Perioperative Medicine

A single hospitalized patient can generate up to several hundred alarm signals each day, causing physicians to quickly become desensitized to the noise. But ignoring these alarms can have fatal consequences for patients, the Joint Commission warns.

Between January 2009 and June 2012, the Joint Commission’s Sentinel Event Alert database recorded 98 alarm-related adverse events, 80 of which resulted in death. Another 13 resulted in permanent loss of function and 5 led to unexpected additional care or an extended stay in the hospital.

The Joint Commission found that inadequate alarms, improper settings, and signals that were not loud enough all contributed to the reported adverse events. Alarms that were improperly turned off also were a problem, according to the Joint Commission.

In the Sentinel Event Alert issued on April 8, the Joint Commission recommended several steps hospital leaders can take to curb the "alarm fatigue" common in hospitals.

– Set up a process for alarm management and response, especially in high-risk areas.

– Perform an inventory of all devices with alarms in high-risk areas and their default settings.

– Establish guidelines for alarm settings in high-risk areas and for high-risk conditions, including situations when alarms are not clinically necessary.

– Establish guidelines for tailoring alarm settings and limits for individual patients.

– Inspect and maintain alarm-equipped devices.

"Alarm fatigue and management of alarms are important safety issues that we must confront," Dr. Ana McKee, executive vice president and chief medical officer at the Joint Commission, said in a statement. "The recommendations in this alert offer hospitals a framework on which to assess their individual circumstances and develop a systematic, coordinated approach to alarms. By making alarm safety a priority, lives can be saved."

The Sentinel Event Alert also calls on hospitals to provide training and education on safe alarm management and response in high-risk areas to all members of the clinical care team.

In addition to the guidance to hospitals, the Joint Commission is considering the creation of a National Patient Safety Goal on the issue of alarm fatigue.

[email protected]

Twitter: @MaryEllenNY

A single hospitalized patient can generate up to several hundred alarm signals each day, causing physicians to quickly become desensitized to the noise. But ignoring these alarms can have fatal consequences for patients, the Joint Commission warns.

Between January 2009 and June 2012, the Joint Commission’s Sentinel Event Alert database recorded 98 alarm-related adverse events, 80 of which resulted in death. Another 13 resulted in permanent loss of function and 5 led to unexpected additional care or an extended stay in the hospital.

The Joint Commission found that inadequate alarms, improper settings, and signals that were not loud enough all contributed to the reported adverse events. Alarms that were improperly turned off also were a problem, according to the Joint Commission.

In the Sentinel Event Alert issued on April 8, the Joint Commission recommended several steps hospital leaders can take to curb the "alarm fatigue" common in hospitals.

– Set up a process for alarm management and response, especially in high-risk areas.

– Perform an inventory of all devices with alarms in high-risk areas and their default settings.

– Establish guidelines for alarm settings in high-risk areas and for high-risk conditions, including situations when alarms are not clinically necessary.

– Establish guidelines for tailoring alarm settings and limits for individual patients.

– Inspect and maintain alarm-equipped devices.

"Alarm fatigue and management of alarms are important safety issues that we must confront," Dr. Ana McKee, executive vice president and chief medical officer at the Joint Commission, said in a statement. "The recommendations in this alert offer hospitals a framework on which to assess their individual circumstances and develop a systematic, coordinated approach to alarms. By making alarm safety a priority, lives can be saved."

The Sentinel Event Alert also calls on hospitals to provide training and education on safe alarm management and response in high-risk areas to all members of the clinical care team.

In addition to the guidance to hospitals, the Joint Commission is considering the creation of a National Patient Safety Goal on the issue of alarm fatigue.

[email protected]

Twitter: @MaryEllenNY

A single hospitalized patient can generate up to several hundred alarm signals each day, causing physicians to quickly become desensitized to the noise. But ignoring these alarms can have fatal consequences for patients, the Joint Commission warns.

Between January 2009 and June 2012, the Joint Commission’s Sentinel Event Alert database recorded 98 alarm-related adverse events, 80 of which resulted in death. Another 13 resulted in permanent loss of function and 5 led to unexpected additional care or an extended stay in the hospital.

The Joint Commission found that inadequate alarms, improper settings, and signals that were not loud enough all contributed to the reported adverse events. Alarms that were improperly turned off also were a problem, according to the Joint Commission.

In the Sentinel Event Alert issued on April 8, the Joint Commission recommended several steps hospital leaders can take to curb the "alarm fatigue" common in hospitals.

– Set up a process for alarm management and response, especially in high-risk areas.

– Perform an inventory of all devices with alarms in high-risk areas and their default settings.

– Establish guidelines for alarm settings in high-risk areas and for high-risk conditions, including situations when alarms are not clinically necessary.

– Establish guidelines for tailoring alarm settings and limits for individual patients.

– Inspect and maintain alarm-equipped devices.

"Alarm fatigue and management of alarms are important safety issues that we must confront," Dr. Ana McKee, executive vice president and chief medical officer at the Joint Commission, said in a statement. "The recommendations in this alert offer hospitals a framework on which to assess their individual circumstances and develop a systematic, coordinated approach to alarms. By making alarm safety a priority, lives can be saved."

The Sentinel Event Alert also calls on hospitals to provide training and education on safe alarm management and response in high-risk areas to all members of the clinical care team.

In addition to the guidance to hospitals, the Joint Commission is considering the creation of a National Patient Safety Goal on the issue of alarm fatigue.

[email protected]

Twitter: @MaryEllenNY

Is sending patients home the same day they undergo percutaneous coronary intervention as safe as watching patients overnight in the hospital? Dr. Kimberly Brayton discusses the results of a meta-analysis, and outlines her own medical center's protocol for post-PCI discharge.

Is sending patients home the same day they undergo percutaneous coronary intervention as safe as watching patients overnight in the hospital? Dr. Kimberly Brayton discusses the results of a meta-analysis, and outlines her own medical center's protocol for post-PCI discharge.

Is sending patients home the same day they undergo percutaneous coronary intervention as safe as watching patients overnight in the hospital? Dr. Kimberly Brayton discusses the results of a meta-analysis, and outlines her own medical center's protocol for post-PCI discharge.

Looking for reliable information to share with patients about the risk for blood clots after surgery? The Agency for Healthcare Research and Quality has developed patient resources to explain the risks and treatments. See the attached PDF file to share with patients and use this link to access additional helpful resources.

Looking for reliable information to share with patients about the risk for blood clots after surgery? The Agency for Healthcare Research and Quality has developed patient resources to explain the risks and treatments. See the attached PDF file to share with patients and use this link to access additional helpful resources.

Looking for reliable information to share with patients about the risk for blood clots after surgery? The Agency for Healthcare Research and Quality has developed patient resources to explain the risks and treatments. See the attached PDF file to share with patients and use this link to access additional helpful resources.

The breakdown and clearance of cortisol are impaired during critical illness, which may account in part for the abnormally high blood levels of cortisol often observed in ICU patients, according to a report published online March 19 in the New England Journal of Medicine.

Hypercortisolemia often accompanies critical illness, but until now it usually has been attributed to increased cortisol production driven by stress-induced activation of the hypothalamic-pituitary-adrenal axis. However, some researchers posited that another possible contributor to hypercortisolemia in this setting might be suppression of the removal of cortisol.

"We hypothesized that cortisol metabolism is reduced during critical illness, contributing to sustained hypercortisolemia with enhanced negative-feedback inhibition of corticotropin," said Dr. Eva Boonen of the clinical division and laboratory of intensive care medicine, Catholic University of Leuven (Belgium), and her associates.

To test their hypothesis, the investigators studied 158 consecutive adults treated for critical illness in a single ICU and 64 demographically matched but not critically ill control subjects. They measured five aspects of cortisol metabolism: daily corticotropin and cortisol levels; plasma cortisol levels reflecting the clearance, metabolism, and production of cortisol during an infusion of deuterium-labeled tracers; plasma clearance of a therapeutic 100-mg IV bolus of hydrocortisone; urinary levels of cortisol metabolites; and levels of major cortisol-metabolizing enzymes in liver and adipose tissue.

Their findings demonstrated that "elevated cortisol levels in critically ill patients were only partially explained by an increase of 83% in cortisol production, as compared with controls." In addition, impaired breakdown and clearance of cortisol contributed to hypercortisolemia, the investigators reported. They found a reduction of more than 50% in cortisol clearance after administration of the 100 mg of hydrocortisone (N. Engl. J. Med. 2013 March 19 [doi: 10.1056/NEJMoa1214969]).

The clinical implications of these study results are important because the findings markedly change "our understanding of the stress response. Reduced inactivation of cortisol may be important not only to increase circulating levels but also to potentiate cortisol levels and activity within the vital tissues that express inactivating enzymes.

"More pragmatically, the data suggest that ‘stress doses’ of hydrocortisone, which are advocated to replace cortisol production in critically ill patients who are presumed to have adrenal failure, are at least 3 times too high," Dr. Boonen and her colleagues said.

The data also suggest that "a low cortisol response to corticotropin stimulation does not necessarily reflect adrenal failure, since cortisol production in critically ill patients is not subnormal, and the suppressed clearance maintains hypercortisolemia. Our results may therefore help to explain why studies investigating the effect of the daily administration of 200 mg of hydrocortisone in patients with sepsis ... have had conflicting results," they added.

This study was supported by the Belgian Fund for Scientific Research, the British Heart Foundation, the Flemish government\'s Methusalem Program, and the European Research Council. No relevant conflicts of interest were reported.

The breakdown and clearance of cortisol are impaired during critical illness, which may account in part for the abnormally high blood levels of cortisol often observed in ICU patients, according to a report published online March 19 in the New England Journal of Medicine.

Hypercortisolemia often accompanies critical illness, but until now it usually has been attributed to increased cortisol production driven by stress-induced activation of the hypothalamic-pituitary-adrenal axis. However, some researchers posited that another possible contributor to hypercortisolemia in this setting might be suppression of the removal of cortisol.

"We hypothesized that cortisol metabolism is reduced during critical illness, contributing to sustained hypercortisolemia with enhanced negative-feedback inhibition of corticotropin," said Dr. Eva Boonen of the clinical division and laboratory of intensive care medicine, Catholic University of Leuven (Belgium), and her associates.

To test their hypothesis, the investigators studied 158 consecutive adults treated for critical illness in a single ICU and 64 demographically matched but not critically ill control subjects. They measured five aspects of cortisol metabolism: daily corticotropin and cortisol levels; plasma cortisol levels reflecting the clearance, metabolism, and production of cortisol during an infusion of deuterium-labeled tracers; plasma clearance of a therapeutic 100-mg IV bolus of hydrocortisone; urinary levels of cortisol metabolites; and levels of major cortisol-metabolizing enzymes in liver and adipose tissue.

