Editorial

In 2004, knowing of my medical interest in arthropods, a resident came to my office to discuss an “unusual case” of pubic louse infestation seen at another hospital: a middle-aged woman had been afflicted for months with a skin eruption with excoriation and impetigo that involved the arms and legs but not the pubic area.

See related article

In a bag, the resident had a dead insect, 5 mm in length, with a brown, lens-shaped body and short hairs on the pronotum that were visible with a hand lens. An attending dermatologist at the other hospital had identified the insect—incorrectly—as a pubic louse.

With deference, I informed the resident that I did not share the opinion that this was a pubic louse, unless the insect represented a new “Cleveland variant” of the species (a reference to the 1975 Bruce Maness sci-fi film, The Tomato That Ate Cleveland). Rather, I stated, “I believe this is a bedbug, but I have not seen many specimens.”

In hindsight, these words were prophetic, for since 2004, the incidence of bedbug infestations has remarkably surged.¹ The trend has not abated, making the review by Ibrahim et al in this issue of the Cleveland Clinic Journal of Medicine timely for all practitioners.²

BEDBUGS ARE BACK…

Bedbugs have plagued man for millennia. In 1939, it was estimated that 4 million Londoners (in a city of 8.5 million) were bitten by bedbugs each night.³ However, as Ibrahim et al describe, long-acting pesticides introduced during World War II dramatically reduced infestation rates. By 1997, some college entomology programs reported difficulty in locating a single teaching specimen.⁴

The modern resurgence of bedbugs is multifactorial, including a ban on long-acting pesticides such as dichlorodiphenyltrichloroethane (DDT), as well as population growth and increased travel. In days past, bedbug infestations may have pertained to hygiene and social status. But today, travel is a major factor in the resurgence, and bedbugs now affect a broader segment of the population, including the affluent—something that must be kept in mind in the clinical setting.⁵

…AND THEY’RE EVERYWHERE

Many prominent US cities are experiencing near-epidemic numbers of bedbug infestations (Table 1). Bedbug infestations occur not only in homes and hotel rooms, but also in hospitals,⁶ office buildings,⁷ movie theaters,⁸ schools,⁹ and even on subways and trains,¹⁰ expanding the number of people potentially exposed.

Understanding that bedbugs affect more than people who are in bed, or with hygiene challenges, Ibrahim et al describe the presentation of bedbug bites—useful information for all practitioners, regardless of medical specialty.

Bedbugs bite skin that is exposed during sleep (ie, the distal extremities and the head, face, and neck). Quasilinear bites, in groups of three (the notorious “breakfast, lunch, and dinner” sign) are a good clue to remember. Unusually exuberant reactions to bedbug bites may be confused with autoimmune bullous conditions or primary vasculitides.¹¹

NOT ALL WHO ARE BITTEN HAVE REACTIONS

Intricate entomologic studies have shown that substances in bedbug saliva drive bite reactions.^12,13 However, as Ibrahim et al mention, not all bites provoke a reaction in all persons.

This fact cannot be overstated, for providers in primary care and urgent and emergency care settings may have learned to ask questions about scabies such as, “Are other persons in the household similarly affected?” While it is uncommon for a person with scabies not to present with visible skin lesions, one does not want to misinterpret this historical detail in the setting of bedbug bites. If one person in a household has lesions and another does not, this does not exclude a bedbug infestation!

Ibrahim et al emphasize that treatment of bedbug bites is supportive in nature. Most often, extermination in the home or any other setting should be conducted by professionals. During travel, prevention by inspection is widely advocated.⁵ There has been interest in using oral ivermectin in affected patients to adversely affect the bedbug colony, but to date, early experiments have encountered daunting pharmacokinetic concerns.¹⁴

PSYCHOLOGICAL AND OTHER SEQUELAE

A final consideration in bedbug infestations is any lasting sequelae beyond the bites themselves. Bedbug infestations severe enough to cause anemia and exacerbate or trigger adverse cardiac events have been reported.¹⁵ While bedbugs carry human pathogens such as methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus faecium, hepatitis B virus, Bartonella quintana, and Trypanosoma cruzi, Ibrahim et al correctly inform the reader that there are no compelling reports of transmission of these diseases via bedbug bites.¹⁶

However, there may be lasting psychological sequelae. Anxiety, hypervigilance, insomnia, avoidance behaviors, and personal dysfunction can persist, even long after the infestation has been eradicated.

Bedbugs are a national and even global health problem worthy of familiarity by all healthcare providers, regardless of specialty. In this regard, Ibrahim et al succinctly and accurately provide a functional and clinically useful guide.

In 2004, knowing of my medical interest in arthropods, a resident came to my office to discuss an “unusual case” of pubic louse infestation seen at another hospital: a middle-aged woman had been afflicted for months with a skin eruption with excoriation and impetigo that involved the arms and legs but not the pubic area.

See related article

In a bag, the resident had a dead insect, 5 mm in length, with a brown, lens-shaped body and short hairs on the pronotum that were visible with a hand lens. An attending dermatologist at the other hospital had identified the insect—incorrectly—as a pubic louse.

With deference, I informed the resident that I did not share the opinion that this was a pubic louse, unless the insect represented a new “Cleveland variant” of the species (a reference to the 1975 Bruce Maness sci-fi film, The Tomato That Ate Cleveland). Rather, I stated, “I believe this is a bedbug, but I have not seen many specimens.”

In hindsight, these words were prophetic, for since 2004, the incidence of bedbug infestations has remarkably surged.¹ The trend has not abated, making the review by Ibrahim et al in this issue of the Cleveland Clinic Journal of Medicine timely for all practitioners.²

BEDBUGS ARE BACK…

Bedbugs have plagued man for millennia. In 1939, it was estimated that 4 million Londoners (in a city of 8.5 million) were bitten by bedbugs each night.³ However, as Ibrahim et al describe, long-acting pesticides introduced during World War II dramatically reduced infestation rates. By 1997, some college entomology programs reported difficulty in locating a single teaching specimen.⁴

The modern resurgence of bedbugs is multifactorial, including a ban on long-acting pesticides such as dichlorodiphenyltrichloroethane (DDT), as well as population growth and increased travel. In days past, bedbug infestations may have pertained to hygiene and social status. But today, travel is a major factor in the resurgence, and bedbugs now affect a broader segment of the population, including the affluent—something that must be kept in mind in the clinical setting.⁵

…AND THEY’RE EVERYWHERE

Many prominent US cities are experiencing near-epidemic numbers of bedbug infestations (Table 1). Bedbug infestations occur not only in homes and hotel rooms, but also in hospitals,⁶ office buildings,⁷ movie theaters,⁸ schools,⁹ and even on subways and trains,¹⁰ expanding the number of people potentially exposed.

Understanding that bedbugs affect more than people who are in bed, or with hygiene challenges, Ibrahim et al describe the presentation of bedbug bites—useful information for all practitioners, regardless of medical specialty.

Bedbugs bite skin that is exposed during sleep (ie, the distal extremities and the head, face, and neck). Quasilinear bites, in groups of three (the notorious “breakfast, lunch, and dinner” sign) are a good clue to remember. Unusually exuberant reactions to bedbug bites may be confused with autoimmune bullous conditions or primary vasculitides.¹¹

NOT ALL WHO ARE BITTEN HAVE REACTIONS

Intricate entomologic studies have shown that substances in bedbug saliva drive bite reactions.^12,13 However, as Ibrahim et al mention, not all bites provoke a reaction in all persons.

This fact cannot be overstated, for providers in primary care and urgent and emergency care settings may have learned to ask questions about scabies such as, “Are other persons in the household similarly affected?” While it is uncommon for a person with scabies not to present with visible skin lesions, one does not want to misinterpret this historical detail in the setting of bedbug bites. If one person in a household has lesions and another does not, this does not exclude a bedbug infestation!

