line: Despite universal heparin thromboprophylaxis, many medical-surgical critically ill patients may develop NLDVT, placing them at higher risk for longer ICU stays and PE.

Citation: Lamontagne F, McIntyre L, Dodek P, et al. Nonleg venous thrombosis in critically ill adults: a nested prospective cohort study. JAMA Intern Med. 2014;174(5):689-696.

Enter text here

Enter text here

Enter text here

Clinical question: How can the model for end-stage liver disease (MELD)-based model be updated and utilized to predict inpatient mortality rates of hospitalized cirrhotic patients with acute variceal bleeding (AVB)?

Background: AVB in cirrhosis continues to carry mortality rates as high as 20%. Risk prediction for individual patients is important to determine when a step-up in acuity of care is needed and to identify patients who would most benefit from preemptive treatments such as a transjugular intrahepatic portosystemic shunt. Many predictive models are available but are currently difficult to apply in the clinical setting.

Study design: Initial comparison data was collected via a prospective study from clinical records. Confirmation of updated MELD model occurred via cohort validation studies.

Setting: Prospective data collected from Hospital Clinic in Barcelona, Spain. Validation cohorts for new MELD model calibration completed in hospital settings in Canada and Spain.

Synopsis: Data was collected from 178 patients with cirrhosis and esophageal AVB receiving standard therapy from 2007-2010. Esophageal bleeding was confirmed endoscopically. The primary endpoint was six-week, bleeding-related mortality. Among all the subjects studied, the average six-week mortality rate was 16%. Models evaluated for validity included the Child-Pugh, the D’Amico and Augustin models, and the MELD score.

Each model was assessed via discrimination, calibration, and overall performance in mortality prediction. The MELD was identified as the best model in terms of discrimination and overall performance but was miscalibrated. The original validation cohort from the Hospital Clinic in Spain was utilized to update the MELD calibration via logistic regression. External validation was completed via cohort studies in Canada (N=240) and at Vall D’Hebron Hospital in Spain (N=221).

Using the updated model, the MELD score adds a predictive component in the setting of AVB that has not been available. MELD values of 19 and higher predict mortality >20%, whereas MELD values lower than 11 predict mortality of 5%.

Bottom line: Utilization of the updated MELD model may provide a more accurate method to identify patients in which more aggressive preemptive therapies are indicated using prognostic predictions of mortality.

Citation: Reverter E, Tandon P, Augustin S, et al. A MELD-based model to determine risk of mortality among patients with acute variceal bleeding. Gastroenterology. 2014;146(2):412-419.

Clinical question: How can the model for end-stage liver disease (MELD)-based model be updated and utilized to predict inpatient mortality rates of hospitalized cirrhotic patients with acute variceal bleeding (AVB)?

Background: AVB in cirrhosis continues to carry mortality rates as high as 20%. Risk prediction for individual patients is important to determine when a step-up in acuity of care is needed and to identify patients who would most benefit from preemptive treatments such as a transjugular intrahepatic portosystemic shunt. Many predictive models are available but are currently difficult to apply in the clinical setting.

Study design: Initial comparison data was collected via a prospective study from clinical records. Confirmation of updated MELD model occurred via cohort validation studies.

Setting: Prospective data collected from Hospital Clinic in Barcelona, Spain. Validation cohorts for new MELD model calibration completed in hospital settings in Canada and Spain.

Synopsis: Data was collected from 178 patients with cirrhosis and esophageal AVB receiving standard therapy from 2007-2010. Esophageal bleeding was confirmed endoscopically. The primary endpoint was six-week, bleeding-related mortality. Among all the subjects studied, the average six-week mortality rate was 16%. Models evaluated for validity included the Child-Pugh, the D’Amico and Augustin models, and the MELD score.

Each model was assessed via discrimination, calibration, and overall performance in mortality prediction. The MELD was identified as the best model in terms of discrimination and overall performance but was miscalibrated. The original validation cohort from the Hospital Clinic in Spain was utilized to update the MELD calibration via logistic regression. External validation was completed via cohort studies in Canada (N=240) and at Vall D’Hebron Hospital in Spain (N=221).

Using the updated model, the MELD score adds a predictive component in the setting of AVB that has not been available. MELD values of 19 and higher predict mortality >20%, whereas MELD values lower than 11 predict mortality of 5%.