Their findings demonstrated that "elevated cortisol levels in critically ill patients were only partially explained by an increase of 83% in cortisol production, as compared with controls." In addition, impaired breakdown and clearance of cortisol contributed to hypercortisolemia, the investigators reported. They found a reduction of more than 50% in cortisol clearance after administration of the 100 mg of hydrocortisone (N. Engl. J. Med. 2013 March 19 [doi: 10.1056/NEJMoa1214969]).

The clinical implications of these study results are important because the findings markedly change "our understanding of the stress response. Reduced inactivation of cortisol may be important not only to increase circulating levels but also to potentiate cortisol levels and activity within the vital tissues that express inactivating enzymes.

"More pragmatically, the data suggest that ‘stress doses’ of hydrocortisone, which are advocated to replace cortisol production in critically ill patients who are presumed to have adrenal failure, are at least 3 times too high," Dr. Boonen and her colleagues said.

The data also suggest that "a low cortisol response to corticotropin stimulation does not necessarily reflect adrenal failure, since cortisol production in critically ill patients is not subnormal, and the suppressed clearance maintains hypercortisolemia. Our results may therefore help to explain why studies investigating the effect of the daily administration of 200 mg of hydrocortisone in patients with sepsis ... have had conflicting results," they added.

This study was supported by the Belgian Fund for Scientific Research, the British Heart Foundation, the Flemish government\'s Methusalem Program, and the European Research Council. No relevant conflicts of interest were reported.

The breakdown and clearance of cortisol are impaired during critical illness, which may account in part for the abnormally high blood levels of cortisol often observed in ICU patients, according to a report published online March 19 in the New England Journal of Medicine.

Hypercortisolemia often accompanies critical illness, but until now it usually has been attributed to increased cortisol production driven by stress-induced activation of the hypothalamic-pituitary-adrenal axis. However, some researchers posited that another possible contributor to hypercortisolemia in this setting might be suppression of the removal of cortisol.

"We hypothesized that cortisol metabolism is reduced during critical illness, contributing to sustained hypercortisolemia with enhanced negative-feedback inhibition of corticotropin," said Dr. Eva Boonen of the clinical division and laboratory of intensive care medicine, Catholic University of Leuven (Belgium), and her associates.

To test their hypothesis, the investigators studied 158 consecutive adults treated for critical illness in a single ICU and 64 demographically matched but not critically ill control subjects. They measured five aspects of cortisol metabolism: daily corticotropin and cortisol levels; plasma cortisol levels reflecting the clearance, metabolism, and production of cortisol during an infusion of deuterium-labeled tracers; plasma clearance of a therapeutic 100-mg IV bolus of hydrocortisone; urinary levels of cortisol metabolites; and levels of major cortisol-metabolizing enzymes in liver and adipose tissue.

Their findings demonstrated that "elevated cortisol levels in critically ill patients were only partially explained by an increase of 83% in cortisol production, as compared with controls." In addition, impaired breakdown and clearance of cortisol contributed to hypercortisolemia, the investigators reported. They found a reduction of more than 50% in cortisol clearance after administration of the 100 mg of hydrocortisone (N. Engl. J. Med. 2013 March 19 [doi: 10.1056/NEJMoa1214969]).

The clinical implications of these study results are important because the findings markedly change "our understanding of the stress response. Reduced inactivation of cortisol may be important not only to increase circulating levels but also to potentiate cortisol levels and activity within the vital tissues that express inactivating enzymes.

"More pragmatically, the data suggest that ‘stress doses’ of hydrocortisone, which are advocated to replace cortisol production in critically ill patients who are presumed to have adrenal failure, are at least 3 times too high," Dr. Boonen and her colleagues said.

The data also suggest that "a low cortisol response to corticotropin stimulation does not necessarily reflect adrenal failure, since cortisol production in critically ill patients is not subnormal, and the suppressed clearance maintains hypercortisolemia. Our results may therefore help to explain why studies investigating the effect of the daily administration of 200 mg of hydrocortisone in patients with sepsis ... have had conflicting results," they added.

This study was supported by the Belgian Fund for Scientific Research, the British Heart Foundation, the Flemish government\'s Methusalem Program, and the European Research Council. No relevant conflicts of interest were reported.

Hospital readmission rates continue to hover at around 16% for medical discharges and 12% for surgical conditions, despite the existence of several proven protocols for improving the discharge process.

A new analysis of Medicare data conducted by the Dartmouth Atlas Project, and supported by the Robert Wood Johnson Foundation, shows that readmission rates are virtually unchanged between 2008 and 2010. This follows an earlier report from the Dartmouth Atlas Project showing that readmission rates failed to improve between 2004 and 2009.

"We still have a very persistent problem," Dr. Risa Lavizzo-Mourey, president and CEO of the Robert Wood Johnson Foundation, said during a panel discussion on the report on Feb. 13 in Washington.

The national rate for 30-day readmissions for medical conditions was 16.2% in 2008 and 15.9% in 2010. Similarly, the 30-day surgical readmission rates were 12.7% in 2008 and 12.4% in 2010. The same trends hold true when looking at readmission rates for heart failure, acute myocardial infarction, and pneumonia, the conditions that held accountable for as part of a new Medicare readmissions penalty that went into effect in October 2012.

Readmission rates for heart failure were dipped slightly from 21.4% in 2008 to 21.1% in 2010. Acute myocardial infarction readmissions went from 18.7% to 18.1% during the same time period. And pneumonia readmission rates stayed at 15.3% in both 2008 and 2010.

The researchers called the progress on readmissions "slow and inconsistent." But while there has been little change nationally among the Medicare population, there is widespread regional variation, according to the analysis.

For instance, 30-day readmission rates following medical discharge ranged from a low of 11.4% in Ogden, Utah, to a high of 18.1% in the Bronx, N.Y., in 2010. There was even greater variation in readmissions following surgery. Surgical readmission rates ranged from 7.6% in Bend, Oregon, to 18.3% in the New York.

"People who have the same illness often have very different chances of being readmitted depending on where they live," Dr. Lavizzo-Mourey said.

Many patients are readmitted simply because their local hospital is the community’s main source of care, the researchers wrote. This trend results in both higher initial hospital admissions and readmissions, they wrote.

But while the report highlights the lack of progress, there are some success stories, Dr. Lavizzo-Mourey said. For instance, some hospitals are establishing 24-hour pharmacies so that patients can get their prescriptions no matter what time they are discharged. Others are setting up clinics to specialize in the care of patients with heart failure, a condition with a high rate of bounce-back to the hospital. And other hospitals are working with community organizations to ensure patients have the care and support they need when they go home, she said.

"This issue of readmissions is firmly on the radar screen of our health care providers," Dr. Lavizzo-Mourey said.

Dr. Eric Coleman, who runs the Care Transitions Program aimed at improving the safety of hand-offs, said one of the issues that leads to readmissions is the poor engagement of patients and family members before discharge.

At the University of Colorado, Denver, where he heads the division of health care policy and research, Dr. Coleman said they try to avoid simply dumping information on patients and families and instead use a process called "skill transfer" to train them to be able to handle their own care at home without the help of health care providers.

But many of the causes of readmissions are beyond the control of the hospital, Dr. Coleman said. He encourages physicians to go the bedside and ask patients why they think they were readmitted to the hospital. The answers are often about a lack of transportation to appointments, struggles to afford medicine and care, or family caregivers who are burning out.

"It may be that hospitals don’t have the resources to address this but a lot of their community partners, such as the area agencies on aging do have that opportunity," Dr. Coleman said.

[email protected]

Hospital readmission rates continue to hover at around 16% for medical discharges and 12% for surgical conditions, despite the existence of several proven protocols for improving the discharge process.

A new analysis of Medicare data conducted by the Dartmouth Atlas Project, and supported by the Robert Wood Johnson Foundation, shows that readmission rates are virtually unchanged between 2008 and 2010. This follows an earlier report from the Dartmouth Atlas Project showing that readmission rates failed to improve between 2004 and 2009.

"We still have a very persistent problem," Dr. Risa Lavizzo-Mourey, president and CEO of the Robert Wood Johnson Foundation, said during a panel discussion on the report on Feb. 13 in Washington.

The national rate for 30-day readmissions for medical conditions was 16.2% in 2008 and 15.9% in 2010. Similarly, the 30-day surgical readmission rates were 12.7% in 2008 and 12.4% in 2010. The same trends hold true when looking at readmission rates for heart failure, acute myocardial infarction, and pneumonia, the conditions that held accountable for as part of a new Medicare readmissions penalty that went into effect in October 2012.

Readmission rates for heart failure were dipped slightly from 21.4% in 2008 to 21.1% in 2010. Acute myocardial infarction readmissions went from 18.7% to 18.1% during the same time period. And pneumonia readmission rates stayed at 15.3% in both 2008 and 2010.

The researchers called the progress on readmissions "slow and inconsistent." But while there has been little change nationally among the Medicare population, there is widespread regional variation, according to the analysis.

For instance, 30-day readmission rates following medical discharge ranged from a low of 11.4% in Ogden, Utah, to a high of 18.1% in the Bronx, N.Y., in 2010. There was even greater variation in readmissions following surgery. Surgical readmission rates ranged from 7.6% in Bend, Oregon, to 18.3% in the New York.

"People who have the same illness often have very different chances of being readmitted depending on where they live," Dr. Lavizzo-Mourey said.

Many patients are readmitted simply because their local hospital is the community’s main source of care, the researchers wrote. This trend results in both higher initial hospital admissions and readmissions, they wrote.

But while the report highlights the lack of progress, there are some success stories, Dr. Lavizzo-Mourey said. For instance, some hospitals are establishing 24-hour pharmacies so that patients can get their prescriptions no matter what time they are discharged. Others are setting up clinics to specialize in the care of patients with heart failure, a condition with a high rate of bounce-back to the hospital. And other hospitals are working with community organizations to ensure patients have the care and support they need when they go home, she said.

"This issue of readmissions is firmly on the radar screen of our health care providers," Dr. Lavizzo-Mourey said.

Dr. Eric Coleman, who runs the Care Transitions Program aimed at improving the safety of hand-offs, said one of the issues that leads to readmissions is the poor engagement of patients and family members before discharge.

At the University of Colorado, Denver, where he heads the division of health care policy and research, Dr. Coleman said they try to avoid simply dumping information on patients and families and instead use a process called "skill transfer" to train them to be able to handle their own care at home without the help of health care providers.

But many of the causes of readmissions are beyond the control of the hospital, Dr. Coleman said. He encourages physicians to go the bedside and ask patients why they think they were readmitted to the hospital. The answers are often about a lack of transportation to appointments, struggles to afford medicine and care, or family caregivers who are burning out.

"It may be that hospitals don’t have the resources to address this but a lot of their community partners, such as the area agencies on aging do have that opportunity," Dr. Coleman said.

[email protected]

Hospital readmission rates continue to hover at around 16% for medical discharges and 12% for surgical conditions, despite the existence of several proven protocols for improving the discharge process.