Ibrahim et al emphasize that treatment of bedbug bites is supportive in nature. Most often, extermination in the home or any other setting should be conducted by professionals. During travel, prevention by inspection is widely advocated.⁵ There has been interest in using oral ivermectin in affected patients to adversely affect the bedbug colony, but to date, early experiments have encountered daunting pharmacokinetic concerns.¹⁴

PSYCHOLOGICAL AND OTHER SEQUELAE

A final consideration in bedbug infestations is any lasting sequelae beyond the bites themselves. Bedbug infestations severe enough to cause anemia and exacerbate or trigger adverse cardiac events have been reported.¹⁵ While bedbugs carry human pathogens such as methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus faecium, hepatitis B virus, Bartonella quintana, and Trypanosoma cruzi, Ibrahim et al correctly inform the reader that there are no compelling reports of transmission of these diseases via bedbug bites.¹⁶

However, there may be lasting psychological sequelae. Anxiety, hypervigilance, insomnia, avoidance behaviors, and personal dysfunction can persist, even long after the infestation has been eradicated.

Bedbugs are a national and even global health problem worthy of familiarity by all healthcare providers, regardless of specialty. In this regard, Ibrahim et al succinctly and accurately provide a functional and clinically useful guide.

In 2004, knowing of my medical interest in arthropods, a resident came to my office to discuss an “unusual case” of pubic louse infestation seen at another hospital: a middle-aged woman had been afflicted for months with a skin eruption with excoriation and impetigo that involved the arms and legs but not the pubic area.

See related article

In a bag, the resident had a dead insect, 5 mm in length, with a brown, lens-shaped body and short hairs on the pronotum that were visible with a hand lens. An attending dermatologist at the other hospital had identified the insect—incorrectly—as a pubic louse.

With deference, I informed the resident that I did not share the opinion that this was a pubic louse, unless the insect represented a new “Cleveland variant” of the species (a reference to the 1975 Bruce Maness sci-fi film, The Tomato That Ate Cleveland). Rather, I stated, “I believe this is a bedbug, but I have not seen many specimens.”

In hindsight, these words were prophetic, for since 2004, the incidence of bedbug infestations has remarkably surged.¹ The trend has not abated, making the review by Ibrahim et al in this issue of the Cleveland Clinic Journal of Medicine timely for all practitioners.²

BEDBUGS ARE BACK…

Bedbugs have plagued man for millennia. In 1939, it was estimated that 4 million Londoners (in a city of 8.5 million) were bitten by bedbugs each night.³ However, as Ibrahim et al describe, long-acting pesticides introduced during World War II dramatically reduced infestation rates. By 1997, some college entomology programs reported difficulty in locating a single teaching specimen.⁴

The modern resurgence of bedbugs is multifactorial, including a ban on long-acting pesticides such as dichlorodiphenyltrichloroethane (DDT), as well as population growth and increased travel. In days past, bedbug infestations may have pertained to hygiene and social status. But today, travel is a major factor in the resurgence, and bedbugs now affect a broader segment of the population, including the affluent—something that must be kept in mind in the clinical setting.⁵

…AND THEY’RE EVERYWHERE

Many prominent US cities are experiencing near-epidemic numbers of bedbug infestations (Table 1). Bedbug infestations occur not only in homes and hotel rooms, but also in hospitals,⁶ office buildings,⁷ movie theaters,⁸ schools,⁹ and even on subways and trains,¹⁰ expanding the number of people potentially exposed.

Understanding that bedbugs affect more than people who are in bed, or with hygiene challenges, Ibrahim et al describe the presentation of bedbug bites—useful information for all practitioners, regardless of medical specialty.

Bedbugs bite skin that is exposed during sleep (ie, the distal extremities and the head, face, and neck). Quasilinear bites, in groups of three (the notorious “breakfast, lunch, and dinner” sign) are a good clue to remember. Unusually exuberant reactions to bedbug bites may be confused with autoimmune bullous conditions or primary vasculitides.¹¹

NOT ALL WHO ARE BITTEN HAVE REACTIONS

Intricate entomologic studies have shown that substances in bedbug saliva drive bite reactions.^12,13 However, as Ibrahim et al mention, not all bites provoke a reaction in all persons.

This fact cannot be overstated, for providers in primary care and urgent and emergency care settings may have learned to ask questions about scabies such as, “Are other persons in the household similarly affected?” While it is uncommon for a person with scabies not to present with visible skin lesions, one does not want to misinterpret this historical detail in the setting of bedbug bites. If one person in a household has lesions and another does not, this does not exclude a bedbug infestation!

Ibrahim et al emphasize that treatment of bedbug bites is supportive in nature. Most often, extermination in the home or any other setting should be conducted by professionals. During travel, prevention by inspection is widely advocated.⁵ There has been interest in using oral ivermectin in affected patients to adversely affect the bedbug colony, but to date, early experiments have encountered daunting pharmacokinetic concerns.¹⁴

PSYCHOLOGICAL AND OTHER SEQUELAE

A final consideration in bedbug infestations is any lasting sequelae beyond the bites themselves. Bedbug infestations severe enough to cause anemia and exacerbate or trigger adverse cardiac events have been reported.¹⁵ While bedbugs carry human pathogens such as methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus faecium, hepatitis B virus, Bartonella quintana, and Trypanosoma cruzi, Ibrahim et al correctly inform the reader that there are no compelling reports of transmission of these diseases via bedbug bites.¹⁶

However, there may be lasting psychological sequelae. Anxiety, hypervigilance, insomnia, avoidance behaviors, and personal dysfunction can persist, even long after the infestation has been eradicated.

Bedbugs are a national and even global health problem worthy of familiarity by all healthcare providers, regardless of specialty. In this regard, Ibrahim et al succinctly and accurately provide a functional and clinically useful guide.

On July 30, 1965, Lyndon B. Johnson signed H.R. 6675 into law, establishing Medicare and Medicaid as Title XVIII and Title XIX of the Social Security Act.¹ Shortly after, Medicare’s “extended care benefit” began, offering Medicare beneficiaries skilled nursing facility (SNF) care after a qualifying stay of 3 or more consecutive inpatient midnights.² Fifty years later, the word “inpatient” remains embedded in statute, limiting SNF coverage for Medicare beneficiaries hospitalized as outpatients under observation for part or all of a 3-midnight stay.³

At the individual Medicare beneficiary level, the financial impact of this policy is clear. The Office of Inspector General (OIG) reported a $10,503 beneficiary out-of-pocket cost per uncovered SNF stay following an observation hospitalization in 2012.⁴ But the actual number of Medicare beneficiaries impacted by this coverage gap is unknown. Using 2009 claims data, Feng et al.⁵ estimated that 0.75% of previously community dwelling Medicare beneficiaries are discharged to a SNF following an observation hospitalization, and the OIG reported 617,702 beneficiary hospital stays of 3 or more midnights not meeting the 3-midnight inpatient requirement in 2012, with 4% of these beneficiaries discharging to SNFs.⁴ Yet these studies based on Medicare claims data only capture actual SNF utilization, failing to answer the critical question: How many Medicare beneficiaries need, but forgo, SNF care following a non-qualifying observation hospital stay? In this issue of the Journal of Hospital Medicine, Goldstein et al.⁶ provide insight to that question. Using chart review of physical therapy and case management recommendations for post-acute SNF care, Goldstein et al.⁶ compare actual discharge rate to SNF or acute inpatient rehabilitation following an observation stay when such disposition is recommended. In their two-hospital system, fewer than 20% of previously community-dwelling hospitalist patients followed recommendation for post-acute facility stay after observation hospitalization, and more than 40% cited financial concerns as the reason for declining. Patients recommended for SNF also were more likely to be rehospitalized in the subsequent 30 days after discharge, confirming this as a vulnerable patient population. Given Medicare’s original intent to improve health care access for seniors, the case for change seems clear, and the repercussions of not addressing the plight of patients hospitalized under observation is having negative financial and overall detrimental health impacts.

But there are other compelling reasons why this 50-year-old law needs to be improved. Hospital care today is vastly different than when Medicare became law. Average hospital length of stay for patients 65 years and older was 14.2 days in 1965⁷ compared to 5.2 days today,⁸ clearly a shift in what 3 days of hospital care means. Most importantly, observation stays have become a major part of hospital care. Between 2006 and 2014, per-beneficiary outpatient visits (which include all observation stays) increased 44.2% nationally, while inpatient discharges decreased 19.9%.⁹ In 2012, the Centers for Medicare & Medicaid Services (CMS) received 1.7 million outpatient observation claims and an additional 700,000 inpatient claims that started with observation days.¹⁰ CMS also expected the 2-midnight rule to reduce outpatient observation stays,⁴ but a recent OIG report¹¹ found that outpatient stays increased 8.1% in the first year (FY 2014) under the new rule, and there were still 748,337 long observation stays (those lasting 2 midnights or longer) in 2014, only a small (2.8%) decrease from the prior year. These factors limit Medicare beneficiary post–acute SNF eligibility in ways that could not have been anticipated when the extended care benefit was created to help seniors access needed health care.