Bottom line: Utilization of the updated MELD model may provide a more accurate method to identify patients in which more aggressive preemptive therapies are indicated using prognostic predictions of mortality.

Citation: Reverter E, Tandon P, Augustin S, et al. A MELD-based model to determine risk of mortality among patients with acute variceal bleeding. Gastroenterology. 2014;146(2):412-419.

Clinical question: How can the model for end-stage liver disease (MELD)-based model be updated and utilized to predict inpatient mortality rates of hospitalized cirrhotic patients with acute variceal bleeding (AVB)?

Background: AVB in cirrhosis continues to carry mortality rates as high as 20%. Risk prediction for individual patients is important to determine when a step-up in acuity of care is needed and to identify patients who would most benefit from preemptive treatments such as a transjugular intrahepatic portosystemic shunt. Many predictive models are available but are currently difficult to apply in the clinical setting.

Study design: Initial comparison data was collected via a prospective study from clinical records. Confirmation of updated MELD model occurred via cohort validation studies.

Setting: Prospective data collected from Hospital Clinic in Barcelona, Spain. Validation cohorts for new MELD model calibration completed in hospital settings in Canada and Spain.

Synopsis: Data was collected from 178 patients with cirrhosis and esophageal AVB receiving standard therapy from 2007-2010. Esophageal bleeding was confirmed endoscopically. The primary endpoint was six-week, bleeding-related mortality. Among all the subjects studied, the average six-week mortality rate was 16%. Models evaluated for validity included the Child-Pugh, the D’Amico and Augustin models, and the MELD score.

Each model was assessed via discrimination, calibration, and overall performance in mortality prediction. The MELD was identified as the best model in terms of discrimination and overall performance but was miscalibrated. The original validation cohort from the Hospital Clinic in Spain was utilized to update the MELD calibration via logistic regression. External validation was completed via cohort studies in Canada (N=240) and at Vall D’Hebron Hospital in Spain (N=221).

Using the updated model, the MELD score adds a predictive component in the setting of AVB that has not been available. MELD values of 19 and higher predict mortality >20%, whereas MELD values lower than 11 predict mortality of 5%.

Bottom line: Utilization of the updated MELD model may provide a more accurate method to identify patients in which more aggressive preemptive therapies are indicated using prognostic predictions of mortality.

Citation: Reverter E, Tandon P, Augustin S, et al. A MELD-based model to determine risk of mortality among patients with acute variceal bleeding. Gastroenterology. 2014;146(2):412-419.

Clinical question: What is the national burden of ED visits and hospitalizations for insulin-related hypoglycemia?

Background: As the prevalence of diabetes mellitus continues to rise, the use of insulin and the burden of insulin-related hypoglycemia on our healthcare system will increase. By identifying high-risk populations and analyzing the circumstances of insulin-related hypoglycemia, we might be able to identify and employ strategies to decrease the risk of insulin use.

Study design: Observational study using national adverse drug surveillance database and national household survey.

Setting: U.S. hospitals, excluding psychiatric and penal institutions.

Synopsis: Using data from the National Electronic Injury Surveillance System–Cooperative Adverse Drug Event Surveillance (NEISS-CADES) Project and the National Health Interview Survey (NHIS), the authors estimated the rates and characteristics of ED visits and hospitalizations for insulin-related hypoglycemia. The authors estimated that about 100,000 ED visits occur nationally and that almost one-third of those visits result in hospitalization. Compared to younger patients treated with insulin, patients 80 years or older were more likely to present to the ED (rate ratio, 2.5; 95% CI, 1.5-4.3) and much more likely to be subsequently hospitalized (rate ratio, 4.9; 95% CI, 2.6-9.1) for insulin-related hypoglycemia.

The most common causes of insulin-induced hypoglycemia were failure to reduce insulin during periods of reduced food intake and confusion between short-acting and long-acting insulin. The authors suggest that looser glycemic control be sought in elderly patients to decrease the risk of insulin-related hypoglycemia and subsequent sequelae. Patient education addressing common insulin errors might also decrease the burden of ED visits and hospitalizations related to insulin.