A new analysis of Medicare data conducted by the Dartmouth Atlas Project, and supported by the Robert Wood Johnson Foundation, shows that readmission rates are virtually unchanged between 2008 and 2010. This follows an earlier report from the Dartmouth Atlas Project showing that readmission rates failed to improve between 2004 and 2009.

"We still have a very persistent problem," Dr. Risa Lavizzo-Mourey, president and CEO of the Robert Wood Johnson Foundation, said during a panel discussion on the report on Feb. 13 in Washington.

The national rate for 30-day readmissions for medical conditions was 16.2% in 2008 and 15.9% in 2010. Similarly, the 30-day surgical readmission rates were 12.7% in 2008 and 12.4% in 2010. The same trends hold true when looking at readmission rates for heart failure, acute myocardial infarction, and pneumonia, the conditions that held accountable for as part of a new Medicare readmissions penalty that went into effect in October 2012.

Readmission rates for heart failure were dipped slightly from 21.4% in 2008 to 21.1% in 2010. Acute myocardial infarction readmissions went from 18.7% to 18.1% during the same time period. And pneumonia readmission rates stayed at 15.3% in both 2008 and 2010.

The researchers called the progress on readmissions "slow and inconsistent." But while there has been little change nationally among the Medicare population, there is widespread regional variation, according to the analysis.

For instance, 30-day readmission rates following medical discharge ranged from a low of 11.4% in Ogden, Utah, to a high of 18.1% in the Bronx, N.Y., in 2010. There was even greater variation in readmissions following surgery. Surgical readmission rates ranged from 7.6% in Bend, Oregon, to 18.3% in the New York.

"People who have the same illness often have very different chances of being readmitted depending on where they live," Dr. Lavizzo-Mourey said.

Many patients are readmitted simply because their local hospital is the community’s main source of care, the researchers wrote. This trend results in both higher initial hospital admissions and readmissions, they wrote.

But while the report highlights the lack of progress, there are some success stories, Dr. Lavizzo-Mourey said. For instance, some hospitals are establishing 24-hour pharmacies so that patients can get their prescriptions no matter what time they are discharged. Others are setting up clinics to specialize in the care of patients with heart failure, a condition with a high rate of bounce-back to the hospital. And other hospitals are working with community organizations to ensure patients have the care and support they need when they go home, she said.

"This issue of readmissions is firmly on the radar screen of our health care providers," Dr. Lavizzo-Mourey said.

Dr. Eric Coleman, who runs the Care Transitions Program aimed at improving the safety of hand-offs, said one of the issues that leads to readmissions is the poor engagement of patients and family members before discharge.

At the University of Colorado, Denver, where he heads the division of health care policy and research, Dr. Coleman said they try to avoid simply dumping information on patients and families and instead use a process called "skill transfer" to train them to be able to handle their own care at home without the help of health care providers.

But many of the causes of readmissions are beyond the control of the hospital, Dr. Coleman said. He encourages physicians to go the bedside and ask patients why they think they were readmitted to the hospital. The answers are often about a lack of transportation to appointments, struggles to afford medicine and care, or family caregivers who are burning out.

"It may be that hospitals don’t have the resources to address this but a lot of their community partners, such as the area agencies on aging do have that opportunity," Dr. Coleman said.

[email protected]

HONOLULU – Just 1% of patients experienced a non-ST-elevation myocardial infarction following carotid-artery stenting or endarterectomy in a retrospective, nationally representative analysis of more than 1 million patients.

When it did occur, however, NSTEMI significantly increased periprocedural neurologic and cardiac complications, inpatient mortality, disability, and resource utilization – adding on average a full 10 days to hospital length of stay and nearly $85,000 in hospital charges, Dr. Amir Khan said during a plenary session at the International Stroke Conference. Dr. Khan is scheduled to present the study results at the annual meeting of the American Academy of Neurology in San Diego on March 20.

Patrice Wendling/IMNG Medical Media

He observed that postoperative evaluation for MI varied in the data set, as it does nationally, but that post hoc analyses from the POISE (Perioperative Ischemic Evaluation) trial revealed that 65% of patients with an MI after noncardiac surgery did not have ischemic symptoms (Ann. Intern. Med. 2011;154:523-8).

"So, we know that hospitals that don’t have active surveillance regimens for non-STEMI will miss a fair amount of this," said Dr. Khan, an endovascular surgical neuroradiology fellow at the University of Minnesota in Minneapolis.

The majority of perioperative MI is NSTEMI. While few studies have parsed out MI types, the SAPPHIRE (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy) trial showed that 80% of carotid endarterectomy (CEA) patients with periprocedural MI and all carotid angioplasty or stenting (CAS) patients with periprocedural MI were NSTEMI (N. Engl. J. Med. 2004;351:1493-1501).

In an effort to assess the frequency of periprocedural NSTEMI following CEA or CAS in practice and its relationship with outcomes, the researchers used data from the Nationwide Inpatient Sample for all adult patients who underwent CEA or CAS from 2002 to 2009. From this, hospital-weighted national estimates were generated using Healthcare Utilization Project algorithms.

Overall, 11,341 patients (1%) experienced an NSTEMI and 1,072,347 did not; 92% of all patients underwent endarterectomy.

Age, gender, and racial distribution were roughly similar between groups, although patients with NSTEMI had significantly higher baseline rates of atrial fibrillation (24% vs. 8%), heart failure (24% vs. 6.5%) and chronic renal insufficiency (16% vs. 5%), Dr. Khan noted.

In terms of health care usage, rates were slightly higher among NSTEMI patients for inpatient diagnostic cerebral angiography (19% vs. 13.5%), gastrostomy (3% vs. 0.4%), and postprocedure mechanical ventilation (0.5% vs. 0.3%; all P less than .0001).

Blood transfusions were conspicuously higher in those with NSTEMI at 20% vs. 3% in those without, he said. The average length of stay also jumped with NSTEMI from 2.8 days to 12.2 days, pushing hospital charges from an average of $29,160 to $113,317 (all P less than .0001).

Neurologic complications were seen in 6% of patients with NSTEMI vs. 1.4% without, while cardiac complications occurred in 31% vs. 1.5%. In addition, 31% of NSTEMI patients were moderately or severely disabled at discharge vs. just 6% without NSTEMI (all P less than .0001), Dr. Khan reported at the conference, sponsored by the American Heart Association.

In-hospital mortality was 6% in the NSTEMI group and 0.5% in the group without. The composite endpoint of cardiac or neurologic complication and/or death was reached by 38% vs. 3% (both P less than .0001).

When these numbers were plugged into a multivariate analysis that adjusted for age, gender, and comorbidities, the odds ratios for patients with NSTEMI were 3.6 for neurologic complications, 23.2 for cardiac complications, 8.6 for in-hospital mortality, 14.6 for the composite end point, and 5.5 for moderate to severe disability (all P less than .0001), he said.

During a discussion following the presentation, an audience member expressed concern about the complication rates, rising to say, "Often we make decisions about stroke treatment based only on what’s good for the brain. Well there’s no point in making the brain better if the person can have a heart attack and die of some other complications, and I really think this [study] emphasizes that."

Dr. Khan replied, "I totally agree and I think that is one of the take-home messages here ... "

Dr. Khan and his coauthors reported no disclosures.

[email protected]

HONOLULU – Just 1% of patients experienced a non-ST-elevation myocardial infarction following carotid-artery stenting or endarterectomy in a retrospective, nationally representative analysis of more than 1 million patients.

When it did occur, however, NSTEMI significantly increased periprocedural neurologic and cardiac complications, inpatient mortality, disability, and resource utilization – adding on average a full 10 days to hospital length of stay and nearly $85,000 in hospital charges, Dr. Amir Khan said during a plenary session at the International Stroke Conference. Dr. Khan is scheduled to present the study results at the annual meeting of the American Academy of Neurology in San Diego on March 20.

Patrice Wendling/IMNG Medical Media

He observed that postoperative evaluation for MI varied in the data set, as it does nationally, but that post hoc analyses from the POISE (Perioperative Ischemic Evaluation) trial revealed that 65% of patients with an MI after noncardiac surgery did not have ischemic symptoms (Ann. Intern. Med. 2011;154:523-8).

"So, we know that hospitals that don’t have active surveillance regimens for non-STEMI will miss a fair amount of this," said Dr. Khan, an endovascular surgical neuroradiology fellow at the University of Minnesota in Minneapolis.

The majority of perioperative MI is NSTEMI. While few studies have parsed out MI types, the SAPPHIRE (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy) trial showed that 80% of carotid endarterectomy (CEA) patients with periprocedural MI and all carotid angioplasty or stenting (CAS) patients with periprocedural MI were NSTEMI (N. Engl. J. Med. 2004;351:1493-1501).

In an effort to assess the frequency of periprocedural NSTEMI following CEA or CAS in practice and its relationship with outcomes, the researchers used data from the Nationwide Inpatient Sample for all adult patients who underwent CEA or CAS from 2002 to 2009. From this, hospital-weighted national estimates were generated using Healthcare Utilization Project algorithms.

Overall, 11,341 patients (1%) experienced an NSTEMI and 1,072,347 did not; 92% of all patients underwent endarterectomy.

Age, gender, and racial distribution were roughly similar between groups, although patients with NSTEMI had significantly higher baseline rates of atrial fibrillation (24% vs. 8%), heart failure (24% vs. 6.5%) and chronic renal insufficiency (16% vs. 5%), Dr. Khan noted.

In terms of health care usage, rates were slightly higher among NSTEMI patients for inpatient diagnostic cerebral angiography (19% vs. 13.5%), gastrostomy (3% vs. 0.4%), and postprocedure mechanical ventilation (0.5% vs. 0.3%; all P less than .0001).

Blood transfusions were conspicuously higher in those with NSTEMI at 20% vs. 3% in those without, he said. The average length of stay also jumped with NSTEMI from 2.8 days to 12.2 days, pushing hospital charges from an average of $29,160 to $113,317 (all P less than .0001).

Neurologic complications were seen in 6% of patients with NSTEMI vs. 1.4% without, while cardiac complications occurred in 31% vs. 1.5%. In addition, 31% of NSTEMI patients were moderately or severely disabled at discharge vs. just 6% without NSTEMI (all P less than .0001), Dr. Khan reported at the conference, sponsored by the American Heart Association.

In-hospital mortality was 6% in the NSTEMI group and 0.5% in the group without. The composite endpoint of cardiac or neurologic complication and/or death was reached by 38% vs. 3% (both P less than .0001).

When these numbers were plugged into a multivariate analysis that adjusted for age, gender, and comorbidities, the odds ratios for patients with NSTEMI were 3.6 for neurologic complications, 23.2 for cardiac complications, 8.6 for in-hospital mortality, 14.6 for the composite end point, and 5.5 for moderate to severe disability (all P less than .0001), he said.