Policymakers must consider cost when considering statutory change. Waiver programs in the 1980s suspending the 3-midnight requirement raised concerns over potential increase in both SNF utilization and associated costs.¹² However, more recent data suggest that altering the 3-midnight requirement may not increase post-acute SNF utilization. From 2006 to 2010, Medicare Advantage programs that waived the 3-midnight requirement saw a decrease in hospital length of stay without increased SNF utilization or SNF length of stay, indicating that access to the right level of care at the right time could be cost-saving.¹³ Recent data from the Bundled Payments for Care Improvement (BPCI) program found savings were largely related to decreased SNF utilization when payments were episode-based,¹⁴ a trend that may continue as Medicare moves away from fee-for-service towards bundled payments for more conditions. And although neither example directly tests changing the 3-midnight requirement to include observation midnights, both studies suggest that innovative health care delivery and modification of SNF access did not result in increased SNF utilization or greater post-acute costs. In fact, as Goldstein et al.⁶ showed, patients recommended for post-acute SNF following observation stay were more likely to be rehospitalized within 30 days, an additional cost that could potentially be avoided if these patients had SNF access. We believe that these correlations strongly support rescinding the 3-midnight requirement, or at least amending it to allow nights spend under observation to count as “inpatient” for the purposes of SNF benefit coverage.

That being said, what can be done? In 2015, the Medicare Payment Advisory Commission (MedPAC) recommended changing the 3-night requirement to require just one of 3 midnights to be inpatient to make a qualifying stay.¹⁰ Although an improvement over current law, this proposal would not help the majority of beneficiaries who are exclusively hospitalized under observation status. The “Improving Access to Medicare Coverage Act of 2015”, to be reintroduced in Congress in the coming weeks, would count any midnight spent in the hospital towards the 3-midnight stay requirement, and has bipartisan, bicameral support and cosponsorship.¹⁵ In 2015, through unanimous bipartisan, bicameral support, Congress passed the NOTICE Act (PL 114-42), which requires hospitals to inform Medicare beneficiaries hospitalized under observation.¹⁶ We believe that the data are clear to both sides of the aisle that Congress should now work together using scientifically-supported research to improve the exact observation policies they felt patients should be informed of. Passing the Improving Access to Medicare Coverage Act is the logical next step in this arena.

Medicare was intended to give seniors access to the healthcare they need. Growth in hospital-based observation care begs for modernization of the statutory 3-inpatient midnight rule. Counting all midnights towards the 3-midnight requirement, whether those midnights are outpatient observation or inpatient, is the right first step.

Disclosures

Representative Courtney is the bill sponsor of the Improving Access to Medicare Coverage Act. The authors report no other conflicts.

On July 30, 1965, Lyndon B. Johnson signed H.R. 6675 into law, establishing Medicare and Medicaid as Title XVIII and Title XIX of the Social Security Act.¹ Shortly after, Medicare’s “extended care benefit” began, offering Medicare beneficiaries skilled nursing facility (SNF) care after a qualifying stay of 3 or more consecutive inpatient midnights.² Fifty years later, the word “inpatient” remains embedded in statute, limiting SNF coverage for Medicare beneficiaries hospitalized as outpatients under observation for part or all of a 3-midnight stay.³

At the individual Medicare beneficiary level, the financial impact of this policy is clear. The Office of Inspector General (OIG) reported a $10,503 beneficiary out-of-pocket cost per uncovered SNF stay following an observation hospitalization in 2012.⁴ But the actual number of Medicare beneficiaries impacted by this coverage gap is unknown. Using 2009 claims data, Feng et al.⁵ estimated that 0.75% of previously community dwelling Medicare beneficiaries are discharged to a SNF following an observation hospitalization, and the OIG reported 617,702 beneficiary hospital stays of 3 or more midnights not meeting the 3-midnight inpatient requirement in 2012, with 4% of these beneficiaries discharging to SNFs.⁴ Yet these studies based on Medicare claims data only capture actual SNF utilization, failing to answer the critical question: How many Medicare beneficiaries need, but forgo, SNF care following a non-qualifying observation hospital stay? In this issue of the Journal of Hospital Medicine, Goldstein et al.⁶ provide insight to that question. Using chart review of physical therapy and case management recommendations for post-acute SNF care, Goldstein et al.⁶ compare actual discharge rate to SNF or acute inpatient rehabilitation following an observation stay when such disposition is recommended. In their two-hospital system, fewer than 20% of previously community-dwelling hospitalist patients followed recommendation for post-acute facility stay after observation hospitalization, and more than 40% cited financial concerns as the reason for declining. Patients recommended for SNF also were more likely to be rehospitalized in the subsequent 30 days after discharge, confirming this as a vulnerable patient population. Given Medicare’s original intent to improve health care access for seniors, the case for change seems clear, and the repercussions of not addressing the plight of patients hospitalized under observation is having negative financial and overall detrimental health impacts.

But there are other compelling reasons why this 50-year-old law needs to be improved. Hospital care today is vastly different than when Medicare became law. Average hospital length of stay for patients 65 years and older was 14.2 days in 1965⁷ compared to 5.2 days today,⁸ clearly a shift in what 3 days of hospital care means. Most importantly, observation stays have become a major part of hospital care. Between 2006 and 2014, per-beneficiary outpatient visits (which include all observation stays) increased 44.2% nationally, while inpatient discharges decreased 19.9%.⁹ In 2012, the Centers for Medicare & Medicaid Services (CMS) received 1.7 million outpatient observation claims and an additional 700,000 inpatient claims that started with observation days.¹⁰ CMS also expected the 2-midnight rule to reduce outpatient observation stays,⁴ but a recent OIG report¹¹ found that outpatient stays increased 8.1% in the first year (FY 2014) under the new rule, and there were still 748,337 long observation stays (those lasting 2 midnights or longer) in 2014, only a small (2.8%) decrease from the prior year. These factors limit Medicare beneficiary post–acute SNF eligibility in ways that could not have been anticipated when the extended care benefit was created to help seniors access needed health care.

Policymakers must consider cost when considering statutory change. Waiver programs in the 1980s suspending the 3-midnight requirement raised concerns over potential increase in both SNF utilization and associated costs.¹² However, more recent data suggest that altering the 3-midnight requirement may not increase post-acute SNF utilization. From 2006 to 2010, Medicare Advantage programs that waived the 3-midnight requirement saw a decrease in hospital length of stay without increased SNF utilization or SNF length of stay, indicating that access to the right level of care at the right time could be cost-saving.¹³ Recent data from the Bundled Payments for Care Improvement (BPCI) program found savings were largely related to decreased SNF utilization when payments were episode-based,¹⁴ a trend that may continue as Medicare moves away from fee-for-service towards bundled payments for more conditions. And although neither example directly tests changing the 3-midnight requirement to include observation midnights, both studies suggest that innovative health care delivery and modification of SNF access did not result in increased SNF utilization or greater post-acute costs. In fact, as Goldstein et al.⁶ showed, patients recommended for post-acute SNF following observation stay were more likely to be rehospitalized within 30 days, an additional cost that could potentially be avoided if these patients had SNF access. We believe that these correlations strongly support rescinding the 3-midnight requirement, or at least amending it to allow nights spend under observation to count as “inpatient” for the purposes of SNF benefit coverage.