Bottom line: Risks of hypoglycemia in patients older than 80 should be considered prior to starting an insulin regimen or prior to increasing the dose of insulin.

Citation: Geller AI, Shehab N, Lovegrove MC, et al. National estimates of insulin-related hypoglycemia and errors leading to emergency department visits and hospitalizations. JAMA Intern Med. 2014;174(5):678-686.

Clinical question: What is the national burden of ED visits and hospitalizations for insulin-related hypoglycemia?

Background: As the prevalence of diabetes mellitus continues to rise, the use of insulin and the burden of insulin-related hypoglycemia on our healthcare system will increase. By identifying high-risk populations and analyzing the circumstances of insulin-related hypoglycemia, we might be able to identify and employ strategies to decrease the risk of insulin use.

Study design: Observational study using national adverse drug surveillance database and national household survey.

Setting: U.S. hospitals, excluding psychiatric and penal institutions.

Synopsis: Using data from the National Electronic Injury Surveillance System–Cooperative Adverse Drug Event Surveillance (NEISS-CADES) Project and the National Health Interview Survey (NHIS), the authors estimated the rates and characteristics of ED visits and hospitalizations for insulin-related hypoglycemia. The authors estimated that about 100,000 ED visits occur nationally and that almost one-third of those visits result in hospitalization. Compared to younger patients treated with insulin, patients 80 years or older were more likely to present to the ED (rate ratio, 2.5; 95% CI, 1.5-4.3) and much more likely to be subsequently hospitalized (rate ratio, 4.9; 95% CI, 2.6-9.1) for insulin-related hypoglycemia.

The most common causes of insulin-induced hypoglycemia were failure to reduce insulin during periods of reduced food intake and confusion between short-acting and long-acting insulin. The authors suggest that looser glycemic control be sought in elderly patients to decrease the risk of insulin-related hypoglycemia and subsequent sequelae. Patient education addressing common insulin errors might also decrease the burden of ED visits and hospitalizations related to insulin.

Bottom line: Risks of hypoglycemia in patients older than 80 should be considered prior to starting an insulin regimen or prior to increasing the dose of insulin.

Citation: Geller AI, Shehab N, Lovegrove MC, et al. National estimates of insulin-related hypoglycemia and errors leading to emergency department visits and hospitalizations. JAMA Intern Med. 2014;174(5):678-686.

Clinical question: What is the national burden of ED visits and hospitalizations for insulin-related hypoglycemia?

Background: As the prevalence of diabetes mellitus continues to rise, the use of insulin and the burden of insulin-related hypoglycemia on our healthcare system will increase. By identifying high-risk populations and analyzing the circumstances of insulin-related hypoglycemia, we might be able to identify and employ strategies to decrease the risk of insulin use.

Study design: Observational study using national adverse drug surveillance database and national household survey.

Setting: U.S. hospitals, excluding psychiatric and penal institutions.

Synopsis: Using data from the National Electronic Injury Surveillance System–Cooperative Adverse Drug Event Surveillance (NEISS-CADES) Project and the National Health Interview Survey (NHIS), the authors estimated the rates and characteristics of ED visits and hospitalizations for insulin-related hypoglycemia. The authors estimated that about 100,000 ED visits occur nationally and that almost one-third of those visits result in hospitalization. Compared to younger patients treated with insulin, patients 80 years or older were more likely to present to the ED (rate ratio, 2.5; 95% CI, 1.5-4.3) and much more likely to be subsequently hospitalized (rate ratio, 4.9; 95% CI, 2.6-9.1) for insulin-related hypoglycemia.

The most common causes of insulin-induced hypoglycemia were failure to reduce insulin during periods of reduced food intake and confusion between short-acting and long-acting insulin. The authors suggest that looser glycemic control be sought in elderly patients to decrease the risk of insulin-related hypoglycemia and subsequent sequelae. Patient education addressing common insulin errors might also decrease the burden of ED visits and hospitalizations related to insulin.

Bottom line: Risks of hypoglycemia in patients older than 80 should be considered prior to starting an insulin regimen or prior to increasing the dose of insulin.

Citation: Geller AI, Shehab N, Lovegrove MC, et al. National estimates of insulin-related hypoglycemia and errors leading to emergency department visits and hospitalizations. JAMA Intern Med. 2014;174(5):678-686.