During a discussion following the presentation, an audience member expressed concern about the complication rates, rising to say, "Often we make decisions about stroke treatment based only on what’s good for the brain. Well there’s no point in making the brain better if the person can have a heart attack and die of some other complications, and I really think this [study] emphasizes that."

Dr. Khan replied, "I totally agree and I think that is one of the take-home messages here ... "

Dr. Khan and his coauthors reported no disclosures.

[email protected]

HONOLULU – Just 1% of patients experienced a non-ST-elevation myocardial infarction following carotid-artery stenting or endarterectomy in a retrospective, nationally representative analysis of more than 1 million patients.

When it did occur, however, NSTEMI significantly increased periprocedural neurologic and cardiac complications, inpatient mortality, disability, and resource utilization – adding on average a full 10 days to hospital length of stay and nearly $85,000 in hospital charges, Dr. Amir Khan said during a plenary session at the International Stroke Conference. Dr. Khan is scheduled to present the study results at the annual meeting of the American Academy of Neurology in San Diego on March 20.

Patrice Wendling/IMNG Medical Media

He observed that postoperative evaluation for MI varied in the data set, as it does nationally, but that post hoc analyses from the POISE (Perioperative Ischemic Evaluation) trial revealed that 65% of patients with an MI after noncardiac surgery did not have ischemic symptoms (Ann. Intern. Med. 2011;154:523-8).

"So, we know that hospitals that don’t have active surveillance regimens for non-STEMI will miss a fair amount of this," said Dr. Khan, an endovascular surgical neuroradiology fellow at the University of Minnesota in Minneapolis.

The majority of perioperative MI is NSTEMI. While few studies have parsed out MI types, the SAPPHIRE (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy) trial showed that 80% of carotid endarterectomy (CEA) patients with periprocedural MI and all carotid angioplasty or stenting (CAS) patients with periprocedural MI were NSTEMI (N. Engl. J. Med. 2004;351:1493-1501).

In an effort to assess the frequency of periprocedural NSTEMI following CEA or CAS in practice and its relationship with outcomes, the researchers used data from the Nationwide Inpatient Sample for all adult patients who underwent CEA or CAS from 2002 to 2009. From this, hospital-weighted national estimates were generated using Healthcare Utilization Project algorithms.

Overall, 11,341 patients (1%) experienced an NSTEMI and 1,072,347 did not; 92% of all patients underwent endarterectomy.

Age, gender, and racial distribution were roughly similar between groups, although patients with NSTEMI had significantly higher baseline rates of atrial fibrillation (24% vs. 8%), heart failure (24% vs. 6.5%) and chronic renal insufficiency (16% vs. 5%), Dr. Khan noted.

In terms of health care usage, rates were slightly higher among NSTEMI patients for inpatient diagnostic cerebral angiography (19% vs. 13.5%), gastrostomy (3% vs. 0.4%), and postprocedure mechanical ventilation (0.5% vs. 0.3%; all P less than .0001).

Blood transfusions were conspicuously higher in those with NSTEMI at 20% vs. 3% in those without, he said. The average length of stay also jumped with NSTEMI from 2.8 days to 12.2 days, pushing hospital charges from an average of $29,160 to $113,317 (all P less than .0001).

Neurologic complications were seen in 6% of patients with NSTEMI vs. 1.4% without, while cardiac complications occurred in 31% vs. 1.5%. In addition, 31% of NSTEMI patients were moderately or severely disabled at discharge vs. just 6% without NSTEMI (all P less than .0001), Dr. Khan reported at the conference, sponsored by the American Heart Association.

In-hospital mortality was 6% in the NSTEMI group and 0.5% in the group without. The composite endpoint of cardiac or neurologic complication and/or death was reached by 38% vs. 3% (both P less than .0001).

When these numbers were plugged into a multivariate analysis that adjusted for age, gender, and comorbidities, the odds ratios for patients with NSTEMI were 3.6 for neurologic complications, 23.2 for cardiac complications, 8.6 for in-hospital mortality, 14.6 for the composite end point, and 5.5 for moderate to severe disability (all P less than .0001), he said.

During a discussion following the presentation, an audience member expressed concern about the complication rates, rising to say, "Often we make decisions about stroke treatment based only on what’s good for the brain. Well there’s no point in making the brain better if the person can have a heart attack and die of some other complications, and I really think this [study] emphasizes that."

Dr. Khan replied, "I totally agree and I think that is one of the take-home messages here ... "

Dr. Khan and his coauthors reported no disclosures.

[email protected]

Yes – Expensive drugs may offset other costs.

As in every aspect of medicine, there is a cost-benefit balance, with the cost of care being weighed against the benefits of a favorable outcome. The debate seems to be complex, but it can really be boiled down to a single question: Is the therapy worth using when compared with alternatives or to current practice?

It is incumbent upon us as clinicians to evaluate the appropriate use of both expensive and inexpensive drugs.

Drug costs in the ICU always involve more than meets the eye. If we take the traditional silo-based perspective and focus only on the acquisition cost of a drug, we’re ignoring the reality that the less expensive drug is not always the best drug for a condition and that health system costs are affected by the total cost of care. If a less expensive drug requires more patient monitoring, it offsets at least some of the cost advantage by adding higher laboratory or imaging costs.

Another consideration for the hospital is the reimbursement climate. Hospitals that receive low scores on pain management under the HCAHPS (Hospital Consumer Assessment of Healthcare Providers and Systems) survey may experience significant reductions in reimbursement. So if, say, an expensive nonopioid analgesic used as part of a multimodal therapy could significantly improve pain control and reduce opioid-related adverse events, the extra cost could be justified.

Acquisition costs are only part of a drug’s total cost, which also includes the costs of preparation, storage, administration (such as infusion devices), lab monitoring, treating adverse drug events, and, of course, failed therapy.

Costly drugs also may pay for themselves by offsetting other costs. A new, costly drug that reduces the patient’s length of ICU stay by 1 day would save $4,000 to $5,000, and a drug that reduces time spent on a mechanical ventilator could reduce costs by about $1,900 for each ventilator-free day. Ventilator-associated pneumonias cost approximately $50,000 more per case ($70,580 vs. $21,620), but prevention strategies, including the use of medications, could reduce these costs.

Our group recently did a study of ICU costs associated with acute kidney injury following coronary artery bypass grafts and found that costs were twice as high in patients with kidney injury ($25,950 vs. $13,830). If patients have even a 1.5-fold increase over baseline in serum creatinine, the associated cost is $21,775, compared with $13,830 in patients whose serum creatinine is controlled. We calculated that an effective drug, if it cost less than $12,000, would offset these costs (Textbook of Critical Care, 6th edition, 2011, pp. 1387-92).

A 2012 analysis of the cost offset of tolvaptan in patients with inappropriate antidiuretic hormone secretion indicated that the cost of treating hyponatremia was $1,694 and that tolvaptan, at a cost of $250 per day for 4 days, reduced the length of stay by an estimated 1.1 days, thereby providing a savings of $694 per patient (Hosp. Pract. 2012;40:7-14).

Similarly, recombinant factor VIIa costs $7,000 to $10,000 per dose, but when used for its approved indication – bleeding episodes in hemophilia A or B patients with inhibitors to factors VIII/IX and for prevention of bleeding during surgical intervention in these patients – costs per resolved bleeding episode were $3,000 to $17,000 lower than for patients given activated prothrombin complex concentrate (Haemophilia 2009;15:405-19).

Clinicians are excited when we have new options for therapy, but we have to figure out where a new, expensive therapy fits. Does it make sense to use it? What is the efficacy of the drug relative to its costs? The key to the appropriate use of drugs, both costly and cheap, is to develop a disease state–based protocol tailored to your institution’s specific usage patterns, case mix, economic climate, and politics.

Dr. Sandra Kane-Gill is associate professor of pharmacy and therapeutics at the University of Pittsburgh School of Pharmacy. She also serves as associate professor for the Center for Pharmacoinformatics and Outcomes Research at the School of Pharmacy.

No – With cost evaluations, the devil is in the details.

Drug-cost evaluations look great on paper, but they often don’t work in the real world. An expensive drug may let you take a patient off a ventilator earlier, but if you can’t send the patient to the floor because there is no available bed and you can’t let that patient’s nurse go home, there may not be a true savings in cost.

As Dr. Kane-Gill points out, the problem is complex and there are many analytic approaches. We can consider whether we have therapeutically equivalent options, balance the cost-effectiveness and cost-benefit ratios of treatments with different outcomes, or consider patient preference measured in cost-utility tradeoff and expressed as quality-adjusted life years (QALYs).

The problem with cost modeling is that it is sensitive to input – garbage in means garbage out. Models are hampered by the limitations of what can be accomplished in clinical trials and by the assumptions made to create the model. Is it based on acquisition costs or on charges? How do practice variations within the institution (between the medical ICU and the surgical ICU, for example), or from one institution to the next, affect the assumptions in the model?

Cost comparisons must somehow reconcile data from conflicting studies and multiple treatment options, and they must be able to quantify the effects over time of a given intervention.

Clinical trials that are used to justify cost evaluations are performed in controlled settings. I wish that I could say that all my patients were uniform, but they are not. There is a substantial difference between a 24-year-old with a head injury and a 90-year-old with a head injury, or between a patient with a broken hip and one with end-stage liver disease. How do you begin to compare the effects of drugs across these populations? How do you judge the effect of a specific drug in an era of polypharmacy, when some patients seen in our unit have been on as many as 27 drugs at the same time?

Time can also fade the bloom of a once-promising drug, such as drotrecogin alfa (Xigris). An analysis of the PROWESS study (Crit. Care Med. 2003;31:12-9) appeared to show that drotrecogin alfa was helpful in patients with severe sepsis, and this drug’s alleged efficacy was balanced against its cost, which was estimated at $48,000 per QALY and considered to be in the acceptable range. As we all know, longer experience with this agent found no overall benefit and an association with higher bleeding risk (Cochrane Database Syst. Rev. 2012 Dec 12;12:CD004388). The drug was pulled from the market in late 2011.

Dr. Kane-Gill correctly notes that factor VIIa, when used for its rare indication, offers a benefit and saves money. But many ICUs were using this agent outside of its labeled indication (Ann. Intern. Med. 2011;154:516-22) and found that it caused emboli in patients already at risk for thromboembolic events (J. Trauma. 2010;69:489-500; N. Engl. J. Med. 2008;358:2127-37).

If a drug is in the formulary, and if it is new and more expensive than other therapeutic options, it is human nature to think that new and expensive must mean better than old and cheap. In Europe, ICUs routinely use injectable acetaminophen for nonopioid pain relief. In the United States, the intravenous formulations of this drug are costly – about $10 per dose, compared with about 50 cents for one dose of percocet. Yet the reduction in opioid use with the injectable agent is modest, there is no evidence to suggest reductions in opioid-related adverse events, and there are conflicting data on patient satisfaction (Cochrane Database Syst. Rev. 2011 Oct 5;(10):CD007126).