That being said, what can be done? In 2015, the Medicare Payment Advisory Commission (MedPAC) recommended changing the 3-night requirement to require just one of 3 midnights to be inpatient to make a qualifying stay.¹⁰ Although an improvement over current law, this proposal would not help the majority of beneficiaries who are exclusively hospitalized under observation status. The “Improving Access to Medicare Coverage Act of 2015”, to be reintroduced in Congress in the coming weeks, would count any midnight spent in the hospital towards the 3-midnight stay requirement, and has bipartisan, bicameral support and cosponsorship.¹⁵ In 2015, through unanimous bipartisan, bicameral support, Congress passed the NOTICE Act (PL 114-42), which requires hospitals to inform Medicare beneficiaries hospitalized under observation.¹⁶ We believe that the data are clear to both sides of the aisle that Congress should now work together using scientifically-supported research to improve the exact observation policies they felt patients should be informed of. Passing the Improving Access to Medicare Coverage Act is the logical next step in this arena.

Medicare was intended to give seniors access to the healthcare they need. Growth in hospital-based observation care begs for modernization of the statutory 3-inpatient midnight rule. Counting all midnights towards the 3-midnight requirement, whether those midnights are outpatient observation or inpatient, is the right first step.

Disclosures

Representative Courtney is the bill sponsor of the Improving Access to Medicare Coverage Act. The authors report no other conflicts.

On July 30, 1965, Lyndon B. Johnson signed H.R. 6675 into law, establishing Medicare and Medicaid as Title XVIII and Title XIX of the Social Security Act.¹ Shortly after, Medicare’s “extended care benefit” began, offering Medicare beneficiaries skilled nursing facility (SNF) care after a qualifying stay of 3 or more consecutive inpatient midnights.² Fifty years later, the word “inpatient” remains embedded in statute, limiting SNF coverage for Medicare beneficiaries hospitalized as outpatients under observation for part or all of a 3-midnight stay.³

At the individual Medicare beneficiary level, the financial impact of this policy is clear. The Office of Inspector General (OIG) reported a $10,503 beneficiary out-of-pocket cost per uncovered SNF stay following an observation hospitalization in 2012.⁴ But the actual number of Medicare beneficiaries impacted by this coverage gap is unknown. Using 2009 claims data, Feng et al.⁵ estimated that 0.75% of previously community dwelling Medicare beneficiaries are discharged to a SNF following an observation hospitalization, and the OIG reported 617,702 beneficiary hospital stays of 3 or more midnights not meeting the 3-midnight inpatient requirement in 2012, with 4% of these beneficiaries discharging to SNFs.⁴ Yet these studies based on Medicare claims data only capture actual SNF utilization, failing to answer the critical question: How many Medicare beneficiaries need, but forgo, SNF care following a non-qualifying observation hospital stay? In this issue of the Journal of Hospital Medicine, Goldstein et al.⁶ provide insight to that question. Using chart review of physical therapy and case management recommendations for post-acute SNF care, Goldstein et al.⁶ compare actual discharge rate to SNF or acute inpatient rehabilitation following an observation stay when such disposition is recommended. In their two-hospital system, fewer than 20% of previously community-dwelling hospitalist patients followed recommendation for post-acute facility stay after observation hospitalization, and more than 40% cited financial concerns as the reason for declining. Patients recommended for SNF also were more likely to be rehospitalized in the subsequent 30 days after discharge, confirming this as a vulnerable patient population. Given Medicare’s original intent to improve health care access for seniors, the case for change seems clear, and the repercussions of not addressing the plight of patients hospitalized under observation is having negative financial and overall detrimental health impacts.

But there are other compelling reasons why this 50-year-old law needs to be improved. Hospital care today is vastly different than when Medicare became law. Average hospital length of stay for patients 65 years and older was 14.2 days in 1965⁷ compared to 5.2 days today,⁸ clearly a shift in what 3 days of hospital care means. Most importantly, observation stays have become a major part of hospital care. Between 2006 and 2014, per-beneficiary outpatient visits (which include all observation stays) increased 44.2% nationally, while inpatient discharges decreased 19.9%.⁹ In 2012, the Centers for Medicare & Medicaid Services (CMS) received 1.7 million outpatient observation claims and an additional 700,000 inpatient claims that started with observation days.¹⁰ CMS also expected the 2-midnight rule to reduce outpatient observation stays,⁴ but a recent OIG report¹¹ found that outpatient stays increased 8.1% in the first year (FY 2014) under the new rule, and there were still 748,337 long observation stays (those lasting 2 midnights or longer) in 2014, only a small (2.8%) decrease from the prior year. These factors limit Medicare beneficiary post–acute SNF eligibility in ways that could not have been anticipated when the extended care benefit was created to help seniors access needed health care.

Policymakers must consider cost when considering statutory change. Waiver programs in the 1980s suspending the 3-midnight requirement raised concerns over potential increase in both SNF utilization and associated costs.¹² However, more recent data suggest that altering the 3-midnight requirement may not increase post-acute SNF utilization. From 2006 to 2010, Medicare Advantage programs that waived the 3-midnight requirement saw a decrease in hospital length of stay without increased SNF utilization or SNF length of stay, indicating that access to the right level of care at the right time could be cost-saving.¹³ Recent data from the Bundled Payments for Care Improvement (BPCI) program found savings were largely related to decreased SNF utilization when payments were episode-based,¹⁴ a trend that may continue as Medicare moves away from fee-for-service towards bundled payments for more conditions. And although neither example directly tests changing the 3-midnight requirement to include observation midnights, both studies suggest that innovative health care delivery and modification of SNF access did not result in increased SNF utilization or greater post-acute costs. In fact, as Goldstein et al.⁶ showed, patients recommended for post-acute SNF following observation stay were more likely to be rehospitalized within 30 days, an additional cost that could potentially be avoided if these patients had SNF access. We believe that these correlations strongly support rescinding the 3-midnight requirement, or at least amending it to allow nights spend under observation to count as “inpatient” for the purposes of SNF benefit coverage.

That being said, what can be done? In 2015, the Medicare Payment Advisory Commission (MedPAC) recommended changing the 3-night requirement to require just one of 3 midnights to be inpatient to make a qualifying stay.¹⁰ Although an improvement over current law, this proposal would not help the majority of beneficiaries who are exclusively hospitalized under observation status. The “Improving Access to Medicare Coverage Act of 2015”, to be reintroduced in Congress in the coming weeks, would count any midnight spent in the hospital towards the 3-midnight stay requirement, and has bipartisan, bicameral support and cosponsorship.¹⁵ In 2015, through unanimous bipartisan, bicameral support, Congress passed the NOTICE Act (PL 114-42), which requires hospitals to inform Medicare beneficiaries hospitalized under observation.¹⁶ We believe that the data are clear to both sides of the aisle that Congress should now work together using scientifically-supported research to improve the exact observation policies they felt patients should be informed of. Passing the Improving Access to Medicare Coverage Act is the logical next step in this arena.

Medicare was intended to give seniors access to the healthcare they need. Growth in hospital-based observation care begs for modernization of the statutory 3-inpatient midnight rule. Counting all midnights towards the 3-midnight requirement, whether those midnights are outpatient observation or inpatient, is the right first step.

Disclosures

Representative Courtney is the bill sponsor of the Improving Access to Medicare Coverage Act. The authors report no other conflicts.

Acute kidney injury (AKI) is a major contributor to morbidity and mortality in hospitalized patients across the world.¹ Affecting up to 20% of all admissions (depending on which definition of AKI is used),² AKI is the most common reason for new-inpatient nephrology consultation. Recent data suggest that AKI incidence has risen rapidly, by up to 10% per year.^3,4

AKI is associated with a variety of serious short- and long-term complications. Approximately 33% to 60% of critically ill patients who develop dialysis-requiring AKI do not survive to hospital discharge, and mortality associated with dialysis-requiring AKI is greater than that associated with other serious conditions such as myocardial infarction or acute respiratory distress syndrome.⁵ Even relatively mild AKI in the acute inpatient setting appears to be an independent risk factor for mortality.⁶

For several decades, many physicians believed that AKI was a self-limited process followed by complete recovery of renal function to pre-AKI levels among survivors. (Numerous trainees have been taught some variant of the old adage: “If the patients survive, so will their kidneys.”) But studies linking AKI with the development of new-onset chronic kidney disease (CKD) or the accelerated progression of pre-existing CKD have changed this view.⁷ One important reason the long-term impact of AKI hasn’t been appreciated is that, traditionally, clinical studies of AKI examined inhospital outcomes such as short-term mortality and resource usage and did not consider what transpired months to years after discharge. More recently, epidemiologic studies linking inpatient events with outpatient outcomes have filled this knowledge gap.⁸ Contemporary animal models of AKI have shed light on potential mechanisms of maladaptive repair after AKI, characterized by fibrosis, vascular rarefaction, tubular loss, glomerulosclerosis, and chronic interstitial inflammation, all of which result in renal function decline. So over the last decade there has been a paradigm shift in how we think about AKI and CKD. Rather than distinct entities, AKI and CKD are now viewed as interconnected syndromes since AKI is a risk factor for CKD progression and CKD is a risk factor for new episodes of AKI.⁹

Two studies published in this issue of the Journal of Hospital Medicine augment our understanding of AKI and its clinical impact in hospitalized patients. Analyzing data from the National Inpatient Sample, Silver et al.¹⁰ found that hospitalizations that include AKI are substantially costlier and associated with longer lengths of stay than hospitalizations without AKI. The authors also highlight that the additional economic costs of AKI exceeded those of many other higher-profile yet less-common acute medical conditions, such as myocardial infarction and gastrointestinal bleeding. These results re-emphasize the important economic burden of AKI at a national level and expand on prior literature by confirming findings previously limited to single-center and regional studies. Better defining the impact AKI has on our healthcare system could help ensure that adequate resources are invested to combat AKI.

The second study, by Rutter et al.,¹¹ found that among hospitalized patients with normal baseline renal function, use of vancomycin in combination with piperacillin-tazobactam is associated with a higher incidence of AKI after antibiotic exposure than use of either agent as monotherapy. This association persisted even after adjusting for potential confounders such as underlying comorbidities, exposure to nephrotoxic agents, documented hypotension, and baseline renal impairment. This study adds to a growing body of literature that suggests synergistic nephrotoxicity between vancomycin and piperacillin-tazobactam. It underscores that any medical intervention—even treatments typically envisioned as non-hazardous and frequently life-saving—involve inherent risks and should prompt the medical community to promote proper antimicrobial stewardship. Whether such exposures to vancomycin or beta-lactam derivatives cause AKI via direct tubular damage, interstitial nephritis, or some other novel mechanism remains to be elucidated. Better delineation of the contemporary causes of AKI, including increased antibiotic exposure, is the first step toward identifying ways to reduce AKI incidence.

Both of these papers serve to highlight the clinical importance of AKI among hospitalized patients. Their findings re-emphasize the need for vigilance in detecting AKI and intervening early to achieve the best clinical outcomes.

Given recent understanding that survivors of AKI are at greater risk for more rapid loss of renal function long after hospital discharge, one goal the US Department of Health and Human Services put forth for Healthy People 2020 is to “increase the proportion of hospital patients who incurred AKI who have follow-up renal evaluation in 6 months post-discharge” (10% improvement targeted).¹² Transitions of care after hospitalizations complicated by AKI require special attention to ensure that patients’ needs are optimally monitored and managed during the critical post-discharge period. One recent study analyzing discharge documentation for hospitalizations including AKI found that fewer than half of the discharge summaries and patient instructions commented on the presence, cause, or course of AKI, indicating clear room for improvement.¹³ And currently, it appears that only a minority of patients with AKI—even AKI severe enough to require dialysis—are seen by a nephrologist within 90 days of discharge.¹⁴

Hospitalists play a crucial role in coordinating care as vulnerable patients transition from the inpatient to outpatient setting. We suggest that AKI should be properly documented in the discharge summary. In addition, patients should be informed that they experienced AKI so they can discuss with future caregivers potential strategies to avoid additional renal insults. Discharge referrals to nephrology should be arranged for high-risk patients, including those whose renal function remains decreased at discharge or those who had recurrent AKI episodes during prior hospitalizations. For patients with pre-hospitalization baseline CKD, nephrology should be consulted before indefinitely discontinuing medications like angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. These medications are indispensable in retarding the progression of proteinuric CKD, even though they may predispose patients to AKI under certain circumstances (eg, in states of decreased renal perfusion). Adopting these simple steps may substantially improve the long-term outcomes of patients who experience AKI during hospitalization.

Acknowledgments

The authors are supported by NIH-NIDDK Grants T32DK007219 (BJL) and K24DK92291 (CYH).

Disclosure

Nothing to report.

Acute kidney injury (AKI) is a major contributor to morbidity and mortality in hospitalized patients across the world.¹ Affecting up to 20% of all admissions (depending on which definition of AKI is used),² AKI is the most common reason for new-inpatient nephrology consultation. Recent data suggest that AKI incidence has risen rapidly, by up to 10% per year.^3,4

AKI is associated with a variety of serious short- and long-term complications. Approximately 33% to 60% of critically ill patients who develop dialysis-requiring AKI do not survive to hospital discharge, and mortality associated with dialysis-requiring AKI is greater than that associated with other serious conditions such as myocardial infarction or acute respiratory distress syndrome.⁵ Even relatively mild AKI in the acute inpatient setting appears to be an independent risk factor for mortality.⁶

For several decades, many physicians believed that AKI was a self-limited process followed by complete recovery of renal function to pre-AKI levels among survivors. (Numerous trainees have been taught some variant of the old adage: “If the patients survive, so will their kidneys.”) But studies linking AKI with the development of new-onset chronic kidney disease (CKD) or the accelerated progression of pre-existing CKD have changed this view.⁷ One important reason the long-term impact of AKI hasn’t been appreciated is that, traditionally, clinical studies of AKI examined inhospital outcomes such as short-term mortality and resource usage and did not consider what transpired months to years after discharge. More recently, epidemiologic studies linking inpatient events with outpatient outcomes have filled this knowledge gap.⁸ Contemporary animal models of AKI have shed light on potential mechanisms of maladaptive repair after AKI, characterized by fibrosis, vascular rarefaction, tubular loss, glomerulosclerosis, and chronic interstitial inflammation, all of which result in renal function decline. So over the last decade there has been a paradigm shift in how we think about AKI and CKD. Rather than distinct entities, AKI and CKD are now viewed as interconnected syndromes since AKI is a risk factor for CKD progression and CKD is a risk factor for new episodes of AKI.⁹

Two studies published in this issue of the Journal of Hospital Medicine augment our understanding of AKI and its clinical impact in hospitalized patients. Analyzing data from the National Inpatient Sample, Silver et al.¹⁰ found that hospitalizations that include AKI are substantially costlier and associated with longer lengths of stay than hospitalizations without AKI. The authors also highlight that the additional economic costs of AKI exceeded those of many other higher-profile yet less-common acute medical conditions, such as myocardial infarction and gastrointestinal bleeding. These results re-emphasize the important economic burden of AKI at a national level and expand on prior literature by confirming findings previously limited to single-center and regional studies. Better defining the impact AKI has on our healthcare system could help ensure that adequate resources are invested to combat AKI.

The second study, by Rutter et al.,¹¹ found that among hospitalized patients with normal baseline renal function, use of vancomycin in combination with piperacillin-tazobactam is associated with a higher incidence of AKI after antibiotic exposure than use of either agent as monotherapy. This association persisted even after adjusting for potential confounders such as underlying comorbidities, exposure to nephrotoxic agents, documented hypotension, and baseline renal impairment. This study adds to a growing body of literature that suggests synergistic nephrotoxicity between vancomycin and piperacillin-tazobactam. It underscores that any medical intervention—even treatments typically envisioned as non-hazardous and frequently life-saving—involve inherent risks and should prompt the medical community to promote proper antimicrobial stewardship. Whether such exposures to vancomycin or beta-lactam derivatives cause AKI via direct tubular damage, interstitial nephritis, or some other novel mechanism remains to be elucidated. Better delineation of the contemporary causes of AKI, including increased antibiotic exposure, is the first step toward identifying ways to reduce AKI incidence.

Both of these papers serve to highlight the clinical importance of AKI among hospitalized patients. Their findings re-emphasize the need for vigilance in detecting AKI and intervening early to achieve the best clinical outcomes.