Economic evaluations of drugs should be viewed with caution because they require knowledge of the literature basis for the model, may exhibit considerable variation in estimates of indirect costs, and are subject to the vagaries of conflicting data as well as changes in data and practice over time. Additionally, estimates of drug cost and benefits can vary by country, region, or facility.

It’s clear that we need much more data about outcomes and the true costs of the care we give.

Dr. Christine C. Toevs is a trauma surgeon and director of the trauma ICU at Allegheny General Hospital in Pittsburgh. She also has a Masters degree in bioethics.

Yes – Expensive drugs may offset other costs.

As in every aspect of medicine, there is a cost-benefit balance, with the cost of care being weighed against the benefits of a favorable outcome. The debate seems to be complex, but it can really be boiled down to a single question: Is the therapy worth using when compared with alternatives or to current practice?

It is incumbent upon us as clinicians to evaluate the appropriate use of both expensive and inexpensive drugs.

Drug costs in the ICU always involve more than meets the eye. If we take the traditional silo-based perspective and focus only on the acquisition cost of a drug, we’re ignoring the reality that the less expensive drug is not always the best drug for a condition and that health system costs are affected by the total cost of care. If a less expensive drug requires more patient monitoring, it offsets at least some of the cost advantage by adding higher laboratory or imaging costs.

Another consideration for the hospital is the reimbursement climate. Hospitals that receive low scores on pain management under the HCAHPS (Hospital Consumer Assessment of Healthcare Providers and Systems) survey may experience significant reductions in reimbursement. So if, say, an expensive nonopioid analgesic used as part of a multimodal therapy could significantly improve pain control and reduce opioid-related adverse events, the extra cost could be justified.

Acquisition costs are only part of a drug’s total cost, which also includes the costs of preparation, storage, administration (such as infusion devices), lab monitoring, treating adverse drug events, and, of course, failed therapy.

Costly drugs also may pay for themselves by offsetting other costs. A new, costly drug that reduces the patient’s length of ICU stay by 1 day would save $4,000 to $5,000, and a drug that reduces time spent on a mechanical ventilator could reduce costs by about $1,900 for each ventilator-free day. Ventilator-associated pneumonias cost approximately $50,000 more per case ($70,580 vs. $21,620), but prevention strategies, including the use of medications, could reduce these costs.

Our group recently did a study of ICU costs associated with acute kidney injury following coronary artery bypass grafts and found that costs were twice as high in patients with kidney injury ($25,950 vs. $13,830). If patients have even a 1.5-fold increase over baseline in serum creatinine, the associated cost is $21,775, compared with $13,830 in patients whose serum creatinine is controlled. We calculated that an effective drug, if it cost less than $12,000, would offset these costs (Textbook of Critical Care, 6th edition, 2011, pp. 1387-92).

A 2012 analysis of the cost offset of tolvaptan in patients with inappropriate antidiuretic hormone secretion indicated that the cost of treating hyponatremia was $1,694 and that tolvaptan, at a cost of $250 per day for 4 days, reduced the length of stay by an estimated 1.1 days, thereby providing a savings of $694 per patient (Hosp. Pract. 2012;40:7-14).

Similarly, recombinant factor VIIa costs $7,000 to $10,000 per dose, but when used for its approved indication – bleeding episodes in hemophilia A or B patients with inhibitors to factors VIII/IX and for prevention of bleeding during surgical intervention in these patients – costs per resolved bleeding episode were $3,000 to $17,000 lower than for patients given activated prothrombin complex concentrate (Haemophilia 2009;15:405-19).

Clinicians are excited when we have new options for therapy, but we have to figure out where a new, expensive therapy fits. Does it make sense to use it? What is the efficacy of the drug relative to its costs? The key to the appropriate use of drugs, both costly and cheap, is to develop a disease state–based protocol tailored to your institution’s specific usage patterns, case mix, economic climate, and politics.

Dr. Sandra Kane-Gill is associate professor of pharmacy and therapeutics at the University of Pittsburgh School of Pharmacy. She also serves as associate professor for the Center for Pharmacoinformatics and Outcomes Research at the School of Pharmacy.

No – With cost evaluations, the devil is in the details.

Drug-cost evaluations look great on paper, but they often don’t work in the real world. An expensive drug may let you take a patient off a ventilator earlier, but if you can’t send the patient to the floor because there is no available bed and you can’t let that patient’s nurse go home, there may not be a true savings in cost.

As Dr. Kane-Gill points out, the problem is complex and there are many analytic approaches. We can consider whether we have therapeutically equivalent options, balance the cost-effectiveness and cost-benefit ratios of treatments with different outcomes, or consider patient preference measured in cost-utility tradeoff and expressed as quality-adjusted life years (QALYs).

The problem with cost modeling is that it is sensitive to input – garbage in means garbage out. Models are hampered by the limitations of what can be accomplished in clinical trials and by the assumptions made to create the model. Is it based on acquisition costs or on charges? How do practice variations within the institution (between the medical ICU and the surgical ICU, for example), or from one institution to the next, affect the assumptions in the model?

Cost comparisons must somehow reconcile data from conflicting studies and multiple treatment options, and they must be able to quantify the effects over time of a given intervention.

Clinical trials that are used to justify cost evaluations are performed in controlled settings. I wish that I could say that all my patients were uniform, but they are not. There is a substantial difference between a 24-year-old with a head injury and a 90-year-old with a head injury, or between a patient with a broken hip and one with end-stage liver disease. How do you begin to compare the effects of drugs across these populations? How do you judge the effect of a specific drug in an era of polypharmacy, when some patients seen in our unit have been on as many as 27 drugs at the same time?

Time can also fade the bloom of a once-promising drug, such as drotrecogin alfa (Xigris). An analysis of the PROWESS study (Crit. Care Med. 2003;31:12-9) appeared to show that drotrecogin alfa was helpful in patients with severe sepsis, and this drug’s alleged efficacy was balanced against its cost, which was estimated at $48,000 per QALY and considered to be in the acceptable range. As we all know, longer experience with this agent found no overall benefit and an association with higher bleeding risk (Cochrane Database Syst. Rev. 2012 Dec 12;12:CD004388). The drug was pulled from the market in late 2011.

Dr. Kane-Gill correctly notes that factor VIIa, when used for its rare indication, offers a benefit and saves money. But many ICUs were using this agent outside of its labeled indication (Ann. Intern. Med. 2011;154:516-22) and found that it caused emboli in patients already at risk for thromboembolic events (J. Trauma. 2010;69:489-500; N. Engl. J. Med. 2008;358:2127-37).

If a drug is in the formulary, and if it is new and more expensive than other therapeutic options, it is human nature to think that new and expensive must mean better than old and cheap. In Europe, ICUs routinely use injectable acetaminophen for nonopioid pain relief. In the United States, the intravenous formulations of this drug are costly – about $10 per dose, compared with about 50 cents for one dose of percocet. Yet the reduction in opioid use with the injectable agent is modest, there is no evidence to suggest reductions in opioid-related adverse events, and there are conflicting data on patient satisfaction (Cochrane Database Syst. Rev. 2011 Oct 5;(10):CD007126).

Economic evaluations of drugs should be viewed with caution because they require knowledge of the literature basis for the model, may exhibit considerable variation in estimates of indirect costs, and are subject to the vagaries of conflicting data as well as changes in data and practice over time. Additionally, estimates of drug cost and benefits can vary by country, region, or facility.

It’s clear that we need much more data about outcomes and the true costs of the care we give.

Dr. Christine C. Toevs is a trauma surgeon and director of the trauma ICU at Allegheny General Hospital in Pittsburgh. She also has a Masters degree in bioethics.

Yes – Expensive drugs may offset other costs.

As in every aspect of medicine, there is a cost-benefit balance, with the cost of care being weighed against the benefits of a favorable outcome. The debate seems to be complex, but it can really be boiled down to a single question: Is the therapy worth using when compared with alternatives or to current practice?

It is incumbent upon us as clinicians to evaluate the appropriate use of both expensive and inexpensive drugs.

Drug costs in the ICU always involve more than meets the eye. If we take the traditional silo-based perspective and focus only on the acquisition cost of a drug, we’re ignoring the reality that the less expensive drug is not always the best drug for a condition and that health system costs are affected by the total cost of care. If a less expensive drug requires more patient monitoring, it offsets at least some of the cost advantage by adding higher laboratory or imaging costs.

Another consideration for the hospital is the reimbursement climate. Hospitals that receive low scores on pain management under the HCAHPS (Hospital Consumer Assessment of Healthcare Providers and Systems) survey may experience significant reductions in reimbursement. So if, say, an expensive nonopioid analgesic used as part of a multimodal therapy could significantly improve pain control and reduce opioid-related adverse events, the extra cost could be justified.

Acquisition costs are only part of a drug’s total cost, which also includes the costs of preparation, storage, administration (such as infusion devices), lab monitoring, treating adverse drug events, and, of course, failed therapy.

Costly drugs also may pay for themselves by offsetting other costs. A new, costly drug that reduces the patient’s length of ICU stay by 1 day would save $4,000 to $5,000, and a drug that reduces time spent on a mechanical ventilator could reduce costs by about $1,900 for each ventilator-free day. Ventilator-associated pneumonias cost approximately $50,000 more per case ($70,580 vs. $21,620), but prevention strategies, including the use of medications, could reduce these costs.

Our group recently did a study of ICU costs associated with acute kidney injury following coronary artery bypass grafts and found that costs were twice as high in patients with kidney injury ($25,950 vs. $13,830). If patients have even a 1.5-fold increase over baseline in serum creatinine, the associated cost is $21,775, compared with $13,830 in patients whose serum creatinine is controlled. We calculated that an effective drug, if it cost less than $12,000, would offset these costs (Textbook of Critical Care, 6th edition, 2011, pp. 1387-92).

A 2012 analysis of the cost offset of tolvaptan in patients with inappropriate antidiuretic hormone secretion indicated that the cost of treating hyponatremia was $1,694 and that tolvaptan, at a cost of $250 per day for 4 days, reduced the length of stay by an estimated 1.1 days, thereby providing a savings of $694 per patient (Hosp. Pract. 2012;40:7-14).

Similarly, recombinant factor VIIa costs $7,000 to $10,000 per dose, but when used for its approved indication – bleeding episodes in hemophilia A or B patients with inhibitors to factors VIII/IX and for prevention of bleeding during surgical intervention in these patients – costs per resolved bleeding episode were $3,000 to $17,000 lower than for patients given activated prothrombin complex concentrate (Haemophilia 2009;15:405-19).

Clinicians are excited when we have new options for therapy, but we have to figure out where a new, expensive therapy fits. Does it make sense to use it? What is the efficacy of the drug relative to its costs? The key to the appropriate use of drugs, both costly and cheap, is to develop a disease state–based protocol tailored to your institution’s specific usage patterns, case mix, economic climate, and politics.

Dr. Sandra Kane-Gill is associate professor of pharmacy and therapeutics at the University of Pittsburgh School of Pharmacy. She also serves as associate professor for the Center for Pharmacoinformatics and Outcomes Research at the School of Pharmacy.

No – With cost evaluations, the devil is in the details.

Drug-cost evaluations look great on paper, but they often don’t work in the real world. An expensive drug may let you take a patient off a ventilator earlier, but if you can’t send the patient to the floor because there is no available bed and you can’t let that patient’s nurse go home, there may not be a true savings in cost.

As Dr. Kane-Gill points out, the problem is complex and there are many analytic approaches. We can consider whether we have therapeutically equivalent options, balance the cost-effectiveness and cost-benefit ratios of treatments with different outcomes, or consider patient preference measured in cost-utility tradeoff and expressed as quality-adjusted life years (QALYs).

The problem with cost modeling is that it is sensitive to input – garbage in means garbage out. Models are hampered by the limitations of what can be accomplished in clinical trials and by the assumptions made to create the model. Is it based on acquisition costs or on charges? How do practice variations within the institution (between the medical ICU and the surgical ICU, for example), or from one institution to the next, affect the assumptions in the model?

Cost comparisons must somehow reconcile data from conflicting studies and multiple treatment options, and they must be able to quantify the effects over time of a given intervention.

Clinical trials that are used to justify cost evaluations are performed in controlled settings. I wish that I could say that all my patients were uniform, but they are not. There is a substantial difference between a 24-year-old with a head injury and a 90-year-old with a head injury, or between a patient with a broken hip and one with end-stage liver disease. How do you begin to compare the effects of drugs across these populations? How do you judge the effect of a specific drug in an era of polypharmacy, when some patients seen in our unit have been on as many as 27 drugs at the same time?

Time can also fade the bloom of a once-promising drug, such as drotrecogin alfa (Xigris). An analysis of the PROWESS study (Crit. Care Med. 2003;31:12-9) appeared to show that drotrecogin alfa was helpful in patients with severe sepsis, and this drug’s alleged efficacy was balanced against its cost, which was estimated at $48,000 per QALY and considered to be in the acceptable range. As we all know, longer experience with this agent found no overall benefit and an association with higher bleeding risk (Cochrane Database Syst. Rev. 2012 Dec 12;12:CD004388). The drug was pulled from the market in late 2011.

Dr. Kane-Gill correctly notes that factor VIIa, when used for its rare indication, offers a benefit and saves money. But many ICUs were using this agent outside of its labeled indication (Ann. Intern. Med. 2011;154:516-22) and found that it caused emboli in patients already at risk for thromboembolic events (J. Trauma. 2010;69:489-500; N. Engl. J. Med. 2008;358:2127-37).

If a drug is in the formulary, and if it is new and more expensive than other therapeutic options, it is human nature to think that new and expensive must mean better than old and cheap. In Europe, ICUs routinely use injectable acetaminophen for nonopioid pain relief. In the United States, the intravenous formulations of this drug are costly – about $10 per dose, compared with about 50 cents for one dose of percocet. Yet the reduction in opioid use with the injectable agent is modest, there is no evidence to suggest reductions in opioid-related adverse events, and there are conflicting data on patient satisfaction (Cochrane Database Syst. Rev. 2011 Oct 5;(10):CD007126).

Economic evaluations of drugs should be viewed with caution because they require knowledge of the literature basis for the model, may exhibit considerable variation in estimates of indirect costs, and are subject to the vagaries of conflicting data as well as changes in data and practice over time. Additionally, estimates of drug cost and benefits can vary by country, region, or facility.

It’s clear that we need much more data about outcomes and the true costs of the care we give.

Dr. Christine C. Toevs is a trauma surgeon and director of the trauma ICU at Allegheny General Hospital in Pittsburgh. She also has a Masters degree in bioethics.

Nearly 2 years after their presentation at a national meeting, the results of MAGELLAN, comparing rivaroxaban to enoxaparin for thromboprophylaxis in critically ill hospitalized patients, have been published online Feb. 6 in the New England Journal of Medicine.

In that large, multicenter trial, rivaroxaban was noninferior to enoxaparin when used for the standard 10-day duration, and superior when used for an extended 35-day duration, for thromboprophylaxis.

However, the rate of clinically relevant bleeding and the incidence of major bleeding events were significantly higher with rivaroxaban than with enoxaparin. This adverse effect apparently balanced out the reduction in venous thromboembolism, as a prespecified analysis of net clinical benefit and harm did not show either one at day 10 or day 35, reported Dr. Alexander T. Cohen and his associates in MAGELLAN (Multicenter, Randomized, Parallel Group Efficacy and Safety Study for the Prevention of Venous Thromboembolism in Hospitalized Acutely Ill Medical Patients Comparing Rivaroxaban with Enoxaparin). The results were first presented by Dr. Cohen, of King's College Hospital, London, at the annual meeting of the American College of Cardiology in spring 2011.

In the 2.5-year study, 8,101 patients at 556 sites in 52 countries were randomized to receive rivaroxaban (4,050 subjects) or enoxaparin (4,051 subjects). Hundreds of patients in both study groups were excluded from the final analyses for various reasons, usually because they could not be assessed for venous thromboembolism using ultrasonography and other imaging techniques in a timely fashion, as required by the study protocol.

At 10 days' follow-up, 2.7% of patients in both groups had a primary outcome event - asymptomatic proximal deep vein thrombosis (DVT), symptomatic nonfatal pulmonary embolism (PE), or thromboembolism-related death - so rivaroxaban met the criteria for noninferiority to enoxaparin.

At the 35-day follow-up, 4.4% of subjects who received extended-duration rivaroxaban and 5.7% of those who received enoxaparin plus placebo had a primary outcome event, so rivaroxaban met the criteria for superiority to enoxaparin, the investigators reported (N. Engl. J. Med. 2013 Feb. 6 [doi: 10.1056/NEJMoa1111096]).

Rivaroxaban (Xarelto)has several indications: for stroke prevention in nonvalvular atrial fibrillation, for the treatment of DVT and PE, for reducing the risk of recurrence of DVT and PE, and for the prophylaxis of DVT in patients undergoing knee or hip replacement surgery. It is not indicated for the condition studied in MAGELLAN, namely prevention of VTE in acutely medically ill patients.

This study was funded by Bayer HealthCare and Janssen, sponsors that also collected and analyzed the study data. Dr. Cohen and his associates reported numerous ties to industry sources.

[email protected]

Nearly 2 years after their presentation at a national meeting, the results of MAGELLAN, comparing rivaroxaban to enoxaparin for thromboprophylaxis in critically ill hospitalized patients, have been published online Feb. 6 in the New England Journal of Medicine.

In that large, multicenter trial, rivaroxaban was noninferior to enoxaparin when used for the standard 10-day duration, and superior when used for an extended 35-day duration, for thromboprophylaxis.

However, the rate of clinically relevant bleeding and the incidence of major bleeding events were significantly higher with rivaroxaban than with enoxaparin. This adverse effect apparently balanced out the reduction in venous thromboembolism, as a prespecified analysis of net clinical benefit and harm did not show either one at day 10 or day 35, reported Dr. Alexander T. Cohen and his associates in MAGELLAN (Multicenter, Randomized, Parallel Group Efficacy and Safety Study for the Prevention of Venous Thromboembolism in Hospitalized Acutely Ill Medical Patients Comparing Rivaroxaban with Enoxaparin). The results were first presented by Dr. Cohen, of King's College Hospital, London, at the annual meeting of the American College of Cardiology in spring 2011.

In the 2.5-year study, 8,101 patients at 556 sites in 52 countries were randomized to receive rivaroxaban (4,050 subjects) or enoxaparin (4,051 subjects). Hundreds of patients in both study groups were excluded from the final analyses for various reasons, usually because they could not be assessed for venous thromboembolism using ultrasonography and other imaging techniques in a timely fashion, as required by the study protocol.

At 10 days' follow-up, 2.7% of patients in both groups had a primary outcome event - asymptomatic proximal deep vein thrombosis (DVT), symptomatic nonfatal pulmonary embolism (PE), or thromboembolism-related death - so rivaroxaban met the criteria for noninferiority to enoxaparin.

At the 35-day follow-up, 4.4% of subjects who received extended-duration rivaroxaban and 5.7% of those who received enoxaparin plus placebo had a primary outcome event, so rivaroxaban met the criteria for superiority to enoxaparin, the investigators reported (N. Engl. J. Med. 2013 Feb. 6 [doi: 10.1056/NEJMoa1111096]).

Rivaroxaban (Xarelto)has several indications: for stroke prevention in nonvalvular atrial fibrillation, for the treatment of DVT and PE, for reducing the risk of recurrence of DVT and PE, and for the prophylaxis of DVT in patients undergoing knee or hip replacement surgery. It is not indicated for the condition studied in MAGELLAN, namely prevention of VTE in acutely medically ill patients.

This study was funded by Bayer HealthCare and Janssen, sponsors that also collected and analyzed the study data. Dr. Cohen and his associates reported numerous ties to industry sources.

[email protected]

Nearly 2 years after their presentation at a national meeting, the results of MAGELLAN, comparing rivaroxaban to enoxaparin for thromboprophylaxis in critically ill hospitalized patients, have been published online Feb. 6 in the New England Journal of Medicine.

In that large, multicenter trial, rivaroxaban was noninferior to enoxaparin when used for the standard 10-day duration, and superior when used for an extended 35-day duration, for thromboprophylaxis.

However, the rate of clinically relevant bleeding and the incidence of major bleeding events were significantly higher with rivaroxaban than with enoxaparin. This adverse effect apparently balanced out the reduction in venous thromboembolism, as a prespecified analysis of net clinical benefit and harm did not show either one at day 10 or day 35, reported Dr. Alexander T. Cohen and his associates in MAGELLAN (Multicenter, Randomized, Parallel Group Efficacy and Safety Study for the Prevention of Venous Thromboembolism in Hospitalized Acutely Ill Medical Patients Comparing Rivaroxaban with Enoxaparin). The results were first presented by Dr. Cohen, of King's College Hospital, London, at the annual meeting of the American College of Cardiology in spring 2011.

In the 2.5-year study, 8,101 patients at 556 sites in 52 countries were randomized to receive rivaroxaban (4,050 subjects) or enoxaparin (4,051 subjects). Hundreds of patients in both study groups were excluded from the final analyses for various reasons, usually because they could not be assessed for venous thromboembolism using ultrasonography and other imaging techniques in a timely fashion, as required by the study protocol.

At 10 days' follow-up, 2.7% of patients in both groups had a primary outcome event - asymptomatic proximal deep vein thrombosis (DVT), symptomatic nonfatal pulmonary embolism (PE), or thromboembolism-related death - so rivaroxaban met the criteria for noninferiority to enoxaparin.