Given recent understanding that survivors of AKI are at greater risk for more rapid loss of renal function long after hospital discharge, one goal the US Department of Health and Human Services put forth for Healthy People 2020 is to “increase the proportion of hospital patients who incurred AKI who have follow-up renal evaluation in 6 months post-discharge” (10% improvement targeted).¹² Transitions of care after hospitalizations complicated by AKI require special attention to ensure that patients’ needs are optimally monitored and managed during the critical post-discharge period. One recent study analyzing discharge documentation for hospitalizations including AKI found that fewer than half of the discharge summaries and patient instructions commented on the presence, cause, or course of AKI, indicating clear room for improvement.¹³ And currently, it appears that only a minority of patients with AKI—even AKI severe enough to require dialysis—are seen by a nephrologist within 90 days of discharge.¹⁴

Hospitalists play a crucial role in coordinating care as vulnerable patients transition from the inpatient to outpatient setting. We suggest that AKI should be properly documented in the discharge summary. In addition, patients should be informed that they experienced AKI so they can discuss with future caregivers potential strategies to avoid additional renal insults. Discharge referrals to nephrology should be arranged for high-risk patients, including those whose renal function remains decreased at discharge or those who had recurrent AKI episodes during prior hospitalizations. For patients with pre-hospitalization baseline CKD, nephrology should be consulted before indefinitely discontinuing medications like angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. These medications are indispensable in retarding the progression of proteinuric CKD, even though they may predispose patients to AKI under certain circumstances (eg, in states of decreased renal perfusion). Adopting these simple steps may substantially improve the long-term outcomes of patients who experience AKI during hospitalization.

Acknowledgments

The authors are supported by NIH-NIDDK Grants T32DK007219 (BJL) and K24DK92291 (CYH).

Disclosure

Nothing to report.

Acute kidney injury (AKI) is a major contributor to morbidity and mortality in hospitalized patients across the world.¹ Affecting up to 20% of all admissions (depending on which definition of AKI is used),² AKI is the most common reason for new-inpatient nephrology consultation. Recent data suggest that AKI incidence has risen rapidly, by up to 10% per year.^3,4

AKI is associated with a variety of serious short- and long-term complications. Approximately 33% to 60% of critically ill patients who develop dialysis-requiring AKI do not survive to hospital discharge, and mortality associated with dialysis-requiring AKI is greater than that associated with other serious conditions such as myocardial infarction or acute respiratory distress syndrome.⁵ Even relatively mild AKI in the acute inpatient setting appears to be an independent risk factor for mortality.⁶

For several decades, many physicians believed that AKI was a self-limited process followed by complete recovery of renal function to pre-AKI levels among survivors. (Numerous trainees have been taught some variant of the old adage: “If the patients survive, so will their kidneys.”) But studies linking AKI with the development of new-onset chronic kidney disease (CKD) or the accelerated progression of pre-existing CKD have changed this view.⁷ One important reason the long-term impact of AKI hasn’t been appreciated is that, traditionally, clinical studies of AKI examined inhospital outcomes such as short-term mortality and resource usage and did not consider what transpired months to years after discharge. More recently, epidemiologic studies linking inpatient events with outpatient outcomes have filled this knowledge gap.⁸ Contemporary animal models of AKI have shed light on potential mechanisms of maladaptive repair after AKI, characterized by fibrosis, vascular rarefaction, tubular loss, glomerulosclerosis, and chronic interstitial inflammation, all of which result in renal function decline. So over the last decade there has been a paradigm shift in how we think about AKI and CKD. Rather than distinct entities, AKI and CKD are now viewed as interconnected syndromes since AKI is a risk factor for CKD progression and CKD is a risk factor for new episodes of AKI.⁹

Two studies published in this issue of the Journal of Hospital Medicine augment our understanding of AKI and its clinical impact in hospitalized patients. Analyzing data from the National Inpatient Sample, Silver et al.¹⁰ found that hospitalizations that include AKI are substantially costlier and associated with longer lengths of stay than hospitalizations without AKI. The authors also highlight that the additional economic costs of AKI exceeded those of many other higher-profile yet less-common acute medical conditions, such as myocardial infarction and gastrointestinal bleeding. These results re-emphasize the important economic burden of AKI at a national level and expand on prior literature by confirming findings previously limited to single-center and regional studies. Better defining the impact AKI has on our healthcare system could help ensure that adequate resources are invested to combat AKI.

The second study, by Rutter et al.,¹¹ found that among hospitalized patients with normal baseline renal function, use of vancomycin in combination with piperacillin-tazobactam is associated with a higher incidence of AKI after antibiotic exposure than use of either agent as monotherapy. This association persisted even after adjusting for potential confounders such as underlying comorbidities, exposure to nephrotoxic agents, documented hypotension, and baseline renal impairment. This study adds to a growing body of literature that suggests synergistic nephrotoxicity between vancomycin and piperacillin-tazobactam. It underscores that any medical intervention—even treatments typically envisioned as non-hazardous and frequently life-saving—involve inherent risks and should prompt the medical community to promote proper antimicrobial stewardship. Whether such exposures to vancomycin or beta-lactam derivatives cause AKI via direct tubular damage, interstitial nephritis, or some other novel mechanism remains to be elucidated. Better delineation of the contemporary causes of AKI, including increased antibiotic exposure, is the first step toward identifying ways to reduce AKI incidence.

Both of these papers serve to highlight the clinical importance of AKI among hospitalized patients. Their findings re-emphasize the need for vigilance in detecting AKI and intervening early to achieve the best clinical outcomes.

Given recent understanding that survivors of AKI are at greater risk for more rapid loss of renal function long after hospital discharge, one goal the US Department of Health and Human Services put forth for Healthy People 2020 is to “increase the proportion of hospital patients who incurred AKI who have follow-up renal evaluation in 6 months post-discharge” (10% improvement targeted).¹² Transitions of care after hospitalizations complicated by AKI require special attention to ensure that patients’ needs are optimally monitored and managed during the critical post-discharge period. One recent study analyzing discharge documentation for hospitalizations including AKI found that fewer than half of the discharge summaries and patient instructions commented on the presence, cause, or course of AKI, indicating clear room for improvement.¹³ And currently, it appears that only a minority of patients with AKI—even AKI severe enough to require dialysis—are seen by a nephrologist within 90 days of discharge.¹⁴

Hospitalists play a crucial role in coordinating care as vulnerable patients transition from the inpatient to outpatient setting. We suggest that AKI should be properly documented in the discharge summary. In addition, patients should be informed that they experienced AKI so they can discuss with future caregivers potential strategies to avoid additional renal insults. Discharge referrals to nephrology should be arranged for high-risk patients, including those whose renal function remains decreased at discharge or those who had recurrent AKI episodes during prior hospitalizations. For patients with pre-hospitalization baseline CKD, nephrology should be consulted before indefinitely discontinuing medications like angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. These medications are indispensable in retarding the progression of proteinuric CKD, even though they may predispose patients to AKI under certain circumstances (eg, in states of decreased renal perfusion). Adopting these simple steps may substantially improve the long-term outcomes of patients who experience AKI during hospitalization.

Acknowledgments

The authors are supported by NIH-NIDDK Grants T32DK007219 (BJL) and K24DK92291 (CYH).

Disclosure

Nothing to report.

The growing elderly population varies widely in functional capacity and mental agility. Age by itself is not a reliable indicator of physiologic performance in patients with cardiovascular disease.¹

See related article

The concept of frailty helps to identify elderly patients most susceptible to adverse outcomes. Frailty is a powerful indicator of disability, loss of independence, hospitalization, and death. In a patient whose health is declining, frailty is an appropriate impetus for the clinician and patient to reevaluate the goals of care.

In this issue of the Journal, Mallery et al² address an important topic: the use of preventive lipid-lowering therapies in frail patients with limited life expectancy. For these patients, they recommend against lipid-lowering therapy for primary prevention, and only in extenuating circumstances for secondary prevention.

No trials have evaluated lipid-lowering therapy specifically in frail older adults, and therefore, these recommendations are based on an evidence-informed appraisal of the literature. Mallery et al² suggest that in the frail elderly, improvement in function and quality of life are more relevant end points than traditional cardiovascular outcomes. They conclude that available evidence does not support lipid-lowering therapy for most patients with advanced frailty.