At the 35-day follow-up, 4.4% of subjects who received extended-duration rivaroxaban and 5.7% of those who received enoxaparin plus placebo had a primary outcome event, so rivaroxaban met the criteria for superiority to enoxaparin, the investigators reported (N. Engl. J. Med. 2013 Feb. 6 [doi: 10.1056/NEJMoa1111096]).

Rivaroxaban (Xarelto)has several indications: for stroke prevention in nonvalvular atrial fibrillation, for the treatment of DVT and PE, for reducing the risk of recurrence of DVT and PE, and for the prophylaxis of DVT in patients undergoing knee or hip replacement surgery. It is not indicated for the condition studied in MAGELLAN, namely prevention of VTE in acutely medically ill patients.

This study was funded by Bayer HealthCare and Janssen, sponsors that also collected and analyzed the study data. Dr. Cohen and his associates reported numerous ties to industry sources.

[email protected]

The ACE inhibitor ramipril substantially improves pain-free walking time and maximum walking time in patients who have peripheral artery disease with intermittent claudication, according to a report in the Feb. 6 issue of JAMA.

In what the investigators described as the first adequately powered randomized controlled trial to demonstrate ramipril’s benefit in this patient population, the magnitude of improvement in walking performance exceeded that reported for all other drug therapies.

The study subjects reported concomitant improvements in their ability to perform daily activities and their health-related quality of life, said Anna A. Ahimastos, Ph.D., of Baker IDI Heart and Diabetes Institute, Melbourne, and her associates.

The only two drugs currently approved in the United States for this indication, pentoxifylline and cilostazol, are reported to increase walking distance by 15% and 25%, respectively. In this trial, ramipril increased pain-free and maximum walking times by 77% and 123%.

Dr. Ahimastos and colleagues enrolled 212 patients with PAD and intermittent claudication in the double-blind trial, randomly assigning 106 to 6 months of ramipril (10 mg/d) and 106 to matching placebo. The mean age of the subjects was 65.5 years, and all were followed at three medical centers in Australia.

All the study subjects were receiving usual care according to their symptoms and risk profiles, which included antiplatelet and lipid-lowering agents. Roughly one-fourth of each group had diabetes, and the cohort included patients with aortoiliac as well as infrainguinal disease.

At 6-month follow-up, ramipril extended the pain-free walking time by a mean of 75 seconds and the maximum walking time by a mean of 255 seconds, compared with placebo. This corresponds to "a clinically significant increase in uphill walking distance of 184 meters," the investigators said (JAMA 2013;309:453-60).

The drug was particularly effective in patients who had femoropopliteal disease, increasing maximal walking time to 286 seconds, compared with patients who had aortoiliac disease, whose maximal walking time improved by 127 seconds.

These increases were independent of the small changes in blood pressure and ankle-brachial index associated with the drug. They exceed the improvements reported in the literature for other conventional PAD drug therapies including pentoxifylline, cilostazol, dipyridamole, ticlopidine, beraprost, iloprost, naftidrofuryl, and statins, Dr. Ahimastos and her associates said.

Patients in the ramipril group also showed improvements on the Walking Impairment Questionnaire in median walking distance, walking speed, and stair-climbing ability, compared with those in the placebo group. Similarly, the ramipril group showed improvement in the physical component of the Short Form–36, a measure of health-related quality of life, relative to the placebo group.

Ramipril did not significantly change any of the laboratory factors measured in the safety monitoring portion of the study. The only adverse events were transient dizziness, which affected 8.5% of the ramipril group and 2.8% of the placebo group, and persistent cough, which prompted seven patients in the ramipril group to withdraw from the study.

It is not yet known how ramipril improves functional capacity in PAD patients with intermittent claudication. Laboratory and animal studies suggest that the drug may increase peripheral blood flow and promote structural and functional changes in skeletal muscle, the researchers said.

This study was limited in that most of the subjects were whites of European descent, and the investigators had to select a population of patients with stable PAD "in whom we could ethically administer either a placebo or an ACE inhibitor" for 6 months. The cohort was thus "restricted to the lower end of the blood pressure spectrum and excluded patients with other major comorbid conditions," so the findings may not be generalizable to patients with higher blood pressure or to ethnically diverse populations, they added.

The ACE inhibitor ramipril substantially improves pain-free walking time and maximum walking time in patients who have peripheral artery disease with intermittent claudication, according to a report in the Feb. 6 issue of JAMA.

In what the investigators described as the first adequately powered randomized controlled trial to demonstrate ramipril’s benefit in this patient population, the magnitude of improvement in walking performance exceeded that reported for all other drug therapies.

The study subjects reported concomitant improvements in their ability to perform daily activities and their health-related quality of life, said Anna A. Ahimastos, Ph.D., of Baker IDI Heart and Diabetes Institute, Melbourne, and her associates.

The only two drugs currently approved in the United States for this indication, pentoxifylline and cilostazol, are reported to increase walking distance by 15% and 25%, respectively. In this trial, ramipril increased pain-free and maximum walking times by 77% and 123%.

Dr. Ahimastos and colleagues enrolled 212 patients with PAD and intermittent claudication in the double-blind trial, randomly assigning 106 to 6 months of ramipril (10 mg/d) and 106 to matching placebo. The mean age of the subjects was 65.5 years, and all were followed at three medical centers in Australia.

All the study subjects were receiving usual care according to their symptoms and risk profiles, which included antiplatelet and lipid-lowering agents. Roughly one-fourth of each group had diabetes, and the cohort included patients with aortoiliac as well as infrainguinal disease.

At 6-month follow-up, ramipril extended the pain-free walking time by a mean of 75 seconds and the maximum walking time by a mean of 255 seconds, compared with placebo. This corresponds to "a clinically significant increase in uphill walking distance of 184 meters," the investigators said (JAMA 2013;309:453-60).

The drug was particularly effective in patients who had femoropopliteal disease, increasing maximal walking time to 286 seconds, compared with patients who had aortoiliac disease, whose maximal walking time improved by 127 seconds.

These increases were independent of the small changes in blood pressure and ankle-brachial index associated with the drug. They exceed the improvements reported in the literature for other conventional PAD drug therapies including pentoxifylline, cilostazol, dipyridamole, ticlopidine, beraprost, iloprost, naftidrofuryl, and statins, Dr. Ahimastos and her associates said.

Patients in the ramipril group also showed improvements on the Walking Impairment Questionnaire in median walking distance, walking speed, and stair-climbing ability, compared with those in the placebo group. Similarly, the ramipril group showed improvement in the physical component of the Short Form–36, a measure of health-related quality of life, relative to the placebo group.

Ramipril did not significantly change any of the laboratory factors measured in the safety monitoring portion of the study. The only adverse events were transient dizziness, which affected 8.5% of the ramipril group and 2.8% of the placebo group, and persistent cough, which prompted seven patients in the ramipril group to withdraw from the study.

It is not yet known how ramipril improves functional capacity in PAD patients with intermittent claudication. Laboratory and animal studies suggest that the drug may increase peripheral blood flow and promote structural and functional changes in skeletal muscle, the researchers said.

This study was limited in that most of the subjects were whites of European descent, and the investigators had to select a population of patients with stable PAD "in whom we could ethically administer either a placebo or an ACE inhibitor" for 6 months. The cohort was thus "restricted to the lower end of the blood pressure spectrum and excluded patients with other major comorbid conditions," so the findings may not be generalizable to patients with higher blood pressure or to ethnically diverse populations, they added.

The ACE inhibitor ramipril substantially improves pain-free walking time and maximum walking time in patients who have peripheral artery disease with intermittent claudication, according to a report in the Feb. 6 issue of JAMA.

In what the investigators described as the first adequately powered randomized controlled trial to demonstrate ramipril’s benefit in this patient population, the magnitude of improvement in walking performance exceeded that reported for all other drug therapies.

The study subjects reported concomitant improvements in their ability to perform daily activities and their health-related quality of life, said Anna A. Ahimastos, Ph.D., of Baker IDI Heart and Diabetes Institute, Melbourne, and her associates.

The only two drugs currently approved in the United States for this indication, pentoxifylline and cilostazol, are reported to increase walking distance by 15% and 25%, respectively. In this trial, ramipril increased pain-free and maximum walking times by 77% and 123%.

Dr. Ahimastos and colleagues enrolled 212 patients with PAD and intermittent claudication in the double-blind trial, randomly assigning 106 to 6 months of ramipril (10 mg/d) and 106 to matching placebo. The mean age of the subjects was 65.5 years, and all were followed at three medical centers in Australia.

All the study subjects were receiving usual care according to their symptoms and risk profiles, which included antiplatelet and lipid-lowering agents. Roughly one-fourth of each group had diabetes, and the cohort included patients with aortoiliac as well as infrainguinal disease.

At 6-month follow-up, ramipril extended the pain-free walking time by a mean of 75 seconds and the maximum walking time by a mean of 255 seconds, compared with placebo. This corresponds to "a clinically significant increase in uphill walking distance of 184 meters," the investigators said (JAMA 2013;309:453-60).

The drug was particularly effective in patients who had femoropopliteal disease, increasing maximal walking time to 286 seconds, compared with patients who had aortoiliac disease, whose maximal walking time improved by 127 seconds.

These increases were independent of the small changes in blood pressure and ankle-brachial index associated with the drug. They exceed the improvements reported in the literature for other conventional PAD drug therapies including pentoxifylline, cilostazol, dipyridamole, ticlopidine, beraprost, iloprost, naftidrofuryl, and statins, Dr. Ahimastos and her associates said.

Patients in the ramipril group also showed improvements on the Walking Impairment Questionnaire in median walking distance, walking speed, and stair-climbing ability, compared with those in the placebo group. Similarly, the ramipril group showed improvement in the physical component of the Short Form–36, a measure of health-related quality of life, relative to the placebo group.

Ramipril did not significantly change any of the laboratory factors measured in the safety monitoring portion of the study. The only adverse events were transient dizziness, which affected 8.5% of the ramipril group and 2.8% of the placebo group, and persistent cough, which prompted seven patients in the ramipril group to withdraw from the study.

It is not yet known how ramipril improves functional capacity in PAD patients with intermittent claudication. Laboratory and animal studies suggest that the drug may increase peripheral blood flow and promote structural and functional changes in skeletal muscle, the researchers said.

This study was limited in that most of the subjects were whites of European descent, and the investigators had to select a population of patients with stable PAD "in whom we could ethically administer either a placebo or an ACE inhibitor" for 6 months. The cohort was thus "restricted to the lower end of the blood pressure spectrum and excluded patients with other major comorbid conditions," so the findings may not be generalizable to patients with higher blood pressure or to ethnically diverse populations, they added.

SAN JUAN, P.R. – The new oral anticoagulant dabigatran is the cardiologist’s darling but the intensivist’s headache and the trauma surgeon’s nightmare, suggested investigators here.