POINTS TO CONSIDER

Mallery et al² effectively articulate the need for frailty-specific care. Multimorbidity, polypharmacy, and increased adverse drug effects require special attention in the frail elderly. The authors make a sound argument against lipid-lowering therapy for primary prevention in the severely frail elderly, in whom the evidence for short-term benefit is not compelling. They also recommend against nonstatin lipid-lowering medications, and against statin therapy for heart failure, which is consistent with major guidelines. In the modern era of reflexive testing and prescribing, the authors’ “less is more” approach provides needed encouragement for thoughtful care in these vulnerable patients.

However, certain points of contention deserve additional consideration, including the imprecise definition of frailty, potential benefits and harms of statin therapy in high-risk patients, and the importance of shared decision-making.

How should frailty be defined?

Frailty biology is a field of ongoing research, and there is a lack of consensus on how best to define the condition.³ Estimates of the prevalence of frailty among older adults with cardiovascular disease range from 10% to 60%, owing to considerable variability in the tools used for frailty assessment.⁴

Mallery et al² consider an individual to be severely frail if he or she requires assistance with basic activities of daily living as the result of any physical or cognitive deficit (derived from the Clinical Frailty Scale or Frailty Assessment for Care Planning Tool). While functional dependence may be a consequence of frailty, this generalized definition does not characterize the clinical phenotype, which includes slowness, weakness, low physical activity, exhaustion, and unintentional weight loss.

Furthermore, this definition offers no insight into the unique characteristics, causes, and clinical course related to frailty. Significant heterogeneity among “frail” patients precludes a uniform treatment approach in this population.

Do statins benefit frail patients at high risk?

Regarding secondary prevention, the authors highlight a meta-analysis by Afilalo et al,⁵ the most comprehensive assessment to date of statin therapy in elderly patients with documented coronary heart disease. This study included nearly 20,000 elderly patients in nine secondary prevention trials, including the secondary prevention subgroup of the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) trial.⁶

Afilalo et al⁵ calculated that statin therapy reduced the rates of all-cause mortality by 22% and coronary death by 30%, with even greater reductions in the rates of nonfatal myocardial infarction, stroke, and revascularization. Furthermore, the absolute risk reduction was higher and the number needed to treat was lower in those over age 80. Overall, these data convincingly showed that high-risk patients ages 65 to 82 enrolled in clinical trials derive substantial benefit from statin therapy.

Mallery et al² contend that many of the secondary prevention statin trials evaluated composite outcomes over many years of follow-up and therefore are not generalizable to the frail elderly. However, the Afilalo meta-analysis⁵ does not provide patient-level data, and therefore the benefit for different clinical and demographic subgroups is unknown. It is only speculative to infer that those with frailty are unlikely to benefit. In fact, the improved outcomes observed with increasing age would argue against this notion.

Given the compelling data supporting statin therapy in the high-risk elderly population, some patients and clinicians may reasonably feel there is value in statin therapy—even in those with advanced frailty.

What about symptoms, disability, quality of life, and short-term benefits? Asymptomatic or “silent” myocardial infarction is associated with angina, congestive heart failure, and subsequent symptomatic myocardial infarction.^7,8 Dismissing the importance of these end points in clinical trials fails to recognize potential downstream effects that are directly relevant to a patient’s overall health status.

The Study Assessing Goals in the Elderly (SAGE) trial⁹ assessed the effect of statin therapy on ischemia burden in patients ages 65 to 85 with stable coronary disease. The results showed that both moderate and intensive statin dosing significantly reduced myocardial ischemia at 3 and 12 months, as detected by continuous electrocardiographic monitoring.

More research is needed to determine the effect of statin therapy on functional capacity and quality of life. Currently, it is premature to conclude that statins have no relevance to these important patient-centered outcomes.

What are the potential harms?

Mallery et al² cite numerous articles that emphasize the potential adverse effects of statin therapy in the elderly. Unfortunately, data supporting the safety of statin therapy in the elderly were not included. This should be stressed, given that older statin-eligible patients are often undertreated in contemporary practice.¹⁰

A 2015 systematic review and meta-analysis indicated that statin-related events are relatively rare in the elderly.¹¹ Another study showed elderly patients who started statin therapy after a myocardial infarction had no change in short-term cognitive or physical function.¹²

Older age and low body mass index are risk factors for statin myopathy, underscoring the need for close monitoring in frail patients. However, it is important to maintain an objective and balanced approach when considering potential harms.

Need for shared decision-making

Mallery et al² make no mention of shared decision-making. Best practice guidelines for the management of frailty support a holistic medical review to establish an individualized care plan for each patient.¹³ Firm recommendations based on indeterminate evidence undermine the patient-physician relationship and do not allow for personal preferences of care. In an environment of uncertain benefit and harm, the patient’s priorities and values should serve as the cornerstone for clinical decisions.

The growing elderly population varies widely in functional capacity and mental agility. Age by itself is not a reliable indicator of physiologic performance in patients with cardiovascular disease.¹

See related article

The concept of frailty helps to identify elderly patients most susceptible to adverse outcomes. Frailty is a powerful indicator of disability, loss of independence, hospitalization, and death. In a patient whose health is declining, frailty is an appropriate impetus for the clinician and patient to reevaluate the goals of care.

In this issue of the Journal, Mallery et al² address an important topic: the use of preventive lipid-lowering therapies in frail patients with limited life expectancy. For these patients, they recommend against lipid-lowering therapy for primary prevention, and only in extenuating circumstances for secondary prevention.

No trials have evaluated lipid-lowering therapy specifically in frail older adults, and therefore, these recommendations are based on an evidence-informed appraisal of the literature. Mallery et al² suggest that in the frail elderly, improvement in function and quality of life are more relevant end points than traditional cardiovascular outcomes. They conclude that available evidence does not support lipid-lowering therapy for most patients with advanced frailty.

POINTS TO CONSIDER

Mallery et al² effectively articulate the need for frailty-specific care. Multimorbidity, polypharmacy, and increased adverse drug effects require special attention in the frail elderly. The authors make a sound argument against lipid-lowering therapy for primary prevention in the severely frail elderly, in whom the evidence for short-term benefit is not compelling. They also recommend against nonstatin lipid-lowering medications, and against statin therapy for heart failure, which is consistent with major guidelines. In the modern era of reflexive testing and prescribing, the authors’ “less is more” approach provides needed encouragement for thoughtful care in these vulnerable patients.

However, certain points of contention deserve additional consideration, including the imprecise definition of frailty, potential benefits and harms of statin therapy in high-risk patients, and the importance of shared decision-making.

How should frailty be defined?

Frailty biology is a field of ongoing research, and there is a lack of consensus on how best to define the condition.³ Estimates of the prevalence of frailty among older adults with cardiovascular disease range from 10% to 60%, owing to considerable variability in the tools used for frailty assessment.⁴

Mallery et al² consider an individual to be severely frail if he or she requires assistance with basic activities of daily living as the result of any physical or cognitive deficit (derived from the Clinical Frailty Scale or Frailty Assessment for Care Planning Tool). While functional dependence may be a consequence of frailty, this generalized definition does not characterize the clinical phenotype, which includes slowness, weakness, low physical activity, exhaustion, and unintentional weight loss.

Furthermore, this definition offers no insight into the unique characteristics, causes, and clinical course related to frailty. Significant heterogeneity among “frail” patients precludes a uniform treatment approach in this population.

Do statins benefit frail patients at high risk?

Regarding secondary prevention, the authors highlight a meta-analysis by Afilalo et al,⁵ the most comprehensive assessment to date of statin therapy in elderly patients with documented coronary heart disease. This study included nearly 20,000 elderly patients in nine secondary prevention trials, including the secondary prevention subgroup of the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) trial.⁶

Afilalo et al⁵ calculated that statin therapy reduced the rates of all-cause mortality by 22% and coronary death by 30%, with even greater reductions in the rates of nonfatal myocardial infarction, stroke, and revascularization. Furthermore, the absolute risk reduction was higher and the number needed to treat was lower in those over age 80. Overall, these data convincingly showed that high-risk patients ages 65 to 82 enrolled in clinical trials derive substantial benefit from statin therapy.

Mallery et al² contend that many of the secondary prevention statin trials evaluated composite outcomes over many years of follow-up and therefore are not generalizable to the frail elderly. However, the Afilalo meta-analysis⁵ does not provide patient-level data, and therefore the benefit for different clinical and demographic subgroups is unknown. It is only speculative to infer that those with frailty are unlikely to benefit. In fact, the improved outcomes observed with increasing age would argue against this notion.

Given the compelling data supporting statin therapy in the high-risk elderly population, some patients and clinicians may reasonably feel there is value in statin therapy—even in those with advanced frailty.

What about symptoms, disability, quality of life, and short-term benefits? Asymptomatic or “silent” myocardial infarction is associated with angina, congestive heart failure, and subsequent symptomatic myocardial infarction.^7,8 Dismissing the importance of these end points in clinical trials fails to recognize potential downstream effects that are directly relevant to a patient’s overall health status.

The Study Assessing Goals in the Elderly (SAGE) trial⁹ assessed the effect of statin therapy on ischemia burden in patients ages 65 to 85 with stable coronary disease. The results showed that both moderate and intensive statin dosing significantly reduced myocardial ischemia at 3 and 12 months, as detected by continuous electrocardiographic monitoring.

More research is needed to determine the effect of statin therapy on functional capacity and quality of life. Currently, it is premature to conclude that statins have no relevance to these important patient-centered outcomes.

What are the potential harms?

Mallery et al² cite numerous articles that emphasize the potential adverse effects of statin therapy in the elderly. Unfortunately, data supporting the safety of statin therapy in the elderly were not included. This should be stressed, given that older statin-eligible patients are often undertreated in contemporary practice.¹⁰

A 2015 systematic review and meta-analysis indicated that statin-related events are relatively rare in the elderly.¹¹ Another study showed elderly patients who started statin therapy after a myocardial infarction had no change in short-term cognitive or physical function.¹²

Older age and low body mass index are risk factors for statin myopathy, underscoring the need for close monitoring in frail patients. However, it is important to maintain an objective and balanced approach when considering potential harms.

Need for shared decision-making

Mallery et al² make no mention of shared decision-making. Best practice guidelines for the management of frailty support a holistic medical review to establish an individualized care plan for each patient.¹³ Firm recommendations based on indeterminate evidence undermine the patient-physician relationship and do not allow for personal preferences of care. In an environment of uncertain benefit and harm, the patient’s priorities and values should serve as the cornerstone for clinical decisions.

The growing elderly population varies widely in functional capacity and mental agility. Age by itself is not a reliable indicator of physiologic performance in patients with cardiovascular disease.¹

See related article

The concept of frailty helps to identify elderly patients most susceptible to adverse outcomes. Frailty is a powerful indicator of disability, loss of independence, hospitalization, and death. In a patient whose health is declining, frailty is an appropriate impetus for the clinician and patient to reevaluate the goals of care.

In this issue of the Journal, Mallery et al² address an important topic: the use of preventive lipid-lowering therapies in frail patients with limited life expectancy. For these patients, they recommend against lipid-lowering therapy for primary prevention, and only in extenuating circumstances for secondary prevention.

No trials have evaluated lipid-lowering therapy specifically in frail older adults, and therefore, these recommendations are based on an evidence-informed appraisal of the literature. Mallery et al² suggest that in the frail elderly, improvement in function and quality of life are more relevant end points than traditional cardiovascular outcomes. They conclude that available evidence does not support lipid-lowering therapy for most patients with advanced frailty.

POINTS TO CONSIDER

Mallery et al² effectively articulate the need for frailty-specific care. Multimorbidity, polypharmacy, and increased adverse drug effects require special attention in the frail elderly. The authors make a sound argument against lipid-lowering therapy for primary prevention in the severely frail elderly, in whom the evidence for short-term benefit is not compelling. They also recommend against nonstatin lipid-lowering medications, and against statin therapy for heart failure, which is consistent with major guidelines. In the modern era of reflexive testing and prescribing, the authors’ “less is more” approach provides needed encouragement for thoughtful care in these vulnerable patients.

However, certain points of contention deserve additional consideration, including the imprecise definition of frailty, potential benefits and harms of statin therapy in high-risk patients, and the importance of shared decision-making.

How should frailty be defined?

Frailty biology is a field of ongoing research, and there is a lack of consensus on how best to define the condition.³ Estimates of the prevalence of frailty among older adults with cardiovascular disease range from 10% to 60%, owing to considerable variability in the tools used for frailty assessment.⁴

Mallery et al² consider an individual to be severely frail if he or she requires assistance with basic activities of daily living as the result of any physical or cognitive deficit (derived from the Clinical Frailty Scale or Frailty Assessment for Care Planning Tool). While functional dependence may be a consequence of frailty, this generalized definition does not characterize the clinical phenotype, which includes slowness, weakness, low physical activity, exhaustion, and unintentional weight loss.

Furthermore, this definition offers no insight into the unique characteristics, causes, and clinical course related to frailty. Significant heterogeneity among “frail” patients precludes a uniform treatment approach in this population.

Do statins benefit frail patients at high risk?

Regarding secondary prevention, the authors highlight a meta-analysis by Afilalo et al,⁵ the most comprehensive assessment to date of statin therapy in elderly patients with documented coronary heart disease. This study included nearly 20,000 elderly patients in nine secondary prevention trials, including the secondary prevention subgroup of the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) trial.⁶

Afilalo et al⁵ calculated that statin therapy reduced the rates of all-cause mortality by 22% and coronary death by 30%, with even greater reductions in the rates of nonfatal myocardial infarction, stroke, and revascularization. Furthermore, the absolute risk reduction was higher and the number needed to treat was lower in those over age 80. Overall, these data convincingly showed that high-risk patients ages 65 to 82 enrolled in clinical trials derive substantial benefit from statin therapy.

Mallery et al² contend that many of the secondary prevention statin trials evaluated composite outcomes over many years of follow-up and therefore are not generalizable to the frail elderly. However, the Afilalo meta-analysis⁵ does not provide patient-level data, and therefore the benefit for different clinical and demographic subgroups is unknown. It is only speculative to infer that those with frailty are unlikely to benefit. In fact, the improved outcomes observed with increasing age would argue against this notion.

Given the compelling data supporting statin therapy in the high-risk elderly population, some patients and clinicians may reasonably feel there is value in statin therapy—even in those with advanced frailty.

What about symptoms, disability, quality of life, and short-term benefits? Asymptomatic or “silent” myocardial infarction is associated with angina, congestive heart failure, and subsequent symptomatic myocardial infarction.^7,8 Dismissing the importance of these end points in clinical trials fails to recognize potential downstream effects that are directly relevant to a patient’s overall health status.

The Study Assessing Goals in the Elderly (SAGE) trial⁹ assessed the effect of statin therapy on ischemia burden in patients ages 65 to 85 with stable coronary disease. The results showed that both moderate and intensive statin dosing significantly reduced myocardial ischemia at 3 and 12 months, as detected by continuous electrocardiographic monitoring.

More research is needed to determine the effect of statin therapy on functional capacity and quality of life. Currently, it is premature to conclude that statins have no relevance to these important patient-centered outcomes.

What are the potential harms?

Mallery et al² cite numerous articles that emphasize the potential adverse effects of statin therapy in the elderly. Unfortunately, data supporting the safety of statin therapy in the elderly were not included. This should be stressed, given that older statin-eligible patients are often undertreated in contemporary practice.¹⁰

A 2015 systematic review and meta-analysis indicated that statin-related events are relatively rare in the elderly.¹¹ Another study showed elderly patients who started statin therapy after a myocardial infarction had no change in short-term cognitive or physical function.¹²

Older age and low body mass index are risk factors for statin myopathy, underscoring the need for close monitoring in frail patients. However, it is important to maintain an objective and balanced approach when considering potential harms.

Need for shared decision-making

Mallery et al² make no mention of shared decision-making. Best practice guidelines for the management of frailty support a holistic medical review to establish an individualized care plan for each patient.¹³ Firm recommendations based on indeterminate evidence undermine the patient-physician relationship and do not allow for personal preferences of care. In an environment of uncertain benefit and harm, the patient’s priorities and values should serve as the cornerstone for clinical decisions.