Dabigatran (Pradaxa) is a direct thrombin inhibitor approved in the United States for the reduction of risk from stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Unlike Coumadin/warfarin, dabigatran’s effects are not reversible.

Neil Osterweil/IMNG Medical Media

Pharmacists at the Scripps Mercy Hospital in San Diego evaluated prescribing patterns for dabigatran among patients in their hospital and found that 13% received it for off-label indications, a practice that has the potential for patient harm, they said at the annual meeting of the Society of Critical Care Medicine.

Of 38 patients prescribed dabigatran during their hospital stay, 33 received it for the Food and Drug Administration–approved indication but 5 (13%) received it for other, unspecified indications, reported Dr. Trevor Perry and Dr. Harminder Sikand, both clinical pharmacists at Scripps. "Prescribing was equally divided between house staff, hospitalists, and cardiologists," researchers reported (Crit. Care Med. 2012 [doi:10.1097/01.ccm.0000424500.73199.04]).

The incidence of gastrointestinal bleeding with the drug in their study was 10.5%, higher than the 6.1% rate for any gastrointestinal bleeding stated in the package insert, Dr. Perry said in an interview.

In addition, pharmacists needed to correct the dabigatran dose in 24% of patients, and dabigatran had noticeable effects on clotting parameters, with 74% of patients having an activated partial thromboplastin time (aPTT) above the upper limit of normal, and 64% of patients having an international normalized ratio (INR) above the upper limit.

This finding suggests that in these patients, the clotting assays "may be useful to determine medication adherence but not to determine the level of anticoagulation," the authors wrote in a poster presentation.

"Clinicians need to be aware of the appropriate indication for use and renal dosing of dabigatran to prevent patient harm, as only 87% of patients were prescribed dabigatran for the FDA-labeled indication," they noted.

Major heparin boost needed

In a separate study, Dr. Thomas Edrich from the department of anesthesiology, perioperative and pain medicine at Brigham & Women’s Hospital in Boston and his colleagues found that for patients scheduled for catheter-based atrial ablation procedures, those who were on dabigatran required an approximately 50% greater dose of heparin to achieve full anticoagulation for the procedure than did patients on warfarin (Crit. Care Med. 2012 [doi:10.1097/01.ccm.0000425177.10736.a4]).

Patients who had been on warfarin until 12 hours before the procedure required about 3,000-4,000 IU of heparin/hr to achieve an activated clotting time of 350 seconds, compared with about 6,500-9,000 IU/hr in patients on dabigatran, Dr. Edrich said. They studied retrospective data for 36 patients on dabigatran, 100 patients on warfarin (53 with an INR above 2.0), and 29 patients on no anticoagulation.

"The interesting finding here is that if you’ve been on dabigatran, you’re going to need twice as much heparin," he said in a poster discussion session.

Patients like it, surgeons don’t

Although patients like the convenience of oral dosing without the need for regular INR monitoring with the new anticoagulants, often they are not told that convenience may come at a very high price if there is no effective therapy to reverse the anticoagulation effect, commented Dr. Christine Toevs, a critical care surgeon at the West Penn Allegheny Health System in Pittsburgh.

"The problem is that patients aren\'t informed enough to make that choice. They understand that they’re not getting their labs drawn once a week or twice a week, and they understand that’s not a cost that they are paying. But if they fall and they have a head injury, that is a life lost, and we cannot stop it," she said during a debate on the costs of new medications.

Dr. Perry’s and Dr. Edrich’s studies were internally funded; they reported having no financial disclosures. Dr. Toevs reported having no financial disclosures.

SAN JUAN, P.R. – The new oral anticoagulant dabigatran is the cardiologist’s darling but the intensivist’s headache and the trauma surgeon’s nightmare, suggested investigators here.

Dabigatran (Pradaxa) is a direct thrombin inhibitor approved in the United States for the reduction of risk from stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Unlike Coumadin/warfarin, dabigatran’s effects are not reversible.

Neil Osterweil/IMNG Medical Media

Pharmacists at the Scripps Mercy Hospital in San Diego evaluated prescribing patterns for dabigatran among patients in their hospital and found that 13% received it for off-label indications, a practice that has the potential for patient harm, they said at the annual meeting of the Society of Critical Care Medicine.

Of 38 patients prescribed dabigatran during their hospital stay, 33 received it for the Food and Drug Administration–approved indication but 5 (13%) received it for other, unspecified indications, reported Dr. Trevor Perry and Dr. Harminder Sikand, both clinical pharmacists at Scripps. "Prescribing was equally divided between house staff, hospitalists, and cardiologists," researchers reported (Crit. Care Med. 2012 [doi:10.1097/01.ccm.0000424500.73199.04]).

The incidence of gastrointestinal bleeding with the drug in their study was 10.5%, higher than the 6.1% rate for any gastrointestinal bleeding stated in the package insert, Dr. Perry said in an interview.

In addition, pharmacists needed to correct the dabigatran dose in 24% of patients, and dabigatran had noticeable effects on clotting parameters, with 74% of patients having an activated partial thromboplastin time (aPTT) above the upper limit of normal, and 64% of patients having an international normalized ratio (INR) above the upper limit.

This finding suggests that in these patients, the clotting assays "may be useful to determine medication adherence but not to determine the level of anticoagulation," the authors wrote in a poster presentation.

"Clinicians need to be aware of the appropriate indication for use and renal dosing of dabigatran to prevent patient harm, as only 87% of patients were prescribed dabigatran for the FDA-labeled indication," they noted.

Major heparin boost needed

In a separate study, Dr. Thomas Edrich from the department of anesthesiology, perioperative and pain medicine at Brigham & Women’s Hospital in Boston and his colleagues found that for patients scheduled for catheter-based atrial ablation procedures, those who were on dabigatran required an approximately 50% greater dose of heparin to achieve full anticoagulation for the procedure than did patients on warfarin (Crit. Care Med. 2012 [doi:10.1097/01.ccm.0000425177.10736.a4]).

Patients who had been on warfarin until 12 hours before the procedure required about 3,000-4,000 IU of heparin/hr to achieve an activated clotting time of 350 seconds, compared with about 6,500-9,000 IU/hr in patients on dabigatran, Dr. Edrich said. They studied retrospective data for 36 patients on dabigatran, 100 patients on warfarin (53 with an INR above 2.0), and 29 patients on no anticoagulation.

"The interesting finding here is that if you’ve been on dabigatran, you’re going to need twice as much heparin," he said in a poster discussion session.

Patients like it, surgeons don’t

Although patients like the convenience of oral dosing without the need for regular INR monitoring with the new anticoagulants, often they are not told that convenience may come at a very high price if there is no effective therapy to reverse the anticoagulation effect, commented Dr. Christine Toevs, a critical care surgeon at the West Penn Allegheny Health System in Pittsburgh.

"The problem is that patients aren\'t informed enough to make that choice. They understand that they’re not getting their labs drawn once a week or twice a week, and they understand that’s not a cost that they are paying. But if they fall and they have a head injury, that is a life lost, and we cannot stop it," she said during a debate on the costs of new medications.

Dr. Perry’s and Dr. Edrich’s studies were internally funded; they reported having no financial disclosures. Dr. Toevs reported having no financial disclosures.

SAN JUAN, P.R. – The new oral anticoagulant dabigatran is the cardiologist’s darling but the intensivist’s headache and the trauma surgeon’s nightmare, suggested investigators here.

Dabigatran (Pradaxa) is a direct thrombin inhibitor approved in the United States for the reduction of risk from stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Unlike Coumadin/warfarin, dabigatran’s effects are not reversible.

Neil Osterweil/IMNG Medical Media

Pharmacists at the Scripps Mercy Hospital in San Diego evaluated prescribing patterns for dabigatran among patients in their hospital and found that 13% received it for off-label indications, a practice that has the potential for patient harm, they said at the annual meeting of the Society of Critical Care Medicine.

Of 38 patients prescribed dabigatran during their hospital stay, 33 received it for the Food and Drug Administration–approved indication but 5 (13%) received it for other, unspecified indications, reported Dr. Trevor Perry and Dr. Harminder Sikand, both clinical pharmacists at Scripps. "Prescribing was equally divided between house staff, hospitalists, and cardiologists," researchers reported (Crit. Care Med. 2012 [doi:10.1097/01.ccm.0000424500.73199.04]).

The incidence of gastrointestinal bleeding with the drug in their study was 10.5%, higher than the 6.1% rate for any gastrointestinal bleeding stated in the package insert, Dr. Perry said in an interview.

In addition, pharmacists needed to correct the dabigatran dose in 24% of patients, and dabigatran had noticeable effects on clotting parameters, with 74% of patients having an activated partial thromboplastin time (aPTT) above the upper limit of normal, and 64% of patients having an international normalized ratio (INR) above the upper limit.

This finding suggests that in these patients, the clotting assays "may be useful to determine medication adherence but not to determine the level of anticoagulation," the authors wrote in a poster presentation.

"Clinicians need to be aware of the appropriate indication for use and renal dosing of dabigatran to prevent patient harm, as only 87% of patients were prescribed dabigatran for the FDA-labeled indication," they noted.

Major heparin boost needed

In a separate study, Dr. Thomas Edrich from the department of anesthesiology, perioperative and pain medicine at Brigham & Women’s Hospital in Boston and his colleagues found that for patients scheduled for catheter-based atrial ablation procedures, those who were on dabigatran required an approximately 50% greater dose of heparin to achieve full anticoagulation for the procedure than did patients on warfarin (Crit. Care Med. 2012 [doi:10.1097/01.ccm.0000425177.10736.a4]).

Patients who had been on warfarin until 12 hours before the procedure required about 3,000-4,000 IU of heparin/hr to achieve an activated clotting time of 350 seconds, compared with about 6,500-9,000 IU/hr in patients on dabigatran, Dr. Edrich said. They studied retrospective data for 36 patients on dabigatran, 100 patients on warfarin (53 with an INR above 2.0), and 29 patients on no anticoagulation.

"The interesting finding here is that if you’ve been on dabigatran, you’re going to need twice as much heparin," he said in a poster discussion session.

Patients like it, surgeons don’t

Although patients like the convenience of oral dosing without the need for regular INR monitoring with the new anticoagulants, often they are not told that convenience may come at a very high price if there is no effective therapy to reverse the anticoagulation effect, commented Dr. Christine Toevs, a critical care surgeon at the West Penn Allegheny Health System in Pittsburgh.

"The problem is that patients aren\'t informed enough to make that choice. They understand that they’re not getting their labs drawn once a week or twice a week, and they understand that’s not a cost that they are paying. But if they fall and they have a head injury, that is a life lost, and we cannot stop it," she said during a debate on the costs of new medications.

Dr. Perry’s and Dr. Edrich’s studies were internally funded; they reported having no financial disclosures. Dr. Toevs reported having no financial disclosures.